Speciality Medicine

Speciality Medicine

Speciality Medicine

🦠 Infectious Disease

‣
🧫 Understanding Bacteria

We classify bacteria into the following:

‣
Gram ⊕ (peptidoglycan cell wall)
‣
What colour do they turn on gram staining?
  • Purple/blue as the cell wall binds to the molecules in the crystal violet stain.

‣
Cocci (spherical/round)
‣
Staphylococci (+ catalase)
‣
S. aureus (+ coagulase)
‣
S. epidermis (- coagulase)
  • Central line infections
‣
Streptococci (- catalase)
‣
α-haemolytic: Partial haemolysis
  • S. pneumonia
  • S. viridans
‣
β-haemolytic: Complete haemolysis
  • Group A: S. pyogenes
    • ‣
    Name 4 infections that the bacteria can cause.
    1. Erysipelas
    2. Impetigo
    3. Cellulitis
    4. Tonsillitis
  • Group B: S. agalactiae
‣
γ-haemolytic: No haemolysis
  • Enterococci
‣
Bacilli (rods)
  • Mycobacteria
  • Corneybacteria
  • Bacillus
  • Nocardia
  • Listeria monocytogenes
‣
Anaerobes
  1. Clostridium (KEY - C. difficile)
  2. Lactobacillus
  3. Actinomyces
  4. Propionibacterium
‣
Gram ⊖
‣
What colour do they turn on gram staining?
  • No reaction to the crystal violet stain as they don’t have a cell wall.
  • Safranin stain turns them red, binding to the cell membrane.

‣
Diplococci (rounded bacteria occurring in pairs)
  1. N. meningitidis
  2. N. gonorrhoea
  3. Moraxella
‣
Coccobacilli (in between)
  1. Haemophilus influenzae
  2. Bordatella pertussis
‣
Bacilli (rod)
  1. E. coli
  2. Pseudomonas
  3. Enterobacteriae:
    1. Klebsiella
    2. Salmonella
    3. Shigella
    4. Campylobacter
    5. V. cholera
‣
Atypical
  1. Legionella
  2. Mycoplasma pneumoniae
  3. Chlamydia psittaci
  4. Chlamydydophila pneumoniae
  5. Q fever: Coxiella burneti
‣
🧪 Antibiotics
‣
Name the 4 ways that antibiotics commonly kill bacteria.
  1. Inhibition of cell wall synthesis
    2. ‣
    How can we classify these further?
    1. With a beta-lactam ring
      2. ‣
      Name 3 examples of these.
      1. Penicillins (e.g. amoxicillin)
      2. Carbapenems (e.g. meropenem)
      3. Cephalosporins (e.g. cefotaxime)
    2. Without a beta-lactam ring
      3. ‣
      Name 2 examples of these.
      1. Vancomycin
      2. Teicoplanin
    ‣
    What type of bacteria do we use these to treat?
    • Gram ⊕ as they have a peptidoglycan cell wall
    ‣
    What percentage of people with a documented ‘penicillin allergy’ have a true allergy?
    • 10% — Ask what the reaction is. If not rash and angioedema, likely not a true allergy.
  2. Inhibition of folic acid metabolism
    3. ‣
    Name 2 examples of antibiotics that use this mechanism.
    1. Trimethoprim
    2. Co-trimoxazole
  3. Inhibition of nucleic acid synthesis
    4. ‣
    What antibiotic uses this mechanism of action?
    1. Metronidazole: Only effective within anaerobic organisms, not effective against aerobic organisms.
  4. Inhibition of protein synthesis (targeting the ribosome)
    5. ‣
    Name 4 examples of antibiotics that use this mechanism.
    1. Macrolides (e.g. clarithromycin)
    2. Clindamycin
    3. Tetracyclines (e.g. doxycycline)
    4. Gentamicin
‣
What antibiotic would you choose to cover the following bacteria:
‣
Pseudomonas
  • Tazocin
‣
Atypical bacteria
  • Doxycycline / clarithromycin
‣
MRSA
  • Vancomycin / teicoplanin
‣
E. coli
  • Co-amoxiclav
‣
Streptococci
  • Amoxicillin
‣
ESBL (extended-spectrum beta-lactamases)
  • Meropenem
‣
🤧 Common Infections

Systemic:

‣
Sepsis
‣
What’s the pathophysiology?
  1. Macrophages, lymphocytes and mast cells recognise bacteria → Cytokine release (TNF, IL)
    1. Cytokines → Nitrous oxide release → Vasodilation
    2. Cytokines → ↑ blood vessel permeability → Oedema & ↓ intravascular volume
  2. Coagulation activation → ↑ platelet & clotting factor consumption → thrombocytopenia & inability to form clots
    3. ‣
    What is this called?
    • Disseminated intravascular coagulopathy (DIC)
  3. Tissue hypoperfusion → Anaerobic respiration
    4. ‣
    How do we measure for tissue hypoperfusion
    • Lactate: Lactic acid is the product of anaerobic respiration.
‣
How would we investigate a septic patient?
  • Bedside:
    • Urinalysis +/- Urine MC&S
    • Lumbar puncture
  • Bloods:
    • FBC: WCC, neutrophils
    • CRP: Inflammation
    • Blood culture: Bacteraemia
    • U&Es: AKI
    • LFTs: Source? (? Cholangitis, ? Cholecystitis)
    • Clotting: DIC to assess for disseminated intravascular coagulopathy (DIC)
    • VBG/ABG: Lactate
  • Imaging (depends on presenting symptoms & signs):
    • CXR: Chest
    • CT abdomen: Abdominal
‣
When would we classify them as being in septic shock?
  • Systolic blood pressure < 90 mmHg (& not responding to fluid resuscitation)
  • ↑ lactate > 4 mmol/L

Management:

‣
What are the immediate management steps for sepsis? (Sepsis 6)

Remember: BUFALO OR 3 in 3 out.

  • Blood cultures
  • Urine output → Urinary catheter (Is it < 0.5 ml/kg/hr?)
  • Fluids (IV) → Fluid challenge (500ml NaCl (0.9%) over 15 mins)
  • Antibiotics (IV) → The choice depends on the cause, severity and local guidelines.
  • Lactate → VBG (if they’re not desaturating) / ABG (if they’re desaturating)
  • Oxygen
‣
What is the first-line empirical antibiotic for neutropenic sepsis?
  • Tazocin (piperacillin & tazobactam)
‣
What score is used to categorise and grade sepsis patients?
  • qSOFA / SOFA score

Bacterial:

‣
Cellulitis
‣
Name the two organisms that commonly cause this.
  • S. aureus
  • S. pyogenes
‣
Cases
‣
A patient presents with severe leg pain, it is erythematous and very swollen. Pain is out of keeping with physical features. What is the potential diagnosis and management of this?
  • Necrotising fasciitis
  • IV antibiotics and surgical debridement of necrotic tissue
‣
A 57 year old patient has a painful butterfly rash that is sharply demarcated across the bridge of the nose & cheeks. She had a 2 week history of coryzal symptoms prior to this. Diagnosis? Organism?
  • Erysipelas caused by S. pyogenes infection.
‣
A patient is bitten by a dog, how is this managed?
  • IV co-amoxiclav
    • Penicillin allergic: Doxycycline & metronidazole
‣
Management
‣
What is the management if there are no signs of systemic toxicity?
  1. PO flucloxacillin
  2. Penicillin allergic: Clarithromycin
‣
What is the management if there is systemic toxicity?
  • Admission to hospital for full assessment
  • IV Co-amoxiclav
‣
How would you treat MRSA cellulitis?
  • Vancomycin
    • ‣
    After initiating a rapid vancomycin infusion, the patient develops a red rash, pruritus and a burning sensation in their upper body. Vitals are normal. Differentials? Management?
    • Differentials:
      • Red man syndrome (normal vitals make this more likely)
      • Anaphylaxis
    • Management: Stop the infusion and restart later at a slower rate
‣
Gastroenteritis
‣
What bacteria have the following incubation periods:
‣
1-6 hours
  • Bacillus cereus
  • S. aureus
‣
12-48 hours
  • Salmonella
  • E. coli
  • Norovirus
‣
48-72 hours
  • Campylobacter
  • Shigella
‣
Name 3 complications that can follow gastroenteritis.
  1. Guillian-Barré syndrome
  2. Reactive arthritis
  3. Lactose intolerance (Giardiasis)

Cases:

‣
A patient being treated for an infective exacerbation of COPD has developed profuse watery diarrhoea. Diagnosis?
  • C. dificile infection
    • ‣
    What is the management?
    1. IV fluids & PO metronidazole
    2. Severe: IV vancomycin
‣
A patient drunk contaminated water on holiday and now has abdominal cramps, bloody diarrhoea & vomiting. Cause?
  • E. coli 0157 producing Shiga toxin
    • ‣
    When bloods are taken she has high creatinine, low Hb and low platelets. What has she now developed?
    • Haemolytic uraemic syndrome
    ‣
    Should patients with E. coli gastroenteritis be given antibiotics?
    • No, it increases the risk of HUS
‣
A patient ate shellfish in India 2 days ago, now has profuse diarrhoea causing him to collapse and OE he is hypoglycaemic. No blood in diarrhoea. Diagnosis?
  • Cholera - Rapid descent into hypovolaemia, acidosis & death.
    • ‣
    How are they managed?
    1. IV fluids
    2. Doxycycline / Co-trimoxazole
‣
A patient had flu-like symptoms 3 days ago followed by crampy abdominal pain, fever and bloody diarrhoea after eating chicken. Cause?
  • Campylobacter jejuni
    • ‣
    How are they managed?
    1. Mostly conservative
    2. Severe: Azithromycin / ciprofloxacin
    ‣
    What complication can occur from this?
    • Guillian-Barré syndrome
‣
A patient presents with vomiting following eating rice left out from the night before. Cause?
  • Bacillus (Gram positive rod)
‣
Patient presents with headache, fever, arthralgia and Rose spots, mum says he may have eaten something 'dodgy'. Diagnosis?
  • Salmonella typhi gastroenteritis - Typhoid
    • ‣
    How is this managed?
    • Ciprofloxacin (Salmonella & Shigella)
‣
Urinary tract infection (UTI)

UTI can be split into:

‣
Cystitis: Infection of the bladder.
‣
Why is this more common in women?
  • Shorter urethra.
‣
How do they present?
  1. Dysuria
  2. Suprapubic pain
  3. Urinary urgency / frequency / incontinence
‣
What would you look for on urinalysis?
  1. Nitrites: Suggests presence of bacteria as they break down nitrates in the urine into nitrites.
  2. Leukocytes: The number of white cells in the urine.
‣
Management:

Name the management options and durations for:

‣
A non-pregnant woman with a UTI.
  • Trimethoprim → 3 days
  • Nitrofurantoin → 3 days
    • ‣
    When would you choose trimethoprim over nitrofurantoin?
    • Reduced renal function: Nirtofurantoin reaches the bladder via the kidneys, therefore in reduced renal function, it will not reach its destination.
‣
A pregnant woman in the first trimester with a UTI.
  • Nitrofurantoin → 7 days
    • ‣
    Why not use trimethoprim?
    • It’s teratogenic.
‣
A pregnant woman in the third trimester with a UTI.
  1. Amoxicillin (only if culture results available and susceptible) → 7 days
  2. Cefalexin → 7 days
‣
A man with a UTI.
  • Trimethoprim → 7 days
‣
Asymptomatic UTI in a catheterised patient.
  • No management needed until symptomatic
‣
Pyelonephritis: Escalation of the infection into the kidney
‣
How do they present?
  1. Fever
  2. Haematuria
  3. Back pain
  4. Vomiting
  5. Loss of appetite
  6. OE: Renal angle tenderness
‣
What antibiotic course would you opt for?

A 7-10 day course of:

  1. Cefalexin or
  2. Co-amoxiclav or
  3. Trimethoprim.
‣
Bacterial Vaginosis
‣
What is the pathophysiology?
  • Overgrowth of anaerobic bacteria → ↓ Aerobic bacteria producing lactic acid → ↑ Vaginal pH
‣
What organism causes it?
  • Gardnerella vaginalis
‣
Name 4 characteristic features of BV.
  1. Thin, white discharge (fishy)
  2. Clue cells on microscopy
  3. Vaginal pH > 4.5
  4. Positive whiff test (add KOH → fishy odour)
‣
How is it managed? Different in pregnancy?
  • PO Metronidazole 5 days
  • No
‣
What risk does it pose in pregnancy?
  • Premature rupture of membranes (PROM)
‣
Tetanus
‣
How is tetanus often contracted?
  • Exposing a wound to contaminated soil
‣
The toxin released by tetanus prevents GABA release, what symptoms does this cause?
  • Muscle spasms (e.g. dysphagia)
  • Lock jaw
‣
How are they managed?

Confirmed tetanus:

  1. IV tetanus immunoglobulin

Tetanus-prone wounds:

  1. IM tetanus immunoglobulin (for high risk wounds) & dose of Td/IPV vaccine
  2. Arrange full tetanus course
‣
How many doses are required in the tetanus vaccination schedule?
  • 5

Viral:

‣
Herpes simplex virus
‣
Name three signs of infection with HSV. How are each of these managed?
  • Genital ulcers
    • ‣
    Management?
    • PO aciclovir
  • Gingivostomatitis
    • ‣
    Management?
    • PO aciclovir
  • Cold sores
    • ‣
    Management?
    • Topical aciclovir
‣
If a woman has a primary attack in pregnancy how is it managed?
  • Elective C-section (if > 28 weeks) & PO aciclovir
‣
How is a woman with recurrent herpes managed in pregnancy?
  • PO aciclovir
‣
Glandular Fever
‣
What is the cause of this in 90% of cases?
  • EBV
‣
What is the classic triad of infectious mononucleosis?
  1. Pyrexia
  2. Lymphadenopathy
  3. Sore throat
‣
Name 3 other features that these patients may have.
  1. Palatal petechiae
  2. Splenic rupture
  3. Cold AIHA
‣
How is the diagnosis confirmed?
  • Monospot test
  • Specific salivary IgM
‣
How is it managed?
  • Supportive
‣
Complications:
‣
Name 2 types of lymphoma associated with EBV.
  1. Burkitt's
  2. Hodgkin's
‣
What other cancer is it associated with?
  • Nasopharyngeal carcinoma
‣
🌴 Tropical Infections

Not comprehensive, only high yield topics:

‣
HIV
‣
How is it transmitted?
  • Horizontal:
    • Membrane: Sexual contact (vaginal, oral, anal)
    • Blood/wound exposure to infected bodily fluids or blood (e.g. needle stick injuries & sharing needles)
  • Vertical: Pregnancy, birth, breastfeeding
‣
How does HIV affect the immune system?
  • HIV (RNA retrovirus) enters the & destroys CD4+ T-helper cells → Immunocompromise

Presentation:

‣
How can they present?
  • Fever
  • Headache
  • Muscle aches and joint pain
  • Rash: Seborrhoeic dermatitis, atopic dermatitis
  • Infections: Sore throat and painful mouth sores, diarrhoea, lymphadenopathy
  • Weight loss
  • Cough
  • Night sweats

Investigations:

‣
How long after the exposure do you have to wait until you can test?
  • 1 month
‣
If this test is negative, do you need to do a second test? If so, when?
  • Yes - 3 months after exposure
‣
How do you test for HIV? (3)
  1. HIV antibody test (commonly used)
  2. P24 antigen test (benefit of this is it can be picked up earlier)
  3. HIV viral load via PCR testing

Management:

‣
A patient is diagnosed with HIV, when should antiretroviral therapy be initiated? Is CD4 count relevant?
  • Immediately: CD4 count not relevant
‣
What makes up 'Highly active antiretroviral therapy (HAART)'?
  1. 2 NRTIs (nucleoside reverse transcriptase inhibitors)
  2. 1 PIs (protease inhibitor - ...navir drugs)
‣
How do you monitor the effectiveness of treatment?
  1. Viral load (Ideally ↓/undetectable)
  2. CD4+ count (Ideally ↔︎)
‣
A HIV positive patient is pregnant. How do you manage this patient to reduce vertical transmission risk to the foetus? (3)
  1. Maternal & neonatal antiretroviral therapy
  2. C-section
  3. Infant bottle feeding

Needle stick:

‣
If you get a needle stick from a HIV positive patient what is the management?
  1. Wash & bleed
  2. PO antiretroviral therapy (within 72 hrs) for 4 weeks
    3. ‣
    If you get a needle stick from a HIV positive patient, what is the probability you will get infected?
    • 0.3%
      • ‣
      What's the transmission rate in HepB & HepC needle sticks?
      • HepB: 20-30%
      • HepC: 0.5-2%

Complications:

‣
Infectious (High-yield)
‣
HIV patient presents with exertional dyspnoea, dry cough and fever. What is your main differential?
  • Pneumocystis jiroveci pneumonia
    • ‣
    How can you investigate this to confirm your differential? (3)
    1. CXR - Bilateral interstitial pulmonary infiltrates
    2. Exercise-induced desaturation (↓ SpO₂)
    3. Histology: Sputum or biopsy then do silver stain or toludine blue will show the cysts
    ‣
    What is the management? (2)
    1. Co-trimoxazole
    2. IV pentamidine
‣
A HIV patient presents with diarrhoea. What is the most common cause of diarrhoea in HIV patients?
  • Cryptospordiosis
‣
Man presents with abnormal movements and a hypodense area in the basal ganglia. CSF shows raised protein but the rest is normal. Diagnosis?
  • Progressive multifocal leukoencephalopathy (PML) - caused by JC virus
‣
A HIV patient has symptoms of meningitis. What organism do you need to consider?
  • Cryptococcus (fungal)
    • ‣
    Investigations?
    • India stain
    • High opening pressure on LP
‣
HIV patient presents with a hard white lesion on the tongue that looks like candidiasis but can’t be rubbed off. What is this?
  • Hairy leukoplakia
    • ‣
    How do you differentiate between hairy leukoplakia and oral candidiasis?
    • Hairy leukoplakia cannot be scraped away from the tongue, candidiasis can.
    ‣
    What is the underlying pathogen causing this?
    • EBV
‣
Neoplastic
‣
A HIV patient presents with headache, confusion and drowsiness. What are your two differentials?
  1. Toxoplasmosis
  2. Primary CNS lymphoma
    3. ‣
    What is the cause of lymphoma in these patients?
    • EBV
    ‣
    How do you differentiate between the two?
    1. Toxoplasmosis
      • Multiple lesions
      • Ring/nodular enhancement
    2. CNS lymphoma
      • Single lesion
      • Solid (homogenous) enhancement
    ‣
    How do you manage each, respectively?
    1. Toxoplasmosis: Sulfadiazine & pyrimethamine
    2. Lymphoma: Dexamethasone, chemotherapy, radiotherapy, surgical excision
‣
A HIV patient presents with the following skin lesions:
‣
What is this?
  • Kaposi sarcoma
‣
What is the cause?
  • Herpes (HHV-8) on background of HIV infection
‣
Where can it present?
  • Skin
  • GI tract
  • Respiratory - Haemoptysis / Pleural effusion
‣
Management?
  • Radiotherapy & resection
OpenStax College, CC BY 3.0
OpenStax College, CC BY 3.0 creativecommons.org/licenses/by/3.0, via Wikimedia Commons. No changes were made.
‣
Tuberculosis

Presentation:

‣
How effective is the bCG vaccination? Name 3 contraindications.
  • Not very effective.
  • Contraindications:
    1. Past TB infection
    2. Pregnancy
    3. Immunosuppression
‣
A patient has been recently diagnosed with TB and has innumerable small spots across the lungs on CXR. What is this suggestive of?
  • Miliary TB
    • ‣
    Which area of the lungs is commonly affected first?
    • Apex of lungs
    ‣
    How has the infection spread from the ghon focus?
    • Pulmonary venous system
    ‣
    Name 2 other manifestations of secondary TB.
    • Meningitis
    • Pott's disease: Vertebral bodies affected

Investigations:

‣
Name the main test used in the diagnosis of TB. How does it work? What is a positive result? When can you get false negative results?
  • Mantoux test: Inject tuberculin into forearm → Look for reaction
    • ≥ 6mm → Positive result.
  • False negatives in: Miliary TB, HIV, sarcoidosis, lymphoma
‣
If you get a false negative result, what other test can be done?
  • Interferon-gamma blood test
‣
The tissue is biopsied. What pathological test is done? What is a positive result?
  1. Ziehl-Neelsen stain / Auramine staining
  2. Positive result: Acid fast bacilli

Management:

‣
How do you manage this over the next 6 months? (High-yield)

2 months:

  1. Rifampicin
    2. ‣
    Side effects?
    • Orange secretions
    • CYP450 inducer
  2. Isoniazid
    3. ‣
    Side effects?
    • Peripheral neuropathy
    ‣
    What can be given with this to minimise SEs?
    • Pyridoxine
  3. Pyrazinamide
    4. ‣
    Side effects?
    • Gout
    • Hepatotoxicity
  4. Ethambutol
    5. ‣
    Side effects?
    • Optic neuritis/neuropathy
    ‣
    What test is needed before initiating this?
    • Check visual acuity

Subsequent 4 months: Rifampicin & isoniazid

‣
Malaria
‣
How do they present?
  1. Fever on-and-off for alternating days
  2. Headache, myalgia, hepatomegaly
  3. History of foreign travel
‣
How is this transmitted?
  • Mosquitos
‣
Name 2 protective factors against malaria.
  • Sickle cell
  • G6PD deficiency
‣
Name the 2 types. Which is more common? Which is more severe? (Follow-on Qs)
  1. Falciparum (More common & more severe)
    2. ‣
    How do you diagnose this?
    • Blood film: Schizonts
    • Parasitaemia > 2%
  2. Non-falciparum
‣
How is uncomplicated malaria managed?
  • Artemisinin-based combination therapies
‣
How is severe malaria managed?
  • IV artesunate
‣
Tropical Viruses

The following patients have returned from a holiday in a tropical country:

‣
Patient presents with a retro-orbital headache, fever, facial flushing and bloods show ↑ ALT. Diagnosis? Transmission? Management?
  • Dengue fever
  • Mosquito
  • Supportive
‣
A week ago, patient describes they had a high fever, rigors and N&V. They felt better for the last few days but now have thrown up blood and are jaundiced. Diagnosis? Transmission? Management?
  • Yellow fever
  • Mosquito
  • Supportive
‣
Patient presents with fever, fatigue and headache followed by D&V and rash. Diagnosis? Transmission?
  • Ebola virus
  • Touching mucous membranes/secretions from infected individuals (clothes, etc.)
‣
Why are these patients predisposed to severe bleeding?
  • Viral haemorrhagic fever (DIC)
‣
Rare infection cases:
‣
A 23 year old woman has recently returned from a lake resort holiday in Africa and has fever, malaise, dry cough, diarrhoea and right upper quadrant pain. She is pyrexic and has an urticarial rash & hepatosplenomegaly. Diagnosis?
  • Schstosomiasis (parasite)
    • ‣
    Management?
    • Praziquantel: Kills adults but not eggs (Give now and after 3 months)
    • Steroids: Suppress hypersensitivity
‣
Patient returns from holiday with abdominal pain & diarrhoea alongside a cough and fever. They have maculopapular rose spots that blanch on pressure. Diagnosis?
  • Typhoid
    • ‣
    What organism causes it?
    • Salmonella typhi
    ‣
    What do FBC & LFT show?
    • FBC: Neutropenia
    • LFT: Raised transaminases
‣
A patient from India presents with hypopigmented hypoesthetic patches of skin and a change in their facial appearance. Diagnosis?
  • Leprosy
    • Hypopigmented: Loss of pigmentation of skin
    • Hypoesthesia: Sensory loss in areas of lost pigment. Thickened peripheral nerves.
      • ‣
      How is it managed?
      • Dapsone, rifampicin and clofazimine for 12-24 months
‣
A patient presents with a ‘bullseye rash’ (erythema migrans). What is this suggestive of?
  • Lyme Disease (Borelliosis)
    • ‣
    How is this spread?
    • Ticks
    ‣
    Name 2 neurological manifestations.
    • Peripheral neuropathy, e.g. facial nerve palsy (can be bilateral)
    • Meningitis
    ‣
    How do you investigate for it?
    • Blood test for ELISA serology
    ‣
    How is it managed in both early and disseminated disease?
    • Early: PO doxycycline
    • Disseminated: Ceftriaxone

Ltshears, CC BY-SA 3.0
Ltshears, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
A patient has been bit by a dog, and now is hypersalvating and has muscle spasms. Diagnosis?
‣
A sewage worker has bilateral conjunctivitis, bilateral calf pains and a high fever. Diagnosis?
  • Leptospirosis
    • Also seen in farmers & vets
    • Renal failure in 50%, liver failure in 10%
      • ‣
      Management?
      • High dose benzylpenicillin / doxycycline
‣
🍆 Sexually Transmitted Infections
‣
Genital ulcers

What is the diagnosis based on the following presentations:

‣
Patient presents with multiple painful ulcers around her vagina.
  • Herpes simplex virus (HSV) infection
    • ‣
    What are the differentials & features of them?
    • Chancroid
      • Tropical disease (look for travel history)
      • Unilateral tender lymphadenopathy
    • Lymphogranuloma venereum (LGV)
      • Small painless pustule → Ulcer → Painful inguinal lymphadenopathy → Proctocolitis (bowel symptoms)
    ‣
    How would you manage them?
    • PO aciclovir
‣
Patient presents with a single painless ulcer. Serological tests show ✅ VRDL and ✅ TPHA.
  • Syphilis
    • ‣
    What causes this?
    • Treponema pallidum
    ‣
    What is the first-line management?
    • IM benzylpenicillin
    ‣
    Patient presents with fever, rash and tachycardia following their first dose of this. What reaction is this?
    • Jarisch-Herxheimer reaction (not worrying, may need antipyretics)
    ‣
    Following treatment, what will the serological tests show?
    • ❌ VRDL
    • ✅ TPHA
‣
A patient is diagnosed with chlamydia and also has an ulcer on his penis and painful inguinal lymphadenopathy.
  • Lymphogranuloma venereum (LGV)
    • ‣
    How would you mange them?
    • Doxycycline (but check local guidelines)
‣
A patient has arrived back from Kenya with multiple eroded genital ulcers, he is systemically well and culture grew Haemophilus ducreyi.
  • Chancroid
‣
Genital warts
‣
What causes these?
  • Human papillomavirus (HPV) infection
‣
What are the 2 different types of warts and how does their management differ?
  • Solitary, keratinised: Cryotherapy
  • Multiple, non-keratinised: Topical podophyllum
‣
Trichomoniasis
‣
What vaginal discharge is seen in this?
  • Frothy yellow/green
‣
How is it diagnosed?
  • Swab & microscopy
‣
How is it managed?
  • PO Metronidazole (5-7 days)
‣
Chlamydia
‣
How long after exposure do you have to wait until you test for this?
  • 2 weeks
‣
How is it investigated? Does it differ in women and men?

NAATs: Nuclear acid amplification tests

  • Men: First-catch urine sample
  • Women: Vulvovaginal swab
‣
Patient presents after their partner told them they have chlamydia. How is this managed?
  • Treat then test
‣
What is the first-line management?
  • Azithromycin (single dose)
‣
Name 3 complications of chlamydia.
  1. PID → Infertility
  2. Epididymitis
  3. Reactive arthritis (Reiter's)
‣
Gonorrhoea
‣
What are the bacteria's characteristics on microscopy?
  • Gram negative diplococci
‣
How do they often present?
  • Genital discharge
  • Dysuria
  • Dermatitis
  • Arthritis
  • Tenosynovitis (synovial membrane inflammation)
‣
How are they managed?
  • IM ceftriaxone

🧫 Haematology

‣
💉 Anaemia

Name the causes of each of the following:

‣
Microcytic anaemia
‣
Thalassaemia
‣
What are the types?
‣
ɑ
  • 4 genes, they need at least one functional copy to be compatible with life
  • Symptomatic when they have ≥ 2 copies
‣
β
  1. Minor: Heterozygous
  2. Intermedia
  3. Major: Homozygous
    4. ‣
    How does this present?
    • Failure to thrive in the first year of life
    • Microcytic anaemia
‣
What facial features may these patients have?
  1. Prominent forehead
  2. Prominent cheek bones
‣
What are the signs on blood film?
  • Marked poikilocytosis (speculated tear‐drop cells)
  • Target cells
  • Numerous erythroblasts
‣
How would you manage them?
  1. Regular blood transfusions: Provide healthy, functional RBCs → Prevents intrinsic, dysfunctional erythropoiesis
  2. Iron chelation therapy (e.g. desferrioxamine) to prevent iron overload
‣
Anaemia of chronic disease

See normocytic, can be microcytic or normocytic.

‣
Iron deficiency anaemia
‣
Name 4 causes of iron deficiency.
  1. Menorrhagia
  2. GI bleed
  3. Low dietary intake
  4. Malabsorption, e.g. Crohn's/Coeliac
‣
Name 7 features of iron deficiency.
  1. Shortness of breath
  2. Fatigue
  3. Palpitations
  4. Koilonychia
  5. Conjunctival pallor
  6. Angular stomatitis
‣
Why may they be struggling to swallow?
  • Oesophageal webs (Plummer-Vinson syndrome)

Investigations:

‣
What is the classic FBC picture in iron deficiency?
  1. Microcytic anaemia
  2. ↓ MCHC (Hypochromia)
  3. ↑ RDW (Anisocytosis)
‣
On iron studies, what would the ferritin, TIBC and transferrin saturation be?
  • ↓ Ferritin (although this is an acute phase reactant so could be normal)
  • ↑ Total iron binding capacity
  • ↓ Transferrin saturation

Management:

‣
What is the transfusion threshold in a patient with & without ACS?

Transfuse the patients if they have a Hb (but check local guidelines):

  • ACS < 80 g/L
  • Without ACS < 70 g/L
‣
Lead poisoning
‣
In what symptoms should this be considered?
  • Abdominal pain & neurological symptoms combined
  • Blue lines on gum margins
‣
Ultimately, what does lead poisoning lead to? What can be seen on investigations because of this?
  • Inability to produce haem → Microcytic anaemia
‣
What is a differential?
  • Intermittent porphyria
‣
Siderblastic anaemia
‣
What is this?
  • Ineffective erythropoiesis → ↑ iron absorption & deposition in bone marrow, liver, heart & endocrine organs
‣
What are the causes?
  1. Congenital: Inherited in many different ways
  2. Drugs: Alcohol, lead poisoning, isoniazid
‣
What is seen on FBC & iron studies?
  • Microcytic anaemia
  • ↑ Ferritin
  • ↑ Iron
‣
What is seen on blood film?
  • Pappenheimer bodies
‣
Normocytic anaemia
‣
Acute blood loss

Blood loss may cause anaemia (but may not initially), if the patient has sufficient iron stores to maintain normal red cell output then it will be normocytic.

‣
Anaemia of chronic disease
‣
Why does this occur?
  • Chronic disease/inflammation → IL-6 release → ↑ hepcidin → ↓ Fe absorption
‣
How does the FBC change over time?
  1. Initially: Normocytic, normochromic
  2. Long-term: Microcytic, hypochromic
‣
What would Fe studies show?
  • ↓ TIBC
  • ↑ Ferritin (acute phase reactant)
‣
How do you differentiate between a mixed micro/macro anaemia and anaemia of chronic disease?
  • ↑ RDW: Red cell distribution width will be increased due to a combination of both macrocytes and microcytes, that average out to be normocytic
  • ↑ Ferritin: High because it is an acute phase reactant so stimulated by disease activity
‣
Name an example of when a mixed micro/macro presentation may occur.

Crohn's disease

  • Micro: Fe deficiency due to blood loss from chronic bleeding.
  • Macro: Low B12 absoption due to terminal ileum inflammation.
‣
Aplastic anaemia
‣
What are the key features?
  • ↓ Hb
  • ↑ reticulocytes
‣
What are the causes?
  1. Idiopathic
  2. Congenital: Fanconi anaemia, dyskeratosis congenita
  3. Drugs: Cytotoxics, chloramphenicol, sulphonamides, phenytoin, gold
  4. Infections: Parvovirus, hepatitis
  5. Radiation
  6. Leukaemia: ALL, AML
‣
Haemolytic anaemia

Types:

‣
Inherited
‣
Hereditary spherocytosis
  • Autosomal dominant inheritance
  • Defect in the erythrocyte membrane → Breakdown by splenic macrophages
  • Aplastic crisis in parvovirus infection
  • Management: Splenectomy
‣
G6PD deficiency
‣
How is it inherited?
  • X-linked recessive
‣
What is the pathophysiology? (2)
  • ↓ G6PD → Oxidative RBC stress → Intravascular haemolysis
‣
What is the classic presentation?
  1. Trigger: Patient ate fava beans, got an infection or started on antimalarial
  2. Result: Develop jaundice & anaemia following this
‣
Name 3 features.
  1. Neonatal jaundice (High prevalence in African, Asian & Mediterranean people)
  2. Splenomegaly
  3. Heinz bodies (blood film)
‣
What investigation gives a definitive diagnosis?
  • G6PD enzyme assay
‣
What drugs can trigger haemolysis?
  • Sulph-drugs: Sulphonamides, sulphasalazine, sulfonylureas
  • Ciprofloxacin
  • Anti-malarials: primaquine
‣
How do you differentiate from hereditary spherocytosis?
  • Gender: G6PD only males
  • Blood film: G6PD Heinz bodies
‣
How are they managed?
  1. Folate supplementation: ↑ RBC production
  2. Consider splenectomy
‣
Sickle cell
‣
Basics
‣
How is it inherited?
  • Autosomal recessive
‣
What is the pathophysiology? (4)
  1. Decreased water solubility of deoxy-Hb
  2. HbS polymerisation → RBC sickle
  3. Sickle cells are fragile → Haemolysis → Blocking of small blood vessels → Infarction
‣
When are homozygotes likely to present?
  • 4-6 months → This is when foetal haemoglobin degrades and they rely on their own
‣
Investigations
‣
How are they investigated initially?
  1. FBC - Microcytic anaemia, reticulocytosis
  2. LFT: Unconjugated hyperbilirubinaemia
  3. Blood film: Sickle cells, target cells, reticulocytes, Howell-Jolly bodies
‣
What is the diagnostic test?
  • Haemoglobin electrophoresis +/- genetic testing
‣
Why might they have Howell-Jolly bodies on blood film?
  • Splenic infarction → Hyposplenism → Howell-Jolly bodies
‣
Name the 5 sickle cell crises.
‣
Vaso-occlusive
‣
Where does this commonly affect (in exams)?
  • Priapism (painful, persistent erection) requiring aspiration of blood
‣
Splenic sequestration: Pooling of blood in the spleen
‣
What does this cause?
  • Severe anaemia
  • Hypovolaemic shock
‣
What can recurrent crises lead to?
  • Splenic infarction
‣
Acute chest syndrome: Dyspnoea, chest pain
‣
What features are required for this? (2)
  1. Fever/respiratory symptoms
  2. New infiltrates on CXR
‣
What causes this?
  1. Infective: Pneumonia/bronchiolitis
  2. Non-infective: Pulmonary vaso-occlusion/fat emboli
‣
Aplastic
‣
What is this?
  • Failure of the bone marrow to produce any RBCs
‣
What infection commonly causes it?
  • Parvovirus B19
‣
Haemolytic

This is rare, Hb drops due to increased haemolysis

‣
Management
‣
How are they managed generally?
  1. Avoid dehydration
  2. PenV prophylaxis
  3. Pneumococcal polysaccharide vaccine every 5 years
‣
A patient has recurrent painful crises, what medication may be helpful?
  • Long-term hydroxyurea (stimulates HbF)
‣
How are sickle cell crises managed?
  • Supportive
    • Treat infection, keep warm, hydrated, analgesia
    • Antibiotics if required
    • Exchange transfusions
‣
Thalassaemia

See microcytic anaemia.

‣
Acquired
‣
Autoimmune haemolytic anaemia (AIHA)
‣
How do you test for it?
  • Direct coombs test

Two types:

‣
Warm AIHA
‣
Where is the haemolysis?
  • Extravascular: Spleen tags cells for phagocytosis
‣
What are the causes?
  • CLL
  • Lymphoma
  • SLE
‣
How is it managed?
  • Steroids: Immunosuppression is effective
‣
Cold AIHA
‣
Where is the haemolysis & what are the causes?
  • Intravascular: IgM causes complement to directly break down RBCs
‣
What are the causes?
  1. Mycoplasma
  2. EBV
  3. Lymphoma
‣
What investigation confirms this?
  • Cold agglutinins (IgM-complement complexes)
  • ↓ serum haptoglobins
‣
How is it managed?
  • Treat the underlying infection
  • Immunosuppression is less effective compared with warm AIHA
‣
Non-immune

Causes:

  1. Transfusion reactions
    2. ‣
    How do you manage a haemolytic reaction?
    • Stop immediately & flush line
    ‣
    How do you manage a febrile non-haemolytic reaction?
    • Slow transfusion & give paracetamol
    ‣
    If a patient has a minor allergic reaction to a blood transfusion, how is it managed?
    • Temporarily stop & antihistamine
  2. Mechanical (e.g. metallic heart valve)
  3. Microangiopathic haemolytic anaemia
    4. ‣
    What are the causes?
    1. HUS: Haemolytic uraemic syndrome
      • Triad: Microangiopathic haemolytic anaemia + thrombocytopenia + AKI
      • Schistocytes on blood film
    2. DIC: Disseminated intravascular coagulation
    3. TTP: Thrombotic thrombocytopaenic purpura
  4. Paroxysmal nocturnal haematuria
    5. ‣
    What is this?
    • Complement system attacks the RBCs due to receptor mutation
    ‣
    What is the typical presentation?
    1. Haematuria in the morning
    2. Predisposed to thrombosis (DVT/PE)
    3. Smooth muscle dystonia
  5. Infectious: Malaria
    6. ‣
    What would you seen on blood film?
    • Plasmodium schizonts
      • Lukas.S at English Wikipedia, Public domain, via Wikimedia Commons
      Lukas.S at English Wikipedia, Public domain, via Wikimedia Commons
  6. Hypersplenism (e.g. in liver cirrhosis)

Investigations:

‣
What bloods would you do and what results would you look for?
  1. FBC
    • Normocytic anaemia
    • ↑ reticulocytes
  2. Blood film:
    • Spherocytes
    • Schistocytes
    • Sickle cells
  3. LDH
  4. LFT: Bilirubin
  5. Serum haptoglobin
    • ↓ in intravascular haemolysis (its role is to mop up excess Hb)
‣
What condition does haemolysis predispose to?

Gout

  • Haemolysis → ↑ urate
‣
Hypothyroidism

See Endocrinology.

‣
Macrocytic anaemia
‣
Name 2 causes of megaloblastic macrocytic anaemia.
‣
B12 deficiency
‣
What are the causes?
  1. Malabsorption
    1. ↓ dietary intake
    2. Crohn's
    3. Coeliac
  2. Pernicious anaemia
    3. ‣
    What is the pathophysiology?
    • Autoimmune parietal cell destruction → ↓ intrinsic factor → ↓ B12 absorption
    ‣
    What do you test for?
    1. Intrinsic factor antibody
    2. Gastric parietal cell antibody
    ‣
    How do you manage this?
    1. Dietary IF replacement
    2. IM B12 injections, 3 monthly
‣
What will the neutrophils show?
  • Hypersegmentation
‣
Folate deficiency
‣
When treating folate deficiency, what is important to know & why?
  • B12 concentration
  • If B12 is low and you replace folate → Subacute combined degeneration of the cord
‣
Name 4 causes of non-megaloblastic macrocytic anaemia.
  1. Alcohol
  2. Liver dysfunction
  3. Pregnancy
  4. Reticulocytosis
‣
🩸 Clotting Cascade
‣
Basics
‣
What part of the coagulation cascade do APTT & PT represent?
  • Intrinsic pathway: APTT
  • Extrinsic: PT
‣
How is this pathway inhibited naturally?
  1. Tissue factor pathway inhibitor (TFPI): Forms complex with Xa which binds to VIIa:TF complex forming an inactive quaternary complex
  2. Anti-thrombin binds to Va/thrombin forming an inactive complex
    • Heparin acts through this channel
  3. Protein C/S: Protein S activates protein C → Protein C inactivates Va & VIIIa

Joe D, CC BY-SA 3.0
Joe D, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0/, via Wikimedia Commons. No changes were made.
‣
How do warfarin, DOACs and heparin work on the coagulation cascade?
  • Warfarin inhibits production of II, VII, IX, X
SteveKong3, CC BY-SA 4.0
SteveKong3, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.
‣
Bleeding
‣
Haemophilia
‣
Von Willebrand disease
‣
Presentation
‣
How is it inherited?
  • Autosomal dominant
‣
What does von Willebrand factor do?
  • Promotes platelet adhesion to damaged endothelium
  • Stabilises factor VIII → Deficiency leads to VIII inactivity
‣
What are the 3 types of vWD?
  1. Partial reduction (80%)
  2. Abnormal vWF
  3. Complete lack of vWF (autosomal recessive) → Very severe
‣
What are common symptoms? (3)

Platelet-pattern superficial bleeding:

  1. Easy bruising: Petechiae / purpurae
  2. Epistaxis
  3. Menorrhagia
‣
What is seen on a coagulation screen? (4)
  1. Normal PT
  2. Prolonged APTT
  3. Factor VIII decreased activity
  4. Prolonged bleeding time
‣
How is it managed?
  • Only managed if the patient has been symptomatic:
    • Tranexamic acid → Mild bleeding
    • Desmopressin → Stimulates vWF release
    • vWF & F.VIII infusion
‣
Haemophilia A/B
‣
What is deficient in haemophilia A & B, respectively?
  • A: Factor VIII
  • B: Factor IX
‣
Presentation
‣
How are they inherited?
  • X-linked recessive
‣
What is a common presentation?

Neonate/young child with severe large deep bleeds into soft tissue, joint & muscle:

  1. Haemarthrosis (bleeding into joints/muscles)
  2. Intracranial haemorrhage/haematoma
  3. Haematuria
‣
Investigations
‣
What is definitive for haemophilia A?
  • Serum factor VIII
‣
What would you see on a clotting screen?
  • ↑ APTT
  • ↔︎ Bleeding time
‣
How would you manage them?
  • Acutely for both: Tranexamic acid

Specifically:

  • Haemophilia A: Cryoprecipitate (Factor VIII, fibrinogen, von Willebrand factor and factor XIII)
  • Haemophilia B: IV infusion of factor IX (Replace the missing clotting factors)
‣
Platelets
‣
Thrombocytopenia

There are two main causes:

‣
Problems with production
  1. B12/folate deficiency
  2. Liver failure: ↓ Thrombopoietin
  3. Disorders affecting bone marrow production, e.g. leukaemia
‣
Problems with destruction
  1. Disseminated intravascular coagulopathy (DIC)
    2. ‣
    How does normal clot homeostasis work?
    • Coagulation cascade → Fibrin formation & polymerisation
    • Fibrin formation → Plasmin formation → Clot breakdown
    ‣
    What is the pathophysiology of DIC?
    • Large insult (e.g. sepsis) → Excessive TF release → Formation of hundreds of small clots using up all platelets
    ‣
    What are you looking for on FBC and clotting screen?
    • ↓ Platelets
    • ↑ APTT
    • ↑ PT
    • ↑ Bleeding time
  2. Immune thrombocytopenia (ITP)
    3. ‣
    What are the common causes of this?
    • Post-viral infection or vaccination
    ‣
    What features may they present with?
    • Petechiae
    • Bleeding (e.g. epistaxis)
    ‣
    How would you investigate it?
    • FBC: Isolated low platelets
    ‣
    How is it managed?
    • Conservative: Natural course 1-2 weeks
    • Platelet transfusion if severe bleeding
  3. Thrombotic thrombocytopenic purpura (TTP)
    4. ‣
    How do they present?
    1. Focal neurology
    2. Haemolysis (Microangiopathic → Schistocytes)
    3. Thrombocytopenia
  4. Haemolytic uraemic syndrome (HUS)
‣
Vitamin K deficiency
‣
When are you likely to get this?
  • Bile duct occlusion → ↓ fat emulsion → ↓ absorption of fat soluble vitamins ADEK
‣
Hereditary haemorrhagic telangiectasia
‣
What are the common presenting features?
  1. Red freckles on lips
  2. Recurrent epistaxis
  3. Other features: Brain, liver, lung bleeds
Michael Sand, Daniel Sand, Christina Thrandorf, Volker Paech, Peter Altmeyer, Falk G Bechara, CC BY 2.5
Michael Sand, Daniel Sand, Christina Thrandorf, Volker Paech, Peter Altmeyer, Falk G Bechara, CC BY 2.5 creativecommons.org/licenses/by/2.5, via Wikimedia Commons. No changes were made.
‣
How is it inherited?
  • Autosomal dominant
‣
What is the pathophysiology?

Arteriovenous malformations (AVMs)

  • Arteries flow directly into veins rather than capillaries → High pressure blood flow in veins → Vein tears and irritation → Bleeding
‣
Clotting
‣
Thrombophilia
‣
What is the simple pathophysiology of thrombophilia?
  • Defect in factors that normally inhibit the coagulation cascade → Excessive coagulation

Types:

  1. Antiphospholipid syndrome
    2. ‣
    What is this?
    • Persistent antiphospholipid antibodies associated with a variety of clinical features characterised by thromboses and pregnancy-related morbidity.
    ‣
    What are the risk factors?
    • History of systemic lupus erythematosus
    • History of other autoimmune rheumatological disorders
    • History of other autoimmune diseases
    • History of autoimmune haematological disorders
    ‣
    What antiphospholipid antibodies would we look for?
    1. Lupus anticoagulant
    2. Anticardiolipin antibody
    3. Anti-β2-glycoprotein I
    ‣
    How are they managed?

    Our main goals are management of acute thrombosis and prevention of thrombosis recurrence and pregnancy morbidity.

    1. LMWH initially before bridging to warfarin (or if pregnant remain on LMWH until after delivery)
    2. Lifelong warfarin:
      1. Target 2-3
      2. Target 3-4 (if VTE while on warfarin)
  2. Factor V Leiden (Most common hereditary)
    3. ‣
    What is Factor V Leiden?
    • Factor V is resistant to deactivation by protein C → Overly active factor V → Increased coagulation
  3. Protein C/S deficiency
    4. ‣
    Who is this common in?
    • Individuals from Southeast Asian heritage
    ‣
    How do proteins C & S work?
    • Protein C → Activated protein C → Breakdown of factor Va & VIIIa

    (via protein S)

  4. Antithrombin deficiency
‣
Deep vein thrombosis (DVT)
‣
How is the risk of DVT quantified?
  • Well's score for DVT (2-level)
    • ‣
    What scores are considered significant?
    • ≥ 2
    ‣
    If 'DVT likely' how is it investigated? (2)
    1. Proximal leg doppler within 4 hours
    2. D-dimer if negative
    ‣
    If 'DVT unlikely' how is it investigated? (3)
    1. D-dimer
    2. Positive: Doppler within 4 hours
      • If this isn't possible give LMWH
‣
How is DVT managed?
  • Initial: LMWH
    • Stop after 5 days or when the INR ≥ 2
    • If using a DOAC, no heparin bridging is needed.
  • Long-term: Warfarin/DOAC
    • Provoked: 3 months
    • Unprovoked: 6 months / lifelong
‣
What conditions need to be tested for in an unprovoked DVT?
  • Thrombophilia
  • Antiphospholipid antibodies
‣
👹 Cancer
‣
Leukaemia (White cells)
‣
General
‣
At what ages do the different leukaemia's present?

ALL CeLLmates have CoMmon AMbitions:

  1. ALL < 5 years / > 45 years
  2. CLL > 55 years
  3. CML > 65 years
  4. AML > 75 years
‣
Name 5 features likely on presentation of any patient with leukaemia.
  1. ↓ WCC (& neutropenic) → Infections
  2. ↓ Hb → Anaemia, lethargy, SOB
  3. ↓ Platelets → Bleeding
  4. Splenomegaly → Abdominal discomfort
  5. Bone pain
‣
What are your differentials for petechiae?
  1. Leukaemia
  2. Meningococcal septicaemia
  3. Vasculitis
  4. ITP
  5. HSP
  6. Non-accidental injury
‣
How does acute and chronic leukaemia differ in terms of cell type?
  • Acute: Blast cells
  • Chronic: Mature cells
‣
How are they managed?
  1. Chemotherapy
    • Risk of tumour lysis syndrome
  2. Steroids

Types:

‣
Acute lymphoblastic leukaemia (ALL)
‣
Who is it more common in?
  • Children - Accounts for 80% of childhood leukaemia - Good prognosis
    • Down's syndrome
  • Adults (> 45 years) - Poor prognosis
‣
What will the FBC look like?
  • High WCC
  • Lymphocytosis
‣
Chronic lymphocytic leukaemia (CLL)
‣
When is this commonly seen?
  • Adults (> 55y)
‣
Patient with known CLL has jaundice, LFT shows high unconjugated bilirubin. Diagnosis?
  • Warm AIHA
‣
What can this transform into? (What is the transformation called?)
  • High-grade lymphoma (Richter's transformation)
‣
What do you find on blood film?
  • Smudge cells - Represent fragile WBCs
‣
Acute myeloid leukaemia (AML)
‣
Who is it more common in?
  • > 75 years - Most common leukaemia in adults
‣
What is seen on blood film?
  • Auer rods
‣
What is APML?
  • Acute promyelotic leukaemia
  • Presents in ~ 30 y/o with AML & DIC features
‣
Chronic myeloid leukaemia (CML)
‣
What is the characteristic feature of this?
  • Philadelphia chromosome [t(9;22) Bcr-Abl translocation]
    • May have pseudo Pelger-Huet cells on blood film
  • Massive splenomegaly
‣
What are the 3 phases?
  1. Chronic (~ 5y): Often asymptomatic
  2. Accelerated: Blast cells take up 10-20% of blood
  3. Blast: > 30% of blast cells in blood → Pancytopenia & symptoms
‣
What can this develop in to?
  • Acute leukaemia - AML (80%)
‣
What is the first-line management?
  • Immunosuppression - Imatinib
‣
Lymphoma (B/T-cells)

Types:

‣
Hodgkin's lymphoma
‣
Feature
‣
When do they present?

Bimodal:

  1. ~ 20 years
  2. ~ 75 years
‣
What is the most common presentation?
  • Asymmetrical, painless lymphadenopathy
    • Can be painful when drinking alcohol
‣
What are the B symptoms? (4)
  1. Night sweats
  2. Fever
  3. Weight loss
  4. Prurius - itching
‣
What symptoms & signs signify a poor prognosis?
  1. B-symptoms
  2. Lymphocyte depletion
  3. Age > 45 years
  4. Male
  5. High WCC
‣
What are the RFs?
  • EBV
  • HIV
  • High socioeconomic class
  • Jewish ancestry
‣
What other features may be seen?
  • Normocytic anaemia of chronic disease
  • Eosinophilia
‣
What's the most common type?
  • Nodular sclerosing
‣
Investigations
‣
What blood test would you do?
  • LDH (non-specific)
‣
Name the 4 Ann-Arbor stages.

CT/MRI showing lymphadenopathy in:

  • Stage 1: 1 area
  • Stage 2: > 1 area, same side of diaphragm
  • Stage 3: > 1 area, opposite sides of diaphragm
  • Stage 4: Extra-nodal sites
‣
Interpret the following lymph node biopsy.
  • Reed-Sternberg cells (multiple nuclei) present in the centre
Ed Uthman, MD, CC BY-SA 2.0
Ed Uthman, MD, CC BY-SA 2.0 creativecommons.org/licenses/by-sa/2.0, via Wikimedia Commons. No changes were made.
‣
How are they managed?
  1. Chemotherapy
  2. Radiotherapy
‣
Non-Hodgkin's lymphoma
‣
How does the presentation of NHL differ from HL?
  • Lymphadenopathy is usually widespread
  • No Reed-Sternberg cells
  • More common in adults
‣
What are the poor prognostic markers? (4)
  1. Raised serum LDH
  2. B-symptoms
  3. Lymphadenopathy/organomegaly
  4. Anaemia

Types:

‣
Burkitt's
‣
What may you see on inspection?
  • Asymmetrical face swelling
Mike Blyth, CC BY-SA 2.5
Mike Blyth, CC BY-SA 2.5 creativecommons.org/licenses/by-sa/2.5, via Wikimedia Commons
‣
What infection is it assoicated with?
  • EBV
‣
What mutation is it associated with?
  • C-myc
‣
What is seen on microscopy?
  • 'Starry sky' appearance
‣
MALT
‣
What causes this?
  • H. pylori chronic stomach inflammation → Mucosa associated lymphoid tissue
‣
How is it managed?
  1. Triple therapy to eradicate H. pylori
‣
Diffuse large B-cell

Most common lymphoma in U.K.

‣
How does this present?
  • Rapidly growing painless mass in > 65y
‣
What infection is it associated with?
  • Hepatitis C
‣
Multiple myeloma (Plasma cells)
‣
How do these patients present?
  1. Calcium: Hypercalcaemia
  2. Renal failure: Antibodies block the tubule flow
  3. Anaemia: Bone marrow infiltration
  4. Bone pain/fractures: ↑ Osteoclast activity caused by cytokines released by plasma cells
  5. Bleeding: Thrombocytopenia
  6. Infection
‣
Investigations
‣
What are the initial diagnostic investigations?
  1. Urine Bence-Jones protein
  2. Serum-free Light-chain assay
  3. Serum Immunoglobulins
  4. Serum Protein electrophoresis
‣
What result will ALP & phosphate show?
  • Normal ALP (differentiates from bone metastases where ALP will be high)
  • Normal phosphate
‣
What is seen on blood film?
  • Rouleaux: Stacks of aggregated RBCs
‣
What is the best diagnostic investigation?
  • Bone marrow aspirate & biopsy: > 10% plasma cells in bone marrow
‣
What X-ray findings may you see?
  • Punched out lytic lesions
  • Raindrop skull
Mikael Häggström, CC0, via Wikimedia Commons
Mikael Häggström, CC0, via Wikimedia Commons
‣
How are pathological fractures prevented?
  • Bisphosphonates: Zolendronic acid
‣
How are they managed?
  1. Suitable for transplant: Allogenic/autologous HPSC transplant
  2. Not suitable: MPT → Melphalan, prednisolone, thalidomide
‣
Myeloproliferative disorders
‣
General
‣
What mutation is common in these patients?
  • JAK-2
‣
What is seen on bloods in each?
  • PV: Hb > 185/165
  • ET: Platelets > 600
‣
What can these develop into?
  • AML

Types:

‣
Primary myelofibrosis (Haematopoietic stem cells)
‣
What is the pathophysiology of this?
  • Cell line proliferation → Fibroblast stimulation → Bone marrow fibrosis → Pancytopenia
  • Haematopoiesis can happen in liver & spleen causing enlargement
‣
What is seen on bone marrow aspiration?
  • 'Dry tap' because the bone marrow is filled with fibrosed tissue
‣
What does the following blood film show?
  • Poikilocytosis (varying sizes)
  • Tear drop RBCs
Dr Graham Beards, CC BY-SA 3.0
Dr Graham Beards, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
Polycythaemia vera (Erythroid cell)
‣
Name 2 classic symptoms.
  1. Pruritus (intense)
  2. Joint pain: Gouty arthritis
‣
What are they predisposed to?
  • Clots: Hyperviscosity of blood
  • AML transformation
‣
What is first-line management?
  • Venesection
  • Aspirin
‣
Name the secondary causes of polycythaemia
  1. Dehydration: Pseudopolycythaemia (high RBC : plasma)
  2. COPD: ↓ SpO₂ → ↑ EPO → Polycythaemia
  3. Obstructive sleep apnoea
  4. Altitude
‣
Essential thrombocythaemia (Megakaryocyte)
‣
What is reactive thrombocytosis?
  • Platelets are an acute phase reactant so are raised in stress e.g. infection/surgery
‣
What is a characteristic symptom?
  • Burning sensation in the hands
‣
What malignancy is associated with thrombocytosis?
  • Lung
‣
🎞 Blood Films
‣
Name all of the blood film findings you may be looking for.
  1. Reticulocytes → Haemolytic anaemia
  2. Spherocytes → AIHA, hereditary spherocytosis
  3. Heinz bodies → G6PD, ɑ-thalassaemia
  4. Auer rods → AML
  5. Smudge cells → CLL
  6. Howell-Jolly bodies → Hyposplenism/splenectomy, severe anaemia
  7. Target cells → Fe deficiency anaemia / splenectomy
  8. Schistocytes (fragmented RBCs) → HUS, DIC, TTP, metallic valves
  9. Anisocytosis (variation in RBC size) → Myelodysplastic syndrome
  10. Sideroblasts (immature RBCs containing Fe blobs) → Myelodysplastic syndrome
‣
Visualising Cell Types
Ed Uthman, S Bhimji and Mikael Häggström, M.D. Consent from the patient or patient's relatives is regarded as redundant, because of absence of identifiable features (List of HIPAA identifiers) in the media and case information (See also HIPAA case reports guidance)., CC BY 4.0
Ed Uthman, S Bhimji and Mikael Häggström, M.D. Consent from the patient or patient's relatives is regarded as redundant, because of absence of identifiable features (List of HIPAA identifiers) in the media and case information (See also HIPAA case reports guidance)., CC BY 4.0 creativecommons.org/licenses/by/4.0, via Wikimedia Commons. No changes were made.

For the following blood films:

  1. Name the features seen on the film.
  2. Name the disease associated with these features.
Ed Uthman from Houston, TX, USA, CC BY 2.0
Ed Uthman from Houston, TX, USA, CC BY 2.0 creativecommons.org/licenses/by/2.0, via Wikimedia Commons. No changes were made.
‣
Film 1
  1. Target cells
  2. Thalassaemia/hyposplenism/sickle cell
Dr Graham Beards, CC BY-SA 3.0
Dr Graham Beards, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
Film 2
  1. 'Tear drop' poikilocytes (poik - oddly shaped RBCs)
  2. Myelofibrosis - Large megakaryocytes stimulate fibroblasts
Paulo Henrique Orlandi Mourao and Mikael Häggström, CC BY-SA 3.0
Paulo Henrique Orlandi Mourao and Mikael Häggström, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
Film 3
  1. Howell-Jolly bodies (remnants of the RBC nucleus, typically removed by the spleen)
  2. Hyposplenism
Prof. Osaro Erhabor, CC0, via Wikimedia Commons
Prof. Osaro Erhabor, CC0, via Wikimedia Commons
‣
Film 4
  1. Schistocytes
  2. Cold AIHA/mechanical heart valve/DIC (Any mechanical trauma)
S Bhimji, MD, CC BY 4.0
S Bhimji, MD, CC BY 4.0 creativecommons.org/licenses/by/4.0, via Wikimedia Commons. No changes were made.
‣
Film 5
  1. Acanthocytes
  2. Abetalipoproteinemia
‣
💊 Drugs
‣
Tumour lysis syndrome
‣
What cancers is it commonly related to?
  • High grade lymphoma
  • Leukaemia
‣
How is it usually triggered? Pathophysiology?
  • Combination chemotherapy
    • Chemotherapy → Tumour cell breakdown → Release of cell contents into blood stream
‣
What would signify this on blood tests?
  1. ↑ K⁺
  2. ↑ PO₄³⁻
  3. ↓ Ca²⁺
  4. ↑ Urea
‣
What do you need to have to confirm the diagnosis?
  • End organ damage:
    • ↑ serum creatinine
    • Cardiac arrhythmia
    • Seizure
‣
What prophylaxis would be given?
  • IV allopurinol
‣
What therapeutic drug should be given?

Treat each individual electrolyte abnormality:

  • IV rasburicase: Breaks down urea OR lactulose (longer acting)
  • Treat other electrolyte abnormalities as normal
‣
Tranexamic acid
‣
How does it work?
  • Binds to plasmin → Plasmin can't break down fibrin clot
‣
What is it most commonly used to treat?
  • Menorrhagia
‣
Where else is it used?
  • Trauma: IV bolus slowly infused
‣
What drugs can cause aplastic anaemia?
  1. Phenytoin
  2. Chloramphenicol
  3. Carbamazepine
  4. Quinine
‣
Blood products
‣
Blood transfusion
‣
What complications can occur?
  1. Immunological:
    • Acute haemolytic
    • Non-haemolytic febrile
    • Allergic/anaphylaxis
  2. Infective
  3. Transfusion-related acute lung injury (TRALI)
  4. Transfusion-associated circulatory overload (TACO)
  5. Other: Hyperkalaemia, iron overload, clotting
‣
How fast is a blood transfusion given in a non-urgent and urgent scenario?
  • Urgent (major haemoorhage): STAT
  • Non-urgent: 90 mins – 2 hours
‣
When do you transfuse platelets in patients with acute haemorrhage and not acutely unwell patients, respectively?
  • Haemorrhage < 100 x 10⁹
  • Not unwell < 30 x 10⁹
‣
What is used for emergency reversal of anticoagulation?
  • Prothrombin complex concentrate
‣
What is used in a 'clinically significant' haemorrhage in patients with an INR > 1.5?
  • Fresh frozen plasma
‣
What is given to replace fibrinogen?
  • Cryoprecipitate

🥴 Endocrinology

‣
🧠 Pituitary
‣
Prolactin
‣
Name features of excess prolactin in both men and women.
  • Men: Galactorrhoea, impotence, loss of libido
  • Women: Galactorrhoea, amenorrhoea
‣
What neurotransmitter inhibits prolactin release?
  • Dopamine
‣
Name 5 causes of raised prolactin
  1. Prolactinoma
  2. Pregnancy
  3. Oestrogens
  4. Physiological: Stress, exercise, sleep
  5. Acromegaly (1/3 of patients)
‣
Name 3 drugs that cause raised prolactin.

Think dopamine antagonists:

  1. Fluoxetine
  2. Metoclopramide
  3. Haloperidol
‣
How are they managed?
  1. Dopamine agonist: Bromocriptine/cabergoline
  2. Trans-sphenoidal hypophysectomy
‣
Growth Hormone
‣
What are the causes of acromegaly?
  1. Pituitary adenoma (95%)
  2. Ectopic production of GHRH - SCLC or pancreatic cancer
‣
Name the common features.
  • Facial: Coarse features, prognathism (gurn), macroglossia, frontal bossing
  • Body: Wedding ring no longer fits spade-like hands, increase in shoe size
  • Pituitary: Bitemporal hemianopia, headache, hypopituitarism
‣
Why may they get galactorrhoea?
  • 1/3 of patients with acromegaly have hyperprolactinaemia
‣
Name 3 investigations you may want to do.
  1. Serum IGF-1: High
  2. Oral glucose tolerance test (OGTT): GH won't be suppressed
    • High glucose normally suppresses GH
  3. MRI brain: Pituitary
‣
Name 3 complications.
  1. Cardiomyopathy (hypertrophic)
  2. Hypertension
  3. T2DM (> 10%)
  4. Colorectal cancer
‣
How are the majority of cases managed?
  • Trans-sphenoidal surgical removal
‣
What medical treatment may be used, and when?
  1. Somatostatin analogue (Octreotide): Directly inhibits GH release
  2. Bromocriptine: Dopamine agonist
‣
ADH
‣
When is ADH released & how does it work?
  • Released when the plasma osmolality is high
  • Inserts aquaporins into the collecting ducts to retain water resulting in lowering the plasma osmolality
‣
SIADH
‣
What is the problem with ADH here?
  • Overproduction
‣
Name 5 causes of SIADH.
  1. Pituitary overpoduction
  2. Small cell lung cancer
  3. Infection - Atypical pneumonia / lung abscess
  4. Head injury
  5. Medications: Thiazide diuretics, carbamazepine, SSRIs, NSAIDs
‣
How would they present?
  • Euvolaemic
  • Headache, fatigue
  • Muscle aches & cramps
  • Confusion
‣
What would you see on U&E?
  • ↓ Na
‣
What could be other causes of this & how would you rule them out?
  • Addison's - Synacthen test
  • Diuretics - MH
  • D&V - History
  • CKD/AKI - Visible on U&E
‣
Management:
‣
What is the definitive treatment?
  • Establish & treat underlying cause
‣
When correcting the sodium what is important to remember?
  • Correct slowly to prevent central pontine myelinolysis (< 10mmol/L per 24h)
‣
How is the sodium corrected?
  1. Fluid restriction
  2. Tolvaptan (ADH receptor blocker) - Cause rapid increase in Na
‣
Diabetes Insipidus
‣
What is the problem with ADH here?
  • Either not produced or not responded to
‣
What symptoms will this individual be experiencing?
  • Polyuria
  • Polydipsia
‣
What are the two types and their common causes?
  1. Cranial
    • Trans-sphenoidal pituitary surgery, head injury
  2. Nephrogenic
    • Lithium therapy
‣
Investigations:
‣
What would be your intitial investigations in primary care?
  1. Bloods: FBC, U&E (↑ Na)
  2. Fasting glucose: Consider DM
  3. Urine & serum osmolality
    • In DI: ↑ serum osmolality, ↓ urine osmolality
‣
What is the diagnostic test for DI?
  • Water deprivation test: Urine osmolality should increase as patient gets dehydrated. If it doesn’t → DI.
‣
What test differentiates between the two types?
  • Desmopressin stimulation test:
    • Cranial: Urine osmolality will increase (more concentrated) - they respond to ADH
    • Nephrogenic: No response
‣
What is the treatment for each type, respectively.
  • Cranial: Vasopressin/desmopressin
  • Nephrogenic: Chlorothiazide diuretic
‣
🥺 Thyroid
‣
Name 10 causes of a goitre.
  • Smooth:
    1. Graves' disease
    2. Hashimoto's thyroiditis
    3. De Quervain's thyroiditis
    4. Iodine deficiency/excess
    5. Drugs: Lithium / amiodarone
    6. Infiltration (sarcoidosis, haemochromatosis)
  • Nodular:
    1. Toxic multinodular goitre
    2. Solitary thyroid nodule (toxic/non-functional)
    3. Cancer
    4. Thyroglossal cyst
‣
Hyperthyroidism
‣
A patient has hyperthyroidism, name the 4 potential thyroid pathologies causing this.
  1. Graves disease: Non-tender goitre
  2. Toxic multinodular goitre
  3. Solitary toxic thyroid nodule
  4. De Quervain's thyroiditis (in subacute hyperthyroid phase of disease): Tender goitre.
‣
Definitions:
‣
What is hyperthyroidism?
  • Over-production of thyroid hormone by the thyroid gland
‣
What is thyrotoxicosis?
  • Excessive quantity of thyroid hormone in the body
‣
What is Graves' disease?
  • An autoimmune condition where TSH receptor antibodies cause a primary hyperthyroidism
‣
What is a toxic multinodular goitre?
  • Nodules develop on the thyroid gland that act independently of the normal feedback system and continuously produce excessive thyroid hormone.
‣
What is a thyroid storm?
  • Severe presentation of hyperthyroidism with pyrexia, tachycardia & delirium
    • ‣
    What events may precipitate it?
    • Infection, thyroid surgery, trauma
‣
Signs & symptoms:
‣
Name symptoms of thyrotoxicosis.
  1. Sweating & heat intolerance
  2. WL
  3. Fatigue
  4. Anxiety & irritability / restlessness
‣
Name 4 signs associated with all hyperthyroidism cases.
  1. Tachycardia
  2. Tremor
  3. Palmar erythema
  4. Lid lag & retraction
  5. Diffuse goitre
‣
Name 4 signs present in Graves, but not all hyperthyroid cases.
  1. Thyroid acropachy
  2. Exophthalmos - TSH antibodies cause eye muscle inflammation, swelling & hypertrophy
  3. Ophthalmoplegia
  4. Pretibial myxoedema
‣
How do you investigate a patient with thyrotoxicosis?
  • TFTs
  • TSH receptor stimulating antibody - Graves
  • Anti-TPO antibody - Graves
  • USS +/- biopsy - Tumour
‣
What are the 3 options for managing thyrotoxicosis?
  1. Carbimazole
    2. ‣
    How does it work?
    • Stops I₂ from being converted to I⁻ reducing thyroid hormone formation.
    ‣
    Complications?
    • Agranulocytosis
    • Teratogenic
  2. Propylthiouracil
    3. ‣
    How does it work?
    • Similar mechanism to carbimazole
    • Stops I₂ from being converted to I⁻ reducing thyroid hormone formation.
    ‣
    When is it first-line?
    • Pregnancy & thyroid storm
    ‣
    Complication?
    • Risk of severe hepatic reaction → Death
  3. Radioiodine (Lugol's iodine)
    4. ‣
    How does it work?
    • Taken up by thyroid cells and the radiation kills them
    ‣
    When is it contraindicated?
    • Pregnancy
    • Age < 16y
    • Thyroid eye disease (worsens it)
    ‣
    Key side effect?
    • Hypothyroidism
‣
Name all of the drugs used in a thyroid storm.
  1. Propylthiouracil
  2. Beta blocker (IV propranolol) - Tachycardia
  3. Antiarrhythmics
  4. Prednisolone - Reduces conversion of T4 to T3
‣
Hypothyroidism
‣
Name the characteristic features.
  • Weight gain, lethargy
  • Dry skin, coarse hair, loss of lateral eyebrow
  • Menorrhagia
  • Constipation
  • May have amenorrhoea because TRH stimulates prolactin release
‣
Management
‣
What are the standard doses of levothyroxine?
  • 50-100 micrograms
‣
How do you monitor if levothyroxine treatment is effective?
  • Serum TSH (keep in normal range)
‣
How do you need to change levothyroxine management in pregnancy?
  • Increase it by 25-50 micrograms
‣
What are the SEs?
  • Hyperthyroidism
  • Reduced bone mineral density
  • Can worsen angina
  • Atrial fibrillation
‣
What does levothyroxine interact with?
  • Iron (reduces absorption), give them 2 hours apart
‣
Myxoedemic coma
‣
What is this?

Severe hypothyroidism leading to low everything: Consciousness, HR, BP, temperature.

  1. Confusion
  2. Bradycardia
  3. Hypotension
  4. Hypothermia
‣
How is it managed?
  1. IV levothyroxine
  2. IV hydrocortisone: Assume that the low thyroid has lead to adrenal insufficiency

Cases:

‣
A woman presents with weight gain, lethargy and menorrhagia, a goitre and anti-TPO antibodies are found, what does she have?
  • Hashimoto's thyroiditis
    • Non-tender goitre
‣
A man who had a cough 3 weeks ago presents with tachycardia and tremor. His symptoms then settle, but 6 weeks later he presents with weight gain and lethargy. What does he have?
  • De Quervain's (subacute) thyroiditis
    • Tender goitre
‣
A patient from Africa who has recently moved to the UK is found to have hypothyroidism on TFT. What is the most likely cause?
  • Dietary iodine deficiency
‣
A patient with bipolar disorder has hypothyroidism. What is the likely cause?
  • Lithium therapy (can also cause a goitre)
  • Amiodarone also causes hypothyridism
‣
TFTs
TSH
Free T4
Diagnosis (See answers below)
↓
↑
A
↑
↓
B
↓
↓
C
↑
↔︎
D
↓
↔︎
E

Answers:

‣
Diagnosis A
  • Primary hyperthyroidism
‣
Diagnosis B
  • Primary hypothyroidism
‣
Diagnosis C
  • Secondary hypothyroidism / sick euthyroid syndrome
‣
Diagnosis D
  • Subclinical hypothyroidism / poor compliance with thyroxine
‣
Diagnosis E
  • Steroid therapy
‣
Thyroid cancer
‣
Do thyroid cancers commonly secrete hormones?
  • No - very rare
‣
What are the two most common thyroid malignancies?
  1. Papillary (70%) - Often young females (good prognosis)
    2. ‣
    What histological sign is diagnostic of this?
    • Orphan Annie cells
  2. Follicular (20%)
‣
A patient presents with a solitary thyroid nodule, what is this likely to be?
  • Follicular adenoma - test to see if it's malignant
‣
A patient presents with MEN-2, what thyroid malignancy are they likely to have?
  • Medullary - Parafollicular
‣
Patient presents with hypocalcaemia and raised serum calcitonin, what malignancy is this?
  • Medullary
  • Malignant C-cells (parafollicular)
‣
How are they usually managed?
  • Total thyroidectomy
  • Followed by radioiodine to mop up residual cells
  • Levothyroxine replacement
‣
🦴 Parathyroid
‣
How does PTH work?

↓ serum Ca²⁺ causes:

  1. PTH release from parathyroid glands stimulating:
    1. ↑ osteoclast activity → ↑ Ca²⁺ absorption from bone
    2. ↑ kidney reabsorption of Ca²⁺
  2. ↑ 1-ɑ-hydroxylase release in the kidney → ↑ calcitritol (active vitamin D) → ↑ intestinal absorption of Ca²⁺
‣
Hormone profile cases:
Calcium
Phosphate
PTH
ALP
Diagnosis
↓/↔︎
↑
↑
↑/↔︎
A
↑
↓
↑
↑
B
↑
↓/↔︎
↑
↑
C
↑
↑
↓
↑
D
↓
↑
↑
↔︎
E
‣
Diagnosis A
  • Secondary hyperparathyroidism (e.g. vitamin D deficiency, CKD)
‣
Diagnosis B
  • Primary hyperparathyroidism
‣
Diagnosis C
  • Tertiary hyperparathyroidism
‣
Diagnosis D
  • Malignancy (non-parathyroid)
‣
Diagnosis E
  • Pseudohyperparathyroidism
‣
Presentation:
‣
What are the features of hypercalcaemia?
  • Bones - Oesteopenia/porosis
  • Stones - Kidney stones
  • Psychic moans - Confusion, depression
  • Abdominal groans - Pancreatitis, constipation
‣
A patient with CKD presents with low calcium and high PTH, what type is this and how is it managed?
  • Secondary
    • Low 1-ɑ-hydroxylase → Low active vitamin D → ↓ Ca2+ → ↑ PTH
  • Vitamin D analogues
‣
This patient is treated, but their PTH continues to be high, what is this and how is it managed?
  • Tertiary: Parathyroid hyperplasia has occurred over time
  • Surgical resection
‣
An elderly female presents with an unquenchable thirst and a raised PTH level. What is it likely to be and what is the management?
  • Primary - Solitary adenoma
  • Total parathyroidectomy
‣
What is a characteristic feature seen on XR?
  • Pepperpot skull
  • Reduced bone mineral density/erosion
‣
What other neoplasias is it associated with?
  • MEN disorders
‣
🍰 Diabetes
‣
What test can differentiate the 2 types?
  • C-peptide: Precursor is broken down into insulin & C-peptide, therefore in T1DM it will be low, in T2DM it will be high

Types:

‣
Type 1 diabetes mellitus
‣
DKA
‣
Name the 3 ketone bodies.
  • Acetone
  • Acetoacetate
  • β-hydroxybutyrate
‣
Name 3 precipitating factors.
  • Infection
  • Missed insulin
  • MI
‣
Name 5 symptoms.
  • Abdominal pain
  • Polyuria
  • Polydipsia
  • Kussmaul's respiration - trying to breathe out CO2 due to acidosis
  • Pear drop breath
‣
What do you need for diagnosis
  1. Acidosis: pH < 7.3 or plasma bicarbonate below 15mmol/litre.
  2. Ketonaemia: Ketones (beta-hydroxybutyrate) > 3 mmol/litre.
  3. Blood glucose is generally high (> 11mmol/litre), but children can develop DKA with normal glucose.
‣
Management:
‣
What is the immediate initial management?
  • IV fluids → NaCl 500mL 0.9%
‣
What needs to be given next & dose?
  • Fixed rate insulin infusion → 0.1 unit/kg/hr (80kg = 8 units/hr)
    • Continue long-acting insulin, stop short acting
‣
What needs to be monitored and corrected throughout treatment and how is this done?
  • Potassium: Risk of hypokalaemia
    • K⁺ 3.5-5.5 → Add 40mg KCl into IV fluids
  • Sodium: Risk of cerebral oedema if going from aggressive fluid resuscitation
‣
Hypoglycaemia
‣
What are the symptoms?
  • Blurred vision
  • Weakness
  • Recurrent headaches
‣
Name 6 causes of this. (EXPLAIN)
  • EXogenous drugs - insulin, sulphonylureas
  • Pituitary dysfunction
  • Liver failure
  • Addison's disease
  • Insulinoma
  • Non-pancreatic neoplasms
‣
How do you differentiate exogenous insulin intake from endogenous production (insulinoma)?
  • Serum C-peptide → High in endogenous production as it's a by-product of the synthesis
    • Give insulin: Normally C-peptide will fall, in insulinoma it will remain the same
‣
How is it managed in hospital & GP, respectively?
  1. Conscious (both): Lucozade drink
  2. Unconscious:
    • Hospital: 200ml 10% IV dextrose
    • GP: IM glucagon
‣
Insulin therapy
‣
What is insulin sliding scale & when is it used?
  • Two separate infusions, one of glucose and one of insulin
  • Rates can be easily adjusted based on BM results so used in medical management of diabetic inpatients
‣
Who doesn't need to inform the DVLA if on insulin?
  • Temporary treatment for ≤ 3 months or less
  • GDM that are taking insulin for < 3 months post-delivery

Give an example of each of the following:

‣
Rapid-acting
  • Novorapid
‣
Short-acting
  • Actrapid
‣
Intermediate-acting
  • Isophane
‣
Long-acting
  • Levemir / Lantus
‣
Type 2 diabetes mellitus
‣
Diagnosis:
‣
How does diagnosis differ between a symptomatic and asymptomatic patient?
  • Symptomatic - 1 HbA1c, fasting BM or random BM reading needed
  • Asymptomatic - 2 HbA1c readings needed
‣
What HbA1c represents pre-diabetes and diabetes?
  • 42-47 - Pre-diabetes
  • ≥ 48 - Diabetes
‣
What do fasting and random BM readings need to be for diabetes?
  • Fasting
    • 6.1-7 → Impaired fasting glucose
    • ≥ 7 → Diabetes
  • 2h glucose
    • ≥ 7.8 → Impaired glucose tolerance
    • ≥ 11 → Diabetes
  • Random
    • ≥ 11 → Diabetes
‣
In what patients can HbA1c not be used?
  • Increased RBC lifespan - Hb higher than reality
    • Anaemia
      • Fe-deficiency
      • Vitamin B12/folate deficiency
    • Splenectomy
  • Decreased RBC lifespan - Hb lower than reality
    • Sickle cell anaemia
    • G6PD deficiency
    • Hereditary spherocytosis
  • Other
    • CKD
    • Children
    • HIV
    • Gestational diabetes (not enough time)
‣
BP targets:
‣
When is it < 140/80?
  • Diabetes without end-organ damage
‣
When is it < 130/80?
  • Diabetes with end-organ damage
‣
Management targets:
‣
Between what HbA1c values should lifestyle and metformin titration be primarily used?
  • 48-58
‣
At what HbA1c value should a second drug be added?
  • ≥ 58
‣
What are the HbA1c targets for metformin management and sulphonylurea management, respectively?
  • Metformin: 48
  • Sulphonylurea: 53
‣
Is there a preferred second-agent in management?
  • No. Any are acceptable.
‣
Drugs:
‣
What is the incretin effect? What 2 drugs enhance this effect?
  • Give PO and IV glucose and more insulin will be produced from PO because intestines secrete GLP-1
    • GLP-1 agonists (Exenatide) - mimic GLP-1
    • DPP-4 inhibitors - Prevent the breakdown of GLP-1 therefore increasing its effect
‣
What insulin regime should they be started on in severe DM?
  • Basal therapy - Isophane insulin. Add a bolus after meals if BM is very high

The following are examples of which classes, and name the common SEs & CIs of each:

‣
Canagliflozin
  • SGLT-2 inhibitor
  • Stops reabsorption of glucose back into blood in the PCT
  • SE: UTI
  • Relies on decent kidney function
‣
Exenatide (Give indications & target)
  • GLP-1 agonist
  • I: BMI ≥ 35 OR BMI < 35 but can't have insulin for occupation
  • T: Drop in HbA1c of 11 & 3% WL over 6 months
  • SE: Pancreatitis
‣
Sitagliptin
  • DPP-4 inhibitor
  • Doesn't cause weight gain so use in very overweight
  • SE: Pancreatitis
‣
Pioglitazone
  • Thiazolidenedione
  • Increases peripheral insulin sensitivity
  • SE: Weight gain, fluid retention, osteoporosis, liver dysfunction
  • CI: Heart failure
‣
Hyperglycaemic Hyperosmolar Syndrome (HHS):
‣
Over what time period does HHS come on?
  • Days - therefore the dehydration & electrolyte abnormalities are very bad
‣
What is the pathophysiology?
  1. Hyperglycaemia → Osmotic diuresis → Electrolyte losses
  2. Dehydration → Hyperviscosity of blood → Vascular complications
  3. Hypertonicity (constriction) of blood vessels compensates so they don't look as ill as they actually are
‣
What factors are used in diagnosis?
  • Hyperglycaemia: usually > 30 (no ketones/acidosis)
  • BP: Hypotension
  • Raised serum osmolality
‣
What are the 3 key management steps for HHS?
  1. IV fluids: Dilutes hyperglycaemia and increases blood volume
  2. Correct electrolytes
  3. Normalise glucose: Usually don't use insulin as it will drop glucose too quickly and cause significant volume depletion. Fluids usually does the job

Complications:

‣
Diabetic neuropathy
‣
What drugs are used for management of diabetic peripheral neuropathy?
  1. Amitryptiline
  2. Duloxetine
  3. Gabapentin
  4. Pregabalin
‣
A patient with poorly controlled diabetes presents with bloating and vomiting and a very high BM. What has occured here and how is it managed?
  • Gastric neuropathy → Gastroparesis
  • Metoclopramide (prokinetic)
‣
Diabetic retinopathy
‣
Non-proliferative
  • Mild: ≥ 1 microaneurysm
  • Moderate:
    • Blot haemorrhage
    • Hard exudates (lipid leakage exudate)
    • Cotton wool spots (damage to nerve fibres → white patches)
  • Severe: Microaneurysms in all 4 quadrants, bleeding in ≥ 2 quadrants
Renátó BesencziJános TóthAndrás Hajdu, CC BY-SA 4.0
Renátó BesencziJános TóthAndrás Hajdu, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.
‣
Proliferative

Abnormal new blood vessels that grow on the surface of the retina.

  • Treatment: Anti–vascular endothelial growth factor therapy (Anti-VEGF).
‣
👹 Adrenals
‣
Cushing's syndrome
‣
General:
‣
Draw the glucocorticoid negative feedback loop.
OpenStax College, CC BY 3.0
‣
What are the two broad causes of Cushing's and which is more common?
  • Exogenous (more common) - steroids
  • Endogenous
‣
Name 4 causes of Cushing's.
  1. Pituitary tumour (most common endo cause)
  2. Adrenal adenoma
  3. SCLC - secretes ACTH
  4. Exogenous steroid use
‣
Name the common features of Cushing's.
  • Striae
  • Weight gain
  • Easy bruising
  • Diabetes
  • Interscapular fat pad
  • Spinal tenderness
  • Hypertension
‣
What is pseudo-Cushing's and how do you differentiate it from Cushing's?
  • Mimics the features of Cushing's but due to excess alcohol intake
  • Insulin stress test → Impaired glucose tolerance in Cushing's but not in pseudo
‣
Investigating:
‣
What test would you do for this in GP?
  • 24 hour urinary cortisol
‣
What electrolyte abnormality may be seen?
  • Hypokalaemic metabolic alkalosis
    • Hypokalaemia → Cortisol stimulates aldosterone receptor
    • Alkalosis → K in tubule is swapped for H
‣
How does the Dexamethasone suppression test work?
  • Give exogenous steroid → Normal response is for ACTH and cortisol to drop due to negative feedback. This doesn't occur in Cushing's syndrome.
  • Low-dose is given first to rule out exogenous use, followed by high-dose to localise the Cushing’s syndrome pathology.

Dexamethasone Suppression Test Results

Dose
Serum Cortisol
ACTH
Result
Low (1mg)
↓
A
↑/↔︎
B
High (8mg)
↓
C
↑/↔︎
↓
D
↑/↔︎
↑
E
‣
Result A
  • Normal response - could be exogenous steroid intake
‣
Result B
  • Cushing's syndrome - Cortisol release is not suppressed
‣
Result C
  • Cushing's disease - Pituitary is suppressed by high dose.
‣
Result D
  • Adrenal Cushing's - Negative feedback from dexamethasone stops pituitary secretion of ACTH, therefore it’s low.
‣
Result E
  • Ectopic ACTH production (e.g. SCLC) - Dexamethasone doesn’t suppress production because cells are malignant.
‣
How is it managed in most cases?
  • Surgical removal of the adenoma/tumour that is causing the problem
  • Medical management until surgery: Metyrapone (blocks steroid synthesis pathway)
‣
Addison's disease
‣
Causes & features:
‣
Name 4 primary causes of hypoadrenalism.
  1. Autoimmune (80%)
  2. Tuberculosis
  3. Metastases to adrenals (e.g. bronchial)
  4. Waterhouse-Friderichsen syndrome
    5. ‣
    What is this?
    • Adrenal gland failure due to bleeding into the adrenal glands, commonly caused by severe bacterial infection, e.g. meningococcal septicaemia.
‣
Name 2 secondary causes.
  1. Pituitary dysfunction: Surgery, infection, Sheehan's syndrome
  2. Congenital pituitary hypoplasia
‣
Name 1 tertiary cause.
  • Exogenous steroid intake (for > 3 weeks) → Hypothalamic suppression of CRH
‣
Name the common features of Addison's.
  • Lethargy
  • Weakness
  • N&V
  • Hyperpigmentation (palm & buccal): Excess ACTH is converted to ɑ-MSH
‣
Investigations:
‣
What electrolyte abnormalities may be seen?
  • Hyperkalaemia
  • Hyponatraemia
  • Metabolic acidosis
  • Hypoglycaemia
‣
What else would you like to test for?
  • BM - Hypoglycaemia
‣
How would you test for this in general practice?
  • 9AM serum cortisol (ACTH, aldosterone & renin)
‣
What is the definitive investigation, and what do they results represent?
  • Synacthen test (synthetic ACTH)
    • Low cortisol - Primary
    • High cortisol - Secondary
‣
Management:
‣
Name 2 medications given to treat this.
  • Hydrocortisone - Glucocorticoid
  • Fludrocortisone - Mineralocorticoid
‣
If the patient has an infection, should treatment change?
  • Yes - Double the glucocorticoid dose
‣
A patient with RA presents for an elective cholecystectomy, after the surgery she is hypotensive and very unwell. What has occurred here and how is it managed?
  • Addisonian crisis - the trauma needed to be accommodated for with additional glucocortocoid.
  • 100mg IV hydrocortisone, repeat 6 hourly (see local guidelines).
    • Fludrocortisone is not needed due to hydrocortisone having enough effects on its receptors in an acute situation.
  • IV fluids (dextrose if hypoglycaemic)
‣
Primary hyperaldosteronism (Conn’s syndrome)
‣
Name the 2 main causes.
  1. Bilateral adrenal hyperplasia (BAH) - 70%
  2. Adenoma (Conn’s) - 30%
‣
Name the 3 main features.
  1. Hypertension
  2. Hypokalaemia
  3. Alkalosis
‣
What result would be seen on an aldosterone : renin ratio?
  • High aldosterone, low renin (negative feedback)
‣
Why do a CT/adrenal vein sampling?
  • Decide whether it’s Conn's or BAH - is it unilateral?
‣
How does management differ between the 2 types?
  • Conn's - Surgical removal
  • Bilateral adrenal hyperplasia - Spironolactone
‣
Pheochromocytoma
‣
What is this a tumour of?
  • Chromaffin cells of the adrenal medulla
‣
When may you consider this as being a cause of HTN?
  • Treatment resistant HTN
‣
Name 3 investigations you may carry out.
  1. Urinary metanephrines (VMA)
  2. Serum metanephrines - High sens & spec
  3. CT/MRI abdomen - Locate lesion
‣
What are the first and second stages in the management?
  1. Acute:
    1. IV phentolamine (ɑ-blocker): Short acting
    2. Phenoxybenzamine (ɑ-blocker): Longer acting
    3. Labetalol: After ɑ-blockade
  2. Adrenalectomy (4-6 weeks after)
‣
🤔 Other
‣
Multiple endocrine neoplasia (MEN)

What neoplasias make up the following conditions?

‣
MEN 1
  • Pituitary
  • Parathyroid
  • Pancreas - Insulinoma (hypoglycaemia following exercise/fasting), gastrinoma
‣
MEN 2A
  • Parathyroid
  • Pheochromocytoma
  • Medullary thyroid (C-cells)
‣
MEN 2B
  • Medullary thyroid (C-cells)
  • Pheochromocytoma
  • Marfanoid habitus
  • Neuromas
‣
Stress response
‣
What are the main hormones raised?
  • Cortisol
  • Aldosterone
  • Adrenaline
  • GH
  • Glucagon
‣
What hormones are suppressed?
  • Insulin - need more glucose in stress situations
  • Testosterone
  • Oestrogen
‣
What hormones don't change?
  • TSH
  • FSH & LH
‣
What drug class suppresses hypothalamic and pituitary hormone secretion?
  • Opioids
‣
Obesity: Medications
‣
What is orlistat?
  • Pancreatic lipase inhibitor causing reduction in appetite
‣
What are the indications for its administration?
  • BMI ≥ 28 & associated RFs
  • BMI ≥ 30
  • Need to show sustained WL and not usually used for > 1 year

🤘🏼 Rheumatology

‣
🦴 Bone & Joint
‣
Cases

What is the diagnosis based on the following presentations:

‣
65 year old obese patient presents with joint pain that is is worse when exercising and relieved by rest.
  • Osteoarthritis
‣
Patient presents with burning sensation over the antero-lateral thigh.
  • Meralgia paraesthetica
    • ‣
    What causes it?
    • Compression of lateral cutaneous nerve (trauma, obesity, tight clothing)
‣
Patient presents with hip pain. O/E: Hip extended with a straight leg and as the knee is bent there is severe pain.
  • Referred lumbar spinal pain to the hip
  • Trapped femoral nerve (L3/4)
‣
70 year old female patient presents with pain & tenderness over the lateral thigh.
  • Greater trochanteric pain syndrome (Trochanteric bursitis)
  • Repeated IT band movement
‣
Pregnant lady presents with pain over the pubic region that radiates into the groins and medial thigh. You notice a waddling gait.
  • Pubic symphysis dysfunction
‣
Patient presents with hand pain worse in the morning that improves when moving it, and also has abnormal nodules on the skin and SOB.
  • Inflammatory arthritis, e.g. rheumatoid
‣
Bone density
‣
Osteoporosis
‣
Name the 2 main risk factors.
  1. Corticosteroids
  2. Menopause
‣
What endocrine disorders can cause osteoporosis?
  1. Premature menopause
  2. Hyperthyroidism
  3. Hyperparathyroidism
  4. Hypogonadism (primary/secondary)
‣
What score can give us a fracture probability percentage?
  • FRAX: FRAX takes clinical risk factors for fracture and bone mineral density scores at the femoral neck to calculate a 10-year fracture probability for men and women.
‣
How do you measure the extent of osteoporosis? How is it quantified?
  • DEXA scan
  • T-score: The number of standard deviations the patient is from an average healthy young adult.
    • Result
    Diagnosis
    T > -1.0
    Normal
    -1.0 > T > -2.5
    Osteopenia
    T < -2.5
    Osteoporosis

Management:

‣
What are the key three considerations in management?

Considerations based on BMJ Best Practice Management Algorithm:

  1. Glucocorticoid-induced or not?
  2. Male or female?
  3. What is their T-score? (How severe is the osteoporosis?)
‣
What are the two key management options?
  1. Lifestyle: Stop smoking, increase exercise, limit alcohol.
  2. Bisphosphonates
    3. ‣
    What do they do?
    • Reduce osteoclast activity and their reabsorption of bone → Increase bone mineral density (BMD) and decrease risk of vertebral and non-vertebral fractures.
    ‣
    What key risk factors do you need to educate them on?
    • Upper GI: Difficulty swallowing, oesophagitis, and gastric ulcers
    • Osteonecrosis of the jaw
    • Atypical femoral fractures
    • Joint and muscular pain
    ‣
    What advice should you give them for taking oral bisphosphonates?
    • Taken them on an empty stomach with a full glass of water. After, sit upright for 30 minutes before moving or eating to reduce the risk of reflux and erosions of the oesophagus.
    ‣
    Name 2 examples.
    1. Alendronic acid (PO)
    2. Zolendronic acid (IV)
    ‣
    If on steroids, how does management of osteoporotic risk differ?
    • < 65 years old: DEXA scan (then treat if T score < - 1.5).
    • > 65 years old: Start alendronate immediately.
‣
What are the other options?
  1. Denosumab: Monoclonal antibody that targets osteoclasts
  2. Romosozumab: Monoclonal antibody that targets sclerostin, a protein in osteocytes that inhibits bone formation.
  3. Teriparatide: Acts as parathyroid hormone
  4. Hormone replacement therapy, particularly in women with early menopause
  5. Raloxifene: Selective oestrogen receptor modulator
‣
Paget's bone disease

Focal areas of increased bone remodelling, resulting in overgrowth of poorly organised bone.

‣
What is the underlying pathophysiology?
  • Overactivity of osteoclasts → Increased bone breakdown → Increased osteoblast activity → Formation of very dense areas of poorly formed bone
‣
How common is this?
  • 5% of the population
  • Only 5% of people with the disease are symptomatic
‣
What is the stereotypical presentation?
  • Older male presents with bone pain and has an isolated ↑ ALP
    • ‣
    What bones are most commonly affected?
    • Long bones: Femur, tibia
    • Skull
    • Pelvis/spine
‣
How is it investigated?
  • X-ray of symptomatic area
  • LFTs: Isolated ↑ ALP
Jmarchn, CC BY-SA 3.0
Jmarchn, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
How is it managed?
  • Bisphosphonates
‣
What are the main complications?
  1. Deafness
  2. Fractures
  3. Bone sarcoma
‣
Osteopetrosis

A group of rare disorders that cause bones to grow abnormally and become overly dense.

‣
How is it inherited?
  • Autosomal recessive
‣
What would you see on X-ray?
  • 'Marble bone'
Konstantinos C Soultanis, Alexandros H Payatakes2, Vasilios T Chouliaras, Georgios C Mandellos, Nikolaos E Pyrovolou, Fani M Pliarchopoulou and Panayotis N Soucacos, CC BY 2.0
Konstantinos C Soultanis, Alexandros H Payatakes2, Vasilios T Chouliaras, Georgios C Mandellos, Nikolaos E Pyrovolou, Fani M Pliarchopoulou and Panayotis N Soucacos, CC BY 2.0 creativecommons.org/licenses/by/2.0, via Wikimedia Commons. No changes were made.
‣
How would you manage them?
  • Depends on severity, symptoms and patient factors
  • Can include vitamin D supplements, steroids, surgery
‣
Osteogenesis imperfecta

This is an autosomal dominant abnormality of collagen metabolism resulting in bone fragility and fractures

‣
What are the characteristic features?
  • Fractures following minor trauma
  • Blue sclera
  • Otosclerosis → Deafness
‣
What do investigations show?
  • They’re NORMAL: Adjusted calcium, phosphate, parathyroid hormone and ALP

Key Conditions:

‣
Rheumatoid arthritis

A chronic inflammatory condition primarily affecting the small joints of the hands and feet.

‣
What are the key features?
  1. Symmetrical distribution (bilateral)
  2. Swollen, painful joints in hands & feet
    3. ‣
    What joints are commonly affected?
    • Proximal interphalangeal (PIP)
      • DIP never affected in RA (think Heberden's nodes in OA/psoriatic)
    • Metacarpophalangeal (MCP)
    • Wrist & ankle
  3. Worse in the morning, improves with movement
  4. Systemic involvement
‣
What deformities can you see on the following hand:
‣
Answer
  • Index, middle & ring finger: Swan neck → Snapped extensor tendon
  • Little finger: Boutonnieré → Snapped flexor tendon
Abdulaziz Alkanderi, CC BY-SA 3.0
Abdulaziz Alkanderi, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
Investigations:
‣
What bloods are needed to investigate?

Bloods:

  • Rheumatoid factor (positive in 60-70%)
  • Anti-CCP antibodies (positive in 70%)
‣
What are the key features on X-Ray?
  1. Loss of joint space
  2. Juxta-articular osteoporosis
  3. Soft-tissue swelling
  4. Periarticular erosions (late): Dark areas
  5. Subluxation: Dislocation (late)
Bernd Brägelmann Braegel Mit freundlicher Genehmigung von Dr. Martin Steinhoff, CC BY 3.0
Bernd Brägelmann Braegel Mit freundlicher Genehmigung von Dr. Martin Steinhoff, CC BY 3.0 creativecommons.org/licenses/by/3.0, via Wikimedia Commons. No changes were made.
Mikael Häggström, CC0, via Wikimedia Commons
Mikael Häggström, CC0, via Wikimedia Commons
‣
What other investigation is useful & why?
  • Joint ultrasound to evaluate synovitis
‣
What is seen on joint aspiration?
  • ↑ WCC (predominantly neutrophils)
  • Yellow & cloudy, no crystals
James Heilman, MD, CC BY-SA 3.0
James Heilman, MD, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
What is the first-line therapy?
  1. DMARD: Methotrexate (7.5mg OW)
    • Folate supplementation
  2. Steroids: Prednisolone (1-10mg PO OD)
    • IM methylprednisolone is another option for acute flare
    • Low dose is required apart from if they develop eye involvement or vasculitis, then higher doses may be needed
    • PPI to prevent GI bleed
‣
How is the response to treatment monitored?
  • Disease activity scoring: DAS28 (Assesses 28 joints)
    • Points for: Swelling, tenderness & ESR/CRP result
  • Monitoring if on DMARD (4-8W at start then 3-4M)
    • FBC: Hb (anaemia), WCC
    • LFT: ALT/AST
‣
What other options are there for treatment resistant RA?
  • Second-line: Add sulfasalazine/leflunomide
  • Third: Methotrexate + Infliximab, adalimumab, etanercept (anti-TNF)
  • Fourth: Methotrexate + Rituximab (anti-CD20)
    • Destroys B-cells
‣
Name 5 complications of RA.
  1. Eyes: Sjogren's syndrome (sicca syndrome), episcleritis, scleritis
  2. Skin: Rheumatoid nodules, vascular lesions
  3. Cardiac: Coronary artery disease, pericarditis
  4. GI: Oesophagitis, gastritis, hepatotoxicity of DMARDs
  5. Haematology: Anaemia, Felty’s syndrome, thrombocytosis
  6. Atlantoaxial subluxation
    7. ‣
    When do you need to consider this?
    • Any surgery under GA: Requires neck movement
    ‣
    How do you investigate for this?
    • Anteroposterior and lateral cervical spine radiographs

What is the diagnosis based on the following presentation:

‣
A 42 year old man with rheumatoid arthritis presents with splenomegaly and neutropenia.
  • Felty's syndrome (SANTA)
    • Splenomegaly
    • Anaemia
    • Neutropenia
    • Thrombocytopenia
    • Arthritis (rheumatoid)
‣
A 48-year-old woman presents with fatigue and you see positive ANA 6 months ago on the computer. She’s presenting with a feeling of sand/gravel in her eyes and a dry mouth that started 3 months ago.
  • Sjogren's syndrome
    • ‣
    What is the pathophysiology of this condition?
    • Antibodies form against exocrine glands → Dry mucosal surfaces
    ‣
    What malignancy are these patients at risk of?
    • Lymphoid malignancy
    ‣
    What systems are affected?

    The following will be dry:

    • Eyes (keratoconjunctivitis sicca)
    • Mouth
    • Vagina
    ‣
    How is it managed?
    • Artificial saliva & tears
    • Pilocarpine: Stimulates saliva production
‣
An 18-year-old healthy woman presents with fingertips that turn white, then blue and red, in the cold.
  • Raynaud’s phenomenon: Vasospasm that causes digits to change colour to white from lack of blood flow, usually brought on by cold temperatures.
    • ‣
    How does primary differ from secondary?
    • Primary:
      • Bilateral
      • Presents in 30-40 year olds
    • Secondary:
      • Unilateral
      • Patient has positive inflammatory markers/comorbidities
    ‣
    What is the pathophysiology?
    • Arterial spasm within the hands → Reduced blood flow (pale skin) → Tissue hypoxia (cyanosed skin) → Reperfusion (Very red skin)
    ‣
    Name 2 secondary causes.
    • Scleroderma (most common)
    • Rheumatoid arthritis
    ‣
    What is first-line management?
    • CCB, e.g. nifedipine
‣
Osteoarthritis
‣
How does osteoarthritis develop?

Wear & tear → Loss of articular cartilage → Bone remodelling → Inflammatory changes

‣
What is a typical presentation? What joints are affected? (4)
  • Elderly individual presents with unilateral joint pain in a large, weight bearing joint
  • Joints:
    • Fingers - DIP (Heberden's node), PIP (Bouchard's nodes), carpometacarpal
    • Knee
    • Hip
      • image
‣
Name 4 X-ray changes.
  1. Loss of joint space
  2. Subchondral sclerosis
  3. Subchondral cysts
  4. Osteophytes
image
‣
What are the 3 conservative management steps?
  1. Paracetamol & topical NSAIDs
  2. Oral NSAIDs + PPI / Opioids
  3. Intra-articular steroids
‣
Seronegative arthropathies

Inflammatory arthritis but without a positive rheumatoid factor, hence seronegative.

‣
Ankylosing spondylitis
‣
Diagram: The pathophysiological process
Senseiwa
Senseiwa, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0/, via Wikimedia Commons. No changes were made.
‣
What age and gender typically present with this?
  • Men between 20-30 years
‣
What symptoms will they have? (2)
  • Lower back pain & stiffness
    • Early sign: Reduced lateral flexion of spine
  • Usually worse in the morning & improves with exercise
‣
What will be seen on examination?
  • Reduced lumbar mobility
    • Reduced lateral spinal movement (first sign)
    • Shöber's test: Distance between lines changes by < 5cm
  • Reduced chest expansion
‣
Name the other features.
  1. Aortic regurgitation
  2. AV node block
  3. Amyloidosis
  4. Apical fibrosis
  5. Anterior uveitis
  6. Achilles tendonitis
‣
What is the key X-ray finding for diagnosis?
  • Sacroiliitis
‣
What features are present on the following X-rays:
‣
X-ray 1
‣
Answer
  • Bamboo spine: Fusion of vertebrae
  • Dagger sign: Ossification of supraspinous and interspinous ligaments
Stevenfruitsmaak, CC BY-SA 3.0
Stevenfruitsmaak, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
X-ray 2
‣
Answer
  • Squaring of lumbar vertebrae: Osteitis of anterior corners
  • Syndesmophytes: Ossification of annulous fibrosus
James Heilman, MD, CC BY-SA 4.0
James Heilman, MD, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.
‣
How would you manage a patient with AS?
  1. NSAIDs & regular exercise
  2. Physiotherapy
  3. Anti-TNF drugs: Etanercept & adalimumab
    • Indicated after 2 NSAIDs have been tried
‣
Psoriatic arthropathy
‣
Why is this difficult to diagnose?
  • Often presents before cutaneous psoriasis
‣
How do you differentiate psoriatic arthropathy from other causes of joint pain? (3)
  1. Look for nail changes: Onycholysis/dactylitis (finger & toe inflammation)
  2. X-ray: Pencil-in-cup deformity
  3. DIP is commonly affected (differential for OA)
  4. Cutaneous rash
image
image
‣
Reactive arthritis/Spondyloarthropathy
‣
What features point towards reactive arthritis?
  • Recent infection within the last 4 weeks
  • 'Can't see, can't pee, can't climb a tree'
    • Conjunctivitis, balanitis, arthritis
  • Invx: No infection seen on joint aspiration (aseptic arthritis)
‣
What rash can be seen on the feet?
  • Keratoderma blenorrhagica
image
‣
Name the 3 stages of management.
  1. Analgesia & NSAIDs
  2. Intra-articular steroids
  3. Methotrexate/sulphasalazine

Uncommon:

‣
Enteropathic arthropathy
‣
What is the typical presentation of this?
  • Peripheral joint inflammation occurring alongside a flare of Crohn's or UC
‣
Still's disease
‣
What are the common features?
  • High pyrexia (> 39°C) at night that settles by the morning
  • Arthralgia that worsens with the fever at night
  • Rash: salmon-pink, maculopapular
‣
What is this called in children?
  • Juvenile idiopathic arthritis (JIA)
‣
How is it managed?
  1. NSAIDs (1W trial)
  2. Steroids
  3. Methotrexate
‣
Crystal arthropathies
‣
Gout
‣
When is urate produced & where is it excreted?
  • Produced during the metabolism of DNA & RNA both of cells and dietary purines
  • Excreted through the kidneys
‣
What joint does this usually present in? Name 3 others. (4)
  1. 1st MTP joint - Great toe
  2. Knee
  3. Ankle
  4. Wrist
‣
What is found on joint aspiration?
  • Strong-negatively birefringent needle-shaped crystals
Gabriel Caponetti, CC BY-SA 3.0
Gabriel Caponetti, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons
‣
What are the radiological features? (3)
  1. Joint space retained
  2. Joint effusion
  3. 'Punched out' erosions (well-defined)
‣
Name 6 RFs for gout.
  • ↑ production: Cell breakdown
    1. Myelo-/lympho-proliferative disease (leukaemia)
    2. Chemotherapy
    3. Severe psoriasis
  • ↓ excretion
    1. Diuretics - thiazide
    2. CKD
    3. Lead toxicity
‣
What is defined as a high urate?
  • > 450
‣
How is it acutely managed?
  1. NSAIDs (naproxen + PPI)

OR

  1. Colchicine - SE: Diarrhoea
  2. PO steroids
  3. Intra-articular steroids
‣
How is it managed in the long-term? When is this indicated?
  • Allopurinol
    • Indicated: After first attack of acute gout
    • Wait for the acute episode to settle before starting as may worsen it
‣
What is the urate target for successful long-term management?
  • Management < 300
‣
Pseudogout
‣
What crystals are seen in the joint?
  • Calcium pyrophosphate
‣
Name 3 risk factors.
  1. Haemochromatosis
  2. Hyperparathyroidism
  3. Acromegaly
‣
What joints are commonly affected? (3)
  • Knee
  • Shoulder
  • Wrist
‣
What is seen on X-ray?
  • Chondrocalcinosis - Linear calcification of the articular cartilage
Taokinesis (Pixabay profile) Annotated by Mikael Häggström, CC0, via Wikimedia Commons
Taokinesis (Pixabay profile) Annotated by Mikael Häggström, CC0, via Wikimedia Commons
‣
What is seen on joint aspiration?
  • Weak-positively birefringent rhomboid-shaped crystals
  • No bacteria (exclude septic arthritis)
Mikael Häggström, M.D., CC0, via Wikimedia Commons
Mikael Häggström, M.D., CC0, via Wikimedia Commons
‣
How is it managed? (2)
  • NSAIDs
  • Steroids (PO → intra-articular)
‣
🧻 Connective Tissue
‣
Systemic lupus erythematosus (SLE)
‣
What age range and gender usually present with this?
  • Women
  • Afro-caribbean
  • 20-40 years
‣
What is the pathophysiology?
  • Antibodies to the cell nucleus & DNA form (type III hypersensitivity) → Systemic inflammation
‣
Features

How does it manifest in the following systems:

‣
Skin
  • Photosensitive malar rash (nasolabial sparing)
  • Scaly, erythematous, well-demarcated rash
‣
Cardiac & respiratory
  • Pericarditis
  • Pleurisy
‣
MSK
  • Arthritis (no XR changes - non-erosive)
  • Arthralgia
‣
Renal
  • Glomerulonephritis
‣
What is a typical presentation of drug-induced lupus?
  • A patient presents with SLE features after starting a drug, commonly arthralgia, myalgia and cutaneous manifestations
    • ‣
    What antibody is diagnostic?
    • Anti-histone
    ‣
    What drugs commonly cause it?
    1. Hydralazine
    2. Procainamide (anti-arrhythmic)
    3. Isoniazid
    4. Phenytoin
‣
How do you investigate it?
  • Antibodies: ANA, anti-dsDNA, anti-smith
  • ↓ complement (C3 & C4)
  • FBC: Normocytic anaemia of chronic disease
  • Urinalysis - Lupus nephritis
‣
How is it monitored?
  • ESR
‣
What is first-line for mild disease?
  • Hydroxychloroquine & avoiding sun/suncream
‣
What may be used in more severe disease?
  • NSAIDs, steroids
  • Methotrexate, azathioprine, tacrolimus
  • Biologics - Rituximab
‣
Systemic sclerosis (Scleroderma)
‣
What does sclerderma mean?
  • Sclero - hardening, derma - skin
‣
What is it?
  • Autoimmune connective tissue disease leading to fibrosis, affecting the skin and internal organs
‣
What are the 2 main patterns of disease?
  1. Limited cutaneous
    2. ‣
    What are the features of this?

    CREST syndrome

    Calcinosis
    Calcium deposits in the skin
    Raynauds
    Spasm of blood vessels in response to cold or stress
    Esophageal dysfunction
    Acid reflux and decrease in motility of esophagus
    Sclerodactyly
    Thickening and tightening of the skin on the fingers and hands
    Telangiectasias
    Dilation of capillaries causing red marks on the surface of the skin
    ‣
    How does sclerodermic skin look?
    • Tight, shiny skin without normal skin folds
    ‣
    How does oesophageal dysmotility present?
    • Heartburn
    ‣
    What is sclerodactyly?
    • Thickening of skin on the fingers reduces their range of motion
    • Skin can become so tight that it breaks & ulcerates
    ‣
    What are telangiectasia?
    • Dilated small blood vessels with a fine, thready appearance
  2. Diffuse
    3. ‣
    How is this different?
    • All of the features above and internal organs are affected
    ‣
    Give examples of effects. (4)

    Connective tissue of organs undergoes fibrosis, therefore causing:

    • Cardiovascular: Hypertension (↑ SVR), coronary artery disease
    • Pulmonary: Pulmonary hypertension/fibrosis (sclerosis)
    • Renal: Glomerulonephritis, scleroderma renal crisis (combination of hypertension & AKI)
‣
What antibodies do you need to test for?
  1. ANA: Positive in most
  2. Anti-centromere antibodies: Limited cutaneous
  3. Anti-SCL-70 antibodies: Diffuse
‣
Why do you do nailfold capillaroscopy?
  • Examines the health of peripheral capillaries
  • Differentiates idiopathic Raynaud's (normal capillaries) from SS (abnormal)
‣
How are they managed?

MDT approach:

  1. Lifestyle: Avoid smoking, skin stretching, emmolients, avoiding cold
  2. Medical:
    • Steroids, immunosuppression
    • Raynauds → Nifedipine
    • Oesophagus → Omeprazole (acid), metoclopramide (motility)
‣
Polymyositis/Dermatomyositis
‣
What symptoms will individuals with these conditions?
  • Proximal muscle weakness
    • As opposed to PMR where these patients will have stiffness but not weakness.
‣
What do you need to consider when seeing a patient with this condition?
  • Is there an underlying malignancy?
    • This is commonly a paraneoplastic condition
    • Lung, breast, ovarian & gastric cancer
‣
What is the difference between the two?

Myositis: Muscle inflammation

  • Poly: Inflammation of the muscles
  • Dermato: Inflammation of the skin & muscles
‣
What does the following picture show:
‣
Answer
  • Gottron's papules
‣
What does this signify?
  • Dermatomyositis
Elizabeth M. Dugan, Adam M. Huber, Frederick W. Miller, Lisa G. Rider, CC BY-SA 3.0
Elizabeth M. Dugan, Adam M. Huber, Frederick W. Miller, Lisa G. Rider, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.

Investigations & Management:

‣
What is the key investigation when diagnosing this & what result are you looking for?
  • Creatine kinase (released from muscles when damaged)
  • > 1000 U/L
‣
What antibodies are found in the two types?
  1. Anti-Jo-1
  2. ANA
‣
What can give a definitive diagnosis?
  • Muscle biopsy
‣
What is the first-line treatment for both?
  • Corticosteroids

Congenital:

‣
Marfan syndrome
‣
What is the inheritance pattern & pathophysiology?
  • Autosomal dominant mutation in the gene coding for fibrillin, an important component of connective tissue → Increased elasticity
‣
Name 4 features.
  1. Arachnodactyly → Long fingers
  2. Hypermobility of joints
  3. Pectus excavatum/carinatum
  4. Tall, slender build
‣
Name 2 cardiac complications & 1 respiratory.
  1. Aortic sinus dilation (90%) (Also: Dissection)
  2. Mitral valve prolapse (75%)
  3. Recurrent pneumothoraces
‣
How is it monitored & managed?
  • Monitored: Annual echocardiogram
  • Managed: Beta-blocker/ACE-i
‣
Ehlers-Danlos syndrome
‣
What is the inheritance pattern?
  • Autosomal dominant
‣
What is the pathophysiology?
  • Type III collagen defect → Tissue elasticity → Hypermobility
‣
What are the features?
  • Skin elasticity
  • Joint hypermobility
‣
What is used to assess hypermobility?
  • Beighton score
‣
Name 2 complications.
  • Recurrent joint dislocation
  • Mitral regurgitation
‣
🌯 Vasculitis
‣
Giant cell arteritis
‣
Temporal arteritis
‣
What are the main features?
  1. Scalp tenderness
  2. Headache
  3. Jaw claudication (headache worse when talking for prolonged periods)
  4. Visual changes (blurred vision)
  5. > 65 years
‣
How is it investigated & what value is diagnostic?
  1. ESR > 50 → GCA
  2. Temporal artery biopsy (skip lesions mean this test isn't specific)
‣
How is it managed?
  • Acute: Prednisolone 60mg STAT → Rapid recovery
  • Urgent review by ophthalmology
‣
Polymyalgia rheumatica (PMR)
‣
What is present on histology?
  • Giant cell vasculitis with infiltration of lymphocytes & inflammation causing a small lumen
‣
What is the characteristic presentation?
  • Proximal limb stiffness without muscle weakness/wasting
    • Shoulder
    • Hip
‣
How do you differentiate this from polymyositis?
  • Weakness: No weakness in PMR, just stiffness. Weakness in polymyositis
  • CK: Normal CK in PMR
‣
How do you investigate this?
  • ESR > 40 → PMR
  • CK (rule out polymyositis) & EMG normal
  • Biopsy for histology
‣
How do you manage this?
  • Prednisolone 60mg STAT → Rapid recovery

What is the diagnosis based on the following presentation:

‣
A 17 year old patient presents with severe asthma and elevated eosinophil levels on FBC. Their pANCA is positive.
  • Eosinophilic granulomatosis with polyangiitis
  • Associated with sinusitis, asthma, purpurae, peripheral neuropathy and glomerulonephritis
‣
A 21-year-old woman goes to the emergency department with some chest pain. The registrar is troubled that he cannot feel either radial pulse, even though the triage sheet shows the patient to be hypertensive.
  • Takayasu’s arteritis ("pulseless disease")
  • Causes large arteries to form aneurysms or become narrowed & blocked
‣
An 8-year-old patient who had tonsillitis 1 week ago presents with joint pain, abdominal pain and the following rash affecting the lower limbs & buttocks:
Peter Rammstein, CC BY 3.0
Peter Rammstein, CC BY 3.0 creativecommons.org/licenses/by/3.0, via Wikimedia Commons. No changes were made.
‣
What’s the diagnosis?
  • Henoch-Schonlein purpura
‣
What investigation is key?
  • U&E to look for renal involvement as he may have IgA nephropathy
‣
A young, male smoker presents with an acutely ischaemic right foot with absent pulses.
  • Buerger's disease (Non-atherosclerotic vasculitis → Occlusive thrombus)
    • Corkscrew-shaped collateral vessels distally
      • ‣
      What is the main management of this?
      • Smoking cessation
‣
A patient with known Hepatitis B presents with the following rash:
‣
Diagnosis?
  • Polyarteritis nodosa - Results in aneurysms & thrombosis
    • Rash: Livedo reticularis
    • Affects skin, GI tract, kidneys & heart
Nantsupawat T et al, CC BY-SA 3.0
Nantsupawat T et al, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons
‣
A patient presents with recurrent epistaxis, crusty nasal secretions & haemoptysis. Their nose looks as follows:
Vw38, CC BY-SA 4.0
Vw38, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.
‣
Diagnosis?
  • Granulomatosis with polyangiitis
‣
What antibodies will she have?
  • c-ANCA
‣
What will the CXR show?
  • Pulmonary infiltrates/consolidation from vascular damage
‣
What other organ does it commonly affect?
  • Kidney causing glomerulonephritis
    • ‣
    This makes it a differential for what condition?
    • Goodpasture’s as can cause glomerulonephritis & haemoptysis
‣
A 28-year-old female presents with recurrent DVT on a history of SLE.
  • Antiphospholipid syndrome
    • ‣
    Antibody?
    • Anti-cardiolipin
    ‣
    Investigations?
    • FBC: Thrombocytopenia
    • Clotting: Prolonged APTT
    ‣
    Management?
    1. Lifelong warfarin: INR target 2-3
    2. DVT occurs on warfarin: Increase target INR to 3-4
‣
A patient has a history of recurrent oral ulcers and genital ulcers. They have now presented with anterior uveitis.
  • Behçets syndrome (clinical diagnosis)
    • ‣
    What else is this associated with?
    • Erythema nodosum
‣
💂🏼‍♂️ Antibodies

Name the condition most commonly associated with the following antibodies:

‣
Anti-CCP
  • Rheumatoid arthritis
‣
Anti-SCL-70
  • Diffuse systemic sclerosis
‣
Anti-centromere
  • Limited cutaneous systemic sclerosis (CREST)
‣
Anti-histone
  • Drug-induced SLE
‣
Anti-Ro & anti-La
  • Sjogren's syndrome
‣
Anti-Jo-1
  • Dermatomyositis
‣
Anti-cardiolipin
  • Anti-phospholipid syndrome
‣
Anti-Smith
  • SLE
‣
pANCA/MPO-ANCA
  • Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)
    • Also can be raised in IBD
‣
cANCA
  • Granulomatosis with polyangiitis (Wegener's)
‣
💊 Drugs
‣
What are the side effects of the following drugs:
‣
All immunosuppressants (1)
  • Myelosuppression → Neutropenia & infection risk
‣
Methotrexate (3)
  1. Pneumonitis
  2. Mucositis
  3. Myelosuppression
    4. ‣
    What needs to be monitored while a patient is on methotrexate?
    • FBC: Myelosuppression, folate deficiency (macrocytic anaemia)
    • LFT: Liver damage
    • U&E
    ‣
    How is methotrexate toxicity managed?
    • Folinic acid
    ‣
    What drug can never be given with methotrexate?
    • Trimethoprim/co-trimoxazole
    ‣
    How long do they need to be off methotrexate before trying for a baby?
    • 6 months
‣
Corticosteroids (5)
  1. Cushing's syndrome (SWEDISH)
  2. Osteoporosis
  3. Addison's (when withdrawn fast)
  4. Hypertension
  5. GORD
  6. Hyperglycaemia
‣
Ciclosporin (5)
  1. Hypertrophy of the gums
  2. Hypertrichosis
  3. Hypertension
  4. Hyperkalaemia
  5. Hyperglycaemia (diabetes)
‣
Leflunomide (2)
  • Hypertension
  • Peripheral neuropathy
‣
Sulfasalazine (1)
  • Male infertility (reduces sperm count)
‣
Hydroxychloroquine (1)
  • Bull's eye retinopathy - may result in severe and permanent visual loss
    • Monitor visual acuity
‣
Anti-TNF (1)
  • Reactivation of TB or HepB
‣
Rituximab (2)
  • Night sweats
  • Thrombocytopenia
‣
Azathioprine (1)
  1. Pancreatitis
    2. ‣
    What should never be prescribed with this?
    • Allopurinol
‣
Which anti-inflammatory drug used for IBD is safe in pregnancy?
  • Azathioprine
‣
Alendronic acid
‣
Name 3 indications for alendronic acid.
  1. Osteoporosis
  2. Paget's disease
  3. Hypercalcaemia
‣
Name 3 adverse effects of alendronic acid.
  1. Pathological fractures along stress lines
  2. Oesophageal reactions: Oesophagitis, ulcers
  3. Osteonecrosis of jaw
‣
What advice needs to be given when prescribing alendronic acid?
  • Give 30 mins before breakfast (empty stomach)
  • Swallow whole with plenty of water
  • Stay sat/stood upright for 30 mins after taking drug

🧠 Neurology

‣
🧠 Central Nervous System
‣
Brain
‣
Headaches
‣
Primary
‣
Migraine
‣
What features can you get?
  • Premonitory phase: Yawning, mood changes etc
  • Unilateral throbbing headache (often)
  • Nausea and vomiting
  • Aura e.g. zig zag lines in vision
  • Photophobia
  • Impairs capacity to function: impairs activities of daily life
  • Can have triggers: varies between patients e.g. coffee, chocolate
‣
Pathophysiology
  • Cortical spreading depression: self-propogating
  • Meningeal nerves affected
‣
How long does it last?
  • 4-72 hours
‣
Management?
  • Stop analgesia (never treat headaches with analgesia) and caffeine
  • Acutely: Triptans
‣
2 options for prophylaxis?
  • Propanalol
  • Topiramate
‣
Trigeminal Autonomic Cephalgia
‣
Cluster headache
‣
What features can you get?
  • Excruciating pain around one eye (always affects same eye)
  • Eye redness, swelling, sweating, lacrimation
  • Runny nose
  • Restlessness- patient cannot sit still
‣
How long does it last, and how often?
  • 15 mins – 2 hours. Clusters occurs every 4 – 12 weeks typically
‣
What is the common trigger?
  • Alcohol
‣
Management?
  • High dose oxygen
  • Sumatriptan
  • High-dose prednisolone over 48h
  • Long term: Verapamil
‣
Name 3 other differentials.
  1. Paroxysmal hemicrania
  2. SUNCT
  3. Hemicrania continua
‣
Trigeminal neuralgia
‣
What is it?
  • Unilateral electric shock-like pains that are quick in both onset and termination, following the distribution of the trigeminal nerve.
    • Common triggers: Light touch, smoking, talking, and brushing teeth
‣
What can cause it?
  • Idiopathic (majority of cases)
  • Secondary: Tumour, vascular issues
    • ‣
    What features are suggestive of a secondary cause?
    • Sensory changes
    • Deafness or other ear problems
    • Pain only in the ophthalmic division of the trigeminal nerve or bilaterally
    • Optic neuritis / family history of MS
    • Age of onset before 40 years
‣
What’s the first-line management?
  • Carbamazepine
‣
Tension
‣
What features can you get?
  • Bilateral headache like a 'tight band across forehead', mild ache, non-disabling
‣
Management?
  • Reassurance
  • Basic analgesia
  • Relaxation techniques, hot towels to local area
‣
Secondary

Covered elsewhere: CNS infection, SAH, temportal arteritis, raised ICP, SOL, glaucoma, instracranial hypotension.

‣
Idiopathic intracranial hypertension (IIH)
‣
Who classically in exams gets this?
  • Obese women
‣
Management?
  1. Weight loss & close monitoring
  2. Carbonic anhydrase inhibitors - Acetazolamide
‣
What are your differentials for facial pain?
  1. Trigeminal neuralgia
  2. Post-herpetic neuralgia
  3. TMJ syndrome
  4. Giant cell arteritis
  5. Dental pain
‣
Vascular
‣
Stroke
‣
What scoring system is useful in recognising stroke?
  • Rosier score: Any score above 0 indicates stroke is likely
    • Lose points: Syncope/seizure
    • Gain points: Weakness
image
‣
A patient presents with stroke, what invstigation is key & why?
  • CT head: Ischaemic or haemorrhagic?

Classifying:

‣
Ischaemic (85%)
‣
Classification
‣
What are the subtypes & features of them?
  • Cerebral - Contralateral hemiplegia (flaccid then spastic), contralateral hemi-sensory loss, dysphasia, contralateral homonymous hemianopia & contralateral visuo-spatial deficit
  • Brainstem - Quadriplegia, cranial nerve deficits & disorders of consciousness (e.g. locked-in syndrome)
  • Lacunar (basal ganglia) 1 of 5 syndromes:
    • Pure motor
    • Pure sensory
    • Sensorimotor
    • Ataxic hemiparesis
    • Dysarthria
‣
Brainstem strokes:

Name the artery affected from the presentation:

‣
Complete quadriparesis and lower cranial nerve dysfunction, with preserved consciousness.
  • 'Locked in syndrome': Basilar artery
‣
Ipsilateral oculomotor nerve palsy and contralateral hemiparesis.
  • Weber syndrome: Branches of upper basilar and proximal posterior cerebral arteries
Madhero88, CC BY-SA 3.0
Madhero88, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
Loss of contralateral pain/temperature on the body, ipsilateral facial paralysis, ipsilateral deafness and tinnitus, ipsilateral ataxia.
  • Lateral pontine syndrome: Anterior inferior cerebellar artery
    • Blood supply to the pons is lost, so these nerves are affected
‣
Ipsilateral Horner's syndrome, ipsilateral loss of pain and temperature sensation on the face, and contralateral loss of pain and temperature sensation over the contralateral body
  • Lateral medullary syndrome: PICA
    • C.N. IX, X & XII affected - Dysphagia (another presentation)
‣
Diagram: Cerebral Vascular Territories
derivative work: Frank Gaillard (talk)Brain_human_sagittal_section.svg: Patrick J. Lynch, medical illustrator, CC BY-SA 3.0
derivative work: Frank Gaillard (talk)Brain_human_sagittal_section.svg: Patrick J. Lynch, medical illustrator, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
derivative work: Frank Gaillard (talk) Brain_stem_normal_human.svg: Patrick J. Lynch, medical illustrator, CC BY-SA 3.0
derivative work: Frank Gaillard (talk) Brain_stem_normal_human.svg: Patrick J. Lynch, medical illustrator, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
What is the Bamford-Oxford classification?

What symptoms are required for:

‣
Total anterior circulation infarct (ACA + MCA)
  • Contralateral hemiplegia or hemiparesis, AND
  • Contralateral homonymous hemianopia, AND
  • Higher cerebral dysfunction (e.g. aphasia, neglect)
‣
Partial anterior circulation infarct (ACA / MCA)
  • 2/3 of the above
  • Higher cerebral dysfunction alone
‣
Lacunar stroke (Deep perforating arteries)

One of the following:

  • Cerebellar dysfunction
  • Conjugate eye movement disorder
  • Bilateral motor/sensory deficit
  • Ipsilateral cranial nerve palsy with contralateral motor/sensory deficit
  • Cortical blindness/isolated hemianopia
‣
Investigations
‣
What is most commonly used investigation?
  • CT head (non-contrast)
‣
What is the gold standard investigation?
  • Diffusion-weighted MRI
‣
How would you investigate if this is secondary to carotid stenosis?
  • Carotid ultrasound
‣
Management
‣
What is the immediate management?
  1. Aspirin 300mg
  2. Thrombolysis with alteplase (if within 4.5 hours of symptom onset)
    3. ‣
    What is alteplase?
    • A tissue plasminogen activator that rapidly breaks down clots, puts patient at risk of intracranial or systemic haemorrhage
  3. Thrombectomy (within 6 hours) - mechanical removal of the clot
‣
When would you need to do a craniectomy?
  • Malignant MCA syndrome - Swelling around area causes midline shift and raised ICP
‣
What secondary prevention may be needed?
  1. Lifestyle: Diet, exercise, smoking cessation
  2. Manage risk factors: Hypertension, DM, etc.
    • Patients with carotid artery disease may need carotid endarterectomy or stenting.
  3. Medications:
    • Clopidogrel 75mg OD for life (or dipyridamole 200mg BD)
    • Atorvastatin 80mg (but not immediately started)
‣
What is the score to classify disability in stroke?
  • Modified Rankin Scale
‣
Haemorrhagic (15%)
‣
What are the key risk factors? (6)
  • Age
  • Male
  • Family history
  • Anticoagulation, sympathomimetic drugs (such as cocaine & amphetamines)
  • Haemophilia, cerebral amyloid angiopathy/hypertension, AVM
  • Alcohol
‣
How would you manage a haemorrhagic stroke if patient is on warfarin?
  1. Stop warfarin
  2. Give IV vitamin K 5mg
  3. Give prothrombin complex concentrate (or FFP if not available)
‣
TIA
‣
What criteria are used to assess a TIA?

ABCD-2

  • Age ≥ 60 years (1)
  • BP > 140/90 (1)
  • Clinical features
    • Unilateral weakness (2)
    • Isolated speech impairment (1)
  • Duration
    • > 60 mins (2)
    • 10 - 59 mins (1)
  • 2
‣
What score in this criteria represents high risk & how are these managed?
  • Score ≥ 4
  • 300mg of aspirin immediately, then assessed by a specialist within 24 hours
‣
How are all TIA patients managed if on anticoagulation?
  • Immediate referral to A&E for CT head to look for bleed
‣
What are the medical management options?
  1. Control RFs: HTN, lipids
  2. Antiplatelets: Aspirin 300mg for 2 weeks followed by clopidogrel 75mg
  3. Anticoagulation: If TIA associated with AF
‣
When is carotid endarterectomy indicated?
  • Stenosis > 70% on doppler
‣
Intracranial bleeds
‣
Epidural
‣
How is this surgically managed?
  • Ligation of the artery
‣
Subdural
‣
How is this surgically managed?
  • Clot not organised: Burr hole craniostomy
  • Clot organised: Craniotomy
‣
Sub-arachnoid
‣
What is this commonly associated with?
  • Polycystic kidney disease (linked to berry aneurysms)
‣
How are they investigated?
  1. Urgent CT head - If positive begin treatment, if negative see below
  2. LP 12 hours after headache onset - Xanthochromia
‣
How is this surgically managed?
  1. Endovascular coiling
  2. Surgical clipping
‣
Why do they start nimodipine after surgery?
  • Used to prevent vasospasm of the cerebral vessels, optimising brain perfusion
‣
Basal skull fracture
‣
What are the key features?
  1. 'Panda/raccoon eyes' - Periorbital ecchymoses
  2. CSF rinorrhoea/otorrhoea
  3. 'Battle sign' - Retroauricular ecchymoses
image
‣
Venous sinus thrombosis
‣
What features are suggestive of this?
  • Prothrombotic RFs: Smoking, FH of DVT/SLE, COCP
  • Sudden onset severe headache - "Thunderclap"
  • Nerve compression → Papilloedema, eye movement disorders
‣
What is the gold-standard investigation?
  • MR venogram
‣
Movement disorders
‣
Parkinson's
‣
Features?
‣
Cardinal motor features?
  • Resting tremor
  • Cogwheel rigidity
  • Bradykinesia
‣
Other features?
  • Shuffling gait
  • Masked facies
  • Hypophonia
  • Autonomic dysfunction
  • Depression
  • Dementia
‣
What is the first-line management, & how is the patient's QoL relevant?
  • Motor symptoms affecting QoL: Levodopa
  • QoL not affected: Dopamine agonist
‣
What are the common SEs of treatment?
  • Hypotension
  • Restlessness
  • GI upset
‣
What personality changes can dopamine agonists cause?
  • Increased impulsiveness
‣
What are the side effects of long-term levodopa treatment?
  • Drug-induced dyskinesias: Writhing and uncoordinated movements of the limbs
  • On-off effect: Random fluctuations in drug effect
  • Wearing off over time: Symptoms return before taking the next dose
‣
What features are suggestive of drug-induced parkinsonism?
  • Bilateral tremor that has come on after taking dopamine antagonists (antipsychotics, antiemetics)
‣
What are the parkinson's plus syndromes? (4)
  1. Lewy body dementia - Fluctuations in cognitive impairment and visual hallucinations, often before parkinsonian features occur
  2. Progressive supranuclear palsy - Vertical gaze palsy
  3. Multiple systems atrophy - Autonomic features: Postural hypotension, incontinence & impotence
  4. Cortico-basal degeneration - Spontaneous activity by an affected limb (alien limb), or akinetic rigidity of that limb
‣
Benign essential tremor
‣
What features allow you to distinguish it from a Parkinsons tremor?
  • Symmetrical (Parkinsons is asymmetrical)
  • 5-8 hertz (Parkinsons is 4-6)
  • Improves at rest (Parksinsons is worse at rest)
  • Improves with alcohol (Parkinsons has no change with alcohol)
‣
Huntington's chorea
‣
What is the cause?
  • Autosomal dominant trinucleotide (CAG) repeat disorder coding for huntingtin protein.
‣
What is the triad?
  1. Dominant inheritance - Family history
  2. Choreoathetosis - Uncontrollable, purposeless movements
  3. Dementia
‣
What is seen on MRI?
  • Atrophy of caudate nucleus & putamen
‣
Dystonia
‣
What is it?
  • Prolonged, often painful, muscle contraction
‣
What medications commonly cause this?
  • Dopamine antagonists: Antipsychotics, antiemetics (metoclopramide)
‣
How does dystonia commonly present? (3)
  • Oculogyric crisis (upward eye deviation)
  • Torticollis (cervical dystonia)
  • Trismus (lockjaw)

Case:

‣
A 17-year-old girl presents with a resting tremor in her left arm. She is dysarthric and ataxic. An ECG reveals first-degree heart block. Diagnosis?
  • Wilson's disease
  • May also have psychiatric and hepatic features due to damage via copper deposition
‣
Epilepsy
‣
What are your differentials & features suggestive of them?
  1. Generalised seziure: Post-ictal confusion, lateral tongue biting, Todd's paresis (focal neurological deficit)
  2. Syncope: No post-ictal confusion, hot, sweaty & lightheaded before
  3. Stokes-Adams attack (arrhythmogenic syncope): Abrupt onset causing significant injury
  4. Psychogenic non-epileptic attack (pseudoseizures) - Often > 30 mins, in front of others, tongue biting is rare / front biting
  5. Hemiplegic migraine
  6. CVA
‣
Features:
‣
How does a myoclonic seizure commonly present?
  • Sudden jerk of a limb, trunk, or face
  • Worse after alcohol and when tired
‣
What lobe is responsible for a focal seizure with the following features:
‣
Automatisms (e.g. lip-smacking); déjà vu or jamais vu, emotional disturbance (eg. sudden terror); olfactory, gustatory, or auditory hallucinations
  • Temporal lobe
‣
Motor features such as Jacksonian features, dysphasia or Todd's palsy.
  • Frontal lobe
‣
Tingling and numbness followed by motor symptoms
  • Parietal lobe
‣
Spots and lines in the visual field.
  • Occipital lobe
‣
What is Todd's paresis?
  • Post-ictal paresis - Weakness after a seizure, can appear like a stroke presentation
‣
What is Hoover's sign?
  • Used to differentiate functional from organic leg paresis
  • Lie on bed, lift leg up, if the leg on the bed pushes down against your hand it's more likely to be psychogenic
‣
Management:
‣
What is first-line for generalised & focal seizures (long-term), respectively?
  • Generalised: Sodium valproate (non-childbearing age) / lamotrigine (childbearing age)
  • Focal: Carbamazepine
‣
Which anti-epileptic is safe to use in pregnancy?
  • Lamotrigine - Use in all women of childbearing age
‣
What anti-epileptics have the following SEs:
‣
Blurred vision, nystagmus and poor coordination
  • Carbamazepine
‣
Hepatotoxicity, pancreatitis, hair thinning, weight gain
  • Sodium valproate
‣
Gingival hyperplasia, acne, hirsutism & peripheral neuropathy
  • Phenytoin
‣
Large blisters (SJS)
  • Lamotrigine (generally well tolerated)
‣
Status epilepticus:
‣
How do you manage this?
  1. ABCDE - Remember BM is very important
  2. Benzodiazepine (Give second dose after 5 mins if seizure doesn't stop):
    • Hospital: IV lorazepam
    • Primary care: Buccal midazolam/rectal diazepam
  3. IV phenytoin / phenobarbital
  4. Intubate & ventilate
‣
Paediatric:
‣
Infantile spasms
‣
Features?
  1. Jacknife flexion of upper limbs
  2. Clusters
‣
First-line management?
  • Digabatrin
‣
West syndrome:
‣
Triad?
  1. Spasms
  2. Hypsarrhythmia
  3. Developmental regression
‣
What are they at risk of in adulthood?
  • Lennox-Gustau: Seizures & mental handicap
‣
Tuberous sclerosis
‣
What are the cutaneous manifestations?
  1. Ash leaf spots
  2. Angiofibromas
  3. Retinal hamartoma
‣
What may be seen on EEG?
  • Hypsarrhythmia in children
‣
How can you trigger an absence seizure?
  • Hyperventilation for 30 seconds
  • Stress
‣
What is a classic presentation of benign rolandic epilepsy?
  • Morning sensory change
  • EEG: Centrotemporal spikes
‣
Space occupying lesion
‣
What tumours commonly metastasise to the brain? (3)
  1. Breast
  2. Lung
  3. Melanoma
‣
What are the common primary CNS tumours?
  1. Meningioma (benign)
  2. Glioblastoma multiforme (malignant)
‣
Cerebral abscess
‣
RFs?
  • URTI in immunosuppressed patient (steroids, HIV etc)
‣
Features?
  • CT head shows ring enhancing lesion
  • Compression of structures causes spastic hemiparesis and confusion
‣
Management of cerebral abscess?
  • IV antibiotics
  • Surgical drainage
‣
Cerebellum
‣
What features are you looking for OE?
  • Dysdiadochokinesia (an inability to perform rapid alternating hand movements)
  • Ataxia (a broad-based, unsteady gait)
  • Nystagmus (involuntary eye movements)
  • Intention tremor (seen when the patient is asked to perform the 'finger-nose test')
  • Slurred speech
  • Hypotonia
‣
An alcoholic patient has Wernicke's encephalopathy. What is the triad?
  1. Opthalmoplegia
  2. Ataxia
  3. Confusion
    4. ‣
    What else can cause Wernicke's?
    • Hyperemesis gravidarum, malnutrition, bariatric surgery
    ‣
    How are they managed?
    • IV pabrinex (B1)
    ‣
    When managing alcoholics with a low BM, what needs to be given first?
    • Give IV pabrinex first as if not done giving glucose can cause Wernicke's
‣
What are your differentals in someone presenting with cerebellar dysfunction?
  • Posterior circulation stroke
  • Traumatic causes include trauma to the posterior fossa
  • MS
  • Metabolic - Alcohol
  • Infective - Lyme disease
  • Neoplastic causes include primary tumours (e.g. cerebellopontine angle tumour, acoustic neuroma) and secondary tumours (metastases e.g. breast cancer, lung cancer)
  • Drugs - phenytoin and carbamazepine
  • Congenital/hereditary causes include Friedrich's ataxia, and the spinocerebellar ataxias
‣
Spinal cord
‣
Acute spinal compression
‣
How do symptoms differ between spinal cord compression and cauda equina?
  • Cauda equina patients have saddle anaesthesia & loss of anal tone, whereas cord compression doesn't
    • Loss of anal tone → Constipation / incontinence
  • Cord ends at L1
‣
What is a common cause of cauda equina?
  • Lumbar disc herniation
‣
How is this definitively investigated?
  • Whole spine MRI
‣
How is it managed?
  • Steroids
  • Surgical decompression within 48 hours
‣
Cervical spondylosis
‣
What features suggest this?
  • Neck pain, radiculopathy (nerve root pinching) causing flaccid upper limb paresis, and myelopathy causing spastic paraparesis (and can involve the upper limbs)
  • Longer history (6-8 months)

Cases:

‣
Following abdominal surgery a patient has loss of pain, temperature, motor and autonomic function below the umbilicus. Proprioception & vibration are preserved. Diagnosis?
  • Anterior spinal artery occlusion
‣
14 year old has a history of falls, his grandad had similar problems. OE he has wasting of the lower limb muscles, spastic hypertonia, reduced power, ankle reflexes, and upgoing plantars. Diagnosis?
  • Friedrich's ataxia - Autosomal recessive neurodegenerative disease of the spinal cord
    • ‣
    Based on the symptoms above, what has been affected?
    • Corticospinal tracts - Spastic hypertonia, upgoing plantars
    • Peripheral nerves - LMN signs of wasting, absent reflexes
    • Spinocerebellar tracts
    • Dorsal columns - Vibration & proprioception
    ‣
    What other features are characteristic?
    • Pes cavus (don't confuse with CMT - only LMN signs)
    • Scoliosis (due to muscle weakness)
‣
25 year old patient has a ‘cape-like’ (neck and arms) loss of sensation to pain and temperature but preservation of light touch, proprioception and vibration
  • Syringomyelia - Spinothalamic tracts affected first, then corticospinal as it progresses, dorsal columns are spared as the syrinx pushes laterally
    • ‣
    What are the common causes?
    • Chiari malformation
    • Trauma
    • Tumour
    ‣
    What area of the spinal cord does the spinothalamic tract sit in?
    • Anterior white commisure
‣
Both
‣
Infection
‣
Meningitis
‣
What organism is likely responsible for neonatal meningitis?
  • Group B Streptococci
‣
Between 6 - 60 years, what are the 2 main bacteria causing meningitis?
  • N. meningitidis
  • S. pneumoniae
‣
Between 3 months - 6 years, what additional organism can cause disease?
  • H. influenzae
‣
An immunocompromised patient has meningitis signs, a very high opening pressure on LP, how do you confirm fungal infection? Management?
  • Cryptococcus infection - India ink staining
  • IV amphoterecin B & PO flucytosine followed by PO fluconazole (8W)
‣
What is the immediate primary care management if meningitis is suspected?
  • IM benzylpenicillin
    • If IV access is available then give this IV
‣
What is the secondary care management? (3)
  1. IV Cefotaxime/ceftriaxone (after blood cultures)
  2. IV Dexamethasone (to reduce oedema)
  3. Lumbar puncture (unless there are signs of raised ICP, in which case ICU referral is needed)
‣
What is the immediate antibiotic management in a 1 month old child with suspected meningitis?
  • IV cefotaxime (covers GBS)
‣
What is given to household for prophylaxis?
  • Ciprofloxacin
‣
Encephalitis
‣
What history features may be suggestive of encephalitis over meningitis?
  • Personality changes
‣
How would you investigate this? (2)
  1. CT head
  2. CSF viral PCR - Confirm HSV presence & subtype
  3. MRI brain - Bilateral involvement of the medial temporal lobes
‣
How is it managed?

2 weeks of:

  • 2g IV ceftriaxone BD
  • 10 mg/kg IV aciclovir TDS
‣
Lumbar puncture
‣
What is a contraindication for LP & how do you investigate for it?
  • ↑ ICP
  • CT head
‣
Defining values:
‣
How do you define low CSF glucose & when is it low?
  • Less than half of the plasma glucose
  • Low in bacterial/TB meningitis & viral encephalitis
‣
What are the common CSF compositions & when are they present?
  • Lymphocytes - Viral encephalitis/TB
  • Mononuclear cells - Viral meningitis
  • Neutrophils/polymorphs - Bacterial meningitis
‣
What is the CSF normal cell count and when is it changed?
  • Normal < 5
  • < 1000 - TB/viral meningitis
  • > 1000 - Bacterial meningitis (although can be lower)
‣
How can you use protein to differentiate?
  • > 1 - Bacterial or TB
  • < 1 - Viral
‣
Results:
‣
↓ glucose, ↑ protein, ↑ lymphocytes
  • TB meningitis
‣
↔︎ glucose, ↔︎/↓ protein, ↑ lymphocytes
  • Viral meningitis
‣
↓ glucose, ↑ protein, ↑ polymorphs
  • Bacterial meningitis
  • High protein & cell count
‣
↓ glucose, ↑ protein, ↑ lymphocytes
  • Viral encephalitis
‣
Micro: Gram negative diplococci
  • N. meningitidis
‣
Micro: Gram positive diplococci
  • S. pneumoniae
‣
MS
‣
What are the different types?
  1. Primary progressive
  2. Relapsing-remitting
  3. Secondary progressive
‣
What features are diagnostic?
  • At least 2 attacks of neurological dysfunction (relapses) over the previous 2 years
    • E.g. Optic neuritis (double vision & loss of colour vision in 1 eye)
‣
What is the triad of optic neuritis?
  1. Visual loss
  2. Periocular pain - Behind eye
  3. Dyschromatopsia - Loss of colour vision
‣
What is seen on LP?
  • Acellular, often with slightly raised protein,
  • Oligoclonal bands: Dark bands on Western Blot of CSF showing IgG
‣
How are relapses treated?
  • IV methylprednisolone
‣
What is used for long-term management?

Disease-modifying drugs:

  1. Interferon-beta
  2. Natalizumab (expensive & lots of SEs)
‣
What is Devic's disease?

Differential for MS, presenting with the triad of:

  1. Optic neuritis
  2. Transverse myelitis
  3. Positive NMO-IgG (an antibody targeting aquaporin 4)
‣
💪🏼 Peripheral Nervous System
‣
Cranial nerves
‣
Oculomotor
‣
What is a medical & surgical third nerve palsy?
  • Medical: Ptosis & down & out pupil - Diabetes, HTN, vasculitis
  • Surgical: Pupil dilation & pain in addition to above
‣
What can cause a surgical third nerve palsy?
  1. Posterior communicating artery aneurysm
  2. Cavernous sinus infection, thrombosis or tumour
‣
Internuclear ophthalmoplegia
‣
What is the medial longitudinal fasciculus?
  • Brainstem structure that coordinates abduction of one eye with adduction of the other. This meant it communicates with CN III & VI
‣
How does it present?
  • Impaired adduction of the eye on the side of the lesion
  • Nystagmus in the abducting eye
‣
What are the common causes?
  • MS
  • Brainstem infarction
‣
Bulbar/pseudobulbar palsy
‣
What is the difference between the two?
  • Both are lesions of the corticobulbar tract, affecting cranial nerves 9, 10 & 12 causing impairment of speech & swallow.
  • Bulbar palsy is a LMN lesion of this tract, whereas pseudobulbar palsy is a UMN lesion
‣
What features suggest bulbar palsy?
  • Dysphagia, choking on solids & liquids
  • Quiet nasal speech, drooling and a flaccid fasciculating tongue

‣
What are the causes?
  • MND
  • MG
  • GBS
  • Lateral medullary syndrome (stroke)
‣
What features suggest pseudobulbar palsy?
  • Spastic tongue
  • Slow "hot potato" speech
  • Brisk jaw reflex
  • May have UMN lesion signs in the limbs
‣
Facial nerve palsy
‣
How does Ramsay Hunt present?
  1. Ear pain, HL, vertigo
  2. LMN facial nerve palsy
  3. May have a vesicular rash around ear
‣
Bell's palsy:
‣
How do you manage a presentation if within 72 hours of onset?
  • Prednisolone 60mg/day for 7-10 days
‣
Sensory & motor
‣
Sensory
‣
What are your differentials for peripheral sensory loss?
  • Alcohol
  • B12/folate deficiency
  • CKD / Carcinoma
  • Diabetes mellitus / Drugs (isoniazid, amiodarone, phenytoin, cisplatin)
  • Every vasculitis
    • Cryoglobulinaemia (HepC related), RA, SLE, polyangiitis
‣
What dermatome is affected:
‣
Reduced sensation over the medial side of the thigh, with weakness of knee extension
  • L3
‣
Motor
‣
Motor neuron disease
‣
What mutation is associated with this?
  • SOD1 mutation associated with ALS
‣
What other disease is commonly associated with this?
  • Frontotemporal dementia
‣
What are the 4 types?
  1. Spinal ALS - Classic presentation
  2. Bulbar ALS - Early tongue and bulbar involvement
  3. Progressive muscular atrophy - Only LMN features
  4. Primary lateral sclerosis - Only UMN features
‣
How do you manage this?
  • Riluzole
    • Needs regular monitoring of FBC & LFT
‣
Myasthena gravis
‣
What muscles are commonly affected?
  • Eye lids - Ptosis
  • Eye muscles - Ophthalmoplegia
  • Bulbar muscles - Nasal speech
‣
In a myasthenic crisis, what is important to monitor?
  • FVC
‣
What is this commonly associated with?
  • Thymus hyperplasia / thymoma
‣
How do you investigate for this?
  1. Serum acetylcholine receptor antibody (+ in 80-90%)
    • If negative then test for muscle-specific tyrosine kinase antibodies
  2. CT chest looking for thymic hyperplasia/thymoma
  3. Repeated nerve stimulation (tensilon) → ↓ Action potential
‣
How are they managed?
  • Steroids and anticholinesterase inhibitors (such as pyridostigmine or neostigmine).
  • Severe: IVIG/plasmapheresis
‣
Lambert-Eaton syndrome
‣
How do they present?
  • Limb weakness - Improves on exercise
  • Autonomic dysfunction - Orthostatic hypotension, dry mouth
‣
What are the RFs?
  • Underlying malignancy - Commonly SCLC
  • Other autoimmune disease
‣
How do you investigate for this?
  1. Anti-voltage-gated calcium channel antibodies
  2. Repeated nerve stimulation → ↑ Action potential
‣
Management?
  • Amifampridine
‣
Mixed
‣
Mononeuritis multiplex
‣
What is this?
  • Simultaneous or sequential peripheral neuropathy affecting both sensory & motor nerves that are not near or associated with one another
  • Often asymmetrical pattern
‣
What causes it?
  • Diabetes
  • Vasculitis: Polyarteritis nodosa, both polyangiitis'
  • RA/SLE
  • Leprosy, lyme disease, parvovirus, HIV
  • Sarcoidosis
‣
Guillian-Barré syndrome
‣
How do they present?
  • Mixed motor & sensory LMN deficit
‣
What is the most important initial investigation if worried about respiratory failure?
  • Forced vital capacity
‣
How else can you investigate?
  • LP: Normal WCC, high protein (albuminocytologic dissociation)
  • Cardiac monitoring
‣
How are severe cases managed?
  • IV immunoglobulin
‣
Charcot-Marie Tooth disease
‣
What is this?
  • AD inherited disease affecting myelin of peripheral motor & sensory nerves
‣
How do they present?
  • Often presents with peripheral neuropathy
    • Often < 10 years but can be delayed until 40 or later
‣
What are the characteristic features?
  • Pes cavus (high-arching foot)
  • Inverted champagne bottle legs (distal muscle wasting)
  • Weakness of ankle dorsiflexion (foot drop)
‣
Neurofibromatosis
  • See Dermatology
‣
Autonomic
‣
What are the 3 broad causes of autonomic dysfunction?
  1. Autonomic neuropathy
    2. ‣
    Name 3 causes.
    1. Diabetes
    2. Amyloidosis / SLE
    3. Infection (HIV, lyme disease)
    4. Lambert-Eaton
  2. Neurodegenerative disease - PD, MSA
  3. Drug-induced
    4. ‣
    What drugs affect the ANS?
    1. β-blockers
    2. Anticholinergics
    3. Tricyclic antidepressants

👊🏽 Dermatology

‣
🧬 Non-Infectious
‣
Name that rash:
‣
Head
‣
Answer
  • SLE: Thickened plaque-like appearance, spares nasolabial folds, photosensitive
M. Sand, D. Sand, C. Thrandorf, V. Paech, P. Altmeyer, F. G. Bechara, CC BY 2.0
M. Sand, D. Sand, C. Thrandorf, V. Paech, P. Altmeyer, F. G. Bechara, CC BY 2.0 creativecommons.org/licenses/by/2.0, via Wikimedia Commons
‣
Answer
  • Allergic contact dermatitis
  • Tx: TOP steroid, PO prednisolone
James Heilman, MD, CC BY-SA 4.0
James Heilman, MD, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.
‣
Answer
  • Seborrhoeic dermatitis
Amras666, CC BY-SA 3.0
Amras666, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0/, via Wikimedia Commons. No changes were made.
‣
Leg
‣
Answer
  • Gravitational/venous eczema
James Heilman, MD, CC BY-SA 4.0
James Heilman, MD, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.
‣
Answer
  • Leg lymphoedema
DocHealer, CC BY-SA 4.0
DocHealer, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.
‣
Dermatitis
‣
Eczema: Atopic dermatitis
‣
Presentation
‣
Rash:
The original uploader was Eisfelder at German Wikipedia., CC BY-SA 3.0
The original uploader was Eisfelder at German Wikipedia., CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0/, via Wikimedia Commons. No changes were made.
‣
What is the typical presentation?
  • Itchy, poorly demarcated rash on flexural surfaces
  • Dry skin with excoriations
‣
What are the common triggers?
  • Atopy - Dust, animals, dairy, pollen
‣
How do you differentiate between eczema and psoriasis?
  • Eczema - poorly demarcated. Psoriasis - well-defined.
  • Eczema - flexor surfaces. Psoriasis - extensor surfaces.
  • Eczema - no silver. Psoriasis - silver plaques.
‣
Why does it happen? (Pathophysiology)
  • Defects in the skin barrier → Fluid loss (dryness) and infiltration of irritants, microbes & allergens → TH2 driven inflammation (↑ IgE)
‣
What nail changes are seen?
  • Irregular horizontal ridging
‣
What is lichenification and why does it develop?
  • Thickening of the skin due to excessive itching
  • Chronic eczema → Lichenification
‣
Investigations
‣
How is it diagnosed and investigated? (2)
  • Clinical diagnosis in primary care
  • Raised IgE
  • RAST testing for specific antigens
‣
Management
‣
What is maintenance management made up of? (2)
  1. Emollients - Create an artificial barrier
    2. ‣
    Name 3 examples of emmolients.
    • Thin: E45, diprobase
    • Thick: Hydromol
  2. Avoid irritants & skin breaking activities (warm baths)
‣
How are flares managed? (3 lines)
  1. Topical steroid / topical tacrolimus
    • Mild eczema: 1% hydrocortisone / eumovate / calcineurin inhibitor (if reaction to the steroid
    • Moderate (lichenification): Betnovate
    • Severe: Dermovate
  2. Phototherapy - UV light suppresses the immune system
  3. Immunosuppression (rare) - PO corticosteroids, methotrexate, azathioprine
‣
Complications
‣
A patient presents with a fever and the following rash:
image
‣
Describe the rash.
  • Widespread (painful) rash containing vesicles & pustules
‣
What are the 2 pathogens that could be causing this?
  1. HSV (Coldsore)
  2. VZV
‣
What is the diagnosis and management?
  • Eczema herpeticum
    • Mild: PO aciclovir
    • Severe: IV aciclovir
‣
The illness gets worse. What is likely to have happened?
  • Bacterial superinfection → Give flucloxicillin
‣
A patient presents with widespread erythema affecting > 90% of the body SA. Diagnosis?
  • Erythroderma
    • ‣
    Name 3 other causes.
    1. Psoriasis
    2. Seborrhoeic dermatitis
    3. Drug allergy - TEN
‣
Contact dermatitis: Irritant & allergic
‣
Rash:
James Heilman, MD, CC BY-SA 4.0
James Heilman, MD, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons

Allergic:

‣
What type of reaction is this?
  • Type IV hypersensitivity
‣
How are they investigated?
  • Skin patch test
‣
What can cause it and how will they present because of that?
  • Nickel
  • Marks on the skin from new jewellery/watches
  • Treatment: Topical potent steroid

Irritant:

‣
Name the common causes of this.
  • Soap
  • Cleaning products
  • Oils
‣
How does it typically present?
  • Itchy, erythematous skin
  • Rare: Crusting & vesicles
‣
Seborrhoeic dermatitis
‣
Rash:
Amras666, CC BY-SA 3.0
Amras666, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0/, via Wikimedia Commons
‣
What is this?
  • Fungus colonisation → Inflammation affecting the sebacious glands affecting scalp, nasolabial folds & eyebrows → Erythema & dry, crusted, scaly skin
‣
What is it a reaction to?
  • Fungus Malassezia furfur
‣
What conditions is it associated with?
  • HIV
  • Parkinson's
‣
How is it managed?

Antifungals:

  • Scalp: Ketoconazole shampoo
  • Face & body: Clotrimazole/miconazole cream
‣
What are the complications of this condition?
  • Otitis externa
  • Blepharitis
‣
Psoriasis
‣
Presentation
‣
Rash:

Plaque psoriasis (Most common type)

Haley Otman, CC BY 3.0
Haley Otman, CC BY 3.0 creativecommons.org/licenses/by/3.0, via Wikimedia Commons
‣
General
‣
How do they typically present?
  • Silver, symmetrical, well defined plaques (dry, flaky, scaly)
  • Affects extensor surfaces, scalp and behind the ears.
‣
Name 6 triggers.
  1. Stress
  2. Skin trauma
  3. Streptococcal infection
  4. Beta blockers
  5. Alcohol
  6. Lithium
‣
Patient with psoriasis presents with pain in her knee, who do you need to consider referring to & why?
  • Rheumatologist
  • Psoriatic seronegative arthritis
‣
What is the pathophysiology of psoriasis?
  • Type IV hypersensitivity reaction → Hyperproliferation of the epithelium → Plaque formation
    • T-cell mediated autoimmunity
‣
Types

Name the type based on the rash:

Bobjgalindo, CC BY-SA 4.0
Bobjgalindo, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.
‣
Answer
  • Guttate (children) - Salmon pink papules on the trunk in children following strep throat infection
    • ‣
    How is it managed?
    • Conservative: Resolves spontaneously in 3-4 months
      1. Symptomatic: Topical agents as per psoriasis
Pangolin06, CC BY-SA 4.0
Pangolin06, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.
‣
Answer
  • Pustular - Sterile pustules on the palms of hands and soles of feet.
  • Systemically unwell, medical emergency → Admit
‣
Investigations
‣
What are the histological features?
  • Acanthosis - Thickening of the epidermis
  • Parakeratosis - Nuclei in the stratum corneum
  • Munro's microabscesses - Neutrophils
Jenny Giang, Marc A. J. Seelen, Martijn B. A. van Doorn, Robert Rissmann,Errol P. Prens and Jeffrey Damman, CC BY 4.0
‣
Management
‣
Name the different steroid potencies. (5)
  1. Hydrocortosone
  2. Eumovate
  3. Betnovate
  4. Dermovate
  5. Clobetasol propionate
‣
How is it managed?

Regular emmolient use is recommended throughout management.

  1. Potent topical steroid (e.g. Betnovate) + Vitamin D analogue (reduces scaling & plaque thickness)
    1. Betnovate OD + calcipotrol OD (Dovobet: Combined)
    2. Calcipotrol BD
    3. Betnovate BD
  2. UV phototherapy
  3. Systemic therapy
    1. Methotrexate / ciclosporin
    2. Infliximab
‣
How is scalp psoriasis managed?
  • Tar shampoo (mild)
  • TOP steroid
‣
Autoimmune
‣
Lichen planus
‣
Rash:
James Heilman, MD, CC BY-SA 3.0
‣
What are the features?
  • Purple, pruritic plaques with white lacy lines on them on wrists/ankles & oral mucosa
  • Burning on eating
  • Can affect scarred areas
‣
What nail changes are seen?
  • Longitudinal ridges
‣
What commonly triggers an eruption?

Presents ~ 2 months after starting the following drugs:

  1. β-blockers
  2. Thiazides
  3. Gold
  4. ACEi
‣
Management?
  • TOP clobetasone
‣
Pemphigoid disease
‣
Which is which:
‣
Answer
  • Bullous pemphigoid
Mohammad2018, CC BY-SA 4.0
‣
Answer
  • Pemphigus vulgaris
Mohammad2018, CC BY-SA 4.0
‣
What is the pathophysiology of both of these conditions?
  • Autoimmunity
    • Vulgaris: against desmoglein 3
    • Bullous: against hemidesmosomes
‣
Which one has intra-epidermal and which has sub-epidermal blisters?
  • Intra-epidermal → Pemphigus
    • Deposition of IgG autoantibodies in the epidermis
  • Sub-epidermal → Bullous
    • Deposition of IgG autoantibodies on the basement membrane
‣
Which has tense & firm blisters?
  • Bullous pemphigoid
‣
Which commonly affects the oral mucosa?
  • Pemphigus vulgaris
‣
What is Nikolsky sign?
  • Top layers of skin shed when rubbed
    • ‣
    Differentials if positive? (3)
    1. Pemphigus vulgaris
    2. TEN
    3. Staphylococcal scalded skin syndrome
‣
Which one has a good prognosis?
  • Bullous pemphigoid
‣
Erythema nodosum
‣
Rash:
James Heilman, MD, CC BY-SA 3.0
‣
What is the pathophysiology & presentation?
  • Hypersensitivity → Inflammation of the subcutaneous fat (panniculitis) on the shins → Red, painful inflamed nodules on shins
‣
What are the causes? (6)
  • NO cause (idiopathic)
  • Drugs - Sulfasalazine
  • OCP
  • Sarcoidosis
  • Ulcerative colitis/Crohn's
  • Micro: Streptococci, TB, toxoplasmosis
‣
How are they investigated?
  • Bedside
    • Stool sample: Gastroenteritis (campy/salmonella)
    • Faecal calprotectin
  • Bloods
    • FBC & CRP: Infection
    • ESR: IBD
  • Imaging
    • CXR: TB, mycoplasma, sarcoidosis
‣
How is it managed?
  • Treat the underlying condition
‣
Pyoderma gangrenosum
‣
Rash:
I, Monopol, CC BY-SA 3.0
‣
Features?
  • Deep painful pustular ulcers on the legs with a blue/red overhanging edge
‣
Causes? (4)
  1. IBD
  2. Autoimmune hepatitis
  3. RA
  4. Leukaemia: AML / myeloproliferative disorders
  5. Lymphoma
‣
Management?
  • Immunosuppression: PO prednisolone/ciclosporin
‣
Genetic
‣
Neurofibromatosis
‣
NF1
‣
Inheritance?
  • Autosomal dominant
‣
Features? (4)
  1. Cafe-au-lait spots (oval coffee-coloured patches)
  2. Lisch nodules (brown patches on the iris)
  3. Axillary/inguinal freckling
  4. Neurofibromas
‣
Complications? (2)
  1. Optic glioma
  2. Scoliosis
‣
NF2
‣
Key feature?
  • Bilateral acoustic neuroma → Bilateral SNHL → HL, tinnitus, vertigo
‣
Tuberous sclerosis
‣
Inheritance?
  • Autosomal dominant
‣
Features? (4)
  • Dermatological:
    1. Angiofibromas: Firm papules forming a butterfly rash across the face
    2. Ashleaf macule: Oval hypopgimented patches
    3. Ungual fibroma: Fleshy tumours growing from nail folds
  • Neurological: Epilepsy
‣
🧫 Infectious
‣
Rash Quiz

Name, describe & treat the following:

James Heilman, MD, CC BY-SA 3.0
James Heilman, MD, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
Answer
  • Tinea (ringworm)
  • Itchy, discoid, scaly lesion
  • Management: Topical antifungal (terbinafine/ketoconazole)
James Heilman, MD, CC BY-SA 3.0
James Heilman, MD, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
Answer
  • Oral candidiasis
  • Mouth: Nystatin. Vagina: Clotrimazole
Grook Da Oger, CC BY-SA 3.0
Grook Da Oger, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
Answer
  • Pityriasis versicolor
  • Common in hot/humid countries
  • Caused by Malassezia - Gives a "spaghetti meatballs" appearance on KOH stain
    • Yeast stop the melanocytes from functioning in certain areas of skin causing depigmentation
  • Mx: Selenium sulphate
James Heilman, MD, CC BY-SA 4.0
James Heilman, MD, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.
‣
Answer
  • Impetigo
  • Mx: Fusidic acid (mild), Flucloxicillin (severe)
Stephen Ewen, CC BY-SA 4.0
Stephen Ewen, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.
‣
Answer
  • Cellulitis/erysipelas
    • Erysipelas: S. pyogenes infection (IV benzylpenicillin)
  • Depends on severity of situation - PO/IV flucloxicillin
Gzzz, CC BY-SA 4.0
Gzzz, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.
‣
Answer
  • Molluscum contagiosum
  • Infants
  • Watch & wait
James Heilman,MD, CC BY-SA 3.0
James Heilman,MD, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
Answer
  • Pityriasis rosea
  • Presentation: ‘Patient has had a mild cold for last few days, developed an initial discoid patch, and now has a series of 3cm discoid rashes on his body.’
  • Management: Conservative, resolves after 6-12 weeks
Mike Blyth, CC BY 3.0
‣
Acne
‣
Vulgaris
‣
Rash:
Roshu Bangal, CC BY-SA 4.0
Roshu Bangal, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.
‣
Why does acne occur?

Pilosebaceous units are made up of hair follicles & sebaceous glands that produce skin oils.

  1. Androgenic hormones → ↑ oil production → Keratin trapping & blocking of the pilosebaceous unit
  2. Swelling & inflammation within the unit
‣
Describe the appearance of acne.
  • Pustules
  • Comedones - Skin-coloured papules representing blocked pilosebaceous units.
‣
Name the 4 stages of acne management.
  1. Benzoyl peroxide (Epiduo) cream - ↓ Inflammation
  2. Add topical antibiotics
  3. PO antibiotics - Tetracycline, doxycycline (3 months)
  4. PO isotretinoin (Roaccutane) - ↓ sebum production
‣
What management is used in women but not men?
  • COCP
‣
What is acne fulminans?
  • Severe acne → Systemic upset (e.g. fever)
  • Admit → Give PO steroids
‣
Rosacea
‣
Rash:
M. Sand, D. Sand, C. Thrandorf, V. Paech, P. Altmeyer, F. G. Bechara, CC BY 2.0
M. Sand, D. Sand, C. Thrandorf, V. Paech, P. Altmeyer, F. G. Bechara, CC BY 2.0 creativecommons.org/licenses/by/2.0, via Wikimedia Commons. No changes were made.
‣
What is the typical presentation?
  • Flushing/erythema, pustules & telangiectasia
  • Affects cheeks, nose & forehead
  • Photosensitive
‣
How is it managed? (2)
  1. Topical metronidazole
  2. PO oxytetracycline
‣
What is a complication of this?
  • Rhinophyma: Large, bulbous nose associated with granulomatous infiltration
M. Sand, D. Sand, C. Thrandorf, V. Paech, P. Altmeyer, F. G. Bechara, CC BY 2.0
M. Sand, D. Sand, C. Thrandorf, V. Paech, P. Altmeyer, F. G. Bechara, CC BY 2.0 creativecommons.org/licenses/by/2.0, via Wikimedia Commons
‣
👹 Neoplastic
‣
Malignant melanoma
‣
Rash:
Dermanonymous, CC BY-SA 4.0
Dermanonymous, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.
Dermanonymous, CC BY-SA 4.0
Dermanonymous, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.
‣
What are the 4 subtypes?
  1. Superficial spreading (70%): Growing moles
  2. Nodular: Red/black lump that bleeds/oozes (most aggressive)
  3. Lentigo maligna: Slower growing
  4. Acral lentiginous: Hutchinson's sign
‣
What are the main RFs? (6)
  1. Fair skin
  2. Excessive sun exposure
  3. Immunosuppression
  4. FH
  5. High number of moles
  6. Increased age
‣
How do you assess a skin lesion? (5)

The following may raise suspicion:

  1. Asymmetry
  2. Borders: Irregular/uneven
  3. Colour: Multiple different shades of colour
  4. Diameter > 6mm
  5. Evolution: Changes in size, shape, colour, associated symptoms
‣
How do you stage MM?
  • Breslow’s depth - Represents how deep the tumour cells have invaded
‣
Where does it commonly metastasise to?
  • Liver
  • Eyes
‣
How do you assess whether it has spread?
  • Sentinel node biopsy: Affects how wide you make the excision
‣
How is it managed?
  • Surgical excision
  • Consider lymphadenectomy & adjuvant chemotherapy
‣
What are satellite lesions? What do they represent?
  • Small lesions around the main melanoma representing local lymph node spread
‣
Squamous cell carcinoma
‣
Rash:
Dermanonymous, CC BY-SA 4.0
Dermanonymous, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.
‣
What are the precursors to an SCC?
  • Stages: Acitinic keratosis → Bowen's (SCC in-situ)→ SCC
    • ‣
    How is acitinic keratosis managed?
    • Fluorouracil cream, sun avoidance.
    ‣
    How is Bowen's disease managed?
    • Fluorouracil cream (destroys sun-damaged cells)
    • Cryotherapy/excision
    Klaus D. Peter, Wiehl, Germany, CC BY 3.0 DE
    Klaus D. Peter, Wiehl, Germany, CC BY 3.0 DE creativecommons.org/licenses/by/3.0/de/deed.en, via Wikimedia Commons
    ‣
    What is a keratoacanthoma?
    • SCC in a hair follicle
    • Usually regress but may be excised
    Dermanonymous, CC BY-SA 4.0
    Dermanonymous, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons
‣
Describe the appearance of an SCC.
  • Hard, raised, everted edges on sun exposed areas
‣
Look at the following rash:
‣
What is it and do you need to worry?
  • Seborrhoeic keratosis - Not worrying, common in elderly people
James Heilman, MD, CC BY-SA 3.0
James Heilman, MD, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons
‣
What are Marjolin ulcers?
  • SCC developing in the site of a chronic ulcer
Raymund E. Horch, G. Bjoern Stark, Justus P. Beier: Unusual explosive growth of a squamous cell carcinoma of the scalp after electrical burn injury and subsequent coverage by sequential free flap vascular connection – a case report In: BMC Cancer 2005, 5:150 doi:10.1186/1471-2407-5-150, CC BY 2.0
‣
What are the main RFs?
  • Immunosuppression (HIV, drugs)
  • Sun exposure
  • Smoking
  • Genetic
    • Xeroderma pigmentosum - Can't repair damage to DNA caused by UV light. Severe sunburn after a few mins in the sun
    • Oculocutaneous albinism (albino) - Reduction or lack of melanin in the skin, hair and eyes
‣
How do you investigate and manage it?
  • Ix: Biopsy
  • Mx: Excision w/ radiotherapy
‣
Basal cell carcinoma
‣
Rash:
James Heilman, MD, CC BY-SA 3.0
James Heilman, MD, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
Describe the characteristic features of a BCC.
  • Rolled edge
  • Telangiectasia
  • May later ulcerate - central crater
‣
How do you investigate and manage it?
  • Ix: Full-thickness biopsy of edge of lesion
  • Mx: Mohs excision (Slice layers until you no longer see tumour tissue) / cryotherapy
‣
🧪 Metabolic / Toxic
‣
Erythema multiforme
‣
Rash:
James Heilman, MD, CC BY-SA 3.0
James Heilman, MD, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons
Grook Da Oger, CC BY-SA 3.0
Grook Da Oger, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons
‣
What is the key description of this rash?
  • Target lesions
  • Usually acute and self-limiting
‣
What are the causes?

Hypersensitivity reaction to the following:

  • Infection:
    1. HSV infection (most common)
    2. Mycoplasma pneumonia
    3. CMV, VZV
  • Drugs (SNAPP):
    1. Sulphonamides (Trimethoprim, sulfasalazine)
    2. NSAIDs
    3. Allopurinol
    4. Penicillin
    5. Phenytoin
‣
Steven-Johnson syndrome
‣
Rash:
James Heilman, MD, CC BY-SA 3.0
James Heilman, MD, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons
‣
What are the causes?
  • Infections:
    • HSV, mycoplasma, CMV, HIV
  • Drugs:
    • Allopurinol, antiepileptics (carbamazepine), antibiotics, NSAIDs
‣
What is the pathophysiology?
  • A disproportional immune response → Epidermal necrosis → Blistering & skin shedding
‣
What sign do you look for?
  • Nicholsky sign: Top layer of epithelium sheds when rubbed
‣
How is it managed?
  • IV fluids, steroids, immunosuppressants
  • Prophylactic antibiotics
‣
What is the extreme form of SJS called?
  • Toxic epidermal necrolysis (> 30% of body SA)
    • Erythema → Epidermal necrosis (loss of large amounts of epidermis) → Dehydration
      • ‣
      How do you differentiate SJS from TEN?
      • It’s classified by the amount of skin blistered during the reaction
        • SJS < 10%
        • SJS/TEN-overlap syndrome (between 10-30%)
        • TEN > 30% of body SA
      ‣
      What is it associated with?
      • HIV infection
Jay2Base, CC BY-SA 4.0
Jay2Base, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.
‣
What are the complications?
  1. Secondary infection → Cellulitis & sepsis
  2. Scarring
  3. Visual → Blindness

🤢 Metabolic Medicine

‣
⚡️ Electrolytes
‣
Na⁺
‣
Hypernatraemia

Na⁺ > 146mmol/L

Name causes of the following:

‣
Decreased H₂O intake (with normal fluid loss)

Dehydration

  • Lack of environmental water
  • Inability to communicate water needs e.g. Coma, children, intubated patients
‣
Hypotonic H₂O loss

H₂O loss > NaCl loss

  • Skin: Excessive sweating, burns
  • GI disturbances: Vomiting, diarrhoea, fistula
  • Renal disease with impaired urine concentrating ability
    • Diabetes insipidus (See 🥴 Endocrinology → 🧠 Pituitary)
    • Osmotic diuresis: chronic renal failure, hyperglycaemia
    • Renal disease: Nephropathy, myeloma
‣
Increased NaCl
  • Acute salt poisoning: Hypertonic saline
  • Primary hyperaldosteronism (See 🥴 Endocrinology → 👹 Adrenals)
  • Cushings syndrome (See 🥴 Endocrinology → 👹 Adrenals)

Management:

‣
What can happen if it is rapidly corrected?
  • Cerebral oedema → Seizures, coma & death
    • Rapid change in plasma osmolality causes water movement into the brain following the osmotic gradient.
‣
Hyponatraemia

Na⁺ < 133mmol/L

‣
① Hypotonic

This occurs due to Na⁺ depletion or Na⁺ dilution.

‣
What key investigations will help to identify the cause?
  • U&E: Na⁺, glucose, renal function
  • Urine : plasma osmolality
  • Urinary Na⁺

Classifying using volume status:

‣
Hypovolaemic

Loss of H₂O and Na⁺ from the ECF → Increased ADH secretion → Decreased H₂O excretion and H₂O retention → Hyponatraemia

‣
Name 4 renal losses of Na⁺
  1. Diuretic excess (thiazide)
  2. Renal tubular acidosis (See 🥠 Nephrology →❓Other)
  3. Metabolic alkalosis
  4. Mineralocorticoids deficiencies
‣
Name 4 pre-renal losses Na⁺
  1. Upper GI: Vomiting
  2. Mid-GI: Pancreatitis, bowel obstruction
  3. Lower GI: Diarrhoea, bowel preparation
  4. Other: Sweat, bleeding, burns

‣
How do you differentiate between them?

Urinary Na⁺

  • Urinary Na⁺ < 20mmoL/L → Extra-renal
    • Appropriate kidney response because it is holding onto the Na⁺ to retain water during this hypovolaemia.
  • Urinary Na⁺ > 20mmol/L → Renal
    • Inappropriate response, meaning that the cause of the hyponatraema is excessive renal excretion of Na⁺
‣
Euvolaemic
‣
Name 3 causes.
  1. Hypothyroidism
  2. Adrenal insufficiency
  3. Hypotonic IV fluid therapy,
  4. SIADH

Case:

‣
Patient presents with SCLC and hyponatraemia, what is the likely diagnosis?

SIADH (Syndrome of inappropriate ADH).

Causes:

‣
What malignancies can cause this?
  • SCLC
  • Pancreas
  • Prostate
‣
What neurological conditions can cause this?
  • Stroke
  • SAH
  • Meningitis
‣
What infections can cause this?
  • TB
  • Pneumonia
‣
What drugs can cause this?
  • SSRIs
  • Tricyclics
‣
Hypervolaemic

Increase in total body Na⁺ and H₂O, where total body H₂O is out of proportion to Na⁺ → Dilutional hyponatraemia

How do the following results change your differentials:

‣
↑ Urinary Na⁺
  1. Heart failure
  2. Liver cirrhosis
  3. Hepatorenal syndrome
  4. Nephrotic syndrome
‣
↓ Urinary Na⁺
  1. Renal failure
  2. Hypertonic saline
  3. Steroids
‣
② Isotonic: Pseudohyponatraemia
‣
What are the causes of this?

Elevated chylomicrons or triglycerides artifactually decrease the apparent concentration of Na⁺ in the serum.

  • Hyperproteinaemia
  • Hyperlipidaemia
‣
③ Hypertonic: Translocational hyponatraemia

H₂O moves from ICF → ECF due to osmotically active particles in the plasma inducing movement. This decreases Na⁺ even though the serum osmolality remains elevated.

‣
What are the osmotically active particles that can cause this?
  • Hyperglycaemia
  • Mannitol
  • Radiocontrast

Management:

‣
What occurs if you correct hyponatraemia too quickly?
  • Central pontine myelinolysis → Potential quadriparesis and bulbar palsy
‣
K⁺
‣
Hyperkalaemia
‣
Causes:
‣
Name a non-pathological reason.
  • Haemolysis of the blood sample → Repeat
‣
Name 4 conditions.
  1. AKI
  2. Rhabdomyolysis
  3. Addison's disease
  4. Metabolic acidosis
‣
Name 3 drugs.
  1. ACE inhibitors
  2. Spironolactone
  3. Heparin
‣
Name 3 ECG changes of hyperkalaemia.
  1. Tall tented T waves
  2. Small P waves
  3. Wide QRS (> 3 small squares)
‣
When do you treat?
  • K⁺ > 6.5
  • ECG changes stated above
‣
How do you manage hyperkalaemia?
  1. IV fluids
  2. Calcium gluconate (stabilise myocardium)
  3. Insulin-dextrose (push K⁺ into cells)
  4. Inhaled salbutamol (push K⁺ into cells)
‣
Hypokalaemia
‣
Name 2 endocrine causes.
  1. Primary hyperaldosteronism (Conn's)
  2. Cushing's disease
‣
Name 3 other causes.
  1. D&V
  2. Loop & thiazide diuretics
  3. Partially treated DKA
‣
What are the ECG features? (4)
  1. ST depression
  2. T-wave inversion
  3. Long QT
  4. U waves
James Heilman, MD, CC BY-SA 3.0
James Heilman, MD, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons
‣
What other electrolyte should be checked?
  • ↓ Magnesium → ↓ K & ↓ Ca
‣
How are they managed?
  • 1L NaCl with 40mmol KCl at a rate of 10mmol/hr
‣
Ca²⁺
‣
Draw the calcium negative feedback loop.
Mkaram19, CC BY-SA 4.0
Mkaram19, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.

Pathologies:

‣
Hypercalcaemia
‣
Name 3 causes of this.
  1. Hyperparathyroidism (Primary: ↓ PO₄³⁻)
  2. Bone metastases
  3. Primary cancer secreting PTH (Lung SCC)
‣
What is seen on ECG?
  • Shortening of the QT
‣
How is it managed? (2)
  1. IV fluids (3-4L over 24h)
  2. IV bisphosphonates (after the patient has been fully hydrated)
    • E.g. Zolendronate
    • Take 2-3 days to work
    • Max effect at 7 days
‣
Hypocalcaemia
‣
What do you see on examination? (2)
image
‣
What is seen on ECG?
  • Prolonged QT
‣
Name 4 key causes.
  1. Vitamin D deficiency: Malnutrition, malabsorption, CKD
  2. Hypoparathyroidism
  3. Hyperphosphataemia: Tumour lysis syndrome, rhabdomyolysis
    • Causes increased calcium bone deposition
  4. Acute pancreatitis (broken down fat binds to calcium)
‣
A patient has ↓ Ca²⁺, ↓ PO₄³⁻, ↑ ALP, ↑ PTH. Diagnosis?
  • Osteomalacia
    • ALP is involved in bone mineralisation, when the mineralisation is low it compensates by increasing in concentration
‣
Mg²⁺
‣
↓ Mg²⁺
‣
What are the common causes?
  1. ↓ Gut absorption:
    • PPI, alcohol, TPN, diarrhoea
  2. Pushing into intracellular spaces
    • Insulin (refeeding syndrome), acute pancreatitis
  3. ↑ Renal excretion
    • Diuretics (L&T), digoxin, gentamicin
‣
PO₄³⁻
‣
↑ PO₄³⁻
‣
What are the common causes?
  • Hypoparathyroidism
  • Liver disease
  • Osteoporosis
  • Vitamin D overuse
‣
↓ PO₄³⁻
‣
How are the causes classified?
  • Decreased intestinal absorption
  • Increased removal through kidneys
  • Moving phosphate from within cells to outside cells
‣
What are the common causes?
  • Anorexia
  • Chronic diarrhoea
  • Fanconi syndrome
  • Vitamin D deficiency
  • Drugs eg diuretics, steroids
‣
Phosphate physiology
  • Calcium and phosphate react in opposite ways. As levels of calcium rise, phosphate falls. This is regulated by PTH and partly then through Vitamin D.
  • Low calcium is detected, this causes PTH release and PTH works in 3 ways to increase calcium, subsequently decreasing phosphate.
  • PTH works by: Drawing calcium from bone, decreasing calcium lost in urine, and through Vitamin D enhances absorption of calcium from intestines.

‣
🧪 Acid-Base Balance
‣
Acidosis
‣
Respiratory
‣
Name 3 causes.
  1. Asthma
  2. COPD
  3. Respiratory depression - Opiates/benzodiazepines
‣
Metabolic
‣
What is the anion gap? When is it used?
  • Difference between positive & negative ions in serum
    • 10-18 mmol/L
  • Used to classify metabolic acidosis
    • HAGMA: High anion gap metabolic acidosis
    • NAGMA: Normal anion gap metabolic acidosis
Dr. Agnibho Mondal, CC BY-SA 4.0
Dr. Agnibho Mondal, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.
‣
Bloods: Na⁺ = 137, K⁺ = 4, Cl⁻ = 100, HCO₃⁻ = 28. Calculate the anion gap.
  • Positive ions - Negative ions = Anion gap (10-18)
  • 13 - Normal

Causes:

‣
Name 6 causes of metabolic acidosis with raised anion gap.
  • K – Ketoacidosis
  • U – Uraemia (including CKD)
  • S – Salicylate poisoning
  • M – Methanol ingestion
  • A – Aldehydes
  • L – Lactic acidosis (inc. metformin use)
‣
Name 3 causes of metabolic acidosis with normal anion gap.
  1. Diarrhoea (lose HCO₃⁻)
  2. Addison's disease
  3. Renal tubular acidosis (RTA)
‣
Alkalosis
‣
Respiratory
‣
Name 4 causes.

Think shallow, fast breathing:

  1. Anxiety
  2. Chest wall trauma
  3. PE
  4. Altitude
  5. Pregnancy
‣
Metabolic
‣
Name 3 causes.
  1. Vomiting
  2. Hypokalaemia
    • Diuretics
    • Primary hyperaldosteronism/Cushing's/CAH
‣
💦 Fluid Therapy
‣
What are the daily maintenance amounts for water, electrolytes and glucose?
  • Water: 25-30 ml/kg
  • Electrolytes (Na, K, Cl): 1 mmol/kg
  • Glucose: 50-100 g/day
‣
When do exceptions need to be made for fluid prescribing?
  • Post-surgery with drains, etc. → Increase fluids
  • HF → Fluid restrict
‣
Over what time period does 1L NaCl (0.9%) with 40mmol Potassium need to be given?
  • Potassium cannot be given any quicker than 10 mmol per hour → 4 hours

Cases:

‣
Patient presents with AKI. What should their initial fluid management be?
  • Bolus: 500ml of NaCl (0.9%) over 15 minutes
‣
If a patient weighs 75kg, what fluids and amount should be given for maintenance per hour?
  • NaCl (0.9%): 75kg x 30 ml/kg = 2,250 ml / 24 = 93.8ml/hr = 100ml/hr (rounded)
‣
A 28kg child needs maintenance fluids, how much needs to be given over 24h?
  • First 10kg = 100 ml/kg
  • Second 10kg = 50 ml/kg
  • Over 20kg = 20ml/kg
  • Answer: 1660 ml over the day
‣
🆘 Vitamin Deficiencies
‣
Table containing all deficiencies, absorption sites & resulting symptoms:
Deficiency
Site of absorption
Deficiency syndrome
A
Small intestine
Night blindness
B1 (thiamine)
Small intestine
Wernicke's encephalopathy
B2
Proximal small intestine
Angular stomatitis
B3
Jejunum
Pellagra
B12
Terminal ileum
Macrocytic anaemia, glossitis
C
Proximal ileum
Scurvy
D
Jejunum
Rickets, osteomalacia
K
Small intestine
Bleeding disorders
Iron
Duodenum and jejunum
Macrocytic anaemia
Zinc
Jejunum
Poor wound healing
Copper
Stomach and jejunum
Menkes' syndrome

Name the deficiency.

‣
Patient has dermatitis, dementia & diarrhoea.
  • Vitamin B3 - Niacin
    • ‣
    How are they managed?
    • Nicotinamide supplementation
‣
Patient has ecchymoses, gingival swelling, tooth loss and coiled hairs.
  • Vitamin C: Scurvy
‣
Which vitamin can be teratogenic in high doses?
  • Vitamin A

🥠 Nephrology

‣
🥠 Kidney Anatomy

It is essential to understand the anatomy of the kidney to understand where each disease effects.

‣
Kidney
  • Interstitium: Intertubular, extraglomerular, extravascular space of the kidney.
  • Tubules: Proximal convoluted tubule, loop of Henle, and distal convoluted tubule, emptying into the collecting duct.
OpenStax College, CC BY 3.0
OpenStax College, CC BY 3.0 creativecommons.org/licenses/by/3.0, via Wikimedia Commons. No changes were made.
OpenStax College, CC BY 3.0
OpenStax College, CC BY 3.0 creativecommons.org/licenses/by/3.0, via Wikimedia Commons. No changes were made.
‣
Nephron Secretion & Reabsorption
OpenStax College, CC BY 3.0
OpenStax College, CC BY 3.0 creativecommons.org/licenses/by/3.0, via Wikimedia Commons. No changes were made.
‣
Glomerulus

Key anatomy to remember:

  • Afferent arteriole: Afferent = artery.
    • Arteries are always before capillaries (basically what the glomerulus is)
    • NSAIDs constrict the afferent arteriole
  • Efferent arteriole: Efferent = exit.
    • ACEi and ARBs dilate the efferent arteriole → Lower pressure within the glomerulus → Less damage to the glomerular membrane
Shypoetess, CC BY-SA 4.0
Shypoetess, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.
‣
⌛️ Chronic Kidney Disease (CKD)

Abnormalities of kidney structure or function, present for ≥3 months, with implications for health.

‣
Pathophysiology of CKD

What problem is caused when the following mechanisms of the kidney are no longer functioning:

‣
Waste excretion
  • Uraemia: Pericarditis, encephalopathy
‣
Regulation of fluid balance
  • Hypertension
  • Peripheral/pulmonary oedema
‣
Acid-base balance
  • Metabolic acidosis (↑ anion gap)
‣
EPO production
  • Anaemia
‣
1-ɑ-hydroxylase production
  • Hypocalcaemia

What is the pathophysiological issue based on the following presentations:

‣
A patient with CKD 4 presents with normochromic normocytic anaemia.
  • ↓ EPO production due to eGFR < 35
    • ‣
    Where is EPO produced?
    • Interstitial fibroblasts of the kidney
    ‣
    How is it managed?
    • Iron replacement (depending on the iron studies)
    • Darbepoietin (EPO) supplementation
‣
A patient with CKD 5 presents with renal osteodystrophy.
  • ↓ 1-ɑ-hydroxylation → ↓ Ca²⁺ → Secondary hyperparathyroidism → Osteoporosis & osteomalacia
    • ‣
    Why do they have a raised phosphate?

    Two reasons:

    • Low calcium → ↑ PTH → Breakdown of hydroxyapatite → High phosphate
    • CKD → Low clearance of phosphate from kidneys
    ‣
    How is it managed?

    Calcium:

    • Alfacalcidol (calcitriol) → Already been hydroxylated so doesn’t require 1-ɑ-hydroxylase

    Phosphate binders:

    • Calcium containing (e.g. calcium carbonate) → If calcium is low and phosphate is high.
    • Non-calcium containing (e.g. sevelamer) → If calcium normal and phosphate high.
‣
Investigations
‣
What key investigations should/could you do?

Bedside:

  • Urinalysis: Haematuria and/or proteinuria

Bloods:

  • U&E: Cr, eGFR, electrolytes
  • FBC: Anaemia
  • Iron studies: Investigating anaemia further
  • Bone profile: Calcium, phosphate

Imaging/other:

  • Renal ultrasound: Small kidneys; obstruction/hydronephrosis; kidney stones
  • AXR: Show calcium-containing stones
  • Renal biopsy: Looking for underlying cause of CKD, e.g. IgA nephropathy
‣
How do we screen for diabetic nephropathy?
  • Albumin : Creatinine Ratio (ACR): Picks up microalbuminuria

eGFR

‣
What factors does eGFR take into account?
  • Creatinine
  • Age
  • Gender
  • Ethnicity
‣
Name 3 factors that may make eGFR results unreliable.
  1. Pregnancy
  2. Muscle mass: Anorexia/muscular
  3. Eating red meat within the last 24h
‣
Stage the following CKD patients:
‣
CKD staging diagram
  • GFR: Times on a clock from G3a–G5.
  • Albumin: All the 3s (3, 30, 300).
National Kidney Foundation
National Kidney Foundation
‣
GFR 47, Albumin 20
  • Stage 3a
  • A1
‣
GFR 18, Albumin 375
  • Stage 4
  • A3
‣
GFR 90, Albumin 225
  • Stage 1 (GFR > 90 w/ evidence of kidney damage)
  • A2
‣
GFR 68, Uraemia
  • Stage 2 (GFR < 90 with signs of kidney damage)

Management:

‣
Advanced CKD
‣
What medications can slow CKD progression?
  1. ACE inhibitor / ARB (e.g. ramipril): Shown to reduce intra-glomerular pressure independently of blood pressure (through vasodilation of the efferent arteriole)
  2. SGLT-2 inhibitor (e.g. dapagliflozin): Shown to have renoprotective effects independent of diabetes status
  3. Statin
‣
What medications can be given to address systemic complications?
  1. Anaemia → EPO-stimulating agent (e.g. darbepoetin)
  2. Hyperphosphataemia → Phosphate binders
    • Sevelamer (non-calcium containing)
    • Calcium acetate (calcium containing)
  3. Hypercalcaemia → Cinacalcet
    • Signals the body to produce less parathyroid hormone (PTH)
‣
Renal replacement therapy (RRT)
‣
What are the indications for dialysis?

AEIOU

  1. Acidosis: pH < 7.2
  2. Electrolytes: Persistent refractory K⁺ > 7
  3. Intoxication: Severe drug damage
  4. Overload: Refractory pulmonary oedema
  5. Uraemia: Encephalopathy / pericarditis

Types:

‣
How does haemodialysis work?
  • Access:
    • Arteriovenous fistula (AVF)
    • Line: Usually a jugular line with two lumens to pull blood to the machine & push blood back
  • Machine:
    • Dialysate: The dialysate is the fluid that the blood is run against that creates osmotic gradients to remove potassium, calcium, etc.
    • Dialyser: The dialyser is the ‘kidney’ that acts as the membrane between the dialysate and blood
    • Ultrafiltration: This is the amount of fluid removed on dialysis
  • Duration: The usual regimen is 3 sessions a week, having 3-5 hours per session
  • Risks:
    • Endocarditis from line / fistula
    • Haemodynamic instability from fluid shifts
‣
What are the two different types of peritoneal dialysis?
  1. Continuous peritoneal dialysis: Dialysate sits in the abdomen for 6-8 hours while the exchanges occur.
  2. Automated peritoneal dialysis: Dialysis at night over 8 hours using an automated machine.
    3. ‣
    What are they at risk of? Primary cause of this?
    • Spontaneous bacterial peritonitis (SBP)
    • S. epidermis is most common cause
‣
Renal transplant
‣
What are the common drugs used for immunosuppression following transplant?
  1. Tacrolimus
  2. Mycophenolate
  3. Prednisolone
‣
What are renal transplant patients at risk of?
  1. Immunosuppression → Risk of SCC due to sun exposure → Sun cream and avoidance
    • Steroids → Osteoporosis
  2. CMV infection
  3. Lymphoma
‣
🥵 Acute Kidney Injury (AKI)

Acute decline in kidney function, leading to a rise in serum creatinine and/or a fall in urine output.

‣
How do we classify AKI?
‣
Pre-renal

Injury due to impaired kidney perfusion

‣
What are the risk factors?
  1. Older age (above 65 years)
  2. Diabetes
  3. Heart failure
  4. Nephrotoxic medications: NSAIDS, ACE inhibitors
  5. Chronic kidney disease
  6. Contrast
‣
Name 5 causes.
  1. Hypovolaemia (e.g. in D&V)
    2. ‣
    How can you see if pre-renal AKI is due to dehydration?
    • Urea : creatinine ratio.
      • If this is high then likely due to dehydration (Urea is more concentrated)
      • Urea will be high because the low intravascular volume means it appears more concentrated within the blood
  2. Haemorrhage
  3. Sepsis
  4. Third-spacing of fluid (e.g. in pancreatitis)
  5. Renal artery stenosis
‣
How does the kidney respond to being under-perfused?
  1. Activation of the RAAS system: Angiotensin II → Aldosterone release → Sodium & water resorption at the collecting duct
  2. Vasoconstriction of the glomerular efferent arteriole and dilation of the afferent arteriole, is intended to maintain glomerular filtration
  3. Hypothalamus → ADH release → Increased tubular water re-absorption
‣
Renal

Direct injury to the kidney parenchyma

‣
Name the 5 causes of interstitial AKI.
  1. Acute tubular necrosis (e.g. from toxins)
  2. Glomerulonephritis
  3. Interstitial nephritis
  4. Haemolytic uraemic syndrome
  5. Thrombosis

What is the diagnosis based on the following presentations:

‣
Patient presented to A&E in status epilepticus, fitting for 25 minutes. They are now in AKI.
  • Rhabdomyolysis (covered in 🚇 Tubule / Interstitium)
‣
Patient presents with oliguria, raised urea, creatinine and potassium and muddy brown casts in their urinalysis.
  • Acute tubular necrosis (covered in 🚇 Tubule / Interstitium)
    • ‣
    Name 4 nephrotoxic agents that could have caused this.
    1. Myoglobin in rhabdomyolysis
    2. Lead
    3. Radiocontrast
    4. Aminoglycosides, e.g. gentamicin
‣
A 9 year old patient presents with anaemia, thrombocytopenia and a fragmented blood film. He mentions that he had a diarrhoea last week.
  • Haemolytic uraemic syndrome: E. coli 0157 infection
‣
A patient presents with fever, rash and arthralgia after starting a course of rifampicin for TB. She has sterile pyuria and white cell casts in her urine.
  • Acute interstitial nephritis (covered in 🚇 Tubule / Interstitium)
‣
A patient presents with fever, rigors, loin pain and white cell casts in her urine.
  • Acute pyelonephritis (covered in 🚇 Tubule / Interstitium)
‣
Post-renal

Injury due to urinary outflow obstruction

‣
Name 4 causes.
  1. Kidney stones
  2. Prostatic hypertrophy / cancer
  3. External ureteric compression
  4. Abdominal malignancy
‣
How does this impact kidney function?
  • Obstruction → Increased intratubular pressure → Tubular ischaemia & atrophy
‣
How do we manage post-renal AKI?
  • Relieve the obstruction: Insert a catheter, remove the kidney stone, etc.

Investigations & Management:

‣
Investigations
‣
Name the 3 criteria that allow for diagnosis of AKI.
  1. A rise in creatinine of ≥ 26 mmol in 48 hours
  2. A rise in creatinine by 1.5X in 7 days
  3. Urine output < 0.5 ml/kg/hr
‣
How are the 3 stages of AKI defined?

Increase in creatinine by the following times of baseline:

  1. 1.5-1.9 X
  2. 2-2.9 X
  3. ≥ 3 X

Urine production:

  1. < 0.5 ml/kg/hr for 6 hours
  2. < 0.5 ml/kg/hr for 12 hours
  3. < 0.3 ml/kg/hr for 24 hours
‣
How do you investigate an AKI of unknown origin?
  • Urinalysis
  • Renal ultrasound
‣
How do you investigate for vesico-ureteric reflux?
  • Micturating cystography
‣
Patient has uraemia. What 2 conditions are you considering and how do you differentiate them?
  1. Acute tubular necrosis
    • Urine Na⁺ > 30 mmol/L
  2. Pre-renal AKI
    • Urine Na⁺ < 20 mmol/L
‣
Management
‣
How are the majority of cases managed?
  • Conservatively: Often with IV fluids or with encouraging oral intake.
‣
What drugs need to be stopped in AKI?
  • Metformin
  • ACEi/ARB
  • NSAIDs
  • Diuretics
  • Aminoglycosides
‣
What are the 3 stages in management of hyperkalaemia?
  1. Membrane stabilisation: IV calcium gluconate
  2. Pushing potassium intracellularly: Insulin/dextrose (& nebulised salbutamol)
  3. Permanent lowering: Calcium resonium (PO/PR)/diuretics/dialysis
‣
🩸 Glomerulus

If you believe there is a disease of the glomerulus, you must differentiate between nephrotic and nephritic syndrome.

‣
How do nephrotic syndrome and nephritic syndrome present, respectively?
  • Nephrotic: Proteinuria (> 3-3.5g/day) → Hypoalbuminaemia → Oedema
    • ‣
    How do you see the extent of the proteinuria?
    • Albumin : creatinine ratio (ACR)
  • Nephritic: Haematuria, hypertension & proteinuria
‣
How would you investigate these patients?

Bedside:

  • Urinalysis: Looking for haematuria and proteinuria
  • Urine microscopy: Looking for red cells and red cell casts
  • 24-hour urine collection: Protein excretion rate ≥3.5 g per 24 hours indicates nephrotic-range proteinuria
  • Urine PCR ≥ 300 mg/mmol → Nephrotic-range

Bloods:

  • FBC: Hb → Anaemia
  • U&E: eGFR, creatinine (? AKI), electrolytes
  • ESR → Inflammation
  • CRP → Inflammation
  • Immunology

    • What differential do these tests point to if positive:

    ‣
    Complement levels
    • Immune complex disease
    ‣
    pANCA
    • Eosinophilic granulomatosis with polyangiitis
    • Microscopic polyangiitis (MPA)
    ‣
    cANCA
    • Granulomatosis with polyangiitis
    ‣
    Anti-GBM
    • Goodpasture’s
    ‣
    ASO
    • Post-streptococcal
    ‣
    Rheumatoid factor
    • Rheumatoid arthritis
    ‣
    Anti-DNase
    • Post-streptococcal
    ‣
    Anti-dsDNA
    • Systemic lupus erythematosus (SLE)
    ‣
    ANA
    • Systemic lupus erythematosus (SLE)

Imaging / Other:

  • Renal ultrasound: Small kidneys (thinning of cortex) or normal
  • Renal biopsy (gold standard): Tells us the underlying cause through looking at histology.
‣
How is glomerulonephritis generally managed?
  1. Treat the underlying cause:
    • Immunosuppression: Reduce the inflammation from inflammatory diseases
      • Corticosteroid (e.g., prednisolone)
      • Corticosteroid-sparing agent (e.g., cyclophosphamide, rituximab, mycophenolate)
    • Stop causative drugs
    • Treat infection with antibiotics / antivirals
  2. Blood pressure management: Block the renin-angiotensin system to manage hypertension

Name causes of the following:

‣
Nephrotic syndrome

Breakdown of glomerular membrane.

‣
Primary
‣
Minimal change disease

Accounts for ~ 90% of cases in children under the age of 10 years.

‣
How do they present?
  • Children presenting to A&E with:
    • periorbital oedema
    • peripheral oedema
    • shortness of breath (pleural effusions and/or pulmonary oedema)
‣
What are the causes?
  1. Primary: Majority are idiopathic
  2. Secondary:
    • Medications, e.g. NSAIDs
    • Malignancy, e.g. lymphoproliferative disorders
    • Infections, e.g. syphilis
‣
How are they managed?
  • High-dose prednisolone
‣
Focal segmental glomerulosclerosis (FSGS)

Sclerosis in parts of at least one glomerulus.

‣
What commonly causes this?
  1. Diabetes mellitus
  2. Buerger's disease
  3. Sickle cell
  4. HIV
‣
How are they managed?
  • Steroids or cylophosphamide/ciclosporin
‣
Membranous nephropathy

Glomerular basement membrane thickening without significant cellular proliferation on histology.

‣
What are the common causes?
  1. Primary: Autoimmune reaction against important antigens (PLA2R) in the filtration barrier
  2. Secondary:
    • Cancer: Breast, lung, colon
    • Systemic disease: SLE, thyroid
    • Infection: HepB
    • Drugs: Gold, penicillamine
‣
What is seen on histology?
  • "Spike & dome" pattern
  • Thickening of the basement membrane
‣
Secondary
‣
Amyloidosis
‣
What is amyloidosis?
  • Build up of amyloid proteins around tissues → Organ dysfunction
  • In the kidney: Amyloid proteins are deposited in the mesangium & capillary loops → Disruption of the glomerular basement membrane
‣
How might they present?
  1. Unexplained weight loss
  2. Fatigue
  3. Oedema resistant to diuretic therapy
‣
How is it diagnosed? (Key exam question)
  • Congo red staining → Apple-green birefringence
‣
Diabetes

Glucose deposits on the basement membrane causing damage (see Endocrine for more diabetes detail)

Why are they predisposed to:

‣
Thrombosis
  • ↑ loss of proteins into urine → ↑ loss of antithrombin III, protein C & protein S → Hypercoagulability
  • Commonly in the renal veins as it clots as soon as it leaves the kidney, but they can also have a VTE due to this.
‣
Infection
  • Loss of immunoglobulins in the urine
‣
Hyperlipidaemia
  • ↓ oncotic pressure → ↑ rate of lipoprotein synthesis in the liver → ↑ cholesterol
‣
Nephritic syndrome

Inflammation of the glomerular membrane: SHARP AIM

‣
Systemic lupus erythematosus (SLE)

Consider this as a differential — See Rheumatology notes for SLE presentation, investigations & management.

‣
Henoch-schönlein purpura (HSP)

This is an IgA vasculitis. It leads to IgA nephropathy, but is also referred to as HSP nephritis.

‣
What are the 4 HSP features?
  1. Purpura
  2. Joint pain
  3. Abdominal pain
  4. Renal involvement: Glomerulonephritis (HSPN) occurs in 30-50% of HSP patients, consider as a differential in those with a clinical presentation of HSP.
‣
Diagram: HSP rash
image
‣
Alport syndrome
‣
How is it inherited?
  • X-linked (most common), but can be autosomal dominant or autosomal recessive
‣
How do they present?
  • Ears: Bilateral sensorineural hearing loss
  • Eyes: Anterior lenticonus / retinitis pigmentosa
  • Kidneys: Microscopic haematuria
‣
Rapidly-progressive
‣
What can cause this?

All causes of nephritic syndrome can also be rapidly progressive but usually aren't.

‣
Granulomatosis with polyangiitis
  • ✚ cANCA.
  • Triad:
    1. Haemoptysis
    2. Systemic vasculitis
    3. RPGN
‣
Eosinophilic granulomatosis with polyangiitis
  • ✚ pANCA (anti-MPO)
  • Triad:
    1. Allergic asthma
    2. Eosinophilia
    3. RPGN
‣
Microscopic polyangiitis (MPA)
  • ✚ pANCA (anti-MPO)
  • Triad:
    1. Pulmonary infiltrates
    2. CNS/MSK abnormalities
    3. RPGN
‣
What is seen on histology?
  • Crescentic glomerulonephritis
‣
Post-streptococcal
‣
How do they present?
  • 10-14 days following an URTI
‣
How would you investigate?
  1. Anti-Streptolysin O (ASO) titre
  2. Anti-DNase antibody
‣
How would you manage them?
  • Antibiotics & conservative management
‣
Anti-GBM (Goodpasture)

Anti-GBM antibodies attack type 4 collagen in the basement membrane of the lungs & kidneys.

‣
How do they present?
  • Lungs → Haemoptysis
  • Kidneys → Haematuria
‣
What is a key differential? How do you differentiate between them?
  • Granulomatosis with polyangiitis
  • Antibodies: cANCA & anti-GBM
‣
How would you manage them?
  1. Plasmapheresis: Remove the circulating antibodies
  2. High dose IV steroids / cyclophosphamide
‣
IgA nephropathy
‣
How do they present?
  • 2 days following an URTI with:
    • macroscopic haematuria or;
    • asymptomatically with microscopic haematuria and proteinuria.
‣
Key exam question: How do you differentiate between IgA nephropathy and post-streptococcal?
  • Time from infection to presentation:
    • Days from infection → IgA nephropathy
    • Weeks from infection → Post-streptococcal
‣
What would you see on histology?
  1. IgA deposits
  2. Glomerular mesangial proliferation
‣
Membranoproliferative

Deposits in the basement membrane causing thickening, with the membrane being rebuilt around them causing ‘team-tracking’.

‣
When does this present?

Bimodal:

  • 20 year olds
  • 60 year olds
‣
What would histology show?
  • Deposits of IgG and complement on the basement membrane
‣
What diseases can cause this?
  • Primary: Majority are idiopathic
  • Secondary:
    • Haemolytic uraemic syndrome
    • Autoimmune diseases: SLE, scleroderma, Sjögrens
    • Cancer: Leukaemia, lymphoma
    • Infections: Hepatitis B/C
‣
🚇 Tubule / Interstitium
‣
Tubule
‣
Acute tubular necrosis

Epithelial death of the renal tubules due to ischaemia or toxins.

‣
Is it reversible?
  • The cells can regenerate in 1-3 weeks therefore it is reversible.
‣
What are the causes?
  • Ischaemia:
    • Sepsis
    • Shock (e.g. hypovolaemic)
    • Dehydration
  • Toxins:
    • NSAIDs
    • Radiology contrast dye
    • Gentamicin
‣
What is the key feature on urinalysis?
  • Muddy brown casts
‣
How would you manage them?
  • Supportive management, e.g. adequate hydration with IV fluids
  • Stop nephrotoxic medications
‣
Renal tubular acidosis
‣
What metabolic abnormality would all of these patients present with?
  • Hyperchloraemic metabolic acidosis (normal anion gap)
‣
Name the disease based on the physiology:
‣
Collecting duct: ↓ Aldosterone → Proximal ammonium excretion
  • Type 4
‣
Proximal tubule: ↓ HCO₃⁻ reabsorption
  • Type 2
‣
Distal tubule: ↓ H⁺ secretion
  • Type 1
‣
What is the potassium in each type?
  • Type 1: ↓
  • Type 2: ↓
  • Type 4: ↑

Common relationships:

‣
Fanconi syndrome causes which type?
  • Type 2
‣
Rheumatoid arthritis and SLE cause which type?
  • Type 1
‣
Nephrocalcinosis is a complication of which type?
  • Type 1
‣
Polycystic kidney disease (PKD)

A genetic disorder causing cysts develop from cells in the tubular portion of the nephron and collecting ducts.

‣
Autosomal dominant (more common)
‣
What genes are affected in this?
  1. PKD 1 — Accounts for more cases and has a more severe phenotype
  2. PKD 2 — Accounts for around 15% of ADPKD and is less severe
‣
What is the pathophysiology?
  • Dilatation and out-pouching of tubule wall → Glomerulus filters fluid into the newly formed cyst → Cysts separate from nephron, isolating them → Impaired renal function.
CDC/ Dr. Edwin P. Ewing, Jr., Public domain, via Wikimedia Commons
CDC/ Dr. Edwin P. Ewing, Jr., Public domain, via Wikimedia Commons
‣
How might they present?

Symptoms:

  • Abdominal pain
  • Renal colic
  • Haematuria
  • Polyuria, polydipsia, nocturia: Unresponsive to ADH → Unconcentrated urine
  • Dysuria

Signs:

  • Abdominal mass
  • Hypertension
  • Hepatomegaly
‣
What other organs can be affected?
  • Liver: Hepatic ducts express the same proteins
  • Pancreas: Pancreatic ducts express the same proteins
  • Brain: Cerebral aneurysms
  • Heart: Valvular disease
‣
How would you investigate?

Bedside:

  • Urinalysis

Bloods:

  • FBC: looking for anaemia if PKD causing CKD
  • U&E: assessing renal function
  • Bone profile: calcium/phosphate regulation given 1-ɑ-hydroxylase produced in the kidney
  • LFT: looking for hepatic impairment
  • CRP: looking for cyst infection

Imaging:

  • Ultrasound abdomen
  • CT KUB: if presenting with renal colic and querying a stone
  • Renal MRI/CT
  • Cerebral imaging
‣
How would you manage them?
  1. Manage hypertension (< 130/80 mmHg)
  2. Vasopressin (V2) receptor antagonists may be used in patients high-risk of progression
  3. Treat UTIs and infected cysts
‣
Autosomal recessive

ARPKD is a rarer and often more severe form of cystic disease, involving the kidneys and biliary tract.

‣
When & how does this present?
  • In utero or in the neonatal period with bilaterally enlarged echogenic kidneys and can be life-threatening.
  • In older children it manifests as portal hypertension or cholangitis.
‣
What gene is affected?
  • PKHD1 gene on chromosome 6 → Codes for fibrocystin/polyductin protein complex (FPC) → Creation of tubules and maintaines healthy renal, hepatic and pancreatic epithelial tissue.
‣
Rhabdomyolysis

Rhabdomyolysis: Injury to skeletal muscle cells → Release of intracellular ions, myoglobin, creatine kinase (CK) & urates → Obstruction & direct toxicity to renal tubules.

‣
What key features would you look for on history & examination?
  1. Recent crush injury: Traumatic injury
  2. Prolonged immobilisation: Long lie
  3. Muscular pain, swelling or weakness
  4. Dark urine
  5. Other risk factors: Alcohol, cocaine, amphetamine, phencyclidine, narcotics, diuretics
‣
What are the key investigations?

Bedside:

  • Urinalysis: + Blood

Bloods:

  • Serum CK > 5 times normal or > 1000 IU/L
  • U&E: ↑ potassium, magnesium, and phosphate; ↓ calcium
  • FBC: ↓ haemoglobin & platelets (looking for DIC)
‣
How would you manage them?
  1. Hydration: IV fluids (400 mL/hour with a range of 200 mL/hour to 1000 mL/hour is considered reasonable as goal-directed therapy)
  2. Correct electrolytes: Correct hyperkalaemia if present
‣
Obstruction
‣
Crystal nephropathy

High concentration of ions and molecules passing through tubules → Precipitation & deposition of crystals → Tubular obstruction → AKI +/- CKD.

‣
What drugs can cause this?
  1. Methotrexate
  2. Aciclovir
  3. Ciprofloxacin
  4. Amoxicillin
‣
Monoclonal gammopathies

Monoclonal gammopathy (e.g. multiple myeloma) → Light-chain deposition in tubules → Light-chain cast nephropathy → Renal insufficiency.

‣
Note: This is rare.
  • Consider this as a differential but it’s rare and unlikely to come up in exams.
  • ~ 20% of patients with multiple myeloma have renal failure at the time of diagnosis.
‣
What features may you expect?
  • Nephrotic syndrome: Oedema, effusions
  • Hepatomegaly
  • Heart failure features if overloaded
‣
How would you investigate?
  1. Serum protein electrophoresis with immunofixation
  2. 24-hour urine for urine protein electrophoresis and immunofixation
  3. Renal biopsy
‣
Interstitium
‣
Acute interstitial nephritis

Acute inflammation of the renal tubulo-interstitium usually triggered by medications.

‣
What is this?
  • Inflammation of the renal interstitium secondary to a hypersensitivity reaction
‣
How do they present?
  • Triggering medication causing hypersensitivity symptoms:
    • Rash
    • Fever
    • Arthralgia
  • Signs & symptoms of renal dysfunction:
‣
What are the two broad causes?
‣
Medications: What medications cause this?
  1. Antibiotics (e.g. penicillins, sulfa drugs, cephalosporins & quinolones)
  2. NSAIDs
  3. Diuretics
  4. Rifampicin
  5. Allopurinol
‣
Chronic inflammatory disease: What diseases cause this?
  1. Vasculitis
  2. Systemic lupus erythematosus
  3. Sjogren syndrome
  4. Sarcoidosis
‣
How would you investigate them?

Bedside:

  • Urinalysis: Sterile pyuria; low-grade proteinuria; WBC casts

Bloods:

  • FBC: May show eosinophilia
  • U&E: Renal dysfunction
  • Antibodies: ANCA, ANA, anti-ds DNA, complement
‣
How do you manage them?
  1. Stop potentially triggering medications: AKI may resolve following this.
  2. Supportive care: Fluid and electrolyte balance.
  3. Diuretics: Use if retaining fluid, e.g. 40-100 mg IV furosemide.
  4. Steroids: If inflammatory cause, steroids are suggested to improve the rate and extent of renal recovery.
‣
Pyelonephritis

Severe infectious inflammatory disease of the renal parenchyma, calices, and pelvis that can be acute, recurrent, or chronic.

‣
What pathogen most commonly causes this?
  • Enteric bacteria (e.g. E. coli) that either:
    • ascend from the lower urinary tract or;
    • spread haematogenously to the kidney
‣
How do they present?
  • Flank pain
  • Costo-vertebral angle tenderness
  • Fever
  • New or different myalgia, or flu-like symptoms
  • Presence of risk factors: UTI, diabetes mellitus, stress incontinence, catheter, renal calculus
‣
How would you investigate?

Bedside:

  • Urinalysis: Leukocytes, nitries, WBC casts
  • Urine culture: Presence of bacteria

Bloods:

  • FBC: Leukocytosis, elevated infection markers.
  • CRP: Elevated
  • U&E: Renal dysfunction

Imaging:

  • Renal ultrasound: Looking for stones & structural abnormalities
  • CT KUB (with contrast): Identify renal stones, consider if kidneys can tolerate contrast
‣
How would you manage them?
  • Antibiotics: Follow local guidance.
    • When considering antibiotics, we need to note whether they’re pregnant, relation to menopause, urological abnormalities or co-morbidities.
    • Antibiotics may include: Cefalexin, amoxicillin, trimethoprim or ciprofloxacin (avoid if pregnant).
  • Supportive care: Fluids & analgesia.
‣
What can complicate pyelonephritis?
  • Underlying medical problems (e.g. diabetes mellitus, HIV)
  • Genitourinary anatomical abnormalities
  • Obstruction (e.g. benign prostatic hypertrophy, calculi)
  • Multi-drug-resistant pathogens, more likely in some patient groups (e.g. pregnant women & men)

🚑 Emergency Medicine

‣
🔠 ABCDE Assessment
‣
Airway
‣
① How do you assess?
  • Look: Chest wall movements, accessory muscles
  • Listen:
    • Partial obstruction
      • Inspiratory stridor: obstruction at the larynx or above
      • Expiratory wheeze: obstruction of the lower airways
      • Gurgling: liquid or semisolid in the upper airways
      • Snoring: pharynx is partially occluded by the tongue or palate
    • Total obstruction (silent).
  • Feel: Feel at the mouth and nose for breath
‣
② Patient’s airway is obstructed, what now?
  • Call for help
  • Apply 15L O₂ via a non-rebreather
  • Head-tilt chin-lift / jaw thrust
  • Suction if there is liquid in the upper airways
‣
③ What airway adjuncts could you use?
  • Oropharyngeal: Patient has to be unconscious, if semi-conscious this could induce vomiting and/or laryngospasm.
  • Nasopharyngeal: Better tolerated in more conscious patients, avoid in basal skull fracture.
‣
④ Patient goes into cardiac arrest, how do you manage the airway?
  • Leave the airway adjunct in place.
  • Ventilate with a self-inflating bag: Patient needs ventilation so remove the O₂ mask and ventilate (2 people).
‣
Breathing
‣
① How do you assess?
  • Look: SpO₂, respiratory rate, chest deformity, cyanosis, accessory muscle use
  • Listen: Noisy breathing? Are breath sounds equal bilaterally?
  • Feel: Chest expansion, tracheal positioning, percussion note
‣
② How do we manage breathing issues?
  1. O₂
  2. Treat underlying cause: Antibiotics, chest drain, nebulisers
  3. Support breathing if needed: Ventilate with a self-inflating bag
‣
Circulation
‣
① How do you assess?
  • Pulse: Rate, rhythm, character
  • Capillary refill for peripheral perfusion
  • Blood pressure
  • ECG
  • Signs of bleeding
‣
② What key differentials could affect this?
  • Primary causes: ACS, arrhythmia, hypertension, valve disease
  • Secondary causes: Asphyxia, hypoxaemia, blood loss, sepsis
‣
③ How would you manage these issues?
  • Insert 2 IV cannulae (if appropriate), and take bloods
  • Treat underlying cause
  • IV fluids
‣
Disability
‣
① How do you assess?
‣
GCS
‣
What are the components?

How do you score each of the following:

‣
Eyes (E4)
  1. Not open
  2. Open to pain
  3. Open to commands
  4. Open spontaneously
‣
Voice (v05)
  1. No response
  2. Incomprehensible sounds
  3. Inappropriate words
  4. Confused
  5. Orientated
‣
Motor (M6)
  1. No response
  2. Extends from pain
  3. Flexion to pain
  4. Withdraws from pain
  5. Localises to pain
  6. Follows commands
‣
If there are different responses on both sides, which do you count?
  • The best response, e.g. flexes on one side, extends on other = M3
  • AVPU
  • PERLA
  • BM
  • Temperature
  • Check drug chart for potential iatrogentic causes
‣
Exposure
‣
① How do you assess?
  • Head-to-toe examination of the patient to look for underlying causes, maintaining patient dignity
‣
🚑 Advanced Life Support
‣
ALS Algorithm
‣
What rhythms are shockable and non-shockable?
  • Shockable:
    • VT
    • VF
  • Non-shockable:
    • PEA (hypoxia/hypovolaemia)
    • Asystole
‣
What are the 8 reversible causes to consider?

4 Hs and 4 Ts.

  • Hypoxia
  • Hypothermia
  • Hypo/hyperkalaemia: Calcium gluconate, insulin/dextrose infusion, salbutamol nebulisers
  • Hypovolaemia: Blood loss, fluid loss, sepsis
  • Thrombosis: ACS/PE
  • Tension pneumothorax: Needle decompression
  • Tamponade: Managed with needle pericardiocentesis or resuscitative thoracotomy
  • Toxins
‣
🧐 General
‣
Important emergencies
‣
Sepsis
‣
What is the immediate management of sepsis?
  • Blood cultures
  • Urine output < 0.5 ml/kg/hr
  • Fluids - 500ml NaCl (0.9%) over 15 mins
  • Antibiotics (IV) - IV tazocin
  • Lactate - VBG/ABG
  • Oxygen
‣
What is the first-line empirical antibiotic for neutropenic sepsis?
  • Tazocin (piperacillin & tazobactam) - Although check local guidelines
‣
What score is used to categorise and grade sepsis patients?
  • qSOFA / SOFA score
‣
Anaphylaxis
‣
What is it?
  • A hypersensitivity reaction causing rapid-onset life-threatening changes to airway, breathing or circulation.
‣
How do you manage it in an adult?
  1. IM adrenaline (0.5ml of 1 in 1000) & IV fluid bolus 500-1000mls
  2. IV chlorphenamine 10mg
  3. IV hydrocortisone 200mg
‣
Why must you monitor the patient for at least 6 hours?
  • Due to the risk of a biphasic reaction.
‣
Status epilepticus
‣
What is it?
  • Seizure lasting longer than 5 minutes, or more than 3 seizures in one hour.
‣
What is the most common cause in children and in adults, respectively?
  • Children: Infection
  • Adults: Diagnosed epilepsy but not taking their medication properly
‣
At what point can a tonic-clonic seizure cause irreversible neuronal damage?
  • After 30 minutes
‣
How do you manage this?

ABCDE approach

  1. IV lorazepam (repeat after 10 mins)
    • Medical options in community: Buccal midazolam, rectal diazepam (can't give anything orally as patients can't swallow)
  2. IV phenytoin or phenobarbitol
  3. RSI/rapid sequence induction e.g. with propofol → Intubation and ventilation → Transfer to ITU
‣
Meningitis
‣
When do you give benzylpenicillin?
  • If you're worried about meningococcal septicaemia, i.e. rash, really unwell, observations are off, can't get to hospital in time.
‣
How do you manage it?
  1. IV cephalosporin e.g. Cefotaxime +/- amoxicillin (if worried about listeria)
    • If you suspect viral: Use Aciclovir (covers HSV or VZV)
  2. Give dexamethasone within 12 hours (improves mortality)
‣
Overdose Cases

Name the diagnosis.

‣
N&V, tinnitus, confusion. Initial respiratory alkalosis then metabolic acidosis.
  • Aspirin (salicylate)
    • ‣
    How would you manage this?
    • IV sodium bicarbonate (prevent acidaemia)
‣
Colour vision disturbance & electrolyte abnormalities.
  • Digoxin
    • ‣
    How would you manage this?
    • Digibind
‣
Decreased consciousness, ataxia, slurred speech & respiratory depression.
  • Benzodiazepines
    • ‣
    How would you manage this?
    • Conservative.
      • Used to be flumazenil but presents risk of precipitating acute benzodiazepine withdrawal and seizures.
‣
Confusion, reduced conscious level, respiratory depression.
  • Opiate
    • ‣
    How would you manage this?
    • Naloxone
‣
Scoring systems

What are the following scoring systems used for:

‣
Child-Pugh
  • Liver cirrhosis severity
‣
Blatchford
  • Initial admission of GI bleed
‣
Rockall
  • Upper GI bleed inclusive of endoscopy findings
‣
ABCD2
  • TIA risk stratification
‣
DAS28
  • Rheumatoid arthritis disease activity
‣
HAD
  • Anxiety
‣
PHQ-9
  • Depression severity
‣
Edinburgh scale
  • Postnatal depression
‣
AUDIT & CAGE
  • Alcohol screening
‣
Epworth
  • Sleepiness scale - Used in OSA
‣
Gleason score / IPSS
  • IPSS: BPH symptom severity score
  • Gleason: Used to grade prostate biopsy from 1 (healthy) to 5 (anaplastic)
‣
Bishop score
  • Whether induction of labour is required
‣
FRAX
  • Severity of osteoporosis
‣
😵 Shock
‣
What is shock?
  • Shock is a state of insufficient blood flow and oxygen delivery throughout the body to keep your organs and tissues functioning properly.
‣
How do you broadly categorise the causes?
‣
Amount: Hypovolaemia

Name causes of the following.

‣
① Intravascular hypovolaemia
  • Loss of Hb: Haemorrhage
    1. External: Traumatic haemorrhage, GI bleeding (oesophageal varices/peptic ulcers).
    2. Internal: Ruptured AAA, ectopic pregnancy.
  • Loss of plasma: Ascites, burns, severe dehydration, pancreatitis.
‣
② Extravascular hypovolaemia
  1. D&V
  2. Renal: Polydipsia
‣
Blockage: Obstruction
  1. Tension pneumothorax
    • High pressure within the mediastinum compresses the heart, IVC & SVC. This decreases stroke volume, therefore cardiac output.
  2. Cardiac tamponade
  3. Pulmonary embolism
    • Clot within the pulmonary circulation can cause decreased preload to the left side of the heart, and/or increased pressure in the right side of the heart due to back-pressure.
‣
Cardiogenic

Shock resulting from the heart being unable to pump enough blood and oxygen to supply tissues.

  1. Arrhythmia (fast or slow)
  2. Systolic LV or RV dysfunction: Ischaemia, cardiomyopathy, drugs (β-blockers)
  3. Diastolic dysfunction: Hypertrophy, restrictive cardiomyopathy, tamponade
  4. Excessive afterload: Pulmonary embolism, aortic stenosis
  5. Valve dysfunction: Papillary muscle rupture, endocarditis
‣
Distributive

Pathological vasodilation reduces the systemic vascular resistance, decreasing blood pressure. There are 3 key causes:

  1. Septic shock
    • Bacteria release exotoxins and/or endotoxins into vessels → Immune system reactions → Vasodilation & increased vascular permeability.
  2. Anaphylactic shock
    • Protein/antigen → Proinflammatory chemical release (histamine, leukotrienes) → Vasodilation & increased vascular permeability.
  3. Neurogenic shock
    • Spinal cord injury (above T6) or anaesthesia → Damage to sympathetic fibres → Overactivity of the vagus nerve → Excessive vasodilation
‣
How do these causes relate to the blood pressure equation?

Blood pressure = Heart rate (HR) * stroke volume (SV) * systemic vascular resistance (SVR).

  • Hypovolaemia → ↓ preload → ↓ SV
  • Obstructive: High mediastinal pressure → ↓ preload → ↓ SV
  • Cardiogenic:
    • Tachyarrhythmia → ↑ HR → No time for ventricular filling → ↓ preload → ↓ SV
    • ↓ contractility → ↓ SV and/or ↓ HR
  • Distributive: Vasodilation → ↓ SVR → ↓ preload → ↓ SV
‣
How would you manage a patient in shock?
  1. Identify and treat acute, reversible causes:
    • Sepsis 6
    • Adrenaline for anaphylaxis
    • Stop bleeding
  2. Restore intravascular volume:
    • IV fluids
    • Blood transfusion
  3. Infuse vasoactive drugs
    • Noradrenaline / dobutamine → ↑ SVR
  4. Supporting vital functions until recovery
    • Intubation and ventilation
    • Venoarterial extracorporeal membrane oxygenation (ECMO)
‣
🫠 Allergy
‣
What is the skin sensitisation theory?

Developing an allergy is dependent on 2 factors:

  1. Exposure to the allergen due to a break in the skin (eczema/skin infection) leads to an inflammatory response, due to the body thinking that they are foreign
  2. Lack of exposure to the allergen through the GI tract. If this happens then the body recognises it as food and doesn't become sensitised

Prevention relies on regular exposure to the allergen through food & minimising the risk of a break in the skin.

‣
What are the types of reaction?

What is the common name & mechanism of the following reactions:

‣
Type I

Anaphylaxis (severe reaction) / urticaria / itching

  • Mechanism: Antigen binds to IgE antibodies → Mast cell degranulation → Histamine release
    • ‣
    How do you differentiate anaphylaxis from non-anaphylactic type I reactions?
    • Anaphylaxis causes compromise of the airway, breathing or circulation
    ‣
    How do you acutely manage them?
    1. ABCDE - Inc. O2, salbutamol, IV fluids, lie flat, expose to look for flushing, urticaria & angioedema
    2. IM adrenaline (0.5ml of 1 in 1000) - Anterolateral aspect of middle third of the thigh, repeat at 5 min intervals
      • > 12 years: 500mcg
      • 6 ≤ x ≤ 12 years: 300mcg
      • < 6 years: 150 mcg
    3. PO cetirizine/chlorphenamine
    4. Steroids - IV hydrocortisone
    ‣
    Why do you need to admit them after treatment if they are stable?
    • Biphasic reaction: Second reaction after successful treatment of the first
    ‣
    How do you confirm that it was anaphylaxis & manage going forward?
    • Serum mast cell tryptase within 6 hours of the event. Tryptase is release during mast cell degraulation
    • Train parents in BLS & give them an epipen
‣
Type II

Cell-bound

  • Mechanism: IgG/IgM react to an allergen activating the complement system, NK cells & macrophages. This leads to direct local cell damage
  • Examples: Pernicious anaemia, AIHA, ITP, Goodpasture's, haemolytic disease of the newborn, transfusion reactions
‣
Type III

Immune complex

  • Mechanism: IgG/IgM immune complexes of antigen-antibody accumulate in tissues → Complement activation & cell destruction
  • Examples: SLE, post-strep glomerulonephritis, RA, HSP
‣
Type IV

Delayed hypersensitivity (48-72 hours)

  • Mechanism: T-cells are inappropriately activated causing inflammation & damage to local tissues
  • Examples: MS, contact dermatitis, organ transplant rejection
‣
Type V

Other

  • Mechanism: Antibody activates or inhibits a receptor that has a function e.g. TSH
  • Examples: Graves, myasthenia gravis
‣
What are the three main ways to test for allergy?
  1. Skin prick testing: Expose the skin to the allergen and make a small break in it, then test the size of the wheal compared to a control.
  2. RAST testing: Total & specific IgE antibodies to that allergen
  3. Food challenge testing: Gold standard, requires a lot of time & resources to be available
    4. ‣
    Why are 1 & 2 unreliable?
    • They test for sensitivity but not allergy, just because the child has the IgE antibodies, it doesn't mean they will definitely form an allergic reaction
‣
What steps are available for prophylaxis of a reaction?
  1. Establishing the allergen causing the reaction is essential, avoid that allergen & minimise exposure
  2. Prophylactic antihistamines
  3. Immunotherapy: Gradual exposure to allergens over months to desensitise them
‣
What are the options for treatment of an allergic reaction?
  1. IM adrenaline (0.5ml of 1:1000) in anaphylaxis
  2. Antihistamines (e.g. cetirizine)
  3. Steroids (PO prednisolone, TOP/IV hydrocortisone)

🧘🏽‍♂️ Oncology & Palliative Care

‣
👹 Oncology

Most cancers are discussed within their relevant specialities, this covers generic oncological concepts.

‣
Diagnosis
‣
What tumours do the following markers indicate:
‣
CA 125
  • Ovarian
‣
CA 19-9
  • Pancreatic
‣
CA 15-3
  • Breast
‣
PSA
  • Prostate
‣
AFP
  • Hepatocellular carcinoma
‣
CEA
  • Colorectal - Used to monitor disease activity
‣
S-100
  • Melanoma
  • Schwannoma
‣
Beta-hCG (w/ AFP)
  • Both raised - Testicular teratoma
  • Low AFP - Seminoma/choriocarcinoma
‣
Calcitonin
  • Medullary thyroid
‣
How does a PET scan show metabolic activity?
  • It has labelled glucose that is taken up into highly metabolically active cells and then it can be imaged.
‣
What is a PET scan used for?
  • Locating primary cancer.
  • Investigating for metastases.
‣
Management
‣
Chemotherapy
‣
Name 5 common adverse effects to chemotherapy.

Early:

  • Mucositis
  • Rash
  • Diarrhoea
  • Fatigue

Late:

  • Alopecia
  • Nail changes
  • Peripheral neuropathy
  • Fatigue

Drug-specific:

‣
Name 2 adverse effects of cyclophosphamide.

Bladder-related:

  • Haemorrhagic cystitis
  • Transitional cell carcinoma
‣
What adverse effect do cisplatin and vincristine have in common?
  • Peripheral neuropathy
    • ‣
    What is vincristine commonly used to treat?
    • Haematological malignancies
    ‣
    What electrolyte needs to be monitored in a patient on cisplatin?
    • Magnesium: Risk of dropping
‣
What side effect do you need to monitor for in a patient on doxorubicin?
  • Cardiomyopathy
‣
What 2 antibiotics are cytotoxic?
  • Doxorubicin
  • Bleomycin
‣
Name 3 adverse effects of methotrexate.
  • Mucositis
  • Myelosuppression
  • Pulmonary fibrosis / pneumonitis
‣
Radiotherapy
  1. External: External beam radiotherapy (commonest)
  2. Internal: Brachytherapy
‣
Immune Checkpoint Inhibitors
‣
How do these drugs work?
  • Boost the immune response by stopping cancer cells from suppressing T-cell function
‣
What are their main side effects?
  • Autoimmunity/inflammatory conditions: Take care in patients at risk/with autoimmune conditions

Oncological Emergencies:

‣
Malignant Spinal Cord Compression (MSCC)
‣
What are the features?
  1. Non-specific back pain (earliest & commonest)
    2. ‣
    When is the back pain likely to be worse? (2)
    1. At night, when lying down
    2. When straining or coughing
  2. Symmetrical leg weakness
  3. Examination:
    • Compression is above L1 → ↑ Tone & reflexes (UMN).
    • Compression is below L1 → ↑ Tone & reflexes (LMN), saddle anaesthesia, urinary retention, bowel incontinence.
‣
What is the gold-standard investigation?
  • MRI whole spine with contrast
‣
How would you manage them?
  1. Dexamethasone 16mg
  2. Consider:
    1. Radiotherapy
    2. Surgery for decompression (if any instability)

Where is the compression?

‣
Patient presents with spasticity and hyperreflexia in the legs and sensory loss up to the umbilicus.
  • T10 due to sensory level up to the umbilicus.
    • Must be above L1 because perianal sensation is intact & showing UMN signs.
‣
Patient presents with hypotonia and fasciculations in the legs and perianal numbness.
  • Below L1 because the compression is on the cauda equina and LMN signs are present.
‣
Superior Vena Cava Obstruction (SVCO)
‣
Name 4 features that may be present in these patients.
  1. Distended head & neck veins, raised JVP
  2. Facial & periorbital oedema
  3. Dyspnoea
  4. Visual disturbance e.g. blurred vision
‣
Name 6 potential causes.
  1. Lung cancer
  2. Lymphoma
  3. Aortic aneurysm
  4. VTE
  5. Sarcoidosis
  6. Goitre or thyroid cancer
‣
How do you manage these patients?
  1. Dexamethasone 16mg PO
  2. Superior vena cava stent
  3. Consider chemotherapy/radiotherapy if indicated
‣
Hypercalcaemia
‣
What are the common features?
  • Bones: Increased bone breakdown & fractures
  • Stones: Renal colic secondary to calcium stones
  • Psychic moans:Depression, confusion and hallucinations
  • Abdominal groans: Anorexia, N&V, constipation and pancreatitis
‣
What are your differentials?
  1. Bone malignancy
  2. Primary hyperparathyroidism
  3. Other:
    • Endocrine: Addison’s, phaeochromocytoma, hyperthyroidism
    • Dehydration
    • Respiratory: Sarcoidosis, TB
    • Drugs: Lithium, thiazides, vitamin D
‣
How do you manage them?
  1. IV Fluids: Rehydration has a dilutional effect
  2. IV bisphosphonates (e.g. pamidronate)
‣
Neutropenic sepsis
‣
What is it?
  • Fever > 38 during in a patient with neutrophil count < 0.5
‣
How would you manage them?
  • Blood cultures
  • Urine output < 0.5 ml/kg/hr
  • Fluids - 500ml NaCl (0.9%) over 15 mins
  • Antibiotics (IV) - IV tazocin
  • Lactate - VBG/ABG
  • Oxygen
‣
🧘‍♀️ Palliative Care
‣
Nausea & vomiting
‣
What 4 areas mediate nausea & vomiting?

Things in the…

‣
Gut: Gut mucosa
‣
What stimulates N&V through this pathway?
  1. GI obstruction
  2. Bowel colic
  3. Mass
  4. Constipation
  5. Pregnancy
‣
Blood: Chemoreceptor trigger zone
‣
What stimulates N&V through this pathway?
  1. Drugs - Antibiotics, cytotoxics, SSRIs, iron, opioids
  2. Toxins
  3. Uraemia
  4. Hypercalcaemia
  5. Pregnancy
‣
Ears: Vestibular apparatus
‣
What stimulates N&V through this pathway?
  • Motion
  • Vertigo
  • Tinnitus
  • ENT tumours
‣
Head: Cortical structures
‣
What stimulates N&V through this pathway?
  1. Emotions
  2. Sights
  3. Smells
  4. Raised ICP
  5. Migraine
‣
What antiemetic should be used in the following situations:
‣
Hiccups and early satiety?
  • Prokinetic: Metoclopramide/domperidone (D2 antagonist)
‣
Vertigo and brain metastases?
  • Cyclizine (H1 antagonist) & dexamethasone
‣
Secondary to chemotherapy?
  • Ondansetron (5-HT3 antagonist) or NK1
‣
Secondary to hypercalcaemia and uraemia?
  • Haloperidol
‣
Not responsive to haloperidol and ondansetron?
  • Levomepromazine (All receptors)
‣
Parkinson’s disease with N&V from uncertain cause?
  • Ondansetron or cyclizine
‣
Bowel obstruction?
  • Partial/gastric stasis: Metoclopramide
  • Complete: Cyclizine (DON'T use metoclopramide- it's prokinetic)
‣
What should you consider if the medications aren’t working?
  1. Is it being given regularly?
  2. Is it being absorbed?
  3. Is the dose optimum?
  4. Is the route appropriate?
    • Most anti-emetics can be given SC
    • Doses usually the same PO, SC and IV
  5. Do you have the correct cause?
‣
Pain
‣
Why is managing pain important?
  • Prevents tachypnoea:
    • Shallow breathing due to pain → pneumonia.
  • Increased mobility → Reduced DVT risk & retained muscle mass.
  • Better sleep, improved mood
‣
Types of opioids:
‣
What are examples of weak opioids?

They are called ‘weak opioids’ because they have a lower ceiling dose, meaning any increase in dose from there wouldn't help their pain management.

  • Codeine
  • Tramadol
  • Buprenorphine
‣
What are examples of strong opioids?
  • Morphine
  • Fentanyl
  • Oxycodone
‣
What opioids can be used in end stage renal failure?
  • Fentanyl
  • Buprenorphine
  • Oxycodone
‣
What do you need to consider before starting opioids?
  1. What have they had before? Are they opioid naive?
  2. Check bloods for renal function.
  3. Always prescribe a laxative.
‣
How is opiate pain management classified?
  1. Maintenance
    2. ‣
    How is this calculated?
    • Current maintenance + breakthrough doses in last 24h
    ‣
    If pain isn't under control at current doses, how much would you increase the dose by?
    • 1/3
    ‣
    How is the dose often split?
    • Total maintenance is often split in half and given BD
  2. Breakthrough
    3. ‣
    How do you calculate the breakthrough dose?
    • 1/6 to 1/10 of total maintenance dose

Calculation:

‣
A patient is prescribed Zomorph 30mg BD PO. What breakthrough analgesia dose is appropriate?

Calculate total daily dose:

  • 30mg x 2 = 60mg

Breakthrough is 1/6th to 1/10th of total daily dose:

  • 60mg / 6 = 10mg.
‣
Confusion
‣
What can cause this?

A few differentials (but there are many more):

  1. Metabolic disturbance (hypoglycaemia, hypercalcaemia)
  2. Infection (pneumonia, UTI)
  3. Brain metastases
  4. Anaemia
  5. Intense pain
  6. Pain medication side effect
  7. Constipation or urinary retention
  8. Dementia
‣
How do you manage this?
  • Conservative: Ensure there is a clock and calendar in the room, the room is well lit during the day, regular family visiting, hearing aids and anything to improve their senses
  • If hallucinating, consider haloperidol.
‣
How would you manage terminal agitation?

Applies when reversible causes have been excluded and patient is in terminal phase of illness:

  1. Midazolam (benzodiazepines)
‣
Secretions
‣
Why does this occur?
  • Patient is too weak to cough and clear them, poor swallowing. They can be salivary or bronchial.
‣
How do you manage this?
  • Positional: Reposition patients more upright
  • Medical: Glycopyronnium bromide, hyoscine hydrobromide
  • Physical: Suction
‣
Constipation
‣
What can cause this?
  • Lifestyle-related
    • Low fibre
    • Dehydration
    • Environment
    • Confusion
  • Disease-related
    • Hypercalcaemia
    • Hypothyroidism
    • Spinal cord compression
    • Mechanical obstruction
  • Drug-related
    • Opioids
    • Anticholinergics
    • TCAs
‣
How do you manage this?
  1. Lifestyle: Increase fibre and fluid intake, mobilisation
  2. Laxative:
    • Stimulant laxative: Senna
    • Osmotic laxative: Macrogol (often requires lots of fluid intake so not always suitable)
    • Stool softener
‣
Breathlessness
‣
What can cause this?
  • Infection
  • Bronchospasm
  • Pleural effusion
  • Pulmonary embolism
  • Heart failure
  • Anaemia
  • Large airway obstruction from malignancy
‣
How do you management the non-reversible causes?
  • Low dose opioids, if already on morphine: Increase dose by 25%
  • Benzodiazepines, e.g. diazepam
‣
Hiccups
‣
What are the causes?
  • Commonest: GI distension from gastric stasis
  • Phrenic nerve irritation
  • GORD
‣
How do you manage this?
  1. Chlorpromazine
  2. Haloperidol

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