General medicine: CL Lai Session 1

Question 1

When there is PUO, what should we think of?

Answer 1

• Infection
• Autoimmune (female)
• Malignancies (elderly)

Question 2

What type of malaria will give rise to methaemoglobinaemia?

Answer 2

Methhaemoglobinaemia: Falciparum

Question 3

What are the causes of cafe au lait complexion?

Answer 3

• Renal failure (au lait (anemia) and cafe (B-MSH which cant be filtered by the kidney)
• Neurofibromatosis: 5-6 spots –> 1.5cm large
• Haematological malignancies
• Infective endocarditis

Question 4

Patient with history of ESRF on CAPD presents with SOB (present CVS first in patient presentation) what PE and Ix to do?

Answer 4

PE
Look for gouty tophi
Signs of fluid retention
Cardiovascular exam: pulse, increased JVP (pulmonary congestion), apex beat, apical impulse (LVH) note if its normal). If RVH –> parasternal heave. If there is added S3 and S4.
Check peritoneal dialyssi tube and peritoneal signs

Ix to prove if there is pulmonary congestion, MI
* CXR
* sO2, pO2
* ECG
* RFT
* Peritoneal tap analysis (appearance, cell count and culture)
* Echocardiogram

Question 5

How is K affected in renal failure?

Answer 5

• HyperK
• As there is metabolic acidosis in chronic kidney disease. Decreased ability of the kidney to produce ammonia is directly related to the inability to uptake glutamine from the proximal tubule in CKD.
• The inability of the kidneys to generate enough ammonia to neutralize the daily acid load leads to non anion gap metabolic acidosis.
• The metabolic acidosis brings out intracellular K+ inducing hyperK

Urinary ammonia produced in the proximal tubule cells from systemically derived gluatmine. In the proximal tubule the conversion of glutamien to glutamate ad then oxaloacetate, produces 2 ammonium and 2 HCO3- ions.
The production of ammonia by the kidneys is the major mechanism of new HCO3- formation in metabolic acidosis and is increased several times more than titratable acid excretion.

Question 6

Patient has AST over 1000, what are the causes?

Answer 6

• Hepatitis: hep E most common (related to pork), than hep A, than hep B (acute and acute on chronic)
  If HBsAg+ve how to differentiate acute vs acute on chronic: ask about sexual history
  IgM Anti HBc+ve: both acute and acute on chronic
  IgM Anti HBc-ve: acute on chronic
  Check HBsAg in 6 months to know status. Acute will clear HBsAg in 6 months. If acute on chronic HBsAg will still be positive
  Hep B: Incubation period of 12-24 weeks
• Drug induced: INH
• Autoimmune hepatitis (can present fulminantly occasionally)
• Wilsons disease (young patient): serum copper and ceruloplasmin
• Cardiac congestion (normally presents with liver congestion)

Question 7

What are the specific complications of short course steroid therapy?

Answer 7

• Hyperglycemia
• HypoK (if given more than 20mg –> prescribe slow K)
• Infection

Question 8

What are the overall complications of corticosteroid therapy?

Answer 8

• Osteoporosis
• Avascular necrosis of femur
• Cushing syndrome (HT, DM, thin skin, abd stirae (due to increased subcutaneous tissue)
• Reactivation of latent infection: hep B (has glucocorticoid responsive element –> increases viral load and suppresses the immune system. When stop steroids –> causes immune rebound that attacks the high viral load infected hepatocytes. This can happen for up to 10 weeks), TB
• Cataracts