MBBS Internal Medicine Flashcards

24 sample cards from the Internal Medicine deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. What antibody serology and imaging are characteristic for the two forms of IBD?

   Ulcerative colitis: p-ANCA positive. Crohn's disease: ASCA (anti-Saccharomyces cerevisiae antibody) positive. Crohn's imaging may show 'string sign' on barium follow-through due to terminal ileal stricturing.

2. Outline the stepwise pharmacological management of inflammatory bowel disease.

   Induction: aminosalicylates (5-ASA, mainly UC) and/or corticosteroids for flares. Maintenance: 5-ASA (UC), immunomodulators (azathioprine, methotrexate), and biologics (anti-TNF e.g. infliximab) for moderate-severe or refractory disease.

3. Name three extraintestinal manifestations common to inflammatory bowel disease.

   Erythema nodosum, pyoderma gangrenosum, anterior uveitis/episcleritis, enteropathic arthritis (peripheral and axial/sacroiliitis), and primary sclerosing cholangitis (strongly associated with ulcerative colitis).

4. Which organism is the most common cause of bloody, invasive bacterial diarrhea associated with pseudoappendicitis, and which is linked to Guillain-Barré syndrome?

   Campylobacter jejuni is the most common cause of bacterial diarrhea and is the classic antecedent infection of Guillain-Barré syndrome. It can cause pseudoappendicitis from mesenteric adenitis/terminal ileitis.

5. What is the most common cause of antibiotic-associated pseudomembranous colitis, and its first-line treatment?

   Clostridioides difficile (toxins A and B). First-line treatment is oral vancomycin or fidaxomicin; stop the offending antibiotic. Fecal microbiota transplant is used for recurrent disease.

6. Differentiate the mechanisms of secretory versus invasive (inflammatory) infectious diarrhea, giving one example each.

   Secretory (non-inflammatory): toxin-mediated water/electrolyte secretion, watery diarrhea, no blood/leukocytes—e.g. Vibrio cholerae, ETEC. Invasive (inflammatory): mucosal invasion causing bloody diarrhea with fecal leukocytes—e.g. Shigella, Salmonella, EHEC.

7. Which gastrointestinal infection is associated with hemolytic uremic syndrome, and what is the responsible toxin?

   Enterohemorrhagic E. coli (EHEC, serotype O157:H7) producing Shiga (verotoxin). HUS is the triad of microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. Antibiotics are avoided as they may increase HUS risk.

8. State the two most common causes of acute pancreatitis.

   Gallstones (biliary) and alcohol account for ~80% of cases. The mnemonic 'I GET SMASHED' covers others: Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion sting, Hypercalcemia/Hypertriglyceridemia, ERCP, Drugs.

9. What are the diagnostic criteria for acute pancreatitis (revised Atlanta classification)?

   Diagnosis requires $\geq 2$ of 3: (1) characteristic epigastric pain radiating to the back; (2) serum lipase or amylase $> 3 \times$ the upper limit of normal; (3) characteristic findings on cross-sectional imaging (CT/MRI/US).

10. Name two clinical signs of severe hemorrhagic acute pancreatitis and what they represent.

    Cullen's sign (periumbilical bruising) and Grey Turner's sign (flank bruising). Both indicate retroperitoneal hemorrhage tracking to the skin in severe necrotizing pancreatitis.

11. List the key features and diagnostic triad/findings of chronic pancreatitis.

    Chronic inflammation causing irreversible fibrosis. Classic triad: pancreatic calcification, steatorrhea, and diabetes mellitus. Features include chronic epigastric pain, exocrine insufficiency (malabsorption), and endocrine insufficiency. Imaging shows calcifications/ductal changes.

12. Define acute kidney injury (AKI) using the KDIGO serum creatinine and urine output criteria.

    AKI is diagnosed by any of: rise in serum creatinine $\geq 0.3$ mg/dL ($26.5\ \mu mol/L$) within 48 h; rise to $\geq 1.5 \times$ baseline within 7 days; or urine output $< 0.5$ mL/kg/h for $\geq 6$ hours.

13. Classify the three major categories of AKI by anatomical site of insult.

    (1) Prerenal—decreased renal perfusion; (2) Intrinsic (intrarenal)—direct damage to renal parenchyma (tubules, glomeruli, interstitium, vessels); (3) Postrenal—obstruction of urinary outflow tract.

14. List the main prerenal causes of AKI.

    True volume depletion (hemorrhage, vomiting, diarrhea, burns, diuretics), reduced effective circulating volume (heart failure, cirrhosis, sepsis/distributive shock), renal artery stenosis, and drugs impairing autoregulation (NSAIDs, ACE inhibitors/ARBs).

15. What is the most common cause of intrinsic AKI, and what causes it?

    Acute tubular necrosis (ATN). It is caused by ischemia (prolonged prerenal hypoperfusion) or nephrotoxins (aminoglycosides, contrast media, myoglobin in rhabdomyolysis, hemoglobin, cisplatin).

16. List the four sub-categories of intrinsic AKI by the renal structure involved.

    (1) Tubular—acute tubular necrosis; (2) Interstitial—acute interstitial nephritis (often drug-induced); (3) Glomerular—glomerulonephritis; (4) Vascular—vasculitis, thrombotic microangiopathy, cholesterol emboli.

17. List the common postrenal (obstructive) causes of AKI.

    Bilateral ureteric obstruction (stones, tumors, retroperitoneal fibrosis), bladder outlet obstruction (benign prostatic hyperplasia, prostate cancer), urethral stricture, and blocked urinary catheter. Obstruction must be bilateral (or unilateral in a single functioning kidney) to cause AKI.

18. Describe the typical clinical features of AKI.

    Often asymptomatic early. Features include oliguria/anuria, fluid overload (edema, pulmonary edema, hypertension), uremic symptoms (nausea, anorexia, confusion, pericarditis, asterixis), and signs of the underlying cause. Severe cases cause arrhythmias from hyperkalemia.

19. How does fractional excretion of sodium ($FE_{Na}$) help differentiate prerenal AKI from ATN? Give the formula and cutoffs.

    $$FE_{Na} = \frac{U_{Na} \times P_{Cr}}{P_{Na} \times U_{Cr}} \times 100\%$$ Prerenal: $FE_{Na} < 1\%$ (avid sodium reabsorption). ATN (intrinsic): $FE_{Na} > 2\%$ (impaired reabsorption). Less reliable if diuretics have been given.

20. Compare urine osmolality, urine sodium, and BUN:creatinine ratio in prerenal AKI versus ATN.

    Prerenal: urine osmolality $> 500$ mOsm/kg (concentrated), urine $Na^+ < 20$ mmol/L, BUN:creatinine ratio $> 20:1$. ATN: urine osmolality $< 350$ mOsm/kg (isosthenuric), urine $Na^+ > 40$ mmol/L, BUN:creatinine ratio $\approx 10-15:1$.

21. Which urine microscopy finding is characteristic of acute tubular necrosis?

    Muddy brown granular casts (and renal tubular epithelial cell casts). In contrast, white cell casts/eosinophils suggest acute interstitial nephritis, and red cell casts suggest glomerulonephritis.

22. Outline the general (supportive) management principles of AKI.

    Treat the underlying cause; optimize volume status (fluids for prerenal, diuretics/restriction for overload); stop nephrotoxic drugs and adjust drug doses; correct electrolyte/acid-base disturbances (especially hyperkalemia); relieve obstruction (catheter/stent); monitor and consider dialysis if needed.

23. List the emergency indications for renal replacement therapy (dialysis) in AKI using the 'AEIOU' mnemonic.

    Acidosis (severe metabolic, refractory), Electrolyte abnormality (refractory hyperkalemia), Intoxication (dialyzable toxins), Overload (refractory fluid/pulmonary edema), Uremia (pericarditis, encephalopathy, bleeding).

24. Describe the emergency management of severe hyperkalemia complicating AKI.

    (1) Stabilize the myocardium with IV calcium gluconate; (2) shift $K^+$ intracellularly with insulin plus dextrose and nebulized salbutamol (and bicarbonate if acidotic); (3) remove $K^+$ from the body with potassium binders or dialysis. Stop potassium-sparing drugs.

What this deck covers

Internal Medicine flashcards FAQ