Examius

🌍 MBBS · subject

MBBS Internal Medicine Syllabus

The Internal Medicine syllabus for MBBS in full: 10 chapters, 42 topics and 85 sub-topics, every one listed below, plus 50 Internal Medicine flashcards with answers.

10Chapters
42Topics
85Sub-topics
50Flashcards

Internal Medicine syllabus: all 10 chapters

Expand any chapter to see its topics and sub-topics.

  1. Ischemic heart disease

     3 topics
    • Acute coronary syndrome
      • STEMI
      • NSTEMI
      • Unstable angina
    • Stable angina
    • Chronic ischemic heart disease

  2. Asthma

     4 topics
    • Pathophysiology
    • Clinical Features
    • Diagnosis
    • Management
      • Inhaled Corticosteroids
      • Bronchodilators
      • Biologics

  3. Gastroenterology

     5 topics
    • Gastrointestinal bleeding
      • Upper gastrointestinal bleeding (peptic ulcer disease, esophageal varices)
      • Lower gastrointestinal bleeding (diverticulosis, colorectal cancer)
    • Liver diseases
      • Hepatitis (viral hepatitis, alcoholic hepatitis)
      • Cirrhosis
      • Non-alcoholic fatty liver disease (NAFLD)
      • Hepatocellular carcinoma
    • Inflammatory bowel disease (IBD)
      • Crohn's disease
      • Ulcerative colitis
    • Gastrointestinal infections
      • Gastroenteritis (viral, bacterial)
      • Clostridium difficile infection
      • Parasitic infections
    • Pancreatic diseases
      • Acute pancreatitis
      • Chronic pancreatitis
      • Pancreatic cancer

  4. Acute kidney injury (AKI)

     6 topics
    • Prerenal causes of AKI
    • Intrinsic causes of AKI
    • Postrenal causes of AKI
    • Clinical features of AKI
    • Diagnosis of AKI
    • Management of AKI

  5. Diabetes mellitus

     5 topics
    • Type 1 diabetes
    • Type 2 diabetes
    • Diabetic ketoacidosis (DKA)
    • Hyperosmolar hyperglycemic state (HHS)
    • Diabetic complications
      • Retinopathy
      • Nephropathy
      • Neuropathy

  6. Anemia

     4 topics
    • Iron deficiency anemia
    • Megaloblastic anemia
      • Vitamin B12 deficiency
      • Folate deficiency
    • Hemolytic anemia
      • Autoimmune hemolytic anemia
      • Hereditary spherocytosis
    • Aplastic anemia

  7. Infectious Diseases

     5 topics
    • Bacterial Infections
      • Sepsis
      • Pneumonia (community-acquired)
      • Pneumonia (hospital-acquired)
      • Urinary Tract Infection (UTI)
      • Skin and Soft Tissue Infections
      • Tuberculosis
    • Viral Infections
      • Human Immunodeficiency Virus (HIV)
      • Viral Hepatitis (Hepatitis B)
      • Viral Hepatitis (Hepatitis C)
      • Influenza
      • Herpes Simplex Virus (HSV)
      • Varicella-Zoster Virus (VZV)
    • Fungal Infections
      • Candidiasis
      • Aspergillosis
      • Cryptococcosis
      • Histoplasmosis
    • Parasitic Infections
      • Malaria
      • Leishmaniasis
      • Toxoplasmosis
      • Schistosomiasis
    • Antimicrobial Therapy
      • Antibiotics (Penicillins)
      • Antibiotics (Cephalosporins)
      • Antibiotics (Fluoroquinolones)
      • Antifungals
      • Antivirals
      • Antiparasitic Drugs

  8. Rheumatology

     4 topics
    • Rheumatoid arthritis
      • Pathophysiology
      • Clinical features
      • Diagnosis (rheumatoid factor, anti-CCP antibodies)
      • Management (disease-modifying antirheumatic drugs, biologics)
    • Systemic lupus erythematosus (SLE)
      • Clinical features
      • Diagnosis (antinuclear antibodies, anti-dsDNA antibodies)
      • Management (corticosteroids, immunosuppressants)
    • Spondyloarthropathies
      • Ankylosing spondylitis
      • Psoriatic arthritis
      • Reactive arthritis
      • Enteropathic arthritis
    • Vasculitis
      • Giant cell arteritis
      • Takayasu arteritis
      • Polyarteritis nodosa
      • Granulomatosis with polyangiitis (Wegener's granulomatosis)

  9. Geriatrics

     3 topics
    • Geriatric syndromes
      • Falls
      • Delirium
      • Dementia
      • Urinary incontinence
      • Frailty
    • Polypharmacy
      • Rational prescribing in elderly patients
      • Drug interactions
      • Adverse drug reactions
    • Geriatric assessment
      • Comprehensive geriatric assessment (CGA)
      • Functional assessment
      • Cognitive assessment

  10. Vaccinations

     3 topics
    • Childhood vaccinations
      • DTaP
      • MMR
      • Varicella
    • Adult vaccinations
      • Influenza
      • Pneumococcal
      • Herpes Zoster
    • Travel vaccinations

MBBS Internal Medicine flashcards — 50 questions with answers

  1. Define acute coronary syndrome (ACS) and list the three clinical entities it encompasses.

    ACS is a spectrum of conditions caused by acute myocardial ischemia from reduced coronary blood flow. The three entities are: (1) unstable angina (UA), (2) non-ST-elevation myocardial infarction (NSTEMI), and (3) ST-elevation myocardial infarction (STEMI).

  2. What is the core pathophysiological event underlying most cases of acute coronary syndrome?

    Rupture or erosion of a vulnerable (lipid-rich, thin fibrous cap) atherosclerotic plaque, exposing thrombogenic material that triggers platelet aggregation and thrombus formation, causing partial or complete coronary occlusion.

  3. Distinguish unstable angina from NSTEMI on the basis of biomarkers and ECG.

    Both show ischemic symptoms without ST elevation (often ST depression/T-wave inversion). Unstable angina has NORMAL cardiac troponin (no myocardial necrosis), whereas NSTEMI has ELEVATED troponin indicating myocyte necrosis.

  4. Which ECG finding defines STEMI, and what is the typical territory-to-artery correlation for an inferior STEMI?

    STEMI is defined by new ST-segment elevation in two contiguous leads (with reciprocal changes). An inferior STEMI shows ST elevation in leads II, III, and aVF, usually due to occlusion of the right coronary artery (RCA).

  5. What is the gold-standard biomarker for diagnosing myocardial infarction, and what is its time course?

    Cardiac troponin (T or I) is the gold standard. It rises within 3-4 hours of injury, peaks at 24-48 hours, and remains elevated for 7-14 days. High-sensitivity troponin allows earlier detection.

  6. State the initial medical management mnemonic 'MONA-BASH' components for ACS.

    Morphine, Oxygen (only if $SpO_2 < 90\%$), Nitrates, Aspirin, plus Beta-blocker, ACE inhibitor, Statin, Heparin (anticoagulation) and a second antiplatelet (P2Y12 inhibitor).

  7. What is the preferred reperfusion strategy for STEMI and the key time targets?

    Primary percutaneous coronary intervention (PCI) is preferred. Target door-to-balloon time $\leq 90$ minutes. If PCI is unavailable, fibrinolysis should be given within 30 minutes (door-to-needle) and ideally within 12 hours of symptom onset.

  8. Define stable angina and describe its classic clinical triad.

    Stable angina is predictable, exertional chest discomfort due to fixed coronary stenosis causing demand-supply mismatch. Classic triad: (1) substernal chest discomfort, (2) provoked by exertion/emotional stress, (3) relieved within minutes by rest or sublingual nitroglycerin.

  9. What is the underlying pathophysiology of stable angina versus unstable angina?

    Stable angina results from a FIXED atherosclerotic stenosis (usually $>70\%$) causing ischemia only when myocardial oxygen demand rises. Unstable angina results from an acute, dynamic event—plaque rupture with non-occlusive thrombus—causing ischemia at rest.

  10. What is the first-line investigation to confirm stable angina in a patient able to exercise, and what defines a positive result?

    Exercise (treadmill) ECG stress testing. A positive (ischemic) result is horizontal or downsloping ST-segment depression $\geq 1$ mm. CT coronary angiography is increasingly first-line for anatomical assessment.

  11. List the first-line anti-anginal drug classes for symptomatic relief in stable angina.

    Beta-blockers and/or calcium channel blockers are first-line. Short-acting sublingual nitrates are used for acute relief. Second-line options include long-acting nitrates, ivabradine, nicorandil, and ranolazine.

  12. Which two drug classes reduce mortality (prognostic benefit) in chronic ischemic heart disease, beyond symptom control?

    Antiplatelet therapy (aspirin, or clopidogrel) and statins (high-intensity) improve prognosis. ACE inhibitors are added in patients with diabetes, hypertension, LV dysfunction, or prior MI.

  13. Define chronic (stable) ischemic heart disease and name its major modifiable risk factors.

    A chronic condition of myocardial ischemia from established coronary atherosclerosis. Major modifiable risk factors: smoking, hypertension, diabetes mellitus, dyslipidemia (high LDL), obesity, physical inactivity, and an atherogenic diet.

  14. What is Prinzmetal (variant) angina and its characteristic ECG finding?

    Angina caused by coronary artery vasospasm, occurring typically at rest and at night, in patients who may have normal/near-normal coronary arteries. ECG shows transient ST-segment ELEVATION during the episode that resolves with vasospasm relief.

  15. Name three mechanical complications of acute myocardial infarction and their typical timing.

    (1) Papillary muscle rupture → acute mitral regurgitation (days 3-5); (2) ventricular septal rupture → VSD (days 3-5); (3) free wall rupture → tamponade (days 3-7). Earlier complications include arrhythmias and cardiogenic shock.

  16. Differentiate upper from lower gastrointestinal bleeding by anatomical landmark and typical presentation.

    The landmark is the ligament of Treitz (duodenojejunal flexure). Upper GI bleeding (proximal) presents with hematemesis and/or melena. Lower GI bleeding (distal) typically presents with hematochezia (fresh blood per rectum).

  17. List the two most common causes of upper GI bleeding.

    (1) Peptic ulcer disease (the most common cause), and (2) esophageal/gastric variceal bleeding (in portal hypertension). Other causes: Mallory-Weiss tear, erosive gastritis/esophagitis, and malignancy.

  18. What scoring systems are used to risk-stratify upper GI bleeding, and what does each assess?

    The Glasgow-Blatchford score (pre-endoscopy) assesses need for intervention/admission; a score of 0 may allow outpatient management. The Rockall score (uses endoscopy findings) predicts rebleeding and mortality.

  19. Outline the acute management priorities for a patient with variceal upper GI bleeding.

    Resuscitate (ABC, IV access, fluids/blood, restrictive transfusion to Hb $\geq 7$ g/dL), give a vasoactive drug (terlipressin/octreotide), prophylactic antibiotics, then urgent endoscopic variceal band ligation. Balloon tamponade or TIPS if refractory.

  20. Define cirrhosis and name its two histopathological hallmarks.

    Cirrhosis is the end-stage of chronic liver disease characterized by diffuse hepatic fibrosis and the replacement of normal architecture by regenerative nodules. The two hallmarks are bridging fibrosis and regenerative nodule formation.

Show the other 30 Internal Medicine flashcards

  1. List the major clinical features (stigmata) of chronic liver disease.

    Spider naevi, palmar erythema, gynecomastia, jaundice, ascites, caput medusae, asterixis (flapping tremor), leukonychia, clubbing, Dupuytren's contracture, and signs of portal hypertension (splenomegaly, varices).

  2. What is the Child-Pugh score and which five parameters does it use?

    It grades severity/prognosis of cirrhosis. The five parameters are: serum Bilirubin, serum Albumin, Prothrombin time (INR), Ascites, and Encephalopathy (mnemonic 'BAP-AE'). Classes A, B, C indicate increasing severity.

  3. Give the formula and components of the MELD score used for liver transplant prioritization.

    MELD uses bilirubin, INR, and creatinine: $$\text{MELD} = 3.78\ln(\text{bilirubin}) + 11.2\ln(\text{INR}) + 9.57\ln(\text{creatinine}) + 6.43$$ Higher scores indicate worse short-term mortality and higher transplant priority.

  4. What is the pathophysiology of hepatic encephalopathy and its first-line treatment?

    Failure of the liver to clear nitrogenous/ammonia from the gut leads to neurotoxicity; precipitants include GI bleeding, infection, and constipation. First-line treatment is lactulose (reduces ammonia absorption); rifaximin is added as a non-absorbable antibiotic.

  5. Compare ulcerative colitis and Crohn's disease in terms of distribution and depth of inflammation.

    Ulcerative colitis: continuous inflammation limited to the colon/rectum, mucosa and submucosa only (superficial). Crohn's disease: skip lesions anywhere from mouth to anus (commonly terminal ileum), transmural (full-thickness) inflammation.

  6. List the characteristic histological features that distinguish Crohn's disease from ulcerative colitis.

    Crohn's: non-caseating granulomas, transmural inflammation, skip lesions, cobblestone mucosa, fistulae. Ulcerative colitis: crypt abscesses, continuous mucosal inflammation, pseudopolyps, and NO granulomas.

  7. 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.

  8. 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.

  9. 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).

  10. 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.

  11. 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.

  12. 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.

  13. 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.

  14. 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.

  15. 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).

  16. 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.

  17. 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.

  18. 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.

  19. 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.

  20. 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).

  21. 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).

  22. 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.

  23. 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.

  24. 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.

  25. 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.

  26. 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 $\approx 10-15:1$.

  27. 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.

  28. 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.

  29. 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).

  30. 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.

Same Internal Medicine syllabus in other exams

The Internal Medicine outline above is identical in these 3 exams:

MBBS Internal Medicine FAQ

What is in the MBBS Internal Medicine syllabus?

MBBS Internal Medicine is split into 10 chapters: Ischemic heart disease, Asthma, Gastroenterology, Acute kidney injury (AKI), Diabetes mellitus, Anemia, Infectious Diseases, Rheumatology, Geriatrics and Vaccinations. Together they contain 42 topics and 85 sub-topics.

How many chapters are in MBBS Internal Medicine?

10 chapters, containing 42 topics and 85 sub-topics. The largest chapter is Acute kidney injury (AKI), with 6 topics.

Are there flashcards for MBBS Internal Medicine?

Yes — a 50-card Internal Medicine deck, printed in full in the flashcards section of this page and available in the Examius app with spaced repetition. The free plan covers one exam of your choice, including its flashcards; Examius Pro, a one-time purchase, unlocks every other exam and deck.