INI CET Internal Medicine Syllabus

Internal Medicine syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Internal Medicine in INI CET, not a summary of it.

1. 1

   Ischemic heart disease

   3 topics

   • Acute coronary syndrome
     • STEMI
     • NSTEMI
     • Unstable angina
   • Stable angina
   • Chronic ischemic heart disease
2. 2

   Asthma

   4 topics

   • Pathophysiology
   • Clinical Features
   • Diagnosis
   • Management
     • Inhaled Corticosteroids
     • Bronchodilators
     • Biologics
3. 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. 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. 5

   Diabetes mellitus

   5 topics

   • Type 1 diabetes
   • Type 2 diabetes
   • Diabetic ketoacidosis (DKA)
   • Hyperosmolar hyperglycemic state (HHS)
   • Diabetic complications
     • Retinopathy
     • Nephropathy
     • Neuropathy
6. 6

   Anemia

   4 topics

   • Iron deficiency anemia
   • Megaloblastic anemia
     • Vitamin B12 deficiency
     • Folate deficiency
   • Hemolytic anemia
     • Autoimmune hemolytic anemia
     • Hereditary spherocytosis
   • Aplastic anemia
7. 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. 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. 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. 10

    Vaccinations

    3 topics

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

Internal Medicine flashcards for INI CET

19 of 51 cards from the Internal Medicine deck — real questions with worked answers.

1. What are the three subtypes of acute coronary syndrome (ACS), and how are they distinguished?

   STEMI (ST-elevation MI: complete coronary occlusion, ST elevation, elevated troponin), NSTEMI (partial occlusion, no ST elevation, elevated troponin), and unstable angina (ischemia at rest/crescendo pattern, no troponin rise). Troponin separates NSTEMI from unstable angina; ST elevation separates STEMI.

2. What ECG criterion defines STEMI requiring emergent reperfusion?

   New ST-segment elevation at the J-point in 2 contiguous leads: greater than or equal to 1 mm in most leads, or greater than or equal to 2 mm (men) / 1.5 mm (women) in V2-V3. A new left bundle branch block with ischemic symptoms is treated as a STEMI equivalent.

3. What is the door-to-balloon time target for primary PCI in STEMI, and the time window for fibrinolysis if PCI is unavailable?

   Door-to-balloon less than 90 minutes for primary PCI. If PCI cannot be done within 120 minutes of first medical contact, give fibrinolysis within 30 minutes (door-to-needle), ideally within 12 hours of symptom onset.

4. What is the classic clinical triad/features of stable angina, and what distinguishes it from unstable angina?

   Stable angina: substernal chest discomfort, provoked by exertion or stress, relieved by rest or nitroglycerin within minutes, with a predictable, reproducible threshold. Unstable angina occurs at rest, is new-onset severe, or is increasing (crescendo) in frequency/severity/duration.

5. What is the Canadian Cardiovascular Society (CCS) grading of angina?

   Class I: angina only with strenuous exertion. Class II: slight limitation of ordinary activity. Class III: marked limitation (angina on walking 1-2 blocks or 1 flight of stairs). Class IV: angina at rest or with any activity.

6. What are the cornerstone medications for chronic ischemic heart disease that reduce mortality versus those that relieve symptoms?

   Mortality-reducing: aspirin (antiplatelet), high-intensity statin, ACE inhibitor/ARB (esp. with diabetes/LV dysfunction), and beta-blocker (post-MI/LV dysfunction). Symptom-relieving (antianginal): beta-blockers, calcium channel blockers, nitrates, and ranolazine.

7. What is the underlying pathophysiology of acute coronary syndrome?

   Rupture or erosion of an atherosclerotic plaque exposes thrombogenic core, triggering platelet aggregation and thrombus formation. This causes partial occlusion (UA/NSTEMI) or complete occlusion (STEMI), leading to myocardial oxygen supply-demand mismatch and ischemia/infarction.

8. How are upper versus lower GI bleeding distinguished anatomically and clinically?

   Upper GI bleed: proximal to the ligament of Treitz (esophagus, stomach, duodenum); presents with hematemesis and melena; elevated BUN/creatinine ratio. Lower GI bleed: distal to the ligament of Treitz; presents with hematochezia (bright red blood per rectum).

9. What are the most common causes of upper GI bleeding?

   Peptic ulcer disease (most common), esophageal/gastric varices, Mallory-Weiss tears, erosive gastritis/esophagitis, and gastric malignancy. Variceal bleeding is the key consideration in cirrhotic patients.

10. What is the initial management of acute variceal bleeding?

    Resuscitation (IV fluids, transfuse to hemoglobin ~7 g/dL), IV octreotide (splanchnic vasoconstriction), prophylactic antibiotics (e.g., ceftriaxone), and urgent endoscopic band ligation. Add non-selective beta-blockers for secondary prophylaxis.

11. What is the Child-Pugh score and what five parameters does it use to assess cirrhosis severity?

    It grades cirrhosis severity/prognosis using: bilirubin, albumin, INR (prothrombin time), ascites, and hepatic encephalopathy. Class A (5-6), B (7-9), C (10-15), with higher classes indicating worse prognosis.

12. Differentiate Crohn disease from ulcerative colitis in inflammatory bowel disease.

    Crohn: any part of GI tract (mouth to anus), skip lesions, transmural inflammation, fistulae/strictures, non-caseating granulomas, cobblestone mucosa. Ulcerative colitis: continuous involvement from rectum proximally, limited to colon, mucosal/submucosal inflammation, crypt abscesses, increased colon cancer risk.

13. Which serologic markers help distinguish ulcerative colitis from Crohn disease?

    p-ANCA is more associated with ulcerative colitis; ASCA (anti-Saccharomyces cerevisiae antibodies) is more associated with Crohn disease.

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

    Clostridioides difficile. First-line treatment is oral vancomycin or fidaxomicin; metronidazole is reserved for mild cases when preferred agents are unavailable. Stop the offending antibiotic.

15. What are the diagnostic criteria (e.g., Ranson/Atlanta) and two most common causes of acute pancreatitis?

    Diagnosis requires 2 of 3: characteristic epigastric pain radiating to back, lipase/amylase greater than 3x upper limit of normal, or imaging findings. The two most common causes are gallstones and alcohol.

16. How are the causes of acute kidney injury (AKI) classified into three categories?

    Prerenal (decreased renal perfusion), intrinsic/intrarenal (direct kidney parenchymal damage), and postrenal (urinary tract obstruction).

17. List common prerenal causes of AKI.

    Hypovolemia (hemorrhage, vomiting, diarrhea, diuretics), decreased cardiac output (heart failure), systemic vasodilation (sepsis), and renal vasoconstriction (NSAIDs constrict afferent arteriole; ACE inhibitors/ARBs dilate efferent arteriole), plus hepatorenal syndrome.

18. What is the most common intrinsic (intrarenal) cause of AKI, and what are its two main etiologic types?

    Acute tubular necrosis (ATN). The two main types are ischemic (prolonged prerenal hypoperfusion) and nephrotoxic (aminoglycosides, contrast, myoglobin from rhabdomyolysis). Urine shows muddy brown granular casts.

19. What are postrenal causes of AKI?

    Obstruction of urinary outflow: bilateral ureteral obstruction (stones, tumors, retroperitoneal fibrosis), bladder outlet obstruction (BPH, prostate cancer, neurogenic bladder), and urethral obstruction. Obstruction must usually be bilateral (or affect a solitary kidney) to cause AKI.

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