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INI CET Internal Medicine Syllabus

The Internal Medicine syllabus for INI CET in full: 10 chapters, 42 topics and 85 sub-topics, every one listed below, plus 51 Internal Medicine flashcards with answers.

10Chapters
42Topics
85Sub-topics
51Flashcards

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

INI CET Internal Medicine flashcards — 51 questions with 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.

  20. How do FENa and urine sodium help distinguish prerenal AKI from ATN?

    Prerenal: FENa less than 1%, urine Na less than 20 mEq/L, BUN/Cr ratio greater than 20, high urine osmolality (concentrated). ATN: FENa greater than 2%, urine Na greater than 40 mEq/L, BUN/Cr ratio ~10-15, isosthenuria, muddy brown casts.

Show the other 31 Internal Medicine flashcards

  1. What are the KDIGO criteria for diagnosing and staging AKI?

    AKI = rise in serum creatinine greater than or equal to 0.3 mg/dL within 48 hours, or 1.5x baseline within 7 days, or urine output less than 0.5 mL/kg/hr for 6+ hours. Staged 1-3 by degree of creatinine rise and oliguria duration.

  2. What are the urgent ('AEIOU') indications for dialysis in AKI?

    Acidosis (refractory metabolic), Electrolytes (refractory hyperkalemia), Intoxications (dialyzable toxins), Overload (refractory fluid/pulmonary edema), and Uremia (encephalopathy, pericarditis, bleeding).

  3. How does the pathophysiology of type 1 diabetes differ from type 2 diabetes?

    Type 1: autoimmune destruction of pancreatic beta cells causing absolute insulin deficiency (anti-GAD, anti-islet antibodies). Type 2: peripheral insulin resistance plus progressive beta-cell dysfunction/relative insulin deficiency, strongly linked to obesity.

  4. What HbA1c, fasting glucose, and OGTT values diagnose diabetes mellitus?

    Diabetes: HbA1c greater than or equal to 6.5%, fasting plasma glucose greater than or equal to 126 mg/dL, 2-hour OGTT greater than or equal to 200 mg/dL, or random glucose greater than or equal to 200 mg/dL with classic symptoms. Prediabetes: HbA1c 5.7-6.4% or fasting 100-125 mg/dL.

  5. What is the diagnostic triad and key laboratory findings of diabetic ketoacidosis (DKA)?

    Triad: hyperglycemia (greater than 250 mg/dL), high anion gap metabolic acidosis (pH less than 7.3, bicarbonate less than 18), and ketonemia/ketonuria. More common in type 1 diabetes; precipitated by infection, non-compliance, or new-onset diabetes.

  6. Outline the management of DKA.

    IV isotonic fluids first (correct dehydration), then continuous IV insulin infusion, and potassium replacement (insulin drives K+ intracellularly; hold insulin if K+ less than 3.3). Monitor glucose, anion gap, and electrolytes; add dextrose when glucose ~200. Treat precipitant.

  7. How does hyperosmolar hyperglycemic state (HHS) differ from DKA?

    HHS: extreme hyperglycemia (often greater than 600 mg/dL), profound dehydration, serum osmolality greater than 320 mOsm/kg, minimal/no ketones, and pH greater than 7.3 (no significant acidosis). Occurs in type 2 diabetes, with higher mortality and more altered mental status than DKA.

  8. What are the main microvascular and macrovascular complications of diabetes?

    Microvascular: retinopathy, nephropathy (microalbuminuria progressing to proteinuria), and neuropathy (distal symmetric polyneuropathy, autonomic). Macrovascular: coronary artery disease, stroke, and peripheral arterial disease.

  9. What are the laboratory findings of iron deficiency anemia?

    Microcytic, hypochromic anemia (low MCV, low MCH) with low serum ferritin (most specific), low serum iron, high total iron-binding capacity (TIBC), low transferrin saturation, and high RDW. Most common cause of anemia worldwide.

  10. What distinguishes the two main causes of megaloblastic anemia (B12 vs folate deficiency)?

    Both cause macrocytic anemia with hypersegmented neutrophils and elevated homocysteine. B12 deficiency also raises methylmalonic acid (MMA) and causes neurologic deficits (subacute combined degeneration); folate deficiency has normal MMA and no neurologic findings.

  11. What lab findings indicate hemolytic anemia?

    Elevated indirect (unconjugated) bilirubin, elevated LDH, low haptoglobin, and reticulocytosis. Direct Coombs (DAT) positive in autoimmune hemolysis; schistocytes suggest microangiopathic hemolysis; spherocytes suggest hereditary spherocytosis or warm AIHA.

  12. What is the characteristic bone marrow and blood picture of aplastic anemia?

    Pancytopenia (anemia, leukopenia, thrombocytopenia) with reticulocytopenia and a hypocellular ('empty,' fat-replaced) bone marrow on biopsy. Causes include idiopathic/autoimmune, drugs, radiation, viruses, and benzene exposure.

  13. Name a classic bacterial infection example for each: gram-positive cocci, gram-negative rod, and an intracellular bacterium.

    Gram-positive cocci: Staphylococcus aureus (clusters), Streptococcus (chains). Gram-negative rod: Escherichia coli. Obligate intracellular: Mycobacterium tuberculosis (acid-fast), Chlamydia, Rickettsia.

  14. What are the classic clinical-lab features distinguishing common viral hepatitis transmission routes?

    Hepatitis A and E: fecal-oral, acute self-limited (E dangerous in pregnancy). Hepatitis B, C, D: bloodborne/sexual, can become chronic. Hepatitis D requires co-infection with B (needs HBsAg envelope).

  15. What is the most common opportunistic fungal infection in AIDS patients with low CD4, and a key invasive mold in neutropenic patients?

    Pneumocystis jirovecii pneumonia (PJP) occurs with CD4 less than 200 (treat/prophylax with TMP-SMX). Aspergillus is the key invasive mold in prolonged neutropenia (galactomannan, halo sign on CT).

  16. Name the parasitic cause and diagnostic hallmark of malaria.

    Plasmodium species (P. falciparum most severe), transmitted by female Anopheles mosquito. Diagnosis: thick and thin blood smears (gold standard) or rapid antigen tests; ring forms and banana-shaped gametocytes suggest P. falciparum.

  17. What are the four mechanisms of antibiotic resistance?

    Enzymatic inactivation (e.g., beta-lactamases), altered target site (e.g., altered PBPs in MRSA, ribosomal mutations), decreased drug uptake/porin loss, and increased efflux pumps.

  18. What is the principle of empiric versus definitive (de-escalation) antimicrobial therapy?

    Empiric therapy is broad-spectrum, started before culture results based on likely pathogens and local resistance. Definitive therapy narrows coverage (de-escalation) once culture and sensitivities identify the organism, reducing resistance and toxicity.

  19. What are the 2010 ACR classification criteria components and key serologies for rheumatoid arthritis?

    Criteria weigh joint involvement (small joints, symmetric), serology (RF and anti-CCP/ACPA), acute-phase reactants (ESR/CRP), and symptom duration greater than 6 weeks. Anti-CCP is most specific. Classic: symmetric small-joint polyarthritis with morning stiffness greater than 1 hour.

  20. What antibody is most sensitive and what antibodies are most specific for systemic lupus erythematosus (SLE)?

    ANA is most sensitive (screening; near 100% sensitive but not specific). Anti-dsDNA (correlates with disease activity/nephritis) and anti-Smith are most specific for SLE.

  21. What defines the seronegative spondyloarthropathies and their shared genetic marker?

    A group including ankylosing spondylitis, psoriatic arthritis, reactive arthritis, and IBD-associated arthritis. They are RF-negative, associated with HLA-B27, and feature axial/sacroiliac involvement, enthesitis, dactylitis, and asymmetric oligoarthritis.

  22. How are vasculitides classified by vessel size, with one example of each?

    Large-vessel: giant cell (temporal) arteritis, Takayasu arteritis. Medium-vessel: polyarteritis nodosa, Kawasaki disease. Small-vessel: granulomatosis with polyangiitis (c-ANCA), microscopic polyangiitis, eosinophilic granulomatosis (Churg-Strauss), IgA vasculitis (HSP).

  23. What are the classic 'geriatric giants' (geriatric syndromes)?

    Multifactorial conditions common in the elderly: immobility, instability (falls), incontinence, and impaired cognition/intellect (delirium and dementia). Often expanded to include frailty, pressure ulcers, and polypharmacy.

  24. What is polypharmacy, and which tools help reduce inappropriate prescribing in the elderly?

    Polypharmacy is the concurrent use of multiple medications (commonly defined as 5 or more), increasing risk of adverse drug events and interactions. The Beers Criteria and STOPP/START criteria identify potentially inappropriate medications to deprescribe.

  25. What domains are assessed in a Comprehensive Geriatric Assessment (CGA)?

    A multidimensional evaluation of medical (comorbidities, medications, nutrition), functional (ADLs/IADLs, gait/balance), cognitive/psychological (cognition, mood), and social/environmental status, to create a coordinated care plan.

  26. What is the typical childhood vaccination schedule highlight for measles and DTaP?

    MMR (measles-mumps-rubella) is given as a 2-dose series, first at 12-15 months and second at 4-6 years. DTaP (diphtheria-tetanus-acellular pertussis) is a 5-dose primary series at 2, 4, 6, and 15-18 months, and 4-6 years.

  27. Which vaccines are routinely recommended for adults aged 65 and older?

    Annual influenza vaccine, pneumococcal vaccines (PCV and/or PPSV23), recombinant zoster (shingles) vaccine (2 doses), and Tdap once then Td/Tdap booster every 10 years. RSV vaccine is also recommended for older adults.

  28. Which vaccines are commonly required or recommended for international travelers?

    Depending on destination: hepatitis A and B, typhoid, yellow fever (required for some African/South American countries with certificate), Japanese encephalitis, rabies (pre-exposure), meningococcal (required for Hajj), and cholera. Ensure routine vaccines are up to date.

  29. What is a live attenuated vaccine and which key patient groups should avoid it?

    A live attenuated vaccine (e.g., MMR, varicella, yellow fever, oral polio, BCG, intranasal influenza) contains weakened but replicating organisms. It is contraindicated in pregnant women and significantly immunocompromised patients due to risk of disease from the vaccine strain.

  30. What are the typical clinical features (symptoms) of acute kidney injury?

    Often asymptomatic early; may show decreased urine output (oliguria/anuria), fluid overload (edema, pulmonary congestion), and symptoms of uremia (nausea, fatigue, confusion, asterixis, pericardial rub) and electrolyte disturbances (hyperkalemia causing arrhythmias).

  31. What is the classic presentation of acute coronary syndrome, including atypical presentations?

    Classic: crushing substernal chest pressure radiating to the left arm or jaw, with diaphoresis, dyspnea, and nausea, lasting greater than 20 minutes and not relieved by rest. Atypical (women, elderly, diabetics): dyspnea, epigastric pain, fatigue, or silent ischemia.

Same Internal Medicine syllabus in other exams

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

INI CET Internal Medicine FAQ

What is in the INI CET Internal Medicine syllabus?

INI CET 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 INI CET 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 INI CET Internal Medicine?

Yes — a 51-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.