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Medicine, Nursing & Clinical English 6 Interactive Flashcard Decks

Organ-Systems Medicine Study Guide I: Cardiology, Pulmonology, Nephrology, GI/Hepatology & Hematology

Master internal medicine organ systems with 192 board-style flashcards covering Cardiovascular Physiology & Pathology, Pulmonology, Nephrology, Gastroenterology, and Hematology/Oncology.

Practice 6 Curated Organ-Systems Medicine I: Cardiology, Pulmonology, Nephrology, GI & Hematology/Oncology Decks ↓ Browse All Organ-Systems Medicine I: Cardiology, Pulmonology, Nephrology, GI & Hematology/Oncology Flashcards →

Master internal medicine organ systems with 192 board-style flashcards covering Cardiovascular Physiology & Pathology, Pulmonology, Nephrology, Gastroenterology, and Hematology/Oncology.

Quick Access: Browse All Cardiology Flashcard Sets on Flashcards World — 6 complete progressive decks (192 verified flashcards) organized across Basic, Intermediate, and Advanced mastery tiers.

1. Complete 6-Deck Progressive Curriculum Matrix (192 Flashcards)

Module Mastery Level Curated Flashcard Deck Cards Direct Study Link
Module 1 Basic Cardiology & Cardiovascular Physiology — Hemodynamics, Cardiac Cycle, Murmurs, Heart Failure & Arrhythmias 32 Cards Practice Deck →
Module 2 Intermediate Cardiology & Vascular Disease: Diagnostic Patterns and Emergencies 32 Cards Practice Deck →
Module 3 Basic Pulmonology — Respiratory Physiology, V/Q Mismatch, Spirometry, Obstructive vs Restrictive Lung Disease & ARDS 32 Cards Practice Deck →
Module 4 Intermediate Nephrology — Renal Physiology, Nephritic vs Nephrotic Syndromes, Acute Kidney Injury (AKI), RTA & Electrolytes 32 Cards Practice Deck →
Module 5 Advanced Gastroenterology & Hepatology — Cirrhosis, Viral/Autoimmune Hepatitis, IBD (Crohn vs UC), Pancreatitis & Jaundice 32 Cards Practice Deck →
Module 6 Advanced Hematology & Oncology — Coagulation Cascade, Microcytic/Macrocytic/Hemolytic Anemias, Leukemias & Lymphomas 32 Cards Practice Deck →

2. Module-by-Module Syllabus & Sample Active-Recall Flashcards

Each of the 6 modules below is engineered using atomic retrieval prompts: every card isolates a single high-yield rule, diagnostic criterion, statutory article, deadline, or clinical mechanism.

Module 1 (BASIC): Cardiology & Cardiovascular Physiology — Hemodynamics, Cardiac Cycle, Murmurs, Heart Failure & Arrhythmias

Deck Overview: Hemodynamic principles, Wiggers diagram, heart sounds and murmurs, pathophysiology of HFrEF vs HFpEF, and core arrhythmia mechanisms

# Front (Active Recall Prompt) Back (Answer & Explanation)
1 How is cardiac output calculated from stroke volume or by the oxygen Fick principle? CO = stroke volume × heart rate. At steady state, CO = whole-body oxygen consumption / (arterial oxygen content − mixed venous oxygen content). Use oxygen content, not saturation alone, and consistent units: mL O₂/min divided by mL O₂/L blood gives L blood/min.
2 What are preload, afterload and contractility, the main determinants of stroke volume? Preload is myocardial stretch at end-diastole, often indexed by end-diastolic volume. Afterload is the load opposing ventricular ejection; arterial pressure, outflow obstruction and ventricular geometry contribute. Contractility is the myocardium’s force-generating state at a given preload and afterload. Afterload is not identical to systemic vascular resistance.
3 How does the Frank–Starling mechanism relate ventricular filling to stroke volume? Within the physiological range, greater end-diastolic filling increases myocardial stretch and usually stroke volume at a given afterload and contractile state. Length-dependent activation, including increased myofilament calcium sensitivity, contributes. The relationship is not an unlimited increase in output with added filling.
4 What event produces the first heart sound (S1), and where is it usually best heard? S1 arises from vibrations associated with mitral and tricuspid valve closure at the start of ventricular systole. It is usually best heard near the apex, normally around the left fifth intercostal space at the midclavicular line.
5 What produces S2, and why does its normal split widen during inspiration? S2 accompanies aortic (A2) and pulmonary (P2) valve closure. A2 normally precedes P2. Inspiration increases right-heart filling and prolongs right ventricular ejection, delaying P2 and widening the physiological split.
6 When is S3 heard, and what does a pathological S3 suggest? S3 is a low-frequency sound during rapid early-diastolic ventricular filling. When pathological, it suggests increased filling volume or ventricular dysfunction, as in heart failure, dilated cardiomyopathy or significant regurgitation. It can be physiological in younger people and does not diagnose a disease by itself.

Module 2 (INTERMEDIATE): Cardiology & Vascular Disease: Diagnostic Patterns and Emergencies

Deck Overview: Coronary artery disease, myocardial infarction localization, cardiomyopathies, endocarditis, aortic dissection, and vasculitides

# Front (Active Recall Prompt) Back (Answer & Explanation)
1 How do STEMI, NSTEMI, and unstable angina differ, and how do they relate to the 2026 MI classification? STEMI and NSTEMI describe the presenting ECG pattern, not the depth of necrosis. STEMI has persistent diagnostic ST elevation or an occlusion-equivalent pattern; NSTEMI lacks persistent diagnostic ST elevation but has acute myocardial injury with evidence of ischemia. Unstable angina has acute ischemic symptoms without MI on serial testing. New LBBB alone is insufficient. The 2026 universal definition separately classifies MI by mechanism: primary, secondary, or procedure-related.
2 Why is serial cardiac troponin preferred to CK-MB for suspected myocardial infarction, including recurrent symptoms? High-sensitivity cardiac troponin I or T is preferred; interpret serial changes using the assay's thresholds, including sex-specific upper reference limits. A raised result alone indicates myocardial injury, not necessarily infarction: ischemic evidence is also needed. New or recurrent symptoms require reassessment with serial troponin, ECG, and appropriate imaging. CK-MB is less sensitive and specific and does not become the preferred test merely because a recent infarction may leave troponin elevated.
3 Which ECG leads reflect inferior-wall infarction, and which coronary artery is usually responsible? Leads II, III, and aVF view the inferior wall. The culprit is commonly the right coronary artery, but the left circumflex can also supply this territory, depending on coronary anatomy. ECG patterns help localize the injury and suggest the culprit; they do not prove the responsible artery. Coronary imaging establishes the anatomy, and right-sided leads help assess associated right ventricular involvement.
4 Why can nitrates worsen hypotension in right ventricular infarction? An injured right ventricle may depend on adequate filling to maintain pulmonary flow and left ventricular preload. Nitrate-induced venodilation can therefore reduce cardiac output and blood pressure. The 2025 AHA/ACC ACS guideline advises avoiding nitrates in suspected RV infarction. Hypotension with elevated jugular venous pressure and relatively clear lungs is a clue, not a required triad. Fluids and other treatments must be guided by perfusion and congestion, not given automatically.
5 What should suggest ventricular septal rupture after myocardial infarction, and how is it confirmed? A new harsh systolic murmur, heart failure, or shock after MI should raise concern for a new left-to-right ventricular shunt. Rupture often develops during the first week, but timing varies. Urgent echocardiography with Doppler identifies the defect and shunt. A right-sided oxygen-saturation step-up supports the diagnosis if catheter measurements are obtained. Prompt specialist assessment is essential; the presentation can range from a murmur to circulatory collapse.
6 Why is the posteromedial papillary muscle more vulnerable to infarction-related rupture? It usually has a single arterial supply from the RCA or circumflex system, depending on dominance, whereas the anterolateral muscle generally has dual supply. Rupture can cause abrupt severe mitral regurgitation, pulmonary edema, and shock, often within days of MI. The murmur may be faint or absent as ventricular and atrial pressures rapidly equalize. Urgent echocardiography is needed; transesophageal imaging may clarify an inconclusive transthoracic study.

Module 3 (BASIC): Pulmonology — Respiratory Physiology, V/Q Mismatch, Spirometry, Obstructive vs Restrictive Lung Disease & ARDS

Deck Overview: Lung mechanics, gas exchange, spirometric patterns, COPD, asthma, interstitial lung diseases, and acute respiratory distress syndrome

# Front (Active Recall Prompt) Back (Answer & Explanation)
1 What four basic lung volumes make up Total Lung Capacity (TLC)? Tidal Volume (TV), Inspiratory Reserve Volume (IRV), Expiratory Reserve Volume (ERV), and Residual Volume (RV). TLC = TV + IRV + ERV + RV.
2 Which lung volumes and capacities cannot be measured by standard spirometry, and why? Residual Volume (RV), Functional Residual Capacity (FRC = ERV + RV), and Total Lung Capacity (TLC) cannot be measured by spirometry because spirometry can only measure inhaled and exhaled air, not the volume remaining in the lungs after maximal expiration.
3 What is the Alveolar Gas Equation, and what is the simplified alveolar PO2 (PAO2) at sea level on room air? PAO2 = (Patm - PH2O) x FiO2 - (PaCO2 / R). At sea level on room air: PAO2 = 150 - (PaCO2 / 0.8).
4 What is the Alveolar-arterial (A-a) oxygen gradient, and what is its normal expected value? The difference between alveolar oxygen tension and arterial oxygen tension: A-a gradient = PAO2 - PaO2. Normal is < 10-15 mmHg in young adults, estimated by (Age / 4) + 4.
5 Which two causes of hypoxemia present with a normal A-a gradient, and which three present with an elevated A-a gradient? Normal A-a gradient: 1) Hypoventilation (e.g. opioid overdose); 2) High altitude (low inspired PO2). Elevated A-a gradient: 1) V/Q mismatch; 2) Right-to-left shunt; 3) Diffusion limitation.
6 How does the hypoxemia of a true right-to-left shunt respond to 100% supplemental oxygen compared to V/Q mismatch? Hypoxemia from a true right-to-left shunt (e.g. Eisenmenger syndrome, pulmonary arteriovenous malformation, complete alveolar collapse) is refractory to 100% supplemental O2 because non-ventilated blood bypasses alveolar gas exchange entirely.

Module 4 (INTERMEDIATE): Nephrology — Renal Physiology, Nephritic vs Nephrotic Syndromes, Acute Kidney Injury (AKI), RTA & Electrolytes

Deck Overview: Glomerular filtration, nephrotic and nephritic glomerulopathies, prerenal vs intrinsic AKI, renal tubular acidoses, and fluid-electrolyte imbalances

# Front (Active Recall Prompt) Back (Answer & Explanation)
1 Which substances are the gold standard for measuring Glomerular Filtration Rate (GFR) and Effective Renal Plasma Flow (ERPF), and why? Inulin measures GFR because it is freely filtered and neither reabsorbed nor secreted; Para-aminohippuric acid (PAH) measures ERPF because it is freely filtered and almost 100% secreted by tubular cells on a single pass.
2 What is the formula for Filtration Fraction (FF), and how do NSAIDs versus ACE inhibitors alter FF? FF = GFR / RPF. NSAIDs constrict afferent arterioles (inhibiting prostaglandins), decreasing both GFR and RPF proportionally -> FF is unchanged; ACE inhibitors dilate efferent arterioles (inhibiting Angiotensin II), decreasing GFR more than RPF -> FF decreases.
3 How is fractional excretion of sodium (FeNa) calculated, and what limits its use in distinguishing causes of acute kidney injury? FeNa = (urine sodium x serum creatinine) / (serum sodium x urine creatinine) x 100%. Values below 1% can support sodium-avid/prerenal physiology; values above 2% can support tubular injury. Neither threshold proves a diagnosis. Diuretics, chronic kidney disease and several intrinsic renal diseases can alter the result, so interpret it with clinical assessment and urine findings.
4 Why is the BUN-to-Creatinine ratio > 20:1 in prerenal azotemia but normal (10-15:1) in intrinsic AKI? In hypovolemia/prerenal states, enhanced proximal tubular sodium and water reabsorption causes passive paracellular reabsorption of urea alongside sodium, raising BUN disproportionately to creatinine; damaged tubules in intrinsic AKI cannot reabsorb urea.
5 What clinical diagnosis is suggested by the presence of: 1) Muddy brown granular casts; 2) RBC casts; 3) WBC casts; 4) Fatty casts? 1) Muddy brown granular casts: Acute Tubular Necrosis (ATN); 2) Red blood cell casts: Glomerulonephritis / nephritic syndrome; 3) White blood cell casts: Acute Interstitial Nephritis (AIN) or pyelonephritis; 4) Fatty casts / oval fat bodies: Nephrotic syndrome.
6 What nephron segments are most vulnerable to ischemic versus nephrotoxic Acute Tubular Necrosis (ATN)? Ischemic ATN selectively damages the straight segment of the proximal tubule (S3) and the medullary thick ascending limb (TAL) due to high metabolic demand in a low-PO2 medulla; nephrotoxic ATN (aminoglycosides, cisplatin) primarily damages the proximal convoluted tubule.

Module 5 (ADVANCED): Gastroenterology & Hepatology — Cirrhosis, Viral/Autoimmune Hepatitis, IBD (Crohn vs UC), Pancreatitis & Jaundice

Deck Overview: Hepatic failure and portal hypertension, viral hepatitis serology, inflammatory bowel disease, biliary disease, and acute/chronic pancreatitis

# Front (Active Recall Prompt) Back (Answer & Explanation)
1 What cell type in the liver is the primary driver of hepatic fibrosis in cirrhosis, and what is the activating mechanism? Hepatic Stellate cells (Ito cells in the space of Disse); chronic injury stimulates them to lose vitamin A storage droplets and transdifferentiate into contractile, proliferative myofibroblasts that synthesize abundant extracellular matrix (Type I and III collagen) driven by TGF-beta.
2 What Hepatic Venous Pressure Gradient (HVPG) defines clinically significant portal hypertension, and what are the three major portosystemic collateral pathways? HVPG >= 10 mmHg; major collateral pathways: 1) Left gastric vein to azygos vein (esophageal varices); 2) Paraumbilical veins to superficial epigastric veins (caput medusae); 3) Superior rectal vein to middle/inferior rectal veins (anorectal varices).
3 How is the Serum-Ascites Albumin Gradient (SAAG) calculated, and what do values >= 1.1 g/dL versus < 1.1 g/dL indicate? SAAG = Serum albumin - Ascitic fluid albumin. SAAG >= 1.1 g/dL indicates portal hypertension (cirrhosis, congestive heart failure, Budd-Chiari); SAAG < 1.1 g/dL indicates non-portal hypertensive causes (peritoneal carcinomatosis, peritoneal tuberculosis, nephrotic syndrome, pancreatitis).
4 What ascitic fluid neutrophil threshold confirms Spontaneous Bacterial Peritonitis (SBP), and what is the standard empirical therapy? Ascitic fluid absolute neutrophil count (ANC) >= 250 cells/mm3 (0.25 x 10^9/L); empirical first-line treatment is intravenous third-generation cephalosporins (e.g. Cefotaxime or Ceftriaxone) plus intravenous albumin (1.5 g/kg on day 1, 1.0 g/kg on day 3) to prevent hepatorenal syndrome.
5 What is the hemodynamic pathophysiology of Hepatorenal Syndrome (HRS) in advanced cirrhosis? Severe portal hypertension triggers excessive splanchnic nitric oxide production, causing profound splanchnic arterial vasodilation; this drops effective arterial blood volume, causing extreme compensatory RAAS and sympathetic activation that produces intense renal vasoconstriction and pre-renal AKI.
6 What neurotoxin drives Hepatic Encephalopathy, and what are the mechanisms of action of lactulose and rifaximin? Ammonia (NH3); lactulose is fermented by gut bacteria into lactic and acetic acids, which acidifies the colonic lumen and converts diffusible NH3 into non-absorbable ammonium (NH4+) trapped in stool; rifaximin is a non-absorbable antibiotic that eradicates ammonia-producing gut bacteria.

Module 6 (ADVANCED): Hematology & Oncology — Coagulation Cascade, Microcytic/Macrocytic/Hemolytic Anemias, Leukemias & Lymphomas

Deck Overview: Hemostasis, microcytic and macrocytic anemias, Coombs-positive and intrinsic hemolytic anemias, acute/chronic leukemias, and lymphoma staging

# Front (Active Recall Prompt) Back (Answer & Explanation)
1 What are the three core steps of primary hemostasis and their key platelet receptor interactions? 1) Adhesion: Platelet GpIb binds to subendothelial von Willebrand Factor (vWF); 2) Activation: Shape change and release of ADP and TXA2; 3) Aggregation: Platelet GpIIb/IIIa receptors bind circulating fibrinogen, cross-linking adjacent platelets to form a primary platelet plug.
2 Which coagulation pathways and factors are evaluated by Prothrombin Time (PT/INR) versus activated Partial Thromboplastin Time (aPTT)? PT/INR assesses the Extrinsic pathway (Factor VII and Tissue Factor) and Common pathway (Factors X, V, II [prothrombin], and I [fibrinogen]); aPTT assesses the Intrinsic pathway (Factors XII, XI, IX, and VIII) and Common pathway.
3 What is the genetic inheritance, laboratory profile, and first-line treatment for von Willebrand Disease (vWD)? Autosomal dominant deficiency or dysfunction of vWF; normal or prolonged aPTT (vWF stabilizes Factor VIII), prolonged bleeding time, abnormal ristocetin cofactor assay, and normal PT/platelet count; treated with Desmopressin (DDAVP), which stimulates vWF release from Weibel-Palade bodies.
4 How are Hemophilia A and Hemophilia B differentiated by factor deficiency, and what are their typical mixing study results? Hemophilia A is an X-linked recessive deficiency of Factor VIII; Hemophilia B is an X-linked recessive deficiency of Factor IX; both present with hemarthroses, deep muscle hematomas, and isolated prolonged aPTT; a 1:1 normal plasma mixing study CORRECCTS the aPTT to normal.
5 What laboratory constellation defines Disseminated Intravascular Coagulation (DIC)? Severe thrombocytopenia, prolonged PT/INR, prolonged aPTT, markedly elevated D-dimer / fibrin degradation products (FDPs), severely decreased serum fibrinogen, and microangiopathic schistocytes on blood smear.
6 What enzyme deficiency causes Thrombotic Thrombocytopenic Purpura (TTP), and what is its classic clinical pentad? Severe deficiency of ADAMTS13 (vWF-cleaving protease) leading to uncleaved ultra-large vWF multimers that cause microvascular thrombosis; classic pentad (FAT RN): Fever, microangiopathic hemolytic Anemia (schistocytes), Thrombocytopenia, Renal insufficiency, and Neurological abnormalities; emergent treatment is plasma exchange.

3. 8-Week Spaced Repetition & Active Recall Study Schedule

To achieve >90% long-term retention before exam day, follow this structured 8-week interleaving schedule across all 6 decks (192 core cards + your personal error-log cards):

Phase Target Decks Daily New Cards Daily SRS Reviews Exam Application Protocol
Weeks 1–2 (Foundation) Module 1 & Module 2 (Basic) 16 cards/day 25–45 reviews Master core definitions, foundational statutes/physiology, and primary classifications.
Weeks 3–4 (Intermediate Application) Module 3 & Module 4 (Intermediate) 16 cards/day 50–85 reviews Interleave Basic & Intermediate decks; drill multi-step clinical vignettes or statutory exceptions.
Weeks 5–6 (Advanced Mastery) Module 5 & Module 6 (Advanced) 16 cards/day 85–120 reviews Focus on high-difficulty differentials, numerical deadlines, contraindications, and edge-case traps.
Weeks 7–8 (Final Consolidation) All 6 Cardiology Decks (Interleaved) 0 new cards 100–140 reviews Full timed mock blocks + rapid spaced-repetition review of flagged/missed cards.

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