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.

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.

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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	Cardiovascular Pathology — Acute Coronary Syndrome (STEMI/NSTEMI), Cardiomyopathies, Valvular & Vascular Disease	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 →

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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

• Direct Deck Link: Cardiology & Cardiovascular Physiology — Hemodynamics, Cardiac Cycle, Murmurs, Heart Failure & Arrhythmias (32 Flashcards)
• Level Filter: Browse all BASIC Cardiology Sets

#	Front (Active Recall Prompt)	Back (Verified Exam Answer & Explanation)
1	What is the formula for cardiac output (CO) using stroke volume, and how does the Fick principle calculate CO?	CO = Stroke Volume (SV) x Heart Rate (HR). Under the Fick principle: CO = Rate of oxygen consumption (VO2) / (Arterial oxygen content [CaO2] - Venous oxygen content [CvO2]).
2	What are the three primary physiological determinants of stroke volume (SV)?	1) Preload (approximated by ventricular end-diastolic volume [EDV]); 2) Afterload (approximated by mean arterial pressure or systemic vascular resistance); 3) Inotropy (myocardial contractility).
3	How does the Frank-Starling law describe the relationship between ventricular preload and stroke volume?	Increasing ventricular end-diastolic volume increases myocyte sarcomere stretch toward optimal actin-myosin overlap (up to ~2.2 micrometers), increasing the force of ventricular contraction and stroke volume.
4	What mechanical event causes the first heart sound (S1), and where is it heard loudest?	Closure of the mitral and tricuspid (atrioventricular) valves at the onset of ventricular systole (isovolumetric contraction); heard loudest at the cardiac apex (5th intercostal space, midclavicular line).
5	What causes the second heart sound (S2), and what is the mechanism behind physiological splitting during inspiration?	Closure of the aortic (A2) and pulmonic (P2) semilunar valves. Inspiration decreases intrathoracic pressure, increasing venous return to the right heart and prolonging right ventricular ejection time, delaying P2 closure.
6	What hemodynamic condition causes a pathological third heart sound (S3), and in which clinical states is it classic?	Sudden deceleration of blood flow into a dilated, volume-overloaded ventricle during rapid early diastolic filling (ventricular gallop); classic in HFrEF, dilated cardiomyopathy, and severe mitral/tricuspid regurgitation.

Module 2 (INTERMEDIATE): Cardiovascular Pathology — Acute Coronary Syndrome (STEMI/NSTEMI), Cardiomyopathies, Valvular & Vascular Disease

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

• Direct Deck Link: Cardiovascular Pathology — Acute Coronary Syndrome (STEMI/NSTEMI), Cardiomyopathies, Valvular & Vascular Disease (32 Flashcards)
• Level Filter: Browse all INTERMEDIATE Cardiology Sets

#	Front (Active Recall Prompt)	Back (Verified Exam Answer & Explanation)
1	How do STEMI, NSTEMI, and Unstable Angina differ by ECG criteria, cardiac biomarkers, and extent of myocardial necrosis?	STEMI shows ST-segment elevation or new LBBB with elevated troponin (transmural necrosis); NSTEMI has elevated troponin with ST depression or T-wave inversions (subendocardial necrosis); Unstable Angina presents with ischemic chest pain without troponin elevation or persistent ST elevation.
2	What are the kinetic profiles of cardiac troponin I/T versus CK-MB, and when is CK-MB clinically useful?	Cardiac troponin rises in 3-4 hours, peaks at 18-24 hours, and remains elevated for 7-14 days; CK-MB rises in 4-6 hours, peaks at 24 hours, and normalizes within 48-72 hours, making CK-MB ideal for detecting early reinfarction.
3	Which ECG leads correspond to inferior wall myocardial infarction, and what coronary artery is most commonly occluded?	Leads II, III, and aVF reflect inferior wall ischemia, most commonly caused by acute occlusion of the Right Coronary Artery (RCA, ~85-90% of cases) or less commonly the Left Circumflex (LCx).
4	What is the classic clinical triad of acute right ventricular infarction, and why are nitrates contraindicated?	Triad of hypotension, elevated jugular venous pressure, and clear lung fields in the setting of inferior STEMI; nitrates and diuretics are contraindicated because the ischemic right ventricle is highly preload-dependent, and venodilation causes catastrophic hypotension.
5	What mechanical complication of myocardial infarction typically occurs 3 to 7 days post-MI presenting with a new harsh holosystolic murmur?	Interventricular septal rupture (VSR) due to macrophage-mediated tissue degradation and coagulative necrosis, presenting with biventricular failure, a harsh holosystolic murmur at the left lower sternal border, and an oxygen saturation step-up from RA to RV.
6	Which papillary muscle is most vulnerable to post-MI rupture, and what is its single-source arterial supply?	The posteromedial papillary muscle of the mitral valve, because it has a single blood supply from the Posterior Descending Artery (PDA); acute rupture (day 2-7 post-MI) causes acute severe mitral regurgitation and cardiogenic pulmonary edema.

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

• Direct Deck Link: Pulmonology — Respiratory Physiology, V/Q Mismatch, Spirometry, Obstructive vs Restrictive Lung Disease & ARDS (32 Flashcards)
• Level Filter: Browse all BASIC Cardiology Sets

#	Front (Active Recall Prompt)	Back (Verified Exam 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

• Direct Deck Link: Nephrology — Renal Physiology, Nephritic vs Nephrotic Syndromes, Acute Kidney Injury (AKI), RTA & Electrolytes (32 Flashcards)
• Level Filter: Browse all INTERMEDIATE Cardiology Sets

#	Front (Active Recall Prompt)	Back (Verified Exam 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	What is the formula for the Fractional Excretion of Sodium (FeNa), and what values distinguish prerenal azotemia from Acute Tubular Necrosis (ATN)?	FeNa = (Urinary Na x Serum Cr) / (Serum Na x Urinary Cr) x 100%. FeNa < 1% indicates prerenal azotemia (intact tubular reabsorption of sodium); FeNa > 2% indicates intrinsic renal failure / ATN (damaged tubules unable to concentrate sodium).
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

• Direct Deck Link: Gastroenterology & Hepatology — Cirrhosis, Viral/Autoimmune Hepatitis, IBD (Crohn vs UC), Pancreatitis & Jaundice (32 Flashcards)
• Level Filter: Browse all ADVANCED Cardiology Sets

#	Front (Active Recall Prompt)	Back (Verified Exam 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

• Direct Deck Link: Hematology & Oncology — Coagulation Cascade, Microcytic/Macrocytic/Hemolytic Anemias, Leukemias & Lymphomas (32 Flashcards)
• Level Filter: Browse all ADVANCED Cardiology Sets

#	Front (Active Recall Prompt)	Back (Verified Exam 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.

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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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4. Direct Links to All Curated Study Decks

• Complete Topic Catalog: Organ-Systems Medicine I: Cardiology, Pulmonology, Nephrology, GI & Hematology/Oncology
• Basic Tier: Basic Cardiology Flashcards
• Intermediate Tier: Intermediate Cardiology Flashcards
• Advanced Tier: Advanced Cardiology Flashcards
• Cardiology & Cardiovascular Physiology — Hemodynamics, Cardiac Cycle, Murmurs, Heart Failure & Arrhythmias
• Cardiovascular Pathology — Acute Coronary Syndrome (STEMI/NSTEMI), Cardiomyopathies, Valvular & Vascular Disease
• Pulmonology — Respiratory Physiology, V/Q Mismatch, Spirometry, Obstructive vs Restrictive Lung Disease & ARDS
• Nephrology — Renal Physiology, Nephritic vs Nephrotic Syndromes, Acute Kidney Injury (AKI), RTA & Electrolytes
• Gastroenterology & Hepatology — Cirrhosis, Viral/Autoimmune Hepatitis, IBD (Crohn vs UC), Pancreatitis & Jaundice
• Hematology & Oncology — Coagulation Cascade, Microcytic/Macrocytic/Hemolytic Anemias, Leukemias & Lymphomas