Medical School Memory Techniques: Flash Cards for MCAT and USMLE Success
Published Mar 12, 2025
The path to becoming a physician is paved with rigorous examinations. From the initial hurdle of the MCAT to the multi-step USMLE process, medical students face the daunting task of memorizing and understanding vast amounts of complex information. Success requires not just hard work, but smart, evidence-based study strategies.
Among the most powerful tools in a medical student's arsenal are flashcards. This seemingly simple learning device—when used correctly—can dramatically improve retention of medical concepts, terminology, and relationships crucial for excelling on high-stakes medical exams.
This comprehensive guide explores how to leverage flashcards effectively for MCAT and USMLE preparation, incorporating cognitive science principles to maximize your study efficiency and examination performance.
Table of Contents
- The Science of Medical Memory Formation
- Why Flash Cards Excel for Medical Education
- Creating High-Yield MCAT Flash Cards
- Designing Effective USMLE Step 1 Flash Cards
- Advanced USMLE Step 2 CK Flash Card Strategies
- Optimizing Your Flash Card System
- Integrating Flash Cards with Other Study Methods
- Common Flash Card Mistakes Medical Students Make
- The Final Push: Exam-Week Flash Card Strategies
- Conclusion: Your Flash Card Path to Medical Excellence
The Science of Medical Memory Formation
Before discussing flashcard techniques, it's crucial to understand how memory works in the context of medical education.
The Memory Pathways for Medical Knowledge
Medical knowledge acquisition follows three primary memory stages:
- Encoding: The initial process of transforming information (like a disease presentation) into a memory.
- Consolidation: The stabilization of that memory trace over time, strengthening neural connections.
- Retrieval: The ability to access and recall that information when needed (such as during an exam).
Medical students often focus exclusively on encoding (reading textbooks, watching lectures) while neglecting consolidation and retrieval—the areas where flashcards excel.
The Forgetting Curve and Medical Information
Hermann Ebbinghaus's research on the "forgetting curve" demonstrated that without reinforcement, we forget:
- 50-80% of newly learned information within 24 hours
- Up to 90% within a week
This presents a significant challenge for medical students facing exams that test cumulative knowledge acquired over months or years of study.
Cognitive Load Theory in Medical Education
Medical students constantly battle cognitive overload. The brain's working memory can typically handle only 4-7 pieces of information simultaneously, yet medical concepts often involve complex interconnections across multiple systems.
Effective flashcards help manage cognitive load by:
- Breaking complex medical concepts into digestible chunks
- Creating schemas that organize related information
- Facilitating the transfer of information from working memory to long-term memory
Why Flash Cards Excel for Medical Education
Flashcards are uniquely suited to the challenges of medical education for several key reasons:
Research shows that actively retrieving information—rather than passively reviewing it—strengthens memory formation. This "testing effect" is precisely what flashcards facilitate.
When you see "What are the cardinal signs of inflammation?" on a flashcard and must recall "redness, heat, swelling, pain, and loss of function," you're engaging in active recall that strengthens those neural pathways far more effectively than re-reading those symptoms in a textbook.
The spacing effect—reviewing information at increasing intervals—is proven to enhance long-term retention. Digital flashcards can implement this automatically, showing you cards just before you're likely to forget them.
For medical students, this means:
- Cards you consistently remember appear less frequently
- Difficult concepts (like complicated metabolic pathways) appear more often
- Study time is optimized for maximum retention per minute spent
Metacognition: Understanding Your Understanding
Flashcards provide immediate feedback on what you know and don't know. This metacognitive awareness allows you to:
- Identify knowledge gaps before they appear on exams
- Adjust study focus based on performance
- Build confidence in well-understood areas
Perfect for Medical Content Types
Medical education involves several distinct types of information, all of which fit perfectly with the flashcard format:
- Terminological knowledge: Medical vocabulary and definitions
- Factual associations: Symptoms associated with conditions
- Procedural knowledge: Step-by-step processes
- Diagnostic reasoning: Differential diagnoses from a set of symptoms
- Visual recognition: Identifying structures, cells, or patterns
Creating High-Yield MCAT Flash Cards
The MCAT tests both content knowledge and its application in passage-based scenarios. Effective MCAT flashcards should address both dimensions.
Biology and Biochemistry Examples
Card 1:
- Front: "What happens to enzyme kinetics as substrate concentration increases, and why does this occur?"
- Back: "As substrate concentration increases, reaction rate increases linearly at first, then levels off to a maximum velocity (Vmax).
- Explanation: At low concentrations, increasing substrate allows more enzyme-substrate complexes to form. At high concentrations, all enzyme active sites become saturated, so adding more substrate cannot increase reaction rate further.
- Application: Used to determine Km (substrate concentration at half Vmax), which indicates enzyme affinity for substrate."
Card 2:
- Front: "Compare and contrast facilitated diffusion and active transport."
- Back:
"Facilitated Diffusion:
- Uses transport proteins
- Moves molecules down concentration gradient
- No ATP required
- Example: GLUT transporters for glucose
Active Transport:
- Uses transport proteins
- Moves molecules against concentration gradient
- Requires ATP energy
- Example: Na+/K+ ATPase pump"
Card 3:
- Front: "How do competitive and noncompetitive enzyme inhibitors differ in their effects on Km and Vmax?"
- Back:
"Competitive Inhibitors:
- Bind to active site
- Increase Km (more substrate needed to reach half Vmax)
- No change in Vmax (can be overcome with high substrate concentration)
- Example: Methotrexate competing with folate
Noncompetitive Inhibitors:
- Bind to allosteric site
- No change in Km
- Decrease Vmax (cannot be overcome with more substrate)
- Example: Lead inhibiting delta-aminolevulinic acid dehydratase"
General Chemistry Examples
Card 1:
- Front: "What happens to gas pressure when volume decreases and temperature remains constant? Which law governs this relationship?"
- Back: "Pressure increases as volume decreases (inverse relationship).
Governed by Boyle's Law: P₁V₁ = P₂V₂
Application: Explains why breathing in (expanding lung volume) pulls air into lungs by decreasing pressure."
Card 2:
- Front: "Define buffer capacity and what determines it."
- Back: "Buffer capacity: The amount of acid or base a buffer can neutralize before significant pH change occurs.
Determined by:
- Concentration of buffer components (higher concentration = higher capacity)
- Relative concentrations of acid and conjugate base (maximum capacity when [acid] = [conjugate base])
- pKa value relative to desired pH (optimal when pKa is within 1 unit of target pH)
Example: Bicarbonate buffer (H₂CO₃/HCO₃⁻) in blood."
Card 3:
- Front: "How do strong and weak acids differ in their dissociation and pH impact?"
- Back:
"Strong Acids:
- Complete dissociation in water
- pH calculation depends only on acid concentration
- Examples: HCl, H₂SO₄, HNO₃
Weak Acids:
- Partial dissociation in water
- pH calculation requires Ka and equilibrium expressions
- Examples: Acetic acid, carbonic acid
- Biological relevance: Most physiological buffers use weak acids"
Organic Chemistry Examples
Card 1:
- Front: "Compare SN1 and SN2 reaction mechanisms, including stereochemistry outcomes."
- Back:
"SN1 (Substitution, Nucleophilic, Unimolecular):
- Two-step mechanism with carbocation intermediate
- Rate depends only on substrate concentration
- Favored by tertiary substrates
- Results in racemization or inversion
- Occurs in polar protic solvents
SN2 (Substitution, Nucleophilic, Bimolecular):
- One-step concerted mechanism
- Rate depends on both nucleophile and substrate concentration
- Favored by primary/secondary substrates
- Always results in inversion of stereochemistry
- Occurs in polar aprotic solvents"
Card 2:
- Front: "How do IR spectroscopy peaks help identify functional groups? List key examples."
- Back: "IR spectroscopy identifies functional groups by their characteristic absorption frequencies:
- C=O (carbonyl): 1670-1780 cm⁻¹ (strong)
- O-H (alcohol): 3200-3550 cm⁻¹ (broad, strong)
- N-H (amine): 3300-3500 cm⁻¹ (medium)
- C≡N (nitrile): 2210-2260 cm⁻¹ (medium)
- C-H (alkane): 2850-3000 cm⁻¹ (strong)
- C=C (alkene): 1620-1680 cm⁻¹ (variable)
Biological relevance: Used to identify drug functional groups and protein secondary structures."
Card 3:
- Front: "What is the significance of Markovnikov's rule, and how does it apply to alkene reactions?"
- Back: "Markovnikov's rule: In the addition of HX to an unsymmetrical alkene, the hydrogen adds to the carbon with more hydrogens, and the halogen adds to the carbon with fewer hydrogens.
- Rationale: Forms the more stable carbocation intermediate
- Example: Addition of HBr to propene produces 2-bromopropane (not 1-bromopropane)
- Biological relevance: Similar regioselectivity principles operate in enzyme-catalyzed reactions"
Physics Examples
Card 1:
- Front: "How does fluid flow velocity relate to pressure according to Bernoulli's principle, and where does this apply in the body?"
- Back: "Bernoulli's principle: As the velocity of fluid flow increases, the pressure exerted by that fluid decreases.
P₁ + ½ρv₁² + ρgh₁ = P₂ + ½ρv₂² + ρgh₂
Physiological applications:
- Blood flow in stenotic (narrowed) vessels - velocity increases, pressure decreases at narrowing
- Venturi effect in breathing - air moving rapidly over airway creates lower pressure, drawing more air in
- Aneurysm formation - widened vessels have slower flow and higher wall pressure"
Card 2:
- Front: "What is the relationship between current, resistance, and voltage in a circuit? How does this apply to nerve conduction?"
- Back: "Ohm's Law: V = IR (Voltage = Current × Resistance)
- Increasing voltage increases current if resistance is constant
- Increasing resistance decreases current if voltage is constant
Nerve Conduction Application:
- Neuronal membrane = resistor and capacitor in parallel
- Ion channels = variable resistors
- Resting potential = battery
- Opening Na⁺ channels decreases membrane resistance, allowing current flow
- Myelination increases resistance between nodes of Ranvier, enabling saltatory conduction"
Card 3:
- Front: "Compare the lenses of the eye and a simple magnifying glass in terms of focal length and image formation."
- Back: "Eye lens:
- Variable focal length (accommodation)
- Forms real, inverted image on retina
- Focal length decreases (becomes stronger) when ciliary muscles contract
- Presbyopia occurs when lens becomes less elastic with age
Magnifying glass:
- Fixed focal length
- Forms virtual, upright, enlarged image when object is within focal length
- Power (diopters) = 1/focal length (meters)
- Relationship to eye: Helps by creating a larger virtual image that subtends larger angle on retina"
Psychology and Sociology Examples
Card 1:
- Front: "Compare and contrast the major perspectives in psychology: psychodynamic, behavioral, cognitive, biological, and humanistic."
- Back:
"Psychodynamic:
- Focus: Unconscious processes, childhood experiences
- Key figures: Freud, Jung, Erikson
- Medical application: Understanding defense mechanisms in patient coping
Behavioral:
- Focus: Observable behavior, environmental influences
- Key figures: Pavlov, Skinner, Watson
- Medical application: Behavior modification for addiction treatment
Cognitive:
- Focus: Mental processes, thinking, perception
- Key figures: Piaget, Beck, Miller
- Medical application: Cognitive-behavioral therapy for depression
Biological:
- Focus: Physiological bases of behavior and mind
- Key figures: Kandel, Damasio
- Medical application: Understanding neurobiological basis of psychiatric disorders
Humanistic:
- Focus: Self-actualization, personal growth, subjective experience
- Key figures: Rogers, Maslow
- Medical application: Patient-centered care approaches"
Card 2:
- Front: "What is social stratification, and how does it impact health outcomes?"
- Back: "Social stratification: The hierarchical arrangement of social groups based on factors like socioeconomic status, race, gender, etc.
Health impacts:
- Access to care (transportation, insurance, availability)
- Quality of care (bias in treatment, communication barriers)
- Environmental exposures (pollution, housing quality)
- Health behaviors (food deserts, exercise opportunities)
- Chronic stress from discrimination and inequality
Examples:
- Lower life expectancy in lower socioeconomic groups
- Higher maternal mortality in Black women across all education levels
- Limited healthcare access in rural communities"
Card 3:
- Front: "Describe Piaget's four stages of cognitive development and their approximate age ranges."
- Back: "Sensorimotor Stage (0-2 years):
- Development of object permanence
- Progression from reflexes to goal-directed activity
- Medical relevance: Assessing developmental milestones in pediatrics
Preoperational Stage (2-7 years):
- Symbolic thinking emerges
- Egocentrism predominates
- Lacks conservation
- Medical relevance: Understanding childhood cognition limitations in pain assessment
Concrete Operational Stage (7-11 years):
- Logical thinking about concrete events
- Conservation and reversibility developed
- Classification skills improve
- Medical relevance: Ability to understand illness causality
Formal Operational Stage (11+ years):
- Abstract reasoning develops
- Hypothetical thinking possible
- Systematic problem-solving emerges
- Medical relevance: Capacity for informed consent, treatment adherence reasoning"
Designing Effective USMLE Step 1 Flash Cards
USMLE Step 1 requires deeper integration of basic science knowledge with clinical applications. Your flashcards should reflect this integration.
Pathology Examples
Card 1:
- Front: "Compare and contrast the pathophysiology and laboratory findings in iron deficiency anemia vs. anemia of chronic disease."
- Back:
"Iron Deficiency Anemia:
- Pathophysiology: Inadequate iron intake, chronic blood loss, or malabsorption
- Labs:
• Low serum iron
• Low ferritin
• High TIBC (Total Iron Binding Capacity)
• Low MCV (microcytic)
• Low reticulocyte count
- Peripheral smear: Microcytic, hypochromic RBCs
Anemia of Chronic Disease:
- Pathophysiology: Inflammatory cytokines increase hepcidin, trapping iron in macrophages
- Labs:
• Low serum iron
• Normal/high ferritin (acute phase reactant)
• Low TIBC
• Normal/low MCV
• Low reticulocyte count
- Associated with: Chronic infections, autoimmune disorders, malignancies"
Card 2:
- Front: "What are the histological features of granulomatous inflammation? List three diseases that exhibit this pattern."
- Back: "Histological Features:
- Organized collection of epithelioid macrophages
- Often surrounded by lymphocytes
- May contain multinucleated giant cells (fused macrophages)
- May show central caseous necrosis (especially TB)
- Fibrosis in later stages
Diseases:
- Tuberculosis: Caseating granulomas with Langhans giant cells
- Sarcoidosis: Non-caseating granulomas with asteroid bodies
- Crohn's disease: Non-caseating granulomas in all layers of bowel wall
- Fungal infections: Histoplasmosis, coccidioidomycosis
- Foreign body reactions: Suture granulomas, berylliosis"
Card 3:
- Front: "Describe the pathophysiology of acute pancreatitis, including common etiologies and complications."
- Back: "Pathophysiology:
- Premature activation of pancreatic enzymes within acinar cells
- Trypsinogen converted to trypsin, activating other zymogens
- Autodigestion of pancreatic tissue
- Release of inflammatory mediators
- Potential progression to systemic inflammatory response syndrome
Common Etiologies (GET SMASHED):
- Gallstones (most common in US)
- Ethanol (alcohol, second most common)
- Trauma
- Steroids
- Mumps/other viruses
- Autoimmune
- Scorpion venom
- Hyperlipidemia/Hypercalcemia
- ERCP complications
- Drugs (thiazides, azathioprine, didanosine)
Complications:
- Local: Pseudocyst, abscess, necrosis
- Systemic: ARDS, shock, renal failure, DIC
- Late: Chronic pancreatitis, diabetes mellitus"
Pharmacology Examples
Card 1:
- Front: "Compare and contrast the mechanisms, indications, and adverse effects of angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs)."
- Back:
"ACE Inhibitors (e.g., lisinopril, enalapril):
- Mechanism: Inhibit conversion of angiotensin I to angiotensin II
- Indications: Hypertension, heart failure, diabetic nephropathy, post-MI
- Adverse effects:
• Dry cough (bradykinin accumulation)
• Angioedema
• Hyperkalemia
• First-dose hypotension
• Teratogenic (contraindicated in pregnancy)
• Acute kidney injury (in bilateral renal artery stenosis)
ARBs (e.g., losartan, valsartan):
- Mechanism: Block AT1 receptors, preventing angiotensin II action
- Indications: Similar to ACEIs; often used when ACEIs not tolerated
- Adverse effects:
• Hyperkalemia
• First-dose hypotension
• Teratogenic (contraindicated in pregnancy)
• Acute kidney injury (in bilateral renal artery stenosis)
• No cough or angioedema (key difference from ACEIs)"
Card 2:
- Front: "Explain the mechanism of action, clinical uses, and toxicities of methotrexate."
- Back: "Mechanism of Action:
- Inhibits dihydrofolate reductase
- Prevents conversion of dihydrofolate to tetrahydrofolate
- Reduces thymidylate and purine synthesis
- Ultimately inhibits DNA synthesis and cell division
Clinical Uses:
- Oncology: Acute lymphoblastic leukemia, lymphomas, choriocarcinoma
- Rheumatology: Rheumatoid arthritis, psoriatic arthritis
- Dermatology: Severe psoriasis
- Obstetrics: Ectopic pregnancy
- Gastroenterology: Inflammatory bowel disease
Toxicities:
- Myelosuppression (leucopenia, thrombocytopenia)
- Mucositis
- Hepatotoxicity
- Pulmonary fibrosis
- Nephrotoxicity
- Teratogenicity
Antidote:
- Leucovorin (folinic acid) - bypass inhibited enzyme"
Card 3:
- Front: "For the antibiotic vancomycin, describe: 1) mechanism of action, 2) spectrum of activity, 3) clinical uses, 4) toxicities, and 5) monitoring parameters."
- Back: "Mechanism:
- Inhibits cell wall synthesis by binding to D-Ala-D-Ala terminus of peptidoglycan precursors
- Prevents cross-linking of peptidoglycan chains
Spectrum:
- Gram-positive bacteria (including MRSA)
- Not effective against gram-negatives (large molecule can't penetrate outer membrane)
- Poor oral absorption (used IV for systemic infections)
Clinical Uses:
- MRSA infections
- C. difficile colitis (oral administration)
- Empiric therapy for suspected gram-positive infections
- Surgical prophylaxis in penicillin-allergic patients
Toxicities:
- Nephrotoxicity (particularly with aminoglycosides)
- Ototoxicity
- Red man syndrome (histamine release with rapid infusion)
- Thrombophlebitis at infusion site
- Neutropenia (with prolonged use)
Monitoring:
- Trough levels (goal 10-15 μg/mL for typical infections, 15-20 μg/mL for severe infections)
- Renal function
- CBC with prolonged therapy"
Microbiology Examples
Card 1:
- Front: "Compare and contrast the virulence factors and clinical presentations of Staphylococcus aureus vs. Streptococcus pyogenes (Group A Strep)."
- Back:
"Staphylococcus aureus:
- Virulence Factors:
• Protein A (binds Fc of antibodies)
• Coagulase (forms fibrin clot)
• Catalase positive (differentiating test)
• Enterotoxins (cause food poisoning)
• TSST-1 (toxic shock syndrome)
• PVL (in community-acquired MRSA)
- Clinical Presentations:
• Skin/soft tissue infections (furuncles, carbuncles)
• Pneumonia (especially post-influenza)
• Endocarditis
• Osteomyelitis
• Food poisoning
• Toxic shock syndrome
Streptococcus pyogenes:
- Virulence Factors:
• M protein (anti-phagocytic)
• Erythrogenic toxins (scarlet fever rash)
• Streptokinase (dissolves clots)
• Streptolysins O and S (hemolysins)
• Hyaluronidase (spreading factor)
• Catalase negative
- Clinical Presentations:
• Pharyngitis ("strep throat")
• Scarlet fever
• Impetigo/erysipelas
• Necrotizing fasciitis
• Post-infectious sequelae (rheumatic fever, glomerulonephritis)"
Card 2:
- Front: "Describe the replication cycle of HIV and indicate where each class of antiretroviral drugs acts."
- Back: "HIV Replication Cycle:
- Attachment to CD4 receptor and CCR5/CXCR4 co-receptors
- Entry inhibitors block here (e.g., maraviroc - CCR5 antagonist)
- Fusion inhibitors block membrane fusion (e.g., enfuvirtide)
-
Reverse transcription of viral RNA to DNA
- Nucleoside reverse transcriptase inhibitors (NRTIs) act as chain terminators (e.g., tenofovir, emtricitabine)
- Non-nucleoside reverse transcriptase inhibitors (NNRTIs) bind directly to enzyme (e.g., efavirenz)
-
Integration of viral DNA into host genome
- Integrase strand transfer inhibitors (INSTIs) block here (e.g., raltegravir, dolutegravir)
-
Transcription and translation of viral proteins
-
Assembly of viral components at cell membrane
- Maturation inhibitors act here (experimental)
-
Budding of immature virion
-
Maturation via protease cleavage of polyproteins
- Protease inhibitors block here (e.g., darunavir, atazanavir)"
Card 3:
- Front: "For Clostridium tetani, describe: 1) key microbiological characteristics, 2) pathogenesis, 3) clinical presentation, and 4) prevention/treatment."
- Back: "Microbiological Characteristics:
- Gram-positive, spore-forming bacillus
- Obligate anaerobe
- Terminal "drumstick" spores
- Soil organism
- Produces exotoxin (tetanospasmin)
Pathogenesis:
- Enters through contaminated wounds
- Spores germinate in anaerobic conditions
- Tetanospasmin travels via retrograde axonal transport to CNS
- Toxin blocks release of inhibitory neurotransmitters (glycine, GABA)
- Results in unopposed excitatory activity and muscle spasms
Clinical Presentation:
- Incubation period: 3-21 days
- Lockjaw (trismus) - initial symptom
- Risus sardonicus (facial grimace)
- Opisthotonus (severe spasm of back muscles)
- Autonomic dysfunction
- Reflex spasms triggered by minimal stimuli
- Consciousness preserved throughout
Prevention/Treatment:
- Prevention: Tetanus toxoid vaccine (DTaP, Tdap, Td)
- Post-exposure: Wound cleaning, tetanus immunoglobulin (TIG)
- Treatment:
• Tetanus immunoglobulin
• Muscle relaxants (benzodiazepines)
• Neuromuscular blockade if needed
• Wound debridement
• Antibiotics (metronidazole or penicillin G)
• Supportive care (often requiring mechanical ventilation)"
Physiology Examples
Card 1:
- Front: "Compare and contrast the physiological changes in different types of shock (hypovolemic, cardiogenic, septic, and anaphylactic)."
- Back:
"Hypovolemic Shock:
- Cause: Blood/fluid loss
- CO: Decreased
- SVR: Increased (compensation)
- PCWP: Decreased
- Treatment: Fluid resuscitation
Cardiogenic Shock:
- Cause: Pump failure (MI, valve dysfunction)
- CO: Decreased
- SVR: Increased (compensation)
- PCWP: Increased (hallmark)
- Treatment: Inotropes, mechanical support
Septic Shock:
- Early: Distributive phase
• CO: Increased
• SVR: Decreased (vasodilation)
• PCWP: Normal/decreased
- Late: Myocardial depression
• CO may decrease
- Treatment: Antibiotics, fluids, vasopressors
Anaphylactic Shock:
- Cause: Severe allergic reaction
- CO: Initially increased, then decreased
- SVR: Markedly decreased (massive vasodilation)
- PCWP: Decreased
- Treatment: Epinephrine, fluid resuscitation, antihistamines, steroids
CO = Cardiac Output, SVR = Systemic Vascular Resistance, PCWP = Pulmonary Capillary Wedge Pressure"
Card 2:
- Front: "Describe the components of the renin-angiotensin-aldosterone system (RAAS) and its role in blood pressure regulation."
- Back: "RAAS Pathway:
- Decreased renal perfusion sensed by juxtaglomerular cells
- Renin released into circulation
- Renin cleaves angiotensinogen to angiotensin I
- Angiotensin-converting enzyme (ACE) converts angiotensin I to angiotensin II
- Angiotensin II effects:
• Potent vasoconstriction (↑ BP)
• Stimulates aldosterone secretion from adrenal cortex
• Increases ADH release from posterior pituitary
• Stimulates thirst
• Promotes cardiac and vascular remodeling
- Aldosterone effects:
• Increases Na⁺ and water reabsorption in distal tubule
• Increases K⁺ and H⁺ excretion
• Expands plasma volume (↑ BP)
Negative Feedback:
- Increased BP inhibits renin release
- ANP/BNP counteract RAAS effects
Clinical Correlations:
- ACE inhibitors/ARBs for hypertension, heart failure, CKD
- Aldosterone antagonists (spironolactone, eplerenone)
- Renal artery stenosis - hyperactivated RAAS
- Primary hyperaldosteronism (Conn's syndrome) - autonomous aldosterone production"
Card 3:
- Front: "Explain the cardiac action potential, including the responsible ion channels and corresponding ECG events for each phase."
- Back: "Phase 0 - Rapid Depolarization:
- Voltage-gated Na⁺ channels open
- Rapid influx of Na⁺
- Corresponds to initial ECG deflection (beginning of QRS)
Phase 1 - Early Repolarization:
- Inactivation of Na⁺ channels
- Transient outward K⁺ current
- Corresponds to J point on ECG
Phase 2 - Plateau:
- Balance between inward Ca²⁺ current (L-type Ca²⁺ channels)
- Outward K⁺ current
- Responsible for prolonged cardiac contraction
- Corresponds to ST segment on ECG
Phase 3 - Rapid Repolarization:
- Increasing outward K⁺ current (delayed rectifier K⁺ channels)
- Decreasing Ca²⁺ current
- Corresponds to T wave on ECG
Phase 4 - Resting Potential:
- Maintained by Na⁺/K⁺ ATPase and inward rectifier K⁺ channels
- Spontaneous depolarization in pacemaker cells (funny current, If)
- Corresponds to isoelectric TP interval on ECG
Refractory Periods:
- Absolute: Phases 0-2 and early Phase 3 (cannot initiate new action potential)
- Relative: Late Phase 3 (stronger than normal stimulus can trigger action potential)
Clinical Correlations:
- Class I antiarrhythmics target Na⁺ channels
- Class II (beta-blockers) reduce sympathetic effects
- Class III (amiodarone, sotalol
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