Your FREE COMLEX Level 1 Flashcards 2026 – 250+ Cards

The four signs of somatic dysfunction: Tissue texture change, Asymmetry, Restriction of motion, Tenderness.

T1–L2 (thoracolumbar) — ALL sympathetic preganglionic cell bodies are here.

Craniosacral: cranial nerves III, VII, IX, X and sacral S2–S4.

1) Body is a unit; 2) self-regulation/self-healing; 3) structure & function interrelated; 4) rational treatment based on these three.

Biomechanical, Respiratory–Circulatory, Neurological, Metabolic–Energy, Behavioral.

Impaired or altered function of related components of the somatic system: skeletal, arthrodial, myofascial structures + their vascular, lymphatic, neural elements.

Sensitivity (tenderness), Tissue texture change, Asymmetry, Restriction of motion — same findings as TART.

Neutral spine; rotation & sidebending to OPPOSITE sides; a GROUP of vertebrae; often chronic compensatory curve.

Flexed or extended spine; rotation & sidebending to the SAME side; usually a SINGLE vertebra; often acute (named FRS or ERS).

Initiating motion in one plane reduces the range of motion in the other two planes.

By the direction of FREEST motion (where the segment moves best), not the restriction.

The point in the range of motion where motion is limited by the dysfunction — short of the anatomic barrier.

The limit of active motion the patient can produce voluntarily.

The limit of passive motion set by bone/ligament — beyond it, injury occurs.

Diseased organ → afferent input at its sympathetic level → paraspinal tissue texture change, tenderness, restriction.

Somatic (musculoskeletal) input that produces an altered visceral function — the reverse of viscerosomatic.

Tender, smooth, firm neurolymphatic nodules at predictable anterior/posterior sites; each points to a specific organ.

A spinal segment held at a lowered firing threshold, perpetuating heightened sympathetic output to related tissues.

T1–T5 — basis of the cardiac viscerosomatic reflex.

T2–T7 — pulmonary viscerosomatic reflex.

T5–T9 (stomach, liver, gallbladder, spleen, proximal duodenum).

T10–T11 (small bowel to proximal colon, kidney, upper ureter).

T12–L2 (descending/sigmoid colon, bladder, reproductive organs).

T1–T4 — fibers ascend the chain to the superior cervical ganglion.

Parasympathetic supply to head, neck, thorax, and abdomen to the splenic flexure (proximal 2/3 of transverse colon).

Parasympathetic supply to the descending colon, pelvis, bladder, and reproductive organs.

Preganglionic sympathetic fibers synapse directly on chromaffin cells (no postganglionic neuron) — they ARE modified neurons.

Acute: warm, boggy, edematous. Chronic: cool, ropy, fibrotic.

Alternating fascial preferences at the 4 transition zones (OA, cervicothoracic, thoracolumbar, lumbosacral): L/R/L/R.

Seated flexion test localizes sacroiliac (sacrum on ilium) dysfunction; standing flexion test localizes iliosacral.

A structural problem can impair function, and altered function can change structure — they are reciprocal.

The cranial articulation between the sphenoid and occiput; central to the cranial concept and cranial strain patterns.

Midline bones (sphenoid, occiput) flex; paired bones externally rotate; the body widens and shortens.

The 5 components: CNS motility, CSF fluctuation, dural membrane mobility, cranial bone motion, and involuntary sacral motion.

Named by axis: e.g., left-on-left; treat with muscle energy, often patient in Sims (lateral) position.

e.g., left-on-right; differs from a forward torsion in the seated flexion test side and the deep sulcus location.

A neutral group curve often arises to compensate for a Type II dysfunction or a structural asymmetry (e.g., short leg).

Anterior Chapman's point classically maps to upper-respiratory/ear congestion problems.

Anterior Chapman's point near the tip of the right 12th rib is associated with the appendix.

Generally found in the paravertebral region (near the transverse processes/spinous processes).

Bogginess, ropiness, edema, temperature change, increased/decreased moisture — the 'T' of TART.

Positional asymmetry of related parts of the musculoskeletal system (the 'A' of TART).

Limited or asymmetric range of motion of a segment (the 'R' of TART).

Address autonomic balance and reduce nociception/facilitation.

Maintain the flow of body fluids — lymph, blood, and cerebrospinal fluid.

Optimize energy expenditure and support immune and metabolic function.

Address mind–body, psychosocial, and lifestyle contributors to health.

First rib held down (exhaled); restricted on inhalation — often involves the anterior/middle scalene.

In a group dysfunction, treat the KEY rib: the TOP rib of an exhaled group, the BOTTOM rib of an inhaled group.

Compensated: fascial preferences ALTERNATE at the transition zones; uncompensated: they do not (suggests trauma/pathology).

A primary dysfunction is the cause; a secondary (reflex) dysfunction follows from visceral or other input.

DIRECT technique: patient actively contracts against the physician's counterforce; post-isometric relaxation lets the barrier be re-engaged.

INDIRECT technique: position into ease away from the tender point, hold ~90 seconds, then slowly return to neutral.

Return the patient to neutral SLOWLY and passively, or the tender point/dysfunction can recur.

High-Velocity, Low-Amplitude — DIRECT: a quick, short thrust through the restrictive barrier, often with an audible cavitation.

Cavitation — release of gas from the synovial joint, NOT a bone moving back into place.

Bony instability: e.g., spinal metastasis, fracture, severe osteoporosis, or atlantoaxial instability (Down syndrome, RA).

Can be DIRECT (load fascia to its barrier) or INDIRECT (move into ease); felt as palpable tissue softening (creep/release).

Based on the primary respiratory mechanism / cranial rhythmic impulse palpated at the sphenobasilar synchondrosis.

A sequenced articulatory treatment for the shoulder (glenohumeral joint), patient in lateral recumbent.

Promotes lymph flow; avoid directly over an acute infection site or in fragile patients who cannot tolerate it.

Combines an INDIRECT start (into ease) with a final DIRECT movement through the barrier.

Indirect: neutral position + compression/torsion to shorten tissue, then move into ease for ~3–5 seconds.

Stretch, kneading, or inhibition of hypertonic muscle — addresses myofascial tissue, not the bony segment directly.

Low-Velocity, High-Amplitude: repetitive springing through the restrictive barrier to restore range of motion.

Direct = engage the restrictive barrier; Indirect = move away from it, into the position of ease.

Contracting a muscle reflexively relaxes its antagonist — the principle some muscle-energy variants use.

Soft-tissue/articulatory technique along the paraspinals thought to normalize sympathetic tone and aid lymphatic flow.

Rib held DOWN; moves freely on exhalation, restricted on inhalation; treat the KEY rib (the top one of a group).

Rib held UP; moves freely on inhalation, restricted on exhalation; treat the BOTTOM rib of the group.

Technique choice is guided primarily by the patient (acuity, age, frailty, contraindications), not personal preference.

Counterstrain to the psoas/iliacus tender point is a gentle, effective approach when direct techniques aren't tolerated.

Diagnose, engage the restrictive barrier, patient contracts ~3–5 s against counterforce, relax, re-engage the new barrier; repeat 3–5×.

Anterior tender points are generally treated with FLEXION (and fine-tuning of rotation/sidebending) into ease.

Posterior tender points are generally treated with EXTENSION into the position of ease.

Vertebrobasilar insufficiency and Down syndrome (atlantoaxial instability) are contraindications to cervical HVLA.

Move toward the position of ease (away from the barrier) to allow the dysfunction to release.

Patient lateral recumbent, affected shoulder up; physician moves the shoulder through a set sequence of motions.

Avoid the lymphatic pump directly over an area of acute infection or a fracture.

Start indirect (into ease), add a compressive/distractive force, then carry the segment through the barrier (direct finish).

Upper trunk injury (C5–C6): 'waiter's tip' posture — arm adducted, internally rotated, forearm pronated.

Lower trunk injury (C8–T1): claw hand from intrinsic hand muscle paralysis.

Mid-shaft humeral fracture or 'Saturday night palsy' → wrist drop (loss of extensors).

Surgical-neck humeral fracture / anterior shoulder dislocation → deltoid weakness, lateral shoulder numbness.

Carpal tunnel / supracondylar fracture → thenar wasting, loss of thumb opposition.

Medial epicondyle or hook of hamate → claw hand, weak grip, sensory loss to digits 4–5.

Fibular neck injury / leg crossing → foot drop (loss of dorsiflexion and eversion).

Interruption of the cervical sympathetic chain: ptosis, miosis, anhidrosis (± enophthalmos).

Facial sensation (3 divisions) + muscles of mastication; trigeminal neuralgia = brief, electric, lancinating facial pain.

C5, C6, C7, C8, T1 → trunks, divisions, cords, branches.

C3, C4, C5 — 'keep the diaphragm alive'; supplies the diaphragm.

Branch of vagus (CN X); injury → hoarseness; loops under the aortic arch (left) and subclavian (right).

C5–C7; injury → winged scapula (serratus anterior palsy).

L1–L2 (genitofemoral nerve); absent reflex is a sign of testicular torsion.

Median nerve + 9 flexor tendons (4 FDS, 4 FDP, 1 FPL); compression → median neuropathy.

Gives the muscles of mastication, malleus & incus, maxillary/mandibular processes (CN V).

T8 IVC (vena cava), T10 esophagus (+ vagus), T12 aorta (+ thoracic duct, azygos).

Lateral → medial: femoral Nerve, Artery, Vein, Empty space, Lymphatics.

Supraspinatus, Infraspinatus, Teres minor, Subscapularis.

Compression below the conus: saddle anesthesia, bowel/bladder dysfunction, lower-limb weakness — a surgical emergency.

L4–S3; the largest nerve; divides into tibial and common peroneal nerves.

Motor to muscles of facial expression; lesion → ipsilateral facial droop (Bell palsy spares the forehead if central).

Parasympathetic to thoracic/abdominal viscera; motor to pharynx/larynx; sensory from the same.

From the upper trunk; injury weakens supraspinatus (abduction initiation) and infraspinatus (external rotation).

Drains lymph from most of the body into the left subclavian/internal jugular junction; enters thorax via the aortic hiatus (T12).

~85% right-dominant: the posterior descending artery arises from the right coronary artery.

Diaphragmatic irritation refers to the shoulder (C3–C5 shared dermatome) — e.g., subphrenic abscess, ruptured spleen.

T4 nipple, T10 umbilicus, L1 inguinal region — quick localization of a spinal level.

Tenderness suggests a scaphoid fracture (risk of avascular necrosis); contents include the radial artery.

Rapid Na⁺ influx → depolarization (in ventricular myocytes).

Plateau: Ca²⁺ influx balances K⁺ efflux — sustains contraction.

Repolarization from K⁺ efflux.

Spontaneous diastolic depolarization ('funny' Na⁺ current + Ca²⁺) — sets heart rate.

High parasympathetic tone keeps the heart rate BELOW the SA node's intrinsic rate (~100/min).

↑ vagal tone → slows AV conduction; can terminate some supraventricular tachycardias.

Reabsorbs the LARGEST fraction of filtered Na⁺, water, glucose, amino acids, and bicarbonate.

Secretes renin in response to ↓ renal perfusion, ↓ NaCl at the macula densa, and sympathetic input.

Renin → angiotensin I → (ACE) → angiotensin II → vasoconstriction + aldosterone → Na⁺/water retention.

Estimates GFR because inulin is freely filtered and neither reabsorbed nor secreted.

Na⁺ − (Cl⁻ + HCO₃⁻); a high anion gap acidosis points to added acid (DKA, lactate, toxins).

Hypokalemic, contraction metabolic alkalosis maintained by volume/chloride depletion + hyperaldosteronism.

Kidneys retain bicarbonate over days (chronic COPD).

Vascular smooth muscle contraction → vasoconstriction, ↑ blood pressure.

↑ heart rate, ↑ contractility, ↑ renin release.

Bronchodilation, vasodilation in skeletal muscle, uterine relaxation.

Acts on NICOTINIC receptors (all preganglionic fibers are cholinergic).

↑ ventricular filling (preload) → ↑ stroke volume, up to a physiologic limit.

Dihydropyridine receptor (T-tubule) triggers the ryanodine receptor to release Ca²⁺ from the SR.

↑ CO₂, ↑ temperature, ↑ 2,3-BPG, ↓ pH (Bohr effect) → easier O₂ unloading to tissues.

↓ CO₂, ↓ temperature, ↓ 2,3-BPG, ↑ pH, fetal hemoglobin → tighter O₂ binding.

Distal nephron: reabsorb Na⁺/water, secrete K⁺ and H⁺.

Inserts aquaporins in the collecting duct → water reabsorption; from the posterior pituitary.

Reabsorbs Na⁺/K⁺/2Cl⁻ (the loop-diuretic target); impermeable to water.

↑ capillary hydrostatic pressure or ↓ plasma oncotic pressure (low albumin) → net filtration → edema.

Change in volume per change in pressure; ↓ in fibrosis, ↑ in emphysema.

Drives K⁺ INTO cells (used to treat hyperkalemia, given with glucose).

↑ BP stretches carotid sinus → ↑ vagal tone, ↓ sympathetic → ↓ HR and ↓ BP.

The loop of Henle establishes the medullary osmotic gradient that lets the kidney concentrate urine.

Afferent arteriole → glomerulus → efferent arteriole; angiotensin II preferentially constricts the EFFERENT arteriole.

Produced by type II pneumocytes; lowers alveolar surface tension; deficiency → neonatal respiratory distress syndrome.

Phosphofructokinase-1 (PFK-1) — the committed step.

Per glucose: 2 ATP + 2 NADH + 2 pyruvate (in the cytoplasm).

3 NADH, 1 FADH₂, 1 GTP, and 2 CO₂ released.

Acetyl-CoA (2 carbons) condenses with oxaloacetate (4 carbons) to form citrate (6 carbons).

NADH/FADH₂ donate electrons to the ETC; the proton gradient drives ATP synthase — most cellular ATP.

Substrate concentration at ½ Vmax; LOW Km = HIGH affinity.

↑ apparent Km, Vmax UNCHANGED (overcome by more substrate).

↓ Vmax, Km UNCHANGED.

Double-reciprocal (1/V vs 1/[S]); x-intercept = −1/Km, y-intercept = 1/Vmax.

Impairs the last ATP step of glycolysis → hemolytic anemia (RBCs rely on glycolysis).

Isocitrate dehydrogenase.

t(9;22) BCR-ABL fusion → constitutive tyrosine kinase; chronic myeloid leukemia.

Lactate from muscle → liver → gluconeogenesis → glucose back to muscle.

Rate rises with temperature only until the enzyme denatures, then falls sharply.

At metaphase→anaphase: ensures all chromosomes are attached to the spindle before separation.

Pyruvate carboxylase, PEP carboxykinase, fructose-1,6-bisphosphatase, glucose-6-phosphatase.

Makes NADPH (biosynthesis, antioxidant) and ribose-5-phosphate (nucleotides); rate-limiting = G6PD.

↓ NADPH → oxidative hemolysis (Heinz bodies, bite cells) after infection, fava beans, or oxidant drugs.

Breaks fatty acids into acetyl-CoA in mitochondria; carnitine shuttles long-chain fatty acids in.

Converts toxic ammonia to urea for excretion; defects cause hyperammonemia.

Vertical transmission, each child 50% risk, both sexes affected (e.g., Marfan, Huntington).

Often skips generations; 25% risk with two carriers; consanguinity raises risk (e.g., cystic fibrosis).

Males mostly affected, no male-to-male transmission (e.g., hemophilia, Duchenne).

Type I (glucose-6-phosphatase deficiency) → severe fasting hypoglycemia, hepatomegaly, lactic acidosis.

Vitamin C is needed for hydroxylation of proline/lysine; deficiency = scurvy (poor wound healing, bleeding gums).

Thick peptidoglycan; retains crystal violet → stains PURPLE.

Thin peptidoglycan + outer membrane with LPS (endotoxin); stains PINK with safranin.

Staphylococcus (catalase +) vs Streptococcus (catalase −).

S. aureus (coagulase +) vs S. epidermidis / S. saprophyticus (coagulase −).

Alpha = partial (green, e.g. S. pneumoniae, viridans); beta = complete clearing (e.g. S. pyogenes).

Gram-positive rod with tumbling motility; grows at cold temperatures; risky in pregnancy/neonates.

Gram-negative, oxidase +, blue-green pigment; resistant; treat with antipseudomonal beta-lactams.

Gram-positive, catalase-negative, alpha-hemolytic; causes dental caries and subacute endocarditis.

Lipid A of gram-negative outer membrane; triggers fever, hypotension, and septic shock.

Immediate, IgE-mediated: anaphylaxis, allergies, atopy, allergic asthma.

Antibody (IgG/IgM) vs cell-surface antigen: autoimmune hemolytic anemia, Goodpasture.

Immune complexes deposit: serum sickness, Arthus reaction, SLE.

Delayed, T-cell mediated (no antibody): PPD/TB test, contact dermatitis, graft rejection.

Hypersensitivity: Anaphylactic (I), Cytotoxic (II), Immune complex (III), Delayed (IV).

Anaphylatoxins; C5a is also a potent neutrophil chemoattractant.

Gradual desensitization shifts response from IgE toward IgG and induces tolerance.

More severe because memory IgE is already bound to mast cells (sensitized).

Detects antibodies on or against red blood cells (direct = on RBCs; indirect = in serum).

Rickettsia, Chlamydia ('stay inside when it's Really Cold').

Bacillus and Clostridium (gram-positive rods).

Exotoxin: secreted protein, often gram-positive, specific effects. Endotoxin: LPS in gram-negative wall, septic shock.

Mycobacterium tuberculosis; apical disease, caseating granulomas; treat with RIPE.

S. pneumoniae, H. influenzae, N. meningitidis — dangerous in asplenic patients; need opsonization.

DNA viruses that establish latency (HSV in sensory ganglia, VZV in dorsal root ganglia).

Innate: fast, non-specific (neutrophils, macrophages, complement). Adaptive: slower, specific, memory (T and B cells).

Class I (all nucleated cells) presents to CD8 T cells; class II (APCs) presents to CD4 T cells.

Th1 (IFN-γ): intracellular pathogens, macrophage activation. Th2 (IL-4/5): humoral, parasites, allergy.

Strong, lasting immunity but contraindicated in pregnancy and immunocompromised (e.g., MMR, varicella).

Most common primary immunodeficiency; recurrent sinopulmonary/GI infections; anaphylaxis risk with blood products.

Treponema (syphilis), Borrelia (Lyme), Leptospira; thin, spiral organisms.

Clostridium, Bacteroides, Actinomyces; foul-smelling, abscess-forming; often below the diaphragm.

Type II: antibody binds a FIXED tissue antigen. Type III: antibody binds a SOLUBLE antigen, forming circulating complexes.

Programmed, ATP-dependent death of single cells WITHOUT inflammation; membrane stays intact.

Unregulated death of groups of cells that DOES incite inflammation; membranes rupture.

Rubor (redness), calor (heat), tumor (swelling), dolor (pain), functio laesa (loss of function).

Neutrophils predominate; short-lived.

Lymphocytes, plasma cells, macrophages; tissue destruction + repair (fibrosis, angiogenesis).

Metastasis — spread to a distant, non-adjacent site.

Benign: well-differentiated, slow, encapsulated, no metastasis. Malignant: poorly differentiated, invasive, metastasizes.

Epithelial origin; spreads FIRST via lymphatics.

Mesenchymal origin; spreads FIRST hematogenously.

Transudate: low protein (↑ hydrostatic / ↓ oncotic). Exudate: high protein/cells (inflammation, ↑ permeability).

Organized collection of activated macrophages (epithelioid) — type IV reaction (TB, sarcoid, fungi).

Cheese-like; classic for tuberculosis.

Hypertrophy = bigger cells; hyperplasia = more cells.

Reversible change of one mature cell type to another (e.g., Barrett esophagus: squamous → columnar).

Loss of function — the fifth cardinal sign of inflammation.

Architecture preserved (ghost cells); ischemic infarcts of most solid organs.

Tissue digested to liquid; brain infarcts and abscesses.

Saponification; classic in acute pancreatitis (elevated lipase).

Vessel-wall necrosis; malignant hypertension, vasculitis.

Misfolded protein deposits; apple-green birefringence with Congo red under polarized light.

TB, sarcoidosis, fungal infections, Crohn disease, cat-scratch — type IV reaction.

Dystrophic: in damaged tissue, normal calcium. Metastatic: in normal tissue, high serum calcium.

Benign prostatic hyperplasia, endometrial hyperplasia — increased cell NUMBER.

Reversible: cell swelling, blebbing. Irreversible: mitochondrial damage, membrane rupture, Ca²⁺ influx.

Reactive oxygen species damage lipids, proteins, DNA; defended by superoxide dismutase, catalase, glutathione.

Intrinsic (mitochondrial, cytochrome c) and extrinsic (death-receptor, Fas/FasL) — both converge on caspases.

↑ hydrostatic pressure, ↓ oncotic pressure (low albumin), ↑ capillary permeability, or lymphatic obstruction.

Muscarinic agonist; treats postoperative urinary retention and neurogenic bladder (stimulates the bladder).

Na⁺ channel blockers (quinidine, lidocaine, flecainide).

Beta-blockers (metoprolol) — rate control + post-MI mortality benefit.

K⁺ channel blockers (amiodarone, sotalol) — prolong repolarization.

Non-dihydropyridine Ca²⁺ channel blockers (verapamil, diltiazem) — rate control in atrial fibrillation.

Beta-1 agonist; ↑ contractility in acute decompensated heart failure.

Strong alpha + beta-1; weak beta-2 → vasoconstriction with some inotropy (first-line in septic shock).

Competitively inhibit HMG-CoA reductase, the rate-limiting enzyme of cholesterol synthesis.

Probenecid blocks renal tubular secretion of penicillin → higher, longer-lasting blood levels.

Constant FRACTION removed per unit time; rate ∝ concentration; constant half-life (most drugs).

Constant AMOUNT removed per unit time (saturated): ethanol, phenytoin, high-dose aspirin.

Time for concentration to fall by half; only constant/meaningful in first-order kinetics.

Rate control in atrial fibrillation and inotropy in heart failure; narrow therapeutic index.

First-line for trigeminal neuralgia; blocks voltage-gated Na⁺ channels.

Excess cholinesterase inhibitor → SLUDGE (salivation, lacrimation, urination, defecation, GI, emesis) + muscle weakness.

Epinephrine reverses the life-threat (airway/BP); antihistamines treat the milder histamine symptoms.

Block angiotensin II formation; ↓ BP, renoprotective; side effects: cough, hyperkalemia, angioedema; avoid in pregnancy.

↓ HR, ↓ contractility, ↓ renin; post-MI and heart-failure mortality benefit; caution in asthma (β2).

Block Na⁺/K⁺/2Cl⁻ in thick ascending limb (furosemide); ototoxicity, hypokalemia.

Block Na⁺/Cl⁻ in distal tubule; hypokalemia, hyponatremia, hyperglycemia, hyperuricemia, hypercalcemia.

Inhibits vitamin K epoxide reductase (factors II, VII, IX, X); monitor PT/INR; many interactions.

Activates antithrombin III; monitor aPTT; reversed by protamine; risk of HIT.

Bind 30S ribosome (bactericidal); nephrotoxic and ototoxic (e.g., gentamicin).

Inhibit cell-wall synthesis (penicillin-binding proteins); penicillins, cephalosporins, carbapenems.

Depletes glutathione → NAPQI hepatotoxicity; antidote is N-acetylcysteine.

Respiratory depression + pinpoint pupils; reverse with naloxone.

First-line for depression/anxiety; risk of serotonin syndrome (autonomic instability, clonus, agitation).

Hyperglycemia, osteoporosis, immunosuppression, Cushingoid features, adrenal suppression with abrupt withdrawal.

Cross-reactivity with cephalosporins is low (especially later generations); avoid all beta-lactams only in severe (anaphylactic) reactions.

Venodilation → ↓ preload; relieve angina; tolerance develops without a nitrate-free interval.

Dihydropyridines (amlodipine) act on vascular smooth muscle → vasodilation, peripheral edema.

Proportion WITH disease who test positive (true-positive rate); a negative SENSitive test rules OUT (SnNout).

Proportion WITHOUT disease who test negative (true-negative rate); a positive SPecific test rules IN (SpPin).

Of those who test positive, the proportion who truly have disease; FALLS as prevalence falls.

Of those who test negative, the proportion who are truly disease-free; RISES as prevalence falls.

Independent of prevalence; LR+ > 10 strongly rules in, LR− < 0.1 strongly rules out.

Risk in exposed ÷ risk in unexposed; used in cohort studies. RR = 1 means no association.

Used in case-control studies; approximates RR when the disease is rare.

NNT = 1 ÷ absolute risk reduction; how many to treat to prevent one outcome.

Rejecting a true null hypothesis (a false positive); its probability is alpha.

Failing to reject a false null (a false negative); its probability is beta; power = 1 − beta.

Probability of seeing the data (or more extreme) if the null were true; < 0.05 is conventionally significant.

If it crosses the null value (1 for RR/OR, 0 for a difference), the result is not significant.

Randomization, restriction, matching (design) and stratification/multivariable analysis (analysis).

Cohort follows exposure → outcome (incidence, RR); case-control starts from outcome → exposure (OR).

A patient with capacity voluntarily agrees after disclosure of risks, benefits, and alternatives.

Incidence = NEW cases over time; prevalence = ALL existing cases at a point in time.

Combines pretest probability with a likelihood ratio to read off the post-test probability.

Plots sensitivity vs (1 − specificity); a larger area under the curve = better overall test discrimination.

Gold standard for causation; randomization controls confounding; blinding reduces bias.

Earlier detection by screening that lengthens apparent survival without changing the outcome.

Differential accuracy of memory between cases and controls — a classic case-control study flaw.

Non-representative sampling distorts the association (e.g., Berkson, healthy-worker effect).

1 − beta; increased by a larger sample, larger effect size, or lower variability.

Statistically pools results of multiple studies to increase power and precision.

Control event rate − treatment event rate; NNT = 1 ÷ ARR.

Protect patient health information; disclose only with consent or a recognized exception (e.g., reportable disease, imminent harm).

A competent patient's right to accept or refuse treatment — the basis of informed consent and refusal.

Beneficence: act in the patient's best interest. Non-maleficence: 'first, do no harm.'