Medical terms, defined.
Browse concise, high-yield explanations covering USMLE Step 1 and Step 2. Every entry is the same definition our Anki add-on serves when you hover a term mid-study, and the add-on explains 7,200+ terms on your cards.
mTOR inhibitor
PharmacologymTOR inhibitors (sirolimus/rapamycin, everolimus, temsirolimus) bind FKBP-12 and inhibit mTORC1, blocking IL-2–driven T-cell proliferation (G1→S arrest). They're used for transplant immunosuppression, certain cancers (RCC, breast, neuroe...
mTOR inhibitors
PharmacologymTOR inhibitors (sirolimus/rapamycin, everolimus, temsirolimus) bind FKBP-12 to block mTORC1, halting the IL-2–driven G1→S cell-cycle progression of T cells. They are used for transplant immunosuppression (sirolimus, everolimus), cancer...
noncompetitive antagonist
Pharmacology (Pharmacodynamics)A noncompetitive antagonist binds either an allosteric site or irreversibly to the active site of a receptor, reducing the maximal effect (Emax) of an agonist that cannot be overcome by adding more agonist. Potency (EC50) is generally un...
topoisomerase inhibitor
PharmacologyTopoisomerase inhibitors are drugs that block enzymes which relieve DNA supercoiling during replication and transcription, causing DNA strand breaks and cell death. Topoisomerase I inhibitors (irinotecan, topotecan) and topoisomerase II...
antimetabolite
Pharmacology (Hematology/Oncology)Antimetabolites are chemotherapeutic (and immunosuppressive) drugs that structurally mimic endogenous purines, pyrimidines, or folate, thereby inhibiting DNA/RNA synthesis. They are S-phase specific and most effective against rapidly div...
full agonist
PharmacologyA full agonist binds a receptor and produces the maximal possible biological response (Emax, intrinsic activity = 1). Potency (EC50) is independent of efficacy, so a full agonist can be more or less potent than other agonists, but it alw...
tyrosine kinase inhibitors
Pharmacology / OncologyTyrosine kinase inhibitors (TKIs) are small-molecule targeted drugs that block ATP binding or activation of receptor or non-receptor tyrosine kinases, which shuts off proliferative signaling. The classic example is imatinib, which inhibi...
microtubule inhibitor
Pharmacology (Hematology/Oncology)Microtubule inhibitors are drugs that disrupt microtubule (α/β-tubulin) dynamics, arresting cells in M phase (mitosis) and triggering apoptosis. Key classes: vinca alkaloids (vincristine, vinblastine; block polymerization), taxanes (pacl...
mixed agonist-antagonist
PharmacologyA mixed agonist-antagonist is an opioid that acts as an agonist at one opioid receptor type (typically kappa) while acting as an antagonist (or weak/partial agonist) at another (typically mu). Examples are nalbuphine, butorphanol, and pe...
irreversible inhibitor
Pharmacology / Biochemistry (Enzyme Kinetics)An irreversible inhibitor binds an enzyme via covalent (or very tight) bonds, permanently inactivating it so function returns only after new enzyme is synthesized. Effects are not overcome by increasing substrate, and it behaves like a n...
reversible inhibitor
Biochemistry / PharmacologyA reversible inhibitor binds an enzyme through noncovalent interactions (H-bonds, ionic, hydrophobic, van der Waals) and can dissociate, so enzyme activity is restored when the inhibitor is removed or diluted. Main types are competitive...
depolarizing neuromuscular blocker
PharmacologyDepolarizing neuromuscular blockers (prototype: succinylcholine) are nicotinic ACh receptor agonists at the motor end plate that cause persistent depolarization, leading to initial fasciculations followed by flaccid paralysis (Phase I bl...
nondepolarizing neuromuscular blocker
PharmacologyNondepolarizing neuromuscular blockers (NDMBs; e.g., rocuronium, vecuronium, cisatracurium, atracurium, pancuronium, tubocurarine) are competitive antagonists of nicotinic acetylcholine receptors (nAChR) at the motor end plate. They caus...
alpha-2 agonist
PharmacologyAlpha-2 agonists (clonidine, dexmedetomidine, guanfacine, methyldopa [via alpha-methylnorepinephrine], tizanidine, brimonidine, apraclonidine) stimulate presynaptic Gi-coupled alpha-2 receptors, decreasing norepinephrine release and symp...
alpha-1 agonist
Pharmacology (Autonomic Pharmacology)Alpha-1 agonists (e.g., phenylephrine, midodrine, norepinephrine, oxymetazoline) activate Gq-coupled α1 receptors on vascular smooth muscle, causing vasoconstriction, increased SVR, and increased BP with reflex bradycardia. Other effects...
nicotinic antagonist
Pharmacology (Autonomic Pharmacology / Anesthesia)Nicotinic antagonists block nicotinic acetylcholine receptors (ligand-gated Na+/K+ channels) at either the neuromuscular junction (NMJ; neuromuscular blockers) or autonomic ganglia (ganglionic blockers). NMJ blockers (e.g., rocuronium, v...
alpha-2 antagonist
PharmacologyAlpha-2 antagonists block presynaptic α2 autoreceptors (Gi-coupled) on noradrenergic neurons, removing negative feedback and increasing norepinephrine release (and increasing sympathetic outflow). Key examples: mirtazapine (antidepressan...
beta-2 agonist
PharmacologyBeta-2 agonists are drugs that stimulate β2-adrenergic receptors (Gs-coupled), increasing cAMP and causing bronchial smooth muscle relaxation (bronchodilation). Short-acting agents (albuterol, levalbuterol, terbutaline) are used as rescu...
beta-1 antagonist
Pharmacology (Autonomic / Cardiovascular)Beta-1 antagonists (β1-blockers) competitively block β1-adrenergic receptors, mainly in the heart and juxtaglomerular cells. They lower heart rate, contractility, AV node conduction, and renin release. They are used for hypertension, ang...
beta-1 agonist
PharmacologyBeta-1 agonists activate β1-adrenergic receptors (Gs-coupled, mainly in the heart and juxtaglomerular cells), increasing heart rate, contractility, conduction velocity, and renin release. Clinically, dobutamine (selective β1) is used for...
H2 blocker
PharmacologyH2 blockers (cimetidine, ranitidine [withdrawn], famotidine, nizatidine) are competitive antagonists of histamine H2 receptors on gastric parietal cells, reducing gastric acid secretion. They are used for GERD, peptic ulcer disease, and...
H2 antihistamine
PharmacologyH2 antihistamines (cimetidine, famotidine, ranitidine*, nizatidine) competitively block histamine H2 receptors on gastric parietal cells, decreasing cAMP-mediated H+/K+ ATPase activity and reducing gastric acid secretion. They are used f...
H1 blocker
PharmacologyH1 blockers (H1 antihistamines) are competitive inverse agonists at histamine H1 receptors that reduce allergic symptoms (itching, rhinorrhea, urticaria). First-generation agents (diphenhydramine, chlorpheniramine, hydroxyzine, promethaz...
alpha-1 antagonist
PharmacologyAlpha-1 antagonists (alpha-1 blockers) competitively block postsynaptic α1-adrenergic receptors on vascular and prostatic/bladder-neck smooth muscle, causing vasodilation and smooth muscle relaxation. They are used for BPH (tamsulosin, a...
beta-2 antagonist
PharmacologyBeta-2 antagonists (beta-2 blockers) block β2-adrenergic receptors, causing bronchoconstriction, vasoconstriction (loss of β2 vasodilation), decreased glycogenolysis/gluconeogenesis, and decreased aqueous humor production (topical agents...
H1 antihistamine
PharmacologyH1 antihistamines are competitive inverse agonists at histamine H1 receptors, used for allergic rhinitis, urticaria, pruritus, motion sickness, and insomnia. First-generation agents (diphenhydramine, chlorpheniramine, hydroxyzine, promet...
ubiquitin-proteasome pathway
Biochemistry / Cell BiologyThe ubiquitin-proteasome pathway is the main ATP-dependent system for selective degradation of intracellular proteins (misfolded, damaged, short-lived regulatory proteins like cyclins). Proteins are tagged with a polyubiquitin chain (≥4...
WPW syndrome
CardiologyWolff-Parkinson-White (WPW) syndrome is a pre-excitation disorder caused by an accessory pathway (bundle of Kent) connecting atria and ventricles, bypassing the AV node. ECG shows a short PR interval (<120 ms), delta wave (slurred QRS up...
hypothalamic-pituitary-adrenal axis
Endocrinology / PhysiologyThe HPA axis is the neuroendocrine cascade in which hypothalamic CRH stimulates anterior pituitary ACTH release, which stimulates adrenal cortex (zona fasciculata) cortisol secretion. Cortisol exerts negative feedback on both the hypotha...
ubiquitin-proteasome
Biochemistry / Cell BiologyThe ubiquitin-proteasome system (UPS) is the major pathway for selective degradation of intracellular proteins in eukaryotes. Target proteins are tagged with a polyubiquitin chain (K48-linked, ≥4 ubiquitins) via an E1→E2→E3 enzymatic cas...
HPG axis
Endocrinology / Reproductive PhysiologyThe hypothalamic-pituitary-gonadal (HPG) axis is the endocrine feedback system in which pulsatile hypothalamic GnRH stimulates anterior pituitary LH and FSH release, which act on the gonads to produce sex steroids (testosterone, estrogen...
Chvostek sign
Endocrinology / Physiology (Electrolyte Disorders)Chvostek sign is twitching of the ipsilateral facial muscles (especially the corner of the mouth/upper lip) elicited by tapping the facial nerve just anterior to the ear, over the parotid gland/zygomatic arch. It indicates neuromuscular...
VHL disease
Genetics / Oncology (Neurocutaneous Syndromes)von Hippel-Lindau (VHL) disease is an autosomal dominant tumor suppressor syndrome caused by loss-of-function mutations of the VHL gene on chromosome 3p25-26. It causes hemangioblastomas (retina, cerebellum, spinal cord), clear cell rena...
HPA axis
Endocrinology / PhysiologyThe HPA (hypothalamic-pituitary-adrenal) axis is the neuroendocrine pathway controlling the stress response and cortisol production: hypothalamic CRH stimulates anterior pituitary ACTH release, which stimulates adrenal cortex (zona fasci...
Bence-Jones protein
Hematology/OncologyBence-Jones proteins are free monoclonal immunoglobulin light chains (kappa or lambda) produced by clonal plasma cells and excreted in urine. They are classically associated with multiple myeloma (and also Waldenström macroglobulinemia,...
Kussmaul breathing
Pathophysiology / Internal Medicine (Acid-Base Disorders)Kussmaul breathing is deep, labored, rapid (often regular) respiration that is a compensatory response to severe metabolic acidosis, classically seen in diabetic ketoacidosis (DKA) and uremia. The increased minute ventilation blows off C...
Cushing triad
Neurology / Neurosurgery (Critical Care)Cushing triad = hypertension (widened pulse pressure), bradycardia, and irregular/depressed respirations. It is a late, ominous sign of raised intracranial pressure (ICP) and impending brain herniation, reflecting brainstem compression a...
hypothalamic-pituitary-thyroid axis
EndocrinologyThe hypothalamic-pituitary-thyroid (HPT) axis is a negative feedback loop regulating thyroid hormone: hypothalamic TRH stimulates anterior pituitary TSH release, which stimulates the thyroid to make and secrete T4 (mostly) and T3 (active...
Kayser-Fleischer ring
Gastroenterology / Genetics (Metabolic Disorders)Kayser-Fleischer rings are golden-brown to greenish-brown rings at the periphery of the cornea. Copper deposits in Descemet's membrane cause them. They are classically seen in Wilson disease (hepatolenticular degeneration), an autosomal...
Virchow triad
Pathology / HematologyVirchow triad describes the three factors that predispose to venous thrombosis: (1) venous stasis, (2) endothelial injury, and (3) hypercoagulability. Any one or more can lead to deep vein thrombosis (DVT) and subsequent pulmonary emboli...
Barrett metaplasia
Gastroenterology / PathologyBarrett metaplasia (Barrett esophagus) is replacement of the normal stratified squamous epithelium of the distal esophagus with metaplastic intestinal-type columnar epithelium containing goblet cells, caused by chronic GERD. It is the ma...
Cheyne-Stokes respiration
Pulmonology / Respiratory Physiology (with Cardiology and Neurology overlap)Cheyne-Stokes respiration is a periodic breathing pattern of cyclic crescendo-decrescendo hyperpnea alternating with central apnea (or hypopnea). It is classically seen in heart failure, stroke/brain injury, and at high altitude, and it...
Whipple triad
EndocrinologyWhipple triad is the set of three criteria that confirms true hypoglycemia as the cause of a patient's symptoms: (1) symptoms/signs consistent with hypoglycemia, (2) a documented low plasma glucose at the time of symptoms, and (3) resolu...
Hutchinson triad
Microbiology / Infectious DiseaseHutchinson triad is the classic triad of late (tardive) congenital syphilis: interstitial keratitis, sensorineural (CN VIII) deafness, and Hutchinson teeth (notched, peg-shaped, widely spaced upper central incisors). It results from tran...
Bruton agammaglobulinemia
ImmunologyBruton (X-linked) agammaglobulinemia is an X-linked recessive primary immunodeficiency caused by BTK (Bruton tyrosine kinase) mutations, which block pre-B cell to mature B cell maturation. It presents in boys after ~6 months (loss of mat...
Sjogren syndrome
Rheumatology / ImmunologySjögren syndrome is an autoimmune disease with lymphocytic (CD4+ T-cell) infiltration and destruction of exocrine glands (lacrimal and salivary). It causes keratoconjunctivitis sicca (dry eyes), xerostomia (dry mouth), and sometimes paro...
hyper-IgE syndrome
ImmunologyHyper-IgE syndrome (Job syndrome) is a primary immunodeficiency, classically from AD-negative dominant STAT3 mutations, causing impaired Th17 differentiation. It presents with the triad of recurrent cold (non-inflamed) staphylococcal ski...
Job syndrome
ImmunologyJob syndrome (Hyper-IgE syndrome) is a primary immunodeficiency, most often caused by an autosomal dominant loss-of-function mutation in STAT3. The mutation impairs Th17 cell differentiation and causes decreased IFN-γ and IL-17. The clas...
Behçet disease
RheumatologyBehçet disease is a chronic, relapsing variable-vessel vasculitis characterized by recurrent painful oral aphthous ulcers, genital ulcers, and uveitis. It is strongly associated with HLA-B51 and the "Silk Road" regions (Turkey, Middle Ea...
alpha-ketoglutarate dehydrogenase
BiochemistryAlpha-ketoglutarate dehydrogenase is a TCA cycle enzyme complex that converts alpha-ketoglutarate to succinyl-CoA, generating NADH and CO2. It is structurally and mechanistically analogous to pyruvate dehydrogenase and requires the same...
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