Pharmacology Flashcards - Epinephrine, Norepinephrine and Related Drugs

A comprehensive set of Q&A flashcards based on the lecture notes covering adrenergic drugs, anticholinergics, anesthetics, psychotropics, antivirals/antibiotics, chemo agents, diabetes meds, GI drugs, and overdose/poisoning treatments.

What receptors does epinephrine activate and what clinical effects does its β2 activity confer?

Non-selective α and β agonist; significant β2 activity → bronchodilation; uses include anaphylaxis, asthma, cardiac arrest; added to local anesthetics.

What is norepinephrine’s receptor profile and its cardiovascular effect at high levels?

Strong α1 > β1 agonist; no β2 effect → no bronchodilation; used for septic shock/hypotension unresponsive to fluids; increases BP with reflex bradycardia.

Explain dopamine’s dose-dependent receptor activation and the corresponding clinical use.

Low-dose: D1/D5 receptors in kidneys (renal vasodilation); Moderate dose: β1 receptors in heart (↑inotropy); High-dose: α1 in blood vessels (vasoconstriction). Use in shock with hypotension and poor renal perfusion; tachycardia limits use.

What is phenylephrine’s mechanism and typical uses?

Pure α1 agonist → peripheral vasoconstriction; uses: nasal decongestant, mydriasis induction, anesthesia-induced or other hypotension; no direct cardiac stimulation; reflex bradycardia possible.

Describe dobutamine’s receptor activity and primary clinical use.

β1 > β2 agonist → ↑inotropy > chronotropy; mild vasodilation; pure inotrope with less vasoconstriction; used in acute heart failure and cardiogenic shock.

What is clonidine’s mechanism and a key consideration during withdrawal?

α2 agonist → ↓ central sympathetic outflow; uses include resistant hypertension, opioid withdrawal, ADHD (off-label); sudden withdrawal → rebound hypertension; does not cause orthostatic hypotension like peripheral α blockers.

What receptors does labetalol block and what are its main indications and caveat for CHF?

Blocks β1, β2, and α1 → ↓ HR and vasodilation; uses include hypertensive emergencies, pregnancy hypertension (safe), pheochromocytoma; unlike many β-blockers, causes vasodilation via α1 block; not ideal for long-term CHF due to reduced β1 selectivity.

What is the mechanism and primary use of tamsulosin?

Selective α1A antagonist (prostate > vessels); use: BPH (relieves LUTS); not for hypertension; minimal orthostatic hypotension compared to nonselectives; also improves urinary flow without major BP drop.

Describe bethanechol’s mechanism and primary uses.

Muscarinic agonist; stimulates bladder and GI smooth muscle; use: non-obstructive urinary retention, neurogenic bladder, post-op ileus; no nicotinic activity; not for obstructive conditions.

What is pilocarpine’s mechanism and its clinical applications?

Muscarinic agonist → ↑ aqueous humor outflow, ↑ secretions; use: acute angle-closure glaucoma, Sjögren’s syndrome; good for emergency IOP reduction; causes miosis and ciliary spasm.

State neostigmine’s mechanism, CNS activity, and key clinical uses.

Reversible acetylcholinesterase inhibitor (does not cross BBB); uses include MG symptom relief, reversal of non-depolarizing NM blockade; safe peripherally; also used in post-op ileus and urinary retention.

What distinguishes physostigmine from neostigmine?

AChE inhibitor that crosses the BBB → restores central ACh; uses: anticholinergic toxicity (e.g., atropine, TCA overdose); treat both central and peripheral symptoms; monitor for seizures and bradycardia.

Describe atropine’s mechanism and typical indications.

Muscarinic antagonist (reversible); no nicotinic effects; uses: bradycardia, organophosphate poisoning, pre-anesthetic; high-yield: reverses muscarinic effects only (bronchorrhea, bradycardia); causes pupillary dilation and cycloplegia.

What is the mechanism and primary uses of ipratropium?

Inhaled muscarinic antagonist → ↓ bronchoconstriction; uses: COPD (first-line), asthma (adjunct), rhinorrhea; no cardiac stimulation; safe in CAD; slower onset but longer effect than β2-agonists.

Describe scopolamine’s mechanism and clinical applications.

Muscarinic antagonist with high CNS penetration; uses: motion sickness, postoperative N/V; greater sedative and antiemetic effects vs atropine; transdermal patch for prophylaxis.

State succinylcholine’s mechanism and major cautions.

Depolarizing NM blocker → sustained depolarization and paralysis; use: rapid intubation (fast onset, short duration); contraindicated in hyperkalemia, burns, neuromuscular disease; risk of malignant hyperthermia.

What is rocuronium’s mechanism and key clinical notes?

Non-depolarizing NM blocker → blocks nicotinic ACh receptor; use: muscle relaxation for surgery/intubation; slower onset than succinylcholine but safer in hyperkalemia; reversed with neostigmine or sugammadex.

Explain botulinum toxin’s mechanism and its common therapeutic and cosmetic uses.

Blocks ACh release at NMJ → flaccid paralysis; uses: blepharospasm, dystonias, hyperhidrosis, chronic migraine; effects are local and temporary; also used for cosmetic wrinkles.

What is donepezil’s mechanism and its clinical role?

Central AChE inhibitor → ↑ ACh in brain; use: mild to moderate Alzheimer’s disease; slows progression but does not reverse disease; monitor for GI upset, bradycardia, insomnia.

Describe memantine’s mechanism and its place in therapy.

NMDA receptor antagonist → ↓ glutamate excitotoxicity; use: moderate to severe Alzheimer's; high-yield: synergistic with AChE inhibitors; fewer side effects; may reduce agitation/progression.

State the mechanism and primary uses of pramipexole and ropinirole.

Direct dopamine D2 receptor agonists; use: Parkinson’s (early or adjunctive), restless leg syndrome; high-yield: useful in younger patients to delay levodopa start; side effects: impulse control issues, hallucinations.

What is selegiline’s mechanism and a key drug interaction risk?

MAO-B inhibitor → ↓ CNS dopamine breakdown; use: adjunct to levodopa in Parkinson’s; slows symptom progression; risk of serotonin syndrome with SSRIs.

Describe benztropine’s mechanism and when it is most effective.

Antimuscarinic → ↓ ACh to balance dopamine loss; uses: Parkinsonian tremor and drug-induced EPS; high-yield: most effective for tremor and rigidity; not ideal in elderly due to delirium risk.

Explain how amantadine works and its clinical role in Parkinson’s.

↑ dopamine release and ↓ reuptake; NMDA receptor antagonist; use: early Parkinson’s, levodopa-induced dyskinesia; side effects: livedo reticularis, ankle edema.

What is haloperidol’s pharmacologic class and key risks?

High-potency D2 receptor antagonist; uses: schizophrenia (positive symptoms), acute agitation, Tourette’s; high-yield: high risk of EPS and tardive dyskinesia; can cause NMS.

What distinguishes atypical antipsychotics from typicals regarding side effects?

Mechanism: D2 + 5-HT2A antagonists (less dopamine blockade); uses: schizophrenia (positive and negative symptoms), bipolar; high-yield: lower EPS risk but higher metabolic side effects (e.g., olanzapine, clozapine); also used as adjunct in treatment-resistant depression.

State clozapine’s mechanism, major risk, and additional adverse effects.

Weak D2, strong 5-HT2A antagonist; uses: schizophrenia unresponsive to other meds; high-yield: agranulocytosis risk (CBC monitoring); also causes seizures, myocarditis, weight gain.

Describe aripiprazole’s mechanism and its clinical advantages.

Partial D2 agonist + 5-HT1A agonist; uses: schizophrenia, bipolar, adjunct in depression; activates D2 when dopamine is low and blocks when high; fewer metabolic and EPS side effects.

What are the receptor actions and uses of quetiapine?

D2 + 5-HT2A blocker; strong H1 antagonism; uses: bipolar depression, psychosis, insomnia (off-label); sedating; risk of metabolic syndrome.

Summarize the mechanism and notable features of SSRIs.

Inhibit serotonin reuptake → ↑ 5-HT in synapse; use: depression, anxiety, PTSD, OCD, panic disorder; takes 2–4 weeks to work; risk of sexual dysfunction and SIADH; safer in overdose vs TCAs.

How do SNRIs differ from SSRIs and what is a notable side effect?

Mechanism: Block reuptake of 5-HT + NE; use: Depression, GAD, neuropathic pain, fibromyalgia; high-yield: may increase BP due to NE inhibition; duloxetine preferred for diabetic neuropathy.

What is bupropion’s mechanism and key clinical considerations?

Inhibits dopamine reuptake (DAT); uses: depression, smoking cessation, ADHD (off-label); high-yield: no sexual side effects; contraindicated in seizures, eating disorders; activating, good for atypical depression.

State mirtazapine’s mechanism and its notable effects on weight and sleep.

α2 antagonist → ↑ NE & 5-HT; also blocks H1, 5-HT2/3; uses: depression with insomnia or weight loss; high-yield: causes weight gain and sedation; minimal sexual dysfunction.

What is the mechanism and clinical concern with MAO inhibitors?

Irreversibly inhibit MAO-A/B → ↑ NE, 5-HT, DA; uses: atypical depression, Parkinson’s (MAO-B), refractory depression; high-yield: risk of hypertensive crisis with tyramine-containing foods; must wait 2 weeks before switching to serotonergic drugs.

Describe the mechanism and major adverse effects of phenytoin.

Na+ channel inactivation → ↓ neuron firing; uses: focal & generalized seizures; status epilepticus after benzodiazepines; narrow therapeutic index; side effects include gingival hyperplasia, hirsutism; nonlinear kinetics.

State the mechanism and key clinical notes for carbamazepine.

Na+ channel blocker; uses: focal seizures, trigeminal neuralgia, bipolar; high-yield: 1st-line for trigeminal neuralgia; risk of SIADH, agranulocytosis, CYP induction.

Summarize valproic acid’s mechanism and its major clinical risks.

Na+ channel blocker +↑ GABA + T-type Ca2+ blockade; uses: generalized seizures, bipolar disorder, migraine prophylaxis; high-yield: teratogenic (neural tube defects), hepatotoxicity, weight gain; broad utility.

What is ethosuximide’s mechanism and its primary indication?

Blocks T-type Ca2+ channels in the thalamus; use: 1st-line for absence seizures; high-yield: side effects include fatigue, GI distress, headache, itching, Stevens–Johnson syndrome; ineffective for tonic-clonic or focal seizures.

Describe the concept of inhaled anesthetic potency (MAC) and factors affecting onset/recovery.

Potency is inversely related to MAC (minimum alveolar concentration); faster onset/recovery with low blood:gas partition; uses: general anesthesia induction/maintenance; examples include nitrous oxide (rapid) and halothane (hepatotoxic).

State the mechanism and key use of propofol in anesthesia.

GABA-A agonist; use: rapid induction and procedural sedation; high-yield: fast onset, short duration; risks: hypotension and respiratory depression; lipid-based formulation requiring monitoring for hypertriglyceridemia.

Explain ketamine’s mechanism and its clinical advantages and side effects.

NMDA receptor antagonist → dissociative anesthesia; uses: analgesia + sedation (trauma, burns, kids); high-yield: preserves airway reflexes and BP; side effects: emergence delirium, ↑ intracranial pressure, dissociative amnesia.

What is etomidate’s mechanism and a notable endocrine effect?

GABA-A agonist; use: induction in hemodynamically unstable patients; high-yield: adrenocortical suppression (inhibits 11β-hydroxylase); not used for prolonged sedation.

Describe how local anesthetics work and a key strategy to reduce systemic absorption.

Block voltage-gated Na+ channels → prevent action potentials; uses: local anesthesia (nerve blocks, infiltration); high-yield: prefer rapidly firing nerves; co-administer with epinephrine to ↓ systemic absorption.

What is the difference between esters and amides in local anesthetics?

ESTER: two i’s in name; Degraded by plasma esterases; short duration; examples: procaine, tetracaine, cocaine, benzocaine, dyclonine. AMIDE: one i in name; Degraded by hepatic amidases; longer duration; examples: lidocaine, mepivacaine, bupivacaine, prilocaine, etidocaine.

Name a few must-know adverse effects associated with local anesthetics.

Prilocaine → methemoglobinemia; Bupivacaine → cardiotoxic; Etidocaine/Mepivacaine have notable duration/toxicity considerations; pregnancy considerations vary.

What is the clinical use and key property of midazolam?

Benzodiazepine → ↑ GABA-A activity; uses: pre-op sedation, amnesia, anxiolysis; short-acting; antagonized by flumazenil; risk of respiratory depression when combined with opioids.

What triggers malignant hyperthermia and what is the antidote?

MH is caused by a mutation in the ryanodine receptor causing ↑ Ca2+ release in muscle; triggers: succinylcholine and volatile anesthetics; treatment: dantrolene; features: hyperthermia, muscle rigidity, acidosis.

State dantrolene’s mechanism and its primary indications.

Inhibits ryanodine receptor → ↓ Ca2+ release from the sarcoplasmic reticulum; uses: malignant hyperthermia and neuroleptic malignant syndrome; note: the only antidote for MH; may cause hepatotoxicity with chronic use.

Summarize the mechanism and key uses of penicillin class drugs.

β-lactams → inhibit transpeptidase → prevent peptidoglycan cross-linking; Penicillin G/V: syphilis, GAS pharyngitis, meningococcus; Ampicillin/amoxicillin: broader gram-negative coverage (e.g., H. influenzae, Listeria); amoxicillin is more orally bioavailable; β-lactamase-sensitive unless combined with clavulanate.

What is the clinical role of piperacillin–tazobactam?

Piperacillin: broad-spectrum antipseudomonal β-lactam; tazobactam: β-lactamase inhibitor; uses: serious gram-negative infections including Pseudomonas and intra-abdominal infections; covers anaerobes + Pseudomonas; common empiric choice for hospital-acquired infections.

Describe cefepime’s spectrum and notable safety concerns.

4th-gen cephalosporin → β-lactamase resistant to many β-lactamases; uses: pseudomonas, febrile neutropenia, severe nosocomial infections; good CNS penetration; risk of neurotoxicity (seizures) in renal failure.

What is vancomycin’s mechanism and primary clinical uses along with major adverse effects?

Binds D-Ala-D-Ala → inhibits cell wall synthesis; uses: MRSA, C. difficile (oral), serious gram-positive infections; not absorbed orally (oral use targets gut); adverse: red man syndrome, nephrotoxicity, ototoxicity.

Name a single flashcard that captures MRSA coverage drugs, based on the MRSA coverage list.

MRSA coverage includes vancomycin, daptomycin, linezolid, ceftaroline/5th-gen cephalosporins, clindamycin, doxycycline, TMP-SMX, rifampin (often in combination), among others; choose based on context and organism susceptibility.

Describe the mechanism and common use of aminoglycosides.

Irreversibly bind 30S → block initiation and misread tRNA; use: severe gram-negative infections (e.g., gentamicin), synergy with β-lactams; requires O2 for uptake; toxicity: ototoxicity, vestibulotoxicity, nephrotoxicity.

State the mechanism and key pregnancy/pediatric considerations for doxycycline.

Binds 30S → blocks aminoacyl-tRNA; uses: atypicals (Chlamydia, Rickettsia, Mycoplasma), acne, Lyme, malaria prophylaxis; high-yield: avoid in pregnancy/children <8 due to tooth discoloration; excellent intracellular penetration.

Summarize macrolide mechanism and major cautions.

Bind 50S → block translocation; uses: CAP (Streptococcus pneumoniae, atypicals), pertussis, chlamydia; high-yield: QT prolongation, CYP450 inhibition (especially erythromycin); azithromycin has long half-life and fewer interactions.

Describe linezolid’s mechanism, uses, and important interactions.

Binds 50S → inhibits initiation complex; uses: VRE, VRSA, resistant gram-positive infections; high-yield: serotonin syndrome risk with SSRIs, bone marrow suppression; oral bioavailability = IV.

What does chloramphenicol do and what are its notable risks?

50S inhibitor → blocks peptidyl transferase; uses: meningitis in developing countries, Rickettsia in pregnancy; risks: Gray baby syndrome, aplastic anemia.

State the mechanism and major cautions of fluoroquinolones.

Inhibit DNA gyrase (topoisomerase II/IV); uses: UTI, CAP, GI infections, prostatitis; risks: tendon rupture, QT prolongation; avoid in pregnancy and children; ciprofloxacin covers Pseudomonas.

Outline metronidazole’s mechanism and its primary anaerobic coverage and notable interaction.

Forms free radicals → DNA damage in anaerobes; uses: anaerobes (Bacteroides, C. difficile), Giardia, Entamoeba, H. pylori; high-yield: disulfiram-like reaction with alcohol.

Explain TMP-SMX’s mechanism, uses, and key safety concerns.

Sequential inhibition of folate synthesis (dihydropteroate + DHFR); uses: UTI, MRSA skin infections, Pneumocystis, Nocardia; high-yield: hyperkalemia, bone marrow suppression, SJS/TEN; avoid in G6PD deficiency and late pregnancy.

Describe rifampin’s mechanism, uses, and a major drug interaction concern.

Inhibits DNA-dependent RNA polymerase; uses: TB, meningococcal prophylaxis, H. influenzae prophylaxis, leprosy; high-yield: CYP450 inducer, orange secretions; resistance develops quickly, thus never used alone.

What is nitrofurantoin primarily used for and a key safety note?

Mechanism: bacterial enzyme reduction → DNA damage; use: uncomplicated UTIs; safe in pregnancy; avoid in renal failure; can cause pulmonary fibrosis with long-term use.

State ganciclovir’s mechanism, uses, and a major toxicity risk.

Similar to acyclovir but activated by CMV UL97 kinase; use: CMV infections (immunocompromised); high-yield: myelosuppression, renal toxicity; valganciclovir offers better oral availability.

Explain oseltamivir’s mechanism, timing of use, and a secondary use.

Neuraminidase inhibitor → blocks viral release; use: influenza A & B within 48 hours of symptoms; high-yield: shortens illness if started early; also used for post-exposure prophylaxis.

Describe fluconazole’s mechanism and its spectrum of activity, including CNS penetration.

Inhibits ergosterol synthesis (14α-demethylase); uses: candidiasis, cryptococcal meningitis maintenance; good CNS penetration; CYP inhibition; not effective against molds (e.g., Aspergillus).

State isoniazid’s mechanism and a key activation requirement and adverse effects.

Inhibits mycolic acid synthesis; use: TB (treatment & latent prophylaxis); high-yield: requires catalase-peroxidase (KatG) for activation; hepatotoxicity, peripheral neuropathy (prevent with B6).

What is pyrazinamide’s notable activity and common adverse effects?

Mechanism: unclear; activated in acidic TB phagolysosomes; use: TB therapy (shortens duration); high-yield: hepatotoxicity, hyperuricemia (gout); most active during intracellular phase.

Summarize methotrexate’s mechanism, uses, and a key rescue strategy.

Inhibits dihydrofolate reductase → ↓ DNA synthesis; uses: cancers (ALL, lymphoma, choriocarcinoma), ectopic pregnancy, RA; high-yield: leucovorin rescue; side effects: myelosuppression, hepatotoxicity, mucositis.

What is 5-fluorouracil’s mechanism and its main therapeutic use with a note on enhancement?

Inhibits thymidylate synthase → ↓ dTMP; uses: colorectal cancer, breast cancer; topical for basal cell carcinoma; high-yield: enhanced by leucovorin; main toxicity: myelosuppression, hand-foot syndrome.

Describe cyclophosphamide’s mechanism and a key prophylaxis to prevent a major toxicity.

Alkylates DNA (crosslinking); uses: solid tumors, leukemias, SLE, vasculitis; adverse: hemorrhagic cystitis; prevention with MESNA; risk: bladder cancer.

State cyclosporine’s mechanism and major toxicities, including drug interactions.

Calcineurin inhibitor → ↓ IL-2 → ↓ T-cell activation; uses: transplant rejection prevention, RA; high-yield: nephrotoxicity, gingival hyperplasia, hirsutism; metabolized by CYP3A4.

Describe tacrolimus’s mechanism and a few key adverse effects.

Calcineurin inhibitor (FKBP binding); uses: transplant rejection, eczema (topical); high-yield: nephrotoxicity but no hirsutism/gingival overgrowth; more potent with ↑ risk of neurotoxicity and diabetes.

What is sirolimus’s mechanism and its main transplant-related benefit and side effects?

mTOR inhibitor → blocks T-cell response to IL-2; use: kidney transplant (especially when nephrotoxicity is a concern); high-yield: no nephrotoxicity but causes hyperlipidemia; synergistic with cyclosporine.

Outline metformin’s mechanism and its main advantages and contraindications.

Activates AMPK → ↓ gluconeogenesis, ↑ insulin sensitivity; use: first-line for type 2 diabetes; high-yield: weight-neutral, no hypoglycemia; contraindicated in renal failure due to risk of lactic acidosis.

Describe GLP-1 agonists’ mechanism and primary benefits and risks.

Mimics incretin → ↑ insulin, ↓ glucagon, slows gastric emptying; use: type 2 diabetes and obesity; high-yield: weight loss, low hypoglycemia risk; risks include pancreatitis and thyroid C-cell tumors.

Explain SGLT2 inhibitors’ mechanism and notable effects and risks.

Block renal glucose reabsorption in proximal tubule; use: type 2 diabetes, heart failure, CKD; high-yield: weight loss, cardiovascular benefit; risks include UTIs, DKA in euglycemia, dehydration.

What do thionamides PTU and methimazole do and what are their pregnancy considerations?

Inhibit thyroid peroxidase (PTU also blocks T4→T3); uses: hyperthyroidism; PTU in first-trimester pregnancy; high-yield: agranulocytosis, hepatotoxicity; methimazole is teratogenic; PTU has hepatotoxicity risk.

State the mechanism and key adverse effects of PPIs like omeprazole.

Irreversibly inhibit H+/K+ ATPase in parietal cells; uses: GERD, ulcers, Zollinger-Ellison, H. pylori regimens; high-yield: risk of hypomagnesemia, B12 deficiency, fractures; delayed onset due to activation in acidic environment.

Describe sucralfate’s mechanism and its limitations with other acid-suppressive therapies.

Binds ulcer base to form a physical barrier; uses: stress ulcers, duodenal ulcers; requires acidic environment to activate; avoid with H2 blockers or PPIs.

What is loperamide’s mechanism and its key safety notes?

μ-opioid receptor agonist → slows gut motility; uses: traveler’s diarrhea, chronic diarrhea; no CNS penetration → no euphoria; overuse may cause ileus or QT prolongation.

Explain ondansetron’s mechanism, indications, and notable side effects.

5-HT3 receptor antagonist in CNS and GI; uses: chemo-induced N/V, postoperative nausea; side effects: QT prolongation, serotonin syndrome; often combined with dexamethasone.

State the mechanism and therapeutic use of lactulose in hepatic encephalopathy.

Guts flora metabolize → ↓ NH3 absorption; use: hepatic encephalopathy; high-yield: traps NH3 as NH4+; side effects: bloating, diarrhea.

Describe N-acetylcysteine’s mechanism and its key overdose and protective uses.

Replenishes glutathione; uses: acetaminophen overdose, mucolytic, contrast nephropathy prevention; high-yield: most effective within 8–10 hours of ingestion; also used in CF for mucus thinning.

What are the roles of atropine and pralidoxime in organophosphate poisoning?

Atropine blocks muscarinic effects; pralidoxime reactivates AChE (if given early); both required; atropine for symptom control, pralidoxime for reversal; must give before enzyme aging occurs.

Explain glucagon’s mechanism and two primary clinical uses.

↑ cAMP → cardiac stimulation; uses: β-blocker overdose, hypoglycemia; can bypass β-receptors for inotropic/chronotropic effects; also used to relax the LES during esophageal foreign body retrieval.

What is flumazenil’s role and a major safety caveat?

GABA-A antagonist; reversal of benzodiazepine sedation; high-yield: may trigger seizures in chronic BZD users; not routinely used unless BZDs are the only substance involved.

Describe sodium bicarbonate’s mechanism in toxicity management and its primary indications.

Alkalinizes plasma → stabilizes cardiac membranes; uses: TCA-induced arrhythmias or widened QRS; high-yield: increases protein binding → ↓ free TCA; also corrects acidosis, which worsens toxicity.