What are the pharmacological class, mechanism of action, and classic adverse effects of Lisinopril and Enalapril?

Class: ACE Inhibitors. MOA: Inhibit angiotensin-converting enzyme, decreasing Angiotensin II and aldosterone while increasing bradykinin. Adverse effects: Dry cough, angioedema, hyperkalemia, teratogenicity, acute creatinine rise in bilateral renal artery stenosis.

What is the mechanism of action of Losartan and Valsartan, and what is their key clinical advantage over ACE inhibitors?

Class: Angiotensin II Receptor Blockers (ARBs). MOA: Selectively block AT1 receptors, preventing angiotensin II-mediated vasoconstriction and aldosterone secretion. Advantage: Because ARBs do not inhibit ACE (kininase II), they do not impair bradykinin degradation and have a much lower incidence of dry cough and angioedema (though rare angioedema can still occur, so caution is warranted in patients with prior ACE-inhibitor angioedema).

What are the mechanism of action and primary bacterial resistance mechanisms for Penicillin G and Amoxicillin?

Bind penicillin-binding proteins (PBPs/transpeptidases) to block peptidoglycan cross-linking in the bacterial cell wall, activating autolysins. Resistance occurs via beta-lactamase cleavage of the beta-lactam ring (overcome by adding clavulanate, sulbactam, or tazobactam) or altered PBPs (e.g., mecA/PBP2a in MRSA).

What are the spectrum of activity and primary excretion pathway of the antistaphylococcal penicillins Nafcillin, Oxacillin, and Dicloxacillin?

Antistaphylococcal penicillins with bulky R-side chains that sterically block staphylococcal beta-lactamase. Active against MSSA and streptococci (no Gram-negative activity). Cleared predominantly via the biliary tract (no renal dose adjustment required).

Albuterol (SABA) vs Salmeterol/Formoterol (LABA) — Beta-2 Agonist Mechanism & GINA Asthma Monotherapy Rule

Stimulate beta-2 adrenergic receptors (Gs -> adenylyl cyclase -> increased cAMP -> bronchial smooth muscle relaxation) and drive K+ into cells (causing hypokalemia and tremor). LABAs must NEVER be used as monotherapy in asthma without an inhaled corticosteroid (ICS) due to increased asthma-related mortality; GINA guidelines recommend ICS-formoterol as preferred reliever.

Ipratropium (SAMA) & Tiotropium/Umeclidinium (LAMA) — Mechanism & Role in COPD vs Asthma

Competitively block M3 muscarinic receptors on airway smooth muscle, preventing vagally mediated bronchoconstriction and mucus secretion. LAMAs are cornerstone maintenance therapy in COPD and severe asthma. Adverse effects: Dry mouth and acute urinary retention in men with BPH.

Volume of Distribution (Vd), Clearance (CL) & Elimination Half-Life (t1/2) — Core Pharmacokinetic Equations

Vd = Amount of drug in body / Plasma concentration (C0); Loading Dose = (Vd x Cp) / F. Maintenance Dose = (CL x Cp x tau) / F. Half-life t1/2 = (0.693 x Vd) / CL. It takes 4 to 5 half-lives for a drug infused at a constant rate to reach 94–97% steady-state concentration (or be completely eliminated).

First-Order vs Zero-Order Elimination Kinetics — Classic Zero-Order Drugs ('PEA')

First-order kinetics: A constant FRACTION of drug is eliminated per unit time (rate is proportional to plasma concentration; t1/2 is constant). Zero-order (capacity-limited) kinetics: Enzymatic pathways are saturated, so a constant AMOUNT of drug is eliminated per unit time (concentration drops linearly; t1/2 increases as concentration rises). Classic zero-order drugs: Phenytoin, Ethanol, and Aspirin (at toxic doses).

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Livello	Fronte (Domanda / Termine)	Retro (Risposta / Spiegazione)
`basic`	What are the pharmacological class, mechanism of action, and classic adverse effects of Lisinopril and Enalapril?	Class: ACE Inhibitors. MOA: Inhibit angiotensin-converting enzyme, decreasing Angiotensin II and aldosterone while increasing bradykinin. Adverse effects: Dry cough, angioedema, hyperkalemia, teratogenicity, acute creatinine rise in bilateral renal artery stenosis.
`basic`	What is the mechanism of action of Losartan and Valsartan, and what is their key clinical advantage over ACE inhibitors?	Class: Angiotensin II Receptor Blockers (ARBs). MOA: Selectively block AT1 receptors, preventing angiotensin II-mediated vasoconstriction and aldosterone secretion. Advantage: Because ARBs do not inhibit ACE (kininase II), they do not impair bradykinin degradation and have a much lower incidence of dry cough and angioedema (though rare angioedema can still occur, so caution is warranted in patients with prior ACE-inhibitor angioedema).
`basic`	What are the mechanism of action and primary bacterial resistance mechanisms for Penicillin G and Amoxicillin?	Bind penicillin-binding proteins (PBPs/transpeptidases) to block peptidoglycan cross-linking in the bacterial cell wall, activating autolysins. Resistance occurs via beta-lactamase cleavage of the beta-lactam ring (overcome by adding clavulanate, sulbactam, or tazobactam) or altered PBPs (e.g., mecA/PBP2a in MRSA).
`basic`	What are the spectrum of activity and primary excretion pathway of the antistaphylococcal penicillins Nafcillin, Oxacillin, and Dicloxacillin?	Antistaphylococcal penicillins with bulky R-side chains that sterically block staphylococcal beta-lactamase. Active against MSSA and streptococci (no Gram-negative activity). Cleared predominantly via the biliary tract (no renal dose adjustment required).
`intermediate`	What are the mechanism of action, therapeutic lag mechanism, and classic adverse effects of the SSRIs Sertraline, Escitalopram, and Fluoxetine?	Selectively inhibit presynaptic serotonin transporter (SERT), increasing synaptic 5-HT; require 4–6 weeks for full antidepressant effect (downregulation of presynaptic 5-HT1A autoreceptors). Adverse effects: Sexual dysfunction (anorgasmia), GI upset, SIADH (hyponatremia in elderly), QT prolongation (citalopram), and serotonin syndrome.
`intermediate`	What are the mechanism of action, pain indications, and cardiovascular adverse effects of the SNRIs Venlafaxine, Desvenlafaxine, and Duloxetine?	Inhibit presynaptic reuptake of both serotonin and norepinephrine. Indicated for MDD, GAD, diabetic peripheral neuropathy, and fibromyalgia (duloxetine). Dose-dependent norepinephrine reuptake inhibition can cause sustained hypertension and diaphoresis; venlafaxine has a severe discontinuation syndrome due to its short half-life.
`intermediate`	How do Rapid-Acting (Lispro, Aspart), Short-Acting (Regular), Intermediate (NPH), and Long-Acting Basal (Glargine, Degludec) insulins compare in pharmacokinetic onset, peak, and duration?	Rapid-acting (Lispro, Aspart, Glulisine): onset 15 min, peak 1h, duration 3–4h (mealtime bolus). Short-acting (Regular): onset 30–60 min, peak 2–3h (only insulin given IV for DKA/hyperkalemia). Intermediate (NPH): peak 4–10h. Long-acting basal (Glargine, Degludec): peakless over 24+ hours.
`intermediate`	What are the mechanism of action, glycemic/weight benefits, and renal/iodinated contrast safety rules for Metformin (Glucophage)?	Biguanide that activates hepatic AMPK and inhibits mitochondrial complex I and glycerophosphate dehydrogenase, suppressing hepatic gluconeogenesis and improving peripheral insulin sensitivity without causing hypoglycemia or weight gain (chronic use can cause vitamin B12 deficiency). Contraindicated if eGFR < 30 mL/min/1.73 m² (do not initiate if eGFR 30–45); temporarily hold metformin at the time of or prior to iodinated IV contrast procedures if eGFR is 30–60 mL/min/1.73 m² (or with liver disease, alcoholism, acute heart failure, or intra-arterial contrast) and recheck eGFR at 48 hours before restarting to prevent Metformin-Associated Lactic Acidosis (MALA).
`advanced`	Albuterol (SABA) vs Salmeterol/Formoterol (LABA) — Beta-2 Agonist Mechanism & GINA Asthma Monotherapy Rule	Stimulate beta-2 adrenergic receptors (Gs -> adenylyl cyclase -> increased cAMP -> bronchial smooth muscle relaxation) and drive K+ into cells (causing hypokalemia and tremor). LABAs must NEVER be used as monotherapy in asthma without an inhaled corticosteroid (ICS) due to increased asthma-related mortality; GINA guidelines recommend ICS-formoterol as preferred reliever.
`advanced`	Ipratropium (SAMA) & Tiotropium/Umeclidinium (LAMA) — Mechanism & Role in COPD vs Asthma	Competitively block M3 muscarinic receptors on airway smooth muscle, preventing vagally mediated bronchoconstriction and mucus secretion. LAMAs are cornerstone maintenance therapy in COPD and severe asthma. Adverse effects: Dry mouth and acute urinary retention in men with BPH.
`advanced`	Volume of Distribution (Vd), Clearance (CL) & Elimination Half-Life (t1/2) — Core Pharmacokinetic Equations	Vd = Amount of drug in body / Plasma concentration (C0); Loading Dose = (Vd x Cp) / F. Maintenance Dose = (CL x Cp x tau) / F. Half-life t1/2 = (0.693 x Vd) / CL. It takes 4 to 5 half-lives for a drug infused at a constant rate to reach ~94–97% steady-state concentration (or be completely eliminated).
`advanced`	First-Order vs Zero-Order Elimination Kinetics — Classic Zero-Order Drugs ('PEA')	First-order kinetics: A constant FRACTION of drug is eliminated per unit time (rate is proportional to plasma concentration; t1/2 is constant). Zero-order (capacity-limited) kinetics: Enzymatic pathways are saturated, so a constant AMOUNT of drug is eliminated per unit time (concentration drops linearly; t1/2 increases as concentration rises). Classic zero-order drugs: Phenytoin, Ethanol, and Aspirin (at toxic doses).

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Settimane 1–2: Fondamenti (basic): Completa i mazzi Base (32 carte/giorno) con 15–20 minuti di ripasso quotidiano.
Settimane 3–5: Approfondimento (intermediate): Aggiungi i mazzi Intermedi (20 nuove carte/giorno) formulando la risposta prima di girare la carta.
Settimane 6–7: Padronanza (advanced): Passa ai mazzi Avanzati (15 nuove carte/giorno) per preparare esami universitari o concorsi.
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Studiare tutto il giorno prima dell'esame: La costanza quotidiana (20 min/giorno) moltiplica la ritenzione.
Ignorare il contesto: Studia gli esempi pratici riportati sul retro di ogni flashcard.

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