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ACE Inhibitors
Inhibit the enzyme ACE, which converts angiotensin I to angiotensin II, leading to vasodilation, reduced blood pressure, and decreased aldosterone. Side Effects: Dry cough.
Beta Blockers
Block β-adrenergic receptors (mostly β1 in the heart), leading to decreased heart rate, reduced myocardial contractility, and lowered blood pressure. Side Effects: Bradycardia (slow HR).
Calcium Channel Blockers
Inhibit L-type calcium channels in vascular smooth muscle and/or cardiac muscle, causing vasodilation and potentially reducing heart rate and contractility. Side Effects: Constipation.
Angiotensin II Receptor Blockers (ARBs)
Block angiotensin II from binding to AT1 receptors, causing vasodilation and reduced aldosterone secretion. Side Effects: Headache.
Opioids
Bind to mu (μ), kappa (κ), and delta (δ) opioid receptors in the CNS and PNS, inhibiting ascending pain pathways and altering pain perception. Side Effects: Respiratory Depression.
Barbiturates
Enhance GABA-A receptor activity by prolonging the duration of chloride channel opening, leading to CNS depression. Side Effects: Sedation.
Benzodiazepines
Enhance GABA-A receptor activity by increasing the frequency of chloride channel opening, causing anxiolysis, sedation, and muscle relaxation. Side Effects: Sedation.
Statins
Inhibit HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis, lowering LDL cholesterol by upregulating LDL receptors in the liver. Side Effects: GI Issues, Rash.
Triptans
Stimulate 5-HT receptors in cerebral arteries, causing vasoconstriction and reducing headache symptoms. Side Effects: Vasoconstriction.
Anticholinergic drugs (ACh blockers/Acetylcholine blockers)
Block acetylcholine (ACh) receptors in the vestibular nuclei (located deep in the brain)/the labyrinth (inner ear) and reticular formation. Side Effects: Dizziness, erythema.
Antihistamines (H1 receptor blockers)
Block H1 receptors, thereby preventing ACh from binding to receptors in the vestibular nuclei. Side Effects: Dizziness, sedation.
Antidote for Heparin
Protamine sulphate can be given as an antidote in case of excessive anticoagulation.
Antidote for Warfarin
Antidote is vitamin K.
Digoxin
A cardiac glycoside derived from the Digitalis plant, increases myocardial contractility by inhibiting the Na+/K+-ATPase pump.
Digoxin Mechanism of Action
Increases myocardial contractility and alters electrical conduction in the heart, decreasing conduction rate and prolonging the refractory period.
Narrow Therapeutic Window (Digoxin)
Requires drug level monitoring (0.8-2 ng/mL) due to risk of toxicity, especially with hypokalemia.
Heart Failure (Left-sided)
Characterized by pulmonary edema, coughing, shortness of breath, and dyspnea.
Heart Failure (Right-sided)
Characterized by systemic venous congestion, pedal edema, jugular venous distension, ascites, and hepatic congestion.
Treatment for Status Epilepticus
Diazepam (Valium) is for immediate treatment.
Common ending for ACE Inhibitors
pril
Common ending for Beta Blockers
lol
Common ending for Calcium Channel Blockers
pine, mil, zem
Common ending for Angiotensin II Receptor Blockers (ARBs)
sartan
Common ending for Barbiturates
tal
Common ending for Benzodiazepines
pam
Common ending for Statins
statin
Common ending for Triptans
tans
Common ending for Anticholinergic drugs (ACh blockers/Acetylcholine blockers)
ine
Common ending for Antihistamines (H1 receptor blockers)
ate, ine