Ανεπιθυμητές ενέργειες Flashcards
CCB MECHANISM
Block voltage-dependent L-type calcium channels of cardiac and smooth muscle muscle
contractility.
Vascular smooth muscle—amlodipine = nifedipine > diltiazem > verapamil.
Heart—verapamil > diltiazem > amlodipine = nifedipine (verapamil = ventricle).
CCB CLINICAL USE
Dihydropyridines (except nimodipine): hypertension, angina (including Prinzmetal), Raynaud
phenomenon.
Nimodipine: subarachnoid hemorrhage (prevents cerebral vasospasm).
Clevidipine: hypertensive urgency or emergency.
Non-dihydropyridines: hypertension, angina, atrial fibrillation/flutter.
CCB ADV ERSE EFFECTS
Non-dihydropyridine: cardiac depression, AV block, hyperprolactinemia, constipation.
Dihydropyridine: peripheral edema, flushing, dizziness, gingival hyperplasia.
Hydralazine
MECHANISM increase cGMP –> smooth muscle relaxation. Vasodilates arterioles > veins; afterload reduction.
CLINICAL USE
Severe hypertension (particularly acute), HF (with organic nitrate). Safe to use during pregnancy.
Frequently coadministered with a β-blocker to prevent reflex tachycardia.
ADV ERSE EFFECTS Compensatory tachycardia (contraindicated in angina/CAD), fluid retention, headache, angina.
Lupus-like syndrome.
Hypertensive
emergency
Hypertensive
emergency
Drugs include clevidipine, fenoldopam, labetalol, nicardipine, nitroprusside.
Nitroprusside
Short acting; increase cGMP via direct release of NO. Can cause cyanide toxicity (releases cyanide
Fenoldopam
Dopamine D1 receptor agonist—coronary, peripheral, renal, and splanchnic vasodilation. lowers BP,
increases natriuresis. Also used postoperatively as an antihypertensive. Can cause hypotension and
tachycardia.
Nitrates
Nitroglycerin, isosorbide dinitrate, isosorbide mononitrate.
MECHANISM Vasodilate by increase NO in vascular smooth muscle –> increase in cGMP and smooth muscle relaxation.
Dilate veins»_space; arteries. preload.
CLINICAL USE Angina, acute coronary syndrome, pulmonary edema.
ADV ERSE EFFECTS Reflex tachycardia (treat with β-blockers), hypotension, flushing, headache, “Monday disease” in
industrial exposure: development of tolerance for the vasodilating action during the work week
and loss of tolerance over the weekend tachycardia, dizziness, headache upon reexposure.
Ranolazine
MECHANISM Inhibits the late phase of sodium current thereby reducing diastolic wall tension and oxygen
consumption. Does not affect heart rate or contractility.
CLINICAL USE Angina refractory to other medical therapies.
ADV ERSE EFFECTS Constipation, dizziness, headache, nausea, QT prolongation
Αλλοπουρινόλη
Competitive inhibitor of xanthine oxidase.
conversion of hypoxanthine and xanthine to
urate. Also used in lymphoma and leukemia
to prevent tumor lysis–associated urate
nephropathy. concentrations of azathioprine
and 6-MP (both normally metabolized by
xanthine oxidase).
The most frequent adverse
effect with either medication is the precipitation of an
acute gouty attack; thus, patients generally should be
receiving prophylactic doses of colchicine.
Hypersensitivity to allopurinol occurs in 2% of cases,
usually within the first few months of therapy, and it can be
life-threatening. The most common sign of hypersensitivity
is a pruritic rash that may progress to toxic epidermal
RHEUMATOLOGIC, IMMUNOLOGIC, & ALLERGIC DISORDERS CMDT 2016 819
necrolysis, particularly if allopurinol is continued; vasculitis
and hepatitis are other manifestations. Patients should
be instructed to stop allopurinol immediately if a rash
develops. Chronic kidney disease and concomitant thiazide
therapy are risk factors. In certain ethnic groups, there
is a strong association between HLA-B5801 and allopurinol
hypersensitivity. Current recommendations are to
screen for HLA-B5801 prior to initiating allopurinol in
Han Chinese, those of Thai descent, and Koreans with
stage 3 or worse chronic kidney disease
