Calcium-channel blockers Alcohol

CALCIUM CHANNEL BLOCKERS ALCOHOL 1. Acute alcohol ingestion may t hypotensive effect. Chronic moderate/heavy drinking 1 hypotensive effect 2. Verapamil may t peak serum concentration and prolong the effects of alcohol 1. Additive hypotensive effect with acute alcohol excess. Chronic alcohol excess is associated with hypertension 2. Uncertain at present, but presumed to be due to an inhibition of hepatic metabolism of alcohol 1. Monitor BP closely as unpredictable responses can occur. Advise patients to drink only in moderation and avoid large variations in the amount of alcohol drunk 2. Warn the patient about the potentiation of the effects of alcohol, particularly the risks of driving... 

If die nitrates are administered witii the antihypertensives, alcohol, calcium channel blockers, or the phe-notiiiazines, there may be an increased hypotensive effect. When nitroglycerin is administered intravenously (IV), die effects of heparin may be decreased. Increased nitrate serum concentrations may occur when the nitrates are administered witii aspirin. 

Uncontrolled hypertension Valvular disorders function sympathomi meti cs) Offending medications (NSAIDs, COX-2 inhibitors, steroids, lithium, (i-blockers, calcium channel blockers, anti-arrhythmics, alcohol, thiazolidinediones)... 

Drugs that may interact with nitrates include alcohol, alteplase, aspirin, beta-blockers, calcium channel blockers, dihydroergotamine, heparin, nondepolarizing muscle relaxants, phenothiazines, phosphodiesterase inhibitors (eg, sildenafil, tadalafil, vardenafil), and vasodilators. 

Certain other drugs also having uterine relaxant property are calcium channel blockers, prostaglandin synthesis inhibitors, progesterone, nitrites, anticholinergics, ethyl alcohol etc. 

Glyceryl trinitrate overdose should be treated with the patient s head lowered. Other measures include respiration maintenance, use of plasma expanders, and electrolyte balance. Withdrawal of heparin treatment or dose reduction should be performed with the overdose of heparin. Protamine sulfate may be used to reduce severe bleeding. Heparin should be used with caution with glyceryl trinitrate, aprotinine, alcohol, tobacco, and ACE inhibitors. Nifedipine should be used with care when coadministering with immunosuppressants, magnesium salts, tobacco, digoxin, antineoplastics, calcium channel blockers, antihistamines, antifungals, antiepileptics, antiarrhythmics, and alcohol. 

Chronic heart failure is typically managed by reduction in physical activity, low dietary intake of sodium (less than 1500 mg sodium per day), and treatment with vasodilators, diuretics and inotropic agents. Drugs that may precipitate or exacerbate CHF—nonsteroidal antiinflammatory drugs (NSAIDs), alcohol, (3-blockers, calcium channel-blockers and some antiarrhythmic drugs—should be avoided if possible. Patients with CHF complain of dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, fatigue, and dependent edema. 

Rush CR, Pazzaglia PJ. Pretreatment with isradipine, a calcium-channel blocker, does not attenuate the acute behavioral effects of ethanol in humans. Alcohol Clin Exp Res 1998 22(2) 539-47. 

Mechanism and susceptibility factors The mechanism of cisplatin-induced neurotoxicity has not been fully explained. Cisplatin appears to affect neurons in the dorsal root ganglia. It has also been suggested that it can act as a calcium channel blocker, altering intracellular calcium homeostasis and leading to apoptosis of exposed neurons, such as those of the dorsal root ganglia. Cisplatin-induced sensory neuropathy is predominantly characterized by symptoms such as numbness and tingling, paresthesia of the upper and lower extremities, reduced deep-tendon reflexes, and leg weakness with gait disturbance. The first symptoms are often observed after a cumulative dose of 300-600 mg/m. Risk factors include diabetes mellitus, alcohol consumption, or inherited neuropathies. Advanced age has not been identified as an independent risk factor when there is no co-morbidity (67-70). 

Calcium-channel blockers Nifedipine and verapamil can increase alcohol serum levels by about 15-50%. The mechanism is speculated to be via inhibition of hepatic alcohol metabolism. Some data suggest that alcohol might also inhibit the metabolism of nifedipine, thus raising its serum levels with consequent effects. 

The bioavailability of felodipine and nifedipine appear to be increased by alcohol. The manufacturers of some calcium-channel blockers warn that inter-individual variations in the response to these drugs can occur and some patients ability to drive or operate machinery may be impaired, particularly at the start of treatment and in conjunction with alcohol. " Patients should therefore be advised about these effects. Note that long-term moderate to heavy drinking can impair the efficacy of antihypertensives. See also Alcohol + Antihypertensives , p.48. 

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