Heart disease Hypothyroidism

These drugp are contraindicated in patients with known hypersensitivity to the drug or to any constituents of the drug, after a recent myocardial infarction (heart attack), or in patients with thyrotoxicosis. When hypothyroidism is a cause or contributing factor to a myocardial infarction or heart disease, the physician may prescribe small doses of thyroid hormone... 

This point of view overlooks the fact that every well and normal individual is potentially an ill individual, and the roots of disease may be present in his make-up years before there is any overt disease. A dozen young men used as normal controls may each have metabolic peculiarities that point toward a different metabolic derangement gout, multiple sclerosis, diabetes, anemia, atherosclerosis, hypertension, nephrosis, hypothyroidism, rheumatoid arthritis, rheumatic heart disease, liver cirrhosis, and myasthenia gravis, for example, and yet at the time of their use as controls these young men may show no symptoms of the disease which is to appear later in life. It seems far from safe to assume that because an individual on clinical examination seems well, all of his blood values, for example, are normal and meaningless so far as disease susceptibilities are concerned. 

In patients with longstanding hypothyroidism and those with ischemic heart disease, rapid correction of hypothyroidism may precipitate angina, cardiac arrhythmias, or other adverse effects. For these patients, replacement therapy should be started at low initial doses, followed by slow titration to full replacement as tolerated over several months. If hypothyroidism and some degree of adrenal insufficiency coexist, an appropriate adjustment of the corticosteroid replacement must be initiated prior to thyroid hormone replacement therapy. This prevents acute adrenocortical insufficiency that could otherwise arise from a thyroid hormone-induced increase in the metabolic clearance rate of adrenocortical hormones. 

Acute and chronic bronchitis, pneumonia, upper respiratory infection, pulmonary emphysema, pulmonary heart disease, heart failure, acute nephritis and renal failure, chronic nephritis, gastritis, hypothyroidism, hypoadrenalism, fibromyalgia, rheumatic arthritis and rheumatoid arthritis. 

There has been a retrospective study of the frequency of amiodarone-associated thyroid dysfunction in adults with congenital heart disease (41). Of 92 patients who had taken amiodarone for at least 6 months (mean age 35, range 18-60 years), 36% developed thyroid dysfunction— 19 became hyperthyroid and 14 hypothyroid. The mean dosage was 194 (100-300) mg/day, and the median duration of therapy was 3 (0.5-15) years. Female sex (OR = 3) and unoperated or palliated cyanotic congenital heart disease (OR = 7) were significant susceptibility factors for thyroid dysfunction. The risk was also dose-related. Although the authors conceded that they may have over-estimated the... 

On the basis of this experimental evidence, it seems likely that in the setting of the ischemic heart disease and hypothyroidism, thyroid hormone replacement may have adverse effects probably due to the loss of the cardioprotection conferred by hypothyroidism and not to the effects of thyroid hormone per se. In support to this notion are clinical observations showing that angina is not uncommon after thyroid hormone replacement in hypothyroid patients. 

It was suggested that the combination of oral erythromycin and carbimazole could lead to torsade de pointes in susceptible individuals. In this case, female sex, presence of valvular heart disease, bradycardia, hypoka-laemia, and hypothyroidism may all have been contributory factors. See also, Drugs that prolong the QT interval + Other drugs that prolong the QT interval , p.257. 

A number of other reports describe very significant reductions in endogenous markers of thyroid function in subjects and patients taking phenytoin or carbamazepine, " but not sodium valproate. However, there seems to be only two cases in which reversible hypothyroidism was seen, one with carbamazepine and phenytoin, and the other with carbamazepine alone. There is also a report of an arrhythmia in a patient with hypothyroidism and rheumatic heart disease given phenytoin this was attributed to the displacement of protein bound levothyroxine by phenytoin leading to an increase in free levothyroxine in the plasma. This report was later criticised by others, who suggested that the arrhythmia, if indeed there was one, was caused directly by the cardiac actions of... 

Cobalt Co Anemia anorexia growth reduction. White liver disease (in sheep) Heart failure hypothyroidism Cobalt is a component of vitamin and involved in the synthesis of hemoglobin... 

A common disorder very strong associations with premature ischaemic heart disease (IHD) children who are homozygotes for the disorder exhibit features of IFID in the first decade of life xanthomas (massive accumulation of cholesterol in the skin) and corneal arcus (white ring in the eyes) are common features of the disease occurs both as a heritable disorder and secondary to hypothyroidism... 

Disulfiram works by irreversibly blocking the enzyme aldehyde dehydrogenase, a step in the metabolism of alcohol, resulting in increased blood levels of the toxic metabolite acetaldehyde. As levels of acetaldehyde increase, the patient experiences decreased blood pressure, increased heart rate, chest pain, palpitations, dizziness, flushing, sweating, weakness, nausea and vomiting, headache, shortness of breath, blurred vision, and syncope. These effects are commonly referred to as the disulfiram-ethanol reaction. Their severity increases with the amount of alcohol that is consumed, and they may warrant emergency treatment. Disulfiram is contraindicated in patients who have cardiovascular or cerebrovascular disease, because the hypotensive effects of the disulfiram-alcohol reaction could be fatal in such patients or in combination with antihypertensive medications. Disulfiram is relatively contraindicated in patients with diabetes, hypothyroidism, epilepsy, liver disease, and kidney disease as well as impulsively suicidal patients. 

Amiodarone Blocks IKr, JNa/ Ica-L channels, adrenoceptors Prolongs action potential duration and QT interval slows heart rate and AV node conduction low incidence of torsade de pointes Serious ventricular arrhythmias and supraventricular arrhythmias Oral, IV variable absorption and tissue accumulation hepatic metabolism, elimination complex and slow Toxicity Bradycardia and heart block in diseased heart, peripheral vasodilation, pulmonary and hepatic toxicity hyper- or hypothyroidism. Interactions Many, based on CYP metabolism... 

Heart or kidney failure, arthritis, dementia, chronic diseases of the digestive system, anemia, hypotension, hypothyroidism, hypoadrenalism, chronic nephritis, infertility, menopause syndrome, impotence. 

Cardiac failure may also affect metabolism by altering hepatic blood flow. However, even after heart attack without hypotension or cardiac failure, metabolism may be affected. For example, the plasma clearance of lidocaine is reduced in this situation. Other diseases such as those, which affect hormone levels hyper-or hypothyroidism, lack of or excess growth hormone, and diabetes can alter the metabolism of foreign compounds. 

Medical conditions based in nearly all physiological systems can produce coincident sleep disturbances and sleep deprivation. This includes disorders of the cardiovascular (chronic heart failure), pulmonary (asthma), gastrointestinal (hepatic failure), renal (urinary tract infections, polyuria), endocrine (diabetes, hypothyroidism, hyperthyroidism), and neurological (Parkinson s disease,... 

Thyroid disorders (hypothyroidism or hyperthyroidism) Cardiovascular disease (arrhythmias, congestive heart failure) Gastrointestinal disease or disorder (sprue or other malabsorption syndromes, peptic ulcer, cohtis)... 

Indications 1) Shaoyin diseases, 2) collapse of yang due to erroneously sweating taiyang diseases. Influenza, intestinal fever, cholera, diarrhea, neurotic vomiting, indigestion, edema, jaundice, hypopituitarism, hypothyroidism, adrenal insufficiency, intractable arthritis, prostration, heart failure, cardiac insufficiency, and coma... 

Hydrocortisone should be used with extreme caution in patients with GI ulceration, renal disease, hypertension, osteoporosis, diabetes mellitus, thromboembolic disorders, seizures, myasthenia gravis, congestive heart failure (CHF), tuberculosis, hypoalbuminemia, hypothyroidism, cirrhosis of the liver, emotional instability, psychotic tendencies, hyperlipidemias, glaucoma or cataracts, because the drug may exacerbate these conditions (see Tables 11 and 14). 

Toxicity Toxicity is that of thyrotoxicosis (Table 38-1). Older patients, those with cardiovascular disease, and those with long-standing hypothyroidism are highly sensitive to the stimulatory effects of T on the heart. Such patients should receive lower initial doses ofT. ... 

Relative active or latent peptic ulcer disease, recent intestinal anastomoses, nonspecific ulcerative colitis (increased risk of perforation), diabetes, adrenocortical insufficiency (may persist for months after discontinuing therapy), active or latent tuberculosis, cerebral malaria, chicken pox, meades, latent amebiasis or strongyloides infection, inactivated viral or bacterial vaccines where antibody response may not be induced, cirrhosis, congestive heart failure, renal failure or hypertension (increased risk of sodium retention, edema and potassium loss), hypokalemia or hypocalcemia, emotional instability or psychotic tendencies, hypothyroidism, growth retardation in infants and children. 

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