Epinephrine hypertension caused

Pheochromocytomas are tumors that produce norepinephrine and epinephrine and cause hypertension. 

During phase I, each seizure causes a sharp increase in autonomic activity with increases in epinephrine, norepinephrine, and steroid plasma concentrations, resulting in hypertension, tachycardia, hyperglycemia, hyperthermia, sweating, and salivation. Cerebral blood flow is also increased to preserve the oxygen supply to the brain during this period of high metabolic demand. Increases in sympathetic and parasympathetic stimulation with muscle hypoxia can lead to ventricular arrhythmias, severe acidosis, and rhabdomyolysis. These, in turn, could lead to hypotension, shock, hyperkalemia, and acute tubular necrosis. 

Pheochromocytoma A tumor arising from chromaffin cells, most commonly found in the adrenal medulla. The tumor causes the adrenal medulla to hypersecrete epinephrine and norepinephrine, resulting in hypertension and other signs and symptoms of excessive sympathetic nervous system activity. The tumor is usually benign but may occasionally be cancerous. 

The major circulating hormones that influence vascular smooth muscle tone are the catecholamines epinephrine and norepinephrine. These hormones are released from the adrenal medulla in response to sympathetic nervous stimulation. In humans, 80% of catecholamine secretion is epinephrine and 20% is norepinephrine. Stimulation of cy-adrenergic receptors causes vasoconstriction. The selective a,-adrenergic receptor antagonist, prazosin, is effective in management of hypertension because it causes arterial and venous smooth muscle to relax. 

The answer is d, (Hardman, pp 855-856.) Propranolol, as well as other non selective beta blockers, tends to slow the rate of recovery in a hypoglycemic attack caused by insulin. Beta blockers also mask the symptoms of hypoglycemia and may actually cause hypertension because of the increased plasma epinephrine in the presence of a vascular beta2 blockade. 

There is evidence that y-aminobutyric acid A receptors may be modified during SE and become less responsive to endogenous agonists and antagonists. Two phases of GCSE have been identified. During phase I, each seizure produces marked increases in plasma epinephrine, norepinephrine, and steroid concentrations that may cause hypertension, tachycardia, and cardiac arrhythmias. Muscle contractions and hypoxia can cause acidosis, and hypotension, shock, rhabdomyolysis, secondary hyperkalemia, and acute tubular necrosis may ensue. 

Overdosage or inadvertent IV injection Overdosage or inadvertent IV injection of conventional subcutaneous epinephrine doses may cause severe or fatal hypertension or cerebrovascular hemorrhage resulting from the sharp rise in blood pressure. Fatalities may also occur from pulmonary edema resulting from peripheral constriction and cardiac stimulation. 

The greatest hazards of accidental overdosage with epinephrine and norepinephrine are cardiac arrhythmias, excessive hypertension, and acute pulmonary edema. Large doses of isoproterenol can produce such excessive cardiac stimulation, combined with a decrease in diastolic blood pressure, that coronary insufficiency may result. It also may cause arrhythmias and ventricular fibrillation. Tissue sloughing and necrosis due to severe local ischemia may follow extravasation of norepinephrine at its injection site. 

Tricyclic antidepressants potentiate the pressor effects of directly acting sympathomimetic amines, such as adrenaline (epinephrine) or noradrenaline (norepinephrine), to cause hypertension. Small amounts of these, such as may be present in local anaesthetic solutions, can be dangerous. Tricyclic antidepressants will inhibit the antihypertensive effects of the older anti hypertensive drugs, such as adrenergic neurone-blocking agents, e.g. guanethidine, a-methyl-DOPA, and clonidine. 

Venlafaxine (Effexor), approved by the FDA in December 1993, was described in more detail early in this chapter. It is one of the newer antidepressants implicated in causing suicidality. It is a NSRI that also strongly inhibits the reuptake of epinephrine. Its profile is very similar to the SSRIs in producing stimulation, including anxiety, nervousness, insomnia, anorexia, and weight loss. It causes the various emotional and behavioral abnormalities that go along with stimulation, such as agitation and mania, and has been associated with hostility, paranoid reaction, psychotic depression, and psychosis. It can cause hypertension. 

BETA-BLOCKERS LIDOCAINE 1. Risk of bradycardia (occasionally severe), 1 BP and heart failure with intravenous lidocaine 2. Risk of lidocaine toxicity due to t plasma concentrations of lidocaine, particularly with propranolol and nadolol 3. t plasma concentrations of propranolol and possibly some other beta-blockers 1. Additive negative inotropic and chronotropic effects 2. Uncertain, but possibly a combination of beta-blocker-induced reduction in hepatic blood flow (due to 1 cardiac output) and inhibition of metabolism of lidocaine 3. Attributed to inhibition of metabolism by lidocaine 1. Monitor PR, BP and ECG closely watch for development of heart failure when intravenous lidocaine is administered to patients on beta-blockers 2. Watch for lidocaine toxicity 3. Be aware. Regional anaesthetics should be used cautiously in patients with bradycardia. Beta-blockers could cause dangerous hypertension due to stimulation of alpha-receptors if epinephrine is used with focal anaesthetic... 

There are two types of MAO MAO-A, found mainly in the liver and gastrointestinal tract, and MAO-B, found mainly in the brain and platelets. MAO-A in the liver is involved in the elimination of ingested monoamines (e.g. tyramine) and inactivates circulating monoamines (e.g. epinephrine, norepinephrine and dopamine) when they pass through the liver. Co-ingestion of these monoamines with MAO inhibitors leads to their unopposed action, which causes severe hypertension, so the former should be avoided. 

Overdose of catecholamines may result in animal death. In test animals, there is evidence that death is the result of respiratory arrest caused by hypertension following overdose of epinephrine. 

Tyrosine can be decarboxylated to tyramine by aromatic L-amino acid decarboxylase of intestinal bacteria. Tyramine, which is present in large amounts in certain foods (e.g., aged cheeses, red wines), is converted by monoamine oxidase (MAO) to the aldehyde derivatives. However, individuals who are receiving MAO inhibitors for the treatment of depression can accumulate high levels of tyramine, causing release of norepinephrine from sympathetic nerve endings and of epinephrine from the adrenal medulla. This results in peripheral vasoconstriction and increased cardiac output, which lead to hypertensive crises that can cause headaches, palpitations, subdural hemorrhage, stroke, or myocardial infarction. 

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