Adrenal infarction

Bilateral adrenal hemorrhage or infarction—usually due to anticoagulant therapy, coagulopathy, thromboembolic disease, or meningococcal infection. Causes acute adrenal insufficiency. 

Approximately 50% of patients with meningococcal meningitis have purpuric lesions, petechiae, or both. Patients may have an obvious or subclini-cal picture of disseminated intravascular coagulation, which may progress to infarction of the adrenal glands and renal cortex and cause widespread thrombosis. 

The decreased work capacity of the in-farcted myocardium leads to a reduction in stroke volume (SV) and hence cardiac output (CO). The fall in blood pressure (RR) triggers reflex activation of the sympathetic system. The resultant stimulation of cardiac 3-adreno-ceptors elicits an increase in both heart rate and force of systolic contraction, which, in conjunction with an a-adren-oceptor-mediated increase in peripheral resistance, leads to a compensatory rise in blood pressure. In ATP-depleted cells in the infarct border zone, resting membrane potential declines with a concomitant increase in excitability that may be further exacerbated by activation of p-adrenoceptors. Together, both processes promote the risk of fatal ventricular arrhythmias. As a consequence of local ischemia, extracellular concentrations of H+ and K+ rise in the affected region, leading to excitation of nociceptive nerve fibers. The resultant sensation of pain, typically experienced by the patient as annihilating, reinforces sympathetic activation. 

Contraindications Uncontrolled adrenal cortical insufficiency, untreatedthyrotoxico-sis, treatment of obesity, uncontrolled angina, uncontrolled hypertension, uncontrolled myocardial infarction, and hypersensitivity to any component of the formulations... 

AT2 receptors are present at high density in all tissues during fetal development, but they are much less abundant in the adult where they are expressed at high concentration only in the adrenal medulla, reproductive tissues, vascular endothelium, and parts of the brain. AT2 receptors are up-regulated in pathologic conditions including heart failure and myocardial infarction. The functions of the AT2 receptor appear to include fetal tissue development, inhibition of growth and proliferation, cell differentiation, apoptosis, and vasodilation. 

Diagnosed, but uncorrected adrenal cortical insufficiency Untreated thyrotoxicosis Hypersensitivity to any component of drug Myocardial infarction... 

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. 

Heparin-induced thrombocytopenia (platelet count <150,000/ml or a 50% decrease from the pretreatment value) occurs in about 0.5% of medical patients 5 to 10 days after initiation of therapy with standard heparin. The incidence of thrombocytopenia is lower with low-molecular-weight heparin. Thrombotic complications that can be life threatening or lead to amputation occur in about one-half of the affected heparin-treated patients and may precede the onset of thrombocytopenia. The incidence of heparin-induced thrombocytopenia and thrombosis is higher in surgical patients. Venous thromboembolism occurs most commonly, but arterial thromboses causing limb ischemia, myocardial infarction, and stroke also occur. Bilateral adrenal hemorrhage, skin lesions at the site of subcutaneous heparin injection, and a variety of systemic reactions may accompany heparin-induced thrombocytopenia. The development of IgG antibodies against complexes of heparin with... 

Thyroid USP is contraindicated in patients with thyrotoxicosis, acute myocardial infarction, or uncorrected adrenal insufficiency. 

In elderly patients, especially those with multisystemic diseases, hypothyroidism may become severe and fife threatening. Myxedema coma represents the most extreme form of severe hypothyroidism. This medical emergency may occur when severe hypothyroidism is complicated by trauma, infection, myocardial infarction, cold exposure, or administration of hypnotics or opiates, medications that suppress central nervous system function, particularly ventilatory drive. It typically presents in older women in winter. The main clinical features are hypothermia and a variable degree of altered consciousness (Iglesias et ai, 1999). Serum T4, TSH and cortisol should be measured to confirm the diagnosis and evaluate adrenal reserve. When there is a reasonably high level of suspicion, treatment should not be delayed to await laboratory results. 

Temporary clamping of the circulation to the rafs adrenal for a period of 1 h gave rise to wedges of infarction in the zona fasciculata and zona reticularis not involving either the zona glomerulose... 

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