Hypothyroidism Mnemonic

[Telly Piatt]

Hypothyroidismis a disorder of the endocrine system where the thyroid gland does not produce enough thyroid hormone. Hypothyroidism can be due to various etiologies including Hashimoto thyroiditis, postpartum thyroiditis, and congenital hypothyroidism. Hypothyroidism can result in a spectrum of neuropsychiatric symptoms, and can also be caused by psychotropic medications such as lithium.

Hashimoto thyroiditis (also known as Hashimoto's Disease) is an autoimmune disorder with antithyroid peroxidase (antimicrosomal) and antithyroglobulin antibodies. It is the most common cause of hypothyroidism in iodine-sufficient regions (i.e. - most Western and affluent nations). On physical exam, individuals may have a moderately enlarged, nontender thyroid.

Postpartum thyroiditis is a self-limiting thyroiditis that can last for up to 1 year after delivery. Individuals can go between transient hyperthyroidism or hypothyroidism. Following the self-limited phase, most individuals will return back to a euthyroid state. On physical exam, the thyroid is typically painless and normal in size.

Self-limited disease often following a viral infection (e.g. - flu). Individuals may be hyperthyroid early in course of illness, followed by hypothyroidism. Hypothyroidism can remain permanent in about 15% of cases. On physical exam, individuals will have jaw pain, and tender thyroid. ESR may also be elevated.

When an individual does not have adequate iodine, the thyroid will progressively enlarge as it tries to keep up with an increased demand for thyroid hormone production. This results in a prominent goiter that develops, and is seen on physical exam. Iodine deficiency is the most common cause of thyroid enlargement and goiter worldwide.

Lithium decreases production and release of thyroxine (T4) from the thyroid gland. It also interferes with de-iodination of T4 to T3 (tri-iodothyronine). T3 is the metabolically active form of thyroid hormone.[1]

The sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC-VI)5 defines four goals for the evaluation of the patient with elevated blood pressure: detection and confirmation of hypertension; detection of target organ disease (e.g., renal damage, congestive heart failure); identification of other risk factors for cardiovascular disorders (e.g., diabetes mellitus, hyperlipidemia); and detection of secondary causes of hypertension. Physicians can use the mnemonic ABCDE to help determine secondary causes in the patient with elevated blood pressure (Table 1).

The first, most practical step in evaluating an elevated blood pressure reading is to investigate its accuracy. A blood pressure cuff that is too small, tight-fitting sleeves that are not removed, or a brachial artery that is noncompressible because of calcification (sometimes seen in the elderly) can cause falsely elevated readings. White-coat hypertension (blood pressure that is elevated in the physician's office but normal at other times) accounts for about 20 percent of patients with elevated readings.3 JNC-VI recommends confirming high blood pressure readings outside of the office setting.

Obstructive sleep apnea (OSA), a repetitive mechanical obstruction of the upper airway during sleep, is an independent risk factor for hypertension.6 At least one half of patients with OSA have hypertension.7 Treatment of OSA with surgery or nasal continuous positive air way pressure reduces hypertension in these patients.8 Daytime somnolence, obesity, snoring, lower-extremity edema (secondary to the right-sided congestive heart failure that occurs after repetitive anoxic insults to the myocardium during sleep), morning headaches, and nocturia suggest OSA.9 There is a high incidence of OSA in patients with chronic obstructive pulmonary disease (COPD). A formal sleep study usually is needed for diagnosis of OSA and determination of corrective interventions.

Primary hyperaldosteronism is defined as overproduction of aldosterone independent of its usual regulator, the renin-angiotensin system.10 The resulting retention of excess salt and water suppresses renin levels (as opposed to elevating renin levels, which causes secondary hyperaldosteronism). Increased urinary excretion of potassium signals hyperal-dosteronism, which should be suspected in all hypertensive patients with unprovoked (i.e., not diuretic-induced) hypokalemia.11 The next diagnostic test should be demonstration of an elevated ratio of plasma aldosterone levels to plasma renin activity.12

Renovascular hypertension is defined as hypertension resulting from compromised arterial supply to the kidneys. About 65 percent of renovascular disease is secondary to atherosclerosis in the renal arteries, usually seen after age 50 in patients at risk for arterial compromise (e.g., smokers, patients with diabetes, patients with known atherosclerotic disease).13 The remainder of patients will demonstrate fibromuscular dysplasia (FMD) and will tend to be younger (25 to 50 years of age) at the time of diagnosis.13

About one half of patients with renovascular hypertension will have an abdominal bruit identifiable on physical examination.13 Bruits heard in both systole and diastole are more suggestive of renovascular hypertension than systolic bruits alone.14 In unselected populations of hypertensive persons, the incidence of renovascular hypertension is less than 1 percent.14 However, identification of this relatively small population can be important because surgery or angioplasty can reverse the hypertension, especially if performed early enough to prevent permanent renal damage.

Magnetic resonance angiography (MRA) is a noninvasive imaging modality with a sensitivity of 100 percent and a specificity of 70 to 90 percent compared with renal arteriography for detection of renal artery stenosis.2,15 MRA best delineates the proximal renal vasculature and is therefore useful as an initial diagnostic tool for patients suspected of having atherosclerotic renal artery stenosis, which usually involves the proximal renal artery.16 Patients suspected of having FMD, which tends to involve the distal renal artery, should undergo conventional angiography or computed tomographic angiography.16

Another initial diagnostic test is the captopril (Capoten)-augmented radioisotopic reno-gram.17 This test is based on the fact that a kidney that is receiving an inadequate blood supply will activate the renin-angiotensin system. Therefore, a single dose of the angiotensin-converting enzyme (ACE) inhibitor captopril will abruptly reduce renal function in the ischemic kidney. A scan is considered positive if there is delayed or decreased uptake of the radioisotope in the stenotic kidney compared with the non-stenotic one, so this test is not as useful if stenosis is present bilaterally.2

Duplex ultrasound scanning is another diagnostic option, but it can be limited by its dependence on operator skill and experience. Renal arteriography remains the gold standard for defining the vessel anatomy but does not always correlate with postprocedural outcomes (i.e., surgical correction of the renal artery stenosis often does not resolve the hypertension).13

Renal parenchymal disease can be a cause or consequence of hypertension. Progressive renal damage is caused by the mechanical and humoral effects of glomerular hypertension. The renal damage decreases the kidneys' ability to excrete salt and excess fluid (resulting in a low renin state, as opposed to the high renin state found in renovascular hypertension), and the hypertension worsens. As renal damage progresses, hyperparathyroidism develops and erythropoietin production increases, exacerbating the hypertension.5,18 Thus, a vicious cycle of worsening renal function and hypertension begins.

Aggressive treatment of hypertension (particularly with ACE inhibitors) in patients with renal parenchymal disease can lower the blood pressure and slow the disease's progression, although it is difficult to effectively control hypertension in chronic renal disease. Early treatment of hypertension and diabetes, the two most common causes of end-stage renal disease, can lower the incidence of long-term renal complications.18

Diagnosis is based on loss of renal cortical function (demonstrated by elevated serum creatinine levels and decreased creatinine clearance), although it may be impossible to tell if the renal dysfunction is primary or secondary to the hypertension.2

Excess catecholamine levels play a role in causing white-coat hypertension and hypertension in pheochromocytoma, OSA, and other diseases discussed in this article. Acute stress induces catecholamine release and often contributes to preoperative or postoperative hypertension. Over-the-counter or prescription decongestants can have sympathomimetic effects, as do nonprescription weight-loss preparations containing ephedra (ma huang).19,20 The hypertensive effects of cocaine and amphetamines also are sympathomimetic.

Many prescription and nonprescription drugs can cause or exacerbate hypertension (Table 2). Immunosuppressive agents such as cyclosporine (Sandimmune), tacrolimus (Prograf), and corticosteroids increase blood pressure in up to 80 percent of solid-organ transplant recipients.5 Nonsteroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase-2 (COX-2) inhibitors elevate blood pressure via their antiprostaglandin effects on the kidneys. Estrogen, in the dosages most often used in oral contraceptive pills (30 to 35 mcg), appears to have only a mild hypertensive effect and no increased risk for overall mortality or myocardial infarction (if smokers over age 35 are excluded).24 The lower doses of estrogen used in postmenopausal hormone-replacement regimens actually can have some antihypertensive effect.25 Nicotine in cigarettes, smokeless tobacco, and cigars causes transient (30 minutes or less) increases in blood pressure, although trans-dermal nicotine preparations do not appear to have this effect.26 Because patients who smoke often have a cigarette just before coming into the physician's office, blood pressure should be rechecked after 30 minutes if initial readings are elevated. Although caffeine can raise blood pressure acutely, tolerance develops rapidly, and there appears to be no direct relationship between caffeine intake and chronic hypertension.27 Chronic overuse of alcohol is a potentially reversible cause of hypertension.4

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