CAMBIO DE BLOG

SOLO COMUNICARLES QUE HE CAMBIADO LA DIRECICION DEL BLOG, AHORA ESTARE EN DRALMANZA-MEMORIA.BLOGSPOT.COM, LOS VEO POR ALLA, GRACIAS

HYPERALDOSTERONISM

PRIMARY: caused by an aldosterone-secreting tumor, resulting in hypertension, hypokalemia, metabolic alkalosis, and low plasma rennin.

Increased aldosterone secretion from adrenal, which results primary from 2 major subtypes:

1)      Unilateral aldosterone-producing adenoma (APA) or Conn’s syndrome, the most common subtype (50-60% of case), usually small <3 cm unilateral, and rennin-unresponsive. This means that aldosterone secretion is not affected by changes en posture. Rarely, the adenoma is rennin-responsive (aldosterone levels increase with standing).

2)      Idiopathic hyperaldosteronism (IHA) or bilateral adrenal hyperplasia. Aldosterone increases in response to postural studies. Rarely, patients are hyperplastic (primary adrenal hyperplasia), and the response of aldosterone to standing is similar to rennin-unresponsive APA

Other subtypes:

3)      Rennin-responsive adenoma

4)      Primary adrenal hyperplasia

5)      Glucocorticoids-remediable aldosteronism.

Aldosterone, by inducing renal distal tubular reabsortion of sodium, enhances secretion of potassium and hydrogen ions, causing hypernatremia, hypokalemia, alkalosis.

Hypokalemia → fatigue, muscle weakness, cramping, headaches, and palpitations.

                            Polydipsia and polyuria from hypokalemia-induced nephrogeni diabetic insipidus.

Treatment: the goal of treatment is to prevent the morbidity and mortality associated with hypertension and hypokalemia. Appropriate treatment depends on the cause e.g. Conn’s syndrome vs. IHA (unilateral or bilateral adrenalectomy).

Medication: spironolactone (aldosterone antagonists).

SECUNDARY: Due to: Renal artery stenosis

                                        Chronic renal failure

                                        CHF

                                        Cirrhosis

                                        Nephrotic syndrome

Kidney perception of low intravascular volume results in an overactive rennin-angioitensin system. Associated with high plasma rennin.

CUSHING SYNDROME

Cushing syndrome is caused by prolonged exposure to elevated levels of either endogenous glucocorticoids or exogenous glucocorticoids.

Etiologies include:

1)      Pituitary adenoma: classic Cushing’s disease (80%); ↑ ACTH.

2)      Adrenal hyperplasia/neoplasia: ↓ ACTH.

3)      Ectopic ACTH production e.g. oat cell carcinoma, small-cell lung carcinoma or carcinoid tumor. ↑ ACTH.

4)      Iatrogenic: most common etiology, chronic steroid use. ↓ ACTH.

Individuals with Cushing Syndrome can develop moon facies, facial plethora, supraclavicular fat pads, buffalo hump, truncal obesity, and purple striae. Often complain of proximal muscle weakness, easy bruising, weigh gain, hisutism, and, in children, growth retardation. Hypertension, osteopenia, diabetes mellitus, and impaired immune function may occur.

Exogenous steroids may cause suppression of the hypothalamus-pituitary-adrenal (HPA) axis, which can last for as long as a year after exogenous steroids administration has ended.

An individual with HPA axis suppression cannot increase steroids production appropriately during a medical illness or other stress, and would need to receive stress doses of steroids to avoid adrenal crisis. Thus, in an emergency, the potential for relative adrenal insufficiency should be considered in any patient with Cushing syndrome.

ADRENAL CRISIS

Adrenal crisis may occur in patients on steroids who stop taking their glucocorticoids or neglect to increase their steroid during an acute illness. It also may occur in patients who have recently undergone resection of an ACTH-producing or cortisol-producing tumor, or who are taking adrenal steroid inhibitors.

Finding: Hypotension, abdominal pain, vomiting, and mental confusion (secondary to low serum sodium or hypotension), hypoglycemia, hyperkalemia, hyponatremia, and metabolic acidosis.

Biochemical evaluation of Cushing syndrome.

Four methods are accepted for the diagnosis:

1)      Urinary free cortisol levels.

2)      Low-doses dexamethasone suppression test.

3)      Evening serum and salivary cortisol levels.

4)      Dexamethasone-corticopropin-releasing hormone test.

Treatment:

The Cushing syndrome treatment is directed by the primary cause of the syndrome.

A culprit tumor should be removed if possible.

For exogenous etiology a gradual withdrawal of glucocorticoids is the way.

THYROID PHYSIO-PATHOLOGY

Thyroid hormones: T3 (triiodothyronine)

                                T4 (tetraiodothyronine = thyroxine)

Both have systemic effects. Abnormal thyroid hormone levels lead to hypothyroid and hyperthyroid states. Inadequate thyroid hormone during the development leads to congenital hypothyroidism; also know as cretinism, with associated irreversible brain damage.

Source: Follicles of thyroid. Most T3 formed in blood.

Function: Bone growth (synergism with GH)

                Brain maturation.

                Beta-adrenergic effects: increases stimulation of β1 receptors in heart = ↑ CO, HR, SV, and contractility.

                Basal metabolic rate ↑ via ↑ Na/K-ATPase activity = ↑ 02 consumption, RR, body temperature.

Regulation: TRH (thyrotropin releasing hormone) from the hypothalamus stimulates TSH (thyroid stimulating hormone) in adenohypophysis, which stimulates follicular cells.

Hypothyroidism: Cold intolerance, hypoactivity, weigh gain, fatigue, lethargy, ↓ appetite, constipation, weakness, ↓ reflex, myxedema (facial/periorbital), dry, cool skin, and coarse, brittle hair.

↑ TSH (sensitive test for 1° hypothyroidism), ↓ total T4, ↓ free T4,↓ T3 uptake.

Hyperthyroidism: Heat intolerance, hyperactivity, weigh loss, chest pain/palpitation, arrhythmias, diarrhea, ↑ reflex, warm, moist skin, and fine hair.

 ↓ TSH (if 1°), ↑ total T4, ↑ free T4, ↑ T3 uptake.

Hashimoto’s thyroiditis: Autoimmune disorder resulting in hypothyroidism (can have thyrotoxicosis during follicular rupture). Slow course, moderately enlarged, nontender thyroid. Lymphocyte infiltrate with germinal centers. Antimicrosomal and antithyroglobulin antibodies. Associated with Hürthle cells on histology.

Subacute thyroiditis (de Quervain’s): Self-limited hypothyroidism often following a flulike illness. Elevated ESR, jaw pain, early inflammation, and very tender thyroid gland. Histology shows Granulomatous inflammation.

May be hyperthyroid early in course. Lymphocytes subacute thyroiditis is painless.

Riedel’s thyroiditis: Thyroid replaced by fibrous tissue (hypothyroid). Presents with fixed, hard, and painless.

Cretinism: Due to several fetal hypothyroidism. Endemic cretinism occurs wherever endemic goiter is prevalent (lack of dietary iodine); sporadic cretinism is caused by defect in T4 formation or developmental failure in thyroid formation.

Finding: Pot-bellied, pale, puffy face child protruding umbilicus and protuberant tongue.

Graves’ disease: An autoimmune hyperthyroidism with thyroid-stimulating/TSH receptor antibodies. Ophthalmopathy (proptosis, extraocular muscle swelling), pretibial myxedema, diffuse goiter. Often presents during stress (e.g. childbirth).

Stress-induced catecholamine surge leading to death by arrhythmia. Seen as a serious complication of Graves’ and other hyperthyroidism disorder.

Graves’ is type II hypersensitivity.

Toxic multinodular goiter: Iodine deprivation followed by Iodine restoration. Causes release of T3 and T4. Nodules are not malignant.

Jod-Basedow phenomenon= thyrotoxicosis if a patient with iodine deficiency goiter is made iodine replete.

Thyroid cancer:

1)      Papillary carcinoma- most common, excellent prognosis, ground-glass nuclei (Orphan Annie), psammoma bodies, nuclear grooves. ↑ Risk with childhood irradiation.

2)      Follicular carcinoma-good prognosis, uniform follicles.

3)      Medullary carcinoma-from parafollicular “C cells”; produces calcitonin, sheets of cells in amyloid stroma. Associated with MEN type 2A and 2B.

4)      Undifferenciated/anaplastic- older patients, very poor prognosis.

Lymphoma – associated with Hashimoto’s thyro