Chapter 22: Alterations in Endocrine system Flashcards
SIADH
Increased ADH usually due to tumors
Can be caused by hypoglycemics, antidepressants, antipsychotics, narcotics, anesthesia, chemo, NSAIDs
S/S SIADH
Hypotonic hyponatremia, hypervolemia, weight gain, peripheral edema absent, lethargy, concentrated urine
Diabetes insipidus
Decreased ADH leading to polyuria and polydipsia
Neurogenic central DI
Insufficient secretion of ADH from hypothalamus
Usually due to pituitary surgery
Nephrogenic DI
Inadequate response of kidney to ADH
Genetic or damage due to drugs
Primary polydipsia
excessive fluid intake lowers plasma osmolarity to a point below threshold for ADH secretion
S.S DI
Polyuria, nocturia, continuous thirst, polydipsia
Causes of hypopituitarism
Inadequate supply of hypothalamic releasing hormones, damage to pituitary stalk, inability of gland to produce hormones
Panhypopituitarism
All hormones deficient
Pituitary gland vulnerable to
Ischemia and infarction due to being highly vascular
ACTH deficiency
Can be life threatening
N/V, anorexia, fatigue, weakness, hypoglycemia
TSH deficiency
Cold intolerance, skin dryness, mild myxedema, lethargy, decreased metabolic rate
Hyperpituitarism is usually due to
Primary adenoma: benign, slow growing tumor of anterior pituitary
Adenomatous tissue secretes the hormone of the cell type from which is arose
Hypersecretion of GH
Acromegaly
Due to GH secreting adenoma
Gigantism in children due to increased bone growth
S/S Acromegaly
Enlarged tongues, intersitital edema, overactive sweat glands, coarse skin and body hair, large joints, large face hands and feet, barrel chest
S/S prolactinoma
Amenorrhea, infertility, galactorrhea
Thyrotoxicosis
Any cause of increased TH levels
Hyperthyroidism
Excess amount of TH secreted by thyroud gland
S/S hyperthyroidism
Increased metabolic rate, heat intolerance, increased tissue sensitivity to stimulation by SNS
Graves disease
Autoimmune
Lymphocyte infiltration and stimulation of thyroid by autoantibodies directed against TSH receptor
Leads to goiter
2 major manifestations of Graves
Ophthalmopathy and dermopathy
Ophthalmopathy
Increased secretion of hyaluronic acid, adipogensis and inflammation and edema of orbital contents leads to exophthalmos
Pretibial myxedema
Subcutaneous swelling on anterior portion of legs characteristic of Graves
Thyrotoxic crisis
Thyroid storm
Death can occur within 48 hours
S/S: hyperthermia, increased HR, high output HF, agitation, delirium
Most common causes of hypothyroidism
autoimmune thyroiditis, loss of thyroid tissue due to treatment of hyperthyroidism, head and neck radiation, iodine deficiency
S/S hypothyroidism
Decreased metabolic rate, cold intolerance, lethargy, tiredness
Characteristic sign of hypothyroidism
Myxedema: swelling of face, alopecia, loss of nails along with hardening of skin
Myxedema
non-pitting boggy edema caused by infiltration of mucopolysaccharides and proteins between connective tissue in the dermis
Myxedema coma
Diminished consciousness due to severe hypothyroidism
Most common cause of primary hypothyroidism
Iodine deficiency most common worldwide
Autoimmune thyroiditis most common in US
Subactue thyroiditis
Uncommon bacterial inflammation of thyroid preceded by viral infection
Fever, tenderness, enlargement of thyroid
Primary hyperparathyroidism
Excess secretion of PTH due to adenomas
Increased Ca + PO4 hallmarks
Secondary hyperparathyroidism
Compensatory response to parathyroid glands to chronic hypocalcemia
Usually due to CKD or vit D deficiency
Tertiary hyperparathyroidism
Due to chronic hypocalcemia
Usually due to renal transplant
Hyperparathyroidism can cause
Kidney stones and increased risk for fractures due to bone resorption
Hypoparathyroidism usually due to
Removal of PT gland with removal of thyroid gland
Hypomagnesia can cause
Decreased PTH
Glycosylated Hemoglobin
HbA1c
Permanent attachment of glucose to Hgb molecules and reflects average plasma glucose exposure over life of RBC
Labs for DM diagnosis
HbA1c >6.5%
Fasting plasma glucose >126
2 hour plasma glucose >200
Random plasma glucose >200
Type 1 DM
Autoimmune
Environmental genetic factors trigger cell mediated destruction of pancreatic beta cells
Decreased insulin leads to
Marked increase in glucagon
What causes DKA
Increased hepatic metabolism of fat causing increased levels of circulating ketones
Risk factors for type 2 DM
Age, obesity, hypertension, physical inactivity, family history, metabolic syndrome
Metabolic syndrome
Central obesity, dyslipidemia, pre-hypertension, increased FPG
Obesity causes of insulin resistance
Increased leptin and decreased adiponectin
Increase in free fatty acids and intracellular deposits of triglycerides and cholesterol
Increased inflammatory cytokines
Maturity onset of diabetes of youth
Noninsulin requiring diabetes in lean individuals <25 with evidence of autosomal dominant inheritance
Somogyi effect
Too much intermediate acting insulin given at dinner followed by rebound hyperglycemia around 3am
Dawn phenomenon
Early morning rise in glucose due to nocturnal elevation of GH, which decreases metabolism of glucose
Diabetic ketoacidosis
Usually in type 1 DM
Due to decrease insulin and increase in levels of insulin counter-regulatory hormones
Most common precipitating factor for DKA
Intercurrent illness
S/S DKA
Kussmal respirations, postural dizziness, CNS depression, ketonuria, anorexia, N/V, abdominal pain, sweet breath, dehydration, thirst, polyuria
Most marked electrolyte imbalance in DKA
Decrease in total K+
Labs in DKA
Glucose >250, serum bicarb >18, ph <7.3, urine and serum ketones present
Hyperosmolar hyperglycemic nonketotic syndrome
High mortality complication of type 2 DM
Similar to DKA but no ketones
Extreme glucosuria and polyuria causing severe volume loss, increased serum osmolarity, intracellular dehydration, and loss of electrolyte
DX criteria for hyperosmolar hyperglycemic nonketotic syndrome
Glucose >600, normal bicarb and ph, osmolarity >320, no ketones
Microvascular disease due to DM
Capillary disease: leads to blindness, ESKF, neurppathies
Diabetic retinopathy, diabetic kidney disease
Diabetic retinopathy
Damage to retinal blood vessels and RBCs, platelet aggregation, relative hypoxemia, hypertension
Diabetic kidney disease
Glomeruli injured by protein denaturation, hyperglycemia with high renal blood flow, activation of RAAS, hypertension
Microalbuminuria first manifestation
Diabetic neuropathies
Nerves are vulnerable to effects of chronic hyperglycemia
Axonal degeneration involving sensory nerve fibers and metabolic activity of schwann cells decreases
Charcot neuroarhtropathy
Progressive degeneration of joint, usually in foot or ankle
Macrovascular disease in DM
Increased risk for hypertension, accelerated atherosclerosis, CV disease, stroke and PVD
Risk for infection in DM
Increased due to decreased senses, hypoxia, pathogens liking glucose, decreased blood supply leading to decreased WBC, decreased immune response, delayed wound healing
Cushing syndrome
Chronic exposure to excess endogenous cortisol
Cushing disease
Excess endogenous secretion of ACTH
2 observations in cushing disease
Do not have diurnal or circadian secretion patterns of ACTH and cortisol
Do not increase ACTH and cortisol in response to stressor
Most common feature of Cushing disease
Weight gain
Central obesity, moon face, buffalo hump
Due to lipolysis and altered fat distribution
S/S cushing disease
Glucose intolerance, protein wasting, increased bone resorption, hypercalciuria and kidney stones, vasoconstriction and hypertension, increased risk for CAD,
Congenital Adrenal hyperplasia
Autosomal, recessive
Deficiency in enzyme critical in cortisol synthesis
Conn syndrome
Primary hyperaldosteronism
Causes hypokalemia, induces insulin resistance, promotes inflammation, endothelial dysfunction and CV remodeling
Secondary hyperaldosteronism
Due to aldosterone secretion from angiotensin II through renin-dependent mechanism
Compensatory due to low blood volume
S/S hyperaldosteronism
Hypertension, hypokalemia, hypervolemia, metabolic alkalosis
Virilization
Development of male sex characteristics due to over secretion of androgens
Addison disease
Primary hypocortisolism
Inability of adrenals to produce and secrete adrenocortical hormones
Decreased aldosterone and cortisol
Biggest concern with addison disease
hypotension–addisonian crisis
Prolonged addison disease usually due to
Prolonged administration of glucocorticoids
Hirsutism
Excessive growth of facial and body hair
Active anterior pituitary adenoma
Causes hypersecretion of hormones from the adenoma itself and hyposecretion of hormones from surrounding pituitary cells
Cretinism
Caused by untreated congenital hypothyroidism
Pheochromocytoma
Chromaffin cell tumors of adrenal medulla
Hypertension, tachycardia, palpitations, severe headache, diaphoresis, heat intolerance, weight loss, constipation
Gastroperesis
Complication of diabetes where patient feels full–microvascular problem of autonomic neuropathy