19. Endocrine Alterations Flashcards
List the 7 hormones released from the anterior pituitary and their target tissues
- Prolactin (mammary gland) - ACTH (adrenal cortex) - GH (bone/muscle/tissues) - TSH (thyroid gland) - LH + FSH (ovaries and testes) - MSH (melanin in skin)
What is the function of the posterior pituitary?
stores ADH and oxytocin produced by the hypothalamus; DOES NOT PRODUCE THEM!
What are the 3 direct targets of the hypothalamus and through what?
- anterior pituitary: through releasing hormones (RH) and inhibiting hormones (IH) - kidneys and uterus/breast: through ADH and oxytocin - adrenal medulla: sympathetic innervation
What do pancreatic B cells secrete?
insulin and C peptide (aka Amylin)
What do pancreatic A cells secrete?
glucagon
What do pancreatic D cells secrete?
somatostatin
What do pancreatic F cells secrete?
pancreatic polypeptide
What causes pituitary dwarfism? What do these people look like?
- hyposecretion of growth hormone - normal body proportion but rarely taller than 4ft
What causes acromegaly? Most common cause?
- caused by continuous exposure to high levels of GH and insulin-like growth factor 1 (IGF-1) - almost always caused by GH-secreting pituitary adenoma
Acromegaly vs gigantism
- acromegaly: occurs in adults (after growth plates have close) - gigantism: occurs in childhood (before growth plates close)
condition that results from any cause of increased TH levels
thyrotoxicosis
form of thyrotoxicosis in which excess amounts of TH are secreted from the thyroid gland
hyperthyroidism
clinical manifestations of hyperthyroidism
- thin hair - tachycardia - weight loss (elevated metabolism) - exophthalmos (protruding eyes) - hyperreflexia - enlarged thyroid
over secretion of T3/T4 due to abnormal antibodies (TSIs) that stimulate TSH receptors (type II hypersensitivity)
Grave’s disease
What causes goiters?
thyroid enlargement due to iodine deficiency - follicles make thyroglobulin but cannot make TH
subcutaneous swelling on the anterior portions of the legs and indurated and erythematous skin; seen w/ high levels of TSI
pretibial myxedema (Grave’s dermopathy)
- occurs when there are several hyper-functioning nodules leading to hyperthyroidism - what is it called when only 1 nodule is hyper-functioning?
- toxic multinodular goiter - toxic adenoma
dangerous worsening of thyrotoxic state in which death can occur within 48 hours without treatment; sxs caused by increased action of T4 and T3 exceeding metabolic demands
thyrotoxic crisis (thyroid storm)
Sxs of thyrotoxic crisis
- hyperthermia - tachycardia - high output heart failure - agitation/delirium - N/V/D
Grave’s diseases is a _____ hyperthyroidism and a TSH-secreting pituitary adenoma is a ____ hyperthyroidism
- primary - secondary
congenital iodine deficiency/hypothyroidism
cretinism
clinical manifestation of cretinism
- difficulty eating - protruding tongue - hypotonia - lethargy - bradycardia - cognitive disability varies
deficient production of TH by the thyroid gland
hypothyroidism
most common form of primary hypothyroidism; gradual inflammatory destruction of thyroid tissue by infiltration of auto reactive T lymphocytes and circulating thyroid antibodies
autoimmune thyroiditis (Hashimoto’s thyroiditis)
rare nonbacterial inflammation of the thyroid gland often preceded by a viral infection; associated w/ transient hypothyroidism
subacute thyroiditis (de Quervain thyroiditis)
clinical manifestations of hypothyroidism
- loss of hair - bradycardia - decreased metabolism - lethargy - cold intolerance - muscle weakness - LE edema
characteristic sign of severe or long-standing hypothyroidism; will see non pitting, boggy edema (around eyes, hands, feet, and supraclavicular fossa), slurred speech, and hoarseness
myxedema
clinical manifestation of myxedema coma (medical emergency)
- hypothermia w/o shivering - hypoventilation - hypotension - hypoglycemia - lactic acidosis
most common endocrine malignancy
thyroid carcinoma
high levels of ADH in the absence of normal physiologic stimuli for release
syndrome of inappropriate ADH secretion (SIADH)
How does SIADH affect the following: - urine output - urine osmolality - serum Na - serum osmolality
- urine output: low - urine osmolality: high - serum Na: low (hyponatremia) - serum osmolality: low (hypoosmolar)
symptoms of SIADH
- water retention - low urine output - N/V - mental changes
What is the overall function of ADH?
increases BP and blood volume, decreases osmolarity
failure of hypothalamus to produce ADH or release it from posterior pituitary; decrease in ADH plasma levels
neurogenic/central diabetes insipidus (DI)
kidneys unable to respond to ADH; increase plasma ADH
nephrogenic diabetes insipidus (DI)
How does DI affect the following: - urine output - urine osmolality - serum Na - serum osmolality
- urine output: high - urine osmolality: low - serum Na: high (hypernatremia) - serum osmolality: high (hyperosmolar)
symptoms of DI
- polyuria - thirst - high urine output - signs of dehydration
treatment of SIADH
- fluid restriction - treat the cause
treatment of DI
- give desmopressin (synthetic analog of ADH) -> central - treat the cause -> nephrogenic
benign, slow-growing tumors that arise from cells in the anterior pituitary
pituitary adenoma
3 most common types of pituitary adenoma
- Prolactinoma (60%) - Acromegaly/giantism (20%) - Cushing’s disease (10%)
characterized by greater than normal secretion of PTH and hypercalcemia
hyperparathyroidism
characterized by inappropriate excess secretion of PTH by one or more of the parathyroid glands
primary hyperparathyroidism
compensatory response of parathyroid glands to chronic hypocalcemia -> can be associated w/ decreased renal activation of vitamin D (renal failure)
secondary hyperparathyroidism
How does hyperparathyroidism affect Ca and Pi
- increased Ca levels (hypercalcemia) -> increases bone resorption to release Ca and GI reabsorption - decreased Pi levels (hypophosphatemia) -> PTH causes Pi to be excreted in urine
clinical manifestations of primary hyperparathyroidism
- fatigue - headache - depression - anorexia - N/V - pathologic fractures
abnormally low PTH levels most commonly caused by damage to parathyroid glands during thyroid surgery
hypoparathyroidism
How does hypoparathyroidism affect Ca and Pi
- decreased Ca levels (hypocalcemia) - increased Pi levels (hyperphosphatemia)
clinical manifestations of hypoparathyroidism
- symptoms of hypocalcemia (ex. tetany and muscle spasms) - dry skin - loss of body and scalp hair - hypoplasia of developing teeth - bone deformities
refers to clinical manifestations resulting from chronic exposure to excess cortisol regardless of cause
Cushing syndrome
hypersecretion of ACTH
Cushing disease
clinical manifestations of Cushing’s syndrome
- fat deposition on neck/back (buffalo hump) - fat deposition on the face (moon face) - ABD fat deposition - bruising (breakdown of collagen) - stretch marks - muscle weakness/wasting - osteoporosis - adrenal hyperplasia
How would Cushing disease affect the following values: - K - Na - glucose
- K: hypokalemia (aldosterone -> K excretion) - Na: hypernatremia (aldosterone -> Na reabsorption) - glucose: hyperglycemia (high cortisol)
primary adrenal insufficiency (hyposecretion of all adrenal steroids) usually due to autoimmune restriction of adrenal gland
Addison’s disease
How would Addison’s disease affect the following values: - K - Na - glucose
- K: hyperkalemia (no aldosterone for K excretion) - Na: hyponatremia (no aldosterone for Na reabsorption) - glucose: hypoglycemia (low cortisol)
clinical manifestations of Addison’s diseases
- weakness/fatigue - skin hyperpigmentation (due to high MSH associated w/ high ACTH) - hypotension - tachycardia - N/V/D - adrenal atrophy
hyper-secretion of aldosterone due to adrenal neoplasm
primary hyperaldosteronism (Conn syndrome)
tumor of chromaffin tissue -> produces excess catecholamines
pheochromocytoma
Symptoms of pheochromocytoma
- persistant HTN - headache - pallor - diaphoresis - tachycardia/palpitations - anxiety
permanent attachment of glucose to hemoglobin and reflects average plasma glucose exposure of life of RBC
glycosylated hemoglobin (HbA1c)
lab value diagnosis criteria for DM
- HbA1c > 6.5% - fasting plasma glucose (FPG) > 126 mg/dl (fasting = at least 8 hours) - 2 hour plasma glucose > 200 mg/dl during oral glucose tolerance test (OGTT) - symptoms of hyperglycemia w/ random plasma glucose > 200 mg/dl
beta cell destruction -> leads to absolute insulin deficiency
type 1 DM (IDDM)
Describe pathophysiology of IDDM
- autoantigens form on B-cells and circulate in bloodstream/lymphatics - activation of cellular immunity (T cells) and humoral immunity (autoantibodies) towards B-cells - destruction of B-cells with decreased insulin secretion
How does a decrease in insulin affect glucagon levels?
causes increase in glucagon (produced by alpha cells of pancreas)
clinical manifestations of IDDM
- polydipsia (water attracted to glucose -> intracellular dehydration) - polyuria (hyperglycemia = osmotic diuretic) - polyphagia (depletion of cellular stores due to lack of glucose -> starvation) - weight loss - fatigue - visual changes - paresthesias
What is one of the most important contributors to insulin resistance and NIDDM
obesity
4 mechanisms that link obesity to insulin resistance
- inflammation changes adipokine levels - elevated levels of serum FFA and intracellular deposit of triglycerides (interfere w/ insulin signaling) - inflammatory cytokines released from adipocytes are cytotoxic to B-cells - obesity is correlated w/ hyperinsulenima and decreased insulin receptor density
combination of insulin resistance and decreased beta cell mass and function
type 2 DM (NIDDM)
clinical manifestations of NIDDM
- some classic sxs (polyuria/polydipsia) - fatigue - pruritus - recurrent infections - visual changes - neuropathy - individual is usually overweight w/ dyslipidemia and HTN
low blood glucose during the night that may lead to rise in morning blood glucose; tx is a nighttime snack to prevent hypoglycemia
Somogyi effect
early morning rise in blood glucose level related to release of GH, cortisol, and catecholamines w/o preceding hypoglycemia; tx is insulin to counter hyperglycemia
dawn phenomenon
symptoms of hypoglycemia
- pallor - tremor - tachycardia/palpitations - diaphoresis - headache - irritability/anxiety - confusion - seizures - coma
serious complication related to deficiency of insulin and increase in levels of insulin couter-regulatory hormones (catecholamines, GH, cortisol, and glucagon)
diabetic ketoacidosis (DKA)
3 main characteristics of DKA
- hyperglycemia - acidosis - ketonuria
Why is DKA more common in IDDM?
insulin is more deficient
Pathophysiology of DKA
- w/ insulin deficiency -> lipolysis is enhanced (increased fatty acid delivery to liver) - increased glyconeogenesis (contribute to hyperglycemia and production of ketone bodies) - increased ketones -> decreased pH -> metabolic acidosis
clinical manifestations of DKA
- Kussmaul respirations - fruity/acetone odor in breath - CNS depression - ketonuria - anorexia - N/V and ABD pain - postural dizziness
more common complication of NIDDM that differs from DKA w/ higher degree of fluid deficiency rather than insulin deficiency
hyperosmolar hyperglycemic nonketoic syndrome (HHNKS)
In which disease are glucose levels higher: DKA or HHNKS?
HHNKS -> due to volume depletion
clinical manifestations of HHNKS
- severe dehydration (from polyuria) - loss of electrolytes (ex. potassium) - neurologic changes (stupor, coma, seizures) - hypotension/hypoperfusion/tachycardia - N/V and ABD pain
List 7 chronic complications of DM
- retinopathy - nephropathy - neuropathy - infection - CAD - stroke - PVD
results from relative hypoxemia, damage to retinal blood vessels, RBC aggregation, and HTN
diabetic retinopathy
glomeruli are injured by hyperglycemia w/ high renal blood flow (hyper filtration) and intraglomerular HTN
diabetic nephropathy
most common complication of DM; hyperglycemia leads to ischemia and demyelination contributing to neural changes and delayed conduction
diabetic neuropathy
clinical manifestation of diabetic neuropathy
- glove and stocking loss of sensation - loss of motor nerve function w/ clawed toes and small muscle wasting in hands - Charcot joints (joint and ligament degeneration; mainly in feet)
How does diabetic neuropathy lead to amputation?
- decrease in sensation -> painless trauma -> ulceration -> infection - muscle atrophy -> changes in gait -> new pressure points -> ulceration -> infection - autonomic neuropathy -> decreased perspiration -> dry skin/cracks/fissures -> infection - All lead to soft tissue infection and osteomyelitis
Other than diabetic neuropathy, what else leads to amputation for diabetics?
angiopathy of both large and small vessels (vessel occlusion -> ischemia -> gangrene)
5 main reasons diabetics have increased risk for infection throughout the body
- impaired senses (neuropathy and retinopathy) - hypoxia (glycosylated Hgb impaired O2 delivery to tissues) - pathogens (some proliferate rapidly due to high glucose levels) - blood supply (vascular changes and reduced supply of WBCs) - suppressed immune response (impaired innate and adaptive immune system)
Goal of treatment for DM
prevent complications by regulating glucose - diet - exercise - medications
Metabolic acidosis (ex. DKA) will do what to serum potassium levels?
increase (hyperkalemia) -> H+ replaces K in the cells
