Endocrine Flashcards
goiter
an enlargement of thyroid gland w/ or w/o s/s of thyroid dysfx
Excess TSH
low iodine levels (these goiters tend to be larger)
goitrogens–ie lithium
Hashimoto’s
thyroid receptor antibodies antithyroglobulin antibody (anti-Tg) antithyroperoxidase antibody (anti- TPO)--hallmark of disorder
Risk factors for hypothyroidism
female age > 50 caucasian pregnancy hx of other autoimmune disorders family hx meds--lithium, amiodarone treatments for hyperthyroidism
hypothyroidism
early manifestations
cold intolerance weight gain lethargy fatigue memory deficits poor attn span increased cholesterol muscle cramps raises carotene levels (yellows skin) constipation decreased fertility puffy face hair loss brittle nails anemia hoarse voice
hypothyroidism
late manifestations
below normal temp. bradycardia weight gain decreased LOC thickened skin cardiac complications (cardiomegaly)
myxedema
life-threatening severe hypo (coma) → undiagnosed or untreated
hypothyroidism treatment
levothyroxine (synthetic T4, converted to T3 in body)
taken for life
take on empty stomach
↑ risk for bleeding with warfarin
hyperthyroidism (Thyrotoxicosis)
excessive secretion of T3 and T4
Primary → Grave’s disease
Secondary (pituitary) → over secretes TSH
Tertiary (hypothalamus)
hyperthyroidism risk factors
family hx of Graves age > 40 female caucasian meds excessive iodine intake pregnancy
Graves’ disease
autoimmune
excess levels of T3 and T4
thyroid-stimulating antibodies → thyroid continues to secrete hormones w/o stimulation from pituitary gland
graves’ disease
clinical manifestations
nervousness insomnia sensitivity to heat weight loss gland usually enlarged and palpable audible bruit may be heard atrial fib myxedema--dermatologic manifestations exophthalmos
Graves’ disease diagnosis
Low TSH ↑ T3 ↑ T4 antithyroglobulin antithyrotropin receptor antibody ultrasound with color doppler eval radioactive iodine scanning and measurements of iodine uptake-- ↑ iodine uptake and distributed diffusely
treatment of hyperthyroidism
- propylthiouracil (PTU) - blocks thyroid hormone synthesis, suppresses conversion of T4-T3
- BLACK BOX - hepatotoxic
- used in 1st trimester with caution
- radioactive iodine treatment
- surgery - hormone replacement needed for life
thyrotoxic crisis
overwhelming release of thyroid hormones that exerts an intense stimulus on the metabolism
reaction to major stressor
life threatening condition most commonly precipitated by surgery, trauma, or infection
body revved up and can result in death if not treated within 48 hours
hypoparathyroidism
s/s r/t insufficient PTH secretion and the resulting ↓ Ca
muscle cramps irritability tetany convulsions trousseau's and chvostek's sign
hypoparathyroidism treatment
replace PTH
normalize serum Ca and vit D levels
if parathyroid removed, replacement treatments are for life
hyperparathyroidism
s/s r/t excessive secretion of PTH with hypercalcemia and bone breakdown
muscle weakness poor concentration neuropathies kidney stones metabolic acidosis osteopenia pathological fractures constipation depression, confusion, subtle cognitive deficits
hyperparathyroidism treatment
↓ Ca levels diuretics calcitonin bisphosphonates Vit D surgical intervention
SIADH etiology
malignant tumors
CNS disorders (trauma, stroke, brain tumors)
drug therapy
misc. (hypothyroidism, infection)
SIADH
↓ serum osmolality dilutional hyponatremia ↑ urine specific gravity & osmolality weight gain ↓ urine ouput
SIADH clinical manifestations
hyponatremia: dyspnea, fatigue dulled sensorium, confusion, lethargy muscle twitching, convulsions impaired taste, anorexia, vomiting, cramps
SIADH treatment
treat the underlying cause
chronic SIADH - demeclocyline
severe cases may call for hypertonic solution
demeclocycline
tetracycline
interferes with renal response to ADH
AE: photosensitivity, teeth staining, nephrotoxic
Neurogenic DI etiology
hypothalamus or pituitary gland damgage
associated disorders: stroke, traumatic brain injury, brain surgery, cerebral infections
sudden onset, usually permanent
treatment: desmopressin (DDAVP) - synthetic ADH replacement therapy, comes in nasal spray; give as small of dose as possible
Nephrogenic DI etiology
loss of kidney function
often drug related ie lithium
CKD
slow onset and progressive
treatment: thiazide diuretics
Cushings clinical manifestations
↑ cortisol
glucose intolerance, hyperglycemia
HTN, capillary friability
muscle wasting, weakness; thinning of skin, osteoporosis and bone pain
redistribution of fat to abd, shoulders and face
impaired wound healing & immune response, risk for infection
mood swings, insomnia
drug therapy for cushings
- treatment dependent on cause
- tumor- surgery or radiation
- exogenous steroids - taper
- drug therapy is not primary, but adjunct w/radiation or surgery; helps with elevated cortisol levels
aminoglutethimide
blocks synthesis of all adrenal steroids
used in ppl awaiting surgery, no longer than 3 months
reduces cortisol levels by 50%
AE: drowsiness, nausea, anorexia, rash
ketoconazole
antifungal that also inhibits glucocorticoid synthesis
adjunct therapy to radiation, surgery
severe liver damage
do not take with ETOH or other hepatotoxic drugs
teratogenic
addison disease clinical manifestations
slow onset early s/s anorexia, weight loss weakness, malaise, apathy electrolyte imbalances skin hyperpigmentation
