endocrine pathology (bikman) Flashcards
describe the hypothalamic-pituitary axis (primary, secondary, tertiary)
feedback regulation of the endocrine system, where the tertiary organ is the hypothalamus, secondary is the ant pit, primary is the end endocrine organ
disorders of the post pit
SIADH, Diabetes Insipidus, Galactorrhea, hyposecretion of oxytocin
SIADH
hypersecretion of ADH
clinical manifestations of SIADH
renal water retention, hyponatremia, hypoosmolarity; water reabsorption without ion reabsorption
actions of SIADH
increase in permeability of renal collecting duct to water, constriction of arterial smooth muscle
causes of SIADH
ectopic production of ADH by cancer cells, surger, drugs, head trauma
treatment of SIADH
water restriction, ADH receptor blockers, remove tumor if present
diabetes insipidus
insufficiency of ADH with polyuria and polydispia
clinical manifestations of diabetes insipidus
high dilute urine flow, drink large amounts of water, generic signs of dehydration
neurogenic DI
damage to the brain causing insufficient ADH
nephrogenic DI
lack of ADH receptors in kidney causing an insufficient ADH response
psychogenic DI
drinking too much water
describe how you test for DI
restrict water for a day and if osmolarity increases its PSYCHOGENIC. If it doesn’t change, give them ADH, if osmolarity increases its NEUROGENIC (decreased ADH production) of it doesn’t change, its NEPHROGENIC (kidney doesn’t respond to ADH
treatment for psychogenic DI
restrict water
treatment for nephrogenic DI
drink lots of water and have a NaCl rich diet
neurogeenic DI treatment
ADH replacement
effects of hyposecretion of oxytocin
lack of milk ejection and prolonged labor, lack of compassion, bonding, etc
galactorrhea
hypersecretion of oxytocin (excessive/inappropriate secretion of milk)
hormones of the ant pit
ACTH, LH, FSH, GH, PRL, TSH
what hypothalamic tropic hormone is an antagonist to PRL?
PIF/dopamine. when dopamine level is low, there is an increase in PRL
how do you determine the origin of a low plasma ant pit hormone problem?
hypothalamic factor stimulation test
what do you do in a hypothalamic factor stimulation test?
- take blood sample 2. inject one or more of the hypothalamic releasing factors 3. take another blood sample 4. compare amounts of the ant pit hormones before and after the hypothalamic factor injection
after a hypothalamic factor stimulation test, if pit hormones increase the problem is the ___, or if the pit hormones do not increase, the problem is the ______.
hypothalamus, pituitary
ant pit disorders
pit infarction, empty sella syndrome, hyperpituitarism
pit infarction
hypopituitarism due to hemorrhage that can manifest with apoplexy (paralysis with loss of consciousness)
sheehan syndrome
postpartum hypopituitarism
empty sella syndrome
hypopituitarism due to a shrunk or flattened pit gland
hyperpituitarism
commonly due to a benign adenoma, destruction of end organ, a hypothalamic disorder, or carcinoma
treatment of pit adenomas
hormone therapies, surgery, radiation
types of pit adenomas
(most common) PRL, GH, ACTH, LH/FSH, TSH (least common)
t/f. the larger a pit tumor grows, the greater the larger the blind spot gets
true.
symptoms of hyperpituitarisms
visual defects, headache, oculomotor palsies (inability to dilate/constrict pupil, follow object, open eyelid)
PRL release is stimulated by
TRH, oxytocin, stress and high estrogen, ovulation, suckling
PRL release is inhibited by
somatostatins and dopamine, estrogen and progesterone together (pregnancy), PRL (when it causes the hypot to release dopamine)
actions of PRL
induces proliferation of glandular tissue and mammary glands, increases Ca from bone and secretion into milk, stimulates immune system
female hypersecretion of PRL
amenorrhea, galactorrhea, hirsutism, osteopenia
male hypersecretion of PRL
hypogonadism, impaired libido, infertility, gynecomastia and galactorrhea
treatment of PRL hypersecretion
dopamine agonist (bromocryptin), somatostatin analogs (octreotide)
diagnosis of PRL hyposecretion
low plasma PRL, TRH stim test to determine is at the pit or hypot
GH release is stimulated by
GHRH, ghrelin (released when we eat to use for fuel), estrogen and testosterone
GH release is inhibited by
somatostain, IGF
actions of GH
stimulates IGF production by liver and other tissues; GF and IGF stimulate growth of long bones at epiph plate, increase aa incorporation into proteins, inhibit protein breakdown, increase lipolysis; inhibit hepatic glucose uptake and promotes gluconeogenesis, stimulates the immune sys
disorders of hypersecretion of GH
gigantism (prepubertal adenoma), acromegaly (post pubertal adenoma)
gigantism is accompanied with an increased risk of
hypertrophic cardiomyopathy
what can cause early death in individuals with acromegaly?
cardiac hypertrophy
treatment for hypersecretion of GH
somatostatin analog (octreotide) that inhibits GH, glucagon and insulin
disorders of hyposecretion of GH
children: dwarf (growth failure with increase % fat and decreased lean mass, thin and fragile bones, poor immune sys); adult: depression, poor lactation, decreased bone mass, poor immune sys, low blood gluc)
at what age does GH fall?
60-65
treatment with hyposecretion of GH
GH or IGF-1 injections depending on where the problem is
t/f. hormones dictate growth
true
thyroid disorders
hyperthyroidism, hypothyroidism, non-neoplastic diseases, neoplastic disease
TH is stimulated by
TRH, cold
TH is inhibited by
somatostatins, dopamine, stress, T3
low TSH, low T3
secondary/tertiary hypothyroidism
high TSH, low T3
primary hypothyroidism
low TSH, normal T3
sublingual hyperthyroidism
normal TSH and T3
euthyroidism
high TSH, normal T3
subclinical hypothyroidism
low TSH, high T3
primary hyperthyroidism
high TSH, high T3
secondary/tertiary hyperthyroidism
what does T3 do
regulates basal activity of most cells and increases mRNA synthesis
t/f. treatment with thyroid increases metabolic rate
true.
another name for hyperthyroidism
thyrotoxicosis
clinical manifestations of hyperhtyroidism
weight loss, heat intolerance, tachycardia/other arrythmias, clots, tremors, warm/moist skin, diarrhea, exopthalamos, lid lag, thyroid storm
common causes of hyperthyroidism
graves, multinodular goiter, thyroid adenoma
clinical manifestations of hypothyroidism
fatigue, weight gain, cold intolerance, bradycardia, impaired contraction, delayed reflexes, lethargy, rough/dry skin, hair loss, reduced appetite, constipation, deepened voice (myxedema)
lack of thyroid in utero causes
congenital cretinism
infant hypothyroidism can cause
developmental cretinism and TH supplements can help normal development
why should a woman get her thyroid check before she gets pregnant?
maternal hypothyroidism can cause a 10-20 IQ drop in infant
causes of acquired hypothyroidism
hashimotos, iatrogenic
non neoplastic thyroid problems
thyroiditis, graves, goiter
neoplastic thyroid problems
adenoma, carcinoma
hashimotos thyroiditis
most common cause of hypothyroidism and is an AI destruction of the thyroid; presence of hurthle cells
dequervain thyroiditis
enlarged sore throat that follows URI, immune cross reaction with thyroid follicles, self limiting; presence of multinucleated giant cells
silent thyroiditis
cycels of hypo and hyper, postpartum or mid age, painless; presence of lymphoid infiltrate
reidels thyroiditis
hypothyroidism, hard mass, rare, tracheal compression; presence of extensive fibrosis
symptoms of graves
hyperthyroidism, exopthalamus, dermopathy
histology of thyroid with graves
hyperplasia of epithelium, scalloped colloid
treatment of graves
beta blockers, iodine blockers, hot iodine, surgery
what is a goiter
enlarged thyroid due to inflammatory or noninflammatory response
t/f. you can determine the exact origin of the problem on the axis with a the presence of a goiter
false. it only tells you that there is a problem because it can be from hypo, hyper, or normal thyroid levels
3 ways to decrease T3/4
no iodine, enzyme defects, unknown reasons
t/f. most thyroid neoplasms are adenomas
true. carcinomas are uncommon
4 types of thyroid carcinoma
papillary, follicular, medullary, anaplastic
papillary thyroid carcinoma
most common, good survival, “orphan annie” tumor; histo: psammoma body
follicular thyroid carcinoma
second most common, good survival, worsens with age, tumor size and invasiveness; histo: vascular invasion
medullary thyroid carcinoma
rare, decent survival if only in the thyroid, pretty bad survival if it metastisized, tumor of parafollicular cells
anaplastic thyroid carcinoma
rarest type, fast growing neck mass, terrible prognosis
levels of adrenal cortex (out to in)
zona glomerulosa, fasciculata, reticularis
what does the zona glomerulosa produce?
mineralcorticoids (salt)
what does the zona fasciculata produce?
glucocorticoids (sugar)
what does the zona reticularis produce?
sex hormones (sex)
what does the adrenal medulla produce?
epi/norepinephrine
cushing syndrome
elevated plasma cortisol
cushing disease
elevated ACTH production due to a pit tumor
t/f. all cushing disease is cushing syndrome; not all cushing syndrome is cushing disesae
true.
cortisol, ACTH, MSH levels in cushing syndrome
high cortisol, low ACTH, low MSH
cortisol, ACTH, MSH levels in cushing disease
high cortisol, high ACTH, high MSH
what will high MSH cause?
hyperpigmentation
clinical manifestations of cortisol hypersecretion
increased resistance to catecholamines (high bp, tachycardia), IR, weight gain, muscle fatigue due to muscle breakdown, osteoporosis, increased inflammation, thin skin
cortisol’s effect on fat metabolism (central and peripheral)
on central fat - decrease HSL/ATGL and increase LPL; on peripheral fat - increase HSL/ATGL and decrease LPL
low dose dexamethasone results in diagnosis of high plasma cortisol
decreased ACTH and cortisol = chronic stress; no change = pit tumor/ectopic ACTH
high dose dexamethasone results in diagnosis of high plasma cortisol
decreased ACTH and cortisol = pit tumor; no change pit tumor
if there is no change in ACTH or cortisol in a low dose dexamethasone test, why would a high dose dexamethasone test tell you where the problem is a pit tumor or ectopic ACTH
ectopic tumors are not sensitive to dexamethasone inhibition of ACTH, so no changes in both low and high dose tests would tell you it could be ectopic ACTH
if ACTH is low and cortisol, it could be from what?
adrenal tumor or injection of excess cortisol
hypersecretion of adrenal androgen and estrogens can cause
feminization or virilization
adrenal medulla hyperfunction is caused by
tumors of chromaffin cells (aka pheochromocytoma)
symptoms of catecholamine hypersecretion
high HR and BP, diaphoresis, weight loss, hyperglycemia/hyperlipidemia
addison disease
adrenal hyposecretion, usually AI origin, with symptoms of skin hyperpigmentation, low BP, weakness, slow onset
waterhouse-friderichsen syndrome
adrenal hyposecretion caused by bacterial infection, bilateral hemorrhage, low BP, shock, DIC (?)
features of MEN disorders
genetic endocrine tumors that are typically found in younger people, are multifocal, and agressive
MEN-1 effects
not really a problem in the thyroid, but hyperplasia, adenoma, and carcinoma of other endocrine organs
MEN-2 effects
thyroid medullary carcinoma, and not really a problem in other organs
features of MEN-1
parathyroid hyperplasia, pancreatic hormone tumors, pit adenoma, duodenal gastrinoma, thyroid and adrenal adenomas, lipomas
MEN-1 gene mutation
turns off gene, encodes menin, is a TSG
features of MEN-2a
meullary thyroid carcinoma, pheochromocytoma, parathyroid hyperplasia
RET gene mutation
turns MEN-2a and 2b on, proto-oncogene, encodes TK receptor
features of MEN-2b
MARFAN, neuromas, medullary thyroid carcinioma, pheochromocytoma
t/f. insulin is the only major hormone that promotes body fat storage and inhibits fat use
true.
castrati
the absence of androgens, leading to a “generic female” fat deposition
