endocrine pathology (bikman) Flashcards
(120 cards)
1
Q
describe the hypothalamic-pituitary axis (primary, secondary, tertiary)
A
feedback regulation of the endocrine system, where the tertiary organ is the hypothalamus, secondary is the ant pit, primary is the end endocrine organ
2
Q
disorders of the post pit
A
SIADH, Diabetes Insipidus, Galactorrhea, hyposecretion of oxytocin
3
Q
SIADH
A
hypersecretion of ADH
4
Q
clinical manifestations of SIADH
A
renal water retention, hyponatremia, hypoosmolarity; water reabsorption without ion reabsorption
5
Q
actions of SIADH
A
increase in permeability of renal collecting duct to water, constriction of arterial smooth muscle
6
Q
causes of SIADH
A
ectopic production of ADH by cancer cells, surger, drugs, head trauma
7
Q
treatment of SIADH
A
water restriction, ADH receptor blockers, remove tumor if present
8
Q
diabetes insipidus
A
insufficiency of ADH with polyuria and polydispia
9
Q
clinical manifestations of diabetes insipidus
A
high dilute urine flow, drink large amounts of water, generic signs of dehydration
10
Q
neurogenic DI
A
damage to the brain causing insufficient ADH
11
Q
nephrogenic DI
A
lack of ADH receptors in kidney causing an insufficient ADH response
12
Q
psychogenic DI
A
drinking too much water
13
Q
describe how you test for DI
A
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
14
Q
treatment for psychogenic DI
A
restrict water
15
Q
treatment for nephrogenic DI
A
drink lots of water and have a NaCl rich diet
16
Q
neurogeenic DI treatment
A
ADH replacement
17
Q
effects of hyposecretion of oxytocin
A
lack of milk ejection and prolonged labor, lack of compassion, bonding, etc
18
Q
galactorrhea
A
hypersecretion of oxytocin (excessive/inappropriate secretion of milk)
19
Q
hormones of the ant pit
A
ACTH, LH, FSH, GH, PRL, TSH
20
Q
what hypothalamic tropic hormone is an antagonist to PRL?
A
PIF/dopamine. when dopamine level is low, there is an increase in PRL
21
Q
how do you determine the origin of a low plasma ant pit hormone problem?
A
hypothalamic factor stimulation test
22
Q
what do you do in a hypothalamic factor stimulation test?
A
- 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
23
Q
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 ______.
A
hypothalamus, pituitary
24
Q
ant pit disorders
A
pit infarction, empty sella syndrome, hyperpituitarism
25
pit infarction
hypopituitarism due to hemorrhage that can manifest with apoplexy (paralysis with loss of consciousness)
26
sheehan syndrome
postpartum hypopituitarism
27
empty sella syndrome
hypopituitarism due to a shrunk or flattened pit gland
28
hyperpituitarism
commonly due to a benign adenoma, destruction of end organ, a hypothalamic disorder, or carcinoma
29
treatment of pit adenomas
hormone therapies, surgery, radiation
30
types of pit adenomas
(most common) PRL, GH, ACTH, LH/FSH, TSH (least common)
31
t/f. the larger a pit tumor grows, the greater the larger the blind spot gets
true.
32
symptoms of hyperpituitarisms
visual defects, headache, oculomotor palsies (inability to dilate/constrict pupil, follow object, open eyelid)
33
PRL release is stimulated by
TRH, oxytocin, stress and high estrogen, ovulation, suckling
34
PRL release is inhibited by
somatostatins and dopamine, estrogen and progesterone together (pregnancy), PRL (when it causes the hypot to release dopamine)
35
actions of PRL
induces proliferation of glandular tissue and mammary glands, increases Ca from bone and secretion into milk, stimulates immune system
36
female hypersecretion of PRL
amenorrhea, galactorrhea, hirsutism, osteopenia
37
male hypersecretion of PRL
hypogonadism, impaired libido, infertility, gynecomastia and galactorrhea
38
treatment of PRL hypersecretion
dopamine agonist (bromocryptin), somatostatin analogs (octreotide)
39
diagnosis of PRL hyposecretion
low plasma PRL, TRH stim test to determine is at the pit or hypot
40
GH release is stimulated by
GHRH, ghrelin (released when we eat to use for fuel), estrogen and testosterone
41
GH release is inhibited by
somatostain, IGF
42
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
43
disorders of hypersecretion of GH
gigantism (prepubertal adenoma), acromegaly (post pubertal adenoma)
44
gigantism is accompanied with an increased risk of
hypertrophic cardiomyopathy
45
what can cause early death in individuals with acromegaly?
cardiac hypertrophy
46
treatment for hypersecretion of GH
somatostatin analog (octreotide) that inhibits GH, glucagon and insulin
47
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)
48
at what age does GH fall?
60-65
49
treatment with hyposecretion of GH
GH or IGF-1 injections depending on where the problem is
50
t/f. hormones dictate growth
true
51
thyroid disorders
hyperthyroidism, hypothyroidism, non-neoplastic diseases, neoplastic disease
52
TH is stimulated by
TRH, cold
53
TH is inhibited by
somatostatins, dopamine, stress, T3
54
low TSH, low T3
secondary/tertiary hypothyroidism
55
high TSH, low T3
primary hypothyroidism
56
low TSH, normal T3
sublingual hyperthyroidism
57
normal TSH and T3
euthyroidism
58
high TSH, normal T3
subclinical hypothyroidism
59
low TSH, high T3
primary hyperthyroidism
60
high TSH, high T3
secondary/tertiary hyperthyroidism
61
what does T3 do
regulates basal activity of most cells and increases mRNA synthesis
62
t/f. treatment with thyroid increases metabolic rate
true.
63
another name for hyperthyroidism
thyrotoxicosis
64
clinical manifestations of hyperhtyroidism
weight loss, heat intolerance, tachycardia/other arrythmias, clots, tremors, warm/moist skin, diarrhea, exopthalamos, lid lag, thyroid storm
65
common causes of hyperthyroidism
graves, multinodular goiter, thyroid adenoma
66
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)
67
lack of thyroid in utero causes
congenital cretinism
68
infant hypothyroidism can cause
developmental cretinism and TH supplements can help normal development
69
why should a woman get her thyroid check before she gets pregnant?
maternal hypothyroidism can cause a 10-20 IQ drop in infant
70
causes of acquired hypothyroidism
hashimotos, iatrogenic
71
non neoplastic thyroid problems
thyroiditis, graves, goiter
72
neoplastic thyroid problems
adenoma, carcinoma
73
hashimotos thyroiditis
most common cause of hypothyroidism and is an AI destruction of the thyroid; presence of hurthle cells
74
dequervain thyroiditis
enlarged sore throat that follows URI, immune cross reaction with thyroid follicles, self limiting; presence of multinucleated giant cells
75
silent thyroiditis
cycels of hypo and hyper, postpartum or mid age, painless; presence of lymphoid infiltrate
76
reidels thyroiditis
hypothyroidism, hard mass, rare, tracheal compression; presence of extensive fibrosis
77
symptoms of graves
hyperthyroidism, exopthalamus, dermopathy
78
histology of thyroid with graves
hyperplasia of epithelium, scalloped colloid
79
treatment of graves
beta blockers, iodine blockers, hot iodine, surgery
80
what is a goiter
enlarged thyroid due to inflammatory or noninflammatory response
81
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
82
3 ways to decrease T3/4
no iodine, enzyme defects, unknown reasons
83
t/f. most thyroid neoplasms are adenomas
true. carcinomas are uncommon
84
4 types of thyroid carcinoma
papillary, follicular, medullary, anaplastic
85
papillary thyroid carcinoma
most common, good survival, "orphan annie" tumor; histo: psammoma body
86
follicular thyroid carcinoma
second most common, good survival, worsens with age, tumor size and invasiveness; histo: vascular invasion
87
medullary thyroid carcinoma
rare, decent survival if only in the thyroid, pretty bad survival if it metastisized, tumor of parafollicular cells
88
anaplastic thyroid carcinoma
rarest type, fast growing neck mass, terrible prognosis
89
levels of adrenal cortex (out to in)
zona glomerulosa, fasciculata, reticularis
90
what does the zona glomerulosa produce?
mineralcorticoids (salt)
91
what does the zona fasciculata produce?
glucocorticoids (sugar)
92
what does the zona reticularis produce?
sex hormones (sex)
93
what does the adrenal medulla produce?
epi/norepinephrine
94
cushing syndrome
elevated plasma cortisol
95
cushing disease
elevated ACTH production due to a pit tumor
96
t/f. all cushing disease is cushing syndrome; not all cushing syndrome is cushing disesae
true.
97
cortisol, ACTH, MSH levels in cushing syndrome
high cortisol, low ACTH, low MSH
98
cortisol, ACTH, MSH levels in cushing disease
high cortisol, high ACTH, high MSH
99
what will high MSH cause?
hyperpigmentation
100
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
101
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
102
low dose dexamethasone results in diagnosis of high plasma cortisol
decreased ACTH and cortisol = chronic stress; no change = pit tumor/ectopic ACTH
103
high dose dexamethasone results in diagnosis of high plasma cortisol
decreased ACTH and cortisol = pit tumor; no change pit tumor
104
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
105
if ACTH is low and cortisol, it could be from what?
adrenal tumor or injection of excess cortisol
106
hypersecretion of adrenal androgen and estrogens can cause
feminization or virilization
107
adrenal medulla hyperfunction is caused by
tumors of chromaffin cells (aka pheochromocytoma)
108
symptoms of catecholamine hypersecretion
high HR and BP, diaphoresis, weight loss, hyperglycemia/hyperlipidemia
109
addison disease
adrenal hyposecretion, usually AI origin, with symptoms of skin hyperpigmentation, low BP, weakness, slow onset
110
waterhouse-friderichsen syndrome
adrenal hyposecretion caused by bacterial infection, bilateral hemorrhage, low BP, shock, DIC (?)
111
features of MEN disorders
genetic endocrine tumors that are typically found in younger people, are multifocal, and agressive
112
MEN-1 effects
not really a problem in the thyroid, but hyperplasia, adenoma, and carcinoma of other endocrine organs
113
MEN-2 effects
thyroid medullary carcinoma, and not really a problem in other organs
114
features of MEN-1
parathyroid hyperplasia, pancreatic hormone tumors, pit adenoma, duodenal gastrinoma, thyroid and adrenal adenomas, lipomas
115
MEN-1 gene mutation
turns off gene, encodes menin, is a TSG
116
features of MEN-2a
meullary thyroid carcinoma, pheochromocytoma, parathyroid hyperplasia
117
RET gene mutation
turns MEN-2a and 2b on, proto-oncogene, encodes TK receptor
118
features of MEN-2b
MARFAN, neuromas, medullary thyroid carcinioma, pheochromocytoma
119
t/f. insulin is the only major hormone that promotes body fat storage and inhibits fat use
true.
120
castrati
the absence of androgens, leading to a "generic female" fat deposition
