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DMD 5248 > endocrine pathology (bikman) > Flashcards

endocrine pathology (bikman) Flashcards

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

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2
Q

disorders of the post pit

A

SIADH, Diabetes Insipidus, Galactorrhea, hyposecretion of oxytocin

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3
Q

SIADH

A

hypersecretion of ADH

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4
Q

clinical manifestations of SIADH

A

renal water retention, hyponatremia, hypoosmolarity; water reabsorption without ion reabsorption

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5
Q

actions of SIADH

A

increase in permeability of renal collecting duct to water, constriction of arterial smooth muscle

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6
Q

causes of SIADH

A

ectopic production of ADH by cancer cells, surger, drugs, head trauma

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7
Q

treatment of SIADH

A

water restriction, ADH receptor blockers, remove tumor if present

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8
Q

diabetes insipidus

A

insufficiency of ADH with polyuria and polydispia

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9
Q

clinical manifestations of diabetes insipidus

A

high dilute urine flow, drink large amounts of water, generic signs of dehydration

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10
Q

neurogenic DI

A

damage to the brain causing insufficient ADH

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11
Q

nephrogenic DI

A

lack of ADH receptors in kidney causing an insufficient ADH response

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12
Q

psychogenic DI

A

drinking too much water

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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

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14
Q

treatment for psychogenic DI

A

restrict water

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15
Q

treatment for nephrogenic DI

A

drink lots of water and have a NaCl rich diet

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16
Q

neurogeenic DI treatment

A

ADH replacement

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17
Q

effects of hyposecretion of oxytocin

A

lack of milk ejection and prolonged labor, lack of compassion, bonding, etc

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18
Q

galactorrhea

A

hypersecretion of oxytocin (excessive/inappropriate secretion of milk)

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19
Q

hormones of the ant pit

A

ACTH, LH, FSH, GH, PRL, TSH

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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

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21
Q

how do you determine the origin of a low plasma ant pit hormone problem?

A

hypothalamic factor stimulation test

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22
Q

what do you do in a hypothalamic factor stimulation test?

A
  1. 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
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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

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24
Q

ant pit disorders

A

pit infarction, empty sella syndrome, hyperpituitarism

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25
Q

pit infarction

A

hypopituitarism due to hemorrhage that can manifest with apoplexy (paralysis with loss of consciousness)

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26
Q

sheehan syndrome

A

postpartum hypopituitarism

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27
Q

empty sella syndrome

A

hypopituitarism due to a shrunk or flattened pit gland

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28
Q

hyperpituitarism

A

commonly due to a benign adenoma, destruction of end organ, a hypothalamic disorder, or carcinoma

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29
Q

treatment of pit adenomas

A

hormone therapies, surgery, radiation

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30
Q

types of pit adenomas

A

(most common) PRL, GH, ACTH, LH/FSH, TSH (least common)

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31
Q

t/f. the larger a pit tumor grows, the greater the larger the blind spot gets

A

true.

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32
Q

symptoms of hyperpituitarisms

A

visual defects, headache, oculomotor palsies (inability to dilate/constrict pupil, follow object, open eyelid)

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33
Q

PRL release is stimulated by

A

TRH, oxytocin, stress and high estrogen, ovulation, suckling

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34
Q

PRL release is inhibited by

A

somatostatins and dopamine, estrogen and progesterone together (pregnancy), PRL (when it causes the hypot to release dopamine)

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35
Q

actions of PRL

A

induces proliferation of glandular tissue and mammary glands, increases Ca from bone and secretion into milk, stimulates immune system

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36
Q

female hypersecretion of PRL

A

amenorrhea, galactorrhea, hirsutism, osteopenia

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37
Q

male hypersecretion of PRL

A

hypogonadism, impaired libido, infertility, gynecomastia and galactorrhea

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38
Q

treatment of PRL hypersecretion

A

dopamine agonist (bromocryptin), somatostatin analogs (octreotide)

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39
Q

diagnosis of PRL hyposecretion

A

low plasma PRL, TRH stim test to determine is at the pit or hypot

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40
Q

GH release is stimulated by

A

GHRH, ghrelin (released when we eat to use for fuel), estrogen and testosterone

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41
Q

GH release is inhibited by

A

somatostain, IGF

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42
Q

actions of GH

A

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

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43
Q

disorders of hypersecretion of GH

A

gigantism (prepubertal adenoma), acromegaly (post pubertal adenoma)

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44
Q

gigantism is accompanied with an increased risk of

A

hypertrophic cardiomyopathy

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45
Q

what can cause early death in individuals with acromegaly?

A

cardiac hypertrophy

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46
Q

treatment for hypersecretion of GH

A

somatostatin analog (octreotide) that inhibits GH, glucagon and insulin

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47
Q

disorders of hyposecretion of GH

A

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)

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48
Q

at what age does GH fall?

A

60-65

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49
Q

treatment with hyposecretion of GH

A

GH or IGF-1 injections depending on where the problem is

50
Q

t/f. hormones dictate growth

A

true

51
Q

thyroid disorders

A

hyperthyroidism, hypothyroidism, non-neoplastic diseases, neoplastic disease

52
Q

TH is stimulated by

A

TRH, cold

53
Q

TH is inhibited by

A

somatostatins, dopamine, stress, T3

54
Q

low TSH, low T3

A

secondary/tertiary hypothyroidism

55
Q

high TSH, low T3

A

primary hypothyroidism

56
Q

low TSH, normal T3

A

sublingual hyperthyroidism

57
Q

normal TSH and T3

A

euthyroidism

58
Q

high TSH, normal T3

A

subclinical hypothyroidism

59
Q

low TSH, high T3

A

primary hyperthyroidism

60
Q

high TSH, high T3

A

secondary/tertiary hyperthyroidism

61
Q

what does T3 do

A

regulates basal activity of most cells and increases mRNA synthesis

62
Q

t/f. treatment with thyroid increases metabolic rate

A

true.

63
Q

another name for hyperthyroidism

A

thyrotoxicosis

64
Q

clinical manifestations of hyperhtyroidism

A

weight loss, heat intolerance, tachycardia/other arrythmias, clots, tremors, warm/moist skin, diarrhea, exopthalamos, lid lag, thyroid storm

65
Q

common causes of hyperthyroidism

A

graves, multinodular goiter, thyroid adenoma

66
Q

clinical manifestations of hypothyroidism

A

fatigue, weight gain, cold intolerance, bradycardia, impaired contraction, delayed reflexes, lethargy, rough/dry skin, hair loss, reduced appetite, constipation, deepened voice (myxedema)

67
Q

lack of thyroid in utero causes

A

congenital cretinism

68
Q

infant hypothyroidism can cause

A

developmental cretinism and TH supplements can help normal development

69
Q

why should a woman get her thyroid check before she gets pregnant?

A

maternal hypothyroidism can cause a 10-20 IQ drop in infant

70
Q

causes of acquired hypothyroidism

A

hashimotos, iatrogenic

71
Q

non neoplastic thyroid problems

A

thyroiditis, graves, goiter

72
Q

neoplastic thyroid problems

A

adenoma, carcinoma

73
Q

hashimotos thyroiditis

A

most common cause of hypothyroidism and is an AI destruction of the thyroid; presence of hurthle cells

74
Q

dequervain thyroiditis

A

enlarged sore throat that follows URI, immune cross reaction with thyroid follicles, self limiting; presence of multinucleated giant cells

75
Q

silent thyroiditis

A

cycels of hypo and hyper, postpartum or mid age, painless; presence of lymphoid infiltrate

76
Q

reidels thyroiditis

A

hypothyroidism, hard mass, rare, tracheal compression; presence of extensive fibrosis

77
Q

symptoms of graves

A

hyperthyroidism, exopthalamus, dermopathy

78
Q

histology of thyroid with graves

A

hyperplasia of epithelium, scalloped colloid

79
Q

treatment of graves

A

beta blockers, iodine blockers, hot iodine, surgery

80
Q

what is a goiter

A

enlarged thyroid due to inflammatory or noninflammatory response

81
Q

t/f. you can determine the exact origin of the problem on the axis with a the presence of a goiter

A

false. it only tells you that there is a problem because it can be from hypo, hyper, or normal thyroid levels

82
Q

3 ways to decrease T3/4

A

no iodine, enzyme defects, unknown reasons

83
Q

t/f. most thyroid neoplasms are adenomas

A

true. carcinomas are uncommon

84
Q

4 types of thyroid carcinoma

A

papillary, follicular, medullary, anaplastic

85
Q

papillary thyroid carcinoma

A

most common, good survival, “orphan annie” tumor; histo: psammoma body

86
Q

follicular thyroid carcinoma

A

second most common, good survival, worsens with age, tumor size and invasiveness; histo: vascular invasion

87
Q

medullary thyroid carcinoma

A

rare, decent survival if only in the thyroid, pretty bad survival if it metastisized, tumor of parafollicular cells

88
Q

anaplastic thyroid carcinoma

A

rarest type, fast growing neck mass, terrible prognosis

89
Q

levels of adrenal cortex (out to in)

A

zona glomerulosa, fasciculata, reticularis

90
Q

what does the zona glomerulosa produce?

A

mineralcorticoids (salt)

91
Q

what does the zona fasciculata produce?

A

glucocorticoids (sugar)

92
Q

what does the zona reticularis produce?

A

sex hormones (sex)

93
Q

what does the adrenal medulla produce?

A

epi/norepinephrine

94
Q

cushing syndrome

A

elevated plasma cortisol

95
Q

cushing disease

A

elevated ACTH production due to a pit tumor

96
Q

t/f. all cushing disease is cushing syndrome; not all cushing syndrome is cushing disesae

A

true.

97
Q

cortisol, ACTH, MSH levels in cushing syndrome

A

high cortisol, low ACTH, low MSH

98
Q

cortisol, ACTH, MSH levels in cushing disease

A

high cortisol, high ACTH, high MSH

99
Q

what will high MSH cause?

A

hyperpigmentation

100
Q

clinical manifestations of cortisol hypersecretion

A

increased resistance to catecholamines (high bp, tachycardia), IR, weight gain, muscle fatigue due to muscle breakdown, osteoporosis, increased inflammation, thin skin

101
Q

cortisol’s effect on fat metabolism (central and peripheral)

A

on central fat - decrease HSL/ATGL and increase LPL; on peripheral fat - increase HSL/ATGL and decrease LPL

102
Q

low dose dexamethasone results in diagnosis of high plasma cortisol

A

decreased ACTH and cortisol = chronic stress; no change = pit tumor/ectopic ACTH

103
Q

high dose dexamethasone results in diagnosis of high plasma cortisol

A

decreased ACTH and cortisol = pit tumor; no change pit tumor

104
Q

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

A

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
Q

if ACTH is low and cortisol, it could be from what?

A

adrenal tumor or injection of excess cortisol

106
Q

hypersecretion of adrenal androgen and estrogens can cause

A

feminization or virilization

107
Q

adrenal medulla hyperfunction is caused by

A

tumors of chromaffin cells (aka pheochromocytoma)

108
Q

symptoms of catecholamine hypersecretion

A

high HR and BP, diaphoresis, weight loss, hyperglycemia/hyperlipidemia

109
Q

addison disease

A

adrenal hyposecretion, usually AI origin, with symptoms of skin hyperpigmentation, low BP, weakness, slow onset

110
Q

waterhouse-friderichsen syndrome

A

adrenal hyposecretion caused by bacterial infection, bilateral hemorrhage, low BP, shock, DIC (?)

111
Q

features of MEN disorders

A

genetic endocrine tumors that are typically found in younger people, are multifocal, and agressive

112
Q

MEN-1 effects

A

not really a problem in the thyroid, but hyperplasia, adenoma, and carcinoma of other endocrine organs

113
Q

MEN-2 effects

A

thyroid medullary carcinoma, and not really a problem in other organs

114
Q

features of MEN-1

A

parathyroid hyperplasia, pancreatic hormone tumors, pit adenoma, duodenal gastrinoma, thyroid and adrenal adenomas, lipomas

115
Q

MEN-1 gene mutation

A

turns off gene, encodes menin, is a TSG

116
Q

features of MEN-2a

A

meullary thyroid carcinoma, pheochromocytoma, parathyroid hyperplasia

117
Q

RET gene mutation

A

turns MEN-2a and 2b on, proto-oncogene, encodes TK receptor

118
Q

features of MEN-2b

A

MARFAN, neuromas, medullary thyroid carcinioma, pheochromocytoma

119
Q

t/f. insulin is the only major hormone that promotes body fat storage and inhibits fat use

A

true.

120
Q

castrati

A

the absence of androgens, leading to a “generic female” fat deposition

DMD 5248 (7 decks)

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