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DT4 Exam 1 > Endo > Flashcards

Endo Flashcards

1
Q

derivation of anterior pituitary

A

Rathke’s pouch from oral cavity

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2
Q

hormones from posterior pituitary

A

oxytocin and ADH

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3
Q

cause of most excess hormones from anterior pituitary

A

adenoma

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4
Q

other causes of hyperpituitarism

A

hyperplasia, carcinoma, non-pituitary tumors, disorders of hypothalamus

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5
Q

clinical presentation hyperpituitarism

A

signs and symptoms from excessive hormone or mass effect
radiologic abnormalities, bitemporal hemanopsia
elevated intracranial pressure
may cause hypopituitarism from compression

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6
Q

radiographic abnormalities of sella turcica

A

sellar expansion, bony erosion, disruption of diaphragma sellae

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7
Q

size macroadenoma and microadenoma

A

macro>1cm

miro<1cm

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8
Q

invasive adenoma

A

nonencapsulated

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9
Q

pituitary apoplexy

A

rapid enlargement due to acute hemorrhage

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10
Q

histological difference of adenoma

A

do not have reticulin

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11
Q

pituitary stone

A

calcified prolactinoma

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12
Q

signs of prolactinoma

A

amenorrhea, galactorrhea, loss of libido, infertility

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13
Q

causes of serum prolactinemia

A

pregnancy, nursing, stress
damaged to pituitary stalk or hypothalamus
drugs-phenothiazine, haloperidol (decrease dopamine)
estrogen, renal failure, hypothyroidism

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14
Q

treatment prolactinoma

A

bromocriptine (dopamine agonist)

transphenoidal surgery

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15
Q

acidophilic adenoma

A

GH

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16
Q

signs of GH adenoma

A

gigantism in pre-pubertal child
acromegaly in adults
abnormal glucose tolerance, DM, muscle weakness, HTN, arthritis, osteoporosis, CHF, increased risk of GI cancer

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17
Q

genetics GH adenoma

A

gsp mutation of alpha subunit of Gs protein

inhibits GTPase

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18
Q

basophilic adenoma

A

corticotroph cell adenoma

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19
Q

Cushing disease

A

due to pituitary/hypothalamic disorder

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20
Q

Cushing syndrome

A

other causes-iatrogenic, primary adrenal cortex, ectopic ACTH

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21
Q

Nelson’s syndrome

A

pituitary corticotroph adenoma due to removal of adrenals for Cushing’s syndrome resulting in a loss of negative feedback
increase ACTH but no cortisol
hyperpigmentation from POMC

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22
Q

results of null cell adenoma

A

mass effect and compress remaining pituitary resulting in hypopituitarism

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23
Q

gonadotroph adenoma

A

diagnosed in middle age men and women

loss of libido in men

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24
Q

hypopituitarism

A

loss of 75% or more of anterior pituitary

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25
Q

hypopituitarism from loss of hypothalamus

A

get loss of ADH too

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26
Q

symptoms of hypopituitarism

A

hypofunction of adrenal cortices, thyroid, and gonads
pallor (decrease MSH)
atrophy of gonads and genitalia leading to amenorrhea, impotence, and loss of libido
loss of axillary and pubic hair

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27
Q

nonsecretory pituitary adenoma

A

enlargement may be gradual or due to acute hemorrhage (pituitary apoplexy)

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28
Q

Sheehan’s syndrome

A

postpartum hemorrhage

most common cause of ischemic necrosis leading to hypopituitarism

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29
Q

less susceptible portion of pituitary

A

posterior pituitary

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30
Q

empty sella syndrome

A

enlarged, empty sella turcica caused by chronic herniation of the subarachnoid space into the sella turcica
obese patients with multiple pregnancies

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31
Q

genetic defects causing hypopituitarism

A

defect in gene encoding pit 1
transcription factor for GH, prolactin, and TSH
resulting protein binds DNA but does not activate target genes

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32
Q

diabetes insipidus

A

lack of ADH

leads to excessive thirst

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33
Q

SIADH

A

too much ADH

most common cause is secretion by malignant neoplasms

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34
Q

craniopharyngiomas

A

slow intracranial tumors
enough calcium to see on x-ray
most are suprasellar and occur in children
endocrine deficiencies in children, visual disturbances in adults

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35
Q

Cushing disease presentation

A

primary hypothalamic-pituitary disease
increase ACTH
females in 30-40s
nodular cortical hyperplasia of adrenals

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36
Q

primary adrenocortical hyperplasia

A

most are neoplasms, adenomas or carcinomas
hyperplasia is less common
increased glucocorticoids leading to decreased ACTH

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37
Q

ectopic ACTH from tumors

A

most common cause small cell carcinoma of lung
others-carcinoid tumors, medullary carcinoma of thyroid, pancreatic islet cell tumors
nodular adrenocortical hyperplasia

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38
Q

dexamethasome test on ectopic ACTH

A

does not suppress ACTH production

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39
Q

signs and symptoms of hypercortisolism

A

HTN and weight gain
truncal obesity, moon faces, buffalo hump
atrophy of fast twitch muscle
hyperglycemia, glucosuria, polydipsia
striae on abdomen and osteoporosis
hirsutism, menstrual irregularities, mental disturbances, poor wound healing

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40
Q

exogenous steroids on adrenal

A

atrophy

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41
Q

ectopic or endogenous ACTH on adrenal

A

bilateral nodular adrenocrotical hyperplasia

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42
Q

Crooke’s hyaline

A

keratin intermediate filaments

pituitary changes from endogenous or exogenous glucocorticoids

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43
Q

pituitary dexamethasone challenge

A

at low dose not suppressed but at high dose suppressed

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44
Q

primary hyperaldosteronism

A

due to neoplasm or hyperplasia

increased aldosterone and decreased renin

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45
Q

secondary hyperaldosteronism

A

due to increase renin activity from CHF, decreased renal perfusion, hypoalbuminemai, or pregnancy
hypertension and hypokalemia

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46
Q

treatment of adenomas

A

surgical correction of hypertension possible

hyperplasia is treated medically

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47
Q

andrenogenital syndromes

A

causes of virilization

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48
Q

congential adrenal hyperpalsia

A

AR defect in biosynthesis of cortisol

most common is 21 hydroxylase deficiency

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49
Q

21 hydroxylase deficiency

A

increased androgen activity

sodium wasting due to lack of mineral-corticoid

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50
Q

17 hydroxylase deficiency

A

androgen deficiency

some sodium retention and hypertension

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51
Q

morphology of congenital adrenal hyperplasia

A

bilateral nodular adrenal hyperlplasia

pituitary-hyperplasia of corticostrophs

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52
Q

treatment congenital adrenal hyperplasia

A

suppress ACTH

at risk of acute adrenal insufficiency

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53
Q

autoimmune chronic adrenocortical insufficiency

A

1/2 restricted to adrenals, rest are plyglandular syndromes

HLA-B8 and DR3

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54
Q

infections that can cause chronic adrenocortical insufficiency

A

tuberculosis
Histoplasm capsulatum
Coccidiodes immitis

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55
Q

metastatic causes of chronic adrenocortical insufficiency

A

lung and breast most common

others-GI, melanoma, hematopoietic

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56
Q

symptoms of Addisons (chronic adrenocortical insufficiency)

A 
weakness and fatigue
anorexia, weight loss, diarrhea
hyperpigmentation
volume depletion and hypotension
hypoglycemia
57
Q

adrenocortical insufficiency without pigmentation

A

pituitary and hypothalamic causes

58
Q

acute adrenal crisis

A

intractable vomiting, abdominal pain, hypotension, coma, vascular collapse
death if corticosteroids not replaced immediately

59
Q

morphology primary autoimmune adrenocortical insufficiency

A

irregularly shrunken adrenals with lymphoid infiltate

medulla preserved

60
Q

morphology secondary autoimmune adrenocortical insufficiency

A

small, flattened

atrophied

61
Q

morphology TB and fungus adrenocortical insufficiency

A

granulomatous inflammation

62
Q

morphology metastatic carcinoma adrenocortical insufficiency

A

adrenals enlarged, architecture obscured by neoplasm

63
Q

acute adrenocrotical insufficiency

A

exogenous steroids may develop acute crisis if rapid withdrawal
massive adrenal hemorrhage

64
Q

Waterhouse Friderichsen syndrome

A

classically from N. meningitidis

others-pseudomonas, pneumococci, H flu

65
Q

classification of adrenocortical neoplasm

A

according to clinical findings not morphology

66
Q

morphology adenomas

A

most nonfunctional

small (1-2 cm)

67
Q

morphology carcinomas

A

more likely to be functional

large, invasive, met by lymphatic and/or bloodstream

68
Q

derivation of adrenal medulla

A

neural crest

chromaffin cells

69
Q

pheochromocytoma rule of 10

A

10% tumor
10% bilateral
10% familial
10% malignant

70
Q

signs and symptoms of pheo

A

hypertension (risk of MI, HF, renal injury, and CVA)

tachycardia, palpitations, HA, sweating, tremor, sense of apprehension

71
Q

sudden death in pheo

A

increase catecholamines leading to myocardial instability and ventricualr arrhythmias

72
Q

morphology pheo

A

hemorrhage, necrotic, cystic
stain with silver stains
benign may have capsular and vascular invasion

73
Q

diagnosis of malignant pheo

A

by mets exclusively

74
Q

laboratory testing pheo

A

increased urinary excretion of free catecholamines, VMa, and dopamine

75
Q

origin neuroblastoma

A

neural crest

may arise anywhere in sympathetic chain

76
Q

signs and symptoms neuroblastoma less than 2 yrs

A

protuberant abdomen with abdomenal mass, fever, and weight loss
catecholamines (less likely to cause HTN)

77
Q

signs and symptoms neuroblastoma older

A

mets leading to hepatomegally, ascites, and bone pain

catecholamines (less likely to cause HTN)

78
Q

histology neuroblastoma

A

small, round blue cell tumors

Homer Wright pseudorosettes

79
Q

laboratory diagnosis neuroblastoma

A

increase serum catecholamines and VMA and HVA in urine

80
Q

prognosis neuroblastoma depending on genetics

A

deletion short arm ch1 aggressive

amplification of N-myc- poor prognosis

81
Q

MEN 1 syndrome

A

pituitary, parathyroid, pancreatic islet cell tumors (insulin, glucagon, gastrin, somatostatin, VIP)

82
Q

genetic mutation MEN 1

A

tumor suppressor on ch 11

83
Q

MEN IIa syndrome

A

medulla-thyroid medullary carcinoma, pheo
medullary carcinoma associated with C-cell hyperplasia
parathyroid disorder

84
Q

genetics MEN IIa

A

mutation RET on ch 10

85
Q

MEN IIb

A

thyroid medullary carcinoma and pheo
no parathyroid disorder
associated with neuromas and/or ganglioneuromas

86
Q

genetics MEN IIb

A

mutation in RET but different mutation than in MEN IIa

87
Q

beta cells islets of langerhans

A

insulin

88
Q

alpha cells islets of langerhans

A

glucagon

89
Q

delta cells islets of langerhans

A

somatostatin (suppresses release of insulin and glucagon)

90
Q

pancreatic polypeptide cells islets of langerhans

A

pancreatic polypeptide

91
Q

signs and symptoms type 1 DM

A

polyuria, polydipsia, polyphagia, ketoacidosis

catbolism leading to weight loss and muscle weakness

92
Q

ketoacidosis in type 1 DM

A

decrease insulin leads to excessive breakdown of fat

free fatty acids go to liver and are oxidized by acetyl coA to ketone bodies

93
Q

ketone bodies in ketoacidosis

A

acetoacetic acid and beta hydroxybuteric acid

94
Q

hyper-osmolar nonketotic coma

A

severe dehydration from sustained hyperglycemia
absence of ketoacidosis and symptoms
occurs in T2DM

95
Q

release of insulin

A

biphasic
release from granules when glucose increases
if persists glucose triggers insulin synthesis

96
Q

major anabolic hormone

A

insulin

97
Q

insulin receptor

A

tyrosine kinase

98
Q

genetic susceptibility T1DM

A

class II MHC most important
DR3/4
DQ302/602 linkage

99
Q

protective against diabetes

A

asparagine 57 on DQ beta chain

100
Q

insulinitis

A 
CD8 T lymphocytes with variable CD4T 
beta cells destroyed 
expression of class II HLA antigens on beta cells (normal is no expression)
101
Q

antibodies in T1DM

A

react to glutamic acid decarboxylase

102
Q

molecular mimicry in T1DM

A

GAD shares sequence with Coxsackie virus

103
Q

deranged beta-cell secretion of insulin in T2DM

A

early-disorder of insulin release (blunted first stage)

later-deficiency of insulin

104
Q

insulin resistance in T2DM

A

decrease in number of insulin receptors and problems in receptor signaling

105
Q

delay in complications of DM

A

control to delay complications

complications mainly due to hyperglycemia

106
Q

nonenzymatic glycosylation

A

glucose attached to free amino acid of protein w/o enzymes

traps LDL in vessel walls leading to atherogenesis

107
Q

complications of hyperglycemia in nerves, lens, kidney, blood vessels

A

do not require insulin for glucose to enter cells

glucose converted to sorbitol, increased influx of water leading to osmotic cell injury

108
Q

morphology islets in T1DM

A

reduction in number and size of islets

insulitis

109
Q

morphology islets in T2DM

A

subtle reduction in beta cell mass and amyloid deposits

110
Q

morphology vascular system DM

A

accelerated atherosclerosis leading to increased risk of MI

hyaline arteriosclerosis and diabetic microangiopathy

111
Q

hyaline arteriosclerosis

A

related to disease duration and degree of HTN

112
Q

diabetic microangiopathy

A

diffuse thickening of basement membrane (especially capillaries of skin, skeeltal muscle, retinas, renal glomeruli, renal medulla)
concentric hyaline of type IV collagen, makes membranes leaky

113
Q

diabetic nephropathy

A

second to MI as cause of death

thickened BM

114
Q

diffuse glomerulosclerosis

A

diffuse increase in mesangial matrix cell proliferation
thickened capillary BM
nephrotic syndrome, also deen in old age and HTN

115
Q

nodular glomerulosclerosis

A

nodules at periphery of glomerulus composed of mucopolysaccharides
impede flow of blood of efferent arterioles (tubular ischemia)
Kimmelstiel-Wislon nodules

116
Q

pyelonephritis

A

acute or chronic inflammation of kidneys beginning in interstitium and affecting tubules
common in diabetics
may lead to acute necrosis of papilla (necrotizing papillitis)

117
Q

nonproliferative diabetic neuropathy

A

intra-retinal or pre-retinal hemorrhages, retinal exudates, microaneurysms
edema and thickening of retinal capillaries (microangiopathy)

118
Q

proliferative diabetic neuropathy

A

neovascularization and fibrosis
may lead to blindness
vitreous hemorrhages can form
can pull retina-retinal detachment

119
Q

sorbitol deposition in eye

A

an lead to glaucoma and cataracts

120
Q

diabetes on the brain

A

microangiopathy
neuronal degradation
predisposed to CVA and brain hemorrhages

121
Q

diagnosis of diabetes fasting blood glucose

A

> 126 on more than 1 occasion

122
Q

prediabetes on fasting blood glucose

A

100-126

123
Q

glucose tolerance test diagnosis of diabetes

A

> 200 after 75 gm of glucose

124
Q

islet cell tumors

A

neuroendocrine origin

125
Q

insulinomas

A

secrete insulin leading to hypoglycemia
precipitated by fasting or exercise
neuropsych symptoms of nervousness, confusion, stupor

126
Q

morphology insulinoma

A

usually benign

look like giant islets

127
Q

differential diagnosis insulinoma

A

insulin sensitivity
liver disease
inherited glycogenoses
retroperitoneal fibromas or fibrosarcomas
factious-inject with insulin (measure C-peptide)

128
Q

Zollinger-Ellison syndrome

A

secrete gastrin-extreme gastric acid secretion

peptic ulcers in unusual locations (jejunum)

129
Q

signs and symptoms Zollinger-Ellison

A

epigastric pain

diarrhea

130
Q

morphology Zollinger-Ellison syndrome

A

may arise in pancreas, peripancreatic region, wall of duodenum
most are malignant

131
Q

laboratory diagnosis Zollinger-Ellison

A

limited rise in gastric acid secretion by gastrin injection

132
Q

treatment Zollinger Ellison

A

histamine (H2) blockers and excision of neoplasm

133
Q

pseudohypoparathyroidism type 1

A

diminished cAMP response resulting in round facies, short stature, short metacarpal and metatarsal bones (Albright Hereditary osteodystrophy)

134
Q

hashimoto

A 
HLA DR5
painless enlargement 
anti-TSH receptor blocks TSH
Germinal centers 
increased risk of B cell lymphomas
135
Q

medullary carcinoma of thyroid

A 
neuroendocrine tumor
secrete calcitonin 
RET protoncogene for MEN IIa/b
may have VIP causing diarrhea 
amyloid deposits, polygonal to spindle shaped cells
136
Q

Graves

A

papillae without fibrovascular core
colloid shows scalloping
due to autoantibodies

137
Q

thyroid adenoma

A

intact capsule but cannot differentiate on FNA so removed

138
Q

papillary carcinoma of thyroid

A

dense fibrovascular core and psammoma bodies

orphan annie nucleus

DT4 Exam 1 (5 decks)

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