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Gen Path > Exam 3 - Endocrine > Flashcards

Exam 3 - Endocrine Flashcards

1
Q

What are the 7 (or 8) major glands of the endocrine system?

A 
pancreas
pituitary
thyroid
parathyroid
adrenal
thymus
ovary/testis
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2
Q

What are/is the etiology of hyposecretion of hormones?

A

agenesis - smaller gland
atrophy - less, no gland
destruction of the gland

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3
Q

What is the etiology of hypersecretion of hormones?

A

tumor

hyperplasia

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4
Q

Which gland is known as the “master gland”?

A

pituitary gland

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5
Q

What connects the pituitary gland to the hypothalamus?

A

infundibulum stalk

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6
Q

Which hormones are produced by the anterior pituitary gland?

A 
TSH
PRL
ACTH
GH
FSH
LH

“FLAT PiG” - mnemonic

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7
Q

What hormones are found in the posterior pituitary?

A

oxytocin

ADH

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8
Q

What cells are making the oxytocin and ADH for the posterior pituitary?

A

glial cells and axonal processes from the hypothalamus

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9
Q

If there is hyperfunction of the anterior pituitary gland, what is associated with that?

A

adenoma

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10
Q

What is the cause of hypofunction of the anterior pituitary?

A

nonfunctional pituitary adenoma
postpartum ischemic necrosis
ablation/destruction via surgery, radiation, adjacent tumor surgery

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11
Q

How much of the anterior pituitary needs to be damaged before you begin seeing affects from postpartum ischemic necrosis?

A

75% damage

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12
Q

What embryonic derivative is the anterior pituitary from?

A

derived from the primitive oral cavity - Rathke’s Pouch

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13
Q

What embryonic derivative is the posterior pituitary from?

A

neuroectoderm

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14
Q

Describe gigantism.

A

Growth that occurs before closure of the epiphyseal plates in the long bones

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15
Q

What causes gigantism?

A

an adenoma in the anterior pituitary that secretes growth hormone

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16
Q

What can you notice clinically in someone with gigantism?

A

generalized increase in body size

arms/legs disproportionally long

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17
Q

Is there any treatment for someone with gigantism? If so, what is it?

A

yes, surgical removal of the ademona

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18
Q

What is the prognosis of gigantism?

A

fair to good

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19
Q

Describe acromegaly.

A

growth after closure of the epiphyseal plates

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20
Q

What is the cause of acromegaly?

A

increase growth hormone due to an adenoma

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21
Q

What is seen clinically in someone with acromegaly?

A

enlarged bones of the hands, feet, and face
prognathism, diastemas
hypertension
congestive heart failure

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22
Q

What is the treatment for acromegaly?

A

removal of adenoma

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23
Q

What is the prognosis for acromegaly?

A

guarded - due to hypertension/congestive heart failure

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24
Q

What are potential causes of pituitary dwarfism?

A

failure to produce growth hormone

lack of response to growth hormone

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25
Q

What is seen clinically in someone with pituitary dwarfism?

A

short stature

small jaws & teeth

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26
Q

Describe treatment for pituitary dwarfism.

A

if lack of production of growth hormone, hormone replacement would be treatment

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27
Q

What is the prognosis for pituitary dwarfism?

A

good

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28
Q

What is the function of the thyroid gland?

A

produce hormones that regulate rate at which body carries out its necessary functions

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29
Q

What are some causes of hyperthyroidism?

A

diffuse toxic hyperplasia (graves disease)
goiter
adenoma
increased ingestion of exogenous thyroid hormone

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30
Q

How is hyperthyroidism diagnosed?

A

increased TH and descreased TSH levels

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31
Q

What are some clinical symptoms of hyperthyroidism?

A 
hypermobility
tachycardia, palpations
exophthalmous (bulding eyes)
heat intolerance
excessive sweating
soft, warm, flushed skin
weight loss
malabsorption, diarrhea
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32
Q

What is a thyroid storm?

A

a sudden onset of hyperthyroidism triggered by stress

pts often die of cardiac arrhythmias

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33
Q

How is hyperthyroidism treated?

A

dependent on cause

reactive iodine can be used to destroy overactive thyroid tissue

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34
Q

Prognosis of hyperthyroidism.

A

good if identified and tx properly

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35
Q

What is the prevalence of Graves disease in women vs men?

A

7:1 more common in females

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36
Q

Describe Graves Disease.

A

Autoimmune disease (genetic component) w/ antibodies to TSH receptor –> so TSH receptor is constantly stimulated

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37
Q

What can occur due to Graves disease?

A

hyperthyroidism
exophthalmos
skin lesions - pretibial myxedema

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38
Q

What is the etiology of hypothyroidism?

A 
iodine deficiency
autoimmune destruction (Hashimotos)
ablation by surgery or radiation
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39
Q

What are some clinical features in someone with hypothyroidism?

A

cretinism (infancy or childhood) - learning disability

myxedema - older children and adults

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40
Q

Describe clinical cretinism.

A

short stature
severe mental retardation
protruding tongue
impaired development of skeleton and CNS

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41
Q

Describe clinical myxedema

A 
generalized apathy
mental sluggishness 
obesity
cold intolerance
enlarged tongue
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42
Q

Is serum TSH increased during hypothyroidism?

A

yes, in primary cases due to loss of feedback. NOT in cases caused by primary hypothalamic or pituitary disease

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43
Q

What is the treatment for hypothyroidism?

A

hormone replacement

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44
Q

What is the prognosis for hypothyroidism?

A

good unless treatment is delayed (CNS damage could be permanent)

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45
Q

What are some facial features of myxedema?

A 
periorbital edema
swollen lips
puffy, pale face
lateral eyebrows thin
sparse, course hair
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46
Q

What is the predominance in female vs male for Hashimoto thyroiditis?

A

10:1 more prominent in females

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47
Q

What is Hashimoto thyroiditis?

A

an autoimmune disease - progressive destruction of the thyroid gland

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48
Q

Will having Hashimotos put you at risk for other autoimmune diseases?

A

yes, and B-cell non-Hodgkin lymphomas

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49
Q

What causes goiters?

A

dietary deficiency of iodine

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50
Q

What is seen clinically from goiters?

A

cosmetic issues (large mass)
airway obstruction
dysphagia
compression of vessels

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51
Q

Who is most likely to have neoplastic thyroid nodules?

A

males and young patients

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52
Q

What commonly contributes to thyroid neoplasms?

A

genetic and environmental factors such as radiation exposure in the first 2 decades

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53
Q

What is the most common thyroid cancer?

A

papillary thyroid carcinoma

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54
Q

Who is affected by papillary thyroid carcinoma?

A

females in their 3rd-5th decade of life

55
Q

What mutation is related with papillary thyroid carcinoma?

A

RET proto-oncogene mutation

56
Q

What is the 10 year survival rate for someone with papillary thyroid carcinoma?

A

95%

57
Q

NOTE:

A

histologically - papillary thyroid carcinoma has “orphan Annie nuclei”
- pathologically there are many nuclear changes

58
Q

Who is affected by follicular thyroid carcinoma?

A

patients older than their 5th decade w/ possible dietary iodine deficiency

59
Q

What is follicular thyroid carcinoma similar to?

A

follicular adenoma, so be sure you see invasion through the capsule or into blood vessels

60
Q

What cell(s) is medullary thyroid carcinoma arising from?

A

parafollicular C cells

61
Q

What is increased in the serum when looking at lab results for medullary thyroid carcinoma?

A

calcitonin

62
Q

What gene is mutated in medullary thyroid carcinoma?

A

RET proto-oncogene

63
Q

What type of cells make up the parathyroid glands?

A

chief cells and oxyphil cells

64
Q

What is the function of chief cells?

A

secrete parathyroid hormone - regulates blood calcium levels

65
Q

What controls parathyroid hormone release?

A

decreased levels of blood calcium - no pituitary or hypothalamic stimulation

66
Q

What happens in the body as a result of PTH?

A

increased renal tubular reabsorption of calcium
increased urinary phosphate excretion
increased renal conversion of vitamin D inot its active form –> increases gastrointestinal calcium absorption
increases osteoclastic activity to release calcium from bones

67
Q

What is an important cause to hypercalcemia?

A

hyperparathyroidism

68
Q

What are the 2 types of hyperparathyroidism?

A

primary

secondary

69
Q

Describe primary hyperparathyroidism.

A

an autonomous spontaneous overproduction of PTH

70
Q

Describe secondary hyperparathyroidism.

A

secondary to chronic renal failure

71
Q

What does primary hyperparathyroidism result from?

A

parathyroid hyperplasia or adenoma

72
Q

Who usually presents with primary hyperparathyroidism?

A

adult females more often than males

73
Q

What are some clinical symptoms of primary hyperparathyroidism?

A

“painful bones, stones, abdominal groans, and psychic moans”
bones - fractures associated w/ osteoporosis
stones - kidney stones
abdominal groans - constipation, peptic ulcers, gallstones
psychic moans - depression, lethargy, seizures

74
Q

In the oral cavity (or other bones), what can happen/appear as a result from primary hyperparathyroidism?

A

ground glass appearance of bone

Brown tumor

75
Q

Can blood tests detect clinically silent hyperparathyroidism?

A

yes

76
Q

Which is often more severe primary or secondary hyperparathyroidism?

A

secondary hyperparathyroidism

77
Q

What does renal insufficiency lead to in secondary hyperparathyroidism?

A

hyperphosphatemia

78
Q

Describe hyperphosphatemia.

A

increased amounts of phosphate in the blood b/c of decreased excretion

79
Q

What results from hyperphosphatemia?

A

decreased serum calcium levels which increases PTH secretion

80
Q

Aside from renal failure, what else can cause secondary hyperparathyroidism?

A

damaged kidneys unable to produce vitamin D

81
Q

What happens due to decreased Vitamin D?

A

reduced calcium absorption in the intestines, PTH secretion is increased

82
Q

Are serum calcium levels normal or decreased in secondary hyperparathyroidism?

A

levels are near normal b/c excess PTH is compensating for lack of calcium

83
Q

What are the clinical symptoms for secondary hyperparathyroidism?

A

same as primary.
Bones, stones, …etc….
you can also get renal osteodystrophy

84
Q

Describe treatment options for hyperparathyroidism.

A

surgical removal of hyperplastic parathyroid glands

kidney transplant

85
Q

Prognosis of hyperparathyroidism

A

typically good

86
Q

What can contribute to causing hypoparathyroidism?

A

DiGeorge’s syndrome;

autoimmune disease

87
Q

What is produced from the exocrine function of the pancreas?

A

gastric enzymes

88
Q

What makes up the endocrine pancreas?

A

islets of Langerhans

89
Q

What cells make up these islets of Langerhans in the endocrine portion of the pancreas?

A

beta cells
alpha cells
delta cells
PP cells

90
Q

What do beta cells produce?

A

insulin

91
Q

What do alpha cells produce?

A

glucagon

92
Q

What do delta cells produce?

A

somatostatin

93
Q

What do PP cells produce?

A

VIP - pancreatic polypeptide

94
Q

What is the function of glucagon?

A

mobilizes carbs stored in the liver into circulation

promotes glycogenolysis and gluconeogenesis

95
Q

What is the function of insulin?

A

allows glucose to be transported and stored in cells within the body after meals

96
Q

What is the function of somatostatin?

A

suppresses both insulin and glucagon release

97
Q

What does VIP do?

A

exerts several GI effects

98
Q

Describe diabetes mellitus.

A

metabolic disorders resulting in hyperglycemia
Type I and II
caused by deficient production or response to insulin

99
Q

What is the range for normal blood glucose levels?

A

70-120 mg/dL

100
Q

Any one of the following criteria qualifies someone as diabetic:

A

random glycemia > or equal to 200 mg/dL
fasting glucose > or equal to 126
abnormal glucose tolerance test

101
Q

What 3 processes is homeostasis dependent upon?

A

gluconeogenesis
glucose uptake by tissues
actions of insulin and glucagon

102
Q

Describe diabetes mellitus type I.

A

chronic autoimmune disease where beta cells are destroyed by self-activated T-cells and autoantibodies

103
Q

What are some clinical features in people with type I diabetes?

A

normal weight
decreased blood insulin
younger than 20 when diagnosed
autoantibodies are detectable in the blood of 70-80% of patients

104
Q

When will someone with type I diabetes see symptoms?

A

Once 90% of beta cells are destroyed

105
Q

What are symptoms of type I diabetes?

A

polydipsia (excessive thirst)
polyuria
polyphagia (excessive hunger)
ketoacidosis - excessive breakdown of fats - accumulation of ketoacids in blood

106
Q

Describe treatment for type I diabetes.

A

insulin

kidney/pancreas transplant (Ab may still attack donor tissue)

107
Q

Prognosis of diabetes type I.

A

guarded —> many complications arise from this

108
Q

How can type II diabetes mellitus arise?

A

insulin resistance

decreased insulin secretion

109
Q

What are some clinical features of someone with type II diabetes?

A

onset after age 40
obesity
normal or increased blood insulin levels
increased susceptibility to infection

110
Q

Describe treatment for type II diabetes.

A

weight loss, improved diet
oral hypoglycemic drugs
insulin

111
Q

What is prognosis for type II diabetics?

A

fair, not as severe as type I diabetes

112
Q

What are some manifestations in the pancreas due to diabetes?

A

destruction of islets
heavy inflammatory infiltrate
amyloid (abnormal protein)

113
Q

What are some vasculopathy manifestations from diabetes that occur?

A 
atherosclerosis
myocardial infarction
stroke
gangrene
thickened basement membrane
114
Q

What are some other manifestations of diabetes?

A 
diabetic nephropathy
glomerular lesions (glomerular sclerosis)
nodular glomerulosclerosis
blindness
neuropathy
115
Q

Is it possible to have an islet cell tumor?

A

Yes, but they are uncommon. Can be functional or non-functional

116
Q

What is an insulinoma?

A

an insulin secreting islet cell tumor

117
Q

What tissues does a gastrinoma arise from?

A

duodenum, peripancreatic tissues, or pancreas

118
Q

Who is susceptible to gastrinomas?

A

90-95% of patients with peptic ulcers get these

119
Q

What is Zollinger-Ellison Syndrome?

A

tumors causing the stomach to produce too much acid.

120
Q

What hormones are produced by the adrenal glands, specifically the adrenal cortex?

A

cortisol/cortisone
aldosterone
estrogen
progesterone

121
Q

What hormones are produced from the adrenal medulla?

A

Catecholamines
epinephrine
norepinephrine
dopamine?

122
Q

What are the two types of hyperadrenalism?

A

hypercortisolism (Cushing’s Syndrome)

hyperaldosteronism

123
Q

What are some causes of Cushing’s Syndrome?

A

Excess administration of exogenous glucocorticoids
primary adrenal hyperplasia/neoplasm
ACTH oversecretion by pituitary microadenoma
Ectopic ACTH secretion by neoplasm

124
Q

What are some short term clinical signs of Cushing’s Syndrome?

A

weight gain
hypertension
moon facies (fat in the face)
buffalo hump

125
Q

What are some long term clinical features of Cushing’s Syndrome?

A 
decreased muscle mass
weakness
diabetes
osteoporosis
cutaneous striae
depression/mood swings
menstrual irregularities
126
Q

What is the prognosis for Cushing’s Syndrome?

A

good

127
Q

What can occur if you have hyperaldosteronism?

A

sodium retention, potassium excretion
hypertension
hypokalemia

128
Q

What are the types of hyperaldosteronism?

A

primary and secondary

129
Q

Describe primary hyperaldosteronism.

A

very rare
decreased levels of plasma renin
hyperplasia, neoplasm

130
Q

Describe secondary hyperaldosteronism.

A

aldosterone release in response to activation of renin - angiotensin system
increased levels of plasma renin

131
Q

What are the different types of hypoadrenalism?

A

primary or secondary

132
Q

What happens during secondary hypoadrenalism?

A

decreased stimulation of adrenals from deficiency of ACTH

90% of glands must be destroyed before seeing symptoms

133
Q

What are some manifestations of hypoadrenalism?

A

weakness
fatigue
GI disturbances (anorexia, nausea, vomiting, weight loss, diarrhea)

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