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
2
Q
What are/is the etiology of hyposecretion of hormones?
A
agenesis - smaller gland
atrophy - less, no gland
destruction of the gland
3
Q
What is the etiology of hypersecretion of hormones?
A
tumor
hyperplasia
4
Q
Which gland is known as the “master gland”?
A
pituitary gland
5
Q
What connects the pituitary gland to the hypothalamus?
A
infundibulum stalk
6
Q
Which hormones are produced by the anterior pituitary gland?
A
TSH PRL ACTH GH FSH LH
“FLAT PiG” - mnemonic
7
Q
What hormones are found in the posterior pituitary?
A
oxytocin
ADH
8
Q
What cells are making the oxytocin and ADH for the posterior pituitary?
A
glial cells and axonal processes from the hypothalamus
9
Q
If there is hyperfunction of the anterior pituitary gland, what is associated with that?
A
adenoma
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
11
Q
How much of the anterior pituitary needs to be damaged before you begin seeing affects from postpartum ischemic necrosis?
A
75% damage
12
Q
What embryonic derivative is the anterior pituitary from?
A
derived from the primitive oral cavity - Rathke’s Pouch
13
Q
What embryonic derivative is the posterior pituitary from?
A
neuroectoderm
14
Q
Describe gigantism.
A
Growth that occurs before closure of the epiphyseal plates in the long bones
15
Q
What causes gigantism?
A
an adenoma in the anterior pituitary that secretes growth hormone
16
Q
What can you notice clinically in someone with gigantism?
A
generalized increase in body size
arms/legs disproportionally long
17
Q
Is there any treatment for someone with gigantism? If so, what is it?
A
yes, surgical removal of the ademona
18
Q
What is the prognosis of gigantism?
A
fair to good
19
Q
Describe acromegaly.
A
growth after closure of the epiphyseal plates
20
Q
What is the cause of acromegaly?
A
increase growth hormone due to an adenoma
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
22
Q
What is the treatment for acromegaly?
A
removal of adenoma
23
Q
What is the prognosis for acromegaly?
A
guarded - due to hypertension/congestive heart failure
24
Q
What are potential causes of pituitary dwarfism?
A
failure to produce growth hormone
lack of response to growth hormone
25
What is seen clinically in someone with pituitary dwarfism?
short stature
| small jaws & teeth
26
Describe treatment for pituitary dwarfism.
if lack of production of growth hormone, hormone replacement would be treatment
27
What is the prognosis for pituitary dwarfism?
good
28
What is the function of the thyroid gland?
produce hormones that regulate rate at which body carries out its necessary functions
29
What are some causes of hyperthyroidism?
diffuse toxic hyperplasia (graves disease)
goiter
adenoma
increased ingestion of exogenous thyroid hormone
30
How is hyperthyroidism diagnosed?
increased TH and descreased TSH levels
31
What are some clinical symptoms of hyperthyroidism?
```
hypermobility
tachycardia, palpations
exophthalmous (bulding eyes)
heat intolerance
excessive sweating
soft, warm, flushed skin
weight loss
malabsorption, diarrhea
```
32
What is a thyroid storm?
a sudden onset of hyperthyroidism triggered by stress
| pts often die of cardiac arrhythmias
33
How is hyperthyroidism treated?
dependent on cause
| reactive iodine can be used to destroy overactive thyroid tissue
34
Prognosis of hyperthyroidism.
good if identified and tx properly
35
What is the prevalence of Graves disease in women vs men?
7:1 more common in females
36
Describe Graves Disease.
Autoimmune disease (genetic component) w/ antibodies to TSH receptor --> so TSH receptor is constantly stimulated
37
What can occur due to Graves disease?
hyperthyroidism
exophthalmos
skin lesions - pretibial myxedema
38
What is the etiology of hypothyroidism?
```
iodine deficiency
autoimmune destruction (Hashimotos)
ablation by surgery or radiation
```
39
What are some clinical features in someone with hypothyroidism?
cretinism (infancy or childhood) - learning disability
| myxedema - older children and adults
40
Describe clinical cretinism.
short stature
severe mental retardation
protruding tongue
impaired development of skeleton and CNS
41
Describe clinical myxedema
```
generalized apathy
mental sluggishness
obesity
cold intolerance
enlarged tongue
```
42
Is serum TSH increased during hypothyroidism?
yes, in primary cases due to loss of feedback. NOT in cases caused by primary hypothalamic or pituitary disease
43
What is the treatment for hypothyroidism?
hormone replacement
44
What is the prognosis for hypothyroidism?
good unless treatment is delayed (CNS damage could be permanent)
45
What are some facial features of myxedema?
```
periorbital edema
swollen lips
puffy, pale face
lateral eyebrows thin
sparse, course hair
```
46
What is the predominance in female vs male for Hashimoto thyroiditis?
10:1 more prominent in females
47
What is Hashimoto thyroiditis?
an autoimmune disease - progressive destruction of the thyroid gland
48
Will having Hashimotos put you at risk for other autoimmune diseases?
yes, and B-cell non-Hodgkin lymphomas
49
What causes goiters?
dietary deficiency of iodine
50
What is seen clinically from goiters?
cosmetic issues (large mass)
airway obstruction
dysphagia
compression of vessels
51
Who is most likely to have neoplastic thyroid nodules?
males and young patients
52
What commonly contributes to thyroid neoplasms?
genetic and environmental factors such as radiation exposure in the first 2 decades
53
What is the most common thyroid cancer?
papillary thyroid carcinoma
54
Who is affected by papillary thyroid carcinoma?
females in their 3rd-5th decade of life
55
What mutation is related with papillary thyroid carcinoma?
RET proto-oncogene mutation
56
What is the 10 year survival rate for someone with papillary thyroid carcinoma?
95%
57
NOTE:
histologically - papillary thyroid carcinoma has "orphan Annie nuclei"
- pathologically there are many nuclear changes
58
Who is affected by follicular thyroid carcinoma?
patients older than their 5th decade w/ possible dietary iodine deficiency
59
What is follicular thyroid carcinoma similar to?
follicular adenoma, so be sure you see invasion through the capsule or into blood vessels
60
What cell(s) is medullary thyroid carcinoma arising from?
parafollicular C cells
61
What is increased in the serum when looking at lab results for medullary thyroid carcinoma?
calcitonin
62
What gene is mutated in medullary thyroid carcinoma?
RET proto-oncogene
63
What type of cells make up the parathyroid glands?
chief cells and oxyphil cells
64
What is the function of chief cells?
secrete parathyroid hormone - regulates blood calcium levels
65
What controls parathyroid hormone release?
decreased levels of blood calcium - no pituitary or hypothalamic stimulation
66
What happens in the body as a result of PTH?
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
What is an important cause to hypercalcemia?
hyperparathyroidism
68
What are the 2 types of hyperparathyroidism?
primary
| secondary
69
Describe primary hyperparathyroidism.
an autonomous spontaneous overproduction of PTH
70
Describe secondary hyperparathyroidism.
secondary to chronic renal failure
71
What does primary hyperparathyroidism result from?
parathyroid hyperplasia or adenoma
72
Who usually presents with primary hyperparathyroidism?
adult females more often than males
73
What are some clinical symptoms of primary hyperparathyroidism?
"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
In the oral cavity (or other bones), what can happen/appear as a result from primary hyperparathyroidism?
ground glass appearance of bone
| Brown tumor
75
Can blood tests detect clinically silent hyperparathyroidism?
yes
76
Which is often more severe primary or secondary hyperparathyroidism?
secondary hyperparathyroidism
77
What does renal insufficiency lead to in secondary hyperparathyroidism?
hyperphosphatemia
78
Describe hyperphosphatemia.
increased amounts of phosphate in the blood b/c of decreased excretion
79
What results from hyperphosphatemia?
decreased serum calcium levels which increases PTH secretion
80
Aside from renal failure, what else can cause secondary hyperparathyroidism?
damaged kidneys unable to produce vitamin D
81
What happens due to decreased Vitamin D?
reduced calcium absorption in the intestines, PTH secretion is increased
82
Are serum calcium levels normal or decreased in secondary hyperparathyroidism?
levels are near normal b/c excess PTH is compensating for lack of calcium
83
What are the clinical symptoms for secondary hyperparathyroidism?
same as primary.
Bones, stones, ...etc....
you can also get renal osteodystrophy
84
Describe treatment options for hyperparathyroidism.
surgical removal of hyperplastic parathyroid glands
| kidney transplant
85
Prognosis of hyperparathyroidism
typically good
86
What can contribute to causing hypoparathyroidism?
DiGeorge's syndrome;
| autoimmune disease
87
What is produced from the exocrine function of the pancreas?
gastric enzymes
88
What makes up the endocrine pancreas?
islets of Langerhans
89
What cells make up these islets of Langerhans in the endocrine portion of the pancreas?
beta cells
alpha cells
delta cells
PP cells
90
What do beta cells produce?
insulin
91
What do alpha cells produce?
glucagon
92
What do delta cells produce?
somatostatin
93
What do PP cells produce?
VIP - pancreatic polypeptide
94
What is the function of glucagon?
mobilizes carbs stored in the liver into circulation
| promotes glycogenolysis and gluconeogenesis
95
What is the function of insulin?
allows glucose to be transported and stored in cells within the body after meals
96
What is the function of somatostatin?
suppresses both insulin and glucagon release
97
What does VIP do?
exerts several GI effects
98
Describe diabetes mellitus.
metabolic disorders resulting in hyperglycemia
Type I and II
caused by deficient production or response to insulin
99
What is the range for normal blood glucose levels?
70-120 mg/dL
100
Any one of the following criteria qualifies someone as diabetic:
random glycemia > or equal to 200 mg/dL
fasting glucose > or equal to 126
abnormal glucose tolerance test
101
What 3 processes is homeostasis dependent upon?
gluconeogenesis
glucose uptake by tissues
actions of insulin and glucagon
102
Describe diabetes mellitus type I.
chronic autoimmune disease where beta cells are destroyed by self-activated T-cells and autoantibodies
103
What are some clinical features in people with type I diabetes?
normal weight
decreased blood insulin
younger than 20 when diagnosed
autoantibodies are detectable in the blood of 70-80% of patients
104
When will someone with type I diabetes see symptoms?
Once 90% of beta cells are destroyed
105
What are symptoms of type I diabetes?
polydipsia (excessive thirst)
polyuria
polyphagia (excessive hunger)
ketoacidosis - excessive breakdown of fats - accumulation of ketoacids in blood
106
Describe treatment for type I diabetes.
insulin
| kidney/pancreas transplant (Ab may still attack donor tissue)
107
Prognosis of diabetes type I.
guarded ---> many complications arise from this
108
How can type II diabetes mellitus arise?
insulin resistance
| decreased insulin secretion
109
What are some clinical features of someone with type II diabetes?
onset after age 40
obesity
normal or increased blood insulin levels
increased susceptibility to infection
110
Describe treatment for type II diabetes.
weight loss, improved diet
oral hypoglycemic drugs
insulin
111
What is prognosis for type II diabetics?
fair, not as severe as type I diabetes
112
What are some manifestations in the pancreas due to diabetes?
destruction of islets
heavy inflammatory infiltrate
amyloid (abnormal protein)
113
What are some vasculopathy manifestations from diabetes that occur?
```
atherosclerosis
myocardial infarction
stroke
gangrene
thickened basement membrane
```
114
What are some other manifestations of diabetes?
```
diabetic nephropathy
glomerular lesions (glomerular sclerosis)
nodular glomerulosclerosis
blindness
neuropathy
```
115
Is it possible to have an islet cell tumor?
Yes, but they are uncommon. Can be functional or non-functional
116
What is an insulinoma?
an insulin secreting islet cell tumor
117
What tissues does a gastrinoma arise from?
duodenum, peripancreatic tissues, or pancreas
118
Who is susceptible to gastrinomas?
90-95% of patients with peptic ulcers get these
119
What is Zollinger-Ellison Syndrome?
tumors causing the stomach to produce too much acid.
120
What hormones are produced by the adrenal glands, specifically the adrenal cortex?
cortisol/cortisone
aldosterone
estrogen
progesterone
121
What hormones are produced from the adrenal medulla?
Catecholamines
epinephrine
norepinephrine
dopamine?
122
What are the two types of hyperadrenalism?
hypercortisolism (Cushing's Syndrome)
| hyperaldosteronism
123
What are some causes of Cushing's Syndrome?
Excess administration of exogenous glucocorticoids
primary adrenal hyperplasia/neoplasm
ACTH oversecretion by pituitary microadenoma
Ectopic ACTH secretion by neoplasm
124
What are some short term clinical signs of Cushing's Syndrome?
weight gain
hypertension
moon facies (fat in the face)
buffalo hump
125
What are some long term clinical features of Cushing's Syndrome?
```
decreased muscle mass
weakness
diabetes
osteoporosis
cutaneous striae
depression/mood swings
menstrual irregularities
```
126
What is the prognosis for Cushing's Syndrome?
good
127
What can occur if you have hyperaldosteronism?
sodium retention, potassium excretion
hypertension
hypokalemia
128
What are the types of hyperaldosteronism?
primary and secondary
129
Describe primary hyperaldosteronism.
very rare
decreased levels of plasma renin
hyperplasia, neoplasm
130
Describe secondary hyperaldosteronism.
aldosterone release in response to activation of renin - angiotensin system
increased levels of plasma renin
131
What are the different types of hypoadrenalism?
primary or secondary
132
What happens during secondary hypoadrenalism?
decreased stimulation of adrenals from deficiency of ACTH
| 90% of glands must be destroyed before seeing symptoms
133
What are some manifestations of hypoadrenalism?
weakness
fatigue
GI disturbances (anorexia, nausea, vomiting, weight loss, diarrhea)
