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Exam 1 - Endocrine > Endocrine Pathology > Flashcards

Endocrine Pathology Flashcards

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1
Q

2 hormones secreted by posterior pituitary (and sites of action)

A

oxytocin (breast) and ADH (kidney)

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2
Q

vascular supply of anterior v. posterior pituitary

A

Anterior only has a single system: portal vascular system that’s a conduit from the hypothalamus.
The posterior has dual circulation (arteries/veins and the portal venous system). Means anterior is more susceptible to ischemia!

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3
Q

What type of cells comprise the posterior pituitary?

A

modified glial cells (pituicytes) and axonal processes (so it’s almost like brain tissue)

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4
Q

embryo derivative of anterior v. posterior

A 
anterior = Rathke's pouch
posterior = floor of the 3rd ventricle
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5
Q

Name the two inhibitory hormones from the hypothalamus. What do they act on?

A

Dopamine - aka PIF: inhibits prolactin release

Somatostatin - aka GIH: inhibits growth hormone release

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6
Q

Name the 2 acidophilic and 3 basophilic cells of the anterior pituitary

A 
Acidophils = Somatotrophs (GH) and Lactotrophs (Prolactin)
Basophils = Corticotrophs (ACTH), Thyrotrophs (TSH), and Gonadotrophs (FSH and LH)
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7
Q

2 ways to know microscopically if there is a pituitary adenoma

A
  1. homogenous appearance of one cell type

2. decreased reticulin fibers (histo slide looks like little islands in a sea of spots)

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8
Q

Function of Dopamine

A

prevents pituitary from releasing prolactin, which is not needed in everyday life. So usually we are in a constant dopamine inhibitory state

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9
Q

Stalk effect

A

less common cause of hyperprolactinemia than an adenoma = mass in suprasellar compt that disturbs the usual hypothalamic inhibitory effect of dopamine on prolactin

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10
Q

(4) presenting sx of prolactinoma

A

amenorrhea, infertility, loss of libido, and galactorrhea (abnormally high flow of milk in lactating woman or secretion of milk from nonlactating person)

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11
Q

Pharm tx of prolactinoma

A

Bromocriptine (dopamine analog)

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12
Q

increased GH in a GH Adenoma stimulates increased secretion of? What does this cause?

A

IGF-1. This is the cause of gigantism in kids and acromegaly in adults

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13
Q

Oral glucose challenge

A

High glucose should suppress GH production. If failure to suppress GH, is a very sensitive test for acromegaly.

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14
Q

Cushing syndrome v. Cushing Disease

A

Syndrome = the general state of excess ACTH leading to hypersecretion of cortisal from adrenals

Disease = specifically a pituitary adenoma as the culprit for the hypercortisolism

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15
Q

Name 4 not so obvious Cushing’s sx

A

osteoporosis, cardiac hypertrophy (HTN), amenorrhea, and skin ulcers with poor wound healing

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16
Q

What is required to dx a pituitary carcinoma?

A

must demonstrate metastases. pituitary carcinomas are very rare

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17
Q

Fxn of Oxytocin

A

stimulates contraction of uterine smooth muscle and cells of lactiferous ducts in mammary glands

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18
Q

Blood Na levels in Diabetes Insipidus pt

A

HYPERnatremia. Urine is dilute w/ low spec gravity

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19
Q

Blood Na levels in SIADH

A

HYPOnatremia - b/c absorbing to much water due to excess ADH

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20
Q

What condition often leads to SIADH?

A

ectopic ADH secretion from small cell carcinoma of the lung (paraneoplastic syndrome)

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21
Q

What lymph node sits behind the thyroid

A

Delphian lymph node

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22
Q

How do T3 and T4 travel in the serum?

A

Bound to thyroxine binding globulin, Albumin, and Transthyretin proteins

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23
Q

Name of the genes that thyroid hormone has an effect on. What effect is it?

A

TREs = the thyroid hormone response elements in target genes upregulating transcription. Think of thyroid hormones as UPregulators

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24
Q

Binding of T4 v. T3 to nuclear receptors

A

T3 binds with 10 x affinity of T4 to the nuclear receptors

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25
(4) effects of thyroid hormones
1. Breaks down lipids and carbs 2. Makes proteins 3. Critical role in brain development (why absence of thyroid hormone during fetal/neonatal development = profound intellectual stunting) 4. Overall: Increased Basal Metabolic Rate!
26
(2) functions of Calcitonin
1. promotes bones to take up Ca out of the blood | 2. inhibits osteoclasts from resorbing bone
27
Thyroid storm
abrupt onset of severe hyperthyroidism. emergent b/c can cause heart arrhythmia
28
Most useful screening test for hypo or hyperthyroidism. Follow up confirmation test?
Serum TSH. Will be low in primary hyperthyroid and high in secondary hyperthyroid. Usually confirmed w/ an elevated serum FT4
29
Grave's Disease Triad
hyperthyroidism, exopthalmos (from infiltrative ophthalmopathy), and infiltrative dermopathy (pretibial myxedema)
30
mechanism of Grave's disease
an autoimmune disease with auto-Abs most commonly to the TSH receptor. Abs could also be against thyroglobulin and thyroid peroxidase
31
(3) gene defects associated w/ Grave's disease
PTPN22 CTLA-4 HLA-DR3
32
(4) reasons for the exopthalmopathy in Graves
1. T cells infiltrate (and take up space) in retro-orbits 2. Inflammation causes edema and swelling of ocular muscles 3. Accumulation of extracellular matrix 4. Increased adipocytes
33
expected lab findings in Grave's for TSH, T3/T4, and Iodine uptake
low TSH, high T3/T4, and high iodine uptake that is DIFFUSE
34
Primary v. Secondary v. Tertiary Hypothyroidism (and 2 examples of primary)
Primary: actual thyroid is problem. Hashimoto's or surgery/radiation Secondary: pituitary is problem = TSH deficiency Tertiary: hypothalamus is problem = TRH deficiency
35
TSH in primary v. secondary/tertiary hypothyroidism
primary hypothyroidism = high TSH | secondary/tertiary = low TSH
36
cretinism
hypothyroidism that develops during infancy or early childhood. most cases due to lack of dietary iodine
37
Effect of cretinism. Name 5 sx
``` Effect = impaired development of skeletal system and CNS. Sx = Severe mental retardation, short stature, wide set eyes, coarse facial features, and large protruding tongue ```
38
Myxedema, def and how it presents
the counterpart to cretinism (hypothyroidism) in older child or adult. It progresses slowly over time w/ slowing of mental and physical activity. Sx = fatigue, cold intolerance, and apathy.
39
(4) physical signs of myxedema
``` Face = edema of face and eyelids, coarsening of facial features Heart = cardiomegaly with slow pulse Hair = dry and brittle ```
40
(3) pathways by which the thyroid epithelium is damaged in Hashimoto's thyroiditis and the unifying pathogenesis behind them
Big idea: breakdown in self-tolerance and autoimmune destruction of thyroid 1. T-cell mediated: CD8+ cytotoxic T cells destroy thyrocytes 2. Cytokine-mediated: excessive T-cell activation makes cytokines (interferon gamma!), which recruits/activates macrophages that damage thyrocytes 3. Ab-mediated: anti-thyroid Abs bind to thyrocytes. Then NKs come along, attach to bound Abs and murder
41
What does Hashimoto's thyroid look like under the microscope? Grossly?
Lots of inflammation seen w/ infiltration of lymphocytes, plasma cells, macrophages w/ germinal center formation Thyroid looks pale and enlarged
42
What are Hurthle cells? 2 associated conditions?
thyroid follicle cells with a crap ton of esoinophilic cytoplasm that look fluffy and pink. Seen in Hashimoto's Thyroiditis AND in thyroid adenomas.
43
Labs seen in clinical course of Hashimoto's Thyroiditis
[may first see a transient hyperthyroidism = low TSH and high FT4/FT3] Once hypothyroidism begins, T4 and T3 levels = low with compensatory high TSH
44
One important association with Hashimoto's Thyroiditis
slightly increased risk of lymphoma
45
2 other name for de Quervain Thyroidits
Subacute Thyroiditis or Granulomatous Thyroiditis
46
etiology of Subacute (granulomatous) Thyroiditis
aka de Quervain Thyroiditis. Believed to be post-viral etiology. Ex. Hx of URI from coxsackie, mumps, measles, or adenovirus
47
microscopic appearance of Subacute Thyroiditis
aka de Quervain or Granulomatous Thyroiditis. Ergo, see multinucleated giant cells surrounding pools of colloid
48
What happens to thyroid hormone in Subacute Thyroiditis?
1st get transient hypERthyroidism, then get transient hyPOthyroidism. Then you completely recover
49
Clinical presentation of Subacute (granulomatous) v. Subacute Lymphocytic Thyroiditis
Granulomatous: neck pain sometimes radiating to throat, jaw, ears, esp w/ swallowing Lymphocytic: PAINLESS thyroiditis with nonspecific lymphoid infiltrate of thyroid
50
Reidel's Thyroiditis
rare disorder of unknown cause. Get fibrosis all up in the thyroid. Can form a fixed mass mimicking a carcinoma. Cause obstruction and, thus, HYPOthyroidism
51
Why does a goiter form?
due to impaired synthesis of thyroid hormone, most common cause is iodine deficiency
52
How does a multinodular goiter form?
starts as a simple goiter that involutes over and over again
53
Plummer syndrome. What is it? Compare to Grave's
occasionally happens w/ a multinodular goiter where a nodule becomes hyperfunctioning and get hyperthyroidism. These "hot" nodules will [ ] the radioiodine v. Grave's that has even iodine uptake
54
(4) clinical criteria for what makes a thyroid nodule more likely neoplastic
1. solitary nodules more likely neoplastic than multiple nodules 2. nodules in younger pts (<40) more likely neoplastic 3. nodules in males more likely neoplastic 4. "hot" nodules (take up radioactive iodine) are more likely BENIGN
55
cell derivation of thyroid adenomas
thyroid follicular epithelium
56
even though thyroid carcinomas are rare, what is the most common type of thyroid carcinoma? How/where does it manifest?
papillary carcinoma. First manifests as a mass in a cervical lymph node. Great prognosis w/ 95% survival rate
57
how the diagnosis made for papillary carcinoma v. follicular carcinoma?
Papillary: dx made on way nucleus looks! Empty nuclei devoid of nucleoli = Orphan Annie eyes Follicular: dx depends on invasion through the capsule!
58
Prognosis of papillary v. follicular carcinoma
papillary: excellent prognosis = 95% survival follicular: not as good, prognosis depends on extend of invasion through capsule = 50% survival
59
what is a medullary carcinoma?
It's a subtype of thyroid carcinoma, only makes up 5% of thyroid Cas. Is a tumor of parafollicular C-cells and secretes calcitonin (but rarely are there manifestations of this secretion)
60
mutations in what gene are particularly important in both sporadic and genetic thyroid tumors?
RET proto-oncogene
61
What's an important microscopic distinction of medullary carcinomas?
will see amyloid (pink) deposits in the STROMA
62
embryo derivative of parathyroid glands
from 3rd and 4th branchial pouches along with the thymus
63
where are the parathyroid glands located?
on posterior side of thyroid (superior and inferior poles)
64
histology of parathyroid glands
see chief cells = small, basaloid nuclei w/ pink cytoplasm, surrounded by stromal fat
65
(5) ways that PTH increases serum Ca++
1. has kidney reabsorb Ca+ (decreased loss of Ca in urine) 2. increase kidney excretion of phosphate 3. has kidney convert to active vitamin D 4. increases GI absorption of Ca+ 5. activates osteoclasts to release bone Ca+
66
most common cause of clinically apparent hypercalcemia
Malignancies, (2) types: 1. bone-destroying malignancies: multiple myeloma, leukemia 2. malignancies that produce a PTH-like hormone = PTHrP
67
what happens to parathyroid glands in diGeorge syndrome?
Agenesis: developmental failure of gland formation
68
(2) causes of primary hyperparathyroidism
Adenoma (most common) Familial hypocalciuric hypercalcemia: where parathyroid glands have decreased sensitivity to Ca+ due to mutations in the calcium sensing receptors (CASRs)
69
How do parathyroid adenomas usually present? Contrast w/ primary hyperplasia, which is another form of primary hyperparathyroidism
almost always solitary, meaning 1 of the 4 glands is enlarged v. primary hyperplasia where all 4 glands usually enlarged
70
histo finding on parathyroid adenoma or hyperplasia
decrease in the stromal fat
71
what is bones, stones, moans, and groans associated with?
primary hyperparathyroidism (adenoma or hyperplasia) bones: bone pain and fx secondary to oxteoporosis stones: renal nephrolithiasis moans: lethargy, eventual seizures groans: GI ulcers, increased gastrin b/c of hyperCa++, pancreatitis, gallstones
72
ACTH stimulation tests for
Adrenal insufficiency
73
3 tests for Cushing's
1. 24 hr urine free cortisol 2. 11pm cortisol (b/c cortisol should be lower in evening and higher in morning, so if high = cushing's) 3. Low dose dexamethasone test
74
Main difference between primary and secondary adrenal insufficiency
Primary = low Na and high K. Defect at adrenals, so low Aldosterone. Secondary (central) = normal Na/K b/c Aldosterone is normal
75
Lab value expected from pt taking exogenous cortisol
Low ACTH
76
K and glucose levels w/ Insulinoma
Low glucose (hypoglycemia) and low K (hypokalemic)
77
Pt w/ low glucose and low K+, but normal kidney/liver fxn tests. What test should be performed next?
ACTH stimulation test (the gold standard test for adrenal insufficiency), then you measure the stimulated cortisol levels.
78
You suspect a pt has acromegaly. In addition to an elevated plasma GH level, what other lab finding would also be expected?
High serum IGF-1 (insulin-like growth factor) of more than 300
79
Why does a prolactinoma cause amenorrhea?
High prolactin feeds back to hypothalamus to inhibit GnRH, which means ant pituitary not stimulated to make FSH/LH, leading to decreased FSH/LH effects on the ovary
80
Why does cushing's do to bones? Why?
Osteoporosis, or decreased bone mineral density. High cortisol causes apoptosis of osteoblasts.
81
What dx best explains sx of cold intolerance, constipation, and fatigue in pt w/ GH-secreting tumor?
Secondary hypothyroidism due to compression by the GH-secreting tumor.
82
Oral glucose tolerance test
Tests for GH suppression (the normal response to hyperglycemia). So looking for GH issues (e.g. Secreting adenoma, acromegaly, etc)
83
Most common cause of GH deficiency (GHD) in child
Craniopharyngioma
84
Explain how a pt with hypopituitarism who is put on exogenous thyroid hormone can develop adrenal crisis? What sx?
Thyroid hormone increases metabolism. If you're hypothyroid, all the drugs/chemicals in your body are not eliminated quickly. So if you're hypopit, may have just enough cortisol hanging around to get by. But when administer thyroid hormone, that gets that little amt of cortisol out of the body and go into adrenal crisis. Sx = n/v, lethargy.
85
Order of lost hormones from first one lost to last in HYPOpituitarism
1st = GH Then FSH/LH, then TSH Last = ACTH
86
If a pt has high TSH and high FT4 with palpitations, diaphoresis, and an enlarged thyroid, what is the next best test to confirm cause?
MRI of the pituitary gland - the only scenario with BOTH high TSH and high FT4 is a TSH-secreting pituitary tumor. (B/c normally high T4 would mean low TSH and vice versa)
87
Another name for Thyrotropin
TSH (Thyroid Stimulating Hormone)
88
Why would you give Levothyroxine to a pt with high TSH and super high prolactin with amenorrhea?
The high TSH is indicative of primary hypothyroidism, so low thyroid hormone. And w/ hypothyroidism, metabolism/excretion of all drugs/hormones in your system is decreased, so that's the cause for the high prolactin, which causes the amenorrhea. (Safe to r/o TSH-secreting tumor for questions b/c it's so rare)
89
MEN 1 syndrome
3 Ps: | Hyperparathyroidism, Prolactinoma, and Gastrin-secreting Pancreatic tumor

Exam 1 - Endocrine (2 decks)

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