Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Exam 1 - Endocrine > Endocrine Pathology > Flashcards

Endocrine Pathology Flashcards

1
Q

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

A

oxytocin (breast) and ADH (kidney)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

embryo derivative of anterior v. posterior

A 
anterior = Rathke's pouch
posterior = floor of the 3rd ventricle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Pharm tx of prolactinoma

A

Bromocriptine (dopamine analog)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Oral glucose challenge

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Name 4 not so obvious Cushing’s sx

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is required to dx a pituitary carcinoma?

A

must demonstrate metastases. pituitary carcinomas are very rare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Fxn of Oxytocin

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Blood Na levels in Diabetes Insipidus pt

A

HYPERnatremia. Urine is dilute w/ low spec gravity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Blood Na levels in SIADH

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What condition often leads to SIADH?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What lymph node sits behind the thyroid

A

Delphian lymph node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How do T3 and T4 travel in the serum?

A

Bound to thyroxine binding globulin, Albumin, and Transthyretin proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Binding of T4 v. T3 to nuclear receptors

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

(4) effects of thyroid hormones

A
  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!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

(2) functions of Calcitonin

A
  1. promotes bones to take up Ca out of the blood

2. inhibits osteoclasts from resorbing bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Thyroid storm

A

abrupt onset of severe hyperthyroidism. emergent b/c can cause heart arrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Most useful screening test for hypo or hyperthyroidism. Follow up confirmation test?

A

Serum TSH. Will be low in primary hyperthyroid and high in secondary hyperthyroid.
Usually confirmed w/ an elevated serum FT4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Grave’s Disease Triad

A

hyperthyroidism, exopthalmos (from infiltrative ophthalmopathy), and infiltrative dermopathy (pretibial myxedema)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

mechanism of Grave’s disease

A

an autoimmune disease with auto-Abs most commonly to the TSH receptor. Abs could also be against thyroglobulin and thyroid peroxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

(3) gene defects associated w/ Grave’s disease

A

PTPN22
CTLA-4
HLA-DR3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

(4) reasons for the exopthalmopathy in Graves

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

expected lab findings in Grave’s for TSH, T3/T4, and Iodine uptake

A

low TSH, high T3/T4, and high iodine uptake that is DIFFUSE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Primary v. Secondary v. Tertiary Hypothyroidism (and 2 examples of primary)

A

Primary: actual thyroid is problem. Hashimoto’s or surgery/radiation
Secondary: pituitary is problem = TSH deficiency
Tertiary: hypothalamus is problem = TRH deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

TSH in primary v. secondary/tertiary hypothyroidism

A

primary hypothyroidism = high TSH

secondary/tertiary = low TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

cretinism

A

hypothyroidism that develops during infancy or early childhood. most cases due to lack of dietary iodine

37
Q

Effect of cretinism. Name 5 sx

A 
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
Q

Myxedema, def and how it presents

A

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
Q

(4) physical signs of myxedema

A 
Face = edema of face and eyelids, coarsening of facial features
Heart = cardiomegaly with slow pulse
Hair = dry and brittle
40
Q

(3) pathways by which the thyroid epithelium is damaged in Hashimoto’s thyroiditis and the unifying pathogenesis behind them

A

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
Q

What does Hashimoto’s thyroid look like under the microscope? Grossly?

A

Lots of inflammation seen w/ infiltration of lymphocytes, plasma cells, macrophages w/ germinal center formation
Thyroid looks pale and enlarged

42
Q

What are Hurthle cells? 2 associated conditions?

A

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
Q

Labs seen in clinical course of Hashimoto’s Thyroiditis

A

[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
Q

One important association with Hashimoto’s Thyroiditis

A

slightly increased risk of lymphoma

45
Q

2 other name for de Quervain Thyroidits

A

Subacute Thyroiditis or Granulomatous Thyroiditis

46
Q

etiology of Subacute (granulomatous) Thyroiditis

A

aka de Quervain Thyroiditis. Believed to be post-viral etiology. Ex. Hx of URI from coxsackie, mumps, measles, or adenovirus

47
Q

microscopic appearance of Subacute Thyroiditis

A

aka de Quervain or Granulomatous Thyroiditis. Ergo, see multinucleated giant cells surrounding pools of colloid

48
Q

What happens to thyroid hormone in Subacute Thyroiditis?

A

1st get transient hypERthyroidism, then get transient hyPOthyroidism. Then you completely recover

49
Q

Clinical presentation of Subacute (granulomatous) v. Subacute Lymphocytic Thyroiditis

A

Granulomatous: neck pain sometimes radiating to throat, jaw, ears, esp w/ swallowing
Lymphocytic: PAINLESS thyroiditis with nonspecific lymphoid infiltrate of thyroid

50
Q

Reidel’s Thyroiditis

A

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
Q

Why does a goiter form?

A

due to impaired synthesis of thyroid hormone, most common cause is iodine deficiency

52
Q

How does a multinodular goiter form?

A

starts as a simple goiter that involutes over and over again

53
Q

Plummer syndrome. What is it? Compare to Grave’s

A

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
Q

(4) clinical criteria for what makes a thyroid nodule more likely neoplastic

A
  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
Q

cell derivation of thyroid adenomas

A

thyroid follicular epithelium

56
Q

even though thyroid carcinomas are rare, what is the most common type of thyroid carcinoma? How/where does it manifest?

A

papillary carcinoma. First manifests as a mass in a cervical lymph node. Great prognosis w/ 95% survival rate

57
Q

how the diagnosis made for papillary carcinoma v. follicular carcinoma?

A

Papillary: dx made on way nucleus looks! Empty nuclei devoid of nucleoli = Orphan Annie eyes
Follicular: dx depends on invasion through the capsule!

58
Q

Prognosis of papillary v. follicular carcinoma

A

papillary: excellent prognosis = 95% survival
follicular: not as good, prognosis depends on extend of invasion through capsule = 50% survival

59
Q

what is a medullary carcinoma?

A

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
Q

mutations in what gene are particularly important in both sporadic and genetic thyroid tumors?

A

RET proto-oncogene

61
Q

What’s an important microscopic distinction of medullary carcinomas?

A

will see amyloid (pink) deposits in the STROMA

62
Q

embryo derivative of parathyroid glands

A

from 3rd and 4th branchial pouches along with the thymus

63
Q

where are the parathyroid glands located?

A

on posterior side of thyroid (superior and inferior poles)

64
Q

histology of parathyroid glands

A

see chief cells = small, basaloid nuclei w/ pink cytoplasm, surrounded by stromal fat

65
Q

(5) ways that PTH increases serum Ca++

A
  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
Q

most common cause of clinically apparent hypercalcemia

A

Malignancies, (2) types:

  1. bone-destroying malignancies: multiple myeloma, leukemia
  2. malignancies that produce a PTH-like hormone = PTHrP
67
Q

what happens to parathyroid glands in diGeorge syndrome?

A

Agenesis: developmental failure of gland formation

68
Q

(2) causes of primary hyperparathyroidism

A

Adenoma (most common)
Familial hypocalciuric hypercalcemia: where parathyroid glands have decreased sensitivity to Ca+ due to mutations in the calcium sensing receptors (CASRs)

69
Q

How do parathyroid adenomas usually present? Contrast w/ primary hyperplasia, which is another form of primary hyperparathyroidism

A

almost always solitary, meaning 1 of the 4 glands is enlarged
v. primary hyperplasia where all 4 glands usually enlarged

70
Q

histo finding on parathyroid adenoma or hyperplasia

A

decrease in the stromal fat

71
Q

what is bones, stones, moans, and groans associated with?

A

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
Q

ACTH stimulation tests for

A

Adrenal insufficiency

73
Q

3 tests for Cushing’s

A
  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
Q

Main difference between primary and secondary adrenal insufficiency

A

Primary = low Na and high K. Defect at adrenals, so low Aldosterone.
Secondary (central) = normal Na/K b/c Aldosterone is normal

75
Q

Lab value expected from pt taking exogenous cortisol

A

Low ACTH

76
Q

K and glucose levels w/ Insulinoma

A

Low glucose (hypoglycemia) and low K (hypokalemic)

77
Q

Pt w/ low glucose and low K+, but normal kidney/liver fxn tests. What test should be performed next?

A

ACTH stimulation test (the gold standard test for adrenal insufficiency), then you measure the stimulated cortisol levels.

78
Q

You suspect a pt has acromegaly. In addition to an elevated plasma GH level, what other lab finding would also be expected?

A

High serum IGF-1 (insulin-like growth factor) of more than 300

79
Q

Why does a prolactinoma cause amenorrhea?

A

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
Q

Why does cushing’s do to bones? Why?

A

Osteoporosis, or decreased bone mineral density. High cortisol causes apoptosis of osteoblasts.

81
Q

What dx best explains sx of cold intolerance, constipation, and fatigue in pt w/ GH-secreting tumor?

A

Secondary hypothyroidism due to compression by the GH-secreting tumor.

82
Q

Oral glucose tolerance test

A

Tests for GH suppression (the normal response to hyperglycemia). So looking for GH issues (e.g. Secreting adenoma, acromegaly, etc)

83
Q

Most common cause of GH deficiency (GHD) in child

A

Craniopharyngioma

84
Q

Explain how a pt with hypopituitarism who is put on exogenous thyroid hormone can develop adrenal crisis? What sx?

A

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
Q

Order of lost hormones from first one lost to last in HYPOpituitarism

A

1st = GH
Then FSH/LH, then TSH
Last = ACTH

86
Q

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?

A

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
Q

Another name for Thyrotropin

A

TSH (Thyroid Stimulating Hormone)

88
Q

Why would you give Levothyroxine to a pt with high TSH and super high prolactin with amenorrhea?

A

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
Q

MEN 1 syndrome

A

3 Ps:

Hyperparathyroidism, Prolactinoma, and Gastrin-secreting Pancreatic tumor

Exam 1 - Endocrine (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions