Brainscape's Knowledge GenomeTM

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


See full index

PATH STORE > PathEndocrine > Flashcards

PathEndocrine Flashcards

1
Q

3 classic symptoms of prolactinoma

A

Galactorrhea, amenorrhea (females) Impotence (males)

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

A typical complication of prolactinoma

A

Fracture

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

Secondary complication of growth cell adenoma (besides growth) and its mechanism

A

Diabetes Mellitus, because growth hormone is gluconeogenic

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

Diagnostic test for GH adenoma

A

Failure of glucose to suppress GH

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

bone condition seen in women with prolactinoma and its mechanism

A

Osteoporosis Prolactin inhibits GnRH = no estrogen = increased osteoclast activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Lab findings of GH cell adenoma GH: Glucose, IGF1, OGTT test

A

Elevated GH, elevated glucose, low IGF-1 in serum and impaired OGTT test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

cell of origin in prolactinoma

A

acidophilic cells of ant. pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Woman gives birth, begins breast feeding and then a week later she notices loss of pubic hair and difficulty with breast feeding

A

Sheehan syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Sheenan syndrome pathogenesis

A

During pregnancy, pituitary swells 2x but doesn’t increase blood flow. If blood is lost during labor, pituitary infarcts (coagulative necrosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Empty sella syndrome defect

A

Herniation of arachnoid and CSF into the sella, destroying the pituitary

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

Sudden onset severe headache and bitemporal hemianopsia and diplopia

A

Pituitary apoplexy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Major cause that central DI

A

Null cell adenoma, hypothalamic injury, etc

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

Lab findings of nephrogenic DI (serum ADH, urine sp. gravity)

A

high, low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Most common site of ectopic ADH production

A

Small Cell Lung Cacner/oat cell carcinoma

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

2 lab values that distinguish SIADH from DI

A

Sodium and serum osmolality SIADH is hyponatremic, low osmolality, the others are hypernatremic, high osmolality

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

Midline anterior neck mass in a child

A

Thyroglossal duct cyst

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

Graves disease defect (name one antibody)

A

IgG stimulates TSH receptor

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

3 PE findings of Graves

A

Goiter Exophthalmos Myxedema and skin pigmentation

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

mechanism of exopthalmos and pretibial myxedema

A

T cells stimulate Fibroblasts release to glycosaminoglycans –> increases osmotic swelling and adipocyte size –> exopthalmos

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

3 major cell types involved in exophthalmos

A

Fibroblasts T cells Fat cells

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

Histology of graves

A

Tall follicular cells, papillary processes with colloid scalloping Scalloped colloid looks like little tombstones –> like…GRAVES

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

Patient with hyperthyroidism undergoes a surgery under general anesthesia. When they wake up they develop severe hyperthermia, Delerium, tachycardia and arrhythmias

Diagnosis?

A

Thyroid Storm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Are hot nodules (with I131 thyroid scan) benign or malignant

A

Benign (mostly)

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

Infant with pot bellly, swollen face, protruding umbilicul, tongue falling out of mouth

A

Cretinism –> congential hypothyroid

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

6 Ps of cretinism

A

Pot belly Protruding umbilicus Protouding tongue Pale Puffy Face Poor brain development

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

Myxedema cause

A

accumulation of glycosaminoglycans in skin and soft tissue

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

Patent states they’ve been gaining weight despite not eating more, feels fatigued and has noticed deepening of voice and feels like their tongue is larger than normal

A

Hypothryoidism

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

Hashimoto defect (3 Ab)

A

IgG ab against thyroid peroxidase, IgG against thyroglobulin, Antimicrosomal Ab

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

HLA association with hashimoto

A

HLA DR5

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

classic paradox in lab findings in Hashimoto

A

Patients initially present with elevated T4 levels and SSx of hyperthyroid, then come back and have SSx of hypothyroid

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

Why do T4 levels initially increase in Hashimoto

A

follicle damage causes release of T4

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

2 unique histology findings of Hashimoto

A

1- Germinal center formation (appears like a lymph node), with plasma cells 2- hurthle cells

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

hurthle cell description

A

Eosinophlic metaplasia that lines the follicles

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

which cancer does hashimotos increase risk for? why?

A

Diffuse large B cell lymphoma b/c germinal cells are being formed

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

Patient has an upper respiratory infection, then develops periodic episodes of tachycardia, sweating, increased appetite. C/o Jaw pain and anterior neck pain.

A

Subacute granulomatous Thyroiditis

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

Subacute granulomatous thyroiditis labs

A

Elevated ESR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

SGT clinical course

A

Hyperthyroidism that may progress to hypothyroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

SGT biopsy

A

Granulomatous inflammation w/ giant cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

20-year-old presents with dysphagia and wheezing. The thyroid is firm when palpated but not painful, and it doesn’t move when palpated.

Diagnosis?

A

Riedel fibrosing thyroiditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

how does I 131 uptake help distinguish hyperthyroid/toxic goiter from cancer

A

Cancer is a cold nodule (doesn’t take up I 131)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

5 classic cancers of the thyroid

A

Follicular Adenoma Follicular Carcinoma Papillary carcinoma Medullary carcinoma Anaplastic carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Hallmark of follicular adenoma on gross exam/histology

A

Follicles are surrounded by a thick fibrous capsule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

CLassic risk factor for developing papillary carcinoma of thyroid

A

Radition to the head and neck area as a child

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Papillary carcinoma histology (2 unique features)

A

Empty nuclei with central clearing (orphan annie cells), Psammoma bodies Papillary = Psammoma and Pupils (eyes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Most common pituitary adenoma

A

Prolactinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Follicular carcinoma mutation and mechanism of invasion

A

RAS, capsular and vascular invasion by collagenase

47
Q

Follicular carcinoma spread and prognosis

A

HEMATOGENOUS SPREAD. it forgot its a carcinoma Good prognosis

48
Q

Dexa test result in pituitary corticotrophic adenoma

1.0 mg and 8.0 mg

A
  1. 0 mg- no change in serum/urine ACTH and cortisol level (remain high)
  2. 0 mg- lower level of serum and urine ACTH and cortisol level
49
Q

Medullary carcinoma is a malignancy of

A

Calcitonin secreting parafollicular C cells

50
Q

medullary carcinoma labs and inheritance

A

Hypocalcemia w/ hypercalciuria (b/c calcitonin increases renal excretion of Ca), Autosomal dominant (MET protooncogene)

51
Q

Classic medullary carcinoma histology

A

sheets of cells in an amyloid (pink) stroma

52
Q

Medullary carcinoma mutation

A

RET mutation (MEN2a 2b)

53
Q

What should be done if pt has RET mutation?

A

Prophylactic thyroidectomy

54
Q

What is the amyloid made of in medullary carcinoma?

A

Calcitonin deposition

55
Q

Patient presents with asymptomatic hypercalcemia

A

Primary hyperparathyroidism

56
Q

histology of papillary carcinoma

A

the papillary process, hypochromatic nuclei, psammoma bodies

57
Q

4 main symptoms of hypercalcemia

A

“Stones, bones, groan, psychiatric overtones” Kidney stones Osteitis fibrosis cystica Constipation, abdominal pain, pancreatitis Depression

58
Q

serum alk phos level in primary hyperPTH. Why?

A

Elevated b/c PTH activates osteoblasts, which secrete alk phos b/c it needs an alkaline environment to make bone

59
Q

Osteitis fibrosa cystica (OFS) cause

A

excessive bone resorption by overactive osteoclasts

60
Q

OFC gross and Xray appearance

A

Cysts full of brown fibrous tissue Multiple cystic spaces on Xray

61
Q

Why is the cyst in OCF is brown?

A

Hemosiderin form macrophages

62
Q

2 most common causes of secondary hyperPTH

A

chronic renal failure Hypovitaminosis D Really, anything that causes low Ca or high Phos

63
Q

Muscle effects of hypocalcemia

A

Muscle spasms and fatigue

64
Q

2 PE findings for hypocalcemia

A

Chovestek sign (tap on facial nerve = twitch) Trousseau (occlude brachail artery = carpal spasm)

65
Q

3 most common causes of hypoparathyroidism

Lab findings in this case:

A

Surgical excision of thyroid Autoimmune DiGeorge!

Low serum PTH, low calcium and high K

66
Q

If ostitis fibrosa cystica like abnormality is seen in a patient in renal failure- the condition is known as:

A

Renal Osteodystrophy

67
Q

inheritance of MEN syndromes

A

Autosomal dominant. “MEN are Dominant”

68
Q

MEN1 mutation

A

menin, a tumor supressor on Ch11

69
Q

MEN1 SSx

A

Pituitary adenoma Pancreatic tumor (ZE, gastrinoma, insulinoma) Parathyroid adenoma

70
Q

MEN2a SSx

A

Parathyroid adenoma Pheochromocytoma Medullary Carcinoma of thyroid

71
Q

MEN2b SSx

A

Pheochromocytoma Medullary carcinoma of thyroid Mucosal neuromas Marfanoid habitus- A TALL PERSON

72
Q

MEN2 defect and pathogenesis

A

RET mutation, which codes for receptor tyrosine kinase

73
Q

embryonic origin of the cells affected Craniopharyngioma

A

Rathke’s pouch

74
Q

MCC (most common cause) of primary hyperaldosteronism

A

Bilateral adrenal hyperplasia, Adrenal adenoma (conn)

75
Q

MCC of secondary hyperaldosteronism

A

Renal artery stenosis, CHF

76
Q

How to differentiate b/w primary and secondary hyperaldo

A

Primary = Low Renin w/o edema Secondary = High Renin + Edema

77
Q

Mechanism of striae in cushing

A

Cortisol inhibits fibroblast prolferation and collagen production

78
Q

Classic triad of symptoms that aren’t related to physical appearance in cushings

A

HTN, hypokalemia and metabolic alkalosis

79
Q

The basis for high dose (8.0 mg overnight) dexa suppression test

A

Pituitary cushings is suppressed with high dose dexa, Ectopic cushings is not

80
Q

imaging findings for exogenous steroid induced cushings

A

bilateral adrenal atrophy

81
Q

2 causes of bilateral adrenal hypertrophy

A

Pituitary Cushings, Ectopic Cushings (Oat cell lung carcinoma)

82
Q

major cause of unilateral adrenal hypertrophy and atrophy of the opposite gland

A

Adrenal adenoma

83
Q

major way to distinguish b/w 21OH and 11OH deficiency

A

21OH = hypotension , hyponatremia, hyperkalemia 11OH= Hypertension, hypernatremia, hypokalemia

84
Q

21OH vs 17OH def (sexual appearance)

A

21OH is precocious puberty in males, ambiguous in females; 17OH is amenorrhea in females and ambiguous in males

85
Q

screening test of choice for any type of congenital adrenal hyperplasia

A

ACTH- will be high

86
Q

SSx of acute adrenal insufficiency

A

acute drop in BP to the point they can’t perfuse organs

87
Q

2 MCC of Addison disease

A

autoimmune destruction of the gland (with polyglandular syndrome, TB and AIDS

88
Q

how to differentiate primary vs secondary adrenal insufficiency

A

Primary causes hyperpigmentation due to high ACTH Secondary doesn’t affect skin b/c ACTH is low

89
Q

which cancer can cause adrenal insufficiency?

A

Lung cancer! remember, lung cancers met to the adrenals; and also RCC

90
Q

Pheochromocytoma is a tumor of

A

chromaffin cells

91
Q

Classic presentation of pheo.

A

EPISODIC Anxiety/panic palpitations headaches sweating

92
Q

screening test for pheo

A

Vannilylmandelic acid (VMA) and catecholamines in the urine and serum

93
Q

the buzzword for the facial appearance of hyperthyroidism

A

“frightened appearance” Refers to staring gaze with lid lag (eyes wide open)

94
Q

Histology of orbital muscles in exophthalmos will show what 2 features?

A

Inflammation (T cells) Increased Adipocytes

95
Q

4 Tx for thyroid storm

A

PTU Prednisone Propanolol Potassium Iodine

96
Q

High Intact PTH, low calcium, dwarfism, blunting of the fourth and fifth knuckles of the hand

A

Pseudohypoparathyroidism (Albright hereditary dystrophy)

97
Q

What is the specific defect in PsHP (Pseudohypoparathyroidism (Albright hereditary dystrophy))?

A

Defective Gs protein in the renal tubular cells –> kidney doesn’t respond to PTH (PsHP is to PTH as Nephrogenic DI is to ADH)

98
Q

Pseudopseudohypoparathyroidism presentation

A

Look like albrights (short stature, short 4th/5th digits) but don’t have end organ PTH resistance…PTH and Ca levels are normal

99
Q

Familial Hypocalciuric Hypercalcemia defect

A

Defective Ca Sensing receptor in the PTH means body can’t respond to high Ca

100
Q

Pseudohypoparathyroidism (Albright hereditary dystrophy) Labs (serum/urine Ca, PTH)

A

High serum Ca High PTH Low urine Ca

101
Q

Relationship of Prolactinoma and Bone in a woman

A

Increases risk for osteoporosis Prolactin inhibits GnRH = low estrogen = increased osteoclasti activity

102
Q

Potassium levels in primary vs secondary adrenal insufficiency. Why?

A

Low in Primary b/c entire adrenal is dead Normal in secondary b/c ACTH doesn’t directly stimulate the zona glomerulosa!!

103
Q

Basis for CRH stimulation test in adrenal insufficiency

A

If CRH stimulates the production of new cortisol, the Dx is Secondary/tertiary adrenal insufficiency (b/c the pituitary wasn’t releasing ACTH) This is the same logic as in pituitary cushings vs ectopic ACTH production

104
Q

Sheehan’s which hormone functions return after a few months

A

ADH

105
Q

The earliest symptom of Sheehan’s

A

difficulty breastfeeding or an inability to breastfeed.

106
Q

Prolactinoma cell of origin

A

acidophilic cells

107
Q

Stalk effect

A

all pituitary hormones are low, but prolactin is high

108
Q

Cause of these findings (visual field defect)

A

Prolactinoma- mass effect- compression on optic optic chiasm superiorly

109
Q

Which hormone defect is seen with the associated image

A

Excess GH

110
Q

Diseases associated with the attached image

A

McCune – Albright syndrome

  1. Female patient common
  2. Polyostotic Fibrous Dysplasia
  3. Café au lait spot
  4. Precocious puberty
  5. Endocrine abnormality (Gigantism, Hyperthyroidism, Cushing syndrome)
111
Q

Likely diagnosis?

A

Probably prolactinoma- macroadenoma

112
Q
  • Blood and urine samples will be sent to measure the concentration at 0900, 1200, 1500 and 1600.
  • 3/4th samples are taken after vasopressin infection.

•

•< 10% increase in urine osmolality following injection vasopressin during the test- ? diagnosis

​

A

nephrogenic DI

113
Q
  • Blood and urine samples will be sent to measure the concentration at 0900, 1200, 1500 and 1600.
  • 3RD/4th samples are taken after vasopressin infection.
  • > 50% increase in urine osmolality following injection vasopressin during the test-? diagnosis

​

A

complete neurogenic DI

PATH STORE (24 decks)

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