Brainscape's Knowledge GenomeTM

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


See full index

PATH STORE > Extra Endocrine > Flashcards

Extra Endocrine Flashcards

1
Q

3 classic symtoms of prlactinoma

A

Galactorrhea, amenorrhea (females)

Impotence (males)

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

why does prolactinoma cause amenorreha

A

Prolactin inhibits GnRH

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

Secondary complication of growth cella denoma (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

Defect in dwarfism

A

Defective GH receptors

Elevated GH and low IGF-1 in serum

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

what endocrine disease can cause a prolactinoma

A

Primary Hypothyroid

TSH backs up, TRH backs up, TRH stimulates Prolactin release

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 doesnt increase blood flow. If blood is lost during labor, pituitary infarcts

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 risk that central DI patients have

A

life threating dehydration

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

Herediatry cause of nephrogenic DI

A

Mutation in neurophysin gene

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

2 drugs that cause neprhogenic DI

A

Lithium

Demococlyine

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

Most common site of ectopic ADH production

A

Small Cell Lung Cacner

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
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
17
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
18
Q

how to differentiate thyroglossal duct cyst from branchial cleft cyst

A

Thyroglossal duct cysts move with tongue and while swallowing.

Brachial cleft cysts dont move and are on the lateral neck

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

Child with mass at the base of the tongue

A

Lingual thyroid

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

What is lingual thyroid composed of

A

Normal thyroid tissue

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

2 receptors that mediate symptoms of hyperthyroidism

A

NaK pump –> increased BMR

B1 receptors –> increased SNS activity

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

3 endocrine changes with hyperthyroid

A

Hypercalcemia (increased bone resorption)
Hyperglycemia (increased gluconeogenesis/glycogenolysis)
Hypocholesterolemia

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

Graves disease defect

A

IgG stimulates TSH receptor

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

3 PE findings of Graves

A

Goiter
Exopthalmos
Myxedema

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

Mechanism of GOiter in graves

A

Constant TSH = thyroid hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
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
27
Q

2 major cell types involved in exopthalmos

A

Fibroblasts

T cells

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

2 specific glycosaminoglycans

A

Chondroitin sulfate

Hyaluronic acid

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

Histology of graves

A

Tall follicular cells 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
30
Q

Thiomide MOA

A

Blocks thyroid peroxidase

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

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

A

Thyroid Storm

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

Toxic multinodular goiter defect

A

Nodules secreating hormone independent of TSH

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

Are hot nodules benign or malignant

A

Benign

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

Jod Basedow phenomenon

A

Patient with iodide deficiency is pumped full of iodide, and then they have thyrotoxicosis

opposite of wolff chaikoff

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
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
36
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
37
Q

Dyshormonogenetic goiter defect

A

It is one of the causes of cretinsm.

Due to low levels of thryoid peroxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
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
39
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
40
Q

Why do hypothryoid patients have deeper voices/large tongues

A

Glycosaminoglycan deposition

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

Hashimoto defect (3 Ab)

A

IgG ab against thryoid peroxidase
IgG against thyroglobulin
Antimicrosomal Ab

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

HLA association with hashimoto

A

HLA DR5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
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
44
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
45
Q

2 unique histology findings of hashimoto

A

1- Germinal center formation (appears like a lymph node)

2- hurthle cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
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
47
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
48
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
49
Q

Subacute granulomatous thyroiditis labs

A

Elevated ESR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
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
51
Q

SGT biopsy

A

Granulomatous inflammation w/ giant cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

20 year old presents with dysphagia and wheezing. Thyroid is firm when palpated but not painful, and it doesnt move when palpated.

A

Riedel fibrosing thyroiditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What must be r/o in fibrosing thyroitis? how?

A

Anaplastic thyroid cancer.

RF is in young patients, cancer is older. RF lacks malignant cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

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

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
55
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
56
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
57
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
58
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
59
Q

Pap. Carcinoma spread and progonisis

A

Cervical llymph nodes

Good prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Follicular carcinoma mutation

A

RAS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Follicular carcinoma spread and prognosis

A

HEMATOGENOUS SPREAD. it forgot its a carcinoma

Good prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Why can’t fine needle aspiration differentiate b/w follicular adenoma and carcinoma

A

FNA only sample cells and not the capsule.

Entire capsule needs to be visualized under microscope to ensure no invasion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Medullary carinoma is a malignancy of

A

Calcitonin secreting parafollicular C cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

medullary carcinoma labs

A

Hypocalcemia w/ hypercalciuria (b/c calcitonin increases renal excretion of Ca)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Classic medullary carcinoma histology

A

sheets of cells in an amyloid (pink) stroma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Medullary carcinoma mutation

A

RET mutation (MEN2a 2b)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What should be done if pt has RET mutation?

A

Prophylactic thyroidectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What is the amyloid made of in med. carcinoma?

A

Calcitonin deposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

70yo pt presents with neck mass, dysphagia, hoarseness

A

Anaplastic carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Patient presents with asymptomatic hypercalcemia

A

Primary hyperparathyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

classic GI symptom that arrises in primary hyperPTH patients

A

Acute pancreatitis –> Ca is an enzyme activator!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

4 main symptoms of hypercalcemia

A

“Stones, bones, groan, psychiatric overtones”

Kidney stones
Osteitis fibrosis cystica
Constipation, abdominal pain, pancreatitis
Depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Osteitis fibrosa cystica cause

A

excessive bone resorption by overactive osteoclasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

OFC gross and Xray appearance

A

Cysts full of brown fibrous tissue

Multiple cystic spaces on Xray

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Why is the cyst brown?

A

Hemosiderin form macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

2 most common causes of secondary hyperPTH

A

chronic renal failure
Hypovitaminosis D

Really, anything that causes low Ca or high Phos

78
Q

Muscle effects of hypocalcemia

A

Muscle spasms and fatigue

79
Q

2 PE findings for hypocalcemia

A 
Chovestek sign (tap on facial nerve = twitch)
Trousseau (occlude brachail artery = carpal spasm)
80
Q

3 most common causes of hypoparathyroid

A

Surgical excision of thyroid
Autimmune
DiGeorge!

81
Q

spatial relationship of alpha and beta cells

A

Alpha cells surround the beta cells

82
Q

hypersensitivity type of DM type 1

A

Type 4 –> T cells against beta cells

83
Q

DM 1 histology vs DM 2

A

DM1 = inflammatory cells in the islet

DM2= Amyloid deposition in islet

84
Q

Polyuria, polydipsia and glycosuria are due to

A

Hyperglycemia causing osmotic diuresis

85
Q

WEight loss, decreased muscle mass and polyphagia are due to

A

Unopposed GLUCAGON. –> Does everything opposite of insulin

Increases lipolysis, protein breakdown, gluconeogenesis (which worsens the hyperglycemic symptoms)

86
Q

SSx of DKA

A

DKA is Deadly

Delerium
Kusmaull respiration
Abdominal pain (N/V)
Dehydration

+ Fruity breath

87
Q

why does DKA occur during illness?

A

Epinephrine is released –> epi causes glucagon release –> overactive lipolysis, glycogenolysis and gluconeogenesis

88
Q

Mechanism for ketone body generation (3 steps)

A

Increaesd liposlysis –> increase FFA production –> liver converts FFAs to ketone bodies

89
Q

2 reasons for hyperkalemia in DKA

A

No insulin = transcellular shift out of cells

AG Metabolic Acidosis = transcellular shift out of cells

90
Q

TOTAL body K levels in DKA

A

Decreased, even though theyre hyperkalemic (all the K is in the blood. none is in the cells)

91
Q

3 Tx for DKA

A

Insulin (treat hyperK and lower glucose)
K+ so they dont become hypokalemic
Glucose so they dont become hypoglycemic

92
Q

Why is DKA not seen in DM2?

A

Endogenous insulin prevents excess lipolysis (less FFAs = less ketone bodies)

93
Q

how does obesity lead to DM 2

A

Adipose down regulates insulin receptors on cells

94
Q

Stronger genetic predisposition b/w DM1 or DM2

A

DM2

95
Q

HLA association in 1 and 2

A

DM1- HLA DR3 and DR4

DM2- none

96
Q

progression of serum insulin in DM2. Why?

A

INitially elevated due to hyperglycemia, but progressively decline as the beta cells burn out

97
Q

3 diagnostic criteria for DM

A

Fasting BGL > 126
Random BGL >200
BGL > 200 2hrs after glucose load

98
Q

hyperosmolar hyperglycemic non ketotic coma mechanism (3 steps)

A

Hyperglycemia –> osmotic diuresis –> dehydration

99
Q

who is HHNS seen in ?

A

Elderly people who DONT DRINK WATER

100
Q

HHNS ssx

A

Polyuria
Thirst
Lethargy
Seizures/neuro defecits

101
Q

HHNS serum osmolarity, glucose and pH

A 
Hyperglycemia 
low osmolarity (water loss)
normal pH (no ketone bodies)
102
Q

Non enzymatic Glycosylization causes which class of comlications

A

Small vessel disease (retinopathy, nephropathy, neuropathy)

Large vessel disease (CAD, PVD, gangrene)

103
Q

Osmotic damage causes which 4 complications

A

Peripheral neuropathy
Impotence
Blindness
Cataracts

104
Q

3 cell types/tissues where osmotic damage occurs

A

Schwann cells
Pericytes of retinal blood vessels
Lens of the eye

105
Q

Mechanism of osmotic damage

A

Accumulation of sorbitol in tissue = osmotic damage

106
Q

2 enzymes responsible for osmotic damage

A

Elevated aldose reductase

Decreased sorbitol dehydrogenase

107
Q

DM can cause cataracts blindness and glaucoma. how are the mechanisms different?

A 
Cataracts = osmotic damage to lens
Blindness = osmotic damage to pericytes
Glaucoma= non enzymatic glycoslylation of retina
108
Q

Type of arteriolosclerosis seen in DM

A

Hyaline (just like HTN)

109
Q

inheritance of MEN syndromes

A

Autosomal dominant. “MEN are Dominant”

110
Q

MEN1 mutation

A

menin, a tumor supressor on Ch11

111
Q

MEN1 SSx

A

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

112
Q

MEN2a SSx

A

Parathyroid adenoma
Pheochromocytoma
Medullary Carcinoma of thyroid

113
Q

MEN2b SSx

A

Pheochromocytoma
Medullary carcinoma of thyroid
Mucosal neuromas
Marfanoid habitus

114
Q

MEN2 defect and pathogenesis

A

RET mutation, which codes for receptor tyrosine kinase

115
Q

embryonic origin of the cells affected by RET mutatino

A

Nueral Crest

116
Q

SSx of Insulinoma

A

Episodic hypoglycemia and AMS that resolves with glucose administration

117
Q

4 SSx of Somatostatinoma

A

Steatorrhea, gallstones (no CCK or secretin)
Glucose intolerance
Achlorhydria (n ogastrin)

118
Q

VIPoma ssx (3)

A

Diarrhea (high VIP = relaxed bowel)
Hypokalemia (diarrhea…may also have NAGMA)
Achlorhydria (VIP inhibits gastrin)

119
Q

Glucagonoma ssx (5)

A 
Dermatitis
Diabetes
DVT
Declining weight
Depression
120
Q

MCC of primary hyperaldosteronism

A 
Bilateral adrenal hyperplasia
Adrenal adenoma (conn)
121
Q

MCC of secondary hyperaldosteronism

A

Renal artery stenosis
CHF

ANything decreasing perfusion to the kidney

122
Q

How to differentiate b/w primary and secondary hyperaldo

A 
Primary = Low Renin w/o edema
Secondary = High Renin + Edema
123
Q

Child with HTN, hypokalemia, elevated aldosterone with low renin

A

Glucocorticoid remediable aldosteronism (GRA)

124
Q

GRA defect

A

Overactive expression of aldosterone synthase

125
Q

confirmatory test for GRA

A

dexamethasone suppression

126
Q

Liddle Syndrome defect

A

loss of ENAC channels = hyponatremia

127
Q

how does Liddle and GRA presentation differ?

A

Liddle has low aldo and low renin

GRA has HIGH aldo and low rening

128
Q

Mechanism of thin extremities in cushing

A

Cortisol causes proteolysis to get AAs for gluconeogenesis

129
Q

Mechanism of obesity in cushing

A

High insulin and and glucose cause lipogenesis

130
Q

Mechanism of striae in cushing

A

Cortisol inhibits fibroblast prolferation and collagen production

131
Q

major eelectroloyte imbalance in cushing

A

Hypokalemia

132
Q

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

A

HTN, hypokalemia and metabolic alkalosis

133
Q

Mechanism for HTN inc ushings

A

cortisol increases catecholamine sensitivity in vessels –> vasoconstriction

Cortisol can increase Na reabsorption by acting like aldo

134
Q

mechanism for hyhpokalemia/metabolic alkalosis in cushings

A

at very high doses, cortisol can actually bind to the aldosterone receptor (K and H secretion, Na reabsorption, HTN)

135
Q

Basis for high dose dex suppression test

A

Pituitary cushings is suppressed with high dose dex

Ectopic cushings is not

136
Q

Basis for CRH stimulation test in cushings

A

If ACTH increases when CRH is administered, it is pituitary cushings

If ACTH doesnt increase with CRH, it is ectopic production

137
Q

imaging findings for exogenous steroid induced cushings

A

bilateral adrenal atrophy

138
Q

2 causes of bilateral adrenal hypertrophy

A

Pituitary Cushings

Ectopic Cushings

139
Q

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

A

Adrenal adenoma

140
Q

2 DDx for Hyperpigmentation of the skin in a person with adrenal dysfunction

A

Adrenal insufficiency
Congential adrenal hyperplasia

Anything causing low cortisol = high ACTH

141
Q

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

A

21OH = hypotension , hyponatremia, hyperkalemia

11OH= Hypertension, hypernatremia, hypokalemia

142
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

143
Q

screening test of choice for any type of congential drenal hyperplasia

A

17-hydroxyprogesterone

144
Q

17OHprogesterone screening results in each case

A

21OH- elevated
11OH - elevated
17OH- decreased

145
Q

complication of over treating someone with cushings

A

they can develop adrenal insufficiency

146
Q

why must corticosteroids must be tapered?

A

Acute withdrawal can lead to acute adrenal failure!

147
Q

SSx of acute adrenal insufficiency

A

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

148
Q

progressive onset of orthostatic hypotension, salt/sugar cravings, fatigue, weight loss

A

addison dz

149
Q

2 MCC of addison disease

A

autoimmune destruction of the gland (DM)

TB in developing countries

150
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

151
Q

which cancer can cause adrenal insufficiency?

A

Lung cancer! remember, lung cancers met to the adrenals

152
Q

Basis for metyropone stimulation test

A

Metyropone inhibits 11-deoxycortisol –> cortisol

Less cortisol should stimulate an increase in ACTH and 11-deoxycoritsol production

153
Q

Metyropone test in primary ad. insuff.

A

ACTH increases, but 11-deoxycortisol does not

154
Q

Metyropone test in secondary/tertiary ad. insuff

A

ACTH and 11deoxycortisol both remain low (b/c pituitary cant make more ACTH in response to the low cortisol)

155
Q

Cell type and embryologic derivative of the adrenal medulla

A

Chromaffin cells

derived from neural crest

156
Q

Pheochromocytoma is a tumor of

A

chromaffin cells

157
Q

Classic presentation of pheo.

A

EPISODIC

Anxiety/panic
palpitations
headaches
sweating

158
Q

screening test for pheo

A

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

159
Q

2 Tx for pheo, and the appropriate order

A

Phenoxybenzamine/phentolamine followed by Bblocker

160
Q

2 Classic extra medullary site for pheochromocytoma

A

Inferior mesenteric artery

Bladder wall

161
Q

Neuroblastoma origin and location

A

chromaffin cells in kids

neural crest origin

162
Q

CLassic neuroblastoma presentation

A

abdominal distention
IRREGULAR shaped mass that CROSSES MIDLINE
HTN +/-
Myoclonus or Opsoclonus (eyes)

163
Q

how to differentiate neuroblastoma from nephroblastoma (wilms)

A

Wilms is smooth and unilateral

164
Q

Histology of neuroblastoma

A

Homer wright rosettes, just like medulloblastoma

165
Q

Neuroblastoma gene defect

A

overexpression of N-myc

166
Q

2 things that suppress GH secretion

A

Somatostatin

GLucose

167
Q

buzzword for the facial apperance of hyperthyroidism

A

“frightened appearance”

Refers to staring gaze with lid lag (eyes wide open)

168
Q

mechanism of hypocholesterolemia in hyperthyroidism

A

Thyroid hormone increases LDL receptor synthesis in the liver –> decreases serum cholesterol

can increase risk of gallstones!!

169
Q

effect of free T3/ rT3 in hypothyroidism

A

Can be low or normal

There is a lot of variability on the effects of T3 b/c it is made peripherally. So in early hypothyroid, T4 will be low, but the T3 can be normal because there isn’t much of it around anyway. But in late disease, T3 will drop b/c T4 is severely low

170
Q

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

A

Inflammation (T cells)

Increased Adipocytes

171
Q

4 Tx for thyroid storm

A

PTU
Prednisone
Propanolol
Potassium Iodine

172
Q

LIgation of superior laryngeal artery during thyroidectomy. Complication?

A

Damage to superior laryngeal nerve –> loss of cricothyroid function (deepening of voice)

173
Q

Ligation of inferior thyroid artery. Post surgical complication?

A

Damage to recurrent laryngeal nerve –> hoarseness

174
Q

Hypocalcemia effects on ECG

A

QT Prolongation

175
Q

what is most likely to be seen in a kidney biopsy in a patient with Primary Hyperparathyroidism?

A

Nephrocalcinosis of the renal tubules

HyperCa = metastatic calcification

176
Q

Knuckle Knuckle Dimple Knuckle sign

A

Turners

177
Q

Knuckle Knuckle Dimple Dimple sign

A

Pseudohypoparathyroidism (Albright heriditary dystrophy)

178
Q

What is the specific defect in PsHP?

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)

179
Q

Which parent is responsible for passing on PsHP? Why?

A

Mom because of genetic imprinting

180
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

181
Q

Which parent causes PsPsHP?

A

Father

182
Q

Familial Hypocalciuric Hypercalcemia defect

A

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

183
Q

FHH Labs (serum/urine Ca, PTH)

A

High serum Ca
High PTH
Low urine Ca

184
Q

Relationship of Prolactinoma and Bone ina woman

A

Increases risk for osteoporosis

Prolactin inhibits GnRH = low estrogen = increased osteoclasti activity

185
Q

2 enzymes implicated in Osmotic damage in diabetes

A

Aldose reductase

ABSENCE of sorbitol dehydrogenase

186
Q

Insulinoma Labs (glucose, insulin, Cpeptide)

A

Low glucose
High Insulin
High C peptide

187
Q

Screening test (besides cpeptide) for insulinoma

A

Symptoms resolve after giving glucose, but then come back several hours later

188
Q

Screening test for gastrinoma

A

Gastrin levels remain elevated after secretin administration

189
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!!

190
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

191
Q

Muscle disease in hypo vs hyperthyroid? how to differentiate?

A

Both get proximal muscle wekness

Hypothyroid = Increased CK
Hyperthyroid = Normal CK

PATH STORE (24 decks)

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