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endocrinology Flashcards

1
Q

high dose dex test-when does it suppress?

A
  1. Suppresses ACTH/cortisol in a pituitary adenoma
  2. Does NOT suppress is ACTH caused by ectopic ACTH (small cell carcinoma)
  3. If adrenal secreting neoplasm, will have high cortisol, low ACTH and NO CHANGE with dexmethasone (ACTH already low and adrenal gland not responsive to it)
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2
Q

PTHrP

A

Squamous cell lung cancer

Breast cancer

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3
Q

branching papillae with a stalk and cuboidal epithelium. Ground glass appearance.
Psamomma bodies

A

papillary thyroid cancer

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4
Q

Sheets of Hurthle cells(eosinophilic cytoplasm) OR follicular cells

A

follicular thyroid cancer

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5
Q

large pleomorphic cells and multinucleated osteoclasts in thyroid histology. Also spindle cells

A

Anaplastic thyroid cancer

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6
Q

Uniform polygonal/spindle cells positive for calcitonin and amyloid

A

MTC

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7
Q

Carpal tunnel associated with:

A

hypothyroidism, diabetes

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8
Q

What is the single best test for hypothyroidism? Why?

A

TSH. Will be high. Because T4 levels can be within normal limits early on. TsH more sensitive. Serum t3 is the last thing to decline, a late indicator.

BUT if a hypothalamic problem, (central) then will not detect….

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9
Q

RANK-L is generated by

A

osteoblasts

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10
Q

Differentiation of osteoclasts is done by

A

RANK-ligand and monocyte CSF

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11
Q

OPG

A

secreted by osteoblasts, acts as a decoy receptor.

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12
Q

Bone turnover increased when:

A

Ratio of RANK-L:OPG is high.

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13
Q

How does PTH work on bone cells?

A

Stimulates secretion of Monocyte CSF and RANK-L BY osteoblasts to stimulate osteoclasts. Does not directly stimulate osteoclasts

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14
Q

How does low estrogen cause breakdown of bone?

A

Overexpression of RANK receptors causes more osteoclastic activity

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15
Q

Side effects of TZDs

A

Liver function–check LFTs.

Also, fluid retention

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16
Q

Signs of hypercalcemia

A

Stones
Groans (GI)
Bones
and psychiatric overtones (mental status)

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17
Q

rT3 made from

A

T4. Converted by hypothalamus and pituitary and also by peripheral tissues. If T4 is low, will have decreased rT3 too.

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18
Q

How does glucocorticoid affect the HPA axis?

A

Suppresses all levels, hypothalamus, pituitary, and adrenal. Can have adrenal crisis.

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19
Q

thyroid diverticulum arises from

A

floor of primitive pharynx

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20
Q

connects thyroid to tongue

A

thyroglossal duct

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21
Q

pyramidal lobe of thyroid=

A

persistence of thyroglossal duct

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22
Q

normal remnant of thyroglossal duct

A

formaen cecum

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23
Q

anterior midline neck mass that MOVES with swallowing

A

thyroglossal duct cyst

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24
Q

lateral neck mass that does not move with swallowing

A

branchial left cyst –from PERSISTENT CERVICAL SINUS

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25
Q

when does fetal adrenal become active

A

secretes cortisol late in gestation

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26
Q

fetal cortisol secretion controlled by

A

ACTH and CRH from fetal pituitary and placenta

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27
Q

Neuroblastoma

A

tumor of adrenal medulla in children

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28
Q

cells in adrenal medulla

A

chromaffin cells

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29
Q

left adrenal drains to

A

left renal vein–>IVC

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30
Q

right adrenal vein drains to

A

IVC

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31
Q

posterior pituitary derived from

A

neuroectoderm

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32
Q

anterior pituitary derived from

A

oral ectoderm (Rathke’s pouch)

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33
Q

Melanotropin secreted by

A

anterior pituitary

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34
Q

acidophils

A

GH and prolactin

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35
Q

Basophils

A

B-FLAT

-FSH, LH, ACTH, TSH

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36
Q

alpha subunit of pituitary hormone

A

TSH, LH, FSH, hCG

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37
Q

B subunit of pituitary hormone determines

A

specificity

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38
Q

alpha cells of pancreas found where?

A

periphery

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39
Q

beta cells of pancreas found where?

A

inside

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40
Q

pathophys of insulin release

A
  1. glucose enters
  2. ATP increase
  3. ATP gated K+ channels open
  4. depolarization of beta cell
  5. VG-Ca channel opens
  6. insulin secretion
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41
Q

Does insulin cross the placenta?

A

No. Ok in pregnancy

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42
Q

which organs uptake glucose independently of insulin?

A 
brain
RBC
intestine
Cornea
Kidney
Liver
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43
Q

GLUT 1 found in

A

RBC and brain (insulin independent)

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44
Q

GLUT 2 found in

A

beta cells, liver, kidney, small intestine

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45
Q

GLUT 4

A

adipose tissue, skeletal muscle

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46
Q

effect on insulin on kidneys

A

increased NA retention

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47
Q

Things that increase insulin

A

hyperglycemia
GH
B2 adrenergic ANTAGONIST

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48
Q

Things that decrease insulin

A

hypoglycemia
somatostatin
a-2 agonist

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49
Q

What type of receptor is insulin receptor?

A

tyrosine kinase

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50
Q

pathophys after insulin binds cell

A

Tyrosine kinase phosphorylates

  • -IP3 causes GLUT-4 vesicles to fuse and glycogen, lipid, and protein synthesis
  • -RAS/MAP kinase causes cell growth
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51
Q

Can RBCs use ketones for energy/

A

NO! they have no mitochondria

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52
Q

effects of glucagon

A

Glycogenolysis
gluconeogenesis
lipolysis
ketone

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53
Q

Glucagon inhibited by

A

somatostatin

and obvi insulin and hyperglycemia

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54
Q

TRH stimulates

A

TSH and prolactin

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55
Q

Dopamine inhibits

A

prolactin

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56
Q

CRH stimulates

A

ACTH
MSH (melanocyte stimulating hormone)
beta endorphin

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57
Q

Somatostatin inhibits

A

GH

TSH

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58
Q

which drugs would stimulate prolactin secretion?

A

Antipsychotics (dopamine antagonist)

Also OCPs

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59
Q

prolactin negative feedback at

A

hypothalamus–increasees dopamine

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60
Q

what stimulates prolactin secretion

A

TRH

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61
Q

Describe how growth hormone works

A

GH stimulates liver to release IGF-1/somatomedin. Causese growth

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62
Q

when is secretion of GH high?

A

exercise and sleep (when glucose is low). Pulsatile secretion.

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63
Q

Gh inhibited by

A

glucose and somatostatin

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64
Q

bilateral adrenal hyperplasia

A

congential adrenal hyperplasia

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65
Q

Boy with ambiguous genitalia

–>hypertension, hypokalemia

A

17a-OH deficiency (“boys are 17 when they hit puberty”)
high aldo
low testosterone

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66
Q

Girl with normal sex organs

–hypertension, hypokalemia

A

17alpha-OH deficiency

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67
Q

Girl with ambigulous genitalia

  • -hypotension, hyperkalemia
  • -High renin
A

21 OH deficiency

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68
Q

Boy with hypotension, hyperkalemia, and increased renin

A

21 OH deficiency

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69
Q

Girl with ambiguous genitalia

–Hypertension

A

11B OH deficiency (“girls are 11 when they hit puberty”)

–will have high 11 deoxycorticosterone

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70
Q

Boy with normal genitalia

–hypertension

A

11B OH deficiency

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71
Q

Cortisol effects

BBIIG

A 
blood pressure
decreased bone formation
Inflammatory (anti)
Insulin resistance
Gluconeogenesis
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72
Q

how does cortisol maintain blood pressure?

A

upregulates alpha 1 receptors on arterioles

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73
Q

how does cortisol effect anti-inflammatory response?

A
  1. inhibit leukotriene and prostaglandin synthesis
  2. inhibit leukocyte adhesion
  3. block histamine release
  4. reduce eosinophil count
  5. block IL-2 production
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74
Q

PTH secreted by what cells

A

chief cells

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75
Q

effects of PTH

A
  1. increased bone resorption Ca and Po4
  2. Increased calcium resabsorption
  3. Decreased phosphate in PCT
  4. Stimulates kidney 1alpha-OH
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76
Q

Overall effect of PTH on serum levels

A

Ca increase
PO4 decrease
urine phosphate increase
PTH=Phosphate trashing hormone

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77
Q

What increases PTH secretion

A

decreased calcium

slight decrease Mg2+

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78
Q

What decreases PTH secretion

A

HUGE decrease in Mg2+

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79
Q

Cause of MG2+ deficiency

A

diarrhea
Aminoglycosides
diuretics
alcohol

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80
Q

Effect of vitamin D?

A

Increases calcium reabsorption in GUT
Increases phosphate release from matrix
Increases intestinal phosphate reabsorption
–>Thus, INCREASES CALCIUM AND PO4

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81
Q

Vitamin D3 from

A

sun exposure

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82
Q

Vitamin D2 from

A

plants

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83
Q

what increases 1, 25 OH2 production

A

Increased PTh
decreased PO4
decreased ca

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84
Q

what cells make calcitonin

A

parafollicular cells

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85
Q

effect of calcitoning

A

decreases bone resorption

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86
Q

t3/T4 receptor

A

steroid

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87
Q

IGF-1, PDGF, EGF (growth factor) receptor

A

Intrinsic tyrosine kinase–>MAP kinase

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88
Q

acidophile and cytokine recptor

A

receptor tyrosine kinase

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89
Q

Nitric oxide, ANP receptor

A

cGMP

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90
Q

vitamin D receptor

A

steroid

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91
Q

GnRH, GHRH signaling pathway

A

IP3

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92
Q

Oxytonin and ADH signaling pathway

A

IP3

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93
Q

TRH signaling pathway

A

IP3

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94
Q

FSH, LH, ACTH, TSH, pathway

A

cAMP

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95
Q

hitamine and gastrin pathway

A

IP3

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96
Q

PTH and calcitonin signaling pathway

A

cAMP

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97
Q

glucagon signaling pathway

A

cAMP

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98
Q

SHBG and testosterone

A

Increase SHBG lowers testosterone.

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99
Q

SHBG levels during pregnancy

A

Increase.

100
Q

Excess iodide temporarily inhibits thyroid peroxidase

A

Wolff Chaikoff effect

101
Q

what converts t4 to t3

A

5’ deiodinase

102
Q

thyroid binding globulin effect

A

binds hormone, preventing it from having any effects

103
Q

When are TBG levels low? high?

A

low: hepatic failure
high: pregnancy

104
Q

how does thyroid hormone increase basal metabolic rate?

A

Upregulates Na/K ATPase

105
Q

peroxidase

A

coupling of MIT and DIT

–oxidation of iodide

106
Q

Methimazole effect

A

Inhibits peroxidase only

‘A MONO EFFECT)

107
Q

propylthiouracil effect

A

Inhibits peroxidase AND peripheral 5’deiodinase

A POLY effect

108
Q

Cushing’s disease

A

INCREASED ACTH causing cushing’s syndrome

109
Q

Other causes of cushing’s syndrome

A

ectopic ACTH

Adrenal hyperplasia/adenoma

110
Q

striae

A

hypercortisolism

111
Q

low dose dex: cortisol elevated

high dose dex: cortisol suppressed

A

cushing’s disease

-ACTH producing tumor

112
Q

low dose dex: coritsol elevated

high dose dex: cortisol elevated

A

Ectopic ACTH OR adrenal hyperplasia/adenoma/carcinoma

113
Q

Conn’s syndrome

A

aldosterone secreting adenoma

114
Q

Treatment for Conn’s or adrenal hyperplasia

A

surgery or spironolactone

115
Q

Cause of secondary hyperaldosteronism

A

renal artery stenosis
CHF
nephrotic syndrome (perception of low intravascular volume)

116
Q

Cause of addison’s

A

Adrenal Atrophy

Absence of hormone

117
Q

hypotension
hyperkalemia
acidosis

A

signs of adrenal insufficiency

118
Q

how to disginguish primary from secondary adrenal insufficiency

A

Primary

  • -High ACTH: skin pigmentation
  • -hyperkalemia (ALSO aldosterone is low!)

Secondary:

  • -No hyperkalemia
  • -ONLY cortisol is low
  • -LOW ACTH
119
Q

how to distinguish primary from secondary hyperaldosteronism?

A

renin levels

120
Q

Pheos associated with:

A

NF-1
MEN2A
MEN2B

121
Q

Treatment for pheo

A
  1. alpha blockade
  2. beta blockade
  3. surgery
122
Q

Rule of 10’s

A

Pheos are 10%:

  • malignant
  • bilateral
  • extra-adrenal
  • calcify
  • kids
123
Q

describe pathway of phenylalanine breakdown

A 
phenylalanine
tyrosine
L-dopa
Dopamine
norepinephrine
epinephrine
124
Q

Breakdown product of dopamine

A

HVA, increased in pheos along with VMAs

125
Q

Waterhouse friederichsen

A

acute primary adrenal insufficiency from adrenal hemorrhage

126
Q

Waterhouse friederichsen is associated with

A

neisseria meningitidis

DIC/Shock

127
Q

dx: neuroblastoma

A

elevated homovanillic acid in the urine.

128
Q

What’s different about neuroblastoma vs a pheo?

A

Less likely to develop hypertension

129
Q

oncogene associated with neuroblastoma

A

n-myc

130
Q

how does a neuroblastoma classically present?

A
  1. abdominal fullness
  2. compression of sympathetic chain (horner’s)
  3. small blue round cells
131
Q

facial/perorbital myxedema

A

sign of hypothyroidism

132
Q

pretibial myxedema

exopthalmos

A

Specific to graves. Not found in other causes of hyperthyroidism

133
Q

dx: hypothyroidism

A 
increased TSH (if primary)
Decreased T4
134
Q

dx: hyperthyroidism

A 
decreased TSH (if primary)
increased free or total T4/T3
135
Q

What is the most sensitive test for primary hypothyroidism?

A

increased TSH

136
Q

hashimotos association

A

HLA-DR5

137
Q

Histology of hashimoto’s

A

Hurthle cells

lymphocytic infiltrate with germinal centers

138
Q

enlarged nontender thyroid

A

hashimoto’s

139
Q

pathophys of hashimotos’

A

anti-thyroglobulin antibodies

140
Q

cretinism caused by

A

severe fetal hypothyroidism

141
Q

Cause of endemic cretinism

A

lack of dietary iodine

142
Q

cause of sporadic cretinism

A

Defect in T4 formation

143
Q

Pot bellied, pale, puffy faced kid with

Protruding umbilicus and Protuberant tongue

A

5P’s of hypocretinism

144
Q

self-limited hypothyroidism after a flu like illness

A

subacute thyroiditis

145
Q

Histology of subacute thyroiditis

A

granulomatous inflammation

146
Q

hypothyroidism with increased ESR, jaw pain, early inflammation, and a tender thyroid

A

subacute thyroiditis

147
Q

hypothyroidism where thyroid is replaced by fibrous tissue

A

riedel’s thyroiditis

148
Q

fixed, hard rock like and painless goiter

A

riedel’s

149
Q

Cause of Riedel’s thyroiditis

A

IgG4 systemic disease

–overproduction of IgG4, causing fibrosis

150
Q

Jod basedow phenomenon

A

thyrotoxicosis if a patient with iodine deficiency goiter is made iodine replete

151
Q

Toxic multinodular goiter etiology

A

mutation in TSH receptor

152
Q

pathophys thyroid storm

A

stress causes a huge catecholamine surge and arrhythmia

153
Q

serious complication of hyperthyroidism

A

thyroid storm.

154
Q

ALP during thyroid storm

A

Increased

155
Q

Hashimoto’s thyroiditis cancer

A

lymphoma

156
Q

orphan annie’s eyes, psamomma bodies, nuclear grooves. Excellent prognosis

A

papillary carcinoma

157
Q

Calcitonin producing tumor with sheet of cells

A

medullary carcinoma

158
Q

who gets anaplastic thyroid cnacer

A

older pts, poor prognosis

159
Q

cystic bone spaces filled with brown fibrous tissue

A

osteitis fibrosa cystica

160
Q

Cause of osteitis fibrosa cystica

A

High PTH

161
Q

cause of primary hyper PTH

A

adenoma

162
Q

lab findings in primary hyperPTH

A

hypercalcemia
hypercalciuria
hypophosphatemia
increased alkaline phosphatase

163
Q

cause of secondary hyperparathyroidism

A

chronic renal disease

164
Q

Labs in secondary hyperparathyroidism

A

hypOcalcemia
hypophosphatemia
increased alkaline phosphatase

165
Q

renal osteodystrophy

A

bone lesions from 2ndary or tertiary hyperparathyroidism

166
Q

Tertiary hyperparathyroidism

A

Autonomous hyperparathyroidism secretion from chronic renal disease.

  • VERY high PTH
  • hyPERcalcemia
167
Q

Causes of hypoPTH

A
  1. DiGeorge
  2. Surgical excision accidnetal
  3. autoimmune destruction
168
Q

Findings of Hypoparathyroidism

A

hypocalcemia
tetany
Chvostek’s sign
Trousseau’s sign

169
Q

Chvostek’s sign

A

tapping of facial nerve=contraction of facial muscles

170
Q

Trousseau’s sign

A

Occlusion of brachial artery with BP cuff

171
Q

Pseudohypoparathyroidism

A

Kidney unresponsive to PTH.

  • -inherited.
  • -hypocalcemia with shortened 4th/5th digits and short stature
172
Q

Inheritance of pseudohypoparathyroidism

A

autosomal dominant

173
Q

Dx of acromegaly

A 
Increased serum IGF-1
OR
Glucose tolerance test-->failure to suppress serum GH
OR
MRI for pituitary mass
174
Q

Treatment for prolactinoma

A

bromocriptine
cabergoline
–dopamine agonists

175
Q

treatment of acromegaly

A

Pituitary adenoma resection

somatostatin analog

176
Q

causes of central DI

A

tumor
trauma/surgery
histiocytosis X

177
Q

causes of nephrogenic DI

A

lithium
hypercalcemia
demeclocycline

178
Q

lab findings of diabetes insipidus

A

Urine specific gravity < 1

serum osmolality > 290

179
Q

dx of diabetes insipidus

A

water deprivation test

180
Q

how to distinguish central vs nephrogenic DI

A

Central: Will respond to Desmopressin
Nephrogenic: No response

181
Q

Treatment for nephrogenic diabetes insipidus

A

hydrochlorothiazide
indomethacin
amiloride

182
Q

Main problem in SIADH

A

hyponatremia from:

  1. High ADH
  2. Low aldosterone
183
Q

treatment of SIADH

A
  1. fluid restriction
    conivaptan
    demeclocycline
184
Q

drugs that can cause SIADH

A

cyclophosphamide

pulmonary dz too

185
Q

Causes of hypopituitarism

A
  1. Pituitary adenoma/craniopharyngioma
  2. Sheehan
  3. empty sella
    radiation and brain injury
186
Q

Cause of coma in type 2 diabetes

A

hyperosmolarity of blood

187
Q

cause of dehydration in insulin deficiency

A

osmotic diuresis with glucose and ketones in the urine

188
Q

Main BUZZWORD FOR DIABETES

A

nonenzymatic glycosylation

189
Q

nonenzymatic glycosylation is responsible for

A

small vessel disease and large vessel disease

  • -retinopathy, glaucoma, renal failure, nephropathy
  • CAD
190
Q

Ostmotic damage in diabetes causes

A

neuropathy and cataracts

191
Q

Histology of T1D

A

islet leukocytic infiltrate

192
Q

Histology of T2D

A

islet amyloid deposit

193
Q

Serum labs in diabetic ketoacidosis

A 
Hyperkalemia (but depleted intracellular K)
Acidosis
Decreased bicarb
(anion gap metabolic acidosis)
194
Q

signs of carcinoid syndrome (labs)

A

Increased 5-HIAA

Niacin deficiency

195
Q

treatment of carcinoid syndrome

A

octreotide (somatostatin analog)

196
Q

Rule of 1/3rds

A

applies to carcinoid syndrome

  • -1/3 metastasize
  • -1/3 present with a second malignancy
  • -1/3 have multiple tumors
197
Q

zollinger ellison associated with

A

MEN type I

198
Q

Men 1 tumor

A

Pituitary, Pancreas, parathyroid (3P’s)

199
Q

Men 2A

A

Parathyroids and pheo(2P)

200
Q

Men 2B

A

Pheo (1P)

201
Q

MEN inheritance

A

autosomal dominant

202
Q

gene mutation in MEN 2A and 2B

A

ret

203
Q

pt with kidney stones and stomach ulcers

A

Men1

  • -Hyperparathyroidism
  • -Zollinger ellison (pancreas)
204
Q

Medullary thyroid cancer seen in

A

MEN2

205
Q

Oral ganglioneuromatosis

A

Men2B

–Associated with marfanoid habitus

206
Q

intermediate insulin

A

NPH

207
Q

Effects of metformin

A

decreased gluconeogenesis
Increased glycolysis
Increased peripheral glucose uptake

208
Q

Most serious adverse effect of metformin

A
  1. lactic acidosis
209
Q

Who is metformin contraindicated in?

A

renal failure

210
Q

can you use metformin in type 1?

A

YES–does not require islet function to work! It enhances glucose uptake without insulin

211
Q

Mechanism of sulfonylureas

A

Increases insulin release

212
Q

tox: sulfonylureas

A

first generation: disulfiram

2nd generation: hypoglycemia

213
Q

Tobultamide

chlorpropamide

A

first generation sulfonylurea

214
Q

glyburide
glimepiride
glipizide

A

second generation sulfonylureas

215
Q

pioglitazone

rosiglitazone

A

TZDs

216
Q

mechanism of TZDs

A

increase insulin sensitivity in peripheral tissue

–Binds PPAR-y nuclear transcription factor

217
Q

Indication of TZDs

A

Type 2 diabetes

218
Q

Side effect of TZD

A

weight gain, edema
hepatotoxicity
heart failure

219
Q

acarbose

miglitol

A

alpha glucosidase inhibitors

220
Q

mech: alpha glucosidase inhibitor acarbose miglitol

A

Inhibit intestinal brush border a-glucosidases

  • -decreased sugar absorption
  • -reuces postprandial hyperglycemia
221
Q

tox: a-glucosidase inhibitors

A

GI disturbances

222
Q

pramlintide

A

amylin analog

223
Q

mechanism pramlintide

A

decreases glucagon

224
Q

Mechanism: exenatide/liraglutide

A

increase insulin

decrease glucagon

225
Q

linagliptin
saxagliptin
sitagliptin

A

DPP-4 inhibitors

226
Q

-gliptin mechanism

A

Increase insulin

decrease glucagon

227
Q

Which oral anti-diabetic agents can be used in type 1?

A

metformin

pramlintide

228
Q

side effect of acarbose/miglitol

A

GI disturbance

229
Q

Side effect of GLP-1

A

GLP-1

230
Q

Side effect of DPP4 gliptins

A

urinary/respiratory infections

231
Q

Side effects of propylthiouracil/methimazole

A

agranulocytosis
aplastic anemia
skin rash

232
Q

side effect of propylthiouracil

A

hepatotoxicity

233
Q

side effect of methimazole

A

teratogen

234
Q

demecoglycline use

A

SIADH

235
Q

octreotide use

A

Somatostatin analog

acromegaly
carcinoid (somatostatin inhibits gastric neuroendocrine cells, gastrin, CCK, 
gastrinoma
glucaonoma
esophageal varices
236
Q

oxytocin use

A 
stimulates labor
milk let down
uterine hemorrhage (contracts spiral arteries?)
237
Q

tox of demeclocycline

A

nephrogenic DI (if too much)
photosensitivity
bone/teeth abnormalities

238
Q

Mechanism glucocorticoids

A

Inhibits phospholipase A2 and Cox2

–decreases leukotrienes and prostaglandins

239
Q

How do you treat addison’s disease

A

Give glucocorticoids

240
Q

What happens if you stop giving glucocorticoids suddenly?

A

Can have adrenal insufficiency (takes time for adrenal to take over, HPA has been suppressed for such a long time)

241
Q

Side effect of glucocorticoids

A

peptic ulcers

diabetes

242
Q

origin of thyroid parafollicular cells

A

neural crest cells

243
Q

classic addison’s presentation

A 
Hyperpigmentation!
Less insulin requirement if diabetic
Orthostatic hypotension
GI symptoms
Fatigue, weight loss
--TYPICALLY LOSS OF CORTISOL AND ALDOSTERONE
244
Q

Leuprolide mechanism

A 
GnRH agonist: 
--Increase testo/DHT
--then DECREASE
a form of androgen deprivation therapy
--abolishes pulsatile secretion
245
Q

Finasteride

A

5a-reductase

  • -increase in testosterone
  • -decrease in DHT
246
Q

flushing
diarrhea
bronchospasm

A

carcinoid syndrome

247
Q

Sarcoidosis results in hypercalcemia from

A

Excess vitamin D (calcitriol)

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