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STEP > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Most common ectopic thyroid tissue site

A

tongue (lingual thyroid). removal may result in hypothyroidism if it is the only thyroid tissue present.

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2
Q

branchial cleft cyst origin

A

persistent cervical sinus

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3
Q

Thyroid tissue origin

A

endoderm

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4
Q

parafollicular cell origin

A

neural crest

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5
Q

adrenal cortex and medulla origin

A

cortex from mesoderm, medulla from neural crest

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6
Q

chromaffin cell regulatory control

A

preganglionic sympathetic fibers

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7
Q

Melanotropin (MSH) origin

A

Intermediate lobe of pituitary.

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8
Q

Anterior pituitary other name

A

adenohypophysis

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9
Q

Anterior pituitary origin

A

oral ectodrm (Rathke pouch)

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10
Q

Hormones that share alpha subunit

A

TSH, LH, FSH, and hCG. Beta subunit determines specificity.

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11
Q

proopiomelanocortin (POMC(

A

ACTH and MSH are derivates of proopiomelanocortin (POMC)

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12
Q

hormones of anterior pituitary

A

FLAT Pig: FSH, LH, ACTH, TSH, PRL, GH.

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13
Q

Basophils

A

B-FLAT: basophils-FSH, LH, ACTH, TSH

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14
Q

Acidophils

A

GH, PRL

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15
Q

posterior pituitary other name

A

neurohypophysis

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16
Q

Origin of ADH and oxytocin

A

supraoptic and paraventricular nuclei

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17
Q

ADH and oxytocin transport

A

carrier proteins called neurophysins.

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18
Q

posterior pituitary embryo origin

A

neuroectoderm

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19
Q

Islets of langerhans

A

collections of alpha, beta, and gamma endocrine cells in the pancreas.

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20
Q

Islets of langerhans origins

A

Arise from pancreatic buds.

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21
Q

Islets of langerhans organizations

A

alpha cells peripherally, beta cells centrally, delta cells interspersed

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22
Q

alpha cells secrete

A

glucagon

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23
Q

delta cells secrete

A

somatostatin

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24
Q

Insulin synthesis

A

preproinsulin synthesized in RER –> cleavage of “presignal” –> proinsulin (stored in secretory granules) –> cleavage of proinsulin –> exocytosis of insulin and C-peptide equally.

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25
Q

C-peptide significance

A

increased in insulinoma and sulfonylurea use, whereas exogenous insulin lacks C-peptide

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26
Q

Insulin receptors

A

tyrosine kinase

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27
Q

insulin MOA

A

activates gene transcription

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28
Q

anabolic effects of insulin

A

1) Increases glucose transport in skeletal muscle and adipose tissue.
2) increases glycogen synthesis and storage
3) increases TG synthesis
4) increases Na+ retention
5) increases protein synthesis
6) increases cellular uptake of K+ and amino acids
7) decreases glucagon release
8) decreases lipolysis in adipose tissue

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29
Q

insulin and placenta

A

doesn’t cross it, unlike glucose

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30
Q

GLUT-4 expression

A

adipose tissue + striated muscle. exercise can also increase GLUT-4 expression

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31
Q

GLUT-1

A

RBCs, brain, cornea, placenta

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32
Q

GLUT-2

A

beta-islet cells, liver, kidney, small intestine

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33
Q

GLUT-3

A

brain, placenta

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34
Q

GLUT-5

A

fructose, spermatocytes, GI tract

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35
Q

insulin-independent glucose uptake pneumonic

A

BRICK L, brain, RBCs, intestine, cornea, kidney, liver

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36
Q

Major regulator of insulin release

A

glucose

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37
Q

Why is there increased insulin sensitivity with oral vs. IV glucose?

A

Incretins such as glucagon-like peptide 1 (GLP-1), which are released after meals + increased beta cell sensitivity to glucose.

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38
Q

Insulin growth pathway

A

insulin binds to receptor –> tyrosine phosphorylation –> RAS/MAP kinase pathway –> cell growth, DNA synthesis

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39
Q

Insulin glucose uptake pathway

A

insulin binds to receptor –> tyrosine phosphorylation –> Phosphoinositide-3 kianse pathway –> vesicles containing GLUT-4 translocate to membrane –> glucose enters via GLUT-4 carriers

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40
Q

Insulin release pathway

A

Glucose enters beta cells through GLUT-2 transporters –> undergoes glycolysis –> increased ATP/ADP ratio–> ATP-sensitive K+ channels close –> membrane depolarized –> voltage-gated Ca2+ channels open –> Ca2+ influx –> exocytosis of insulin vesicles.

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41
Q

glucagon effects

A

1) glycogenolysis, gluconeogenesis

2) lipolysis, ketone production

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42
Q

glucagon inhibitors

A

insulin
hyperglycemia
*somatostain

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43
Q

CRH function

A

increases ACTH, MSH, beta-endorphin

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44
Q

CRH and steroids

A

chronic exogenous steroids decrease CRH

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45
Q

dopamine effects

A

decrease prolactin, decrease TSH

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46
Q

tesamorelin

A

GHRH analog used to treat HIV-associated lipodystrophy

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47
Q

prolactin endocrine effects

A

decreases GnRH (which explains amenorrhea/hypogonadism in pituitary prolactinoma)

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48
Q

somatostatin endocrine efects

A

decreases GH, TSH

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49
Q

TRH affects

A

increases TSH + *prolactin

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50
Q

prolactin structure

A

homologous to GH

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51
Q

Prolactin regulation

A

1) tonically inhibited by dopamine from hypothalamus. 2) Prolactin in turn inhibits its own secretion by increasing dopamine synthesis and secretion from hypothalamus. 3) TRH increases prolactin secretion.
4) renal failure increases prolactin release via reduced prolactin elimination
5) pregnancy –> estrogen –> increased prolactin

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52
Q

TRH and hypothyroidism and amenorrhea

A

TRH increases prolactin secretion in hypothyroidism –> hyperprolactinemia inhibits GnRH

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53
Q

cry of baby and prolactine mechanism

A

cry of baby activates higher cortical centers –> inhibit hypothalamus from secreting dopamine

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54
Q

somatotropin

A

GH

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55
Q

somatomedin C

A

IGF-1

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56
Q

GH actions

A

1) stimulates linear growth and muscle mass through IGF-1 secretion
2) increased insulin resistance

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57
Q

GH regulation and secretion

A
  • released in pulses in response to GHRH.
  • secretion increases during exercise, deep sleep, puberty, hypoglycemia.
  • secretion inhibited by glucose and somatostatin release via negative feedback by somatomedin.
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58
Q

orexigenic

A

means stimulates hunger

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59
Q

positive ghrelin regulation

A

sleep deprivation + Prader-Willi

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60
Q

Ghrelin effects

A

stimulates hunger + GH release

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61
Q

leptin source

A

adipose tissue

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62
Q

endocannabinoids and munchies mechanism

A

act at cannabinoid receptors in hypothalamus and nucleus accumbens, two key brain areas for the homeostatic and hedonic control of food intake, thus increasing appetite.

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63
Q

source of ADH

A

supraoptic nuclei

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64
Q

V1 vs. V2 ADH receptors

A

V2 regulate serum osmolarity, V1 regulate BP

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65
Q

ADH level in Central and nephrogenic DI

A

down in central, normal or increased in nephrogenic

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66
Q

nephrogenic DI etiology

A

mutation in V2 receptor

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67
Q

desmopressin acetate 1) MOA, 2) clinical use

A

ADH analog

central DI + nocturnal enuresis

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68
Q

ADH regulation

A

osmoreceptors in hypothalamus; hypovolemia

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69
Q

17alpha-hydroxylase lab profile

1) mineralocorticoids
2) cortisol
3) sex hormones
4) BP
5) potassium
6) other

A

1) increased
2) decreased
3) decreased
4) increased
5) decreased
6) decreased andostenedione

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70
Q

21-hydroxylase lab profile

1) mineralocorticoids
2) cortisol
3) sex hormones
4) BP
5) potassium
6) other

A

1) down
2) down
3) up
4) down
5) up
6) increased renin activity + increased 17-hydroxy-progesterone

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71
Q

11beta-hydroxylase lab profile

1) mineralocorticoids
2) cortisol
3) sex hormones
4) BP
5) potassium
6) other

A

1) decreased aldosterone, but increased 11-deoxycorticosterone so increased Bp
2) down
3) up
4) up
5) down
6) decreased renin

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72
Q

Cortisol carrier protein

A

corticosteroid-binding globulin (CBG)

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73
Q

cortisol and immunology caveat

A

exogenous corticosteroids can cause reactivation of TB and candidiasis by blocking IL-2 production

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74
Q

cortisol and BP mechanism

A

1) Upregulates alpha1-receptors on arterioles, increasing sensitivity to NE and E.
2) At high concentrations, can bind to mineralocorticoid (aldosterone) receptors.

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75
Q

cortisol actions

A

BIG FIB.
Increases BP
Increases Insulin resistance
Increases Gluconeogenesis, lipolysis, and proteolysis
Decreases Fibroblast activity (causes striae)
Decreases Inflammatory and Immune responses
Decreases Bone formation (by decreasing osteoblast activity)

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76
Q

Cortisol and immune modification mechanism

A

1) inhibits production of leukotrienes and PGs
2) inhibits WBC adhesions –> neutrophilia
3) blocks histamine release from mast cells.
4) reduces eosinophils
5) blocks IL-2 production

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77
Q

cortisol regulation

A

CRH –> ACTH –> cortisol production. Excess cortisol deceases CRh, ACTH, etc.

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78
Q

Plasma calcium forms

A

1) ionized (45%)
2) bound to albumin (40%)
3) bound to anions (15%)

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79
Q

calcium and pH mechanism

A

increased pH increases affinity (negative charge) of albumin for Ca –> hypocalcemia (cramps, pain, paresthesias, carpopedal spasm).

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80
Q

D3 sources

A

sun, fish, plants

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81
Q

D2 sources

A

Ingestion of plants, fungi, yeasts

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82
Q

Vitamin D negative regulation

A

1,25-(OH)2 feedback inhibits its own production

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83
Q

PTH and urine cAMP

A

PTH increases urine cAMP

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84
Q

RANK-L

A
  • receptor activator of NH-kB ligand.
  • secreted by osteoblasts and osteocytes.
  • Binds RANK (receptor) on osteoclasts and their precursors to stimulate osteoclasts and increase calcium, leading to bone resportion.
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85
Q

other regulator of PTH

A

decreased serum Mg increases PTH, but severely decreased Mg decreases PTH secretion.

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86
Q

Common causes of hypomagnesemia

A

diarrhea, aminoglycosides, diuretics, alcohol abuse.

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87
Q

PTH and vitamin D mechanism

A

positive regulator of 1alpha-hydroxylase

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88
Q

calcitonin source

A

parafollicular cells (C cells) of thyroid

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89
Q

Source of T3/T4

A

Follicles of thyroid. Most T3 formed in target tissues.

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90
Q

T3 functions

A

4 B’s –> Brain maturation, Bone growth (synergistic with GH), Beta-adrenergic affects (increases beta1 receptor expression in heart), increases Basal metabolic rate.
*also increases glycogenolysis, gluconeogenesis, lipolysis.

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91
Q

How does T3 increase basal metabolic rate?

A

via increased Na+/K+-ATPase activity, leading to increased O2 consumption, RR, body temperature

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92
Q

TSI

A

thyroid-stimulating immunoglobulin. Graves disease.

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93
Q

Wolff-Chaikoff effect

A

Excess iodine temporarily inhibits thyroid peroxidase, leading to decreased iodine organification, and decreased T3/T4 production.

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94
Q

When is TBG (thyroxine-binding globuline) increased and decreased?

A

Decreased –> hepatic failure, steroids.

Increased –> pregnancy (via estrogen), OCP use.

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95
Q

what converts T4 to T3?

A

5’-deiodinase

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96
Q

T3 vs. T4 potency

A

T3 binds nuclear receptor with greater affinity

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97
Q

Thyroid peroxidase functions

A

1) oxidation and organification of iodide

2) coupling of monoiodotyrosine (MIT) and di-iodotyrosine (DIT).

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98
Q

T4 structure

A

DIT + DIT

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99
Q

T3 structure

A

DIT + MIT

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100
Q

propylthiouracil and methimazole and thyroxine actions

A

Propylthiouracil inhibits both thyroid peroxidase and 5’deiodinase. Methimazole inhibits thyroid peroxidase only.

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101
Q

T3/T4 synthesis

A

Thyroglobulin secreted into follicular lumen –> organification of I2 by thyroid peroxidase –> T4 endocytoses back into epithelial cell –> coupling reaction, T4, T3 to circulation

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102
Q

thyroglobulin derived from

A

tyrosine

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103
Q

Iodine uptake mechanism

A

cotransport with Na

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104
Q

hormones that act through cAMP pathway

A

FLAT ChAMP –> FSH, LH, ACTH, TSH, CRH, hCG, ADH (V2), MSH, PTH.
ALSO –> calcitonin, GHRH, glucagon.

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105
Q

hormones that act through cGMP

A

Think vasodilators. BNP, ANP, EDRF (NO)

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106
Q

other name for NO

A

EDRF, endothelium-derived relaxation factor.

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107
Q

Hormones that act through IP3 pathway

A

GOAT HAG.

GnRH, Oxytocin, ADH (V1), TRH, Histamine (H1-receptor), Angiotensin II, Gastrin

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108
Q

hormones that act through an intracellular receptor

A

Progesterone, estrogen, testosterone, cortisol, aldosterone, T3/T4, vitamin D

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109
Q

hormones that act through receptor tyrosine kinase (MAP kinase pathway)

A

Insulin, IGF-1, FGF, PDGF, EGF

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110
Q

hormones that act through nonreceptor tyrosine kinase (JAK/STAT)

A

Prolactin, immunomodulators (eg, IL-2, IL-6, IFN), GH, G-CSF, Epo, thrombopoietin.

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111
Q

steroid transport

A

lipophilic. thus must be bound to specific binding globulins to increase their solubility

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112
Q

affect of SHBG in men

A

Sex hormone binding globulin. Lowers free testosterone causing gynecomastia.

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113
Q

Cause of hirsutism in women

A

Decreased SHBG raises free testosterone.

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114
Q

SHBG increased with…

A

OCPs, pregnancy

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115
Q

steroid signaling pathway

A

Hormone binds to receptor in nucleus or cytoplasm –> transformation of receptor to expose DNA-binding domain –> bidns to enhancer-like element in DNA –> activates gene transcription.

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2
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116
Q

Most common cause of cushings

A

exogenous corticosteroids (resulting in decreased ACTH and bilateral adrenal atrophy)

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117
Q

Causes of cushings

A

1) exogenous corticosteroids
2) primary adrenal adenoma, hyperplasia, or carcinoma – result in decreased ACTH, atrophy of uninvolved adrenal gland. Can also present with pseudohyperaldosteronism.
3) ACTH-secreting pituitary adenoma (Cushing disease).
4) paraneoplastic ACTH secretion

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118
Q

what causes most endogenous Cushings?

A

ACTH-secreting pituitary adenoma.

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119
Q

Cushing disease

A

ACTH-secreting pituitary adenoma

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120
Q

Cushing’s presentation

A

HTN, weight gain, moon facies, abdominal striae, truncal obesity, buffalo hump, skin changes, osteoporosis, hyperglycemia (insulin resistance), ammenorrhea, immunosuppression

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121
Q

Cushing’s screening tests

A

1) increased free cortisol on 24-hr urinalysis
2) increased midnight salivary cortisol
3) NO suppression with overnight low-dose dexamethasone test.
4) measure serum ACTH

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122
Q

What is the use of a high-dose dexamethasone suppression test?

A

Suppression = Cushing disease

No suppression = ectopic ACTH secretion

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123
Q

What is the use of a CRH stimulation test?

A

Increased ACTH, cortisol = Cushing disease

No increased ACTH, cortisol = ectopic ACTH secretion

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124
Q

Lab findings for exogenous glucocorticoids or adrenal tumor

A

ACTH will be LOW

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125
Q

Adrenal insufficiency presentation

A

weakness + fatigue + orthostatic hypotension + muscle aches + weight loss + GI disturbances + sugar and/or salt cravings

126
Q

Adrenal insufficiency diagnosis

A

1) measurement of serum electrolytes
2) morning/random serum cortisol and ACTH
3) ACTH/cosyntropin stimulation test
4) metyrapone stimulation test

127
Q

difference in labs between primary and 2/3 adrenal insufficiency

A

low cortisol, high ACTH in primary adrenal insufficiency; low cortisol, low ACTH in secondary/tertiatry due to pituitary, hypothalamic disease

128
Q

metyrapone stimulation test + analyzing results

A

Metyrapone blocks last step of cortisol synthesis (11-deoxycortisol to cortisol). Normal response is decreased cortisol and compensatory increased ACTH and 11-deoxycortisol. In primary adrenal insufficiency, ACTH is increased but 11-deoxycortisol remains low after test. In secondary/tertiary adrenal insufficiency, both ACTh and 11-deoxycortisol remain decreased after test.

129
Q

primary adrenal insufficiency labs

A

hypotension (hyponatremic volume contraction) + hyperkalemia + metabolic acidosis.

130
Q

Why do you have skin hyperpigmentation in primary adrenal insufficiency?

A

Increased MSH, byproduct of ACTH production from proopiomelanocortin (POMC).

131
Q

primary adrenal insufficiency association

A

Autoimmune polyglandular syndromes.

132
Q

Acute adrenal insufficiency cause and presentation

A

Massive hemorrhage. Shock.

133
Q

Waterhouse-Friderichsen syndrome

A

Acute, primary adrenal insufficiency due to adrenal hemorrhage with septicemia (usually neisseria), DIC, endotoxic shock.

134
Q

Addison’s causes

A

autoimmune in Western world, TB in developing.

135
Q

Secondary adrenal insufficiency

A

Decreased pituitary ACTH production.

136
Q

Difference in presentation with secondary adrenal insufficiency

A

No skin/mucosal hyperpigmentation, no hyperkalemia (aldosterone synthesis preservd). (secondary spares the skin/mucosa)

137
Q

Cause of tertiary adrenal insufficiency

A

Chronic exogenous steroid use, precipitated by abrupt withdrawal. Aldosterone synthesis unaffected.

138
Q

Why is there no edema in hyperaldosteronism?

A

Aldosterone escape.

139
Q

causes of primary hyperaldosteronism

A

adrenal adenoma (Conn syndrome) or idiopathic adrenal hyerplasia.

140
Q

Causes of secondary hyperaldosteronism

A

1) renovascular hypertension

2) juxtaglomerular cell tumor (due to independent activation of RAAS)

141
Q

secondary hyperaldosteronism labs

A

Increased aldosterone + increased renin.

142
Q

origin of neuroendocrine tumors

A

Kulchitsky and enterochromaffin-like cells.

143
Q

examples of neuroendocrine tumors

A

1) medullary thyroid
2) small cell carcinoma
3) islet cell tumor in pancreas

144
Q

hormones secreted by neuroendocrine tumors

A

5-HIAA, neuron-specific enolase (NSE), chromogranin A

145
Q

What do neuroendocrine cells contain?

A

amine precursor uptake decarboxylase (APUD)

146
Q

neuroblastoma origin

A

neural crest cells

147
Q

Neuroblastoma location

A

can occur anywhere along the sympathetic chain.

148
Q

Most common presentation of neuroblastoma

A

Firm, irregular mass that can cross the midline (vs. wilms, which is smooth and unilateral).

149
Q

urine metabolites in neuroblastoma

A

increased HVA and VMA

150
Q

neuroblastoma tumor markers

A

Bombesin + NSE positive.

151
Q

neuroblastoma classification

A

APUD tumor

152
Q

pheochromocytoma genes

A

Up to 25% associated with germline mutations (NF-1, VHL, RET [MEN 2A, 2B]0

153
Q

pheochromocytoma rule of 10s

A

10% malignant, bilateral, extra-adrenal, calcify, kids

154
Q

pheochromocytoma management and caveat

A

Irreversible alpha-antagonists (eg phenoxybenzamine) followed by beta-blockers prior to tumor resection. alpha-blockade must be achieved before giving beta-blockers to avoid a hypertensive crisis.

155
Q

hypothyroid myopathy

A

proximal muscle weakness, increased CK associated with hypothyroidism

156
Q

hypothyroidism derm presentation

A

Myxedema (facial/periorbital)

157
Q

appetite in hypo/hyperthyroidism

A

decreased in hypo, increased in hyper

158
Q

thyrotoxic myopathy

A

hyperthyroidism – proximal muscle weakness, normal CK

159
Q

hyperthyroidism derm presentation?

A

pretibial myxedema (Graves), periorbital edema

160
Q

skin and hair findings in hyperthyroidism

A

warm, moist skin; fine hair

161
Q

adrenergic response to hyperthyroidism

A

increased number and sensitivity of beta-adrenergic receptors

162
Q

hyper/hypocholsterolemia in hyper and hypothyroidism

A

Hypercholesterolemia in hypothyroidism (decreased LDL receptor expression); hypocholesterolemia in hyper (increased LDL receptor expression).

163
Q

Causes of smooth/diffuse goiter

A

1) Graves disease
2) Hashimoto thyroiditis
3) Iodine deficiency
4) TSH-secreting pituitary adenoma

164
Q

Causes of nodular goiter

A

1) Toxic multinodular goiter
2) Thyroid adenoma
3) thyroid cancer
4) thyroid cyst

165
Q

antibodies in hashimoto’s

A 
antithyroid peroxidase (antimicrosomal)
antithyroglobulin
166
Q

HLA hashimoto’s association

167
Q

hashimoto and cancer

A

Increased risk of non-Hodgkin lymphoma (typically of B-cell origin)

168
Q

Hashimoto’s caveat

A

May be hyperthyroid early in course due to thyrotoxicosis during follicular rupture

169
Q

Hashimoto’s histology

A

Hurthle cells, lymphoid aggregates with germinal centers

170
Q

hashimoto’s findings

A

moderately enlarged, NONTENDER thyroid.

171
Q

Causes of cretenisism

A

1) maternal hypothyroidism
2) thyroid agenesis
3) thyroid dysgenesis
4) iodine deficiency
5) dyshormonogenetic goiter

172
Q

most common cause of cretinism in US

A

thyroid dysgenesis

173
Q

subacute granulomatous thyroiditis progression

A

Can be hyper early in course, followed by hypo

174
Q

subacute granulomatous thyroiditis findings

A

Elevated ESR + jaw pain + *****very tender thyroid.

175
Q

Riedel’s etiology

A

Thyroid replaced by fibrous tissue with inflammatory infiltrate. Fibrosis may extend to local structures (eg, trachea, esophagus), mimicking anaplastic carcinoma.

176
Q

Riedel’s caveat

A

1/3 are hypothyroid

177
Q

Riedel’s association

A

IgG4-related systemic disease (eg, autoimmune pancreatitis, retroperitoneal fibrosis, noninfectious aortitis).

178
Q

Riedel goiter

A

fixed, hard (rock-like), PAINLESS.

179
Q

other causes of hypothyroidism

A

1) iodine deficiency
2) goitrogens (amiodarone, lithium)
3) Wolff-Chaikoff effect

180
Q

cause of pretibial myxedema in graves

A

thyroid-stimulating immunoglobulin stimulates dermal fibroblasts

181
Q

common presentation of graves

A

during stress (eg, pregnancy)

182
Q

Graves histology

A

Tall, crowded follicular epithelial cells; scalloped colloid.

183
Q

Exophthalmos in Graves mechanism

A

Infiltration of retroorbital space by activated T-cells –> increased cytokines (TNF-alpha, IFN-gamma) –> increased fibroblast secretion by hydrophilic GAGs –> increased osmotic muscle swelling, muscle inflammation, and adipocyte count –> exophthalmos.

184
Q

etiology of toxic multinodular goiter

A

Focal patches of hyperfunctioning follicular cells working independently of TSH usually due to TSH receptor mutations.

185
Q

Hot vs. cold nodules

A

Hot nodules are rarely malignant.

186
Q

Thyroid storm

A

uncommon but serious complication that occurs when hyperthyroidism is incompletely treated/untreated and then significantly worsens in the setting of acute stress such as infection, trauma, surgery.

187
Q

thyroid storm presentation

A

agitation + delirium + fever + diarrhea + coma + tachyarrhythmia (cause of death).

188
Q

thyroid storm labs

A

can see increased LFts

189
Q

thyroid storm treatment

A

4 P’s: propranolol, propylthiouracial, prednisolone, potassium iodide

190
Q

lugol iodine

A

potassium iodide

191
Q

Jod-Basedow phenomenon

A

thyrotoxicosis if a patient with iodine deficiency is made iodine replete. opposite of Wolff-Chaikoff.

192
Q

cold thyroid adenoma

A

nonfunctional, becomes “hot” or “toxic” via autonomous thyroid hormone production (rare)

193
Q

Most common histology of thyroid adenoma

A

follicular

194
Q

*Differentiating thyroid adenoma from follicular carcinoma

A

Absence of capsular or vascular invasion in thyroid adenoma.

195
Q

complication of ligating superior laryngeal artery

A

transection of superior laryngeal nerve

196
Q

complication of ligating inferior thyroid artery

A

transection of recurrent laryngeal nerve

197
Q

genetics associated with increased risk of papillary carcinoma

A

RET + BRAF mutations

198
Q

histology of papillary carcinoma

A

Empty-appearing nuclei with central clearing (orphan annie eyes), psammoma bodies, nuclear grooves.

199
Q

follicular carcinoma characteristics

A

Invades thyroid capsule and vasculature (unlike follicular adenoma), uniform follicles; hematogenous spread is common.

200
Q

follicular carcinoma genetics

A

associated with RAS mutation

201
Q

undifferentiated/anaplastic carcinoma and prognosis

A

older patients; invades local structures. very poor prognosis.

202
Q

familial hypocalciuric hypercalcemia pathophys

A

Defective Ca2+-sensing receptor (CaSR) in multiple tissues (eg parathyroids, kidneys). Higher than normal Ca2+ levels required to suppress PTH.

203
Q

familial hypocalciuric hypercalcemia labs

A

mild hypercalcemia + hypocalciuria + normal to elevated PTH

204
Q

Pseudohypoparathyroidism pathophys

A

unresponsiveness of kidney to PTH –> hypocalcemia despite elevated PTH levels. Due to defective Gs protein alpha subunit causing end-organ resistance to PTH. Defect must be inherited from mother due to imprinting.

205
Q

Pseudopseudohypoparathyroidism pathophys and presentatoin

A

physical exam features of Albright hereditary osteodystrophy but without end-organ PTH resistance. Occurs when defective Gs protein alpha-subunit is inherited from father.

206
Q

Laron syndrome

A

Dwarfism, caused by a mutation in the GH receptor.

207
Q

Labs in Laron syndrome

A

Increased GH, decreased IGF-1

208
Q

Laron syndrome presentation

A

Short height + small head circumference + characteristic facies with saddle nose and prominent forehead + delayed skeletal maturation + small genitalia.

209
Q

acromegaly cause

A

usually pituitary adenoma

210
Q

acromegaly presentation

A

large tongue with deep furrows + deep voice + large hands and feet + coarsening of facial features with aging + frontal bossing + diaphoresis (excessive sweating) + impaired glucose tolerance (insulin resistance) + increased risk of colorectal polyps and cancer.

211
Q

acromegaly labs

A

increased IGF-1

212
Q

Nelson syndrome

A

Enlargement of existing ACTH-secreting pituitary adenoma after bilateral adrenalectomy of refractory Cushing disease (due to removal of cortisol feedback mechanism).

213
Q

Nelson syndrome presentation

A

Hyperpigmentation+ headaches + bitemporal hemianopia.

214
Q

Nelson syndrome treatment

A

pituitary irradiation or surgical resection.

215
Q

prolactinoma arises from..

A

lactotrophs

216
Q

treatment for prolactinoma

A

dopamine agonists (ergot alkaloids such as bromocriptine, cabergoline), transsphenoidal resection.

217
Q

brown tumor

A

consists of osteoclasts and deposited hemosiderin from hemorrhages. Causes bone pain.

218
Q

tertiary hyperparathyroidism

A

refractory (autonomous) hyperparathyroidism resulting from chronic renal disease.

219
Q

tertiary hyperparathyroidism labs

A

Very hight PTH + hypercalcemia

220
Q

cause of primary hyperparathyroidism

A

usually parathyroid adenoma or hyperplasia.

221
Q

Primary hyperaparathyroidism labs

A

hypercalcemia, hypercalciuria, hypophosphatemia, increased PTH, increased ALP, increased cAMP in urine.

222
Q

17,20-lyase

A

17-hydroxypregnenolone –> dehydroepiandosterone (DHEA
and
17-hydroxyprogesterone –> adrostenedione

223
Q

17alpha-hydroxylase action

A

Pregnenolone –> 17-hydroxypregnenolone
and
Progesterone - 17-hydroxyprogesterone

224
Q

Aromatase action

A

Androstenedione –> Estrone
and
Testosterone –> Estradiol

225
Q

How would you differentiate pituitary apoplexy from sheehan’s?

A

apoplexy is hemorrhaging vs. sheehan’s, which is ischemic infarct, so you get more of a mass effect presentation with apoplexy.

226
Q

Lab findings in central DI

1) urine SG
2) serum osmolality
3) other

A

1) Less than 1.006
2) Greater than 290 mOsm/kg
3) Hyperosmotic volume contraction

227
Q

Mechanism of gynecomastia in liver disease

A

Decreased SHBG

228
Q

Mechanism of hirsutism in PCOS

A

insulin resistance –> excess insulin lowers SHBG –> increased free testosterone levels.

229
Q

Water deprivation test in central DI vs. nephrogenic DI

A

Central –> Greater than 50% increase in urine osmolality only after administration of ADH analog.
Nephrogenic –> Minimal change in urine osmolality, even after administration of ADH analog.

230
Q

other causes of nephrogenic DI

A

Hypercalcemia, hypokalemia, lithium, demeclocycline (ADH antagonist)

231
Q

Lab values in nephrogenic DI

1) urine SG
2) serum osmolality
3) other

A

1) less than 1.006
2) greater than 290 mOsm/kg
3) hyperosmotic volume contraction

232
Q

nephrogenic DI treatment

A

HCTZ, indomethacin, amiloride. hydration, avoidance of offending agent.

233
Q

when do you give desmopressin for DI?

A

1) serum osmolality greater than 295-300
2) hypernatremic
3) urine osmolality doesn’t rise despite a rising plasma osmolality.

234
Q

Why is SIADH euvolemic?

A

Body responds with decreased aldosterone and increased ANP/BNP –> increased urinary sodium secretion –> this normalizes ECF fluid volume.

235
Q

Causes of hypopituitarism

A

1) pituitary adenoma
2) carniopharyngioma
3) Sheehan
4) Empty sella
5) pituitary apoplexy
6) brain injury
7) radiation

236
Q

sheehan presentation

A

failure to lactate + absent menstruation + cold intolerance

237
Q

empty sella syndrome and epidimiology

A

Atrophy or compression of pituitary gland, which lies in the sella turcica. Common in obese women.

238
Q

Other causes of DM

A

1) unopposed secretion of GH and epinephrine.

2) glucocorticoid therapy (steroid diabetes).

239
Q

vascular presentation of DM

A

arteriolosclerosis, leading to HTN + chronic renal failure. Also large vessel atherosclerosis, CAD, and peripheral vascular occlusive disease.

240
Q

Most common cause of death in diabetes

241
Q

Diabetic neuropathy

A

motor, sensory (glove and stocking distribution) and autonomic degeneration.

242
Q

Cause of cataracts in DM

A

sorbitol accumulation in organs with aldose reductase and decreased or absent sorbitol dehydrogenase.

243
Q

DM diagnosis

A

1) HbA1c greater than 6.5
2) Fasting plasma glucose greater than 126 mg/dL
3) 2-hour oral glucose tolerance test, greater than 200 mg/dL

244
Q

Fasting plasma glucose procedure

A

Need to fast for at least 8 hours

245
Q

OGTT procedure

A

Test 2 hours after consumption of 75 g of glucose in water.

246
Q

Why are diabetics thirsty?

A

hyperglycemia –> increased plasma osmolality –> stimulation of thirst

247
Q

coma/death pathophys in DM

A

hyperglycemia –> osmotic diuresis –> sodium and potassium wasting –> hypovolemia –> circulation failure and decreased tissue perfusion –> coma/death

248
Q

pathophys of ketogenesis in DM

A

increased lipolysis –> increased plasma free fatty acids –> ketogenesis, ketonemia, ketonuria –> vomiting.

249
Q

Hyperosmolar hyperglycemia nonketotic syndrome

A

State of profound hyperglycemia-induced dehydration and increased serum osmolarity, classically seen in elderly type 2 diabetics with limited ability to drink.

250
Q

Hyperosmolar hyperglycemia nonketotic syndrome pathophys

A

Hyperglycemia –> excessive osmotic diuresis –> dehydration.

251
Q

Hyperosmolar hyperglycemia nonketotic syndrome pathophys

A

hyperglycemia + increased serum osmolarity + ***no acidosis (ketone production inibited by presence of insulin).

252
Q

Hyperosmolar hyperglycemia nonketotic syndrome treatment

A

IV fluids, insulin therapy.

253
Q

glucagonoma presentation

A

dermatitis (necrolytic migratory erythema) + diabetes + DVT + declining weight + depression.

254
Q

glucagonoma treatment

A

octreotide + surgery

255
Q

Whipple triad

A

low blood glucose + symptoms of hypoglycemia (lethargy, syncope, diplopia) + resolution of symptoms after normalization of glucose levels.

256
Q

How would you differentiate insulinoma from exogenous insulin use?

A

Increased C-peptie levels.

257
Q

Insulinoma treatment

A

surgical resection

258
Q

insulinoma association

A

10% of cases associated with MEN 1

259
Q

Somatostatinoma labs

A

Decreased secretion of secretin + CCK + glucagon + insulin + gastrin.

260
Q

Somatostatinoma presenation

A

diabetes/glucose intolerance + steatorrhea + gallstones

261
Q

Somatostatinoma treatment

A

surgical resection; octreotide for symptom control

262
Q

carcinoid syndrome rule of 1/3’s

A

1/3 metastasize
1/3 present with 2nd malignancy
1/3 are multiple

263
Q

Most common malignancy in the small intestine

264
Q

Menin and location

A

tumor suppressor gene on chromosome 11

265
Q

parathyroid presentation of MEN 1 vs. MEN 2A

A

parathyroid adenomas in MEN 1, parathyroid hyperplasia in MEN 2A

266
Q

Managing type 1 DM

A

low-carb diet + insulin

267
Q

Managing type 2 DM

A

dietary modification and exercise for weight loss + oral agents, non-insulin injectables, insulin replacement.

268
Q

Managing gestational DM (GDM)

A

dietary modifications, exercise, insulin replacement if lifestyle modification fails

269
Q

Rapid acting insulin drugs

A

Lispro, Aspart, Glulisine (no LAG)

270
Q

Rapid acting insulin drugs SE’s

A

hypoglycemia + lipodystrophy + hypersensitivity reactions

271
Q

Insulin type for DKA

A

Regular insulin (short acting)

272
Q

Long acting insulins

A

detemir + glargine

273
Q

biguanides, metformin metabolic actions

A

Decreased gluconeogenesis
Increased glycolysis
Increased peripheral glucose uptake

274
Q

Metformin contraindication

A

Renal insufficiency (causes metabolic acidosis)

275
Q

weight loss or gain with biguanides?

A

modest weight loss

276
Q

1st generation sulfonylureas

A

clorpropamide, tolbutamide

277
Q

2nd generation sulfonylureas

A

glimepiride, glipizide, glyburide

278
Q

SE’s in first vs. 2nd generation sulfonylureas

A

1st generation: disulfiram-like effects

2nd: hypoglycemia

279
Q

thiazolidinediones clinical use

A

monotherapy in type 2 DM or combined with other agents.

280
Q

meglitinides

A

nateglinide, repaglinide

281
Q

meglitinides clinical use

A

Monotherapy in type 2 DM or combined with metformin

282
Q

meglitinides SE’s

A

Hypoglycemia (increased risk with renal failure) + weight gain

283
Q

GLP-1 analogs

A

exenatide, liraglutide (sc injection)

284
Q

GLP-1 analogs MOA

A

increase glucose-dependent insulin release, decrease glucagon release, decrease gastric emptying, increase satiety

285
Q

GLP-1 analogs SE’s

A

Nausea, vomiting, pancreatitis; modest weight loss

286
Q

DPP-4 inhibitors

A

Lingaliptin, saxagliptin, sitagliptin

287
Q

DPP-4 inhibitors MOA

A

Inhibit DPP-4 enzyme that deactivates GLP-1, thereby increasing glucose-dependent insulin release, decreasing glucagon release, decreasing gastric emptying, and increasing satiety.

288
Q

DPP-4 inhibitors SE’s

A

mild urinary or respiratory infections; weight neutral

289
Q

Amylin analogs

A

pramlintide (sc injection)

290
Q

Amylin analogs MOA

A

decrease gastric emptying = decrease glucagon

291
Q

Amylin analogs SE’s

A

Hypoglycemia in setting of mistimed prandial insulin + nausea

292
Q

Amylin analogs clinical use

A

DM1 and DM2

293
Q

Sodium-glucose co-transporter 2 (SGLT-2) inhibitors

A

Canagliflozin, dapagliflozin, empagliflozin

294
Q

Sodium-glucose co-transporter 2 (SGLT-2) mechanism

A

Block reabsorption of glucose in PCT

295
Q

Sodium-glucose co-transporter 2 (SGLT-2) SE’s

A

glucosuria + UTIs + vaginal yeast infections + hyperkalemia + dehydration (orthostatic hypotension)

296
Q

PPAR–gamma

A

Genes regulate fatty acid storage and glucose metabolism. Activation increases insulin sensitity + increases levels of adiponectin

297
Q

alpha-glucosidase inhibitors

A

acarbose + miglitol

298
Q

alpha-glucosidase inhibitors MOA

A

Inhibit intestinal brush-border alpha-glucosidases. Delayed carbohydrate hydrolysis and glucose absorption, thus decreasing postprandial hyperglycemia.

299
Q

alpha-glucosidase inhibitors SE’s

A

GI disturbances

300
Q

thionamides

A

PTU + methimazole

301
Q

PTU pnemonic

A

Ptu blocks Peripheral conversion

302
Q

thionamide safe for pregnancy

303
Q

Drug to use to control uterine hemorrhage

304
Q

octreotide uses

A

1) acromegaly
2) carcinoid syndrome
3) gastrinoma
4) glucagonoma
5) esophageal varices

305
Q

Glucocorticoids mechanism

A

1) Most effects mediated by interactions with GC response elements.
2) inhibite phospholipase A2
3) inhibite transcription factors, such as NF-kappaB

306
Q

GC’s SE’s

A

1) iatrogenic cushing syndrome
2) adrenocortical atrophy (when stopped abruptly after chronic use)
3) peptic ulcers
4) peptic ulcers
5) steroid diabetes
6) steroid psychosis
7) cataracts

307
Q

fludrocortisone

A

synthetic analog of aldosterone with little GC effects

308
Q

fludrocortisone clinical use

A

Mineralocorticoid replacement in primary adrenal insufficiency

309
Q

fludrocortisone AE’s

A

similar to GC’s + edema, exacerbation of HF, hyperpigmentation

310
Q

cinacalcet MOA

A

sensitizes Ca2+ sensing receptor (CaSR) in parathyroid gland to circulating Ca2+

311
Q

cinacalcet clinical use

A

primary or secondary hyperparathyroidism

312
Q

cinacalcet AE’s

A

hypocalcemia

STEP (85 decks)

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