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Endocrinology_1 Flashcards

1
Q

Thyroid diverticulum arises from what?

A

floor of primitive pharynx–> descends into neck

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2
Q

thyroid connected to tongue by what?

A

thyroglossal duct, which normally disappears but may persist as pyramidal lobe of the thyroid

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3
Q

foramen cecum is what?

A

normal remnant of thyroglossal duct

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4
Q

most common ectopic thyroid tissue site is where?

A

tongue

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5
Q

thyroglossal duct cyst presents as what?

A

an anterior midline neck mass that moves with swallowing

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6
Q

thyroglossal duct cyst must be dDx from what?

A

persistent cervical sinus leading to branchial cleft cyst in lateral neck

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7
Q

fetal adrenal gland consists of what?

A

an outer adult zone and an inner active fetal zone

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8
Q

features of adult zone of fetal adrenal gland?

A

dormant during early fetal life, but begins to secrete cortisol late in gestation

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9
Q

control of cortisol secretion in fetus?

A

controlled by ACTH and CRH from fetal pituitary and placenta.

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10
Q

role of cortisol in fetal development?

A

cortisol is responsible for fetal lung maturation and surfactant production

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11
Q

adrenal cortex is derived from which germ layer?

A

mesoderm

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12
Q

adrenal medulla is derived from which germ layer?

A

neural crest

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13
Q

layers of adrenal gland from outer to inner?

A

Capsule –>• Zona Glomerulosa–>• Zona Fasciculata –>• Zona Reticularis–>• Medulla- Chromaffin cells

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14
Q

in adrenal gland, GFR corresponds with what?

A

Salt (Na+), Sugar (glucocorticoids), Sex (androgens)• The deeper you go the sweeter it gets

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15
Q

secretory product of Zona Glomerulosa of adrenal gland?

A

Aldosterone

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16
Q

secretory product of Zona Fasciculata of adrenal gland?

A

cortisol, sex hormones

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17
Q

secretory product of the zona reticularis of the adrenal gland?

A

Sex hormones (androgens)

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18
Q

secretory products of chromaffin cells?

A

catecholamines

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19
Q

Primary regulatory control of the Zona Glomerulosa?

A

Renin-Angiotensin

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20
Q

primary regulatory control of the Zona Fasciculata?

A

ACTH• hypothalamic CRH

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21
Q

primary regulatory control of the Zona Reticularis?

A

ACTH, hypothalamic CRH

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22
Q

primary regulatory control of adrenal medulla?

A

preganglionic sympathetic fibers

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23
Q

most common tumor of the adrenal medulla in adults?

A

pheochromocytoma

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24
Q

most common tumor of the adrenal medulla in children?

A

neuroblastoma

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25
Q

difference in the presentation between pheochromocytoma and neuroblastoma?

A

pheochromocytoma causes episodic hypertension and neuroblastoma does not

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26
Q

what is the venous drainage of the left adrenal gland?

A

left adrenal –> left adrenal vein –> left renal vein –> IVC

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27
Q

what is the drainage of the right adrenal gland?

A

right adrenal –> right adrenal vein –> IVC

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28
Q

function of the posterior pituitary (neurohypophysis)?

A

Secretes ADH and oxytocin, made in the hypothalamus and shipped to the posterior pituitary via neurophysins (carrier proteins).

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29
Q

posterior pituitary is derived from which germ layer?

A

neuroectoderm

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30
Q

function of the anterior pituitary?

A

Secretes FSH, LH, ACTH, TSH, prolactin, GH, melanotropin (MSH)

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31
Q

anterior pituitary is derived from which germ layer?

A

derived from oral ectoderm (rathke’s pouch)

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32
Q

α subunit is the hormone subunit common to which hormones?

A

TSH• LH• FSH• hCG

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33
Q

function of the β subunit of anterior pituitary hormones?

A

determines hormone specificity

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34
Q

acidophils of the anterior pituitary secrete what?

A

GH • prolactin

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35
Q

how do you remember the hormones secreted by basophils of the anterior pituitary?

A

B-FLAT• Basophils- FSH, LH, ACTH, TSH

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36
Q

how do you remember the hormones secreted by the anterior pituitary?

A

FLAT PiG: • FSH, LH, ACTH, TSH, Prolactin, GH

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37
Q

Islets of Langerhans are collections of what types of cells?

A

α, β, δ endocrine cells

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38
Q

Islets of Langerhans arise from what?

A

pancreatic buds

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39
Q

what is the position and major product of the α cells of the pancreas?

A

glucagon (peripheral)

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40
Q

what is the position and major product of the β cells of the pancreas?

A

insulin (central)• INSulin INSide

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41
Q

what is the position and major product of the δ cells of the islets of Langerhans?

A

somatostatin (interspersed)

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42
Q

what is the major regulator of insulin release?

A

glucose

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43
Q

how is insulin released?

A

ATP generated by glucose metabolism closes K+ channels and depolarizes β cell membrane –> opens voltage gated Ca++ channels. • Ca++ influx stimulates insulin secretion

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44
Q

does insulin cross the placenta?

A

no

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45
Q

what are the tissues that have insulin-dependent glucose uptake?

A

Brain, RBC’s, Intestine, Cornea, Kidney, Liver• BRICK L

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46
Q

what are the insulin dependent glucose transporters?

A

GLUT-4

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47
Q

what is the bidirectional glucose transporter?

A

GLUT2

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48
Q

what is the distribution of GLUT-1?

A

RBC’s Brain

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49
Q

what is the distribution of GLUT-2?

A

β islet cells• liver• kidney• small intestine

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50
Q

what is the distribution of GLUT-4?

A

adipose tissue, skeletal muscle

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51
Q

what are the anabolic effects of insulin?

A
  1. increase glucose transport in skeletal muscle and adipose• 2. increase glycogen synthesis and storage• 3. increase triglyceride synthesis and storage• 4. increase Sodium retention in the kidney• 5. increase protein synthesis in the muscles• 6. increase cellular uptake of K+ and amino acids• 7. decrease glucagon release
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52
Q

which regulators lead to an increase in insulin?

A

hyperglycemia• GH• β2 antagonists

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53
Q

which regulators lead to a decrease in insulin?

A

hypoglycemia• somatostatin• α2- agonists

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54
Q

which is the insulin independent transporter?

A

GLUT-1

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55
Q

which tissues depend on insulin for increased glucose uptake?

A

resting skeletal muscle and adipose tissue (GLUT-4)

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56
Q

which tissues take up glucose independent of insulin levels?

A

Brain and RBC (GLUT-1)

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57
Q

Brain depends on what substances for energy?

A

depends on glucose for metabolism under normal circumstances and uses ketone bodies in starvation

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58
Q

RBC’s depend on what substance for energy?

A

RBC’s always depend on glucose because they have no mitochondria for aerobic metabolism

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59
Q

what is the source of glucagon?

A

made by α cells of the pancreas

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60
Q

what are the catabolic effects of glucagon?

A

glycogenolysis• gluconeogenesis• lipolysis• ketone production

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61
Q

how is glucagon regulated?

A

secreted in response to hypoglycemia• inhibited by insulin, hyperglycemia, and somatostatin

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62
Q

what stimulates the release of TSH and prolactin?

A

TRH

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63
Q

what inhibits the release of prolactin?

A

dopamine

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64
Q

what is the function of CRH?

A

stimulates the release of ACTH, MSH, β-endorphin

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65
Q

what is the function of GHRH?

A

stimulate the release of GH

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66
Q

what inhibits the release of GH and TSH?

A

somatostatin

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67
Q

what is the function of GnRH?

A

stimulate the release of FSH and LH

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68
Q

what inhibits the release of GnRH?

A

prolactin

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69
Q

what is the source of prolactin?

A

secreted mainly by anterior pituitary

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70
Q

what is the function of prolactin?

A

stimulates milk production in breast; inhibits ovulation in females and spermatogenesis in males by inhibiting GnRH synthesis and release

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71
Q

prolactin secretion from anterior pituitary is tonically inhibited by what?

A

dopamine from hypothalamus

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72
Q

how does prolactin inhibit its own secretion?

A

by increasing dopamine synthesis and secretion from hypothalamus

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73
Q

what hormone increases prolactin secretion?

A

TRH

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74
Q

what inhibits prolactin secretion and can be used in treatment of prolactinoma?

A

dopamine agonists (bromocriptine)

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75
Q

which drugs stimulate prolactin secretion?

A

dopamine antagonists (most antipsychotics)• estrogens (OCP’s, pregnancy)

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76
Q

what is the source of growth hormone?

A

secreted mainly by anterior pituitary

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77
Q

what is the function of growth hormone?

A

stimulates linear growth and muscle mass through IGF-1/somatomedin secretion

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78
Q

what is the effect of GH on blood sugar?

A

increases insulin resistance (diabetogenic)

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79
Q

GH is released in pulses in response to what?

A

GHRH

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80
Q

when does GH secretion increase?

A

during exercise and sleep

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81
Q

secretion of GH is inhibited by what?

A

glucose and somatostatin

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82
Q

what can cause excess secretion of GH?

A

pituitary adenoma

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83
Q

excess secretion of GH can cause what?

A

acromegaly in adults or gigantism in children

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84
Q

which hormone activates cholesterol desmolase?

A

ACTH

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85
Q

which drug inhibits cholesterol desmolase?

A

ketoconazole

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86
Q

what is the function of desmolase?

A

converts cholesterol into pregnenolone

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87
Q

what is the function of 3β-hydroxy steroid dehydrogenase?

A
  1. converts pregnenolone to progesterone• 2. converts 17-hydroxypregnenolone into 17-hydroxyprogesterone• 3. converts dihydroepiandosterone (DHEA) into androstenedione
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88
Q

what is the function of 17α-hydroxylase?

A

converts pregnenolone to 17-hydroxypregnenolone and converts progesterone into 17-hydroxyprogesterone

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89
Q

what is the function of 21-hydroxylase?

A
  1. converts progesterone into 11-deoxycorticosterone• 2. converts 17-hydroxyprogesterone into 11-deoxycortisol
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90
Q

what is the function of 11β-hydroxylase?

A
  1. converts 11-deoxycorticosterone into corticosterone• 2. converts 11-deoxycortisol into cortisol
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91
Q

what is the function of aldosterone synthase?

A

converts corticosterone into aldosterone

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92
Q

what hormone activates aldosterone synthase?

A

angiotensin II

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93
Q

what is the function of aromatase?

A
  1. converts androstenedione to estrone• 2. converts testosterone to estradiol
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94
Q

what is the function of 5α-reductase?

A

converts testosterone into DHT

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95
Q

all congenital adrenal enzyme deficiencies are characterized by what?

A

enlargement of both adrenal glands due to high ACTH stimulation because of low cortisol

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96
Q

what are the hormone levels seen in 17α-hydroxylase deficiency?

A

high mineralocorticoids• low cortisol• low sex hormones

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97
Q

how does 17α-hydroxylase deficiency present in both sexes?

A

hypertension, hypokalemia

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98
Q

what are the presenting features of 17α-hydroxylase deficiency that are unique to males?

A

low DHT–> pseudohermaphroditism (variable, ambiguous genitalia; undescended testes)

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99
Q

what are the presenting features of 17α-hydroxylase deficiency unique to females?

A

external phenotypic female with normal internal sex organs, lacks 2ndary sex characteristics

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100
Q

what is the most common form of congenital bilateral adrenal hyperplasia?

A

21-hydroxylase deficiency

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101
Q

what are the hormone levels seen in 21-hydroxylase deficiency?

A

low mineralocorticoids• low cortisol• high sex hormones

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102
Q

how does 21-hydroxylase deficiency present?

A

hypotension, hyperkalemia, increase renin activity, volume depletion• - masculinization, leading to pseudohermaphrodtism in females

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103
Q

what are the hormone levels seen in 11β-hydroxylase deficiency?

A

low aldosterone• high 11-deoxycorticosterone• low cortisol• high sex hormones

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104
Q

how does 11β-hydroxylase deficiency present?

A

hypertension (11-deoxycorticosterone is a mineralocorticoid and secreted in excess)• masculinization

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105
Q

what is the source of cortisol?

A

adrenal zona fasciculata

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106
Q

cortisol is bound to what in the blood?

A

corticosteroid-binding globulin

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107
Q

what are the functions of cortisol?

A
  1. maintains blood pressure• 2. decreases bone formation• 3. anti-inflammatory/immunosuppressive• 4. increases insulin resistance• 5. increases gluconeogenesis, lipolysis, proteolysis• 6. inhibits fibroblasts
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108
Q

how does cortisol act to maintain blood pressure?

A

upregulates α1 receptors on arterioles –> increased sensitivity to NE and Epi

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109
Q

what are the anti-inflammatory/immunosuppressive functions of cortisol?

A
  1. inhibits production of leukotrienes and prostaglandins• 2. inhibits leukocyte adhesion–> neutrophilia• 3. blocks histamine release from mast cells• 4. reduces eosinophils• 5. blocks IL-2 production
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110
Q

what is the effect of chronic stress on cortisol levels?

A

chronic stress induces prolonged secretion

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111
Q

what is the effect of CRH on cortisol?

A

CRH (hypothalamus) stimulates ACTH release (pituitary), causing cortisol production in adrenal zona fasciculata.

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112
Q

what is the effect of excess cortisol on the hypothalamic pituitary axis?

A

leads to decreased CRH, ACTH, and cortisol secretion

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113
Q

what is the source of PTH?

A

Chief cells of the parathyroid

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114
Q

what is the effect of PTH on serum Ca2+, PO4, and urine PO4?

A

increase serum Ca++• decrease serum PO4• increase urine PO4

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115
Q

what are the functions of PTH?

A
  1. increase bone resorption of calcium and PO4• 2. increase kidney resorption of calcium in DCT• 3. decrease resorption of PO4 in PCT• 4. increase 1,25-OH2VitD production by stimulating kidney 1α-hydroxylase• 5. increase production of M-CSF and RANK-L in osteoblasts, stimulating osteoclasts
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116
Q

what is the effect of decreased serum calcium on PTH?

A

increase PTH secretion

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117
Q

what is the effect of decreased serum magnesium on PTH secretion?

A

increase PTH secretion

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118
Q

what is the effect of a dramatic decrease in serum magnesium on PTH?

A

decrease PTH secretion

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119
Q

what are the common causes of decreased Mg2+?

A

diarrhea• aminoglycosides• diuretics• alcohol abuse

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120
Q

what is the source of Vitamin D?

A
  1. D3 from sun exposure in skin• 2. D2 ingested from plants• - Both converted to 25-OH in liver and to 1,25-(OH)2 (active form) in kidney.
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121
Q

what is 24,25-(OH)2D3?

A

an inactive form of vitamin D

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122
Q

Vitamin D deficiency causes what?

A

rickets in kids and osteomalacia in adults

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123
Q

what is the function of vitamin D?

A
  1. increase absorption of dietary Ca and PO4• 2. increase bone resorption of Ca and PO4
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124
Q

which regulators cause an increase in 1,25-OH2 Vit D production?

A
  1. high PTH• 2. low [Ca++]• 3. low PO4
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125
Q

what regulators cause a decrease in 1,25-OH2 Vit D production?

A

1,25-OH2 Vit D feedback

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126
Q

what is the difference between PTH and Vitamin D?

A

PTH leads to increase Ca++ reabsorption and decrease PO4 reabsorption in the kidney, whereas 1,25-OH2 Vit D leads to increased absorption of both Ca++ and PO4 in the gut.

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127
Q

what is the source of calcitonin?

A

parafollicular cells (C cells) of the thyroid

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128
Q

what is the function of calcitonin?

A

decrease bone resorption of calcium• opposes actions of PTH• not important in normal calcium homeostasis.

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129
Q

how is calcitonin regulated?

A

high serum calcium causes calcitonin secretion

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130
Q

which endocrine hormones act via the cAMP signaling mechanism?

A

FSH, LH, ACTH, TSH, CRH, hCG, ADH (V2 receptor), MSH, PTH, calcitonin, GHRH, glucagon• - FLAT ChAMP

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131
Q

which hormones act via the cGMP signaling mechanism?

A

ANP• NO (EDRF)• think vasodilators

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132
Q

which hormones act via the IP3 signaling mechanism?

A

GnRH, GHRH, Oxytocin, ADH (V1 receptor), TRH, histamine (H1), ATII, gastrin• GGOAT

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133
Q

which hormones act via the steroid receptor mechanism?

A

Vitamin D, Estrogen, Testosterone, T3/T4, Cortisol, Aldosterone, Progesterone• VETTT CAP

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134
Q

which hormones act via the intrinsic tyrosine kinase signaling mechanism?

A

insulin• IGF-1• FGF• PDGF• EGF• MAP kinase pathway• Think growth factors

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135
Q

which hormones act via the Receptor-associated tyrosine kinase signaling mechanism?

A

Prolactin, Immunomodulators (cytokines, IL2, IL6, IL8, IFN), GH• JAK/STAT pathway• Think acidophiles and cytokines

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136
Q

what is the effect of high sex hormone-binding globulin in men?

A

lowers free testosterone–> gynecomastia

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137
Q

what is the effect of low SHBG in women?

A

raises free testosterone–> hirsutism

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138
Q

when do SHBG levels increase in women?

A

during pregnancy

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139
Q

what are T3/T4?

A

iodine- containing hormones that control the body’s metabolic rate

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140
Q

what is the source of T3/T4?

A

follicles of thyroid. most T3 formed in target tissues

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141
Q

what is the function of T3/T4?

A
  1. bone growth (synergism with GH)• 2. CNS maturation• 3. increase β1 receptors in heart–> high CO, HR, SV, contractility• 4. increase basal metabolic rate via high Na/K ATPase activity = high O2 consumption, RR, body temperature• 5. increases glycogenolysis, gluconeogenesis, lipolysis
142
Q

what binds thyroid hormones?

A

thyroxine binding globulin binds most T3/T4 in blood; only free hormone is active

143
Q

when is TBG low?

A

hepatic failure

144
Q

when is TBG high?

A

pregnancy/OCP• estrogen increases TBG

145
Q

what is the major thyroid product?

A

T4 is major thyroid product

146
Q

how is T3 made?

A

T4 is converted to T3 in peripheral tissue by 5’-deiodinase

147
Q

which thyroid hormone has the higher receptor affinity?

148
Q

thyroid peroxidase is responsible for what?

A

oxidation and organification of iodide as well as coupling of MIT and DIT

149
Q

propylthiouracil inhibits what?

A

both peroxidase and 5’-deiodinase

150
Q

methimazole inhibits what?

A

peroxidase

151
Q

what are the functions of T3

A

4B’s• Brain Maturation• Bone growth• Beta-adrenergic effects• Basal metabolic rate

152
Q

function of TBG?

A

binds most T3/T4 in blood; only free hormone is active

153
Q

what is cushings syndrome?

A

high cortisol due to a variety of causes

154
Q

what is the #1 cause of Cushings syndrome?

A

exogenous (iatrogenic) steroids• (presents with low ACTH)

155
Q

what are the endogenous causes of Cushing’s syndrome?

A
  1. Cushing’s disease• 2. Ectopic ACTH• 3. Adrenal adenoma
156
Q

what fraction of endogenous Cushing’s syndrome is caused by ACTH secretion from pituitary adenoma?

157
Q

what fraction of endogenous Cushing’s syndrome is caused by ectopic ACTH from nonpituitary tissue making ACTH?

158
Q

what fraction of endogenous Cushing’s syndrome is caused by adrenal adenoma, carcinoma, nodular adrenal hyperplasia?

159
Q

ACTH level in Cushings disease?

160
Q

ACTH level in Cushings syndrome from small cell lung cancer or bronchial carcinoids?

161
Q

ACTH level in Cushing’s syndrome caused by adrenal adenoma, carcinoma, nodular adrenal hyperplasia?

162
Q

what are the findings in Cushing’s syndrome?

A
  1. HTN• 2. weight gain• 3. moon facies• 4. truncal obesity• 5. buffalo hump• 6. hyperglycemia• 7. skin changes• 8. osteoporosis• 9. amenorrhea• 10. immunosuppresion
163
Q

what is the effect of dexamethasone suppression test on cortisol in a normal individual?

A
  1. Low dose= suppressed• 2. high dose= suppressed
164
Q

what is the effect of the dexamethasone suppression test on cortisol in individuals with ACTH-pituitary tumor?

A
  1. low= remains elevated• 2. high= suppressed
165
Q

what is the effect of the dexamethasone suppression test on cortisol in an individual with ectopic ACTH producing tumor?

A
  1. low= remains elevated• 2. high= remains elevated
166
Q

what is the effect of the dexamethasone suppression test on cortisol in an individual with cortisol-producing tumor?

A
  1. low= remains elevated• 2. high= remains elevated
167
Q

primary hyperaldosteronism is caused by what?

A

adrenal hyperplasia or an aldosterone-secreting adrenal adenoma (Conn’s syndrome) • - may be bilateral or unilateral

168
Q

primary hyperaldosteronism results in what?

A

hypertension• hypokalemia• metabolic acidosis• low plasma renin

169
Q

what is the treatment for primary hyperaldosteronism?

A

surgery to remove the tumor and/or spironolactone, a K+ sparing diuretic that works by acting as an aldosterone antagonist

170
Q

what happens in secondary hyperaldosteronism?

A

renal perception of low intravascular volume results in an overactive renin-angiotensin system.

171
Q

what causes secondary hyperaldosteronism?

A

renal artery stenosis• chronic renal failure• CHF• cirrhosis• nephrotic syndrome

172
Q

what is the renin level in secondary hyperaldosteronism?

173
Q

what is the treatment for secondary hyperaldosteronism?

A

spironolactone

174
Q

what is Addison’s disease?

A

Chronic primary adrenal insufficiency due to adrenal atrophy or destruction by disease (autoimmune, TB, metastasis)–> deficiency of aldosterone and cortisol

175
Q

deficiency of aldosterone and cortisol in Addison’s causes what?

A

hypotension (hyponatremic volume contraction)• hyperkalemia• acidosis• skin hyperpigmentation

176
Q

why is there hyperpigmentation in Addison’s?

A

MSH, a by-product of high ACTH production from POMC

177
Q

Addison’s involves which parts of the adrenals?

A

all 3 cortical divisions• medulla spared

178
Q

Addison’s must be distinguished from what?

A

secondary adrenal insufficiency (low pituitary ACTH production), which has no skin hyperpigmentation and no hyperkalemia

179
Q

what is Waterhouse-Friderichsen syndrome?

A

Acute primary adrenal insufficiency due to adrenal hemorrhage associated with Neisseria meningitidis septicemia, DIC, and endotoxic shock

180
Q

what is the most common tumor of the adrenal medulla in adults?

A

pheochromocytoma

181
Q

pheochromocytoma is derived from what?

A

chromaffin cells (arise from neural crest)

182
Q

what is the rule of 10’s for pheochromocytoma?

A

10% malignant• 10% blateral• 10% extra-adrenal• 10% calcify• 10% kids

183
Q

most pheochromocytomas secrete what?

A

Epi• NE• dopamine• which can cause episodic hypertension

184
Q

lab findings in pheochromocytoma?

A

Urinary VMA and plasma catecholamines are elevated

185
Q

pheochromocytoma is associated with which conditions?

A

NF1• MEN2A• MEN2B

186
Q

what is the treatment for pheochromocytoma?

A

tumor surgically removed only after effective α and β blockade is achieved:• irreversible α-antagonists (phenoxybenzamine) must be given first to avoid a hypertensive crisis. β blockers are then given to slow the heart rate

187
Q

what are the episodic hyperadrenergic symptoms of pheochromocytoma?

A

5 P’s:• Pressure• Pain• Perspiration• Palpitations• Pallor

188
Q

what is the most common tumor of the adrenal medulla in children?

A

neuroblastoma

189
Q

where can neuroblastoma occur?

A

anywhere along the sympathetic chain

190
Q

lab values for neuroblastoma?

A

elevated urine homovanillic acid (HVA)

191
Q

which out of the common tumors of the adrenal medulla is more likely to cause hypertension?

A

pheochromocytoma > neuroblastoma

192
Q

what is associated with rapid tumor progression in neuroblastoma?

A

overexpression of N-myc oncogene

193
Q

signs/symptoms of hypothyroidism?

A
  1. Cold intolerance (low heat production)• 2. Weight gain, decreased appetite• 3. hypoactivity, lethargy, fatigue, weakness• 4. constipation• 5. decreased reflexes• 6. myxedema (facial/periorbital)• 7. dry cool skin; coarse brittle hair• 8. bradycardia, dyspnea on exertion
194
Q

signs/symptoms of hyperthyroidism?

A
  1. heat intolerance (high heat production)• 2. weight loss, increased appetite• 3. hyperactivity• 4. diarrhea• 5. high reflexes• 6. pretibial myxedema (Graves)• 7. warm moist skin; fine hair• 8. chest pain, palpitations, arrhythmias, increased β-adrenergic receptors
195
Q

lab findings in hypothyroidism?

A

high TSH• low free T4

196
Q

lab findings in hyperthyroidism?

A

low TSH• high free or total T4• high free or total T3

197
Q

what is the most common cause of hypothyroidism?

A

Hashimoto’s thyroiditis

198
Q

what are the autoantibodies in Hashimoto’s thyroiditis directed at?

A

thyroid peroxidase• antithyroglobulin

199
Q

Hashimoto thyroiditis is associated with which haplotype?

200
Q

people with hashimoto thyroiditis have an increased risk of what?

A

Hodgkin’s lymphoma

201
Q

what is the histology seen in Hashimoto thyroiditis?

A

Hurthle cells• lymphocytic infiltrate with germinal centers

202
Q

what are the PE findings in Hashimoto thyroiditis?

A

moderately enlarged nontender thyroid

203
Q

when can Hashimoto thyroiditis present as hyperthyroidism?

A

early in the course

204
Q

what causes hyperthyroid Hashimoto thyroiditis?

A

thyrotoxicosis during follicular rupture

205
Q

Cretinism happens due to what?

A

severe fetal hypothyroidism

206
Q

where does endemic cretinism occur?

A

where ever endemic goiter is prevalent

207
Q

sporadic cretinism is caused by what?

A

defect in T4 formation or developmental failure in thyroid formation

208
Q

what are the PE findings in cretinism?

A

5P’s:• Pot belly• Pale• Puffy faced child• Protruding umbilicus• Protuberant tongue

209
Q

what is subacute thyroiditis (de Quervain’s)?

A

self limited hypothyroidism often following a flu like illness

210
Q

what is the histology seen in de Quervan’s thyroiditis?

A

granulomatous inflammation

211
Q

what are the findings in de Quervain’s thyroiditis?

A

high ESR• jaw pain• early inflammation• very tender thyroid

212
Q

what is Riedel’s thyroiditis?

A

thyroid replaced by fibrous tissue

213
Q

Riedel’s thyroiditis is considered a menifestation of what?

A

IgG4 related systemic disease

214
Q

what are the findings in Riedel’s thyroiditis?

A

fixed hard painless goiter

215
Q

what are the other causes of hypothyroidism?

A

congenital hypothyroidism• iodine deficiency• goitrogens• Wolff-Chaikoff effect• painless thyroiditis

216
Q

what happens in toxic multinodular goiter?

A

focal patches of hyperfunctioning follicular cells working independently of TSH due to mutation in TSH receptor–>• increased release of T3/T4

217
Q

which type of thyroid nodules are less likely to be malignant?

A

hot nodules

218
Q

what is the Jod-Basedow phenomenon?

A

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

219
Q

what is Grave’s disease?

A

an autoimmune hyperthyroidism with thyroid-stimulating immunoglobulins

220
Q

findings in Grave’s disease?

A

Ophthalmopathy (proptosis, EOM swelling)• pretibial myxedema• increase in connective tissue deposition• diffuse goiter

221
Q

Grave’s disease often presents when?

A

during stress (child birth)

222
Q

what is thyroid storm?

A

stress-induced catecholamine surge leading to death by arrhythmia.

223
Q

thyroid storm is seen as a complication of what?

A

Grave’s and other hyperthyroid disorders

224
Q

what lab level may be seen in Grave’s disease?

A

high ALP due to high bone turn over

225
Q

what is the most common thyroid cancer?

A

papillary carcinoma

226
Q

prognosis for papillary carcinoma thyroid is what?

227
Q

what are the histologic features of papillary carcinoma of thyroid?

A

empty appearing nuclei (Orphan Annie’s eyes) psammoma bodies, nuclear grooves

228
Q

increased risk of papillary carcinoma of thyroid is associated with what?

A

childhood irradiation

229
Q

what is the prognosis associated with follicular carcinoma of the thyroid?

230
Q

how does follicular carcinoma of the thyroid appear histologically?

A

uniform follicles

231
Q

cellular origin of medullary carcinoma of thyroid?

A

from parafollicular C cells

232
Q

medullary carcinoma of thyroid produces what?

A

calcitonin

233
Q

histologic appearance of medullary carcinoma of thyroid?

A

sheets of cells in amyloid stroma

234
Q

medullary carcinoma of the thyroid is associated with which conditions?

A

MEN types 2A and 2B

235
Q

features of anaplastic undifferentiated carcinoma of thyroid?

A
  • older patients• - very poor prognosis
236
Q

thyroid lymphoma is associated with what condition?

A

Hashimoto’s thyroiditis

237
Q

primary hyperparathyroidism is usuallly caused by what?

A

usually an adenoma

238
Q

findings in primary hyperparathyroidism?

A
  1. hypercalcemia• 2. hypercalciuria (renal stones)• 3. hypophosphatemia• 4. high PTH• 5. high ALP• 6. high cAMP in urine
239
Q

clinical presentation of primary hyperparathyroidism?

A

often asymptomatic, or may present with weakness and constipation

240
Q

what is the skeletal complication of primary hyperparathyroidism?

A

Osteitis fibrosa cystica

241
Q

what causes secondary hyperparathyroidism?

A

secondary hyperplasia due to decreased gut Ca++ absorption and increased phosphate, most often in chronic renal disease

242
Q

how does chronic renal disease cause secondary hyperparathyroidism?

A

causes hypovitaminosis D –> low Ca++ absorption

243
Q

what are the findings in secondary hyperparathyroidism?

A

hypocalcemia, hyperphosphatemia in chronic renal failure (hypophosphatemia in most other causes), high ALP, high PTH

244
Q

what is the skeletal complication associated with secondary or tertiary hyperparathyroidism?

A

Renal osteodystrophy

245
Q

what is seen in osteitis fibrosa cystica?

A

cystic bone spaces filled with brown fibrous tissue (bone pain)

246
Q

what is renal osteodystrophy?

A

bone lesions due to secondary or tertiary hyperparathyroidism due in turn to renal disease

247
Q

what is tertiary hyperparathyroidism?

A

refractory (autonomous) hyperparathyroidism resulting from chronic renal disease

248
Q

findings in tertiary hyperparathyroidism?

A

very high PTH• high Ca++

249
Q

hypoparathyroidism is due to what?

A

accidental surgical excision, autoimmune destruction, or DiGeorge syndrome

250
Q

what are the findings in hypoparathyroidism?

A

hypocalcemia• tetany

251
Q

what is Chvostek’s sign?

A

tapping of facial nerve –> contraction of facial muscles

252
Q

what is Trousseau’s sign?

A

occlusion of brachial artery with BP cuff–> carpal spasm

253
Q

what is the eponym of pseudohypoparathyroidism?

A

(Albright’s hereditary osteodystrophy)

254
Q

what is pseudohypoparathyroidism?

A

autosomal dominant kidney unresponsiveness to PTH

255
Q

what are the findings in pseudohypoparathyroidism?

A

hypocalcemia• shortened 4th/5th digits• short stature

256
Q

what is the diagnosis when there is high calcium and high-normal/high PTH?

A

primary hyperparathyroidism (hyperplasia, adenoma, carcinoma)

257
Q

what is the diagnosis when there is high calcium and low PTH?

A

PTH-independent hypercalcemia (excess calcium ingestion, cancer)

258
Q

what is the diagnosis when there is low calcium and high-normal/high PTH?

A

secondary hyperparathyroidism (chronic renal failure)

259
Q

what is the diagnosis when there is low calcium and low PTH?

A

hypoparathyroidism (surgical removal, autoimmune destruction)

260
Q

pituitary adenomas are most commonly what?

A

prolactinoma

261
Q

what are the findings in prolactinoma?

A

amenorrhea, galactorrhea, low libido, infertility (low GnRH).

262
Q

prolactinoma can impinge on what structure?

A

optic chiasm–> bitemporal hemianopsia

263
Q

what is the treatment for prolactinoma?

A

dopamine agonists (bromocriptine or cabergoline) cause shrinkage of prolactinoma

264
Q

what causes acromegaly?

A

excess GH in adults

265
Q

excess GH in adults is typically caused by what?

A

pituitary adenoma

266
Q

findings in acromegaly?

A

large tongue with deep furrows• deep voice• large hands and feet• coarse facial features• impaired glucose tolerance

267
Q

increased GH in children leads to what?

A

gigantism ( increased linear bone growth)

268
Q

how is acromegaly diagnosed?

A

high serum IGF-1• failure to suppress serum GH following oral glucose tolerance test• pituitary mass seen on MRI

269
Q

what is the treatment for acromegaly?

A

pituitary adenoma resection followed by somatostatin analog if not cured

270
Q

Diabetes insipidus is characterized by what?

A

intense thirst and polyuria together with an inability to concentrate urine owing to lack of ADH or to a lack of renal response to ADH

271
Q

what causes central DI?

A

lack of ADH• - pituitary tumor• - trauma• - surgery• - histiocytosis X

272
Q

what causes nephrogenic DI?

A

hereditary• or• secondary to hypercalcemia, lithium, demeclocycline

273
Q

what is demeclocycline?

A

ADH antagonist

274
Q

what are the findings in diabetes insipidus?

A

urine specific gravity <1.006; serum osmolality >290 mOsm/L

275
Q

how is diabetes insipidus diagnosed?

A

Water deprivation test- urine osmolality doesn’t increase.• Response to desmopressin distinguishes central DI from nephrogenic DI

276
Q

what is the treatment for central DI?

A
  1. adequate fluid intake• 2. intranasal desmopressin (ADH analog)
277
Q

what is the treatment for nephrogenic DI?

A

HCTZ/• Indomethacin/• amiloride/

278
Q

what are the findings in SIADH?

A
  • excessive water retention• - hyponatremia with continued urinary Na+ excretion• - urine osmolarity > serum osmolarity
279
Q

how does the body respond to SIADH?

A

decrease aldosterone (hyponatremia) to maintain near normal volume status

280
Q

very low sodium levels in SIADH can lead to what?

A

seizures (correct slowly)

281
Q

causes of SIADH include what?

A
  1. Ectopic ADH (small cell lung cancer)• 2. CNS disorder/head trauma• 3. pulmonary disease• 4. drugs like cyclophosphamide
282
Q

what is the treatment for SIADH?

A

fluid restriction• IV saline• conivaptan• tolvaptan• demeclocycline

283
Q

hypopituitarism is what?

A

undersecretion of pituitary hormones

284
Q

undersecretion of pituitary hormones can be due to what?

A
  1. nonsecreting pituitary adenoma, craniopharyngioma• 2. Sheehan’s syndrome• 3. Empty sella syndrome• 4. brain injury; hemorrhage• 5. radiation
285
Q

what is the treatment for hypopituitarism?

A

substitution therapy (corticosteroids, thyroxine, sex steroids, human growth hormone)

286
Q

what is Sheehan’s syndrome?

A

ischemic infarct of pituitary following postpartum bleeding; usually presents with failure to lactate

287
Q

what is Empty sella syndrome?

A

atrophy or compression of pituitary, often idiopathic, common in obese women

288
Q

what are the acute manifestations of diabetes mellitus?

A
  1. polydipsia• 2. polyuria• 3. polyphagia• 4. weight loss• 5. DKA (type 1), hyperosmolar coma (type 2)• 6. unopposed secretion of GH and epinephrine (exacerbating hyperglycemia
289
Q

in the acute manifestations of diabetes mellitus, insulin deficiency and glucagon excess lead to what?

A
  1. decreased glucose uptake• 2. increased protein catabolism• 3. increased lipolysis
290
Q

in the acute manifestations of diabetes mellitus, decreased glucose uptake leads to what?

A
  1. hyperglycemia• 2. glycosuria• 3. osmotic diuresis• 4. electrolyte depletion• –>dehydration, acidosis• –> coma, death
291
Q

in the acute manifestations of diabetes mellitus increased protein catabolism leads to what?

A

increased plasma amino acids, nitrogen loss in the urine• –>• 1. hyperglycemia• 2. glycosuria• 3. osmotic diuresis• 4. electrolyte depletion• –>dehydration, acidosis• –> coma, death

292
Q

in the acute manifestations of Diabetes mellitus, increased lipolysis leads to what?

A
  1. increased plasma FFA’s• 2. ketogenesis• 3. ketonuria• 4. ketonemia• –>dehydration, acidosis• –> coma, death
293
Q

what are the 2 major causes of the chronic manifestations of Diabetes mellitus?

A

Nonenzymatic Glycosylation• Osmotic damage

294
Q

what happens in small vessel disease caused by nonenzymatic glycosylation in DM?

A

diffuse thickening of basement membrane –> retinopathy, glaucoma, nephropathy

295
Q

what are the features of DM retinopathy that occurs as a result of nonenzymatic glycosylation in small vessels?

A

hemorrhage, exudates, microaneurysms, vessel proliferation

296
Q

what are the features of DM nephropathy caused by nonenzymatic glycosylation of small vessels?

A

nodular sclerosis• progressive proteinuria• chronic renal failure• arteriosclerosis leading to hypertension• Kimmelstiel-Wilson nodules

297
Q

what are the chronic effects of nonenzymatic glycosylation of large vessels in DM?

A

large vessel atherosclerosis• CAD• peripheral vascular occlusive disease• gangrene • –> limbloss, cerebrovascular disease

298
Q

what causes osmotic damage in chronic DM?

A

sorbitol accumulation in tissues with aldose reductase

299
Q

what are the features of neuropathy caused by chronic osmotic damage in DM?

A

motor, sensory, and autonomic degeneration

300
Q

what are the ophthalmic effects of chronic osmotic damage in DM?

301
Q

what are the tests to monitor chronic diabetes?

A

fasting serum glucose• oral glucose tolerance test• HbA1C

302
Q

HbA1C reflects what?

A

average blood glucose over prior 3 months

303
Q

what is the primary defect in DM1 vs. DM2?

A

DM1: autoimmune destruction of β cells• DM2: increased resistance to insulin, progressive pancreatic β cell failure

304
Q

is insulin necessary in treatment of DM1 and DM2?

A

DM1: always• DM2: sometimes

305
Q

what is the age of onset of DM1 vs. DM2?

A

DM1: <30• DM2: >40

306
Q

do DM1 and DM2 have an association with obesity?

A

DM1: no• DM2: yes

307
Q

are DM1 and DM2 associated with a genetic predisposition?

A

DM1: relatively weak, polygenic• DM2: relatively strong, poly genic

308
Q

what is the concordance between identical twins for DM1?

309
Q

what is the concordance between identical twins for DM2?

310
Q

Are DM1 and DM2 associated with the HLA system?

A

DM1: yes- HLA-DR3/4• DM2: No

311
Q

what is the degree of glucose intolerance in DM1 and DM2?

A

DM1: severe• DM2: mild to moderate

312
Q

what is the degree of insulin sensitivity in DM1 and DM2?

A

DM1: high• DM2: low

313
Q

what is the frequency of ketoacidosis in DM1 and DM2?

A

DM1: common• DM2: rare

314
Q

what are the β cell numbers in the islets in DM1 and DM2?

A

DM1: decreased• DM2: variable (with amyloid deposits)

315
Q

what are the serum insulin levels in DM1 and DM2?

A

DM1: low• DM2: variable

316
Q

what is the frequency of the classic symptoms of polyuria, polydipsia, polyphagia and weight loss in DM1 and DM2?

A

DM1: common• DM2: sometimes

317
Q

what is the histology in DM1 and DM2?

A

DM1: islet leukocytic infiltrate• DM2: islet amyloid (AIAPP) deposit

318
Q

ketoacidosis is one of the most important complications of what?

A

DM (usually type I)

319
Q

diabetic ketoacidosis is usually due to what?

A

increased insulin requirements from increased stress

320
Q

what is the biochemical basis of diabetic ketoacidosis?

A

excess fat break down and increased ketogenesis from increased free fatty acids, which are then made into ketone bodies

321
Q

which are the most common ketone bodies in diabetic ketoacidosis?

A

β-hydoxybutyrate > acetoacetate

322
Q

what are the signs/symptoms of diabetic ketoacidosis?

A

Kussmaul breathing (rapid/deep breathing), nausea/vomiting, abdominal pain, psychosis/delirium. fruity breath odor

323
Q

what are the lab values seen in diabetic ketoacidosis?

A
  1. hyperglycemia• 2. high H+• 3. low HCO3- (anion gap metabolic acidosis)• 4. high blood ketone levels• 5. leukocytosis• 6. hyperkalemia, but depleted intracellular K+ due to transcellular shift from decreased insulin
324
Q

what are the complications of diabetic ketoacidosis?

A

Life threatening mucor mycosis• Rhizopus infection• cerebral edema• cardiac arrhythmia• heart failure

325
Q

what is the treatment for diabetic ketoacidosis?

A

IV fluids• IV insulin• K+ (to replete intracellular stores)• glucose if necessary to prevent hypoglycemia

326
Q

what is carcinoid syndrome?

A

rare syndrome caused by carcinoid tumors (neuroendocrine cells), especially metastatic small bowel tumors which secrete high levels of serotonin

327
Q

carcinoid syndrome is not seen if what?

A

the tumor is limited to GI tract (5-HT undergoes first- pass metabolism in liver)

328
Q

carcinoid syndrome results in what?

A

recurrent diarrhea, cutaneous flushing, asthmatic wheezing, and right sided valvular disease

329
Q

what are the lab values seen in carcinoid syndrome?

A

high 5-HIAA in urine• niacin deficiency

330
Q

what is the treatment for carcinoid syndrome?

A

somatostatin analog (octreotide)

331
Q

what is the rule of 1/3’s for carcinoid syndrome?

A

1/3 metastasize• 1/3 present with second malignancy• 1/3 multiple

332
Q

what is the most common tumor of the appendix?

333
Q

what causes Zollinger-Ellison syndrome?

A

Gastrin secreting tumor of pancreas or duodenum

334
Q

what does the stomach look like in ZES?

A

stomach shows rugal thickening with acid hypersecretion

335
Q

ZES causes what?

A

recurrent ulcers

336
Q

ZES may be associated with what?

A

MEN type 1

337
Q

what are the characteristic tumors seen in MEN 1 (Wermer’s syndrome)?

A
  1. Parathyroid tumors• 2. Pituitary tumors• 3. Pancreatic endocrine tumors
338
Q

what are the pituitary tumors seen in MEN1?

A

prolactin or GH secreting

339
Q

what are the pancreatic endocrine tumors associated with MEN1?

A

ZES• insulinoma• VIPomas• glucagonomas (rare)

340
Q

MEN1 commonly presents with what?

A

kidney stones and stomach ulcers

341
Q

what are the tumors seen in MEN 2A (Sipple’s syndrome)?

A
  1. Medullary thyroid carcinoma• 2. Pheochromocytoma• 3. Parathyroid tumors
342
Q

medullary thyroid tumors in MEN2A/B secrete what?

A

calcitonin

343
Q

what tumors are characteristic MEN2B?

A
  1. medullary thyroid• 2. pheochromocytoma• 3. oral/intestinal ganglioneuromatosis
344
Q

oral/intestinal ganglioneuromatosis in MEN2B is associated with what?

A

marfanoid habitus

345
Q

what is the mnemonic for MEN1?

A

3P’s• Pituitary• Parathyroid• Pancreas• (diamond)

346
Q

what is the mnemonic for MEN2A?

A

2 P’s• Parathyroids• Pheochromocytomas• (square)

347
Q

what is the mnemonic for MEN2B?

A

1P• Pheochromocytoma• (triangle)

348
Q

what is the inheritance of all MEN syndromes?

A

autosomal dominant

349
Q

MEN is associated with which gene mutation?

A

MEN2A and MEN2B are associated with ret gene mutation

350
Q

what is the treatment strategy for DM1?

A

low sugar diet, insulin replacement

351
Q

what is the treatment strategy for DM2?

A

dietary modification and exercise for weight loss; oral hypoglycemics and insulin replacement

► Med Notes (62 decks)

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