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Endo USMLE Flashcards

1
Q

woman presents with diffuse goiter and hyperthyroidism. What are the expected values of TSH and thyroid hormones?

A

low TSH & hight thyroid hormones

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2
Q

48y/o female presntes with progressive lethargy and extreme sensitivity to cold temperatures. What is the diagnosis

A

hypothyroidism

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3
Q

pt with elevated serum cortisol levels undergoes a dexamethasone does not decrease cortisol levels, but 8 mg does. What is the dz?

A

pituitary tumor

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4
Q

50y/o man complains of diarrhea. On physical exam his face is plethoric and a heart murmur is detected. What is the dx?

A

carcinoid syndrome

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5
Q

woman of short stature presents with shortened 4th and 5th metacarpals. What endocrine d/o comes to mind?

A

Albright hereditary osteodystrophy or pseudohypoparathyroidism

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6
Q

Nondiabetic pt presents with hypoglycemia but low levels of C pepetide. What is the dx?

A

Surreptitious insulin injection

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7
Q

cortex of the adrenal glands comes from what embryologic source?

A

mesoderm

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8
Q

medulla of the adrenal glands comes from what embryologic source?

A

neural crest

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9
Q

GFR corresponds to

A

Salt (Na+)
Sugar (glucocorticoids) and
Sex (androgens)

mneu: the deepr you go the sweeter it gets

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10
Q

What does GFR stand for?

A

zona glomerulosa
zona fasciculata
zona reticularis

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11
Q

what does the zona glomerulosa secrete

A

aldosterone

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12
Q

what is the primary regulatory control of the zona glomerulosa

A

renin-angiotensin

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13
Q

what does the zona fasciculata secrete

A

cortisol, sex hormone

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14
Q

what is the primary regulatory control of the zona fasciculata

A

ACTH, hypothalamic CRH

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15
Q

what does the zona reticularis secrete

A

sex hormones (e.g., androgens)

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16
Q

what is the primary regulatory control of the zona reticularis

A

ACTH, hypothalamic CRH

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17
Q

what do the chromaffin cells cells of the medulla secrete

A

catecholamines (epi, NE)

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18
Q

what is the primary regulatory control of the medulla

A

preganglionic sympathetic fibers

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19
Q

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

A

pheochromocytoma

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20
Q

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

A

neuroblastoma

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21
Q

out of pheochromocytoma and neuroblastoma which one causes episodic hyperension

A

pheochromocytoma

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22
Q

how does the left adreanal gland drain blood

A

left adrenal ->left adrenal vein -> left renal vv -> IVC

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23
Q

how does the right adreanal gland drain blood

A

right adrenal ->right adrenal vein -> IVC

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24
Q

posterior pituitary is derived from what embryological origin

A

neuroectoderm

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25
Q

posterior pituitary secretes what

A

vasopressen and oxytoxin

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26
Q

where are vasopressen and oxytoxin made

A

hypothalamus

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27
Q

where are vasopressen and oxytoxin shipped

A

pituitary

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28
Q

where is the anterior pituatary derived from

A

oral ectoderm

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29
Q

what does the anterior pituitary secrete

A

FLAT Pig

FSH
LSH
ACTH, Melanotropin (MSH)
TSH
Prolactin
GH
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30
Q

alpha subunit is a common subunit to

A

TSH, LH, FSH, & hCG

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31
Q

Beta subunit determines this

A

hormone specificity

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32
Q

islet of Langerhans are collections of these three types of cells.

A

alpha, beta, delta cells

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33
Q

what part of the pancreas are the alpha, beta, & delta cells most numerous

A

tail

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34
Q

from where do the islets of Langerhans arise

A

pancreatic buds

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35
Q

alpha cells secrete

A

glucagon

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36
Q

beta cells secrete

A

insulin

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37
Q

delta cells secrete

A

somatostatin

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38
Q

prolactin ____ dopamine synthesis and secretion from the hypothalamus.

A

increases

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39
Q

dopamine subsequently _______ prolactin secretion

A

decreases

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40
Q

dopamine agonists (e.g., bromocriptine) ______ prolactin secretion. Dopamine antagonist (e.g., most antipsychotics) __________prolactin secretions.

A

decreases

increases

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41
Q

in females prolactin inhibits_______ synthesis and release, which inhibits ovulation

A

GnRH

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42
Q

___________ this is commonly seen in prolactinomas

A

amenorrhea

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43
Q

what is the congenital adrenal hyperplasia: Female that is not maturing presents with HYPERTENSION, hypokalemia, she has decreased sex hormones, decrease cortisol, increased mineralocorticoids

A

17 alpha hydroxylase deficiency

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44
Q

this congenital adreanal hyperplasia is the most common form. It results in decreased cortisol (increased ACTH), decreased mineralocorticoids, increased sex hormones. Complications include masculinization, female psuedohermaphroditism, HYPOtension, hyponatremia, hyperkalemia, increased plasma renin activity, and volume depletion. Salt wasting can need to hypovolemic shock int he newborn

A

21 beta hydroxylase deficiency

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45
Q

this congenital adreanal hyperplasia results in low cortisol, low aldosterone and corticosterone and high sex horones. Complicatons include masculinization and (HYPERtension (11-deoxycorticosterone acts as a weak mineralocorticoid)

A

11 beta hydroxylase deficiency

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46
Q

where does PTH come from (cells and tissue)

A

chief cells of parathyroid

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47
Q

what are the 4 fxs of PTH

A

1) increased bone resorption of Ca++ & phosphate
2) increased kidney resorption of Ca++ in the distal convoluted tubule
3) decreased kidney resoption of phosphate
4) increased 1,25 (OH)2 vitamen D (cholecalciferol) production by stimulating kidney 1 alpha hydroxilase

mneu: PTH increases serum CA, decreases serum PO, increases urine PO4, and stimulates both osteoclasts and osteblasts

PTH: phosphate trashing hormone

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48
Q

what causes PTH secretion

A

decreased serum Ca++

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49
Q

image p. 250 actions of PTH and 1,25 OH D in maitenence of Ca++ & phosphate homeostasis

A

shown are the main actions of PTH & 1,25 (OH)2 D in the maintenance of Ca++ and phosphate homeostasis

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50
Q

source of vit D3

A

sun exposure in skin

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51
Q

source of D2

A

plants

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52
Q

where are D2 & D3 converted to 25 OH vit D

A

liver

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53
Q

where is 25 OH vit D converted to 1,25 (OH)2 vit D (active form)

A

kidney

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54
Q

what is the fx of vit D

A

1) increased absorption of dietary Ca++
2) increased absorption of dietary phosphate
3) increased bone resorption of Ca++ & (PO4)3-

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55
Q

what dz do you get if you don’t get enough vit D (kids and adults)

A

kids-rickets

adults-osteomalacia

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56
Q

what is 24,25-(OH)2 vit D

A

inactive form of vit D

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57
Q

in the regulation of vit D, what does increased PTH cause

A

increase 1,25-(OH)2 vit D formation

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58
Q

in the regulation of vit D, what does decreased [Ca++]cause

A

increase 1,25-(OH)2 vit D production

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59
Q

in the regulation of vit D, what does increased 1,25-(OH)2 vit D cause

A

increase 1,25-(OH)2 vit D inhibits its own production

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60
Q

What dz?
Ca++: ↑
Phosphate:↓
Alk Phos:↑

A

hyperparathyroidism

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61
Q

What dz?
Ca++: N/↑
Phosphate:N
Alk Phos:↑↑↑

A

paget’s dz of bone

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62
Q

What dz?
Ca++: ↑
Phosphate:↑
Alk Phos:N/↑

A

vit D intoxication

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63
Q

What dz?
Ca++: N
Phosphate:N
Alk Phos:N

A

osteoporosis

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64
Q

What dz?
Ca++: ↓
Phosphate:↑
Alk Phos:N

A

renal insufficiency

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65
Q

where does calcitonin come from

A

parafolicular cells (C cells) of thyroid

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66
Q

what is the fx of calcitonin

A

↓ bone resorption of calcium

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67
Q

calcitonin opposes the action of what hormone

A

PTH

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68
Q

what stimulates calcitonin secretion

A

increased serum Ca++

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69
Q

the need for gene transcription and protein synthesis delays the onset of action of these steroid/thyroid hormones

A

mneu: PET CAT

Progesterone
Esterogen
Testosternone
Cortisol
Aldosterone
Thyroxine and T3
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70
Q

these hormones are lipophilic and insoluble in plasma; therfore, they must circulate bound to specific binding globulins, which increase solubility and allows for increased delivery of steroid to the target organ.

A

steroid

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71
Q

increased levels of sex hormone-binding globulin (SHBG) leads to lower levels of free testosterone and results in this physical exam finding

A

gynecomastia

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72
Q

decreased SHBG raises free testosterone leading to this finding

A

hirsutism

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73
Q

these are iodine containing hromones taht control the body’s metabolic rate

A

thyroid hormones (t3/t4)

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74
Q

source of thyroid hormones

A

follicles of thyroid. Most T3 formed in the blood

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75
Q

fx of thyroid hormones

A

1) bone growth (synergism w/ GH
2) CNS maturation
3) beta adrenergic effects (increased CO,HR,SV, contractility
4) increase BMR via increased Na+/K+ ATPase activity -> increased O2 consumption, RR, increased body temp
5) increased glycogenolysis, gluconeogesis, lipolysis

mneu: T3 fx--4Bs
Brain maturation
Bone growth
Beta adrenergic effects
BMR incrase
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76
Q

what globulin binds most T3/T4 in blood

A

Throxine-binding globulin (TBG)

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77
Q

is free or bound thyroid hromone active

A

free

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78
Q

in what dz would you see decreased TBG

A

hepatic failure

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79
Q

in what condition would you see increase TBG

A

pregnancy

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80
Q

what hromone stimulates TSH secretion from the pituitary

A

TRH (hypothalamus

81
Q

what cells does TSH stimulate to secrete thyroid hormone

A

follicular cells

82
Q

negative feedback by this hormone to the anterior pituitary decreases sensititvity to TRH.

A

T3

83
Q

in Graves dz it is this TSH analog that stimulates follicular cells

A

TSI

84
Q

what organs depend on insulin for glucose uptake

A

skeletal mm and adipose tissue

85
Q

what organs take up glucose independent of insulin levels (GLUT-1)

A

brain and RBC

86
Q

what fuel can the brain use in starbation states

A

ketone bodies

87
Q

this syndrome refers to increased cortisol levels due to a variety of causes. The clinical picture includes hypertension, weight gain, moon facies, truncal obesity, buffalo hump, hyperglycemia (insulin resistance), skin changes (thinning, striae), osteoporosis, amenorrhea, and immune suppression

A

cushing syndrome

88
Q

If you’re pt presents with cushings syndrome you have to identify the source, if the pt has increased ACTH levels because of a pituitary adenoma the pt has

A

Cushing’s dz

89
Q

If you’re pt presents with cushings syndrome you have to identify the source, if the pt has decreased ACTH levels due to causes that are not iatrogenic, the pt has

A

primary adrenal hyperplasia/neoplasia

90
Q

If you’re pt presents with cushings syndrome you have to identify the source, if the pt has decreased ACTH levels due to iatrogenic causes, the pt may be taking

A

steroids (chronic)

91
Q

describe the dexamethasone suppression test in a healthy person

A

low cortisol after low dose

92
Q

describe the dexamethasone suppression test in a person with a ACTH-producing tumor

A

high cortosol after low dose; low cortisol after high dose

93
Q

describe the dexamethasone suppression test in a person with a cortisone producing tumor

A

high cortisol after low and high dose

94
Q

this dz is caused by an aldosterone-secreting tumor, resulting in HTN, hypokalemia, metabolic alkalosis, and LOW plasma renin

A

primary hyperaldosteronism (Conn’s syndrome)

95
Q

this dz is due to renal artery stenosis, chronic renal failure, cHF, cirrhosis, or nephrotic syndrome. Kidney perception of low intravascular volume results in an overactive renin0angiotensin system. Therefore, it is associated with HIGH plasma renin

A

secondary hyperaldosteronism

96
Q

what is the tx for hyperaldosteronism

A

spironolactone (a K+ sparing diuretic that works by acting as an aldosterone antagonist)

97
Q

this is a primary deficiency of aldosterone and cortisol due to adrenal atrophy, causing hypotension (hyponatremic volume contraction) and skin hyperpigmentation (due to MSH, a byproduct of increased ACTH production from POMC). It is characterized by Adrenal Atrophy and Absence of hormone production. It involves All 3 cortical divisions.

A

Addison’s dz

98
Q

How you distinguish Addison’s dz (primary aldosterone/cortisol deficiency[renal problem]) from secondary aldosterone/cortisol deficiency [pituitary problem]

A

Secondary insufficency has no skin hyperpigmentation

99
Q

this is the most common tumor of the adrenal medulla in adults. It is derived from chromaffin cells which arise from the neural crest

A

pheochromocytoma

100
Q

what can pheochromocytomas be associated with if they occur in pts whith MEN types II & III

A

neurofibromatosis

101
Q

this is the most common tumor of the adrenal medulla in children, but it can occur anywhere along the sympathetic chain

A

neuroblastoma

102
Q

what do pheochromocytomas secrete

A

epi, NE, dopamine

103
Q

how do you dx a pheo

A

urinary VMA and plasma catecholamines are elevated

104
Q

what endocrine d/os are pheos assoc with

A

MEN types II & III

105
Q

how do you tx pheos

A

alpha antagonists, especially phenoxybenzamine, a nonselective, IRREVERSABLE alpha blocker

106
Q

symptoms of pheos occur in “spells”–meaning they often relapse and remit. What are the 5 “P”s of a pheo

A 
Pressure (elevated BP)
Pain (headache)
Perspiration
Palpitations (tachycardia)
Pallor
107
Q

give the rule of 10s associated with pheos

A 
10% malignant
10% bilateral
10% extraadrena
10% calcify
10% kids
10% familial
108
Q

this MEN type involves the 1) PANCREAS (e.g., Zollinger-Ellison syndrome, insulinomas, VIPomas) 2)PARATHYROID 3) PITUITARY TUMORS. It often presents with kidney stones and stomach ulcers

A

MEN I (Wermer’s syndrome)= 3 “P” organs (Pancreas, Pituitary, and Parathyroidism)

109
Q

this MEN type involves 1) MEDULLARY CARCINOMA OF THE THYROID 2)PHEOCHROMOCYTOMA 3) PARATHYROID TUMOR.

A

MEN type II (Sipple’s syndrome)

110
Q

this MEN type involves 1) MEDULLARY CARCINOMA OF THE THYROID 2)PHEOCHROMOCYTOMA 3) ORAL AND INTESTINAL GANGLIONEUROMATOSIS (MUCOSAL NEUROMAS).

A

MEN type III ( formerly MEN type IIb )

111
Q

all MEN have this type of inheritance

A

autosomal dominant

112
Q

what gene are MEN type II & III associated with

A

ret gene

113
Q

this d/o often manifests itself with cold intolerance, hypoactivity, weight gain, fatigue, lethargy, decreased appitite, constipation, weakness, decreased reflexes, facial/periorbital myxedema, dry, cool skin, and coarse, brittle hairr

A

hypothyroidism

114
Q

what will the labs show in hypothyroidism

A

increased TSH (most sensitive test for primary hypothyroidism)
decreased total T4
decreased free T4
decreased T3 uptake

115
Q

in this dz the pt presents hypothyroid. It results because thyroid is replaced by fibrous tissue

A

Riedel’s thyroiditis

116
Q

this d/o manifests itself with heat intolerance, hyperactivity, weight loss, chest pain/palpitations, arrhythmias, diarrhea, increased reflexes, warm moist skin, and fine hair

A

hyperthyroidism

117
Q

this is an autoimmune hyperthyroidism with thyroid stimulating/TSH receptor antibodies. It often presents during stress (e.g., childbirth) with opthalmopathy (proptosis, EOM swelling), pretibial myxedema, diffuse goiter.

A

graves dz

118
Q

what type of hypersensitivity rxn in graves dz

A

type II

119
Q

what lab results will you see in hyperthyroidism

A

decreased TSH (if primary)
increased total T4
increased free T4
increased T3 uptake

120
Q

this is an autoimmune d/o resulting in hypothyroidism. It has a slow course and often you will see a moderately enlarged, nontender thyroid. Microscopically you will see a lymphocytic infiltrate with germinal genters. Pt will test positive for antimicrosomal and antithyroglobulin antibodies

A

Hashimoto’s thyroiditis

121
Q

this is a self-limited hypothyroidism which often follows a flulike illness. Pt will presents with jaw pain and a very tender thyroid gland. Labs will show signs of early inflammation and elevated ESR.

A

Subacute thyroiditis (de Quervain’s)

122
Q

this is the most common thyroid cancer. It has an excellent prognosis. Microscopically you will see “ground glass” nuclei and psammoma bodies

A

papillary carcinoma

123
Q

this thyroid cancer has a good prognosis. microscopically you will see uniform follicules

A

follicular carcinoma

124
Q

this thyroid cancer arises from parafollicular “C cells”. It produces calcitonin. Microscopicallly you may see sheets of cells in amyloid stroma. It is seen in MEN types II & III

A

medullary carcinoma

125
Q

this thyroid cancer occurs in older pts. It carries a very poor prognosis

A

undifferentiated/anaplastic

126
Q

this occurs wherever endemic goiter is prevalent (lack of dietary iodine). It is common in china. It can also be caused by a defect in T4 formation or developmental failure in thyroid formation. You may see a pot-bellied, pale, puffy-faced child with protruding umbilicus and protuberant tongue

A

cretinism

127
Q

adult pt presents with large tongue, deep furrows, deep voice, large hands and feet, coarse facial features, impared glucose tolerance (insulin resistance). What is the d/o and what hormone is in excess

A

acromegly

increased growth hormone

128
Q

what does increased GH in children cause

A

gigantism

129
Q

how do you tx increased GH either in acromegly or gigantism

A

octreotide

130
Q

give some natural states in which you might have increased GH

A

stress, exercise, and hypoglycemia

131
Q

this is usually caused by an ademona. labs will show hypercalemia, hypercalciuria (RENAL STONES), hypophosphatemia, increased, PTH & cAMP in urine. While it is often asymptomatic it may present with weakness and constipation (“GROANS”)

A

primary hyperparathyroidism

132
Q

this d/o is due to decreaesed serum Ca++, most often due to chronic renal dz. Labs will show hypocalcemia, hyperphosphatemia, and increased PTH

A

secondary hyperparathyroidism (hyperplasia)

133
Q

this complication of primary hyperparathyroidism results when cystic bone speaces are filled with brown fibrous tissue causing BONE PAIN

A

Osteitis fibrosa cystica (von recklinghausen’s syndrome)

134
Q

this complication of secondary hyperparathyroidism, results in bone lesions due to renal dz

A

renal osteodystrophy

135
Q

give the rhyme that describes hyperparathyroidism

A

stones, bones, and groans

136
Q

pt presents with hypocalcemia or tetany. what dz

A

hypoparathyroidism.

137
Q

give 2 causes of hypoparathyroidism

A

accidental surgical excision (thyroid sx)

DiGeorge syndrome

138
Q

Chvostek’s sign is a sign of hypoparathyroidism. What is it?

A

tap facial nn results in contraction of facial mm

139
Q

trousseau’s sign is a sign of hypoparathyroidism. What is it?

A

occlusion of brachial artery w/ BP cuff results in carpal spasm

140
Q

pt presents w/ hypocalcemia, shortened stature and shortened 4th & 5th digits.

A

pseudohypoparathyroidism

141
Q

what is pseudohypoparathyroidism

A

kidneys are unresponsive to PTH

142
Q

what is the inheritance of pseudohypoparathyroidism

A

autosomal-recessive

143
Q

give 5 causes of hypercalcemia

A

mneu: CHIMPANZEES

Calcium ingestion, Hyperparathyroid, Hyperthyroid,, Iatrogenic (thiazides, Multiple myeloma, Paget’s dz, Addison’s dz, Neoplasms, Zollinger-Ellison syndrome, Excess vit D, Excess vit A, Sarcoidosis

144
Q

give some acute manifestations of diabetes mellitus

A

polydipsia, polyuria, polyphagia, weight loss, DKA (type 1), hyperosmolar coma (type 2), unopposed secretion of GH and epinephrine (exacerbating hyperglycemia)

145
Q

image p. 256 –Diabetes mellitis

A

–

146
Q

Give some chronic manifestations of Diabetes Mellitus

A

small vessel dz (diffuse thickening of basement membrane) ->retinopathy (hemorrhage, exudates, microaneurysms, vessel proliferation), claucoma, nephropathy (nodular sclerosis, progressive protinuria, chronic renal failure, arteriosclerosis leading to HTN)
2. Large vessel atherosclerosis, CAD, peripheral vascular occlusive dz and gangrene, cerebrovascular dz
Neuropathy (motor, sensory, and autonomic degeneration)
Cataracts (sorbitol accumulation

147
Q

what tests should you run in dbts

A

fasting serum glucose
glucose tolerance test
HbA1c

148
Q

what does HbA1c meausre

A

long term diabetic control

149
Q

what is the primary defect in type 1–juvenile onset (IDDM)

A

viral or immune destruction of beta cells

150
Q

what is the primary defect in type 2–adult onset (NIDDM)

A

increased resistance to insulin

151
Q

is insulin necessary for tx in type 1–juvenile onset (IDDM)

A

always

152
Q

is insulin necessary for tx in type 2–adult onset (NIDDM)

A

sometimes

153
Q

at what age does type 1–juvenile onset (IDDM)usually strike [many exceptions]

A

<30

154
Q

at what age does type 2–adult onset (NIDDM)usually strike [many exceptions]

A

> 40

155
Q

is type 1–juvenile onset (IDDM)associated with obesity

A

no

156
Q

is type 2–adult onset (NIDDM)associated with obesity

A

yes

157
Q

is there a genetic predisposition to type 1–juvenile onset (IDDM)

A

weak, polygenic

158
Q

is there a genetic predisposition to type 2–adult onset (NIDDM)

A

strong, polygenic

159
Q

is there an HLA association to type 1–juvenile onset (IDDM)

A

yes (HLA-DR3 &4)

160
Q

is there an HLA association to type 2–adult onset (IDDM)

A

no

161
Q

describe the glucose intolerance associated with type 1–juvenile onset (IDDM)

A

severe

162
Q

describe the glucose intolerance associated with type 2–adult onset (NIDDM)

A

mild-moderate

163
Q

Is ketoacidosis associated with type 1–juvenile onset (IDDM)

A

commonly

164
Q

Is ketoacidosis associated with type 2–adult onset (NIDDM)

A

rarely

165
Q

describe the beta cell numbers in the islets associated with type 1–juvenile onset (IDDM)

A

low

166
Q

describe the beta cell numbers in the islets associated with type 2–adult onset (NIDDM)

A

variable

167
Q

describe the serum insulin associated with type 1–juvenile onset (IDDM)

A

low

168
Q

describe the serum insulin associated with type 2–adult onset (NIDDM)

A

variable

169
Q

are the classic symptoms of polyuria, polydipsia, thirst, and weight loss associated with type 1–juvenile onset (IDDM)

A

commonly

170
Q

are the classic symptoms of polyuria, polydipsia, thirst, and weight loss associated with type 2–adult onset (NIDDM)

A

sometimes

171
Q

diabetic ketoacidosis is one of the most important complications of type 1 dbts describe its pathology

A

excess fat breakdown and increased ketogenesis from increase in free fataty acids, which are then made into ketone bodies.

172
Q

what is ketoacidosis usually due to

A

an increase in insulin requirements due to an increase in stress (e.g., infection)

173
Q

give some signs and symptoms of diabetic ketoacidosis

A

kussmaul respirations (rapid/deep breathing), hyperthermia, nausea/vomiting, abdominal pain, psychosis/dementia, dehydration. Fruity breath odor (due to exhaled acetone)

174
Q

what will the labs of a pt in diabetic ketoacidosis show

A

hyperglycemia, increase H+, decreased HCO3-, (anion gap metabolic acidosis, increased blood ketone levels, leukocytosis. Hyperkalemia, but depleted intracellular K+

175
Q

what are some complications of diabetic ketoacidosis

A

life-threatening mucormycosis, rhizopus infxn, cerebral edema, cardiac arrhythmias, heart failure

176
Q

how do you tx a pt in diabetic ketoacidosis

A

fluids, insulin, and potassium; glucose if necessary to prevent hypoglycemia

177
Q

this d/o is characterized by intensive thirst and polyuria together with aninability to concentrate urine owing to lack of ADH

A

diabetes insipidus

178
Q

this type of diabetes insipidus may be caused by a pituitary tumor, trauma, surgery, histiocytosis

A

central DI

179
Q

this type of diabetes insipidus may be caused by hereditary factors, hypercalcemia, lithium, demeclocycline

A

nephrogenic DI (lack of renal response to ADH)

180
Q

how do you dx DI

A

water deprivation test –urine specific gravity 290mOsm/L

181
Q

how do you tx central DI

A

intranasal despopressin (ADH analog

182
Q

how do you tx central DI

A

hydrochlorothiazide, indomethacin, or amiloride

183
Q

this d/o results in

1) excessive water retention
2) hyponatremia
3) urine osmolarity>serum osmolarity

A

syndrome of inappropriate antiduiuretic hormone secretion

184
Q

how do you tx SIADH

A

demeclocycline or H2O restriction

note: tx slowly

185
Q

in SIADH very low serum sodium levels can lead to this

A

seizures

186
Q

give some causes of SIADH

A

1) ectopic ADH (small cell lung CA)
2) CNS disorders/head trauma
3) pulmonary dz
4) Drugs (e.g., cyclophosphamide)

187
Q

this is a rare syndrome that results in recurrent diarrhea, cutaneous flushing, asthmatic wheezing, and right sided valvular dz.

A

carcinoid syndrome

188
Q

what will you find in the urine of a pt with carcinoid syndrome

A

increased 5-HIAA in urine

189
Q

carcinoid tumor is the most common tumor in this part of large intestine

A

appendix

190
Q

carcinoid tumors result from this type of cell

A

neuroendocrine cells

191
Q

carcinoid tumor secretes high levels of this

A

5-HT (seratonin)

192
Q

if carcinoid tumor is limited to here you wont see symptoms

A

GI tract

5-HT undergoes 1st pass metabolism in liver

193
Q

give the rule of 1/3 for carcinoid tumors

A

1/3 metastasize
1/3 present w/ 2nd malignancy
1/3 multiple

194
Q

where to carcinoid tumors derive from

A

neuroendocrine cells of GI tract

195
Q

how do you tx carcinoid tumors

A

octreotide

196
Q

this is a gastrin secreting tumor of pancreas or duodenum. It causes recurrent ulcrs

A

Zollinger-Ellison syndrome

197
Q

what MEN syndrome is ZE syndorme associated with

A

MEN type I

198
Q

what is the tx strategy for type 1 DM

A

low sugar diet, insulin replacement

199
Q

what is the tx strategy for type 2 DM

A

dietary modification, exercise for weight loss, and oral hypoglycemics

Step 1 Complete (29 decks)

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