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Flashcards in Endo USMLE Deck (199):
1

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

low TSH & hight thyroid hormones

2

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

hypothyroidism

3

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

pituitary tumor

4

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

carcinoid syndrome

5

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

Albright hereditary osteodystrophy or pseudohypoparathyroidism

6

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

Surreptitious insulin injection

7

cortex of the adrenal glands comes from what embryologic source?

mesoderm

8

medulla of the adrenal glands comes from what embryologic source?

neural crest

9

GFR corresponds to

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

mneu: the deepr you go the sweeter it gets

10

What does GFR stand for?

zona glomerulosa
zona fasciculata
zona reticularis

11

what does the zona glomerulosa secrete

aldosterone

12

what is the primary regulatory control of the zona glomerulosa

renin-angiotensin

13

what does the zona fasciculata secrete

cortisol, sex hormone

14

what is the primary regulatory control of the zona fasciculata

ACTH, hypothalamic CRH

15

what does the zona reticularis secrete

sex hormones (e.g., androgens)

16

what is the primary regulatory control of the zona reticularis

ACTH, hypothalamic CRH

17

what do the chromaffin cells cells of the medulla secrete

catecholamines (epi, NE)

18

what is the primary regulatory control of the medulla

preganglionic sympathetic fibers

19

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

pheochromocytoma

20

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

neuroblastoma

21

out of pheochromocytoma and neuroblastoma which one causes episodic hyperension

pheochromocytoma

22

how does the left adreanal gland drain blood

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

23

how does the right adreanal gland drain blood

right adrenal ->right adrenal vein -> IVC

24

posterior pituitary is derived from what embryological origin

neuroectoderm

25

posterior pituitary secretes what

vasopressen and oxytoxin

26

where are vasopressen and oxytoxin made

hypothalamus

27

where are vasopressen and oxytoxin shipped

pituitary

28

where is the anterior pituatary derived from

oral ectoderm

29

what does the anterior pituitary secrete

FLAT Pig

FSH
LSH
ACTH, Melanotropin (MSH)
TSH
Prolactin
GH

30

alpha subunit is a common subunit to

TSH, LH, FSH, & hCG

31

Beta subunit determines this

hormone specificity

32

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

alpha, beta, delta cells

33

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

tail

34

from where do the islets of Langerhans arise

pancreatic buds

35

alpha cells secrete

glucagon

36

beta cells secrete

insulin

37

delta cells secrete

somatostatin

38

prolactin ____ dopamine synthesis and secretion from the hypothalamus.

increases

39

dopamine subsequently _______ prolactin secretion

decreases

40

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

decreases
increases

41

in females prolactin inhibits_______ synthesis and release, which inhibits ovulation

GnRH

42

___________ this is commonly seen in prolactinomas

amenorrhea

43

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

17 alpha hydroxylase deficiency

44

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

21 beta hydroxylase deficiency

45

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)

11 beta hydroxylase deficiency

46

where does PTH come from (cells and tissue)

chief cells of parathyroid

47

what are the 4 fxs of PTH

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

48

what causes PTH secretion

decreased serum Ca++

49

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

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

50

source of vit D3

sun exposure in skin

51

source of D2

plants

52

where are D2 & D3 converted to 25 OH vit D

liver

53

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

kidney

54

what is the fx of vit D

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

55

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

kids-rickets
adults-osteomalacia

56

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

inactive form of vit D

57

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

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

58

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

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

59

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

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

60

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

hyperparathyroidism

61

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

paget's dz of bone

62

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

vit D intoxication

63

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

osteoporosis

64

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

renal insufficiency

65

where does calcitonin come from

parafolicular cells (C cells) of thyroid

66

what is the fx of calcitonin

↓ bone resorption of calcium

67

calcitonin opposes the action of what hormone

PTH

68

what stimulates calcitonin secretion

increased serum Ca++

69

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

mneu: PET CAT

Progesterone
Esterogen
Testosternone
Cortisol
Aldosterone
Thyroxine and T3

70

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.

steroid

71

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

gynecomastia

72

decreased SHBG raises free testosterone leading to this finding

hirsutism

73

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

thyroid hormones (t3/t4)

74

source of thyroid hormones

follicles of thyroid. Most T3 formed in the blood

75

fx of thyroid hormones

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

76

what globulin binds most T3/T4 in blood

Throxine-binding globulin (TBG)

77

is free or bound thyroid hromone active

free

78

in what dz would you see decreased TBG

hepatic failure

79

in what condition would you see increase TBG

pregnancy

80

what hromone stimulates TSH secretion from the pituitary

TRH (hypothalamus

81

what cells does TSH stimulate to secrete thyroid hormone

follicular cells

82

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

T3

83

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

TSI

84

what organs depend on insulin for glucose uptake

skeletal mm and adipose tissue

85

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

brain and RBC

86

what fuel can the brain use in starbation states

ketone bodies

87

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

cushing syndrome

88

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

Cushing's dz

89

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

primary adrenal hyperplasia/neoplasia

90

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

steroids (chronic)

91

describe the dexamethasone suppression test in a healthy person

low cortisol after low dose

92

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

high cortosol after low dose; low cortisol after high dose

93

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

high cortisol after low and high dose

94

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

primary hyperaldosteronism (Conn's syndrome)

95

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

secondary hyperaldosteronism

96

what is the tx for hyperaldosteronism

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

97

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.

Addison's dz

98

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

Secondary insufficency has no skin hyperpigmentation

99

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

pheochromocytoma

100

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

neurofibromatosis

101

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

neuroblastoma

102

what do pheochromocytomas secrete

epi, NE, dopamine

103

how do you dx a pheo

urinary VMA and plasma catecholamines are elevated

104

what endocrine d/os are pheos assoc with

MEN types II & III

105

how do you tx pheos

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

106

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

Pressure (elevated BP)
Pain (headache)
Perspiration
Palpitations (tachycardia)
Pallor

107

give the rule of 10s associated with pheos

10% malignant
10% bilateral
10% extraadrena
10% calcify
10% kids
10% familial

108

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

MEN I (Wermer's syndrome)= 3 "P" organs (Pancreas, Pituitary, and Parathyroidism)

109

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

MEN type II (Sipple's syndrome)

110

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

MEN type III ( formerly MEN type IIb )

111

all MEN have this type of inheritance

autosomal dominant

112

what gene are MEN type II & III associated with

ret gene

113

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

hypothyroidism

114

what will the labs show in hypothyroidism

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

115

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

Riedel's thyroiditis

116

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

hyperthyroidism

117

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.

graves dz

118

what type of hypersensitivity rxn in graves dz

type II

119

what lab results will you see in hyperthyroidism

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

120

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

Hashimoto's thyroiditis

121

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.

Subacute thyroiditis (de Quervain's)

122

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

papillary carcinoma

123

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

follicular carcinoma

124

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

medullary carcinoma

125

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

undifferentiated/anaplastic

126

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

cretinism

127

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

acromegly

increased growth hormone

128

what does increased GH in children cause

gigantism

129

how do you tx increased GH either in acromegly or gigantism

octreotide

130

give some natural states in which you might have increased GH

stress, exercise, and hypoglycemia

131

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")

primary hyperparathyroidism

132

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

secondary hyperparathyroidism (hyperplasia)

133

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

Osteitis fibrosa cystica (von recklinghausen's syndrome)

134

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

renal osteodystrophy

135

give the rhyme that describes hyperparathyroidism

stones, bones, and groans

136

pt presents with hypocalcemia or tetany. what dz

hypoparathyroidism.

137

give 2 causes of hypoparathyroidism

accidental surgical excision (thyroid sx)

DiGeorge syndrome

138

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

tap facial nn results in contraction of facial mm

139

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

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

140

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

pseudohypoparathyroidism

141

what is pseudohypoparathyroidism

kidneys are unresponsive to PTH

142

what is the inheritance of pseudohypoparathyroidism

autosomal-recessive

143

give 5 causes of hypercalcemia

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

give some acute manifestations of diabetes mellitus

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

145

image p. 256 --Diabetes mellitis

--

146

Give some chronic manifestations of Diabetes Mellitus

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

what tests should you run in dbts

fasting serum glucose
glucose tolerance test
HbA1c

148

what does HbA1c meausre

long term diabetic control

149

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

viral or immune destruction of beta cells

150

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

increased resistance to insulin

151

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

always

152

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

sometimes

153

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

<30

154

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

>40

155

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

no

156

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

yes

157

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

weak, polygenic

158

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

strong, polygenic

159

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

yes (HLA-DR3 &4)

160

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

no

161

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

severe

162

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

mild-moderate

163

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

commonly

164

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

rarely

165

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

low

166

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

variable

167

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

low

168

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

variable

169

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

commonly

170

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

sometimes

171

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

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

172

what is ketoacidosis usually due to

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

173

give some signs and symptoms of diabetic ketoacidosis

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

174

what will the labs of a pt in diabetic ketoacidosis show

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

175

what are some complications of diabetic ketoacidosis

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

176

how do you tx a pt in diabetic ketoacidosis

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

177

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

diabetes insipidus

178

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

central DI

179

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

nephrogenic DI (lack of renal response to ADH)

180

how do you dx DI

water deprivation test --urine specific gravity 290mOsm/L

181

how do you tx central DI

intranasal despopressin (ADH analog

182

how do you tx central DI

hydrochlorothiazide, indomethacin, or amiloride

183

this d/o results in
1)excessive water retention
2)hyponatremia
3)urine osmolarity>serum osmolarity

syndrome of inappropriate antiduiuretic hormone secretion

184

how do you tx SIADH

demeclocycline or H2O restriction

note: tx slowly

185

in SIADH very low serum sodium levels can lead to this

seizures

186

give some causes of SIADH

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

187

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

carcinoid syndrome

188

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

increased 5-HIAA in urine

189

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

appendix

190

carcinoid tumors result from this type of cell

neuroendocrine cells

191

carcinoid tumor secretes high levels of this

5-HT (seratonin)

192

if carcinoid tumor is limited to here you wont see symptoms

GI tract
5-HT undergoes 1st pass metabolism in liver

193

give the rule of 1/3 for carcinoid tumors

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

194

where to carcinoid tumors derive from

neuroendocrine cells of GI tract

195

how do you tx carcinoid tumors

octreotide

196

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

Zollinger-Ellison syndrome

197

what MEN syndrome is ZE syndorme associated with

MEN type I

198

what is the tx strategy for type 1 DM

low sugar diet, insulin replacement

199

what is the tx strategy for type 2 DM

dietary modification, exercise for weight loss, and oral hypoglycemics