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Step2CK > Endo step Up > Flashcards

Endo step Up Flashcards

1
Q

when is insuline released

A

response to glucose intake

secreted by pancreatic beta islet cell

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2
Q

effects of insulin

A

induce glucose and aa uptake by muscle, adipose and liver
glucose to glycogen fatty acids and pyruvate
inhibits lipolysis

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3
Q

where and when is glucagon released

A

by alpha islet cells in response to decreased glucose and protein intake
promotes breakdown of glycogen and fatty acids

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4
Q

What HLA is assoc with DM I

A

HLA DR3 DR4 and DQ

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5
Q

signs of DM I

A

polyuria polydipsia, polyphagia, weight loss

rapid onset

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6
Q

labs of DMI I

A

hyperglycemia, glycosuria, serum and urine ketones, increase HbA1c

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7
Q

what happens if DM I patient gives too much insulin

A

hypoglycemia

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8
Q

what illnesses are associated with onset beta cell destruction

A

rubella

coxsackie virus and mumps

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9
Q

risk factors DM II

A

FMH obesity metabolic syndrome, lack of exercise, gestational DM

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10
Q

Dx criteria DM

A

random plasma glucose >200 with Sx
fasting glucose >126 on 2 separate occasions
plasma glucose >200 2 hrs after 75 g oral glucose load
HbA1c>6.5%

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11
Q

what are the rapid acting insulin

A

lispro, asoart and glulisine

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12
Q

what are the long acting insulins

A

NPH, glargine and detemir

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13
Q

diabetic ketoacidosis is complication of what

A

DM I only

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14
Q

complication dM II

A 
hyperosmolar hyperglycemic nonketotic syndrome
retinopathy
nephropathy
neuropathy
atherosclerosis
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15
Q

what leads to DKA

A

low insulin
glucagon excess leading to dehydration of TG that eventually turn to ketoacids
so not taking insuline or have infection,stress, MI or high alcohol use

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16
Q

signs DKA

A

weakness, polyuria, polydipsia, abdominal pain, vomiting, dry mucous membranes, decreased skin turgor, fruity odor on breath, hyperventilation, kussmaul breathing, mental status changes from dehydration

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17
Q

how does metformin work

A

decrease hepatic gluconeogenesis

increase insulin sensitivity

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18
Q

side effects metformin

A

GI
dec B12 absorption
CI in those with hepatic or renal insufficiency

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19
Q

what are the sulfonylurea drug names

A

glyburide glimepriride, glipizide

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20
Q

how do sulfonlyureas work

A

stimulate insulin release from beta cells, reduce serum glucagon, increase binding insulin to tissue R

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21
Q

adverse effects of sulfonylureas

A

hypoglycemia. CI in those with hepatic or renal insufficiency

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22
Q

Mechanism of thiazolidinediones

A

decrease gluconeogenesis

increase insulin sensitivity

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23
Q

thiazolidinediones are CI in what patients

A

CHF

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24
Q

what are the gliptins

A

DDP-IV inhibitors that inhibit degradation of incretin. cause decreased glucagon and increased insulin
delay gastric emptying so can cause diarrhea or constipation

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25
Q

what are the gliflozins

A

SGLT-2 inhibitors that inhibit renal reabsorption of glucose, lowering BP
can cause fungal infections or recurrent UTI

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26
Q

how does acarbose work

A

alpha glucosidase inhibitor that decrease GI absorption of starch
cause flatulance

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27
Q

what drugs stimulate insulin release

A

meglitinides
can cause hypoglycemia
and sulfonylureas

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28
Q

what drug promotes satiety in DM

A

pramlintide, delays gastric emptying

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29
Q

labs in DKA

A 
high glucose like 300-800, decreased Na
normal or inc K (total body K decreased) so pseudohyperkalemia
dec phosphate
high anion gap acidosis
serum and urine ketones
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30
Q

Tx DKA

A

IV saline, insulin, KCl

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31
Q

labs in hyperosmolar hyperglycemic state

A

glucose >800 and commonly above 1000

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32
Q

what are signs of DM retinopathy

A

AV nicking, hemorrhages, edema and infarcts

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33
Q

type of nephropathy in DM

A

glomerulosclerosis, mesangial expansion and BM degeneration

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34
Q

signs of DM nephropathy

A

proteinuria, renal insufficiency later turns into nephrotic

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35
Q

labs in DM nephropathy

A

hypoalbuminemia, increased Cr, increased BUN, UA showing proteinuria and microalbuminuria, EM show thickening and kimmelstiel wilson nodules

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36
Q

Autonomic neuropathy in DM

A

postural hypotension, impotence and incontenence and gastroparesis

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37
Q

why are DM at highger risk silent MI

A

altered pain sensation from neuropathy

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38
Q

greatest cause of death in DM patients

A

cardiac

macrovascular disease

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39
Q

signs of hypoglycemia

A

fainting, weakness, diaphoresis, palpitations (from epinephrine release)
headache, confusion, mental changes, decreased consciousness

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40
Q

causes of hypoglycemia

A 
reactive- post eating
iatrogenic (too much insulin)
insulinoma (beta islet cell tumor)
fasting (under production glucose)
alcohol induced
pituitary/adrenal insufficiency- decreased cortisol leads to insuffiecient hepatic gluconeogenesis
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41
Q

what stiulates and inhibits TRH

A

cold stimulates

stress inhibits

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42
Q

TSH comes from where

A

ant pituitary

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43
Q

which thyroid hormone is more potent

A

T3

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44
Q

what increase TBG levels

A

pregnancy and OCP

free T4 stays same

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45
Q

what decrease TBG levels

A

nephrotic syndrome and androgen use

normal free T4

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46
Q

signs of thyroid storm

A

severe diaphoresis, vomiting, diarrhea, tachy, fever and mental changes

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47
Q

what happens in graves

A

autoimmune TSI Ab bind to TSH R and stimulate hormone production

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48
Q

what is toxic multinodular goiter or toxic adenoma

A

single or multiple
produce excess thyroid hormones
increased uptake at nodules on scan

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49
Q

What is subacute thyroiditis

A 
de quervain
enlarged thyroid maybe from virus
painful goiter
neck pain, fever, increased ESR
decreased uptake!!!!
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50
Q

Tx subacute thyroiditis

A

NSAIDs, beta blockers

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51
Q

silent thyroiditis

A 
temporary may follow pregnancy
low uptake on scan
Bx will show inflammation
beta blockers for sx.
self limited
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52
Q

factitious hyperthyroid

A

taking hormones for thyroid

53
Q

how does IV sodium iodine help hyperthyroid

A

block thyroid hormone release

54
Q

how does hydrocortisone help hyperthyroid

A

inhibits conversion T4 to T3

55
Q

Hashimoto

A

Autoimmune antithyroid peroxidase anti-TPO and antithyroglobulin Ab
also have lymphocytic infiltrates

56
Q

thyroid scan of hashimoto

A

decreased uptake “cold”

57
Q

chronic use of what can cause hypothyroidism

A

chronic lithium and chronic iodide

58
Q

which type thyroid nodules have higher risk malignancy

A

cold nodule and solid on US

59
Q

signs of thyroid carcinoma

A

nontender mass in neck. dysphagia hoarseness and maybe lymphadenopathy

60
Q

Tx thyroid carcinoma

A

surgery, radioablation and postop replacement of hormones
malignant need resection and radioiodine ablation
chemo for mets

61
Q

decreased TSH and hypothyroid

A

pituitary or hypothalamic

62
Q

complications thyroid surgery

A

hypoCa from loss PTH

hoarseness from recurrent laryngeal nerve

63
Q

most common thyroid carcinoma

A

papillary
has follicular variant
follicular has worse prognosis

64
Q

which thyroid CA produces calcitonin

A

medullary in parafollicular cells

!! MEN 2A and 2B

65
Q

most aggressive thyroid CA

A

anaplastic

66
Q

PTH is screted in response to what and what does it do

A 
low Ca
reabsorb bone and increase Ca
induce kidneys to conver Vit D
decrease phosphate reabsorption (lose phosphate)
increase Ca reabsorption
67
Q

active Vit D does what

A

increase intestinal reabsorption Ca

68
Q

calcitonin does what

A

inhibits bone reabsorption

69
Q

hypercalcemia

A

bones stones abdominal groans and psychiatric overtones

70
Q

labs in primary hyper PTH

A

increase Ca, decreased phosphate, increased urine Ca, increased PTH

71
Q

decreased Ca. but high PTH

A

hyperparathyroidism secondary to malnutrition, malabsorption, renal disease or Ca wasting drugs

72
Q

Tx hypercalcemia

A

IV fluids and bisphosphonates

73
Q

most common cause hypoPTH

A

surgery

74
Q

signs hypoPTH

A

hypo Ca
tingling in lips and fingers, dry skin, weakness, abdominal pain, tetany, dyspnea, tachycardia, seizures, movement disorders, cataracts, dental hypoplasia, Trousseau sign, Chvostek sign
increased phosphate, decreased PTH

75
Q

Tx hypoPTH

A

Ca and Vit D

76
Q

pseudohypo PTH

A

tissue does not respond to elevated PTH

Albright hereditary osteodystrophy

77
Q

Sx of pseudohypo PTH

A

hypoCa symptoms, short stature, seizure, poor mental development

78
Q

labs in pseudohypo PTH

A

decreased Ca, increased phosphate and increased PTH!!

79
Q

Tx pseudohypo PTH

A

Ca and Vit D

80
Q

ant pituitary secretes

A

ACTH, TSH, GH, FSH and LH

81
Q

post pituitary secretes

A

ADH and oxytocin

82
Q

what drugs can cause hyperprolactinemia

A

phenthizines, risperidone, haloperidol, methyldopa, verapamil

83
Q

Tx prolactinoma

A

dopamine agonists like cabergoline and bromocriptine and pergolide

84
Q

most common pituitary tumor

A

prolactinoma

85
Q

acromegaly

A

excess secretion GH from anterior pituitary

86
Q

effect of glucose on GH

A

should decrease it

87
Q

Tx for acromegaly

A

surgical resection adenoma, dopamine agonists or octreotide to lessen effects

88
Q

complications acromegaly

A

cardiac failure, DM, spinal cord compression, vision loss

89
Q

child with advanced growth

A

check GH for gigantism

90
Q

why do those with acromegaly have higher risk DM

A

also have increased insulin R

91
Q

decreased LH FSH causes what

A

no estrogen
no testosterone in men impotence and testicular atrophy
decreased libido, infertility, decreased pubic hair, amenorrhea and genital atrophy in women

92
Q

how to check for hypopituitary

A

no menstruation after medroxyprogesterone
no GH after give insulin
dec TSH
dec prolactin
cortisol does not increase after insulin from no ACTH

93
Q

Sx low ACTH MSH

A

adrenal insufficiency causing fatigue, weight loss, dec appetite, poor response to stress, decreased skin pigment!!!!

94
Q

how to determine cause of cortisol excess

A

low DXM test
low cortisol is usually found
if there is no decrease in cortisol then cushings
high dose DXM test– determine cause of cortisol excess

95
Q

what causes cushings

A

excess corticosteroid- most common
pituitary adenoma
paraneoplastic from ACTH production
adrenal tumor

96
Q

signs cushing

A

weakness, depression, menstural irregularities, polydipsia, polyuria, increased libido, impotence, HTN, acne, increased hair growth, central obesity - buffalo hump and moon facies
purple striae on abdomen and cataracts

97
Q

labs in cushings

A

hyperglycemia, glycosuria and decreased K

98
Q

complications cushings

A

increased risk CV or DVTs
increased infection
increased avascular necrosis of hip
hypopituitarism or adrenal insufficiency post surgery

99
Q

conn syndrome

A

primary hyperaldosteronism from adenoma

100
Q

secondary hyperaldosteronism

A

activation RAAS from perceived LBP from kidneys (renal a stenosis, heart failure cirrhosis, nephrotic syndrome)

101
Q

signs of hyperaldosteronism

A

HA, weakness, paresthesias, recalcitrant HTN, tetany

102
Q

labs hyperaldosteronism

A 
DECREASED K
metabolic alkalosis
increased Na
decreased renin in conns
increased 24 urine aldosterone
high ratio plasma aldosterone to plasma renin
103
Q

Addison

A

primary adrenal insufficiency

autoimmune destruction adrenal cortices

104
Q

secondary corticoadrenal insufficiency

A

insufficient ACTH production by pituitary

105
Q

tertiary corticoadrenal insufficiency

A

deficient CRH release from hypothalamus

usually from chronic corticosteroid

106
Q

signs of adrenal insufficiency

A

weakness, fatigue, anorexia, weight loss, nausea and vomiting
myalgia arthralgias
decreased libido, memory impairment and depression
hypotension
increased skin pigmentation!!!(only addison)

107
Q

labs adrenal insufficiency

A

decreased Na
increased K from low aldosterone
decreased cortisol
increased ACTH if addisons

108
Q

ACTH in secondary and tertiary adrenal insufficiency

A

decreased

109
Q

give ACTH and if cortisol increases

A

secondary or tertiary insufficiency

110
Q

what is addisonian crisis

A

severe weakness, fever, mental status changes, vascular collapse

111
Q

what is congenital adrenal hyperplasia

A

defect in synthesis cortisol causing low cortisol

increased ACTH, adrenal hyperplasia and androgen excess from shunting

112
Q

17 a hydroxylase deficiency

A

get cortisol androgen and estrogen deficiency so see amenorrhea, ambiguous genitalia in men
HTN
decreased K, increased Na

113
Q

21 alpha hydroxylase deficiency

A

insufficient cortisol and aldosterone,
most common form!!!!
shifts to androgen
ambiguous genitalia in female, virilization
mactogenitosomiand precocious puberty in men
dehydration and hypotension in more severe cases

114
Q

labs in 21 alpha hydroxylase def

A

decreased Na and increase K

115
Q

what causes ambiguous genitialia in women, precocious puberty in men and HTN

A

11 beta hydroxylase deficieny from excess deoxycorticosterone

116
Q

Tx 17 a hydroxylase def

A

cortisol replacement to suppress ACTH

117
Q

Tx 21 a hydroxylase def

A

cortisol for ACTH suppresion.

fludorcortisone for mineralocorticoids

118
Q

Tx 11 b hydroxylase def

A

cortisol replacement and anti-HTN

119
Q

mutation in RET

A

most MEN 2A 2B

120
Q

Tx pheo

A

alpha and beta blockers before and durign surgical resection

give alpha before beta!!!!!!!!!!!! to avoid HTN crisis

121
Q

MEN1

A

Parathyroid hyperplasia
Pituitary
Pancreas

possible zollinger ellison

122
Q

Men2A

A

Medullary thyroid hyperplasia
Parathyroid hyperplasia
Pheo

123
Q

MEN2B

A

Medullary thyroid
Mucosal neuroma
Pheo

can have marfinoid body habitus

124
Q

Cretinism

A

congenital hypothyroid froms evere iodide deficiency or hereditary

125
Q

signs cretinism

A

poor feeding, lethargy, large fontanelles, thick tongue, constipation, umbilical hernia, poor growth, hypotonicity, dry skin, hypothermia and jaundice

126
Q

labs in cretinism

A

decreased T4 increased TSH

127
Q

Tx cretinism

A

levothyroxine shortly after birth

128
Q

prolonged jaundice

A

first sign cretinism

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