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Pharm Unit 4 - Endo > Pharmacology Unit 4 - Endocrine Pt. 2 > Flashcards

Pharmacology Unit 4 - Endocrine Pt. 2 Flashcards

1
Q

more than ____________ of glucocorticoid therapy can cause adrenal suppression

A

2 weeks

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2
Q

stress dose steroids with minor stress give _______x the dose for ____________ hours

A

2; 23-48

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3
Q

stress dose steroids with severe stress (accidental trauma, major surgery), give up to ________x the normal dose for _____________ hours

A

10; 48-72

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4
Q

if a patient receives stress dose steroids, it takes ____________ months for HPA function to return to normal and an additional ____________ months for cortisol levels to return to normal

A

2-12; 6-9

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5
Q

corticosteroids increase pepsin and gastrin which puts patients at risk for _______________

A

peptic ulcers

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6
Q

how do you treat chronic adrenocortical insufficiency (addisons disease)

A

hydrocortisone and fludrocortisone

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7
Q

how do you treat acute adrenocortical insufficiency (addisons)

A
  1. high dose glucocorticoid therapy IV (100 mg Q8h until stable)
  2. correct fluid and electrolytes
  3. taper glucocorticoid (hydrocortisone) therapy and initiate mineralcorticoid (fludrocortisone) when stable
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8
Q

describe the synthesis of thyroid hormone

A
  1. symporter pulls iodide from the gut and diet into thyroid gland
  2. in the follicular cell iodide is converted to iodine via thyroidal peroxidase (organification)
  3. thyroglobulin is cleaved into T3/T4
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9
Q

how is iodide converted into iodine in the thyroid gland?

A

via thyroidal peroxidase (organification)

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10
Q

which thyroid hormone is the most potent

A

which thyroid hormone is the most potent

T3

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11
Q

T3 is ___________ x more potent/active than T4

A

2-3

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12
Q

for T4 to be utilized it has to be _______________ by ______________ enzymes to T3

A

deiodinated; 5’ deiodinase (D1,D2,D3)

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13
Q

what is the primary pathway for the metabolism of thyroxine (T4)

A

deiodination

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14
Q

what drugs block the metabolism of T4 by blocking the three 5’deiodinase enzymes ?

A
  1. amiodarone
  2. contrast dye
  3. beta blockers
  4. corticosteroids
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15
Q

_____________ and _______________ are physiologic conditions that block the three 5’ deiodinase enzymes responsible for the metabolism of T4 to t3

A

severe illness; starvation

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16
Q

out of T3 and T4, which is most released from the thyroid gland

A

T4

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17
Q

ratio of release T4:T3

A

5:1

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18
Q

_________% of circulating T3 is d/t the metabolism of T4, and ___________% is from the direct thyroid secretion

A

80; 20

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19
Q

__________ is the inactive form of thyroid hormone, and _______ is the active form

A

T4; T3

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20
Q

large doses of iodine inhibit ___________________, which leads to a(n) ___________ in thyroid hormone levels

A

organification; reduction

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21
Q

_______________ influences the synthesis of T3 and T4

A

iodide levels

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22
Q

what conditions have a stimulatory effect on the hypothalamus to release TRH

A
  1. cold (hypotherm)
  2. acute psychosis
  3. circadian and pulsatile rhythm
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23
Q

what inhibits the release of TRH from the hypothalamus

A
  1. increased T3/T4
  2. severe stress
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24
Q

what inhibits the release of TSH from the AP

A
  1. somatostatin
  2. dopamine
  3. corticosteroids
  4. increased T3/T4
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25
Q

what stimulates the release of TSH from the AP

A

TRH

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26
Q

how bioavailable is T4 (thyroxine) in the body?

A

70-80% bioavailable

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27
Q

how bioavailable is T3 in the body?

A

95%

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28
Q

T4 is best absorbed where?

A

ileum and duodenum

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29
Q

what route is preferred for the administration of exogenous T3 and T4 ?

A

IV

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30
Q

____________ function is impacted by multiple drugs

A

thyroid function

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31
Q

Thyroid hormones are important for __________, _______________, _____________, and ___________________

A

optimal growth; development; function; all body tissue maintenance

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32
Q

_______________ hormones are integral to homeostasis

A

thyroid

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33
Q

exogenous T3 has implications in the tx of ________________, but not _____________

A

myxedema coma; thyroid storm

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34
Q

T/F: giving T4 will also supply T3

A

true; due to the T4 conversion to T3

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35
Q

what are the 3 types of anti-thyroid drugs?

A
  1. thioamides
  2. iodides
  3. radioactive iodine
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36
Q

in the thioamide drugs, the ______________ group in their chemical structure is essential for antithyroid activity

A

thiocarbamide

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37
Q

what are your thioamide antithyroid agents ?

A
  1. PTU
  2. Methimazole
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38
Q

which antithyroid drug would you use in pregnant women in their first trimester?

A

PTU

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39
Q

when is PTU the appropriate anti-thyroid med to administer?

A
  1. 1st trimester
  2. thyroid storm
  3. adverse reaction to methimazole
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40
Q

what is the black box warning for PTU

A

severe hepatitis

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41
Q

_____________________ is 10x more potent than PTU

A

methimazole

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42
Q

what is the thioamide drug of choice in children and adults?

A

methimazole

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43
Q

if a pregnant woman needs an anti-thyroid agent, which medication would you use in the 2nd and 3rd trimesters?

A

methimazole

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44
Q

absorption of PTU = _____________ bioavail

A

50-80%

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45
Q

absorption of methimazole

A

completely absorbed

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46
Q

both thioamide drugs are excreted in the ____________; however, ______________ is excreted slower

A

kidney; methimazole

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47
Q

half life of PTU

A

1.5 hours

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48
Q

half life of methimazole

A

6 hours

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49
Q

100 mg dose of PTU will inhibit _____________ by 60% for 7 hours; should be administered q _____-____h

A

organification; 6-8

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50
Q

30 mg dose of methimazole exerts ________________ effects for > 24 hours

A

anti-thyroid

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51
Q

thioamides MOA

A
  1. prevents hormone synthesis by inhibiting thyroid peroxidase catalyzed reactions
  2. blocks iodine organification
  3. blocks the coupling of iodotyrosines
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52
Q

additional MOA of PTU from methimazole

A

inhibits the diodination of T4 and T3

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53
Q

Thoamide toxicity sx

A
  1. maculopapular pruiritic rash
  2. severe fatal hepatitis
  3. agranulocytosis (granulocyte count < 500)
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54
Q

what is the most dangerous complication of thioamides

A

agranulocytosis

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55
Q

what is the most common adverse effect of thioamides

A

maculopapular pruritic rash

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56
Q

T/F: if patient has a severe adverse reaction to PTU you should switch them to methimazole

A

false; cross sensitivity is 50% btwn PTU and methimazole; therefore do not switch drugs in patients with severe reactions

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57
Q

PTU should be avoided in ______________

A

children

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58
Q

___________ is the only isotope used for tx of thyrotoxicosis

A

131 I (radioactive iodine)

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59
Q

MOA of radioactive iodine

A

rapidly accumulates in the thyroid and emits beta rays to destroy the thyroid parenchyma

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60
Q

T/F: radioactive iodine in the tx of hyperthyroidism is very painful

A

false; not painful

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61
Q

how is radioactive iodine administered?

A

orally

62
Q

what is the most widely used B-Blocker for thyrotoxicosis

A

propranolol

63
Q

what is the purpose of using adrenoceptor blocking agents in the tx of hyperthyroidic states?

A

tx the hypermetabolic sx (HR, BP, etc)

64
Q

what is the most common cause of hypothyroidism in the US

A

hashimotos thyroiditis

65
Q

pathogenesis of hashimotos thyroiditis

A

autoimmune destruction of thyroid

66
Q

with hashimotos thyroiditis, the goiter is ____________ early and ________ later

A

present; absent

67
Q

degree of hypothyroidism with hashimotos thyroiditis

A

mild to severe

68
Q

which hypothyroidism causes will have the presence of a goiter?

A
  1. early hashimotos
  2. drug induced hypothyroidism
  3. dyshormogogenesis
  4. congenital (cretinism)
69
Q

which causes of hypothyroidism will a goiter not be present?

A
  1. late hashimotos
  2. radiation
  3. congential (cretinism)
  4. secondary (TSH deficit)
70
Q

s/sx of hypothyroidism

A
  1. pale cool skin
  2. periorbital edema, drooping eyelids
  3. decreased HR
  4. lethargy
  5. decreased BMR
  6. Stiffness and muscle fatigue, decreased DTR
71
Q

s/sx of hyperthyroidism

A
  1. warm, moist skin
  2. periorbital edema
  3. increased HR
  4. dyspnea
  5. increased appetite w/ wt loss
  6. nervousness
  7. increased BMR
72
Q

what is the pharmacologic tx for hypothyroidism

A

levothyroxine

73
Q

what foods should be avoided with levothyroxine d/t it impairing absorption

A

grapefruit

74
Q

s/sx of thyroxine toxicity in children (2ndary to levothyroxine tx or hyperthyroidism)

A
  1. restless
  2. insomnia
  3. accelerated bone maturation and growth
75
Q

s/sx of thyroxine toxicity in adults (2ndary to levothyroxine tx or hyperthyroidism)

A
  1. nervousness
  2. heat intolerance
  3. episodes of palpitations and tachycardia
  4. unexplained weight loss
76
Q

the _______________ is very sensitive to circulating levels of thyroxine and can lead to __________, __________

A

heart; a.fib; dysrhythmias

77
Q

if a patient on levothyroxine develops dysrhythmias or angina, how should you proceed?

A

stope or reduce levothyroxine immediately

78
Q

T/F: in myxedema coma, the low levels of circulating thyroid hormone is cardio protective against increased demands that could lead to angina or MI

A

true

79
Q

________________ is a medical emergency and is d/t untreated hypothyroidism

A

myxedema coma

80
Q

tx of myxedema coma

A
  1. loading dose of levothyroxine (300-400 mcg IV)
  2. followed by 50-100 mcg daily
  3. IV T3 can also be added
81
Q

what is the most common cause of hyperthyroidism

A

graves disease

82
Q

what is the tx of choice for graves disease

A

thyroidectomy

83
Q

what is the pathogenesis of graves dz?

A

lymphocytes secrete TSI which stimulates the TSH receptor with longer duration of stimulation, causing thyroid hormone excess

84
Q

which Dz would present with a + TSI on labs?

A

graves disease

85
Q

what is the tx of choice for Graves Dz in those over 21 years of age

A

radioactive iodine 131

86
Q

Tx for graves disease

A
  1. antithyroid drug therapy (methimazole, PTU)
  2. thyroidectomy (1st line)
  3. radioactive iodine
  4. adjunct therapy: propranolol or metoprolol
87
Q

the pancreas consists of approximately _________________ islets of langerhan

A

1 million

88
Q

within the islets of langerhan, there are at least _____________ hormone producing cells are present

A

5

89
Q

what cells secrete insulin in the pancreas

A

beta

90
Q

what are the pancreatic hormones?

A
  1. insulin
  2. islet amyloid polypeptide
  3. glucagon
  4. somatostatin
  5. pancreatic peptide
  6. Ghrelin
91
Q

what pancreatic hormone is the storage and anabolic hormone of the body

A

insulin

92
Q

what is the pancreatic hormone that is the hyperglycemic factor that moblizes glycogen stores

A

glucagon

93
Q

which pancreatic hormone is the universal inhibitor of secretory cells

A

somatostatin

94
Q

which pancreatic hormone is a small protein that facilitates digestive processes

A

pancreatic peptide

95
Q

what is the pancreatic hormone which increases GH release

A

Ghrelin

96
Q

which pancreatic hormone modulates appetite, gatric empyting, glucagon, and insulin secretion

A

islet amyloid polypeptide (IAPP, amylin)

97
Q

how do you confirm a dx of DM?

A

plasma glucose level > 126 more than once after at least 8 hours of fasting

98
Q

what is the first line tx for DM II?

A

diet

99
Q

which type of diabetes is usually seen with obesity

A

T2DM

100
Q

insulin dependent diabetes that is d/t selective beta cell destruction and severe or absolute insulin deficiency

A

T1DM

101
Q

insulin dependent diabetes that is d/t selective beta cell destruction and severe or absolute insulin deficiency

A

T1DM

102
Q

which type of DM is immune or idiopathic

A

T1DM

103
Q

which type of DM is is due to pancreatectomy, pancreatitis, nonpancreatic dz, corticosteroid therapy?

A

T3DM

104
Q

which type of DM is d/t placental hormones/placenta creating an insulin resistance

A

T4DM

105
Q

when does T4DM (gestational DM) typically occur

A

3rd trimester

106
Q

which DM type is d/t tissue resistance to insulin action, combined with relative deficiency in insulin secretion

A

T2DM

107
Q

the release of insulin requires the utilization of ____________

A

ATP

108
Q

insulin in the cell –> increases _____________ use –> decrease in _________ efflux –> depolarization –> _______ influx –> opens the gate for insulin to be released via exocytosis

A

ATP; K; Ca

109
Q

insulin is released from the pancreatic ____________ cells at a _____________ rate

A

beta; low basal

110
Q

what causes increase in insulin release

A
  1. increased glucose
  2. B-SNS activity
  3. high concentration of fatty acids
  4. certain hormones (glucocorticoids, growth hormone)
  5. glucagon increase
  6. cholecystokinin
111
Q

what are the causes of a decrease in insulin release?

A
  1. increased insulin
  2. leptin
  3. amalyn
  4. somatostatin
  5. alpha-SNS activity
  6. Chronic increase in glucose
  7. low concentration of fatty acids
112
Q

insulin promotes the storage of __________ & ______________

A

fat; glucose

113
Q

glucocorticoids _____________ the affinity of the insulin receptor for insulin

A

decrease

114
Q

which tissues have the highest expression of insulin receptors ?

A
  1. skM
  2. fat
  3. liver

*those that are most sensitive to glucose

115
Q

insulin is primarily metabolized in the __________, but 35-40% excreted in the ______________

A

liver; kidney

116
Q

what are the 4 principal types of insulin preparations

A
  1. rapid acting
  2. short acting
  3. intermediate acting
  4. long-acting
117
Q

with the administration of insulin, you are aiming for a serum glucose level of ________________

A

80 mg/dL

118
Q

which type of insulin preparation permits more physiologic prandial insulin replacement

A

rapid acting

119
Q

_____________ insulin has a fast onset and short duration of <4-5 hours

A

rapid-acting

120
Q

short acting insulin onset: __________, peaks at ____________; and DOA: ___________

A

30 min; 2-3 hours; 5-8 hours

121
Q

intermediate acting insulin has an onset of ____________; and a DOA of ____________

A

2-5 h; 4-12 h

122
Q

long acting insulin has an onset of ___________; and a DOA of ____________

A

1-2 h; 11-24 h

123
Q

________________ is a long acting insulin with a smooth background insulin level with BID dosing

A

detemir

124
Q

duration of action of insulin detemir

A

12 hrs

125
Q

for surgery, we only tx if BG is > ____________

A

200

126
Q

what complication of DM typically occurs with T1DM?

A

DKA

127
Q

which complication of DM typically occurs with T2DM

A

HHS

128
Q

what is the starting dose tx of insulin for DKA

A

regular insulin @ 0.1 IU/kg/h IV

129
Q

this complication of DM has profound hyperglycemia and dehydration and seen especially in the elderly

A

HHS

130
Q

what is the tx for HHS

A

low dose insulin therapy with fluid resuscitation

131
Q

__________________ insulin is a fast-acting preparation and is preferred in tx the abrupt onset of hyperglycemia or the appearance of DKA

A

regular

132
Q

what is the dose of insulin that should be given to tx metabolic derangements of blood glucose

A

1-5 U IV or 0.5-2 U/h IV infusion

133
Q

what is the most popular route of administration for insulin

A

SubQ

134
Q

regular insulin can be administered ______ or ________

A

IV or SQ

135
Q

what is the most common complication of insulin therapy

A

hypoglycemia

136
Q

sulfonylureas bind to a sulfonylurea receptor and stimulate _____________________

A

insulin secretion

137
Q

MOA of sulfonylureas

A
  1. binds to sulfonylurea receptor –> inhibits efflux of K
  2. depolarization of the cell
  3. voltage gate Ca channel opens –> Ca influx
  4. insulin released
138
Q

what are your first generation sulfonylureas

A

“-amide”

  1. Tobutamide
  2. chlorpropamide
  3. tolazamide
139
Q

which oral anti-diabetic agent is the safest for elderly diabetics

A

tobutamide

140
Q

what are your 2nd generation sulfonylureas

A

“-ide”

  1. glyburide
  2. glimepiride
  3. glipizide
141
Q

1st and 2nd generation sulfonylurea’s are metabolized where?

A

liver

142
Q

which generation of sulfonylureas are prescribed more frequently due to the decrease in adverse effects and drug interactions

A

2nd generation (“-ide”)

143
Q

biggest risk 2ndary to taking sulfonylureas

A

hypoglycemia

144
Q

what drug is a sulfonylurea, but has no sulfur and is referred to as a meglitinide analog?

A

repaglinidine

145
Q

repaglinidine is hepatically cleared via ______________

A

CYP3A4

146
Q

meglitinide analogs, like repaglinidine must be taken when?

A

just before eating

147
Q

an antidiabetic agent like a meglitinide analog, such as repaglinidine may be considered for those with a ____________ allergy

A

sulfur

148
Q

sulfonylurea drug that is a D-phenylalanine derivative

A

nateglinide

149
Q

which sulfonylurea drugs are okay for elderly with renal issues

A
  1. repaglinidine
  2. nateglinide
150
Q

nateglinide is a sulfonylurea that is a D-phenylalanine derivative, it is hepatically cleared via ___________ & ____________

A

CYP2C9 ; CYP3A4

Pharm Unit 4 - Endo (4 decks)

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