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Pharm Unit 4 - Endo > Pharmacology Unit 4 - Endocrine Pt. 3 > Flashcards

Pharmacology Unit 4 - Endocrine Pt. 3 Flashcards

1
Q

which sulfonylurea has the lowest incidence of hypoglycemia?

A

nateglinide (D-phenylalanine derivative)

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2
Q

what pharmacologic agent is the first line therapy for DM II

A

metformin

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3
Q

black box warning of metformin

A

lactic acidosis

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4
Q

due to the black box warning with metformin, it is c/i in who?

A
  1. any renal dz
  2. etoh-ism
  3. hepatic disease
  4. any condition that predisposes to tissue anoxia
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5
Q

which anti-diabetic agent is described as a “euglycemic agent” due to less fasting, and less postprandial hyperglycemia, and hypoglycemia?

A

metformin

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6
Q

MOA of biguanides (metformin)

A

reduces hepatic glucose production through the activation of AMP-activated protein kinase

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7
Q

_____________ is an antidiabetic agent that is excreted by the kidneys as the active compound

A

meformin

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8
Q

1/2 life of metformin

A

1.5-3 hours

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9
Q

toxicity of metformin

A
  1. lactic acidosis
  2. vitamin B12 deficiency
  3. GI: anorexia, N/V/D, abdominal pain
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10
Q

if a patient presents for contrast study on metformin, the drug should be stopped ________ days prior

A

2-3

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11
Q

which antidiabetic agents are thiazolidinediones

A

“-glitazone”

  1. rosiglitazone (Avandia)
  2. Piogllitazone (Actos)
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12
Q

toxicity of thiazolidinediones

A
  1. fluid retention
  2. edema
  3. weight gain
  4. anemia
  5. bone fractures in women
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13
Q

c/i of thiazolidinediones

A
  1. CHF
  2. hepatic disease
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14
Q

what is the biggest contraindication with Rosiglitazone (avandia)?

A

heart disease, d/t it worsening the condition

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15
Q

Thiazolidinediones MOA

A
  1. regulates gene expression by binding to PPAR-Y
  2. reduces insulin resistance in T2DM
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16
Q

Thiazolidinediones are long acting oral antidiabetic agents. Effects last > __________ hours

A

24

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17
Q

which meds are alpha glucosidase inhibitors

A

Acarbose and Miglitol

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18
Q

which type of oral antidm agents reduce the post meal excursion by delaying the digestion and absorption of starch and disaccharides?

A

alpha glucosidase inhibitors (Acarbose & miglitol)

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19
Q

why must hypoglycemia secondary to alpha-glucosidase inhibitors have to be treated with glucose?

A

bc the metabolism of sucrose might be blocked

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20
Q

which oral anti-dm agent is a bile acid sequestrant?

A

colesevelam HCL

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21
Q

what is the MOA of bile-acid sequestrants (colesevelam hcl) in the tx of dm?

A

unknown

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22
Q

bile acid sequestrants like colesevelam hcl are approved as a _______________ antihyperglycemic therapy

A

DMII

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23
Q

pharmacological effect of glucagon

A

increases cAMP –> catabolism of stored glycogen, increases gluconeogenesis, and ketogenesis

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24
Q

glucagon has potent ____________ and ____________ effects on the heart

A

inotropic; chronotropic

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25
Q

what are the clinical uses of glucagon

A
  1. hypoglycemia
  2. dx of endocrine d/o
  3. B-blocker OD
  4. radiological procedure of the bowel
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26
Q

why is glucagon used in radiological procedures of the bowel

A

it relaxes the intestines.

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27
Q

what are the 3 primary hormones for Ca and Phos homeostasis

A
  1. Fibroblast Growth Factor 23 (FGF23)
  2. PTH
  3. Vitamin D
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28
Q

which hormone for Ca and Phos homeostasis is considered a “prohormone,” meaning it requires further metabolism to gain biologic activity

A

Vitamin D

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29
Q

Net effect of PTH on serum levels

A

increased calcium, decreased phos

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30
Q

net effect of FGF23 of serum levels

A

decreased phos

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31
Q

net effect of Vitamin D on serum levels

A

increased Calcium and Phos

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32
Q

________________ and ____________ regulate bone formation and resorption, BOTH are capable of stimulating both processes

A

PTH; vitamin D

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33
Q

osteoblasts = ___________________

A

bone forming cells

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34
Q

Vitamin D is produced in the ______________ when stimulated by __________

A

kidney; PTH

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35
Q

what inhibits the production of Vitamin D

A

FGF 23

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36
Q

Vitamin D inhibits the production of ______________ and stimulates the release of _________________

A

PTH; FGF23

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37
Q

____________________ is the principal regulator of intestinal Ca nd P absorption

A

Vitamin D

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38
Q

what are 2 of the most important minerals for general cellular function?

A

Ca and Phos

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39
Q

Ca and P enter the body from the ________________

A

intestine

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40
Q

Ca and P are excreted via _______________, which balances the intestinal absorption

A

kidneys

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41
Q

Actions of Calcitonin

A
  1. lowers serum Ca and P through bone and kidney action
  2. inhibits osteoclastic bone resorption
  3. reduces Ca and P reabsorption in the kidney
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42
Q

Calcitonin is used the tx of

A
  1. pagets Dz
  2. hypercalcemia
  3. osteoporosis
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43
Q

Glucocorticoid effect on Calcium levels

A
  1. antagonizes Vitamin D stimulated intestinal calcium transport
  2. stimulates calcium excretion in the kidneys
  3. blocks bone formation
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44
Q

_______________ prevents accelerated bone loss during the post menopausal period

A

estrogen

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45
Q

what are your non-hormonal agents that affect bone mineral homeostasis

A
  1. Bisphonates
  2. RANK lingand inhibitors
  3. Calcium receptor agonists
  4. Thiazide diuretics
  5. Plicamycin
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46
Q

bisphonate drugs end in ?

A

”- dronates”

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47
Q

MOA of bisphonates

A
  1. inhibit bone resorption (decreases serum calcium which stimulates PTH –> increased serum calcium and decreased phos)
  2. inhibits secondary bone formation
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48
Q

what type of drug is Denosumab

A

a RANK-L inhibitor

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49
Q

MOA of Denosumab

A

interferes with RANK-L fx –> inhibition of osteoclast formation and activity

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50
Q

Cinacacet is what type of drug

A

calcium receptor agonist

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51
Q

what is the MOA of Cincalcet

A

activates Ca receptors of the PTH gland which inhibits the release of PTH

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52
Q

Cinacalcet is approved for the treatment of ?

A
  1. secondary hyperparathyroidism
  2. secondary CKD
  3. parathyroid carcinoma
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53
Q

how do thiazide diuretics affect calcium homeostasis

A

increases the reabsorption of Calcium, thus increasing serum calcium levels

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54
Q

Plicamycin is a ____________________, which is (rarely) used in the tx of _____________ & ________________

A

cytotoxic Abx; pagets dz; hypercalcemia

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55
Q

major causes of hypercalcemia

A
  1. hyperparathyroidism
  2. Cancer with or without bone mets
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56
Q

___________________ can lead to CNS depression, which can lead to coma without treatement

A

hypercalcemia

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57
Q

Tx of hypercalcemia

A
  1. 500-1L/h saline + lasix
  2. bisphonates
  3. calcitonin
  4. gallium nitrate
  5. plicamycin
  6. IV phosphate
  7. glucocorticoids
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58
Q

what is the fastest and surest way to reduce serum calcium levels?

A

IV phosphate

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59
Q

if IV phosphate is administered too fast, what can happen?

A

deplete calcium –> arrhythmias and cardiac arrest

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60
Q

__________________ IV will lower serum calcium substantially within 24-48 hours; however, it is not the drug of choice because of toxicity

A

plicamycin

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61
Q

s/sx of hypocalcemia

A
  1. tetany
  2. parasthesias
  3. muscle cramps
  4. seizures
  5. LARYNGOSPASM
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62
Q

causes of hypocalcemia

A
  1. hypoparathyroidism
  2. Vitamin D deficiency
  3. CKD
  4. malabsorption
63
Q

Tx of hypocalcemia

A
  1. Calcium (IV, IM, PO)
  2. Vitamin D (calcitrol)
64
Q

_________________ takes 24-48 hours to increase serum calcium levels

A

Vitamin D (Calcitrol)

65
Q

________________ delivers 3x more elemental calcium than _____________

A

CaCl; Ca-gluconate

66
Q

what is the benefit of Calcium gluconate in the tx of hypocalcemia

A

less irritating to veins

67
Q

_________________ is a common complication of renal failure

A

hyperphosphatemia

68
Q

tx of hyperphosphatemia

A
  1. dietary restrictions
  2. phosphate binders: sevelamer
  3. calcium supplements
69
Q

causes of hypophosphatemia

A
  1. primary hyperparathyroidisim (increased PTH = dec P)
  2. vitamin D deficiency (dec Vit D = dec P)
  3. idiopathic hypercalciuria
  4. increased FGF23 (inc FGF23 = dec P)
  5. renal phosphate wasting (Fanconi’s syndrome)
  6. over use of phosphate binder
  7. TPN with inadequate phosphate content
70
Q

conditions that cause increase in FGF23 –> decreased phos

A
  1. rickets
  2. tumor induced osteomalacia
71
Q

acute hypophosphatemia can decrease ________________, which decreases _________________, causing a ________________ shift in the oxyhgb dissociation curve –> ______________

A

ATP; 2,3 DPG, left; rhabdomyolysis

72
Q

what is the primary tx of symptomatic primary hyperparathyroidism with hypercalcemia?

A

surgical tx

73
Q

CKD will cause retention of _________ and excretion of ______________

A

phosphorus; ionized calcium

74
Q

tx of secondary hyperparathyroidism of CKD

A

calcitrol analogs (doxercalciferol and paricacitol)

75
Q

s/sx of chronic adrenocortical insufficiency (addisons dz)

A
  1. weakness
  2. fatigue
  3. wt loss
  4. hypotn
  5. hyperpigmentation
  6. inability to maintain blood glucose during fasting
76
Q

congenital adrenal hyperplasia is a defect in the synthesis of __________

A

cortisol

77
Q

in congenital adrenal hyperplasia there will be a __________ cortisol level that is equal to a ____________ in ACTH levels

A

decrease; increase

78
Q

if you know a fetus has congenital adrenal hyperplasia, ______________ can be given to the mom to prevent the baby being born in acute crisis

A

decadron

79
Q

tx of congenital adrenal hyperplasia

A
  1. stress dose glucocorticoids
  2. stabilization doses of glucocorticoids and mineralcorticoids
80
Q

causes of cushings syndrome

A
  1. bilateral adrenal hyperplasia (ACTH secreting pituitary adenoma)
  2. chronic, excessive glucocorticoids
81
Q

tx for cushings

A
  1. surgical removal of ACTH or cortisol producing tumor
  2. irradiation of adrenal gland(s)
82
Q

with surgical tx of cushings syndrome, large doses of ______________ must be administered before and after surgery

A

cortisol (up to 300 mg of hydrocortisone)

83
Q

what is chrousos syndrome?

A

a genetic inactivating mutation of the GR gene which causes primary generalized glucocorticoid resistance

84
Q

chrousos syndrome the HPA compensates causing _________ ACTH, __________ cortisol, ___________ androgens, and ___________ mineracorticoid activity

A

increased; increased; increased; increased

85
Q

how do you tx chrousos syndreom

A

dexmethasone

86
Q

HPA compensation with increased ACTH will cause what s/sx

A
  1. htn
  2. potassium imbalance
  3. hyperandrogenism (male characteristics)
87
Q

tx for aldosteronism

A

spironolactone

88
Q

______________ is responsible for 50% production of aldosterone, and ____________ is responsible for the other 50%

A

ACTH; Angiotensin

89
Q

aldosterone has a negative feedback effect on _____________

A

ACTH

90
Q

MOA of mineralcorticoid drugs

A

bind to mineralcorticoid receptors in the cytoplasm of target cells in the DCT and CD

91
Q

aldosterone increases Na reabsorption in what cells?

A
  1. CD and DCT of kidney
  2. sweat and salivary glands
  3. GI mucosa
  4. across cell membranes
92
Q

increased aldosterone results in…

A
  1. hypokalemia
  2. metabolic alkalosis
  3. increased plasma volume
    4 HTN
93
Q

mineralcorticoids are metabolized in the _______________

A

liver

94
Q

what are your mineralcorticoid drugs? (i.e. aldo agonists)

A
  1. deoxycorticosterone (DOC)
  2. fludrocortisone
95
Q

__________________ is mineralocorticoid that is a precursor of aldosterone

A

dexoxycorticosterone

96
Q

which mineralcorticoid drug is endogenous

A

deoxycorticosterone

97
Q

which mineralcorticoid drug is exogenous

A

fludrocortisone

98
Q

which drug is used to tx adrenocortical insuffciency

A

fludrocortisone

99
Q

which mineralcorticoid agonist has a potent salt retaining activity

A

fludrocortisone

100
Q

what is aldosteronism

A

excessive production of aldosterone via adrenal adenoma causing HTN and Hypok

101
Q

what are your adrenocortical antagonist drugs

A
  1. steroid synthesis inhibitors
  2. glucocorticoid antagonists
  3. mineralcorticoid antagonists
102
Q

which drugs are your steroid synthesis inhibitors (adrenocortical antagonists)

A
  1. aminoglutethimide
  2. ketoconazole
  3. arbiraterone
103
Q

which drugs are your glucocorticoid antagonists

A

Mifepristone

104
Q

1/2 life of mifepristone

A

20 hours

105
Q

mifepristone has a high affinity for the _____________ Receptor, and has extensive binding to _______________

A

glucocorticoid; albumin

106
Q

Mifepristone is only recommended for tx of ___________________ or ____________ that have failed other tx

A

ACTH secretion; adrenal cancer

107
Q

what are your mineralcorticoid antagonists

A

spironolactone and epleronone

108
Q

which mineralcorticoid antagonist drug is more selective

A

epleronone

109
Q

which mineralcorticoid antagonist also fx as an androgen antagonists

A

spironolactone

110
Q

action of spironolactone lasts ___________ days

A

2-3

111
Q

adverse effects of estrogen therapy

A
  1. thromboemboli
  2. MI
  3. HTN
  4. HA
  5. peripheral edema
  6. nausea
112
Q

what are the steps of rational prescribing?

A
  1. make a specific diagnosis
  2. consider the pathophysiologic implications of the Dx
  3. select a specific therapeutic objective
  4. select a drug of choice
  5. determine the appropriate dosing regimen
  6. devise a plan for monitoring the drugs action
  7. determine an endpoint of therapy
  8. plan a program of patient education
113
Q

what are the 17 elements that must be included on an outpatient prescription?

A
  1. prescriber name
  2. prescriber license classification
  3. prescribers address
  4. prescribers telephone number
  5. date script is written
  6. patients name
  7. patients address
  8. name of the medication
  9. strength of the medication (metric units)
  10. quantity to be dispensed
  11. complete directions for use
  12. number of refills and expiration date of script
  13. waiver of the requirement for childproof containers
  14. additional instructions/warnings
  15. prescribers signature
  16. prescribers national provider identification number
  17. state licensce number
114
Q

which elements are required for an inpatient prescription

A
  1. date script is written
  2. name of medication
  3. strength of medication
  4. quantity to be dispensed
  5. compete directions for use
  6. prescribers signature
115
Q

with inpatient computer prescription writing (charting); ______________ must be present for the order to be valid

A

all elements

116
Q

if the duration of therapy or the number of total doses is not specified, the medication is continued until….

A
  1. prescriber discontinues the order
  2. order is terminated per matter of policy
117
Q

what are common omissions with prescription writing ?

A
  1. not D/C prior med when new one has begun
  2. not stating whether regular or long acting form should be used
  3. fail to specify a strength or notation for long acting forms
  4. “PRN” but fail to state what conditions justify the needs
118
Q

“resume pre-op meds”; “continue present IV fluids”; “continue eye drops”

these are all what type of prescribing erros

A

omission of information

119
Q

when writing prescriptions, these rules should be followed to prevent errors:

A
  1. always precede decimal points with a zero
  2. do not follow whole numbers with a zero
  3. “units” should always be written out
  4. “micrograms” should always be written out
  5. Avoid acronyms and drug abbreviations
120
Q

which is appropriate in prescription writing?

A. “one ampule of furosemide”
B. Furosemide 40 mg

A

B - 40 mg furosemide

121
Q

T/F: “OD” is often mistaken for QD therefore you should write out “for right eye only”

A

true

122
Q

which is appropriate in prescription writing?

A. QD
B. Q.D.
C. once daily

A

C - write out once daily

123
Q

how do inappropriate drug prescriptions get written?

A
  1. failure to recognize C/i from other conditions the patient has
  2. failure to obtain information about the other drugs the patient is taking
  3. failure to recognize possible physiochemical incompatibilities between drugs
124
Q

how do you avoid errors in prescribing like: inappropriate drug prescriptions

A
  1. do a thorough H & P
  2. check physicians desk reference
  3. consult handbook of injectable drugs
125
Q

what is the electronic flow of information with E-prescribing

A

Prescriber <–> Intermediary <–> Pharmacy <–> Health insurance

126
Q

components of E-prescribing

A
  1. must be HIPAA compliant
  2. prescribers have information readily available
  3. prescriptions are clearly written
  4. renewals can be processed electronically
127
Q

what is the disadvantage to e prescribing

A

pull down drugs lists create new errors (wrong drug, wrong dose, regimen)

128
Q

what are the 4 ways a patient be noncompliant with meds?

A
  1. patient fails to obtain the medication
  2. patient fails to take the medication as prescribed
  3. patient prematurely D/Cs the medication
  4. patient (or someone else) takes the medication inappropriately
129
Q

ways to improve medication compliance

A
  1. communication
  2. assess personal, social, and economic conditions
  3. assist in the development of a routine for taking medications
  4. mailing refill reminders
130
Q

factors which encourage medication noncompliance

A
  1. dz with no sx
  2. changing medications in hopes of finding one that works better
  3. multiple doses per day
  4. living alone
  5. packaging
  6. transportation
  7. social or personal beliefs
131
Q

what schedule drug is there no accepted medical use, and is there lack of accepted safety as a drug?

A

I

132
Q

this schedule of drug has current accepted medical use, high potential for abuse, and abuse may lead to psychological and/or physical dependence

A

II

133
Q

T/F: all generic drugs are the equivalent to the trade name (proprietary) drug

A

False

134
Q

what is the benefit to generic drugs

A
  1. offer flexibility in filling an order
  2. cost reduction
135
Q

“________________” must be written on the prescription or the generic drug will be used

A

dispense as written

136
Q

what is a generic substitution

A

when the pharmacist substitutes the generic drug for the trade

137
Q

what is a therapeutic substitution

A

when a drug within the same class is substituted for the prescribed drug. pharmacist must have permission of the provider to do this.

138
Q

under what condition can a pharmacist make a therapeutic substitution without the approval of the prescriber?

A

in managed care organizations with a specific formulary

139
Q

T/F: Herbal and dietary supplements are regulated by the FDA

A

false

140
Q

herbal and dietary supplements are considered __________________, not _____________

A

part of the diet; medications

141
Q

WHO estimated in 2011 that ___________% of the worlds population is still dependent on herbal meds

A

80

142
Q

ASA recommends that patients discontinue all herbal medications _____________ weeks prior to surgery

A

2-3

143
Q

T/F: herbals are legally considered medications/drugs

A

false

144
Q

T/F: FDA approval is required prior herbals being sold

A

false

145
Q

T/F: there is no proof of efficacy or safety prior to marketing of herbals

A

true

146
Q

common s/e attributed to herbal medicines

A
  1. CV instability
  2. Electrolyte disturbances
  3. coagulation d/o
  4. endocrine effects
  5. hepatotoxicity
  6. renal failure
147
Q

T/F: herbals are available without a prescription

A

true

148
Q

_____________________ was established to reaffirm that herbals and dietary supplements were a part of the diet, and prohibit manufactures from making false claims (i.e. est of good manufacturing practice [GMP])

A

Dietary supplement health and Education Act 1994 (DSHEA)

149
Q

in 2006, the ______________________________ Act requires mandatory reporting by manufacturers, packers, and distributors, to the FDA of serious adverse events

A

Dietary Supplement and non-prescription drug consumer protection act

150
Q

what was the goal of the 2006 Dietary supplement & non-prescription drug consumer protection act

A

to identify trends to alert the public to potential safety issues with supplements

151
Q

What are examples of serious events that were now required to be reported d/t the 2006 Dietary supplement and non-prescription drug consumer protection act

A
  1. death
  2. life threatening event
  3. hospitalization
  4. persistent disability or incapacity
  5. congenital anomaly or birth defect
  6. adverse event requiring medical or surgical intervention
152
Q

what year did the FDA release the final Good manufacturing Practice (GMP) standards for supplements?

A

2007

153
Q

________________ is a botanical supplement that should not be used longer than 10-14 days d/t immunosuppression

A

Echinacea

154
Q

What are the uses of Echinacea ?

A
  1. immune modulation
  2. Anti-inflammatory
  3. Antibacterial
  4. antifungal
  5. antiviral
  6. antioxidant

Pharm Unit 4 - Endo (4 decks)

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