Exam 3 Review FC Flashcards

1
Q

What is the first line recommendation for non-cancer pain?

A

NSAIDs

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2
Q

what are the three effects of NSAIDs?

A

analgesic, antipyretic, antiinflammatory

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3
Q

ibuprofen- class?

A

NSAID

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4
Q

naproxen- class?

A

NSAID

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5
Q

aspirin- class?

A

NSAID

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6
Q

toradol- class?

A

NSAID

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7
Q

mobic-class?

A

NSAID

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8
Q

two GI adverse effects of NSAIDs?

A

nausea, heartburn

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9
Q

non-GI side effects of NSAIDs? (2)

A

dizziness, mild headaches

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10
Q

hypertension taking NSAIDs?

A

no

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11
Q

history of ulcers taking NSAIDs?

A

no

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12
Q

history of Crohn’s taking NSAIDs?

A

no

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13
Q

GI bleeding taking NSAIDs?

A

no

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14
Q

liver disease- NSAIDs?

A

contraindicated

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15
Q

kidney disease- NSAIDs?

A

contraindicated

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16
Q

pregnancy- NSAIDs?

A

contraindicated

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17
Q

bleeding or platelet disorders- NSAIDs?

A

contraindicated

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18
Q

heart disease- NSAIDs?

A

contraindicated

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19
Q

three drug interactions with NSAIDs?

A

Warfarin, antihypertensives, digoxin (WAD)

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20
Q

antihypertensives, warfarin, digoxin- these are contraindicated with what class?

A

NSAID

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21
Q

N/V, diaphoresis, tinnitus, hypertenvilation (respiratory alkalosis)- these are symptoms of what?

A

salicylate toxicity

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22
Q

salicylates are WHAT-based?

A

aspirin

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23
Q

respiratory alkalosis- early or late signs of salicylate toxicity?

A

early

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24
Q

what is the physiologic manifestation of respiratory alkalosis?

A

hyperventilation

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25
Q

2005 black box warning for NSAIDs? (all prescription and OTC NSAIDs)

A

increased risk of CV events and serious GI bleeding

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26
Q

2015 black box warning for NSAIDs? (all nonaspirin NSAIDs)

A

emphasized increased risk of heart attack and stroke

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27
Q

a nonopioid, non-NSAID analgesic?

A

acetaminophen

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28
Q

when is acetaminophen used?

A

treatment of mild pain and fever

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29
Q

does acetaminophen have anti-inflammatory properties?

A

no

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30
Q

what are the three contraindications for acetaminophen?

A

alcohol abuse, liver/kidney disease, malnutrition

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31
Q

acetaminophen with ETOH abuse?

A

no

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32
Q

acetaminophen with liver disease?

A

no

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33
Q

acetaminophen with kidney disease?

A

no

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34
Q

acetaminophen with malnutrition?

A

no

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35
Q

acetaminophen toxicity causes what effects on the liver?

A

liver damage or failure

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36
Q

four signs of acetaminophen toxicity?

A

abdominal pain, N/V, dark urine, jaundice

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37
Q

abdominal pain, N/V, dark urine, jaundice- symptoms of what?

A

acetaminophen toxicity

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38
Q

how does acetaminophen toxicity manifest?

A

liver damage or failure

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39
Q

what is the definition of analgesia?

A

absence of pain

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40
Q

term? Absence of pain

A

analgesia

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41
Q

what is the effect/definition of an opioid analgesic?

A

analgesia (absence of pain) without resulting in loss of consciousness

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42
Q

what are the three categories of opioid analgesics?

A

full agonists, partial agonists, and antagonists

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43
Q

what is the prototype opioid agonist?

A

morphine

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44
Q

when do we use opioids?

A

serious/acute pain, post-surgery, chronic cancer pain

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45
Q

what type category of opioids activate the opioid receptor fully?

A

full agonists

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46
Q

what category of opioids interact with receptor to achieve a response?

A

full agonists

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47
Q

morphine- category of opioids?

A

full agonists

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48
Q

methadone- category of opioid?

A

full agonists

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49
Q

codeine- category of opioid?

A

full agonists

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50
Q

affinity plus efficacy- category of opioid?

A

full agonists

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51
Q

category of opioid? Activate opioid receptor to a lesser degree

A

partial agonists

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52
Q

category of opioid? Tramadol

A

partial agonists

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53
Q

category of opioid? Buprenorphine

A

partial agonists

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54
Q

category of opioid? Bind to opioid receptors without activating them

A

opioid antagonists

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55
Q

narcan- category of opioid?

A

opioid antagonists

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56
Q

naloxone- category of opioid?

A

opioid antagonists

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57
Q

category of opioid- affinity but no efficacy?

A

opioid antagonists

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58
Q

example of opioid antagonist?

A

naloxone

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59
Q

two examples of partial opioid agonists?

A

buprenorphine, tramadol

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60
Q

three examples of full opioid agonists?

A

morphine, codeine, methadone

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61
Q

hydromorphone- category of opioid?

A

full agonist

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62
Q

why doesn’t tramadol work as well as codeine?

A

affinity but low efficacy

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63
Q

hydrocodone- category of opioid?

A

full agonist

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64
Q

efficacy- think WHAT?

A

effectiveness

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65
Q

opioid antagonists bind to receptor but does not WHAT?

A

activate the receptor

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66
Q

when do we use opioid antagonists?

A

opioid overdose

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67
Q

opioid antagonists occupy the receptor so that full agonists cannot WHAT?

A

attach to the receptor

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68
Q

heroin- category of opioid?

A

full agonist

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69
Q

what are the three goals of therapy for gout?

A

1) management of pain associated with acute attacks 2) lower uric acid level 3) lifestyle management

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70
Q

example medication used for urate lowering therapy?

A

allopurinol

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71
Q

allopurinol- specific class?

A

xanthine oxidase inhibitor

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72
Q

example xanthine oxidase inhibitor?

A

allopurinol

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73
Q

what does allopurinol do?

A

inhibit the enzyme responsible for conversion of hypoxanthine and xanthine to uric acid

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74
Q

what is the first line medication for urate lowering therapy?

A

allopurinol

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75
Q

what medication? Inhibit the enzyme responsible for the conversion of hypoxanthine to xanthine to uric acid?

A

allopurinol

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76
Q

liver-related adverse effect of allopurinol?

A

hepatotoxicity

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77
Q

gout flare at initiation of therapy- associated with what medication?

A

allopurinol

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78
Q

what FIVE labs should be monitored with allopurinol?

A

LFT, BUN, creatinine, uric acid level, CBC

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79
Q

drug interactions with allopurinol?

A

multiple

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80
Q

what gout medication can cause a skin rash?

A

allopurinol

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81
Q

how to manage gout flare with initiation of allopurinol therapy?

A

treat proactively

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82
Q

what is the gout flare when starting allopurinol associated with?

A

shrinking the crystals- makes them active

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83
Q

when does gout flare happen with allopurinol?

A

initiation of therapy

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84
Q

three types of meds used for gout flares?

A

colchicine, NSAIDs, glucocorticoids

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85
Q

what are the two goals of medication for acute gout flares?

A

reduce pain and severity of gout flare

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86
Q

low-dose or high-dose colchicine preferred for gout flare?

A

low-dose

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87
Q

is low-dose colchicine effective for a gout flare?

A

yes

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88
Q

where are corticosteroid hormones produced?

A

adrenal cortex

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89
Q

the adrenal cortex produces what?

A

corticosteroid hormones

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90
Q

when does disease result re: corticosteroids?

A

inadequate or excess secretion

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91
Q

when do we use short-term corticosteroids?

A

self-limiting, acute conditions

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92
Q

self-limiting, acute conditions- use what?

A

short-term corticosteroids

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93
Q

when do we use long-term corticosteroids?

A

life-threatening conditions or severe/disabling symptoms

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94
Q

local over WHAT steroid therapy should be used when possible?

A

local over systemic

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95
Q

can you abruptly stop corticosteroids?

A

no

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96
Q

effect of corticosteroids on bones?

A

osteoporosis

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97
Q

effect of corticosteroids on wound healing?

A

poor wound healing

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98
Q

effect of corticosteroids on sleep?

A

insomnia

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99
Q

effect of corticosteroids on skin?

A

thinning of skin

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100
Q

effect of corticosteroids on mood?

A

mood changes/depression

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101
Q

effect of corticosteroids on blood sugar?

A

hyperglycemia

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102
Q

effect of corticosteroids on vision?

A

cataracts

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103
Q

effect of corticosteroids on infection risk?

A

increased risk for infection

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104
Q

effects of corticosteroids on GI?

A

peptic ulcers; GI upset

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105
Q

why do we not abruptly withdraw corticosteroids?

A

HPA axis suppression

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106
Q

what is suppressed with longer-term corticosteroids?

A

HPA axis suppression

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107
Q

brand name for metformin?

A

glucophage

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108
Q

generic name for glucophase?

A

metformin

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109
Q

other than T2DM, when is metformin used?

A

metabolic-syndrome type disorders such as PCOS

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110
Q

route of metformin administration?

A

orally

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111
Q

metformin- monotherapy?

A

yes

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112
Q

metformin- used with other drugs?

A

yes

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113
Q

first line treatment for T2DM?

A

metformin

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114
Q

metformin- specific drug glass?

A

biguanides

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115
Q

example of biguanide medication?

A

metformin

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116
Q

adverse effects of metformin, are mostly what?

A

GI

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117
Q

how can patients avoid GI side effects of metformin?

A

take with food

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118
Q

four GI adverse effects of metformin?

A

nausea, diarrhea, abdominal cramping, and bloating

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119
Q

how should metformin dose be titrated?

A

slowly

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120
Q

why do we titrate metformin dose slowly?

A

to minimize GI adverse effects

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121
Q

what is the black box warning with metformin?

A

lactic acidosis

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122
Q

what three situations is lactic acidosis with metformin more likely? RED

A

renal impairment, dehydration, elderly

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123
Q

renal impairment, dehydration, and elderly- increased risk for WHAT with metformin? (RED)

A

lactic acidosis

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124
Q

renal impairment predisposes patients to what adverse effect of metformin?

A

lactic acidosis

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125
Q

dehydration predisposes patients to what adverse effect of metformin?

A

lactic acidosis

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126
Q

elderly- predisposes patients to what adverse effect of metformin?

A

lactic acidosis

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127
Q

prevalence of lactic acidosis with metformin?

A

rare

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128
Q

rare, serious adverse effect with metformin?

A

lactic acidosis

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129
Q

two examples of TZDs?

A

pioglitazone and rosiglitazone

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130
Q

pioglitazone- specific class?

A

thiazolidinediones

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131
Q

rosiglitazone- specific class?

A

thiazolidinediones

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132
Q

when are TZDs used?

A

type 2 diabetes mellitus

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133
Q

route of administration- TZDs?

A

orally

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134
Q

can TZDs be used alone?

A

yes

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135
Q

can TZDs be used with other drugs?

A

yes

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136
Q

effect of TZDs on insulin resistance?

A

decreased insulin resistance

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137
Q

what must be present for TZDs to decrease insulin resistance?

A

insulin

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138
Q

what do TZDs activate?

A

peroxisome proliferator-activated receptor gamma

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139
Q

what antidiabetic class acts on the peroxisome proliferator activated receptor gamma?

A

thiazolidinediones

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140
Q

what antidiabetic class regules gene transcription?

A

thiazolidinediones

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141
Q

gene transcription is regulated by TZDs so that WHAT are produced in the cell?

A

proteins

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142
Q

what do the proteins do with TZDs?

A

help insulin act in the cell

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143
Q

brand name for pioglitazone?

A

actos

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144
Q

generic name for actos?

A

pioglitazone

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145
Q

brand name- rosiglitazone?

A

avandia

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146
Q

generic name for avandia?

A

rosiglitazone

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147
Q

is a TZD an insulin secretagogue?

A

no

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148
Q

do TZDs cause the pancreas to produce more insulin?

A

no

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149
Q

why do TZDs cause weight gain and edema?

A

fluid retention and plasma volume expansion

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150
Q

what are the two symptoms of fluid retention and plasma volume expansion with TZDs?

A

weight gain and edema

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151
Q

what two things have decreased excretion with TZDs?

A

sodium and water

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152
Q

what is the effect of PPAR-gamma in the vasculature?

A

increased vascular permeability

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153
Q

what happens to vascular permeability with TZDs?

A

increased

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154
Q

why is vascular permeability increased with TZDs?

A

effects of PPAR-gamma on the vasculature

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155
Q

TZDs- lactation?

A

avoid

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156
Q

TZDs in pregnancy?

A

avoid unless benefits clearly outweigh risks

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157
Q

TZDs can cause anovulatory women to what?

A

ovulate

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158
Q

what antidiabetic class should have pregnancy prevention precautions?

A

TZDs

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159
Q

why can ovulation occur in anovulatory women with TZDs?

A

because of decreased insulin resistance

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160
Q

alpha glucosidase inhibitor- example?

A

acarbose

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161
Q

acarbose- specific class?

A

alpha glucosidase inhibitor

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162
Q

precose- generic name?

A

acarbose

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163
Q

acarbose- brand name?

A

precose

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164
Q

acarbose- monotherapy?

A

no

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165
Q

acarbose- route of administration?

A

orally

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166
Q

where do alpha glucosidase inhibitors act?

A

at the brush border of the small intestine

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167
Q

what is the main effect of alpha glucosidase inhibitors?

A

lower postprandial blood glucose

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168
Q

what do alpha glucosidase inhibitors compete with?

A

complex carbohydrates for digestion

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169
Q

what antidiabetic drug competes with complex carbohydrates for digestion?

A

alpha glucosidase inhibitor

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170
Q

what antidiabetic drug should not be used with intestinal adsorbents?

A

alpha glucosidase inhibitor

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171
Q

what are three examples of intestinal adsorbents?

A

kaolin, pectin, bismuth-subslicylate

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172
Q

when should alpha glucosidase inhibitors be taken?

A

with the first bite of the meal

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173
Q

alpha glucosidase inhibitors- pregnancy?

A

contraindicated

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174
Q

alpha glucosidase inhibitors- lactation?

A

contraindicated

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175
Q

alpha glucosidase inhibitors- renal impairment?

A

contraindicated

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176
Q

alpha glucosidase inhibitors- inflammatory bowel disease?

A

contraindicated

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177
Q

alpha glucosidase inhibitors- history of bleeding ulcers?

A

contraindicated

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178
Q

alpha glucosidase inhibitors- intestinal obstruction?

A

contraindicated

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179
Q

primary type of adverse effects of alpha glucosidase inhibitors?

A

GI symptoms (titrate slowly)

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180
Q

alpha glucosidase inhibitors- any serious GI stuff?

A

contraindicated

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181
Q

SGLT2 inhibitors- route of admin?

A

orally

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182
Q

what antidiabetic med causes osmotic fluid loss?

A

SGLT2 inhibitors

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183
Q

class? Inhibit the reabsorption of glucose in the kidney proximal tubule

A

SGLT2 inhibitors

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184
Q

can SGLT2 inhibitors be used as monotherapy?

A

yes

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185
Q

what is the ultimate result of SGLT2 inhibitors?

A

increased excretion of glucose in the urine

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186
Q

canagliflozin- specific class?

A

SGLT2 inhibitors

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187
Q

dapagliflozin- specific class?

A

SGLT2 inhibitors

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188
Q

empagliflozin- specific class?

A

SGLT2 inhibitors

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189
Q

genital infections- adverse effect of which antidiabetic class?

A

SGLT2 inhibitors

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190
Q

fungal genital infections- adverse effect of which antidiabetic class?

A

SGLT2 inhibitors

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191
Q

bacterial genital infections- adverse effect of which antidiabetic class?

A

SGLT2 inhibitors

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192
Q

UTI- adverse effect of which antidiabetic class?

A

SGLT2 inhibitors

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193
Q

hypovolemia- adverse effect of which antidiabetic class?

A

SGLT2 inhibitors

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194
Q

hypotension- adverse effect of which antidiabetic class?

A

SGLT2 inhibitors

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195
Q

osteoporosis- adverse effect of which antidiabetic class?

A

SGLT2 inhibitors

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196
Q

lower extremity infection/amputation- associated with which antidiabetic class?

A

SGLT2 inhibitors

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197
Q

Fournier’s gangrene- precaution with what antidiabetic class?

A

SGLT2 inhibitors

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198
Q

leg and foot amputations- precaution with what antidiabetic class?

A

SGLT2 inhibitors

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199
Q

ketoacidosis- precaution with what antidiabetic class?

A

SGLT2 inhibitors

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200
Q

fractures- adverse effect associated with what antidiabetic class?

A

SGLT2 inhibitors

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201
Q

sitagliptin- specific class?

A

DPP4 inhibitors/gliptins

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202
Q

DPP4 inhibitors- monotherapy?

A

yes

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203
Q

what class slows the breakdown of glucagon-like peptide 1?

A

DPP4 inhibitors/gliptins

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204
Q

sitagliptin- brand name?

A

januvia

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205
Q

DPP4 inhibitors- route of administration?

A

orally

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206
Q

are DPP4 inhibitors insulin secretagogues?

A

yes

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207
Q

do DPP4 inhibitors have a risk of hypoglycemia?

A

yes

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208
Q

metformin and TZDs and hypoglycemia?

A

least likely

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209
Q

antidiabetic class most likely to cause hypoglycemia?

A

sulfonylurea (not glucose-dependent)

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210
Q

DPP4 inhibitors- glucose dependent insulin secretion?

A

yes

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211
Q

sulfonylurea- glucose dependent insulin secretion?

A

no (hypoglycemia)

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212
Q

GLP1s- glucose dependent?

A

yes

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213
Q

effect of DPP4s on insulin synthesis?

A

increased

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214
Q

effect of DPP4s on beta cell mass?

A

increased- multiple mechanisms

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215
Q

effect of DPP4s on glucagon secretion?

A

suppression

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216
Q

effect of DPP4s on gastric emptying?

A

slowed

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217
Q

effect of DPP4s on appetite?

A

decreased (weight loss)

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218
Q

arthralgia- seen with which antidiabetic class?

A

DPP4 inhibitors/gliptins

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219
Q

pancreatitis- seen with which antidiabetic class?

A

DPP4 inhibitors/gliptins

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220
Q

skin rash- seen with which antidiabetic class?

A

DPP4 inhibitors/gliptins

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221
Q

renal impairment- DPP4 inhibitors?

A

caution

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222
Q

heart failure- DPP4 inhibitors?

A

caution

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223
Q

incretin mimetics?

A

GLP1 receptor agonists

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224
Q

exenatide- specific class?

A

GLP1 receptor agonists

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225
Q

dulaglutide- specific class?

A

GLP1 receptor agonists

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226
Q

semaglutide- specific class?

A

GLP1 receptor agonists

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227
Q

GLP1 agonists- monotherapy?

A

yes

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228
Q

GLP1 agonists with other medications?

A

yes

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229
Q

GLP1 agonists- MOA?

A

act as endogenous GLP1

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230
Q

effect of GLP1 on triglycerides?

A

reduction

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231
Q

effect of GLP1 on systolic blood pressure?

A

reduction

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232
Q

why is there weight loss with GLP1 agonists?

A

reduced appetite and reduced food intake

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233
Q

which GLP1 can be given orally?

A

semaglutide (rybelsus)

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234
Q

another name for GLP1 agonists?

A

incretin mimetics

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235
Q

what is the first oral GLP1 for T2DM only?

A

semaglutide (rybelsus)

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236
Q

most common adverse effects with GLP1 agonists?

A

GI- N/V

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237
Q

gallbladder dysfunction- adverse effect of which antidiabetic class?

A

GLP1 receptor agonists

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238
Q

thyroid dysfunction- adverse effect of which antidiabetic class?

A

GLP1 receptor agonists

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239
Q

pancreatitis or pancreatic duct metaplasia- which antidiabetic class?

A

GLP1 receptor agonists

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240
Q

adverse GLP1 agonist effect on kidneys?

A

kidney failure/injury

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241
Q

route of admin- GLP1 agonists?

A

subcutaneous injection

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242
Q

personal or family history of medullary thyroid carcinoma- contraindication for which antidiabetic class?

A

GLP1 receptor agonists

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243
Q

endocrine neoplasia- contraindication for what antidiabetic class?

A

GLP1 receptor agonists

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244
Q

moderate or greater renal disease- contraindication for what antidiabetic class?

A

GLP1 receptor agonists

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245
Q

history of GI disease is a contraindication GLP1 agonists

A

don’t give

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246
Q

mild renal disease- GLP1?

A

this is ok, but moderate or greater is a contraindication

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247
Q

what condition is treated with levothyroxine?

A

hypothyroidism

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248
Q

what medication acts like the body’s endogenous thyroid hormone?

A

levothyroxine

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249
Q

what three things does thyroid hormone regulate?

A

heart rate, respiratory rate, metabolic rate

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250
Q

heart rate, respiratory rate, metabolic rate- regulated by what?

A

thyroid hormone

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251
Q

five adverse effects of levothyroxine therapy?

A

diarrhea, weight loss, cardiac arrhythmias, menstrual irregularity, heat intolerance

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252
Q

what population is at risk of cardiac arrhythmias with thyroid hormone therapy?

A

elderly

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253
Q

adverse effects of thyroid hormone therapy mirror what condition?

A

hyperthyroidism

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254
Q

weight gain or loss with hyperthyroidism?

A

weight loss

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255
Q

what medication is used to treat hypothyroidism?

A

levothyroxine

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256
Q

too much levothyroxine in the elderly can cause what?

A

cardiac arrhythmias

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257
Q

when should levothyroxine be taken?

A

on an empty stomach at least 30 minutes before breakfast

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258
Q

levothyroxine relative to meals?

A

on an empty stomach at least 30 minutes before breakfast

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259
Q

what three labs should be monitored with levothyroxine?

A

TSH, T3, and free T4

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260
Q

levothyroxine should be taken when?

A

on an empty stomach at least 30 minutes before breakfast

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261
Q

definitive lab for monitoring levothyroxine?

A

TSH

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262
Q

graves disease causes what thyroid imbalance?

A

hyperthyroidism

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263
Q

toxic multi-nodular goiter- causes what thyroid imbalance?

A

hyperthyroidism

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264
Q

agranulocytosis- seen with what endocrine drug?

A

anti-thyroid drugs

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265
Q

aplastic anemia- seen with what endocrine drugs?

A

anti-thyroid drugs

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266
Q

what is the black box warning with propylthiouracil?

A

liver failure

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267
Q

hair loss- seen with what endocrine drugs?

A

anti-thyroid drugs

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268
Q

propylthiouracil- specific class?

A

anti-thyroid drugs

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269
Q

methimazole- specific class?

A

anti-thyroid drugs

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270
Q

how to anti-thyroid drugs work?

A

block synthesis of thyroid hormone by preventing iodination of tyrosine

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271
Q

how does propylthiouracil work?

A

block synthesis of thyroid hormone by preventing iodination of tyrosine

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272
Q

how does methimazole work?

A

block synthesis of thyroid hormone by preventing iodination of tyrosine

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273
Q

what class? Block synthesis of thyroid hormone by preventing iodination of tyrosine?

A

anti-thyroid drugs

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274
Q

another name for anti-thyroid class?

A

thionamides

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275
Q

another name for thionamide class?

A

anti-thyroid drugs

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276
Q

agranulocytosis and aplastic anemia- adverse effects of what class?

A

thionamides

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277
Q

what thionamide should be used in first trimester of pregnancy?

A

propylthiouracil

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278
Q

what thionamide should be used in second and third trimesters of pregnancy?

A

methimazole

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279
Q

what thionamide should be used in second trimester of pregnancy?

A

methimazole

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280
Q

what thionamide should be used in third trimester of pregnancy?

A

methimazole

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281
Q

patient education with thionamides?

A

report infections

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282
Q

what lab monitors for agranulocytosis with thionamides?

A

CBC

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283
Q

when should CBC be drawn with thionamides?

A

at initiation of therapy and if s/s infection d/t r/f agranulocytosis

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284
Q

hashimotos thyroiditis may be seen in what condition/state?

A

pregnancy

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285
Q

hashimotos thyroiditis is a potential indication for what class of drugs in pregnancy?

A

anti-thyroid drugs

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286
Q

propylthiouracil must be used in which trimester of pregnancy?

A

first trimester

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287
Q

what lab should be drawn with initiation of thionamide therapy?

A

CBC

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288
Q

what lab should be drawn if s/s of infection with thionamide therapy?

A

CBC

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289
Q

lisinopril- class?

A

angiotensin-converting enzyme inhibitor

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290
Q

enalapril- class?

A

angiotensin-converting enzyme inhibitor

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291
Q

two examples of ACE inhibitors?

A

lisinopril and enalapril

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292
Q

indications for ACE inhibitors?

A

HTN, diabetic proteinuric states, CAD with ischemia, post MI, heart failure

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293
Q

how do ACE inhibitors work?

A

block the conversion of AT I to AT II and less aldosterone produced

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294
Q

which CV drug results in less aldosterone being produced?

A

angiotensin-converting enzyme inhibitor

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295
Q

what causes vasodilation with ACE inhibitors?

A

increased bradykinin

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296
Q

effect of ACE inhibitors on bradykinin?

A

increased

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297
Q

increased bradykinin with ACE inhibitors leads to what physiologic effect?

A

vasodilation

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298
Q

what is the likely culprit for cough with ACE inhibitors?

A

increased bradykinin (vasodilation)

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299
Q

what is the likely culprit for angioedema with ACE inhibitors?

A

increased bradykinin (vasodilation)

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300
Q

cough and angioedema- associated with what CV drug class?

A

angiotensin-converting enzyme inhibitor

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301
Q

effect of ACE inhibitors on intravascular volume?

A

decreased

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302
Q

effect of ACE inhibitors on vasculature?

A

vasodilation

303
Q

bradykinin causes what with ACE inhibitors?

A

cough and angioedema

304
Q

losartan- class?

A

angiotensin II receptor blocker

305
Q

valsartan- class?

A

angiotensin II receptor blocker

306
Q

indications for ARBS?

A

HTN, diabetic proteinuric states, CAD with ischemia, post MI, heart failure

307
Q

what two CV classes have the same indications?

A

ACE inhibitors and ARBs

308
Q

two example drugs of ARBs?

A

valsartan and losartan

309
Q

valsartan and losartan- class?

A

angiotensin II receptor blocker

310
Q

how to ARBs work?

A

block binding of angiotensin II to receptor

311
Q

what is the difference in the MOA/effects of ACE inhibitors and ARBs?

A

no bradykinin increase with ARBs so less risk of cough or angioedema

312
Q

why do ARBs not affect bradykinin?

A

working down further in the pathway

313
Q

if a patient has a dry cough on an ACEI- what should I do?

A

switch to an ARB

314
Q

adverse blood pressure effect with ACEI and ARBs?

A

hypotension

315
Q

does angioedema usually occur with an ARB?

316
Q

tachyphylaxis- seen with what two CV med classes?

A

ACEI and ARBs

317
Q

ACE inhibitors- pregnancy?

A

absolute contraindication

318
Q

ARBs, pregnancy?

A

absolute contraindication

319
Q

bilateral renal artery stenosis- ACE inhibitors?

A

absolute contraindication

320
Q

bilateral renal artery stenosis- ARBs

A

absolute contraindication

321
Q

angioedema hx- ACE inhibitors?

A

absolute contraindication

322
Q

angioedema hx- ARBs?

A

absolute contraindication

323
Q

effect of ACEIs on potassium?

A

risk for retention of potassium

324
Q

effect of ARBs on potassium?

A

risk for retention of potassium

325
Q

what three labs should be monitored with ACEIs?

A

BUN, creatinine, potassium

326
Q

what three labs should be monitored with ARBs?

A

BUN, creatinine, potassium

327
Q

bilateral renal artery stenosis is a contraindication for what classes of CV meds?

A

ACEI and ARBs

328
Q

pregnancy is an absolutely contraindication for what classes of CV meds?

A

ACEI and ARBs

329
Q

angioedema is an absolute contraindication for what classes of CV meds?

A

ACEI and ARBs

330
Q

three absolute contraindications for ACEIs and ARBs?

A

pregnancy; bilateral renal artery stenosis; angioedema

331
Q

ACEIs and ARBs are protective of what?

A

renally-protective

332
Q

why should we monitor K+ with ACEIs?

A

retention of potassium

333
Q

why should be monitor K+ with ARBs?

A

retention of potassium

334
Q

when should we check renal function after starting ACE or ARB?

A

three-ish weeks

335
Q

hyperkalemia is a sign of what with ACEI or ARBS?

A

kidneys not tolerating

336
Q

two major categories of calcium channel blockers?

A

dihydropyridines and non-dihydropyridines

337
Q

class? Bind to voltage gated L-type channels in the heart and blood vessels preventing calcium from entering the cells

A

calcium channel blockers

338
Q

where do calcium channel blockers bind?

A

voltage gated L-type channels in the heart and blood vessels

339
Q

calcium channel blockers prevent what from entering the cells?

340
Q

why do CCBs cause vasodilation?

A

relaxation of smooth muscle

341
Q

effect of CCBs on arterial beds?

342
Q

effect of CCBs on afterload?

343
Q

chronic and unstable angina is an indication for what CV drug class?

A

calcium channel blockers

344
Q

vasospastic angina is an indication for what CV drug class?

A

calcium channel blockers

345
Q

migraine prophylaxis is an indication for what CV drug class?

A

calcium channel blockers

346
Q

what type of arrhythmias may be managed with CCBs?

A

some supraventricular arrhythmias

347
Q

Raynaud’s syndrome is an indication for what CV drug class?

A

calcium channel blockers

348
Q

CAD with ischemia- is an indication for what CV drug class?

A

calcium channel blockers

349
Q

which category of CCBs are used in hypertension?

A

dihydropyridines

350
Q

amlodipine- specific class?

A

dihydropyridine CCB

351
Q

nifedipine- specific class?

A

dihydropyridine CCB

352
Q

felodipine- specific class?

A

dihydropyridine CCB

353
Q

three examples of dihydropyridine CCBs?

A

amlodipine, nifedipine, felodipine

354
Q

when treating angina, what forms are preferred? Of Ccbs

A

long-acting forms of dihydropyridine CCBs

355
Q

hypotension, dizziness, lower extremity edema, headache, reflex tachycardia- adverse effects of what specific class?

A

dihydropyridine CCB

356
Q

lower extremity edema- associated with what CV drug class?

A

dihydropyridine CCB

357
Q

reflex tachycardia- associated with what CV drug class?

A

dihydropyridine CCB

358
Q

verapamil- specific class?

A

non-dihydropyridine CCB

359
Q

diltiazem- specific class?

A

non-dihydropyridine CCB

360
Q

what category of CCBs are used for supraventricular tachyarrhythmias?

A

non-dihydropyridine CCB

361
Q

three adverse effects of non-dihydropyridine CCBs?

A

fatigue, dizziness, constipation

362
Q

fatigue, dizziness, constipation- adverse effects of what CV class?

A

non-dihydropyridine CCB

363
Q

inotropic effect of non-dihydropyridine CCBs?

A

negative inotropic effect

364
Q

chronotropic effect of non-dihydropyridine CCBs?

A

negative chronotropic effect

365
Q

can verapamil be used in HFrEF?

366
Q

can diltiazem be used in HFrEF?

367
Q

why should we NOT use non-dihydropyridines in HFrEF?

A

negative inotropic and negative chronotropic effects

368
Q

two examples of non-dihydropyridines?

A

verapamil and diltiazem

369
Q

effect of non-dihydropyridines on contractility?

370
Q

effect of non-dihydropyridines on heart rate?

371
Q

very common side effect with non-dihydropyridine CCBs?

A

constipation

372
Q

CCBs in liver dysfunction?

373
Q

CCBs in pregnancy?

A

contraindicated

374
Q

CCBs in lactation?

A

contraindicated

375
Q

how to decide which CCB to use?

A

indication, actions, side effects, specific patient characteristics

376
Q

HMG-CoA reductase inhibitors- broad class?

A

antilipidemics

377
Q

cholesterol absorption inhibitors- broad class?

A

antilipidemics

378
Q

fenofibrates- broad class?

A

antilipidemics

379
Q

another name for statins?

A

HMG-CoA reductase inhibitors

380
Q

another name for HMG- CoA reductase inhibitors?

381
Q

rosuvastatin- specific class?

A

HMG-CoA reductase inhibitors

382
Q

atorvastatin- specific class?

A

HMG-CoA reductase inhibitors

383
Q

two examples of HMG CoA reductase inhibitors?

A

rosuvastatin and atorvastatin

384
Q

what are the two uses for statins?

A

LDL and hypertryglyceridemia

385
Q

what is HMG CoA reductase?

A

an enzyme required in cholesterol synthesis in the liver

386
Q

what is the enzyme required for cholesterol synthesis in the liver?

A

HMG CoA reductase

387
Q

where does HMG CoA reductase work?

A

in the liver

388
Q

what antilipidemic works to prevent atherosclerosis?

A

HMG CoA reductase inhibitors

389
Q

what antilipidemic has pleotropic effects?

390
Q

what antilipidemic class has a decreased production of pro-inflammatory cytokines?

391
Q

what antilipidemic class results in increased activity of endothelial nitric oxide?

392
Q

effect of statins on pro-inflammatory cytokines?

A

decreased production

393
Q

effect of statins on activity of endothelial nitric oxide?

A

increased activity

394
Q

effect of statins on platelet activity?

395
Q

effect of statins on synthesis of thromboxane A2?

396
Q

what antilipidemic class has reduced platelet activity?

397
Q

what antilipidemic class has reduced synthesis of thromboxane A2?

398
Q

common general adverse effect of statins?

A

myopathies

399
Q

four common GI adverse effects of statins?

A

nausea, constipation, indigestion, flatulence

400
Q

what antilipidemic class is associated with flu-like symptoms?

401
Q

what antilipidemic class is associated with memory loss?

402
Q

memory loss with statins is WHAT?

A

reversible if drug stopped

403
Q

myalgia is common with what antilipidemic class?

404
Q

myositis can be seen with what antilipidemic class?

405
Q

rhabdomyolysis can be seen with what antilipidemic class?

406
Q

effect of statins on liver?

A

liver dysfunction

407
Q

what lab should be drawn to check for rhabdomyolysis?

A

creatinine kinase

408
Q

why should we check creatinine kinase with statins?

A

make sure the patient does not have significant elevation (i.e. rhabdo, myositis)

409
Q

headache with statins?

410
Q

type 2 DM and memory loss have been associated with antilipidemic class?

411
Q

statins- active liver disease?

A

contraindicated

412
Q

statins- current ETOH abuse?

A

contraindicated

413
Q

statins- history of liver disease?

A

contraindicated

414
Q

statins- pregnancy?

A

contraindicated

415
Q

statins- lactation?

A

contraindicated

416
Q

ezetimibe- brand name?

417
Q

zetia- generic name?

418
Q

what is ezetimibe used for?

A

reduction of LDL

419
Q

ezetimibe- specific class?

A

cholesterol absorption inhibitor

420
Q

ezetimibe- active liver disease?

A

contraindicated

421
Q

in addition to statins, myalgia, myopathy, rhabdo can be seen with what drug?

422
Q

antilipidemic associated with acute liver injury?

423
Q

what two types of cholesterol does ezetimibe inhibit absorption of?

A

dietary and biliary sources

424
Q

what two sources of cholesterol does ezetimibe act on?

A

dietary and biliary sources

425
Q

what antilipidemic drug acts on dietary and biliary sources of cholesterol?

426
Q

where do cholesterol absorption inhibitors work?

A

brush border of the small intestine

427
Q

what antilipidemic class works at the brush border of the small intestine?

A

cholesterol absorption inhibitor

428
Q

ultimate action of ezetimibe?

A

decreased delivery of intestinal cholesterol to the liver

429
Q

class? Decreased delivery of intestinal cholesterol to the liver

A

cholesterol absorption inhibitor

430
Q

inhibits absorption of cholesterol (dietary and biliary sources) at the brush border of the small intestine- class?

A

cholesterol absorption inhibitor

431
Q

example of cholesterol absorption inhibitor?

432
Q

most common adverse effects with cholesterol absorption inhibitor?

433
Q

most common adverse effects with ezetimibe?

434
Q

primary contraindication of ezetimibe?

A

active liver disease

435
Q

gemfibrozil- specific class?

A

fibric acid derivative

436
Q

fenofibrate- specific class?

A

fibric acid derivative

437
Q

gemfibrozil- brand name?

438
Q

fenofibrate- brand name?

439
Q

lopid- generic name?

A

gemfibrozil

440
Q

tricor- generic name?

A

fenofibrate

441
Q

fibric acid derivatives reduce WHAT?

A

hypertriglyceridemia

442
Q

what antilipidemic class has indirect elevation of HDLs?

A

fibric acid derivative

443
Q

why do fibric acid derivatives cause indirect elevation of HDLs?

A

d/t lowering of triglyceride levels

444
Q

lowering of tridlyceride levels indirectly lowers WHAT with fibric acid derivatives?

A

HDL levels

445
Q

what class helps to avoid pancreatitis in hypertriglyceridemia?

A

fibric acid derivative

446
Q

class? Act by causing an increase in lipolysis of triglycerides by using lipoprotein lipase

A

fibric acid derivative

447
Q

class? Decreases VLDL synthesis by the liver

A

fibric acid derivative

448
Q

liver synthesis of WHAT is affected by fibric acid derivatives?

449
Q

fibric acid derivatives help to avoid WHAT in hypertriglyceridemia?

A

pancreatitis

450
Q

term? Inhibit coagulation cascade and fibrin formation

A

anticoagulants

451
Q

what two things do anticoagulants inhibit?

A

coagulation cascade and fibrin formation

452
Q

term? Inhibit clot formation by preventing platelet activation and aggregation

A

antiplatelets

453
Q

how do antiplatelets inhibit clot formation?

A

by preventing platelet activation and aggregation

454
Q

two types of antithrombotic drugs?

A

anticoagulants and antiplatelets

455
Q

anticoagulants and antiplatelets are types of what?

A

antithrombotic drugs

456
Q

what kind of drugs inhibit coagulation cascade?

A

anticoagulants

457
Q

what kind of drugs inhibit fibrin formation?

A

anticoagulants

458
Q

example- anticoagulant?

A

dabigatran

459
Q

dabigatran- brand name?

460
Q

pradaxa- generic name?

A

dabigatran

461
Q

drug? Decreases risk of stroke and PE associated with non-valvular atrial fibrillation

A

dabigatran

462
Q

when is dabigatran used to decrease risk of stroke and PE?

A

non-valvular atrial fibrillation

463
Q

what type of a fib is dabigatran used in?

A

non-valvular atrial fibrillation

464
Q

dabigatran reduces risk of what two things?

A

stroke and PE

465
Q

when is dabigatran used to treat DVT and PE?

A

in patients who have been treated with a parenteral anticoagulant for 5-10 days

466
Q

when is dabigatran used for DVT and PE prophylaxis?

A

patients after hip surgery

467
Q

patients after hip surgery may receive what medication?

A

dabigatran

468
Q

reversible competitive thrombin inhibitor- drug?

A

dabigatran

469
Q

directly inhibits thrombin’s conversion of fibrinogen to fibrin- drug?

A

dabigatran

470
Q

four GI adverse effects of dabigatran?

A

heartburn, diarrhea, nausea, belching

471
Q

heartburn, diarrhea, nausea, belching- adverse effects of what drug?

A

dabigatran

472
Q

is dabigatran reversible?

473
Q

idarucimab/praxbind- is the reversal agent for what?

A

dabigatran

474
Q

what is the reversal agent for dabigatran?

A

idarucizumab/praxbind

475
Q

IV monoclonal antibody that binds to dabigatran?

A

idarucizumab/praxbind

476
Q

neutralizes anticoagulant effect for immediate surgical procedure or life-threatening bleed?

A

idarucizumab/praxbind

477
Q

bleeding disorders- dabigatran?

A

contraindicated

478
Q

history/active bleeding ulcers- dabigatran?

A

contraindicated

479
Q

mechanical heart valve- dabigatran?

A

contraindicated

480
Q

recent spinal epidural procedure- dabigatran?

A

contraindicated

481
Q

kidney disease- dabigatran?

A

contraindicated

482
Q

clopidogrel- drug type?

A

antiplatelets

483
Q

brand name for clopidogrel?

484
Q

generic name for plavix?

A

clopidogrel

485
Q

drug? Reduces the risk of MI in patients with ACS, STEMI

A

clopidogrel

486
Q

drug? Reduces risk of MI in stroke or established PAD?

A

clopidogrel

487
Q

drug? Prodrug that selectively inhibits the binding of ADP to its platelet receptor

A

clopidogrel

488
Q

drug? Affects the subsequent ADP-mediated activation of the glycoprotein GPIIb/IIIa complex

A

clopidogrel

489
Q

drug? Ultimately inhibits platelet aggregation

A

clopidogrel

490
Q

can everyone take clopidogrel?

A

no- some people are unable to effectively metabolize it

491
Q

bleeding, headache, taste disorders- adverse effects of what drug?

A

clopidogrel

492
Q

clopidogrel- black box warning?

A

antiplatelet activity is dependent on conversion to an active metabolite by the CYP2C19 enzyme

493
Q

why is genetic testing recommended with clopidogrel?

A

to make sure the patient is not a CYP2C19 poor metabolizer

494
Q

clopidogrel- renal dysfunction?

A

contraindicated

495
Q

clopidogrel- hepatic dysfunction?

A

contraindicated

496
Q

clopidogrel- active bleeding?

A

contraindicated

497
Q

sacubitril/valsartan- specific class?

498
Q

what do ANRIs inhibit?

A

RAAS system

499
Q

another name for sacubitril/valsartan?

500
Q

what two classes of drugs inhibit the SNS? (HF)

A

beta blockers (metoprolol) and alpha-beta blockers (Carvedilol)

501
Q

eplerenone- class?

A

mineralocorticoid receptor antagonists

502
Q

are loop diuretics first line therapy for HF?

503
Q

is ivabradine first line therapy for HF?

504
Q

is hydralazine plus a nitrate first line therapy for HF?

505
Q

amiodarone- specific class?

A

class III antiarrhythmic

506
Q

drug? Used to treat a fib and ventricular arrhythmias

A

amiodarone

507
Q

how does amiodarone work?

A

prolong cardiac myocyte repolarization through blockade of potassium channels

508
Q

what channels does amiodarone block?

A

potassium channels

509
Q

lung damage- associated with what CV drug?

A

amiodarone

510
Q

thyroid dysfunction- associated with what CV drug?

A

amiodarone

511
Q

other side effects of amiodarone?

A

N/V, fatigue

512
Q

why should we check thyroid function on amiodarone?

A

can affect thyroid function

513
Q

what labs should be checked on amiodarone?

A

thyroid labs

514
Q

HFrEF reflects what type of dysfunction?

515
Q

what is the normal EF?

516
Q

what is the EF of HFrEF?

517
Q

systolic dysfunction where the heart is not able to meet the perfusion needs of the body’s tissues (term?)

518
Q

what two things determine cardiac output?

A

HR and stroke volume

519
Q

what does EF estimate?

A

stroke volume

520
Q

what three things determine stroke volume?

A

contractility, preload, and afterload

521
Q

when does contractility decrease?

A

anything that causes myocyte dysfunction or death

522
Q

anything that causes myocyte dysfunction or death leads to what?

A

decreased contractility

523
Q

preload increases with volume WHAT?

524
Q

preload increases with increased/decreased heart contractility?

525
Q

what type of valve disease can increase afterload?

526
Q

aortic valvular disease can do what to afterload?

527
Q

an elevated peripheral vascular resistance leads to increased what?

528
Q

volume overload does what to preload?

529
Q

aortic stenosis does what to afterload?

530
Q

what three avenues of neurohormonal activation occur with HFrEF?

A

SNS activation, RAAS activation, natriuretic peptide release

531
Q

what receptors activate the SN?

A

central baroreceptors

532
Q

when do central baroreceptors activate the SNS?

A

due to decreased perfusion of the tissues in HF

533
Q

decreased perfusion of tissues in heart failure result in activation of what?

A

central baroreceptors activate the SNS

534
Q

SNS activation leads to more WHAT?

A

vasoconstriction

535
Q

SNS simulation of what receptors lead to increased work of the heart?

A

beta 1 receptors

536
Q

SNS activation does what to heart rate?

537
Q

SNS activation attempts to do what to contractility?

538
Q

activation of WHAT also leads to ADH production?

A

baroreceptors

539
Q

ADH causes further increase in WHAT?

A

intravascular volume, vasoconstriction, and hyponatremia

540
Q

increases in intravascular volume, vasoconstriction, and hyponatremia- caused by what hormone?

541
Q

catecholamines are toxic to what?

A

myocardium

542
Q

what hormones are toxic to the myocardium?

A

catecholamines

543
Q

what happens to sodium with ADH?

A

hyponatremia

544
Q

why is the RAAS system activated in HFrEF?

A

decreased cardiac output with decreased perfusion of the kidneys

545
Q

decreased cardiac output with decreased perfusion of the kidneys leads to activation of what?

546
Q

why do preload and afterload increase with RAAS activation?

A

ATII and aldosterone production

547
Q

vasoconstriction and extracellular volume increases with neurohormonal activation of what system?

548
Q

(term?) these peptides attempt to compensate for the pathophysiologic processes of HFrEF

A

natriuretic pepties

549
Q

can natriuretic peptides overcome the pathophysiologic processes of HFrEF?

550
Q

what does BNP do?

A

works to excrete more salt and water into the urine to offset the effects of aldosterone and ADH

551
Q

what hormone works to excrete more salt and water into the urine to offset the effects of aldosterone and ADH?

A

brain natriuretic peptide

552
Q

compensatory attempt for HFrEF is completed by what neurohormal systems?

A

natriuretic peptides

553
Q

what process is mediated in part by the neurohormonal activation and multiple other factors such as inflammation

A

cardiac remodeling

554
Q

angiotensin II and aldosterone are directly toxic to the WHAT?

A

myocardium

555
Q

what two chemicals lead to cardiac remodeling, myocyte death, and fibrosis?

A

angiotensin II and aldosterone

556
Q

what vascular effect does ATII cause?

A

vasoconstriction

557
Q

angiotensin II and aldosterone do what to afterload?

558
Q

what do metabolic diseases like frank DM contribute to? (what process of HFrEF)

A

cardiac remodeling

559
Q

what do inflammatory cytokines damage in cardiac remodeling?

560
Q

alterations of myocyte metabolism lead to what?

A

inability to produce the energy needed for contraction and more toxic metabolites are released

561
Q

term? Patient must sit up to breathe

562
Q

term? Patient suddenly wakes up and must sit up to breathe

A

paroxysmal nocturnal dyspnea

563
Q

describe cough with HFrEF?

A

productive of frothy material

564
Q

why is there edema and increase in weight with HFrEF?

A

volume overload

565
Q

why is there decreased urine output in HFrEF?

A

decreased renal perfusion

566
Q

what happens to urine output in HFrEF?

567
Q

dyspnea and fatigue are seen in what disorder?

568
Q

orthopnea definition?

A

patient must sit up to breathe

569
Q

paroxysmal nocturnal dyspnea- definition?

A

patient suddenly wakes up and must sit up to breathe

570
Q

cardiac cachexia is due to what?

A

inflammatory cytokines damage the myocytes and cause weight loss systemically

571
Q

term? Inflammatory cytokines damage the myocytes and cause weight loss sytemically

A

cardiac cachexia

572
Q

diabetes mellitus predisposes patients to what condition?

A

heart failure

573
Q

heart failure can precipitate what condition?

A

diabetes mellitus

574
Q

what condition causes DIRECT TOXICITY to the heart causing cardiomyopathy/HF?

A

diabetes mellitus

575
Q

effect of DM on contractility?

576
Q

effect of DM on cellular calcium efflux?

A

less efficacy

577
Q

formation and deposition of WHAT in the myocardium with DM?

A

advanced glycation end products

578
Q

advanced glycation end products cause what?

A

hypertrophy and fibrosis of the myocardium

579
Q

effect of DM on ATP formation?

580
Q

what is the alternative to ATP formation?

A

depend on fatty acid oxidation (much less efficient)

581
Q

fatty acid oxidation is much less WHAT?

582
Q

impaired ATP formation causes an increase in what?

A

oxygen demand

583
Q

toxic lipid depositions can result from what?

A

impaired ATP formation (DM and HFrEF)

584
Q

what is the SNS dysfunction seen with DM/HFrEF?

A

autonomic neuropathy

585
Q

SNS dysfunction/autonomic neuropathy and inflammation of the heart lead to increased WHAT?

A

myocyte dysfunction

586
Q

endothelial dysfunction pushes the patient to development of WHAT?

587
Q

when may autonomic neuropathy occur?

588
Q

diabetes promotes what in the arteries?

A

atherosclerotic change

589
Q

neurohormonal activation causes increased WHAT metabolism?

A

free fatty acid

590
Q

what is postulated as a cause of increased insulin resistance in DM/HFrEF?

A

Neurohormonal activation causes increased free fatty acid metabolism

591
Q

with direct therapy for HF, should also treat what?

A

any reversible cause/contributing factor

592
Q

reverse myocardial ischemia- example of what?

A

any reversible cause/contributing factor

593
Q

cardioversion for a-fib- example of what?

A

any reversible cause/contributing factor

594
Q

reduction of WHAT is a goal of HFrEF therapy?

595
Q

decrease of WHAT is a goal of HFrEF therapy?

596
Q

reduction of morbidity and decrease in mortality- goals of WHAT?

597
Q

decrease in symptoms, improve quality of life/overall function, decrease in hospitalization- goals of what?

598
Q

how to loop diuretics decrease preload?

A

by decreasing extracellular fluid by increased excretion of sodium and water through the kidneys

599
Q

what class of medications? Decrease preload via decreasing extracellular fluid by increased excretion of sodium and water through the kidneys

A

loop diuretics

600
Q

example of loop diuretic?

A

furosemide

601
Q

furosemide class?

A

loop diuretics

602
Q

effect of loop diuretics on afterload?

603
Q

effect of loop diuretics on preload?

604
Q

how do loop diuretics decrease afterload?

A

decreasing PVR

605
Q

sodium, water, and WHAT are eliminated renally?

606
Q

what three things are eliminated renally with loop diuretics?

A

sodium, water, and potassium

607
Q

what electrolyte imbalance can occur with loop diuretics?

A

hypokalemia

608
Q

MRAs do what with potassium?

A

hold onto it

609
Q

MRA effect on afterload?

610
Q

MRA effect on preload?

611
Q

what three classes of drugs can be used to inhibit RAAS in HFrEF?

A

ARNI, ACE, OR ARBs

612
Q

example ANRI drug?

A

sacubitril/valsartan

613
Q

what is the preferred class of drug to inhibit RAAS in HFrEF?

614
Q

inhibiting the RAAS has what effect on preload?

615
Q

why does RAAS inhibition lead to reduced preload?

A

less aldosterone

616
Q

what does RAAS inhibition lead to reduced afterload?

A

less aldosterone and less ATII

617
Q

what effect does RAAS inhibition have on afterload?

618
Q

ACEIs and ARBs assist with preventing what?

A

cardiac remodeling processes that become maladaptive

619
Q

what two drug classes assist with preventing cardiac remodeling processes that become maladaptive?

A

ACEIs and ARBs

620
Q

less AT II production and actions with what drug class?

621
Q

less AT II actions with what drug class?

622
Q

drug? A prodrug that acts to prevent the breakdown of natriuretic peptides by inhibiting neprilysin

A

sacubitril

623
Q

what is the action of sacubitril?

A

a prodrug that acts to prevent the breakdown of natriuretic peptides by inhibiting neprilysin

624
Q

what chemical does sacubitril inhibit?

A

neprilysin

625
Q

sacubitril prevents the breakdown of what?

A

natriuretic peptides

626
Q

ARNI enhance what two things?

A

natriuresis and vasodilation

627
Q

natriuresis results in what effect on preload?

628
Q

natriuresis results in what effect on afterload?

629
Q

natriuresis results in what two things?

A

decreased preload and afterload

630
Q

vasodilation has what effect on afterload?

631
Q

RAAS inhibition results in decreased hypertrophy and fibrosis of the WHAT?

A

myocardium

632
Q

inhibition of SNS is accomplished with what two drug classes?

A

beta blockers and alpha-beta blockers

633
Q

example of beta blocker used in HFrEF?

A

metoprolol

634
Q

example of alpha-beta blocker used in HFrEF?

A

carvedilol

635
Q

metoprolol drug class?

A

beta blocker

636
Q

carvedilol drug class?

A

alpha-beta blocker

637
Q

what drug class? Decreased myocardial oxygen demand and decreased wall tension

A

beta/alpha-beta blockers

638
Q

decreased myocyte apoptosis- what drug class?

A

beta/alpha-beta blockers

639
Q

inhibition of downregulation of beta receptors- what drug class?

A

beta/alpha-beta blockers

640
Q

beta/alpha-beta blockers have what effect on afterload?

641
Q

decreased tachycardia- what class of HFrEF?

A

beta/alpha-beta blockers

642
Q

improved diastolic filling times- what drug class HFrEF?

A

beta/alpha-beta blockers

643
Q

prevention of dysrhythmias- what drug class HFrEF?

A

beta/alpha-beta blockers

644
Q

rate control if a fib present- what drug class HFrEF?

A

beta/alpha-beta blockers

645
Q

alpha-1 blockade with alpha-beta blockers causes what?

A

vasodilation

646
Q

what drug class promotes osmotic diuresis?

A

SGLT2 inhibitors

647
Q

what drug class promotes more glucose excreted in the urine?

A

SGLT2 inhibitors

648
Q

natriuresis does what to preload?

649
Q

osmotic diuresis does what to preload?

650
Q

SGLT2 inhibitors cause what?

A

osmotic diuresis

651
Q

how may SGLT2 inhibitors lower BP?

A

decreased afterload via vasodilation

652
Q

metabolic modulation occurs with what drug class?

A

SGLT2 inhibitors?

653
Q

lowered blood glucose is a result of WHAT with SGLT2 inhibitors?

A

metabolic modulation

654
Q

possible improved efficiency of myocardial metabolism- what drug class?

A

SGLT2 inhibitors

655
Q

what drug class- increased contractility and increased CO?

A

cardiac glycosides

656
Q

what do cardiac glycosides do to contractility?

657
Q

what do cardiac glycosides do to cardiac output?

658
Q

what class of medications is not generally used in HFrEF?

A

calcium channel blockers

659
Q

what category of CCBs should not be used in HFrEF?

A

non-dihydropyridines

660
Q

two examples of non-dihydropyridines?

A

diltiazem and verapamil

661
Q

why do we not use non-dihydropyridines in heart failure?

A

due to their negative inotropic effects

662
Q

what two CCBs are neurtral re: inotropy?

A

almlodipine and felodipine

663
Q

when might amlodipine and felodipine be used in HFrEF?

A

if additional control of HTN or angina is needed

664
Q

why can amlodipine and felodipine be used in HFrEF?

A

neutral re: inotropy

665
Q

are cardiac glycosides considered a first line therapy?

666
Q

do cardiac glycosides affect mortality?

667
Q

at what EF are cardiac glycosides used?

668
Q

when are cardiac glycosides used in HFrEF?

A

EF<40% and are on other standard therapy

669
Q

drug? Slows conduction through the sinoatrial node

A

ivrabradine

670
Q

what does ivrabradine do?

A

slows conduction through the sinoatrial node

671
Q

at what heart rate is ivabradine contraindicated?

A

pre-treatment heart rate <60 bmp

672
Q

pre-treatment HR <60 bpm is a contraindication for what drug?

A

ivrabradine

673
Q

what drug assists with keeping heart rate out of the 70-100 bpm range?

A

ivrabradine

674
Q

elevation of what correlates with worse outcomes in HF?

A

heart rate

675
Q

when is hydralazine + a nitrate used?

A

vasodilation for those intolerant to the ARNI, ACEIs, or ARBs

676
Q

what effect does hydralazine + a nitrate have on afterload?

A

decrease afterload

677
Q

what two effects does hydralazine + a nitrate have?

A

decrease afterload and open coronary arteries for those with myocardial ischemia

678
Q

what does opening of coronary arteries improve?

A

improved oxygen delivery

679
Q

where does ivrabradine slow conduction?

A

sinoatrial node

680
Q

dietary considerations for HFrEF?

A

avoid all simple carbohydrates and sodium

681
Q

maintain lean body weight, avoid all simple carbohydrates, regular strength training, aerobic exercise- nonpharm therapy for what?

682
Q

what are two examples of myocardial toxins that should be avoided?

A

ETOH, cocaine

683
Q

smoking cessation is important in what disease process?

684
Q

unstable bronchospastic disorders like asthma, contraindication for what drug class?

A

beta blockers

685
Q

what drug class? Gold standard to help reduce second cardiac event post-MI

A

beta blockers

686
Q

why should beta blockers be used for patients with diabetes who have major blood glucose variation ranges?

A

they decrease insulin secretion and may mask many signs of hypoglycemia

687
Q

what drug inhibits the enzyme that converts T4 to T3 and has iodine as a major component?

A

amiodarone

688
Q

what drug has a major risk for patients with underlying predisposition to thyroid disease?

A

amiodarone

689
Q

patients taking amiodarone are at risk for what two thyroid disorders?

A

thyrotoxicosis and hypothyroidism

690
Q

what drug inhibits the enzyme that converts T4 to T3?

A

amiodarone

691
Q

what enzyme does amiodarone inhibit?

A

the enzyme that converts T4 to T3

692
Q

what side effect does hydralazine sometimes induce?

A

lupus-like syndrome

693
Q

per the ADA, when might a less stringent A1C goal be used?

A

extensive comorbid conditions

694
Q

what might be the A1c goal for a patient with extensive comorbid conditions?

695
Q

when is nasally inhaled human insulin contrindicated?

A

patients who smoke or have a history of chronic lung disease

696
Q

do biguanides affect gastric emptying?

697
Q

are meglitinides insulin secretagogues?

698
Q

do meglitinides affect gastric emptying?

699
Q

do sulfonylureas cause an increase in endogenous insulin secretion by the beta cells of the pancreas?

700
Q

do sulfonylureas delay gastric emptying?

701
Q

what class should not be used if these conditions? Bowel disease, IBD, r/f bowel obstruction, colonic ulceration, chronic intestinal disease associated with marked digestive disorders; conditions that may deteriorate w/ increased gas in intestine

A

alpha-glucosidase inhibitors

702
Q

class? Delaying the absorption of complex carbohydrates

A

alpha-glucosidase inhibitors

703
Q

class? Inhibit the reabsorption of glucose in the kidney

A

SGLT2 inhibitors

704
Q

term? Inhibiting glucose production in liver and muscle cells

A

glycogenolysis

705
Q

drug? Enhancing fat storage and prevents mobilization of fat for energy

706
Q

drug? Lowers blood glucose levels by stimulating glucose entry into the cell

707
Q

migraine prophylaxis is an off-label indication for what class?

708
Q

what CCB is most commonly used for migraine prophylaxis?

709
Q

Raynaud’s is an off-label indication for what class?

A

Type 2 CCBs

710
Q

which type of CCBs are used for Raynaud’s?

A

Type 2 CCBs

711
Q

why are type 2 CCBs choice drug for Raynauds?

A

because of their peripheral vasodilating effects and some platelet inhibition

712
Q

what is the drug of choice for Raynauds? (specific drug)

A

long-acting nifedipine

713
Q

off-label use of what class? Mild esophageal spasm- transient improvement

714
Q

what drug can be used off label for mild esophageal spasm?

715
Q

what drug can worsen GERD when treating mild esophageal spasm?

716
Q

what type of CCBs are effective in treatment of stable and exertional angina?

A

type 1 and type 2

717
Q

CCBs- peripheral vasodilation and negative inotropism- reduce what?

A

oxygen demand

718
Q

CCBs- dilation of coronary arteries increases what?

A

oxygen supply

719
Q

does decreasing the dose of an ACEI minimize the dry hacking cough?

720
Q

switching to WHAT from an ACEI can help with dry cough?

721
Q

what is a rare, life-threatening condition that can occur with metformin?

A

lactic acidosis

722
Q

why can metformin cause lactic acidosis?

A

accumulation of lactic acid during treatment

723
Q

what is the most common adverse reaction of metformin?

A

GI disturbance

724
Q

what is the only oral agent approved for use in children by the FDA?

725
Q

DPP-4 inhibitor in children?

726
Q

meglitinides in children?

727
Q

metformin in children?

728
Q

can a basal insulin be used for hyperglycemia in children?

A

yes, but would not be an initial medication for T2DM

729
Q

what two drug classes are most associated with erectile dysfunction?

A

beta blockers and thiazide diuretics

730
Q

what is the beta blocker LEAST likely to cause ED and may even improve ED symptoms?

731
Q

diffuse myalgias, muscle tenderness, weakness, and elevations in CK- consider what diagnosis?

732
Q

impaction is associated with what drug class?

A

bile-acid sequestrants

733
Q

what drug class blocks synthesis of cholesterol in the liver by competitively inhibiting HMG-CoA reductase activity?

734
Q

what drug class induces an increase in high-affinity LDL receptors, resulting in increased catabolism of LDL and increase in liver’s extraction of LDL precursors

735
Q

drug class? Increase lipolysis of triglycerides via lipoprotein lipase

A

fibric acid derivatives

736
Q

decrease in VLDL related to decreased secretion by the liver- class?

A

fibric acid derivatives

737
Q

class? Exchange chloride ions for negatively charged bile acids

A

bile acid sequestrants

738
Q

class? Promoting a 10-fold increase in bile acid excretion

A

bile acid sequestrants

739
Q

class? Increased clearance results in enhanced conversion of cholesterol to bile acids by the liver

A

bile acid sequestrants

740
Q

class? Increased uptake of LDL from plasma results from the upregulation of high-affinity LDL receptors on cell membranes, especially in the liver

A

bile acid sequestrants

741
Q

what isoenzymes are involved in the metabolism of CCBs?

742
Q

why should grapefruit juice be avoided with CCBs?

A

drugs like CCBs that inhibit CYP3A4 isoenzymes may increase free drug levels

743
Q

what drug class has the most potential for hypoglycemia?

A

sulfonylureas

744
Q

DPP4 risk for hypoglycemia?

745
Q

what is the purpose of antithyroid agents?

A

inhibit the synthesis of thyroid hormones

746
Q

what happens to TSH in hyperthyroidism?

A

elevated TSH

747
Q

what drug inhibits the peripheral conversion of thyroxine (T4) to T3?

A

propylthiouracil

748
Q

canagliflozin- urine dipstick for glucose?

A

expected to show positive (intended consequence of the medication)

749
Q

for patients with a history of gout or renal calculi, why is cautious use of diuretics suggested?

A

potential for hyperuricemia

750
Q

high levels of WHAT may occur with all diuretics?

751
Q

what three diuretic classes are most likely to cause hyperuricemia?

A

thiazide, loop, spironolactone

752
Q

what is the least likely diuretic to cause hyperuricemia?

A

indapamide/lozol

753
Q

persistent, severe abdominal pain that may be accompanied by vomiting are hallmark symptoms of what?

A

pancreatitis

754
Q

what two labs are used to monitor thyroid function in hypothyroidism?

A

TSH and free T4