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Pharmacology > Exam 2 Drug Classes > Flashcards

Exam 2 Drug Classes Flashcards

1
Q

MOA of antacids

A
  • neutralize gastric acidity
  • increases stomach pH from 1.3-3.5
  • symptomatic relief and some ulcer healing
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2
Q

antacids medications

A

calcium carbonate (Tums)

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3
Q

AE of antacids

A
  • motility of gastric system
  • DDI, increased pH reduces absorption of acidic groups
  • electrolyte imbalance
  • do not take within 2 hours of other oral meds
  • take with foods
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4
Q

MOA of H2 receptor antagonists

A

reduce the secretion of stimulated acid

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5
Q

indication for H2 receptor agonist

A

treats acid reflux and heal ulcers

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6
Q

H2 receptor agonist medications

A

ranitidine (Zantac)

famotidine (Pepcid)

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7
Q

AE of H2 receptor agonists

A
  • diarrhea
  • muscle pain
  • rashes
  • cimetidine inhibits P450 enzymes and can cause gynecomastia
  • take on empty stomach
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8
Q

MOA of PPI

A

irreversibly inhibits ATPase pump and blocks final steps in acid secretion into stomach

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9
Q

indication of PPI

A

treat acid reflux and heal ulcers (most effective)

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10
Q

PPI medications

A

omeprazole (Prilosec)

esomeprazole (Nexium)

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11
Q

AE of PPIs

A
  • generally well tolerated
  • long term use gastric polyps, altered calcium reabsorption, cvd abnormalities
  • take on empty stomach
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12
Q

what are the 3 mucosal protectors

A
  1. bismuth chelate
  2. sucralfate
  3. misoprost
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13
Q

MOA of bismuth chelate

A
  • coat ulcers
  • increase gastric mucous
  • protects against H. pylori induced ulcers
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14
Q

MOA of sucralfate

A
  • aluminum salt that coats the ulcer
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15
Q

indication of sucralfate

A

high-risk cases

  • trauma
  • burns
  • ARDS
  • major surgery
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16
Q

MOA of misoprostol

A

PGE2 that inhibits acid secretion

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17
Q

indication of misoprostol

A

prevent NSAID induced ulcers

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18
Q

what is the combo therapy used to treat H. plylori infection

A

acid controlling drug + antibiotic

(usually PPI + 2 antibiotics)
- can eliminate bacterium within one week

  • if NSAID ulcer use GI friendly COX2 inhibitor)
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19
Q

MOA anticholinergics

A

binds to ACh receptor on vestibular nuclei and blocks communication

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20
Q

indication of anticholinergics

A

motion sickness related vomiting

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21
Q

AE of anticholinergics

A
  • dizziness
  • drowsiness
  • dry mouth
  • blurred vision
  • dilated pupils
  • cant see, spit, pee or poo
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22
Q

anticolinergic antiemetic medication

A

scopolamine (Transderm Scop)

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23
Q

MOA antiemetic antihistamines

A

inhibit vestibular input to CTZ

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24
Q

indication antiemetic antihistamines

A

motion-sickness related vomiting

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25
Q

antiemetic antihistamine medications

A

meclizine

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26
Q

AE antiemetic antihistamines

A

dizziness and sedation

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27
Q

MOA neuroleptic drugs

A

block dopamine receptors in CTZ

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28
Q

indication for neuroleptic drugs

A

post op N/V and chemo-induced vomiting

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29
Q

AE of neuroleptic drugs

A
  • OH
  • tachycardia
  • blurred vision
  • dry eyes
  • urinary retension
  • long term use can lead to extrapyramidal sx
    TONS
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30
Q

MOA of prokinetic drugs

A
  • block dopamine in CTZ

- produce central and peripheral antiemetic effects

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31
Q

indicator of prokinetic drugs

A

nausea and vomiting

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32
Q

AE of prokinetic drugs

A
  • diarrhea, weakness, prolactin release
  • prolonged use causes extrapyramidal signs, motor restlessness
  • hypo- and hypertension, tachycardia
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33
Q

MOA of serotonin blockers

A

block serotonin receptors in GI tract, CTZ, and vomiting center

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34
Q

Indication of serotonin blockers

A

used to prevent vomiting

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35
Q

prokinetic medications

A

metoclopramide

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36
Q

serotonin blockers medications

A

ondansetron

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37
Q

AE of serotonin blockers

A
  • HA
  • dizziness
  • diarrhea
  • no extrapyramidal signs
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38
Q

what may be used in combo with serotonin blockers to control chemo-induced emesis

A

corticosteroids

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39
Q

neurokin - 1 receptor blockers MOA

A

blocks substance p from binding, prevents both central and peripheral

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40
Q

indication for neurokinin-1 receptor blockers

A

used to prevent emesis from chemotherapy

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41
Q

AE of neurokinin-1 receptor blockers

A
  • sedation
  • GI issues
  • stevens johnson syndrome (life threatening rash)
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42
Q

MOA of cannabinoids

A

is unclear

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43
Q

indication for cannabinoids

A
  • used to block acute and delayed emesis

- used for chemo-induced n/v

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44
Q

AE of cannabinoids

A
  • ataxia
  • light headedness
  • blurred vision
  • dry mouth
  • weakness
  • tachycardia or bradycardia
  • CNS sx (being stoned)
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45
Q

indication of phosphorated carbohydrate solution (Emetrol)

A

used for mild cases of intestinal flu or food-borne causes

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46
Q

MOA of phosphorated carbohydrate solution (Emetrol)

A

relaxes GI tract smooth muscle

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47
Q

Drug classes used to treat Nausea and vomiting

A
  • anticholinergics
  • antihistamines
  • neuropletic drugs
  • pro kinetic drugs
  • serotonin blockers
  • neuokinin-1 receptor blockers
  • cannabinoids
  • phosphorated carbohydrate solution (Emetrol)
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48
Q

indication for absorbents

A

diarrhea

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49
Q

MOA of absorbents

A

binds to bacteria causing diarrhea to carry them out with feces

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50
Q

absorbent medications

A

bismuth subsalicylate (Pepto-Bismol)

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51
Q

AE of absorbents

A
  • aspirin products: so use with caution in children recovering from the flu/chickenpox bc of Reye’s syndrome
  • increased bleeding time
  • GI bleed
  • tinnitus
  • decrease effectiveness of many drugs
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52
Q

MOA antidiarrheal anticholinergics

A

reduce peristalsis of GI tract, inhibits the PNS

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53
Q

AE of antidiarrheal anticholinergics

A

tons of anticholinergic AEs

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54
Q

MOA of intestinal flora modifiers

A

resides in intestines to keep “bad” bacteria in check . helps restore normal gut balance

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55
Q

indications of intestine flora modifiers

A

good to use while taking antibiotics for diarrhea

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56
Q

MOA of opiates

A
  • decrease GI motility and propulsion

- slows transit time in intestines

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57
Q

indication of opiates

A
  • can be used to reduce pain

- diarrhea

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58
Q

opiates for antidiarrheal - medications

A

dipenoxylate (Lomotil)

- has added atropine to prevent recreational opioid use

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59
Q

AE of opiates

A
  • sedation
  • dizziness
  • constipation
  • nausea
  • vomiting
  • respiratory depression
  • bradycardia
  • hypotension
  • urinary retention
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60
Q

classes of antidiarrheal agents

A
  • absorbents
  • anticholinergics
  • intestinal flora modifiers
  • opiates
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61
Q

classes of medications for constipations

A
  • bulk forming laxatives
  • hyperosmotic laxatives
  • saline laxatives
  • emollient laxatives
  • stimulant laxatives
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62
Q

MOA of bulk forming laxatives

A

increases water absorption to soften and increase bulk of intestinal contents

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63
Q

bulk forming laxatives medications

A
  • methycellulose (Citrucel)
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64
Q

hyperosmotic laxatives MOA

A

draws fluid into the colon to increase stool fluid content

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65
Q

hyperosmotic medications

A
  • lactulose

- polyethylene glycol 3350 (Miralax)

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66
Q

AE of hyperosmotic medications

A
  • abdominal bloating
  • rectal irritation
  • electrolyte imbalance: dont use with heart issues
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67
Q

MOA of saline laxatives

A

pushes water/electrolytes into intestines

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68
Q

AE of saline laxatives

A

salts may cause issues with individuals with diminished cardiac or renal failure

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69
Q

MOA of emollient laxatives

A

facilitate water and fat absorption into the stool, lubricates

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70
Q

emollient laxative medications

A

decussate sodium (Colace)

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71
Q

AE of emollient laxatives

A
  • skin rash
  • decreased vitamin absorption
  • electrolyte imbalance
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72
Q

MOA of stimulant laxatives

A

stimulates peristalsis through enteric nervous system

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73
Q

Stimulant laxative medications

A

Senna

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74
Q

AE of stimulant laxative medications

A

dependence with long term use and damage to intestinal cells/loss of colon function

NOT best for long term constipation issues

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75
Q

what nervous system are anticholinergics associated with?

A

PNS

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76
Q

what neurotransmitter bings cholinergic receptors?

A

acetylecholine

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77
Q

what are the two types of cholinergic receptors?

A
  • muscarinic

- nicotinic

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78
Q

what are the AEs of anticholinergic drugs

A 
- cant see, spit, pee, shit
ABCDs
- agitation
- blurred vision
- constipation and confusion
- dry mouth
- stasis of urine and sweat
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79
Q

what are contraindications to taking an anticholinergic drug

A

avoid (esp systemic use) if history of urinary retention, narrow angle closure glaucoma

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80
Q

Indication of atropine

A
  • pre-surgery or end of life care of decrease saliva and secretions
  • mydriasis for eye exams
  • treat poisoning from muscarinic-containing mushrooms, organophosphates, insecticides, or nerve agents
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81
Q

MOA inhaled anticholinergic (aka antimuscarinics)

A

primarily bind M3 in airway smooth muscle to bronchodilate

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82
Q

indication of an inhaled anticholinergic

A

asthma and COPD

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83
Q

anticholinergic medications

A
  • SAMA

- LAMA or LAAC

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84
Q

AE of inhaled anticholinergics

A

dry mouth, but generally well tolerated

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85
Q

MOA of anticholinergics used to treat overactive bladder (patch)

A

antagonize muscarinic receptors on bladder smooth muscle = decrease contraction

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86
Q

what are the uses for anticholinergic drugs

A

COPD, asthma, parkinson’s disease, OAB, motion sickness, decreasing saliva/secretions pre-surgery, treating poisonings, ophthalmic exams

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87
Q

AE of anticholinerics for Parkinson’s

A

may produce extrapyramidal sx

- aka drug induced movement disorders

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88
Q

moa of anticholinergics for parkinson’s

A

block M1 receptors in CNS, may also increase dopamine which plays a role in PD

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89
Q

what receptor types do antihistamines act on?

A

histamine and muscarinic

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90
Q

1st generation antihistamines (H1 antagonists) AEs

A
  • bind to histamine receptors in periphery and CNS (more sedation)
  • bind muscarinic receptors (anticholinergic AE)

(Crosses BBB)

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91
Q

indication of 1st gen H1 antagonists (antihistamines)

A

used for allergies, sleep aid, motion sickness, N/V

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92
Q

2nd generation antihistamines AE

A

Does not cross BBB so not as many sedative effects. generally well tolerated

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93
Q

indication of anticholinergic - antidepressants

A

TCAs (tricyclic antidepressants)

- used for depression, OCD, bulimia, neuropathy and more

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94
Q

MOA anticholinergic antidepressants

A

varies by product
- primarily act by increasing serotonin and NE

H1 antagonists (sedating) 
muscarinic antagonists
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95
Q

AE anticholinergic antidepressants

A
  • can have anticholinergic AEs

- prolong QTc (deadly in overdose)

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96
Q

MOA anticholinergic muscle relaxers

A

serotonin antagonism, also binds muscarinic receptors

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97
Q

MOA anticholinergic antipsychotics

A

antagonize alpha adrenergic, serotonin, dopamine, histamine, and muscarinic receptors to varying degrees

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98
Q

MOA anticholinergic anti arrhythmics

A

primary action is to inhibit sodium channels but also binds muscarinic receptors

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99
Q

when to avoid anticholinergics in elderly

A
  • be aware all the time!!

- avoid in delirium, dementia, cognitive impairment, urinary retention, lower urinary tract sx, BPH

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100
Q

MOA direct acting cholinergic drugs

A

act directly on muscarinic receptors

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101
Q

MOA indirect acting cholinergic drugs

A

inhibit acetylcholinesterase (AChE)

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102
Q

uses of cholinergic drugs

A

glaucoma, GI disorders, urinary retention, alzheimer’s disease, diagnosis of myasthenia graves

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103
Q

MOA cholinergic drugs for glaucoma

A

meds stimulate muscarinic receptors in the eye

  • miosis
  • constrict ciliary muscle
  • decrease resistance to aqueous humor outflow
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104
Q

when to use cholinergic drugs for urinary retention

A
  • neurogenic bladder

- post surgery (potentially due to atropine given before surgery)

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105
Q

why take cholinergic drugs for alzheimers?

A

alzheimer’s is associated with decreased levels of ACh

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106
Q

MOA cholinergic drugs for Alzheimer’s

A

reversibly bind AChE so it does not break down ACh

- overtime may be less effective bc of disease progression (decrease in cholinergic receptors)

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107
Q

AE of cholinergic drugs from alzheimers

A
  • varies some by product
  • GI (n/v/d)
  • less AEs with patch
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108
Q

what are the off-label uses for alzheimer’s disease medication

A

Lewy-Body dementia

traumatic brain injury cognitive impairment

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109
Q

what is myasthenia gravis

A

antibodies bind nicotinic ACh receptors in neuromuscular junction = inability to maintain muscular contractions

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110
Q

how to cholinergic drugs help dx of myasthenia gravis

A

edrophonium is administered and if muscle strength temp improves this assist dx

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111
Q

cholinergic AEs

A

SLUDGE
- sweating, lacrimation, urination, diarrhea, GI cramping, emesis

DUMBELLS
- diarrhea, urination, mitosis, bradychardia, emesis, lacrimation, lethargy, salvation/sweating

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112
Q

contraindications to cholinergic medications

A
  • hx of COPD or asthma
  • urinary tract obstruction
  • PD
  • PUD
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113
Q

therapeutic concerns with direct and indirect acting muscarinic agents (cholinerginic drugs)

A
  • significant CVD effects
  • decreased CO
  • hypotension
  • GI issues
  • lungs
  • frequent urination
  • increase secretions
  • cholinesterase inhibitors - syncope - pacemaker placement
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114
Q

therapeutic effects of anticholinergic drugs

A

atropine

  • dry mouth in low doses
  • blurred vision in higher doses
  • blocked vagal effects
  • constipation, urinary retention
  • high doses have CNS effects

tachycardia and hyperthermia

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115
Q

what nervous system to adrenergic drugs act on

A

SNS

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116
Q

adrenergic agonists =

A

sympathomimetic

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117
Q

adrenergic antagonists =

A

sympatholytic

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118
Q

amphetamine MOA

A
  • sympathomimetic indirect acting adrenergic drug

- taken up by NE receptors which leaves more NE available to have effect

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119
Q

indications of amphetamine

A

used for ADHD and narcolepsy

- increases alertness and decreases fatigue

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120
Q

amphetamine AE

A
  • increased BP and HR
  • decreased appetite
  • enters the CNS and stimulates dopamine receptors = euphoria = abuse potential
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121
Q

cocaine MOA

A

sympathomimetic indirect acting adrenergic drugs

- inhibits reuptake of NE

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122
Q

indication of cocaine

A

used topically during nasal surgeries

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123
Q

cocaine AEs

A

significant vasoconstriction = hypertensive crisis

  • MI
  • stroke
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124
Q

ephedrine MOA

A

sympathomimetic indirect acting adrenergic drugs

  • stimulates adrenergic receptors, facilitates NE release, enters CNS - similar impact to amphetamine
  • synthetic in chinese herbal remedies
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125
Q

indication of ephedrine

A

marketed for increased energy, not regulated by FDA

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126
Q

classes of antihypertensive drugs

A
  • diuretics
  • calcium channel blockers
  • beta blockers
  • ACE inhibitors
  • ARBs
  • central acting alpha agonist
  • nitrates
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127
Q

MOA diuretics

A

act directly on the nephron to limit water and sodium reabsorption

  • increase excretion of NA and water by kidneys
  • increases amount of urine formed
  • decreases blood volume
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128
Q

what is the recommended initial therapy for all HTN pts

A

diuretics

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129
Q

loop diuretics MOA

A

act primarily on ascending loop of Henle and inhibit reabsorption of Na/K/Cl which prevents reabsorption of water
- increases urine production

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130
Q

loop diuretic classification

A

moderate antihypertensive, strong diuretic

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131
Q

thiazide diuretic classification

A

powerful antihypertensive, moderate diuretics

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132
Q

what are the 3 major classifications of diuretics

A
  • loop
  • thiazide
  • potassium-sparing
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133
Q

examples of loop diuretics

A

furosemide (Lasix)

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134
Q

AE loop diuretics

A

dehydration, hypokalemia, hyponatremia, hypocalcemia, toxicity, hyperglycemia, increased LDLs

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135
Q

thiazide diuretics MOA

A
  • act on early part of distal convoluted tubule

- Na and K excretion and reabsorption of Ca

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136
Q

what type of diuretic is the primary choice for HTN

A

thiazide diuretics

- lowers systolic BP more than other classes of antihypertensive drugs

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137
Q

in what populations are thiazide diuretics especially indicated?

A
  • better for individuals prone to renal calculi

- favored for older adults to reduce Ca loss and maintain bone mass

138
Q

examples of thiazide diuretic drugs

A

hydrochlorothiazide (Microzide)

HCTZ

139
Q

AE of thiazide diuretics

A
  • dehydration
  • hyponatremia
  • hypercalcemia
  • significant K loss
  • increased LDLs
140
Q

MOA potassium sparing diretics

A
  • interferes with the sodium-potassium exchange in distal convoluted tubules
  • limits reabsorption of Na
  • reabsorbes more K
141
Q

indication for potassium sparing diuretics

A
  • someone with electrolyte imbalance
142
Q

AE of potassium sparing diuretics

A
  • hyperkalemia
  • lethargy, mental confusion
  • gynecomastia in males
  • menstrual irregularities in females
143
Q

potassium sparing diuretic medications

A

spironolactone

144
Q

indication of direct vasodilators

A

used to treat hypertensive crisis

ex. diastolic over 120

145
Q

MOA of direct vasodilators

A

directly vasodilates the peripheral vasculature

- inhibits smooth muscle contraction in the arterioles

146
Q

AE of direct vasodilators

A

dizziness, OH

147
Q

MOA of calcium channel blockers

A

block Ca entrance into vascular smooth muscles

  • reduces smooth muscle tone which allows for vasodilation
  • decreases contractility, CO, and energy demands on the heart
148
Q

indication for calcium channel blockers

A

HTN, angina, arrhythmias

- useful when beta blockers are contraindicated (asthma, DM, PVD)

149
Q

AE of calcium channel blockers

A
  • HA
  • dizziness
  • hypotension
  • bradycardia
  • reflex tachycardia
  • sweating
  • tremor
  • flushing
  • constipation
150
Q

what are the three classes of calcium channel blockers

A
  1. dihydropyridines
    - reduce arterial tone
  2. phenylklylamines
    - affects the heart
  3. benzodiazepines
    - affects heart and vasculature
151
Q

calcium channel blocker medications

A
  • amlopdipine

- diltiazem

152
Q

indication for b blockers

A

HTN, angina, arrhythmia, post-MI survival

153
Q

b blocker effects on the heart

A
  • reduced contractility
  • reduced HR
  • reduced peripheral vascular resistance

and in return reduced BP!

154
Q

non selective b blockers act on….

A

block b1 and b2 adrenoceptors

155
Q

selective b blockers act on….

A

block only b1 receptors

  • selectivity is lost at high doses
  • use if pt has pulmonary issues
156
Q

b blocker MOA

A
  • lol
  • reduce sympathetic influences
  • prevents normal ligand from binding to receptor by competing for the site
157
Q

non selective b blocker medication

A

propranolol (Inderal)

158
Q

selective b blocker medications

A

metoprolol (Lopressor)

carvedilol (Coreg)

159
Q

non selective b blocker AEs

A

related to receptor blocking action

  • peripheral vasoconstriction
  • bronchoconstriction
  • bradycardia
  • reduce exercise capacity
  • abrupt withdrawal drug triggers arrythmia, angina, MI
  • dizziness
  • OH
  • depression
  • fatigue
  • sexual disfunction
160
Q

cardoselective b blockers AEs

A

related to receptor blocking action

  • peripheral vasoconstriction
  • bradycardia
  • reduce exercise capacity
  • abrupt withdrawal drug triggers arrythmia, angina, MI
  • dizziness
  • OH
  • depression
  • fatigue
  • sexual disfunction
161
Q

a-adrenoceptor blockers MOA

A
  • azosin
  • reduce sympathetic tone of blood vessels to decrease peripheral vascular resistance
  • shown to lower LDL and triglyceride levels
162
Q

indication of a-adrenoceptor blockers

A

used as add-on drugs to reduce BP, never used first

163
Q

AE of a-adrenoceptor blockers

A
  • OH
  • nasal stuffiness
  • reflex tachycardia
  • arrhythmia
164
Q

indication for dual a and b blockers

A

used for individuals who have increased PVR with pure b-blockers

165
Q

dual a and b blocker medication

A

carvedilol

4:1 beta to alpha blockade

166
Q

central acting a2 agonists for HTN

A
  • clonidine

- methyldopa

167
Q

central acting a2 agonists MOA

A

a2 receptor on presynaptic neurons, stimulates CNS, decreases NE production to decrease peripheral resistance, renal vascular resistance, HR and BP

168
Q

AE of central acting a2 agonist

A
  • dizziness
  • drowsiness
  • fatigue
  • headache
169
Q

indication for central acting a2 agonist - clonidine

A
  • used for resistant HTN

- ADHD, vasomotor menopausal sx, tourettes syndrome, adjust pain control

170
Q

AE specific to central acting a2 agonist - clonidine

A
  • dry mouth

- rash with patch but patch typically decreases AEs

171
Q

indication for central acting a2 agonist - methyldopa

A

first line option for HTN in pregnancy

172
Q

ACEi indication

A

HTN, rEF HF, post MI, post stroke, kidney disease

173
Q

MOA ACEi

A
  • pril
  • block conversation of angiotensin I to angiotensin II to increase blood vessel vasodinaltion to ultimately decrease Na and H2O retention

ONLY blocks angiotensin II by RAAS pathway

174
Q

AEs of ACEi

A
  • dry cough
  • angioedema
  • hypotension
  • hyperkalemia
  • acute renal failure
175
Q

ARB MOA

A
  • sartan

- antagonist at AT1 receptor to block binding of angiotensin II

176
Q

ACEi medications

A

lisinopril
enalapril
ramipril

177
Q

indication of ARBs

A

use as alternative if ACEi-intolerant in HTN, kidney disease, HF

178
Q

AE of ARBs

A
  • similar to ACEi but no dry cough
  • hypotension
  • hyperkalemia
  • acute renal failure
179
Q

ARB medications

A

losartan

valsartan

180
Q

what are the sympathomimetics - indirect acting adrenergic drugs?

A

cocaine
amphetamine
ephedrine

181
Q

MOA of sympathomimetics - indirect acting adrenergic drugs

A

release store NE or inhibit reuptake

182
Q

drug classes used for angina treatment

A
  • nitrates
  • b blockers
  • calcium channel blockers
183
Q

Nitrates MOA

A

unknown BUT thought to vasodilate by acting on smooth muscle

- decrease preload and after load to reduce the workload of the heart and lower O2 demands

184
Q

what forms can nitrate be given

A
  • IV
  • sublingual spray, chewable, oral tablets
  • topical transdermal
185
Q

what is the drug of choice for acute angina attacks

A

sublingual nitrates

  • immediate sx releif
  • can be administered before activity to prevent sx
186
Q

nitrate medications

A

nitroglycerin

isosorbide mononitrate

187
Q

how to store nitrates

A
  • limit light exposure
  • short shelf life (6 mo unopened, 3 mo once opened)
  • tingling sensation to know it is active
188
Q

dosing of nitrates

A
  • after 1 dose, relief should onset w/ in 1-2 mins
  • 2nd dose if sx still present after 5 mins
  • up to 3 doses in a 15 min period
189
Q

AE of nitrates

A
  • reflex tachycardia
  • dizziness
  • OH
  • weakness
190
Q

what drug classes are used to predict angina (not used when angina occurs)

A
  • b blockers

- calcium channel blockers

191
Q

when a cardiac event is suspected immediately take…

A

chew 325mg non-enteric coated aspirin

- will prevent clots from forming

192
Q

what are the three classes of antithrombotics

A
  • antiplatelets
  • anticoagulants
  • fibrinolytics
193
Q

antiplatelets…

A

prevent thrombus from happening

194
Q

anticoagulants…

A

prevent initial thrombus and prevent extension of current thrombus

195
Q

fibrinolytics…

A

lyse active thrombus

- clot busters

196
Q

antiplatelet classes

A
  • aspirin
  • ADP receptor inhibitors (irreversible)
  • ADP receptor inhibitors (reversible)
197
Q

aspirin MOA

A

inhibits COX 1 and 2 to inhibit platelet aggregation

- at low doses (81mg) primarily inhibits COX 1 for cardiovascular protection

198
Q

aspirin AE

A

BLEEDING RISK

199
Q

ADP receptor inhibitors (irreversible) MOA

A
  • P2Y12 inhibitors
  • prevents platelet aggregation by blocking ADP binding
  • irreversibly blocks P2Y12 receptor on platelets
  • decreases platelet aggregation for lifespan of platelet (7-10 days)
200
Q

indication for ADP receptor inhibitors (irreversible)

A

used after acute coronary syndrome with PCI (stent placement)

201
Q

ADP receptor inhibitors (irreversible) AEs

A
  • generally well tolerated
  • BLEEDING RISK
  • decreased efficacy in 50% of asians, 30% AA, 25% caucasians
202
Q

ADP receptor inhibitors (irreversible) medications

A

clopidorgrel (Plavix)

- pro drug!! CYP2C19 to active metabolite

203
Q

ADP receptor inhibitors (reversible) MOA

A
  • blocks ADP mediated activation to decrease platelet aggregation
  • reversibly binds P2Y12 receptor on platelet surface
204
Q

ADP receptor inhibitors (reversible) indication

A

used with acute coronary syndrome

- up to 1 year or more after NSTEMI or STEMI

205
Q

ADP receptor inhibitors (reversible) AEs

A

BLEEDING RISK

206
Q

classes of anticoagulants

A
  • heparin
  • LMWH
  • fondaparinux
  • direct thrombin inhibitors
  • vitamin K antagonist
  • factor XA inhibitors
207
Q

what are the DOAC drugs

A

all really eliminated
direct oral anticoagulant
- direct thrombin inhibitor
- factor XA inhibitor

208
Q

heparin MOA

A

increases action of antithrombin which prevents conversion of fibrinogen to fibrin

209
Q

heparin routes

A

IV or subut

210
Q

heparin AEs

A
  • requires platelet monitoring except when using for prophylaxis
  • heparin induced thrombocytopenia
211
Q

heparin reversal agent

A

protamine sulfate

- binds to inactivate heparin

212
Q

LMWH

low molecular weight heparin MOA

A
  • increases antithrombin but has a greater effect on inhibiting FXa than thrombin
213
Q

LMWH medications

A

enoxaparin (Lovenox)

214
Q

LMWH routes

A

IV or subut

215
Q

LMWH compared to heparin

A
  • shorter drug molecule

- preferred bc more simple dosing, no monitoring required, decreased HIT risk

216
Q

LMWH reversal agent

A
  • protamine sulfate (less effective)

- new agent: andexanet alfa (Andexxa), structurally similar to FXa so acts as a decoy

217
Q

fondaparinux (Atrixtra) MOA

A

causes antithrombin-mediated selective inhibition of FXa

218
Q

fondaparinux (Atrixtra) advantages

A
  • once daily dosing

- no hit risk

219
Q

fondaparinux (Atrixtra) routes

A

IV or subut

220
Q

vitamin K antagonist medications

A

warfarin (Coumadin)

221
Q

vitamin K antagonist MOA

A

depletes vitamin K stores to inhibit synthesis of factors VII, IX, X, and II and protein C and S

222
Q

vitamin K antagonist reversal agent

A

vitamin K

223
Q

vitamin K antagonist AEs

A
  • NTI drug
  • frequent INR monitoring
  • genetic variants can increase bleeding risk
  • MANY DDI and food interactions
  • cannot eat too many vitamin K foods
224
Q

INR too low… what is the risk?

A

clotting

225
Q

INR too high… what is the risk?

A

bleed

226
Q

if a pt on vitamin K antagonist eats too much vitamin K…

A

INR will go down which will increase clotting risk

227
Q

PO direct thrombin inhibitor MOA

A

inhibits conversion of fibrinogen to fibrin

228
Q

PO direct thrombin inhibitor AEs

A
  • less intracranial bleeding than warfarin but more GI bleeding
  • beers list for increased risk of GI bleed in 75+
  • dyspepsia (take w food)
229
Q

PO direct thrombin inhibitor reversal agent

A

idarucizumab (Praxbind)

230
Q

factor XA inhibitors MOA

A
  • xaban

- selectively and reversibly binds FXa to prevent fibrinogen from becoming fibrin

231
Q

factor XA inhibitors medications

A

rivaroxaban (Xarelto)

apixaban (Eliquis)

232
Q

factor XA inhibitors AEs

A
  • less intracranial bleeding than warfarin, but Xarelto has more GI bleed (on beers list)
  • Apixaban has the lowest bleeding risk
  • less DDI than warfarin
    xarelto must be taken w food
233
Q

factor XA inhibitors indication

A

usually used with high risk individuals

234
Q

factor XA inhibitors reversal agent

A

andexanet alfa (Andexxa), structurally similar to FXa so acts as a decoy

235
Q

factor XA inhibitors as a DOAC

A

shorter duration of action than warfarin so not preferred if pt is noncompliant
- but more convenient if using before a procedure

236
Q

all antithrombotics…

A

monitor bleeding v clotting

- understand when med is working “too well” or not enough

237
Q

fibrinolytics MOA

A
  • aka thrombolytics

- mimic endogenous TPA, plasmin breaks fibrin links in the thrombus

238
Q

fibrinolytics indication

A

use immediately after a stroke, MI, PE

- aren’t really used long term.. will be transitioned to another drug

239
Q

fibrinolytics route

A

IV

240
Q

VTE treatment in acute setting at diagnosis

A

may start with LMWH or heparin and bridge to PO meds

241
Q

VTE long term treatment

A

1st line: DOAC

2nd: VKA
3rd: LMWH

exceptions

  • use LMWH as 1st line in its with cancer
  • questionable efficacy of DOACs in its with BMI > 40
242
Q

AF treatment

A

1st line: DOAC

2nd: VKA
3rd: aspirin

243
Q

HMG Coa Reductase Inhibitors…

A

“Statins”

244
Q

statin medications

A

atorvastatin (Lipitor)
rosuvastatin (Crestor)
simvastatin
pravastatin

245
Q

statin MOA

A

blocks HMG-CoA reductase = blocks cholesterol sysnthesis

246
Q

statin AEs

A

myalgia

  • usually symmetrical
  • less likely with lower doses
  • less likely with pravastatin and rosuvastatin bc they are hydrophilic
myopathy and rhabomyolysis 
dyspnea
HA
increase liver function enzymes
tendonopathy
247
Q

in what populations is myalgia more likely

A
  • elderly female
  • low BMI
  • asian descent
  • excess alcohol
  • high PA level
  • trauma
  • in combo with other meds
248
Q

what is rhabomyolosis

A

breakdown of muscle, dies and sends toxins to the kidneys

- can cause kidney failure

249
Q

cholesterol absorption inhibitor MOA

A
  • ezetimibe (Zetia)

inhibits absorption of cholesterol in small intestine

250
Q

statin indication

A

atherosclerosis

251
Q

cholesterol absorption inhibitor indication

A

atherosclerosis

252
Q

cholesterol absorption inhibitor AEs

A

generally well tolerated

  • not metabolized in CYP enzymes so far less DDIs
  • less common than statins though bc has not been proven to reduce MI and stroke risk
253
Q

Fibrates

A
  • for atherosclerosis

- generally well tolerated but may increase myopathy risk with statins

254
Q

PCSK9 inhibitor

A
  • for atherosclerosis
  • subcut injection
  • emerging role to reduce mortality in high risk patients .. doesn’t yet do this
255
Q

bempedoic acid (Nexletol)

A
  • 1st non-statin PO in 20 yrs
  • approved adjunct to statin for those with ASCVD who need additional LDL lowering
  • not sure if it decreases risk of MI and stroke yet
  • blocks cholesterol synthesis in the liver
  • AEs: hyperuricemia and tendon rupture
256
Q

atheroclerosis treatment

A

1st line: statin

2nd: ezetimibe added on if uncontrolled or cant have statin
3rd: bile acid sequestrates can be added or PCSK9 inhibitor if very high risk

257
Q

what medication class will decrease edema and congestion

A

diuretics

258
Q

what medication will increase contractility

A

digoxin

259
Q

what medication class will decrease preload and after load

A

vasodilators, ACEi, ARB

260
Q

ARNI (angiotensin receptor-neprilysin inhibitor) medication

A

sacubitril/valsartan (Entresto)

261
Q

sacubitril/valsartan (Entresto) MOA

A

valsartan: vasodilation
sacubitril: inhibits neprilysin enzyme to vasodilate

262
Q

sacubitril/valsartan (Entresto) AEs

A

ARB AEs but higher risk of angioedema

263
Q

Digoxin MOA

A

inhibits Na/K/ATPase pump to increase contractility

ionotripic drug

264
Q

digoxin indication

A

not usually used first bc it does not reduce mortality, but used as an add on in heart failure

265
Q

sacubitril/valsartan (Entresto) indication

A

heart failure combo product

- reduced mortality more than ACEi

266
Q

digoxin AEs

A

NTI

affects Gi, CV, CNS

267
Q

indication of amiodarone

A

used for ventricular arrhythmias

268
Q

amiodarone MOA

A

prolong duration of action potential, blocks K, Na, and Ca channels
- some b blocker activity

269
Q

amiodarone AEs

A
  • VERY long half life
  • TONS of side effects
  • GI problems
  • thyroid disfunction
  • blurred vision
  • ataxia
  • liver toxicity
  • neuropathy
  • bradycardia
  • blue effect
270
Q

classes of drugs used to treat respiratory tract

A
  • decongestants
  • antitussives
  • antihistamines
  • mucolytics and expectorants
271
Q

indication for decongestants

A

nasal stuffiness, allergies, common cold, respiratory tract infections

272
Q

MOA decongestants

A
  • alpha 1 adrenergic agonists
  • cause vasoconstriction
  • reduce blood flow and outflow of capillaries
273
Q

decongestant AEs

A
  • HA, dizziness, nervousness, nausea, CV irregularities, can mimic increased SNS activity
274
Q

contraindications to decongestants

A

HTN

275
Q

indication of antitussives

A

cough suppression
ONLY for dry cough
- recommended for short term use

276
Q

MOA of antitussives

A

decrease afferent nerve activity or decrease coughs center sensitivity

  • acts centrally
  • thicken sputum, reduce clearance
277
Q

antitussive medications

A

codeine and other opioid derivatives

278
Q

antitussive AEs

A

sedation, dizziness, GI upset

- opioid like sx (consultation)

279
Q

antihistamines indication

A

used to manage respiratory and seasonal allergies
(hay fever, cedar fever)
- may be used in asthma

280
Q

antihistamines MOA

A

block histamine receptors on respiratory mucosa OR acts as local anesthetic on respiratory epithelium

  • acts locally
  • reduces sneezing and nasal congestion
281
Q

antihistamines first generation AEs

A

crosses BBB

- sedation, fatigue, dizziness, blurred vision, incoordination

282
Q

antihistamines second generation AEs

A

doesn’t easily cross the BBB

- less side effects, but great amount of variability

283
Q

antihistamines medications

A

1st gen: benadryl

2nd gen: zyrtec, calritin, clarinem, allegra

284
Q

mucolytics indication

A

difficultly cleaving mucous from airway

- nasal congestion

285
Q

mucolytics MOA

A

split disulfide bonds

  • decrease the viscosity of mucus
  • loosens and clears mucus from the airways
286
Q

MOA of expectorants

A

thins mucus and lubricates the irritated respiratory tract

287
Q

indication of expectorants

A

acute and chronic conditions from colds to emphysema or chronic bronchitis

288
Q

inhaled b agonist indication

A

COPD

289
Q

inhaled b agonist MOA

A
  • terol

- agonize b2 receptors to bronchodilate

290
Q

two types of inhaled beta agonists

A

short acting SABAs

long acting LABAs

291
Q

inhaled b agonist medication

A

albuterol (Proventil, Pro Air Ventolin)

SABA

292
Q

SABA

A
  • onset: 5 mins
  • 4-6 hours duration
  • PRN use for SOB
293
Q

LABA

A
  • 12-14 hour duration
  • used for maintenance
  • dose once/twice daily
294
Q

inhaled b agonist AEs

A
  • generally well tolerated

- can cause tachycardia, tremor, hypokalemia, hyperglycemia

295
Q

inhaled antimuscarinics indication

A

COPD

296
Q

inhaled antimuscarinics MOA

A
  • aka antimuscarinics

binds M3, antagonizes ACh to bronchodilate

297
Q

two types of inhaled antimuscarinics

A

short acting SAMA

long acting LAMA

298
Q

SAMA

A

short acting muscarinic antagonist

  • onset: 15-20 mins
  • 6-8 hour duration (longer with neb)
299
Q

inhaled antimuscarinics medications

A

LAMA

tiotropium (Spiriva)

300
Q

LAMA

A

long acting muscarinic antagonist

  • used for maintenance
  • dosed once/twice daily
301
Q

inhaled corticosteroid medication

A

fluticasone (Flovent)

302
Q

inhaled corticosteroid indication

A

COPD, typically used for exacerbations or more severe disease
- unclear safety if used for > 3 years

303
Q

inhaled corticosteroid MOA

A

anti-inflammatory

304
Q

inhaled corticosteroid AE

A
  • if med is stopped monitor!
  • PO steroids have many AE and no evidence of benefit in stable COPD
  • oral candidiasis
  • hoarse voice
  • skin bruising
  • increase risk of pneumonia
    in elderly on high doses
  • osteoporosis
  • cataracts
305
Q

what are the combo products used to treat COPD

A
  • SABA and SAMA
  • LABA and LAMA
  • LABA/ICS
  • LABA/LAMA/ICS
306
Q

SABA/SAMA medication

A

albuterol/ipratopium (Combivent)

307
Q

LABA/ICS medications

A

formoterol/budesonide (Symbicort)

salmeterol/fluticasone (Advair)

308
Q

when are antibiotics used in COPD

A
  • used in acute exacerbations

- extended treatment only in its prone to exacerbations

309
Q

ICS used in asthma - meds

A
  • in peds it may slow growth rate, but also many be due to asthma
310
Q

LABA used in asthma

A
  • used ONLY in combo with ICS
  • helps to lower ICS dose to prevent ICS AEs
  • used for sx reduction, improved lung function and to decrease exacerbatins
311
Q

medication classes used to treat asthma

A
  • ICS
  • SABA and LABA (inhaled b agonist)
  • luekotriene modifiers
  • immunomodulators
312
Q

leukotriene modifies - 2 types

A
  • leukotriene receptor antagonist (LTRA)

- 5-lipoxygenase inhibitor

313
Q

MOA of leukotriene receptor antagonist (LTRA)

A

competitively antagonize leukotriene receptors

314
Q

leukotriene receptor antagonist (LTRA) medications

A

montelukast (Singulair)

- take once daily in the evening for asthma and in the morning for allergies

315
Q

leukotriene receptor antagonist (LTRA) AEs

A
  • very well tolerated
316
Q

leukotriene receptor antagonist (LTRA) indication

A

used as an alternative agent for kids and adults

- often used for asthma+allergies

317
Q

5-lipoxygenase inhibitor MOA

A

inhibits 5-lipoxygenase

318
Q

5-lipoxygenase inhibitor indication

A

used only as an asthma alternative for adults

319
Q

5-lipoxygenase inhibitor AEs

A
  • rare hepatoxicity (monitor LFTs)
320
Q

Immunomodulators: Anti-IgE medications

A

omalizumab (Xolair)

321
Q

Immunomodulators: Anti-IgE MOA

A
  • mab

- binds IgE antibody, limits activation and release of allergic response mediators

322
Q

Immunomodulators: Anti-IgE AEs

A

injection site reaction

- rare by anaphylactic allergic reaction may occur, must be administered in doctors office

323
Q

Immunomodulators: Interleukin Antagonists MOA

A
  • mab

- monoclonal antibodies bind interleukins, decrease eosinophils which are associated with asthma pathologies

324
Q

Immunomodulators: Interleukin Antagonists AEs

A

injection site reaction

325
Q

drug classes used to treat cystic fibrosis

A
  • inhaled b agonist (SABA and LABA)
  • CFTR modulators
  • mucolytics
  • inhaled/PO antibiotics
326
Q

when will bronchodilators be used in CF

A

use LABAs for maintenance

SABAs used prior to

  • chest physiotherapy
  • other inhaled meds that may induce bronchospasm
  • exercise
327
Q

CFTR

A
  • transmembrane regulator protein that regulates sodium and water to keep mucus thin
  • genetic mutations stop CFTR from getting to cell surface
  • ALL over the body
328
Q

MOA of CFTRs

A
  • chloride channels open longer to increase CFTR activity

- facilitates CFTR to cell membrane which will increase chloride transport

329
Q

CFTR medications

A

tezacaftor/ivacaftor (Symdeco)

lumacaftor/ivacaftor (Orkambi)

330
Q

administration of CFTRs

A

PO twice daily or twice weekly

- must take with high fat meals to increase absorption

331
Q

CFTR AEs

A
  • HA
  • GI (pain, N/D)
  • respiratory
    okrambi
  • dizziness and hypertension
332
Q

mucolytics indication

A

used to decrease risk of CF exacerbations, increase lung function and quality of life

333
Q

2 types of mucolytics

A
  • hypertonic saline
  • dornase alfa (Pulmozyme)

use both if you can afford

334
Q

hypertonic saline

A

type of mucolytic

  • neb 2-4 times daily
  • increases hydration of airway mucus
335
Q

dornase alfa (Pulmozyme)

A

type of mucolytic

  • neb daily or twice daily
  • cleaves DNA to decrease mucus viscosity to improve airway
  • AE: chest pain, cough, voice disorder, skin rash
336
Q

indication of inhaled antibiotics

A

CF

  • to decrease risk of exacerbations and increase function and QOL
  • used long term if P. aeruginosa is persistent in cultures

benefit > risk

337
Q

inhaled antibiotics administration

A

neb twice or three times daily x28 days and then 28 days off

338
Q

PO antibiotics for CF

A
  • used to decrease risk of exacerbations
  • can be used w out without P. aeruginosa
  • AE: macrolide AEs
339
Q

nutritional support for CF

A

use fat soluble vitamins that have poor absorption

340
Q

pancreatic enzyme replacement therapy (PERT) for CF

A

take with H2 blockers or PPI to maintain an alkaline environment in the stomach as it can reach the small intestine where it is broken down
- needed prior to every meal or snack

Pharmacology (11 decks)

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