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DPT Semester 1 > Pharmacology Test 2 > Flashcards

Pharmacology Test 2 Flashcards

1
Q

the nervous system can be divided into what two minor systems?

A

CNS and PNS

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2
Q

two subsystems of the PNS

A

1). Autonomic Nervous System 2). Somatic Nervous System

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3
Q

two subsystems of the Somatic Nervous System

A

Sensory (afferent), Motor (efferent)

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4
Q

two divisions of the Autonomic Nervous System

A

Sympathetic and Parasympathetic

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5
Q

what type of receptors does the sympathetic nervous system utilize?

A

Adrenergic

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6
Q

what type of receptors does the parasympathetic nervous system utilize?

A

cholinergic receptors

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7
Q

what are the types of adrenergic receptors?

A

alpha-1, alpha-2, beta-1, and beta-2

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8
Q

what are the types of cholinergic receptors?

A

muscrainic (1, 2, and 3) and nicotinic (neural and muscular)

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9
Q

cholinergic drugs mimic _______

A

the PNS

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10
Q

anticholinergic drugs suppress ______

A

the PNS

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11
Q

adrenergic drugs mimic ______

A

the SNS

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12
Q

alpha and beta-blockers supress _____

A

the SNS

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13
Q

T/F: within the ANS, two neurons link the CNS to the effector organ

A

True

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14
Q

Pre/postganglionic fiber length comparision between SNS and PNS

A

PNS: long mylinated pre and short post

SNS: short mylinated pre and long post

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15
Q

T/F: the synapse between the preganglionic and postganglionic fiber within the ANS is always nicotinic?

A

True

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16
Q

the sympathetic division can be found exiting which region of the spinal cord?

A

thoracolumbar (T1-L2)

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17
Q

the parasympathetic division can be found exiting which regions of the spinal cord?

A

carniosacral (CN 3, 7, 9 and 10; S2-4)

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18
Q

what is the only exception to the 2 neuron rule within the ANS?

A

adrenal gland within the sympathetic division

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19
Q

which division of the ANS will have more extensive branching?

A

sympathetic

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20
Q

which division of the ANS tends to create/cause more discrete reactions affecting only 1 organ/tissue?

A

parasympathetic

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21
Q

effect of SNS on heart?

A

increased HR (beta-1 and beta2),

increased contractility (beta-1 and beta-2)

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22
Q

effect of PNS on heart

A

decreased HR (M2)

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23
Q

SNS effect on lung airway muscles

A

bronchodilation (beta-2)

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24
Q

effect of SNS on lung bronchial secretions

A

increased secretion (beta-2)

decreased secretion (beta-1)

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25
Q

effect of PNS on lung airway smooth muscles

A

bronchoconstriction (M3)

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26
Q

effect of PNS on lung bronchial secretions

A

increased secretion (M3)

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27
Q

effect of SNS on arterioles

A

vasoconstriction of skin and visera (alpha-1, alpha-2)

vasodilation of skeletal muscle and liver (beta-2)

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28
Q

effect of SNS on liver

A

glycogenolysis, gluconeogensis (alpha and beta-2)

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29
Q

effect of PNS on liver

A

glycogen synthesis (M)

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30
Q

catecholamine neurotransmitters

A

dopamine, epinephrine, norepinephrine

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31
Q

if activated an excitatory ligand-gated ion channel would cause ______

A

Na+ or Ca2+ to flow into cell;

K- to flow out

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32
Q

if activated an inhibitory ligand-gated ion channel would cause ______

A

Cl- to flow into cell

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33
Q

Additional neurotransmitters

A

Glutamate, GABA, Dopamine, Serotonin, and Histamine

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34
Q

cholinergic muscarnic receptor primary locations

A

1) . visceral and bronchiole smooth muscle,
2) . Cardiac muscle,
3) . Exocrine glands, salivary,intestinal, lacrimal,
4) . sweat glands

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35
Q

cholinergic muscurinic response to stimulation

A

1) . viseral/bronchiole smooth muscle - contraction
2) . cardiac - decreased HR
3) . glands - increased secretions

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36
Q

alpha-1 receptor locations

A

1) . vascular smooth muscle
2) . intestinal smooth muscle
3) . radial muscle iris
4) . Urinary sphincter
5) . Spleen capsule

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37
Q

stimulation of alpha-1 receptors results in ______ everywhere except ______

A

contraction;

intestinal smooth muscle (relaxation)

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38
Q

location of alpha-2 receptors

A

CNS inhibitory neurons

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39
Q

response of alpha-2 receptors

A

decreased sympathetic discharge from CNS

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40
Q

location of beta-1 receptors?

A

cardiac muscle, kidneys, and fat cells

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41
Q

respones of beta-1 receptors

A

1) . cardiac muscle - increased HR and contractility
2) . kidney - increased renin secretion
3) . fat cells - increased lipolysis

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42
Q

location of beta-2 receptors

A

bronchiole smooth muscles, liver and skeletal muscle arterioles and cell, GI smooth muscle, uterus, gallbladder

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43
Q

response of beta-2 receptors in gallbladder and uterus

A

relaxation

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44
Q

response of beta-2 receptors in skeletal muscle and liver

A

arterioles - vasodilation

cells - increased metabolism and mass

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45
Q

other responses of beta-2 receptors

A

bronchiole smooth muscle - bronchodilation

GI smooth muscle - decreased motility

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46
Q

broad function of anticholinergic drugs?

A

suppress PNS

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47
Q

Key AE of anticholinergic drugs

A

ABCDs

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48
Q

what does ABCDs stand for?

A

agitation, blurred vision, constipation/confusion, dry mouth, stasis or urine and sweat

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49
Q

when should an anticholinergic drug be avoided?

A

1). history of urinary retention, 2). narrow angle closure glaucoma

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50
Q

what are some indications for anticholinergic drugs?

A

COPD, asthma, Parkinson’s, OAB, motion sickness, decreasing saliva/secretions pre-surgery, treating poisoning, opthalmic exams

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51
Q

Atropine indications

A

1). decrease saliva/secretions pre-surgery, 2). treat poisoning

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52
Q

MOA of anticholinergic drugs that treat OAB

A

antagonize muscarinic receptors on bladder smooth muscle => decrease contractions

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53
Q

general MOA of 1st gen antihistamines

A

bind histamine receptors in periphery and CNS = more sedation

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54
Q

general MOA of 2nd gen antihistamines

A

less muscarinic receptor binding = less anticholinergic effects

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55
Q

general MOA of antidepressants

A

primarily increases serotonin and NE; H1 antagonists (sedating) and muscarinic antagonists

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56
Q

anticholinergic drug that is an antidepressant

A

TCA (tricyclic antidepressants)

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57
Q

What is the Beers List?

A

list of potentially inappropriate meds on older adults

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58
Q

drugs on Beers list may worsen what symptoms?

A

delirium, CNS-effect (confusion), urinary retention

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59
Q

two general types of Cholinergic Drugs?

A

Direct Acting, Indirect Acting

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60
Q

Direct Acting cholinergic drugs do what?

A

act directly on muscarinic receptors

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61
Q

Indirect Acting cholinergic drugs do what?

A

inhibit Acetylcholinesterase (AChE)

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62
Q

indications for Cholinergic Drugs

A

glaucoma, GI disorders (paralytic ileus), urinary retention, Alzheimer’s, diagnosis of myasthenia gravis

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63
Q

what is Alzheimer’s Disease associated with?

A

decreased levels of Ach

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64
Q

general MOA of Alzheimer’s drugs

A

reversibly bind AChE so it does not break down ACh (indirect acting)

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65
Q

AE of Alzheimer’s drugs

A

varies but mostly GI (N/V/D)

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66
Q

Cholinergic drugs will do what?

A

enhance the PNS (increase secretions)

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67
Q

Cholingeric AE

A

SLUDGE or DUMBELLS

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68
Q

what does SLUDGE stand for?

A

Sweating, Lacrimation, Urination, Diarrhea, GI cramping, Emesis (vomiting)

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69
Q

What does DUMBELLS stand for?

A

Diarrhea, Urination, Miosis, Bradycardia, Emesis, Lacrimation, Lethargy, Salivation/Sweating

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70
Q

who should avoid Cholinergic drugs?

A

ppl w/history of COPD or asthma, urinary tract obstruction, Parkinson’s, Peptic ulcer disease (PUD)

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71
Q

Therapeutic Concerns for Direct/Indirect acting muscarinic agents?

A

CV effects (bradycardia, decreased CO, syncope, hypotension), GI issues, bronchoconstriction, frequent urination, increased secretions

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72
Q

Atropine AE

A

low doses: dry mouth, high doses: blurred vision, hallucinations, confusion, coma

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73
Q

other Atropine AE

A

tachycardia, decreased bronchial secretions, constipation, urinary retention

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74
Q

where are alpha-1 receptors?

A

vascular smooth muscle

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75
Q

where are alpha-2 receptors?

A

presynaptic junction

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76
Q

where are beta-1 receptors?

A

heart, kidneys

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77
Q

where are beta-2 receptors?

A

Lungs, skeletal muscle blood vessels

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78
Q

where are beta-3 receptors

A

adipose tissue

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79
Q

stimulation of alpha-1 receptors results in what response?

A

vasoconstriction/vasodilation

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80
Q

stimulation of alpha-2 receptors results in what responses?

A

influence of NE release

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81
Q

stimulation of beta-1 receptors results in what responses?

A

HR, contractility, renin secretion

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82
Q

stimulation of beta-2 receptors results in what respones?

A

vasoconstriction/vasodilation, bronchoconstriction/bronchodilation

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83
Q

stimulation of beta-3 results in what?

A

impacts lipolysis

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84
Q

a positive iontropic effect does what?

A

increase stroke volume

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85
Q

a positive chronotropic effect does what?

A

increase heart rate

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86
Q

what are the general effects of catecholamines?

A

sympathommetic - they mimic the SNS

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87
Q

vascular effects of cataecholamines

A

EPI: peripheral vascular resistance (low = reduced; high = increased) NE: elevates BP

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88
Q

CNS effects of catecholamines

A

anxiety, tremors, headache

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89
Q

non-vascular smooth muscle effects of catecholamines

A

relax smooth muscles of GI tract, urinary retention, bronchodilation

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90
Q

metabolic effects of catecholamines

A

increase blood glucose, fatty acid levels, insulin secretion inhibition, increase glycogenolysis/glycuneogensis

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91
Q

net effect of epinephrine on all alpha and beta receptors

A

vasoconstriction & cardiac stimulation

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92
Q

what would epinephrine be used to treat?

A

anaphylactic shock, cardiogenic shock

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93
Q

how does epinephrine effect alpha receptors?

A

alpha-1: smooth muscle vasoconstriction alpha-2: presynaptic receptor

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94
Q

how does epinephrine effect beta-1 receptors?

A

increase strength/rate of cardiac contractions

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95
Q

how does epinephrine effect beta-2 receptors?

A

relaxes bronchial smooth muscle, activates glycogenolysis, dilates skeletal muscle blood vessels

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96
Q

how does epinephrine effect beta-3 receptors

A

activates lipolysis

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97
Q

NE mainly effects which receptors?

A

mainly alpha-1 but will also effect alpha-2 and beta-1

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98
Q

NE has little effect on which receptor?

A

beta-2

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99
Q

main effect of NE

A

increases BP, increases peripheral resistance, minimally increased HR

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100
Q

NE used to treat ___

A

severe hypotension septic shock

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101
Q

Dopamine is a precursor to ____

A

NE

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102
Q

Dopamine mainly activates ______

A

alpha-1 and beta-1 receptors

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103
Q

T/F: catecholamines can be used as vasopressors?

A

true

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104
Q

main effect of vasopressors

A

increase vasoconstriction –> increases BP and MAP

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105
Q

MOA of direct acting adrenergic drugs (DAADs)

A

directly stimulate the alpha or beta receptors

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106
Q

DAADs suffix

A

end in -rine

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107
Q

MOA of indirect acting adrenergic drugs (IAADs)

A

enhance effect of NE or Epi by inhibiting their reuptake or degradation; or increasing the release of NE

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108
Q

IAADs are sympatho_____

A

mimetic –> sympathomimetic –> they mimic the SNS

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109
Q

examples of IAADs

A

1). adderall (amphetamine) 2). Focalin 3). Vyvanse 4). cocaine 5). ephedrine

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110
Q

How does Cocaine work?

A

inhibits re-uptake of NE, significant vasoconstriction = hypertensive crisis, MI, stroke

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111
Q

how do mixed acting adrenergic drugs (MAADs) work?

A

work on direct and indirect pathways

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112
Q

rehab concerns for sympathomimetics

A

1). OTC cold remedies may contain phenylephrine 2). may induce: HTN, cardiac arrhythmias, angina 3). ephedra (weight loss products): cerebral hemorrhage, seizures, and death

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113
Q

effect of SNS on HR and SV

A

increase

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114
Q

mean arterial pressure (MAP) = _________

A

CO * peripheral resistance

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115
Q

General MOAs for antiHTN meds

A

affect variables in CO and MAP to alter BP

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116
Q

AntiHTN meds effect on variables of CO and MAP

A

1). reduce HR –> decrease CO and AP 2). decrease contractility –> decrease SV –> decrease BP 3). increase vasodilation –> lower peripheral vascular resistance –> decrease BP 4). reduce plasma volume –> decrease SV –> decrease bP

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117
Q

Classes of AntiHTN meds

A

1). diuretics 2). direct vasodilators 3). calcium-channel blocking vasodilators 4). beta-blockers 5). α1-Adrenoceptor Blockers6). Dual α- & β- blockers7). alpha agonists 8). RAAS inhibitors

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118
Q

what is the recommended initial therapy for all HTN patients?

A

Diuretics

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119
Q

Types of Diuretics

A

1). Loop 2). Thiazide 3). K+ sparring

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120
Q

which diuretic is the most frequently used?

A

Thiazide

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121
Q

MOA of loop diuretics

A

inhibits reabsorption of Na+, K+, chlorine – prevents reabsorption of water

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122
Q

AE of Loop Diuretics

A

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

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123
Q

PK/PD considerations for Loop Diuretics

A

may be taken along with supplemental K+ or K+ sparing diuretics to reduce risk of hypokalemia and metabolic alkalosis

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124
Q

Loop diuretics suffix

A

-ide

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125
Q

MOA for Thiazide diuretics

A

inhibits mechanism that favors Na+ reabsorption –> result in Na+ and K+ excretion and reabsorption of Ca2+

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126
Q

AE of Thiazide diuretics

A

similar to loop diuretics, may cause hypercalcemia and significant loss of K+

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127
Q

PK/PD considerations for Thiazide Diuretics

A

1). may be given along w/loop diuretics in cases of CHF, severe edema 2). favored for older adults to reduce Ca+ loss and maintain bone loss

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128
Q

which Diuretic is better choice for individuals prone to renal calculi?

A

Thiazide Diuretics

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129
Q

Thiazide Diuretic suffix

A

-azide

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130
Q

MOA for K+ sparring diuretics

A

inhibits the Na+/K+ exchange mechanism and limits the reabsorption of Na+ and excretion of K+. Limits osmotic gradient which drives reabsorption of water from tubule

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131
Q

AE of K+ sparring diuretics

A

hyperkalemia, nausea, lethargy, mental confusion

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132
Q

PK/PD considerations for K+ sparring diuretics

A

1). less effective at producing diuresis but are K+ sparring 2). Prevents hypokalemia (good for arrythmias)

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133
Q

Therapeutic Concerns with Diuretics

A

1). look for signs of hypokalemia or hyperkalemia 2). hyperglycemia and abnormal lipid levels 3). dehydration 4). DDIs with NSAIDs

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134
Q

T/F: there is a fall risk with diuretics

A

True: mental status can change due to hypo/hyperkalemia, dehydration

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135
Q

T/F: risk of orthostatic hypotension with diuretics

A

True, increased TPR

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136
Q

effect of NSAIDs in DDIs with diuretics

A

NSAIDs cause Na+ retention and decreases in renal perfusion –> cause diuretics to be less effective

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137
Q

MOA of direct vasodilators

A

inhibit smooth muscle contraction in arterioles to directly vasodilate the peripheral vasculature

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138
Q

AE of direct vasodilators

A

dizziness, orthostatic hypotension (reflex tachycardia - to compensate for fall in BP)

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139
Q

examples of direct vasodilators

A

apresoline and Loniten

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140
Q

T/F: direct vasodilators are commonly used

A

FALSE

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141
Q

MOA of Calcium-channel blocking vasodilators

A

block Ca2+ entrance into vascular smooth muscle, reducing smooth muscle tone and allowing for vasodilation

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142
Q

Classes of Ca-channel blocking vasodilators

A

1). dihydropyridines 2). phenylakylamines 3). benzothiazepines

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143
Q

effect of dihydropyridines

A

reduce arteriole tone

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144
Q

effect of phenylalkylamines

A

affect the heart

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145
Q

effect of benzothiazepines

A

affect heart and vasculature

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146
Q

AE of Ca-channel blocking vasodilators

A

HA, dizziness, hypotension, bradycardia, reflex tachycardia, sweating, tremor, flushing, constipation

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147
Q

PK/PD considerations for Ca-Channel blocking vasodilators

A

1). useful when beta-blockers are contraindicated (asthma, DM, PVD) 2). originally developed for treating cardiac disease

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148
Q

MOA for beta-blockers

A

competitive antagonist, binds to beta receptors and prevents NE from binding, results in decrease HR, contractility and conduction

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149
Q

types of beta-blockers

A

1). non-selective 2). cardioselective

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150
Q

AE of Non-selective beta-blockers

A

contribution to peripheral vasoconstriction, bronchoconstriction, bradycardia, reduced exercise tolerance, dizziness, OH, depression, fatigue, sexual dysfunction

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151
Q

abrupt withdrawl of Non-selective Beta-blockers results in ______

A

arrhythmia, angina, MI

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152
Q

Non-selective beta-blockers suffix

A

-lol

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153
Q

MOA of cardioselective beta-blockers

A

selectively block beta-1 receptors without causing bronchoconstriction

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154
Q

AE of cardioselective beta-blockers

A

same as non-selective but no pulmonary effects

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155
Q

therapeutic concerns for beta-blockers

A

1). depresses HR and CO during exercise 2). may contribute to orthostatic hypotension 3). may cause CHF 4). masks symptoms of hypoglycemia in diabetic pts.

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156
Q

MOA of alpha-1 adrenoceptor blockers

A

reduces sympathetic tone of blood vessels causing VD and decreased peripheral vascular resistance

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157
Q

AE of alpha-1 adrenoceptor blockers

A

orthostatic hypotension, nasal stuffiness, reflex tachycardia, arrhythmia

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158
Q

seletive alpha-1 blockers suffix

A

-azosin

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159
Q

therapeutic concerns for alpha-1 adrenoceptor blockers

A

fall risk increased risk of CHF

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160
Q

types of alpha agonists

A

alpha-1 receptor agonists alpha-2 receptor agonists

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161
Q

alpha-2 receptor agonists indications

A

HTN, anxiety/PTSD, spasticity

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162
Q

central-acting alpha-2 agonist for HTN MOA

A

decrease sympathetic output from CNS (decrease NE) by binding to presynaptic

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163
Q

AE of central-acting alpha-2 agonists

A

dizziness, drowsiness, fatigue, headache

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164
Q

PT concerns for central-acting alpha-2 agonists

A

orthostatic hypotension, rebound hypertension

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165
Q

central-acting alpha-2 agonist that is in the form of a weekly patch

A

clonidine

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166
Q

clonidine indication

A

reserved for resistance HTN, ADHD, adjunct pain control

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167
Q

AE of clonidine

A

dry mouth, rash

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168
Q

what centrally acting alpha-2 agonist will be used with pregnant women w/HTN?

A

methyldopa

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169
Q

AE of methyldopa

A

sexual dysfunction, sodium/water retention with long-term use

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170
Q

Types of RAAS inhibitors

A

1). Direct renin inhibitor (DRI) 2). Angiotension 1 converting inhibitor (ACEi)3). Angiotensin II receptor blocker (ARB)

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171
Q

DRI MOA

A

block conversion of angiotensinogen to angiotensin I

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172
Q

AE of DRI

A

similar to ACEi and ARB

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173
Q

ACEi MOA

A

blocks conversion of angiotensin I and angiotensin II

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174
Q

downstream effects of ACEi

A

1). increases blood vessel VD, bradykinin >> increases VD 2). decreases aldosterone secretion >> decreases Na+ and H20 retention

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175
Q

ACEi indications

A

HTN, reduced ejection fraction heart failure, post-MI, post-stroke, kidney disease

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176
Q

Common ACEi AE

A

dry cough, hypotension/dizziness, hyperkalemia

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177
Q

rare ACEi AE

A

acute renal failure, angioedmea

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178
Q

PT concerns with ACEi

A

coughing, DDI with NSAIDs

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179
Q

ACEi suffix

A

-pril

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180
Q

ARB MOA

A

antagonist at receptor which blocks the binding of angiotensin II from the RAAS and other pathways

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181
Q

ARB indications

A

alternative if ACEi intolerant in HTN, kidney disease, HF

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182
Q

Common AE of ARB

A

hypotension/dizziness, hyperkalemia

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183
Q

Rare AE of ARB

A

acute renal failure, angioedema

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184
Q

ARB suffix

A

-sartan

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185
Q

which RAAS inhibitor is the best tolerated?

A

ARB

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186
Q

Therapeutic concerns about ACEi

A

cough (instant referral), NSAIDs are contraindicated

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187
Q

General therapeutic concerns for hypertensive agents

A

1). orthostatic hypotension 2). dehydration 3). caution w/heat 4). cannot use HR as exercise tolerance determinant 5). depletion of electrolytes 6). poly pharmacy

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188
Q

What are the 3 types of ischemic heart disease?

A

1). Arteriosclerosis 2). Angina3). MI

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189
Q

3 major forms of angina

A

1). exertional (stable) 2). Variant (Prinzmetal’s) 3). Unstable

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190
Q

Which type of of angina occurs prior to an MI?

A

Unstable, pain will increase with frequency, severity, and/or duration

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191
Q

Two common drug types used to treat angina pectoris?

A

Vasodilators and Cardiac Depressants

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192
Q

what are the subtypes of vasodilators?

A

Nitrates and Ca2+ blockers

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193
Q

what are the subtypes of cardiac depressants?

A

Beta-blockers and Ca2+ blockers

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194
Q

general goal of drugs treating angina pectoris?

A

relieve vasoconstriction and workload of the heart (reduce the O2 requirement)

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195
Q

where do nitrates work?

A

directly on vascular smooth muscle (not a receptor!)

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196
Q

general result of Nitrates

A

decrease preload/afterload –> reduce workload of heart -> reduce O2 demand

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197
Q

T/F: nitrates are DOC for acute angina attacks?

A

True, especially sublingual

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198
Q

Important patient education concerning Nitrates

A

proper storage and dosing

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199
Q

AE Nitrates

A

1). reflex tachycardia 2). dizziness 3). OH4). weakness

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200
Q

what type of angina requires beta-blockers to treat?

A

stable angina along with short-acting nitrates

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201
Q

how do Ca2+ blockers work?

A

block Ca2+ channels resulting in decreased smooth muscle contractility

202
Q

what are the zones injury MI?

A

1). zone of ischemia 2). zone of hypoxic injury 3). zone of infarction

203
Q

two types of MI based on ECG interpretation?

A

STEMI and NSTEMI

204
Q

how is STEMI treated?

A

thrombolytic agent, aspirin, nitrates, beta-blockers

205
Q

how is NSTEMI treated?

A

heparin

206
Q

Peripheral vascular disease (PVD) can result in what?

A

development of venous thrombosis (VT)

207
Q

a VT can result in what?

A

pulmonary embolism (PE)

208
Q

what is a VT?

A

partial/complete occlusion of a vein by a thrombus

209
Q

two types of VTs

A

superficial and deep

210
Q

a DVT can result in what?

A

pulmonary embolism

211
Q

Signs and symptoms of a pulmonary embolism?

A

1). possible sudden death 2). chest pain 3). tachypnea 4). hemoptysis 5). anxiety, restlessness, apprehension 6). dyspnesa 7). persistent cough

212
Q

Vascular injury results in what 2 immediate things?

A

1). exposure of collagen and VWF 2). Tissue factor exposure

213
Q

exposure of collagen and VWF results in what?

A

platelets adhesion and release of ADP and thromboxane A2

214
Q

once platelets adhere and release what happens?

A

more plates are recruited and activated

215
Q

as more platelets are recruited and activated what results

A

platelet aggregation and ultimately platelet-fibrin thrombus formation

216
Q

when tissue factors are exposed due to a tissue injury what is triggered?

A

coagulation pathways and thrombin generation

217
Q

what does thrombin do?

A

recruit more platelets and convert fibrinogen to fibrin

218
Q

how is fibrin important?

A

it binds platelets together to form a thrombus

219
Q

primary hemostasis results in what?

A

platelet plug formation

220
Q

secondary hemostasis results in what?

A

fibrin formation which is used to stabilize the platelet plug

221
Q

What is artherosclerosis?

A

narrowing and hardening of the arteries

222
Q

basic mechanism of artherosclerosis

A

injury occurs to arterial wall -> cholesterol begins to build up in the wall

223
Q

what can atherosclerosis eventually cause?

A

thrombus formation -> MI, stroke, or other ischemic issues

224
Q

what type of cholesterol is “good”?

A

High-density HDL

225
Q

what are the 3 basic classes of drugs used to treat Artheroscerlosis?

A

1). Statins 2). PCSK9 inhibitors 3). Cholesterol Absorption Inhibitor

226
Q

true name of statins?

A

HMG-CoA reductase inhibitors

227
Q

T/F: even with low LDL some populations must take a statin to reduce risk of stroke

A

TRUE

228
Q

basic MOA statins

A

block cholesterol synthesis

229
Q

statins common AE

A

myalgia

230
Q

other Statins AE

A

dyspepsia, headache, increased liver enzymes, tendinopathy and tendon rupture?

231
Q

Rare AE of Statins

A

rhabdo and myopathy

232
Q

T/F: statins have a decreased risk of drug-drug interactions?

A

FALSE, increased risk (especially fibrates)

233
Q

how does grapefruit juice effect statins?

A

inhibits CYP enzymes - linked to statin rhabdo -> increased 6x hosptialization rate

234
Q

what are the 3 types of antithrombotic drugs classes?

A

1). Antiplatelets 2). anticoagulants 3). fibrinolytics

235
Q

general concerns with antithrombotics as a whole?

A

bleeding or clotting

236
Q

what do antiplatelets do?

A

prevent thrombus

237
Q

basic MOA of antiplatelets

A

decrease platelet secretion and adhesion

238
Q

which antithrombotic class has boxed warnings?

A

antiplatelets, warning against CYP interaction, increase risk of bleeding

239
Q

suffix for antiplatelets

A

-gel/-grelor

240
Q

what do anticoagulants do?

A

prevents thrombus & thrombus growth

241
Q

LMWH and Heparin basic MOA

A

increase antithrombin to decrease thrombin

242
Q

Heparin and Direct thrombin inhibitor basic MOA

A

prevents conversion of fibrinogen -> fibrin

243
Q

Arixtra basic MOA

A

selectively inhibits factor Xa

244
Q

Anticoagulants that are administered via IV

A

LMWH, Heparin, Direct thrombin inhibitor, Arixtra

245
Q

Anticoagulants that are administered via PO

A

Direct thrombin inhibitor, Factor Xa inhibitor, and Warfarin (VKa)

246
Q

Direct thrombin inhibitor and Factor Xa are further classified as what?

A

DOAC

247
Q

DOAC has less of a risk of what?

A

intercranial bleeding

248
Q

Warfarin basic MOA

A

inhibits vitamin K - inhibits coagulation cascade indirectly (reduces factor formation)

249
Q

Atrixtra is what type of anticoagulant?

A

factor Xa inhibitor

250
Q

AE of Warfarin

A

intercranial bleeding , rare: skin necrosis, DDI with leafy green

251
Q

Fibrinolytics generally do what?

A

lyse active thrombus

252
Q

Fibrinolytics basic MOA

A

breaks fibrin links in active thrombus

253
Q

when are Fibrinolytics prescribed?

A

immediately following stroke, MI, and PE

254
Q

Fibrinolytics suffix

A

-kinase/-plase

255
Q

what is the continuum from least to most risk of HIT(heparin induced thrombocytopenia) (for anticoagulants)

A

Atrixtra - direct thrombin inhibitor - LMWH - Heparin

256
Q

Cholesterol Absorption Inhibitor MOA

A

inhibits absorption of cholesterol in small intestine

257
Q

When might a cholesterol absorption inhibitor be used?

A

if a pt. is experiencing a lot of myalgia from statins

258
Q

Cholesterol absorption inhibitors DDI

A

not metabolized by CYP enzymes, less DDI

259
Q

basic MOA for PCSK9 Inhibitors

A

increase LDL uptake for degradation

260
Q

PCSK9 common AE

A

injection site reactions

261
Q

what is CHF?

A

heart is unable to pump sufficient blood to supply the needs of the body

262
Q

How is CHF progressive?

A

structural changes over time lead to reduced cardiac contractility

263
Q

Conditions that can lead to CHF

A

ischemic and hypertensive heart disease, cardiomyopathy, valve disease

264
Q

What is compensated CHF?

A

pt is med stable. Combined efforts of 3 compensatory phases achieve a normal CO

265
Q

what is decompensated CHF?

A

unable to maintain adequate circulation. Life-threatening: fluid overload and total heart failure

266
Q

clinical manifestation of L ven CHF

A

1). dyspnea 2). fatigue and muscular weakness 3). renal changes 4). nocturia

267
Q

in general R ven CHF deals with what?

A

fluid build up in the periphery

268
Q

in general L ven CHF deals with what?

A

fluid build up in the lungs

269
Q

which ventricular failure can result in pulmonary edema?

A

Left ventricle heart failure

270
Q

HF with preserved ejection fraction results from what?

A

diastolic heart failure, cardiac hypertrophy -> reduced volume capacity in L ven

271
Q

HF with reduced ejection fraction is caused by what?

A

systolic heart failure, heart unable to adequately contract

272
Q

which HF is more often related to aging and cardiac hypertrophy?

A

HFpEF (preserved heart failure)

273
Q

goals of HFpEF

A

1). treat underlying comorbidities 2). give diuretics 3). may add aldosterone antagonist

274
Q

general goal of HFpEF?

A

get rid of fluid, can’t fix just treat symptoms

275
Q

Goals of HFrEF

A

improve QOL and prolong survival

276
Q

corresponding meds for HFrEF

A

diruretics, + inotropic drugs (digoxin), vasodilators

277
Q

Entresto is what?

A

a type of ARB (higher risk of angioedema than other ARBS)

278
Q

T/F: Digoxin reduces mortality?

A

FALSE

279
Q

T/F: Digoxin is an NTI

A

TRUE

280
Q

rEF Baseline Trx

A

ACEi or ARB, + beta-blocker, + diuretic (prn)

281
Q

when is digoxin prescribed?

A

as a last resort if sympotoms not controlled on other therapy

282
Q

what is an arrhythmia?

A

disturbance of HR due to SA node irregularities (origin, pattern, speed/rate)

283
Q

Overall symptoms of arrhythmias

A

increase/decrease in HR palpitations

284
Q

general symptoms of arrhythmias

A

fatigue, dyspnea, syncope, dizziness, angina, diaphoreseis (profuse sweating)

285
Q

Anti-arrhythmic drug therapeutic concerns

A

also causes arrhythmia, take HR for 60s, decreases exercise tolerance, 30-60% efficacy

286
Q

Amiodarone MOA

A

prolong duration of AP by blocking ion channels (K+, Na+, Ca2+)

287
Q

Amiodrone indication

A

ventricular arrhytmia

288
Q

Amiodarone AEs

A

LFTs, TFT, PFTs, bluish discoloration

289
Q

considerations for Amiodrone

A

50 day half life

290
Q

Digoxin MOA

A

increase contractility (Na+/K+ ATPase)

291
Q

Digoxin indication

A

arrhythmia & CHF (last resort)

292
Q

Digoxin AE

A

GI (Beer’s list)CNS - blurred vision, confusion, lethargy Arrhythmia

293
Q

Digoxin considerations

A

avoid pt who has kidney dysfunction (metabolized by kidneys) *medical emergency if given to them

294
Q

what controls respiration?

A

1). medullary rhythmic center 2). Vagal input from lungs 3). ABGs

295
Q

effect of PNS on respiration?

A

produces mainly bronchoconstriction and mucus secretion

296
Q

effect of SNS on respiration?

A

beta-2 receptors relax smooth muscles, increase mucocilliary clearance

297
Q

what is a healthy V/Q ratio?

A

0.8(Ventilation to perfusion ratio)

298
Q

difference between volumes and capacities in the lungs?

A

capacities are when you add volumes up/together

299
Q

drugs that can be used to treat respiratory tract irritation & control of secretions

A

1). Decongestants 2). Antitussives 3). Antihistamines 4). Mucolytics 5). Expectorants

300
Q

what do decongestants do?

A

counter mucous discharge from upper respiratory tract (nasal stiffness)

301
Q

decongestants MOA

A

usually alpha-1 adrenergic agonist –> causes vasoconstriction –> reduces blood flow = “dry up” mucosal tracts

302
Q

what do antitussives do?

A

used to suppress cough (dry unproductive cough)

303
Q

Antitussives MOA

A

decrease afferent nerve activity or decrease cough center sensitivity

304
Q

Antitussive drugs can include what?

A

Codeine and antihistamines

305
Q

What are antihistamines used for?

A

to manage respiratory allergic responses to seasonal allergies

306
Q

general MOA for antihistamines

A

act on nasal mucosa H1 receptor

307
Q

what do H1 receptors blockers do?

A

reduce nasal congestion, mucosal irritation, and cough by reducing secretions

308
Q

difference between 1st and 2nd generation antihistamines

A

1st generation cross the BBB which results in more drowsiness

309
Q

general AEs for antihistamines

A

dry mouth, sore throat, cough, nausea, HA, diarrhea, and nervousness

310
Q

Mucolytics MOA

A

split disulfide bonds –> decreases viscosity of respiratory secretions making it easier to clear mucus from the airway

311
Q

what do expectorants do?

A

facilitate the production and ejection of mucus.

312
Q

issues with cold remedies and hypertension

A

decongestants can mimic effects of increased sympathetic activity, thus hypertensive individuals should avoid them

313
Q

COPD is an umbrella term for what conditions?

A

1). emphysema 2). chronic bronchitis 3). asthma

314
Q

what is emphysema?

A

pathologic accumulation of air in the tissues, particularly in the lungs

315
Q

pathophysiology of emphysema?

A

alveoli are damaged and create large air spaces which reduce the SA for gas exchange.

316
Q

clinical manifestations of emphysema

A

1). barrel chests 2). clubbed fingers 3). tachypnea 4). marked exertional dyspnea 5). hypertrophied neck muscles 6). anxiety related to dyspnea or fear of dyspnea

317
Q

what is chronic bronchitis?

A

inflammation of airway and irritation that results in excess mucus production

318
Q

hallmark of chronic bronchitis?

A

very productive cough that lasts for at least 3 months for 2 consecutive years

319
Q

clinical manifestations of chronic bronchitis

A

1). SOB 2). persistent cough 3). prolonged expiration 4). recurrent infection due to increased mucus in airways 5). late effects include pulmonary hypertension

320
Q

goals of trx for COPD

A

reduce airway edema secondary to inflammation and bronchospasm

321
Q

how to achieve trx goals for COPD

A

1). facilitate the elimination of bronchial secretions 2). prevent and treat respiratory infections 3). increase exercise tolerance

322
Q

Drug classes used to treat COPD

A

1). Bronchodilators 2). Anti-inflammatory 3). Antibiotics

323
Q

Types of Bronchodilators

A

1). inhaled beta agonists 2). inhaled antimuscarinics

324
Q

MOA of inhaled beta-agonists

A

agonize beta-2 receptors –> increase bronchodilation

325
Q

suffix for inhaled beta-agonists

A

-terol

326
Q

what are SABAs?

A

short acting beta-agonists

327
Q

what are SABAs used for?

A

acute exacerbations, works within 5 minutes and lasts 4-6 hours

328
Q

what are LABAs?

A

long acting beta-agonists

329
Q

what are LABAs used for?

A

chronic managements, 12-24 hour duration, must be dosed once or twice daily

330
Q

AE for inhaled beta-agonists

A

generally well tolerated. AE can include: tachycardia, tremor, hypokalemia

331
Q

MOA for Inhaled antimuscarinics

A

primarily bind M3 in airway smooth muscle which antagonizes ACh actions at those sites resulting in bronchodilation

332
Q

what are SAMA/LAMAs?

A

short/long acting antimuscarinics

333
Q

AE for inhaled antimuscarinics?

A

generally well tolerated other than dry mouth

334
Q

Anti-inflammatory drugs used to treat COPD

A

1). inhaled corticosteriods (-asone or -sonide) 2). PDE-3 inhibitor

335
Q

typical use for ICS?

A

acute exacerbation of COPD or more severe disease

336
Q

ICS AEs?

A

oral candidiasis (prevent by rinsing mouth)

337
Q

MOA for PDE-3 inhibitor

A

decrease breakdown of intracellular cyclic AMP –> decreases inflammation

338
Q

when would PDE-3 inhibitors be used?

A

when a pt has a more severe COPD case, this drug is used in to the hopes to decrease the amount of exacerbations

339
Q

what is asthma?

A

reversible obstructive lung disease characterized by inflammation and increased smooth muscle reaction of the airways to various stimuli

340
Q

types of asthma?

A

1). extrinsic 2). intrinsic 3). exercise-induced 4). asthma associated with COPD

341
Q

Asthma Pathogenesis?

A

1). abnormal airway response 2). mediators cause thickening of airway walls and increased contractile response of bronchial smooth muscle 3). mucous plug can become significant and block up the airways that are in spasm and swollen (traps air distally)

342
Q

Clinical manifestations of Asthma

A

1). sensation of chest constriction 2). inspiratory and expiratory wheezing 3). nonproductive cough 4). prolonged expiration 5). tachycardia and tachypnea

343
Q

Goals for Asthma trx?

A

1). decrease impairments 2). decrease risk (prevent exacerbations, need for emergency care, prevent loss of lung function, decrease AE for therapy)

344
Q

1st line (maintenance trx) for Asthma

A

1). ICS solo 2). LABAs only in combo with ICS

345
Q

1st line trx for acute exacerbations of Asthma

A

PO ICS

346
Q

Alternative trx for Asthma

A

1). Leukotriene Modifiers 2). Immunomodulators 3). Cromolyn Sodium 4). Methylxanthines

347
Q

what are Leukotrienes?

A

released from mast cells eosinphils, they play a role in airway edema, smooth muscle contraction and inflammatory process

348
Q

types of Leukotriene modifiers

A

1). Leukotriene receptor antagonist (LTRA) 2). 5-lipoxygenase inhibitor

349
Q

MOA for LTRA

A

competitively antagonize leukotriene receptors

350
Q

Types of Immunomodulators

A

1). Anti-IgE 2). Interleukin Antagonist

351
Q

MOA of Anti-IgE?

A

binds IgE antibody –> prevents IgE binding to receptors on mast cells and basophils –> limits activation and release of allergic response mediators

352
Q

AE of Anti-IgE

A

HA, injection site reactions; very rare anaphylactic allergic reactions

353
Q

Interleukin antagonist MOA

A

monoclonal antibodies that binds interleukins results in decrease inflammatory response

354
Q

Common interleukin antagonist AE

A

injection site reactions, HA, increase creatine kinase

355
Q

What drugs are used for acute symptom relief and exacerbations of Asthma?

A

1). SABAs2). SAMAs 3). PO steroids

356
Q

what is used for acute symptom relief and EIB?

A

SABAs. typically used up to 3 trx at 20 min intervals

357
Q

when would SAMAs be used?

A

in combo with SABA in emergency care setting or as monotherapy if SABA not tolerated

358
Q

when would PO steroids be used to treat Asthma?

A

moderate to severe exacerbations

359
Q

what is a BPTs?

A

bronchial provocation test. Used to diagnose asthma in atheltes

360
Q

What is cystic fibrosis?

A

gene defect that doesn’t allow Cl- to pass in and out of the plasma membrane of epithelial cells. More commonly known for its copious amounts of mucus but is a multi-system disease

361
Q

CF complications

A

1). CFRD 2). bone disease 3). liver disease 4). lung transplants

362
Q

CF trxs

A

1). Bronchodilators 2). CFTR modulators 3). Mucolytics 4). Anti-inflammatory 5). Inhaled Antibiotics 6). PO Antibiotics 7). Nutritional support

363
Q

Bronchodilators used in CF trx

A

may use LABAs for maintenance; SABAs used prior to chest physiotherapy

364
Q

what is a CF trans-membrane regulator?

A

membrane protein and Cl- channel –> regulates sodium and water which helps keep mucous thin

365
Q

how does CF effect CFTRs?

A

genetic mutations cause closing and/or narrowing of CFTR or prevents CFTR from getting to the cell surface

366
Q

purpose of CFTR modulators

A

decrease risk of exacerbation, increase lung function and QOL

367
Q

common AE for CFTR modulators

A

HA, GI issues, respiratory issue

368
Q

less common AE of CFTR modulators

A

dizziness and hypertension

369
Q

why are mucolytics used in trx of CF?

A

decrease risk of exacerbations, improve lung function and QOL

370
Q

type of mucolytic used ideally?

A

hypertonic saline and dornase alfa

371
Q

MOA of hypertonic saline?

A

increase salt in airways which draws more water into airways -> increases hydration of airway mucus secretions, increases mucucillary functions

372
Q

MOA of dornase alfa (Pulmozyme)

A

cleaves DNA –> decrease mucus viscosity –> improved airflow

373
Q

what is a red flag for a pt on dornase alfa?

A

chest pain -> merits an automatic referral to a physician

374
Q

what is a red flag for a pt on dornase alfa?

A

chest pain -> merits an automatic referral to a physician

375
Q

Anti-inflammatory used to trx CF

A

Chronic high dose ibuprofen if <18 years old - has been proven to slow the loss of lung function

376
Q

Inhaled Antibiotics used to trx CF

A

1). Tobramycin (Tobi) 2). Aztreonam

377
Q

when would an inhaled antibiotic be used chronically for CF trx?

A

if P. aeruginosa persistently present in cultures

378
Q

prescription instructions for Tobramycin

A

nebulized 2-3x daily for 28 days on and then 28 days off

379
Q

AE of Tobramycin (9)

A

voice disorder, HA, fever, respiratory issue, ototoxicity, pharyngolarngeal pain, cough, nasal congestion, wheezing

380
Q

additional AE for aztreonam

A

fever

381
Q

supplemental vitamins used for nutritional support in pts with CF?

A

Vitamins A, D, E, and K

382
Q

what is PERT?

A

pancreatic enzyme replacement therapy

383
Q

Therapeutic concerns with Anti-cholinergic drugs used to trx respiratory conditions?

A

dry mouth, HTN and tachycardia

384
Q

Therapeutic concerns with steroids used to trx respiratory conditions?

A

1). inhaled: oral candidiasis and thrush 2). increased infection risk, HTN, Osteoporosis (muscle weakness, skin atrophy)

385
Q

Therapeutic concerns with Beta-2 agonists used to trx respiratory conditions

A

tremor, trachycardia, hypokalemia, hyperglycemia, reduced exercise capacity

386
Q

what are the phases of digestion?

A

cephalic phase

gastric phase

intestinal phase

387
Q

what occurs during the intestinal phase of digestion?

A

chyme enters the duodenum release of bicarbonate solution and pancreatic enzymes

388
Q

T/F: the neuronal control of digestions is mostly cholinergic and excitatory?

A

True

389
Q

what is peptic ulcer disease (PUD)?

A

ulcerations of the mucosal lining of the esophagus, stomach and/or duodenum

390
Q

T/F: H pylori infection can cause chronic gastritis, PUD, GERD, and gastric cancer?

A

TRUE

391
Q

how is H pylori infection treated?

A

antacid + antibiotic

392
Q

T/F: one should discontinue use of NSAIDs during H. pylori infection if possible

A

TRUE

393
Q

what regulates vomiting?

A

chemoreceptor trigger zone (CTZ) and the Vomiting center

394
Q

where is the CTZ?

A

floor of the 4thh ventricle in cerebrum

395
Q

what does the CTZ respond to?

A

toxins/drugs in blood and CSF

396
Q

what does the vomiting center do?

A

integrates signals from multiple places including: CTZ, GI tract, pharynx, vestibular system

397
Q

what is the typical cause of diarrhea?

A

from water and electrolyte imbalance in intestinal tract

398
Q

common pathologies that can lead to diarrhea?

A
  1. IBS
  2. Crohn’s disease
  3. Ulcerative colitis
  4. Bowel impaction with overflow
  5. Bacterial overgrowth
  6. Bile acid malabsorption
  7. Celiac disease
  8. Short bowel syndrome
  9. Laxative abuse can lead to diarrhea
399
Q

what is constipation?

A

movement disorder of the colon; infrequent/painful defecation, hard stools, incomplete evacuation

400
Q

what are some causes of constipation?

A
  1. Bowel impaction
  2. Endocrine or neurogenic condition
  3. Sedentary lifestyle
  4. Poor diet (limited roughage, dehydration)
  5. Medications
401
Q

drug classes indicated for acid reflux

A
  1. antacid
  2. H2 receptor antagonist
  3. proton pump inhibitors (PPI)
402
Q

Drug classes that heal/treat ulcers that form from gastric acid

A
  1. H2 receptor antagonists
  2. PPI
  3. Mucuosal protectors
403
Q

which drug classes that treat acid reflux also help heal ulcers?

A
  1. H2 receptor blocker
  2. PPI (more effective of the two)
404
Q

MOA of antacids

A

neutralizes stomach acidity by increasing stomach pH

405
Q

AE of antacids

A
  1. Effervescent types (i.e. Alka-Seltzer) have high Na+ content – if pt has hypertension they should probably avoid this one
  2. Magnesium products à diarrhea
  3. Aluminum and calcium à constipation
  4. Drug-Drug interactions
  5. Alters absorption of electrolytes from GI tract à electrolyte imbalance
  6. Avoid taking within 2 hours of other oral medications
406
Q

how do antacids have DDIs?

A

↑ absorption of basic drugs and ↓ absorption of acidic drugs

407
Q

MOA of H2 receptor anatagonists

A

reduce secretion of stimulated acid

408
Q

T/F: H2 receptor antagonists are best taken HS (at bedtime)

A

TRUE

409
Q

H2 receptor antagonist AE

A
  1. diarrhea
  2. muscle pain
  3. rashes
410
Q

PPI MOA

A

irreversibly inhibit H+/K+ ATPase pump on parietal cell membrane which blocks final step in acid secretion into lumen of stomach

411
Q

PPI AE

A

generally well tolerated

long term: gastric polyps, altered Ca2+ metabolism (↓ bone mineralization), some cardiovascular abnormalities.

412
Q

what are the types of mucosal protectors?

A
  1. Bismuth chelate
  2. Sucralafate
  3. Misoprostol
413
Q

how do bismuth protectors works?

A

coats ulcer, enhances prostaglandin synthesis, ↑ gastric mucous epithelial cell growth to protect against H. pylori-induced ulcers

414
Q

how do sucralfates work?

A

an Al salt of sucrose that forms a protective coating over the ulcer; used for high-risk causes (trauma, burns, ARDS, major surgery, etc.)

415
Q

How does misprostol work?

A

synthetic prostaglandin analog (PGE2) that inhibits acid secretion; used to prevent NSAID-induced ulcers.

416
Q

Types of Antiemitic drugs

A
  1. Anticholinergics
  2. Antihistamines
  3. Neuroleptic drugs
  4. Prokinetic drugs
  5. Serotonin blockers
  6. Neurokinin-1 receptor blockers
  7. Cannabinoids
417
Q

MOA for anticholinergic antiemetics

A

binds to ACh receptors on vestibular nuclei, blocks communication

418
Q

Anticholinergic antiemetics AE

A
  1. dizziness,
  2. drowsiness
  3. dry mouth
  4. blurred vision
  5. dilated pupils
  6. difficulty with urination
419
Q

Antihistamine antiemetic MOA

A

inhibit vestibular input to the CTZ

420
Q

Neuroleptic antiemetic drugs MOA

A

block dopamine receptors in CTZ

421
Q

most important AE for neuroleptic antiemetic drugs

A

tardive dyskinesia

422
Q

Prokinetic antiemetic drugs MOA

A

block dopamine in CTZ

423
Q

Prokinetic antiemetic drugs AE

A
  1. sedation
  2. diarrhea
  3. weakness
  4. prolactin release
  5. prolonged use causes extrapyramidal signs, motor restlessness
424
Q

Serotonin blockers antiemetic drug MOA

A

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

425
Q

Neurokinin-1 receptor blocker antimetic drug MOA

A

blocks substance P from binding to NK-1 receptor, prevents both central and peripheral stimulation of vomiting centers

426
Q

Which antiemetic drugs are used to prevent vomiting from motion sickness?

A
  1. Anticholinergics
  2. Antihistamines
427
Q

Which antiemetic drugs are antipsychotic agents, some have anticholinergic actions and are good for postop vomiting?

A

Neuroleptic antiemetics

428
Q

Which antiemetic drugs are used to treat vomiting resulting from chemotherapy?

A
  1. Neurokinin-1 receptor blockers
  2. Cannabinoids
429
Q

Which antiemetic drug can cause Steven-Johnsons syndrome?

A

Neurokinin-1 receptor blockers

430
Q

Types of antidirraheal drugs

A
  1. Absorbents
  2. Anticholinergics
  3. Intestinal flora modifiers
  4. Opiates
431
Q

Absorbents MOA

A

binds to bacteria causing diarrhea and carry them out with feces

432
Q

Absorbents AE

A

*aspirin product: use with caution in children recovering from flu/chickenpox, increased bleeding time, GI bleed, tinnitus

*decrease effectiveness of many drugs (digoxin, hypoglycemic drugs, anticoagulants)

433
Q

Anticholinergic Antidirrheal MOA

A

reduce peristalsis of GI tract

434
Q

Opiates Antidirrheal MOA

A

decrease GI motility and propulsion (in small doses)

Slowing transit time in intestines = absorption of water and electrolytes

435
Q

Opiates antidirrheal AE

A
  1. sedation
  2. dizziness
  3. constipation
  4. nausea
  5. vomiting
  6. respiratory depression
  7. bradycardia
  8. hypotension
  9. urinary retention
436
Q

Types of Laxatives

A
  1. Bulk-forming
  2. Hyperosmotic
  3. Saline
  4. Emollient
  5. Stimulant
437
Q

Bulk forming laxatives MOA

A

increase water absorption à softens and increases bulk of intestinal contents

Distention of colon increases peristalsis

438
Q

hyperosmotic laxatives MOA

A

creates gradient that draws fluid into colon to increase stool fluid content and stimulate peristalsis

439
Q

Hyperosmotic laxatives AE

A
  1. abdominal bloating
  2. rectal irritation
  3. electrolyte imbalance
440
Q

Concerns with hyperosmotic laxatives

A

do not take if a pt is on diuretics or is at CV risk.

The electrolyte imbalance puts them at risk for cardiac arrhythmias

441
Q

Saline laxatives MOA

A

similar to hyperosmotic – osmotic pressure pushed water/electrolytes into intestines

442
Q

Saline Laxatives AE

A

salts may cause issues with individual with diminished cardiac or renal function

443
Q

Emollient laxatives MOA

A

facilitate water and fat absorption into stool, lubricate fecal matter and intestinal wall

444
Q

what are emollient laxatives also known as?

A

stool (fecal) softeners or lubricant laxatives

445
Q

Emollient laxatives AE

A

*generally well tolerated

  1. skin rash
  2. decrease vitamin absorption
  3. electrolyte imbalance
446
Q

Stimulant laxatives MOA

A

stimulates peristalsis through enteric nervous system

447
Q

Important consideration with stimulant laxatives

A

Danger of long-term use:

dependence and damage to intestinal cells/loss of colon function

448
Q

Therapeutic concerns with GI agents

A
  1. patient positioning
  2. Dehydration
  3. Constipation
  4. Drug interactions
449
Q

T/F: exercise can facilitate bowel movements and improve gastric emptying?

A

TRUE

450
Q

T/F: smoking can decrease effectiveness of H2 receptor blockers?

A

TRUE

451
Q

DDI for Climetidine (tagemet)

A

Climetidine (tagemet) inhbits CYP450 enzymes

452
Q

Antihypertensive Drug classes

A
  1. Diuretics
  2. Calcium channel blockers
  3. Beta-blockers (-lol)
  4. ACE Inhibitors (-pril)
  5. ARB (-sartan)
  6. Central acting alpha agonist
  7. Nitrates
453
Q

Diuretic Drugs

A
  1. Furosemide (Lasix) - loop diuretic
  2. Hydrochlorothiazide (HCTZ) - thiazide diuretic
  3. Spironolactone - k+ sparring diuretic
454
Q

Furosemide (Lasix) is what type of diuretic?

A

loop diuretic

455
Q

what type of diuretic is Hydrochlorothiazide (HCTZ)?

A

Thiazide diuretic

456
Q

what type of diuretic is Spironolactone?

A

K+ sparring diuretic

457
Q

Calcium channel blocking diuretics

A
  1. Amlodipin
  2. Diltiazem
458
Q

Beta blockers (-lol)

A
  1. Metoprolol
  2. Propanolol
  3. Carvedilol
459
Q

ACE inhibitors (-pril)

A
  1. Lisinopril
  2. Enalapril
  3. Ramipril
460
Q

ARBs (-sartan)

A
  1. Losartan
  2. Valsartan
461
Q

Central acting alpha agonist

A

Clonidine

462
Q

Nitrates

A
  1. Nitroglycerin
  2. Isosorbide mononitrate
463
Q

What are the 3 types of antithrombotics (drug classes)

A
  1. Antiplatelets
  2. Anticoagulants
  3. Fibrinolytics
464
Q

Antiplatelet drugs

A
  1. Aspirin
  2. Clopidogrel (Plavix)
465
Q

Anticoagulants drugs

A
  1. Enoxaparin (Lovenox)
  2. Apixaban (Eliquis)
  3. Rivaroxaban (Xarelto)
  4. Warfarin
466
Q

Factor Xa inhibitors (-xaban)

A
  1. Apixaban (Eliquis)
  2. Rivaroxaban (Xarelto)
467
Q

Statins are also called what?

A

HMG CoA Reductase Inhibitors

468
Q

Statins

A
  1. Atorvastatin (Lipitor)
  2. Rosuvastatin (Crestor)
  3. Simvastatin
  4. Pravastatin
469
Q

Other Cardiac Meds

A
  1. Sacubitril/valsartan (Entresto)
  2. Digoxin
  3. Amiodarone
470
Q

what type of drug is Sacubitril/valsartan (Entresto)?

A

ARNI

471
Q

comparison of ARBs with ARNI

A

ARNI have a higher risk of angioedema

472
Q

Inhaled medication classes

A
  1. Inhaled beta agonist
  2. Inhaled antimuscarinic
  3. Inhaled corticosteroids
  4. Combination inhaled meds
  5. Inhaled mucolytics
473
Q

Bronchodilators

A
  1. Inhaled beta agonists
  2. Inhaled antimuscarinics
474
Q

Inhaled beta agonsits (-terol)

A
  1. Albuterol (ProAir, Ventolin)
475
Q

Inhaled Antimuscarinics

A
  1. Tiotropium (Spiriva)
476
Q

Inhaled Corticosteroids

A
  1. Fluticasone (Flovent)
477
Q

Combo inhaled medications

A
  1. Fluticason + salmeterol (Adavir) – (ICS with an LABA
  2. Formoterol + budesonide (Symbicort) – (LABA with an ICS)
  3. Albuterol + ipratropium (Combivent) – (SABA with a SAMA)
478
Q

Inhaled Mucolytics

A
  1. Hypertonic saline
  2. Dornase alfa (Pulmozyme)
479
Q

Other Pulmonary Drugs

A
  1. Leukotriene modifiers
  2. Immunomodulators
  3. CFTR modulators
480
Q

Leukotriene Modifiers

A
  1. Montelukast (Singulair)
481
Q

Immunomodulator (Anti-IgE)

A
  1. Omalizumab (Xolair)
482
Q

CFTR Modulators

A
  1. Orkambi
  2. Symdeco
483
Q

Drug classes that treat gastric reflux

A
  1. Antacids
  2. H2 receptor blockers
  3. Proton pump inhibitors (PPI)
484
Q

Antacid Drugs

A
  1. Calcium Carbonate (Tums)
485
Q

H2 Blocker

A
  1. Ranitidine (Zantac)
  2. Famotidine (Pepcid)
486
Q

Proton Pump Inhibitor (PPI)

A
  1. Omeprazlone (Prilosec)
  2. Esomeprazolone (Nexium)
487
Q

Antiemetic Drug Classes

A
  1. Anticholinergics
  2. Antihistamines
  3. Neuroleptic drugs
  4. Prokinetic drugs
  5. Serotonin blockers
  6. Neurokinin-1 receptor blockers
  7. Cannabinoids
488
Q

Antiemetic Drugs

A
  1. Scopolamine (Transderm Scop patch)
  2. Meclizine
  3. Ondansetron (Zofran)
  4. Metoclopramide
489
Q

Anticholinergic antiemetics

A
  1. Scopolamine (Transderm Scop Patch)
490
Q

Antihistamine antiemetics

A
  1. Meclizine
491
Q

Serotonin blocker antiemetic

A
  1. Ondansetron (Zofran)
492
Q

Prokinetic antiemetic

A
  1. Metoclopramide
493
Q

Antidirrheal drugs

A
  1. Bismuth subsalicylate (Pepto-Bismol)
  2. Diphenoxylate (opiate)/atropine (Lomotil)
494
Q

Antidirrheal drug classes

A
  1. Absorbents
  2. Anticholinergics
  3. Intestinal flora modifiers
  4. Opiates
495
Q

Absorbent antidirrheal drugs

A
  1. Bismuth subsalicylate (Pepto-Bismol)
496
Q

Types of Laxative drugs

A
  1. Bulk-forming
  2. Hyperosmotic
  3. Saline
  4. Emollient
  5. Stimulant
497
Q

Hyperosmotic laxatives

A
  1. Polyethylene glycol 3350 (Miralax)
  2. Lactulose
498
Q

Emollient Laxative

A
  1. Docusate sodium (Colace)
499
Q

Bulk forming laxative

A
  1. Methycellulose (Citrucel)
500
Q

Stimulant Laxative

A
  1. Senna glycoside (Senna)

DPT Semester 1 (12 decks)

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