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Pharm 5 > Other > Flashcards

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1
Q

Dx of CHF

A

EF

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2
Q

Causes of high output failure?

A

Secondary (cancer medicines, thiamine deficiency, anemia, hyperthyroidism)

Treat underlying cause

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3
Q

Harmful reflex responses of CHF?

A
  • baroreceptor reflex (activation of SNS)

- activation of RAS/kidneys

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4
Q

Short term responses of SNS reflex in CHF?

A

Compensation to increase CO & BP

  • tachycardia
  • increased contractility
  • increased vascular tone
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5
Q

Long term responses of SNS reflex in CHF?

A
  • increased after load
  • decreased contractility
  • decreased CO
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6
Q

Affects of SNS & RAS in CHF

A
  • arterial vasoconstriction (decreased CO)
  • cardiac remodeling
  • ventricular wall thinning/fibrosis
  • reduced CO/increased circulatory congestion
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7
Q

Life prolonging treatment goal? Other options?

A

suppress compensatory mechanisms

increase contractility

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8
Q

Life prolonging drugs?

A

vasodilators: ACEI, ARBs, hydralazine, isosorbide dinitrate

aldosterone antagonists: spironolactone & eplerenone

beta blockers: carvedilol, bisoprolol, metoprolol

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9
Q

Positive ionotropes?

A
  • digoxin
  • phosphodiesterase inhibitor
  • adrenoceptor agonist
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10
Q

MOA of digoxin?

A
  1. increase Ca
  2. shortens AP/increases contractility
  3. slow conduction thru AV node
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11
Q

Digoxin has a ____ therapeutic window.

A

Narrow; can get toxic effects easily

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12
Q

arrhythmic ADR of digoxin

A
  • bigeminy (two contractions for one SA node impulse)
  • ventricular tachycardia
  • fibrillation
  • death
  • worsens WPW
  • any arrhythmia
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13
Q

GI ADR of digoxin

A 
earliest signs of toxicity
anorexia
nausea
vomiting
diarrhea
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14
Q

CNS ADRs of digoxin

A

hallucinations
disorientation
visual changes (yellow & green)

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15
Q

Other ADRs of digoxin

A

gynecomastia

seizures (severe)

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16
Q

Potassium & digoxin

A

want K on high side of normal to prevent arrhythmias

check frequently

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17
Q

Ca & digoxin

A

want on low side of normal to prevent arrhythmias

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18
Q

Mg & digoxin

A

want on low side of normal to prevent arrhythmias

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19
Q

Tx for toxicity of digoxin

A

GI: lower dose
Arrhythmias: check K, Mg, Ca, digoxin levels, & EKG
… severe give monoclonal antibodies (Digibind: binds and inactivates digoxin)

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20
Q

Clinical uses of Digoxin

A

CHF & Afib

3rd line Afib

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21
Q

MOA of milrinone?

A

inhibits PDE-3
increases Ca
increases contractility
vasodilation

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22
Q

ADRs of milrinone

A 
Nausea
Vomiting
arrhythmias
low platelets
liver enzyme changes
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23
Q

Use of milrinone?

A

acute CHF, severe exacerbation of CHF

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24
Q

MOA of dobutamine

A

increases CO by stimulating B1 receptors (increases contractility)

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25
Q

ADRs of dobutamine

A

tachycardia, angina, arrhythmias, tachyphlaxis (over compensation by body)

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26
Q

Diuretics used to relieve symptoms of CHF?

A
  • loops

- K sparing (ALD antagonists)

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27
Q

MOA of loop diuretics

A

remove fluid
decrease edema
decrease SOB

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28
Q

ADRs of loops

A 
hypotension
worsened renal fxn (increased Cr)
hypokalemia
hypokalemic metabolic alkalosis
hyperuricemia
hypomagnesaemia 
hypocalcium 
ototoxicity (hearing loss)
allergic rxn to sulfa 
Bad with NSAIDs
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29
Q

MOA of ALD antagonists

A

stop RAS reflex
increase Na excretion
decrease K excretion
remove fluid

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30
Q

how do ALD antagonists decrease mortality in CHF?

A

prevent myocardial and vascular fibrosis, baroreceptor dysfunction, & renal effects

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31
Q

ADRs of ALD antagonists

A
  • gynocomastia & menstrual irregularities (Spironolactone)
  • hyperkalemia
  • hypercholremic metabolic acidosis
  • kidney stones
  • Bad with NSAIDs & K pills
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32
Q

MOA of ACEI

A 
block RAS
vasodilation
decrease ALD production
decrease volume 
decrease edema
decrease cardiac remodeling

increases symptoms in 4-12 weeks
decreases incidence of hospitalization

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33
Q

ADRs of ACEI

A 
dry cough
rash
hyperkalemia
hypotension
renal failure
angioedema
TERATOGEN
bad with K pills& NSAIDS
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34
Q

MOA of ARBs

A

decrease fluid & edema & BP

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35
Q

MOA of hydralazine (aa) & isosorbide nitrate (vv) (direct vasodilators) in CHF

A 
reduce preload (vv) & after load (aa)
decrease cardiac remodeling
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36
Q

Population that benefits from direct vasodilators?

A

African Americans

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37
Q

S/E of direct vasodilators?

A

HA, nausea, anorexia, palpitations, sweating, flushing, edema, SLE, peripheral neuropathy, drug fever

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38
Q

What should all STABLE CHF pt receive?

A

BBlocker & ACEI (40% reduction in mortality & hospitalization)

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39
Q

MOA of Bblockers

A

decrease SNS activation (decrease HR & O2 demand)

decrease RAS activation

decreases cardiac cytokines that lead to fibrosis & ventricular wall stiffening

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40
Q

How to dose blockers?

A

start low & increase over 2 weeks to highest tolerated dose

takes 3-6 mo to see symptom improvement in CHF

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41
Q

contraindications of BBlockers?

A

bradycardia
asthma
unstable CHF

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42
Q

MOA of ivabradine

A

Inhibition of (HCN) channels (f-channels) within the SA node

prolongs diastolic depolarization (slows firing of SA nose & reduces HR)

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43
Q

MOA of sacubitril & valsartan

A

sacubitril inhibits neprilysin & increases levels of natriuretic peptides & bradykinin… decreases vasoconstriction, Na retention, & remodeling

valsartan blocks ATII & ALD release

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44
Q

ARRs of sacubitril & valsartan

A

hypotension
hyperkalemia
increased Cr
angioedema

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45
Q

How to treat asymptomatic CHF (structural heart changes)?

A

treat secondary diseases that make CHF worse (HTN, DM, obesity, & hyperlipidemia)

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46
Q

How to treat symptomatic CHF?

A

decrease work load of heart, restrict Na intake

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47
Q

How to treat symptomatic CHF that is worsening? (stage C & D)

A

First line: ACEI, bblocker, loop diuretic

ALD antagonist, vasodilators, digoxin

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48
Q

How to treat CHF when normal treatments fail?

A

resynchronization or transplant

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49
Q

What do you need to monitor with loop diuretics in CHF?

A

Weight

Gain of 3-5 lbs in one week = increase dosage

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50
Q

MOA of warfarin

A

blocks carboxylation/inhibits synthesis of coagulation factors II, VII, IX, X, protein C & S

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51
Q

Why does warfarin often required a heparin bridge?

A

Warfarin has delayed onset, takes 6-50 hours to break down circulating clotting factors (max effect observed 3-5 days after therapy)

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52
Q

What do you monitor for warfarin?

A

PT/INR (prothrombin time)

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53
Q

What is the normal range of INR?

A

2 to 3

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54
Q

What is the ideal INR for mechanical prosthetic heart valves or recurrent systemic embolization?

A

3 to 4.5

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55
Q

Indications for warfarin?

A

LT treatment of:

  • deep vein thrombosis
  • a fib
  • artificial heart valve (mechanical and biprosthetic)
  • mitral valve repair
  • mitral valve stenosis
  • used with heparin for MI
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56
Q

How is heparin administered? warfarin?

A

Heparin - parenteral (IV or SQ)

Warfarin - oral

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57
Q

When do you start heparin and warfarin? When do you stop heparin?

A

Start both together… stop heparin when PT is therapeutic

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58
Q

ADRs of warfarin

A 
TERATOGEN
bleeding
allergies (urticaria)
alopecia 
necrosis of skin if low protein C
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59
Q

Absolute contraindications of warfarin?

A

pregnancy
bleeding
recent surgery

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60
Q

What drugs inhibit the metabolism of warfarin and increase risk of bleeding?

A 
amiodarone
cimetidine
erythromycin
fluconazole
gemfibrozil
isoniazide
metronidazole
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61
Q

what drug inhibits warfarin absorption and increases patients risk of clots?

A

cholestyramine

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62
Q

How to dose warfarin?

A

start 2-5 mg/day
check PT regularly
small dose changes until reach goal PT (usually 5-7 days)

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63
Q

A high PT puts you at a risk for bleeding; what do you give to reverse high PT if no bleeding or emergent surgery?

A

Lower or hold dose

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64
Q

what do you give to reverse high PT in bleeding or emergent surgery situation?

A

subcutaneous vit K

Fresh frozen plasma

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65
Q

MOA of indirect thrombin inhibitors

A

Bind antithrombin and increase its function (to inhibit clotting factors IX, X, II)

Inhibits clotting

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66
Q

Why is Heparin called unfractionated heparin?

A

It is a mixture of similar molecules with binding site for antithrombin

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67
Q

Why is heparin measured in units and not mg?

A

Each molecule has a different number of binding sites for antithrombin, therefore different amount of activity from each molecule

Report in units to standardize the level of thinning the blood

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68
Q

Why isn’t unfractionated heparin given IM?

A

it is traumatic and can bleed into muscle

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69
Q

ADRs of unfractionated heparin?

A

bleeding
alopecia (reversible)
osteoporosis (LT use)
Heparin induced thrombocytopenia

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70
Q

How often does heparin induced thrombocytopenia occur in pt taking unfractionated heparin? When is it usually reversible?

A

25% of the time

It is usually mild and reversible in 4 days

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71
Q

What type of reaction is HIT?

A

Type I hypersensitivity rxn

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72
Q

What is the result of HIT?

A

Up to 4% of pt develop hypercoaguable state due to immune response

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73
Q

What are the symptoms of HIT?

A

decreased platelet count
new blood clots in vv & aa
skin necroses

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74
Q

What should you monitor frequently to avoid HIT in pt receiving unfractionated heparin?

A

platelet count

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75
Q

How do you treat HIT?

A

stop heparin

give direct thrombin inhibitor

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76
Q

contraindications for unfractionated heparin?

A
  • Type 2 HIT
  • allergy
  • active bleeding
  • conditions that increase risk of bleeding (severe HTN - can bleed in head, recent surgery, thrombocytopenia, hemophilia, advanced kidney or liver disease, active TB, peptic ulcer disease)
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77
Q

Indications for unfractionated heparin?

A
  • venous thrombosis
  • arterial thrombosis
  • a fib
  • emboli
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78
Q

How can unfractionated heparin be rapidly reversed?

A

protamine sulfate binds to and inactivates heparin

stop drug and effect goes away in a few hours

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79
Q

Why isn’t unfractionated heparin obsolete?

A

not cleared by kidneys

reversed by protamine

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80
Q

How is unfractionated heparin used prophylactically?

A

to prevent development of clot in high risk pt (venous thrombosis, afib)

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81
Q

how is unfractionated heparin used for treatment of venous thrombosis?

A

to prevent thrombosis from embolization & going to lungs, or from getting bigger

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82
Q

What do you monitor for unfractionated heparin?

A

platelet count
aPTT
clotting factor used to assess activity

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83
Q

what is the normal aPTT range?

A

1.5-2x normal

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84
Q

How does LMWH differ from unfractionate heparin?

A

it is fragments of heparin with antithrombin binding sites (weighs less, shorter chains)

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85
Q

MOA of LMWH

A

binds to antithrombin to increase its inhibition effects on IX, Xa (more than regular heparin), II (less then regular heparin)

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86
Q

How is LMWH dosed?

A

SQ 1-2x/day (longer 1/2 life)

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87
Q

What is the advantage of LMWH?

A
  • greater bioavailability (more predictable response)
  • less frequent dosing
  • less thrombocytopenia
  • less monitoring
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88
Q

Indications for LMWH

A

VTE (DVT & PE)

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89
Q

Cons of LMWH?

A
  • more expensive

- protamine sulfate does not reverse effect as well

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90
Q

what type of drug is fondaparinux?

A 
Factor Xa inhibitor
Synthetic heparin (made in lab): resembles heparin binding sites
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91
Q

Pros of fondaparinux?

A

SQ 1x/d

less HIT

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92
Q

cons of fondaparinux?

A

$$$
protamine sulfate doesn’t reverse it
accumulates in pt with renal impairment (bad for old ppl)

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93
Q

Indications of fondaparinux?

A
  • acute DVT
  • prophylaxis of DVT after hip replair/replacement, knee replacement, or abdominal surgery
  • PE
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94
Q

MOA of direct thrombin inhibitors? (lepirudin, argatroban, bivalirudin, desirudin)

A

bind to active site on thrombin blocking effect of thrombin and preventing clotting

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95
Q

Pros of direct thrombin inhibitors?

A

inhibit clot- bound thrombin and circulating thrombin

more predictable anticoagulation effect than heparin

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96
Q

Indications for direct thrombin inhibitors?

A
  • HIT with thrombosis

- percutaneous transluminal coronary angioplasty

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97
Q

How are direct thrombin inhibitors administered?

A

parentally

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98
Q

How do you monitor effect of direct thrombin inhibitors?

A

PTT

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99
Q

ADRs for direct thrombin inhibitors?

A

bleeding

allergic rxn

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100
Q

What is the significance of dabigatran?

A

first oral direct thrombin inhibitor

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101
Q

indications of dabigatran?

A
  • reduce risk of stroke
  • reduce risk of systemic embolism in pt with nonvalvular AF

(Pt with AF with one additional risk factor for stroke)

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102
Q

Cons of dabigatran vs. warfarin?

A

twice a day dosing of dabigatran reduces compliance

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103
Q

Pros of dabigatran vs. warfarin?

A

Dabigatran does not require INR monitoring

lower risk of intracranial & extra cranial bleeding in pt under 75

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104
Q

Summarize the dosing adjustments needed for dabigatran in pt with renal dysfunction.

A

CrCl > 30mL/min = 150 mg BID (Normal)

CrCl 15-30mL/min = 75 mg BID

CrCl

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105
Q

What is the stability in months of an open dabigatran bottle?

A

4 months

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106
Q

When converting a pt from warfarin to dabigatran what steps should be taken?

A
  • stop warfarin

- start dabigatran when INR is below 2.0

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107
Q

Drug interactions of Dabigatran?

A

Don’t use with pt with renal failure
dronedarone
ketoconazole

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108
Q

extracranial bleeding risk in patients >75 yo with dabigatran is _____ to warfarin.

A

similar

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109
Q

what is used to reverse effects of dabigatran? dose?

A

idarucizumab; give 2-2.5g IV q15minutes

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110
Q

MOA of idarucizumab?

A

humanized monoclonal Ab fragment that binds to dabigatran & its metabolites with higher affinity than thrombin

it neutralizes dabigatran & its anticoagulation effects in minutes

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111
Q

Indications of rivaroxaban?

A

active factor Xa inhibitor
used for prevention of
- DVT, blood clots, & PE after knee or hip replacement
- stroke prevention in AFib

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112
Q

What is the benefits of rivaroxaban?

A

no monitoring
given once daily
more effective than enoxaparin in preventing VTE (DVT & PE) after knee or hip replacement

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113
Q

Dose adjustments for rivaroxaban with renal dysfunction?

A

CrCl > 50 = 20 mg/d with dinner

CrCl 15-50 = 15 mg/d with dinner

CrCl

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114
Q

Steps for converting warfarin to rivaroxaban?

A

stop warfarin

start rivaroxaban when INR is below 3

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115
Q

Drug interactions of rivaroxaban?

A 
ketoconazole
itraconazole
carbamazepine
phenytoin
rifampin
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116
Q

Indications for apixaban?

A

stroke prevention in Afib patient

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117
Q

dosing of apixaban?

A

5 mg 2x/d

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118
Q

When is the dose of apixaban reduced to from 5mg BID to 2.5 mg 2x/day?

A

> 80 yo

1.5

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119
Q

Steps for converting from warfarin to apixaban?

A

stop warfarin

start apixaban when INR is below 2

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120
Q

Drug interactions of apixaban?

A

ketoconazole
itraconazole
ritonavir
clarithromycin

Absolute contraindicated:
rifampin
carbamazepine
phenytoin
phenobarbital
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121
Q

What type of clots to anti platelet drugs work best at preventing?

A

arterial clots (MI & CVA)

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122
Q

what is the anti platelet dose of ASA?

A

low dose

81-325 mg/d

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123
Q

MOA of ASA?

A

inhibits synethesis of thromboxane A2, permanently (for life of platelet or 10 d)… stops it from making platelets release granules that support platelet aggregation

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124
Q

How long does ASA prevent platelet aggregation?

A

10 days, the entire life of the platelet it bines

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125
Q

ADRs of ASA

A

increased bleeding
allergic rxn
epigastric pain
heart burn

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126
Q

Contraindications of ASA?

A

asthma

hypersensitivity rxns

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127
Q

Indications of ASA?

A
  • primary and secondary prevention of MI (decreases incident of death by 15-25%)
  • after transient ischemic attack (prevent 2nd one)
  • after minor stroke (prevent 2nd one)
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128
Q

What is primary prevention of MI?

A

No Hx of MI, trying to prevent it

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129
Q

What is secondary prevention of MI?

A

Hx of MI, want to prevent a 2nd one

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130
Q

MOA of clopidogrel & ticlopidine?

A

IRREVERSIBLY blocks ADP membrane receptor on platelet needed for aggregation

inhibits expression of GP IIb/IIIa receptors to prevent platelet aggregation

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131
Q

clopidogrel & ticlopidine _____ bleeding time

A

prolong

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132
Q

How long do clopidogrel and ticlopidine affect platelets they bind to?

A

life of platelet (10d)

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133
Q

ADRs of ticlopidine?

A
  • nausea
  • diarrhea
  • bleeding
  • severe neutropenia (low white cell count)
  • TTP (thrombotic thrombocytopenic purpura)
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134
Q

What is TTP? What causes it?

A

Thrombotic thrombocytopenic purpura

causes wide-spread coagulation and low platelet count

clopidogrel & ticlopidine

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135
Q

Major ADR of clopidogrel?

A

bleeding
TTP
avoid in slow metabolizers
avoid with drugs that inhibit CYP2C19 (proton pump inhibitors… omeprazole & esomeprazole)

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136
Q

What is the black box warning for clopidogrel?

A

Avoid in pt that have poor metabolism (CYP2C19 dysfunction) … won’t get anti platelet affect

Avoid drugs that inhibit CYP2C19 (omeprazole & esomeprazole)

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137
Q

MOA of dipyridamole?

A

inhibits platelet uptake of adenosine & blocks ADP induced platelet aggregation

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138
Q

ADRs of dipyridamole

A 
nausea
diarrhea
epigastic
dizziness
SEVERE headache
rash
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139
Q

Dipyridamole is not strong enough to be used alone; what is it often combined with?

A

Aspirin & warfarin

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140
Q

What is the MOA of glycoprotein IIb/IIIa antagonists?

A

prevent platelet aggregation by competing with fibrinogen & vWF for platelet receptors

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141
Q

indications of glycoprotein IIb/IIIa receptor antagonists?

A

ST for ACS & PCI

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142
Q

ADRs of glycoprotein IIb/IIIa receptor antagonists?

A

bleeding

acute thrombocytopenia

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143
Q

What are anti platelet drugs used for?

A

arterial clots (CVA & MI)

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144
Q

What is the first line anti platelet drug?

A

aspirin 80-325 mg/d

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145
Q

What is second line anti-platelet drug? when is it indicated?

A

clopidogrel

when can’t use aspirin or have an event on aspirin

unstable angina
stroke
transient ischemic attack
coronary stent placement

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146
Q

what is third line anti-platelet drug?

A

ticlopidine use if can’t take aspirin or clopidogrel

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147
Q

do you have to monitor anti platelets?

A

no

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148
Q

how are fibrinolytic administered?

A

IV

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149
Q

MOA of fibrinolytic?

A

convert plasminogen to plasmin

plasmin degrades fibrin & fibrinogen

dissolves clot

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150
Q

Cons of fibrinolytic?

A

will dissolve clots everywhere not just bad ones, fragile state

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151
Q

ADRs of fibrinolytic?

A

bleeding

allergic rxns

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152
Q

What drug can be used to stop bleeding caused by fibrinolytic?

A

aminocaproic acid

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153
Q

who often receives aminocapronic acid?

A

pt with hemophilia that take fibrinolytics

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154
Q

indications for fibinolytics?

A
  • PE WITH hemodynamic instability
  • SEVERE DVT (SVC syndrome)
  • acute MI when NO ACCESS to cath lab
  • acute ISCHEMIC stroke within 3 hours of onset
  • Arterial embolism
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155
Q

What fibrinolytic should a pt with an acute ischemic stroke take within 3 hours of onset of symptoms?

A

alteplase

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156
Q

Contraindications of fibrinolytic?

A
  • recent surgery
  • Hx of brain bleed
  • active internal bleed
  • brain cancer
  • suspected aortic dissection
  • head or facial trauma in last 3 mo
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157
Q

MOA of nitrates

A

release NO in vascular smooth muscle, decreases Ca & contractility

venous smooth muscle relaxation, venous pooling, decreased preload, decreased CO, decreased BP

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158
Q

Do nitrates affect cardiac or skeletal muscle?

A

no

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159
Q

What is the order of vessel relaxation with nitrates?

A

veins than arteries

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160
Q

How do nitrates help angina?

A

decrease O2 demand, decrease work of heart = decreased angina

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161
Q

what are the indirect effects of nitrates?

A

tachycardia
bronchi relaxation
GI & GU tract relaxation

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162
Q

What removes nitrates from body?

A

large amounts lost during first pass effect in liver, must use large oral dose

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163
Q

How is mononitrate administered?

A

orally

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164
Q

how is dinitrate administered?

A

orally, chewable tablet or sublingual

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165
Q

how is NTG administered

A

sublingual, spray, buccal tablet, ointment, parenterally, orally

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166
Q

What should you use to relieve immediate chest pain?

A

Sublingual or spray (if dry mouth)

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167
Q

what should you use to long term treatment of angina?

A

buccal absorption (avoids first pass)
transdermal patch
tablets or capsules

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168
Q

what is the drug free period required for transdermal nitrate patches?

A

10 hours per day or tolerance occurs

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169
Q

ADR of nitrates?

A

caused be excessive vasodilation:

  • orthostatic hypotension
  • HA
  • dizziness
  • tachycardia
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170
Q

When are nitrates contraindicated?

A
  • increased ICP
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171
Q

How can you prevent reflex tachycardia with nitrates?

A

BBlocker

172
Q

If you are giving nitrates through continuous IV infusion what is the maximum amount of time you should administer it?

A

24 hours

173
Q

How often should oral XL nitrates be dosed?

A

1-2x/d

174
Q

Indications for Nitrates?

A
  • chronic stable angina
  • variant angina (spasms)
  • unstable angina
175
Q

What CCB are used in stable angina?

A

verapamil
diltiazem
dihydropyridines

176
Q

MOA of CCB in stable angina?

A

decrease O2 required by heart by:

  1. inhibiting Ca influx (leads to vasodilation & lower PVR)
  2. slows conduction of heart
  3. slows contractility of heart
177
Q

Other than stable angina, when can CCB be used?

A

to prevent spasms of the aa in the brain (after subarachnoid hemorrhage or stroke)

178
Q

ADRs of CCB?

A

Caused by vasodilation & hypotension:

  • fatigue
  • headache
  • dizziness
  • flushing
  • peripheral edema
  • bradycardia
  • CHF
  • conduction blocks
179
Q

Drug interactions with CCB?

A

bblocker (bradycardia)

drugs metabolized by P450 (digoxin)

180
Q

When should bepridil be used?

A

when pt fails to response to other abtianginal medications (may be used with nitrates & bblockers)

181
Q

Indications for diltiazem & verapamil?

A

typical angina

variant angina

182
Q

Use caution in pt with ____ when using CCB.

A

CHF

183
Q

If you are pt is on a BBlocker what type of CCB should you use?

A

dihydropyridine (less effect on heart rate)

184
Q

If a pt has angina, AND a Hx of atrial arrhythmias, what CCB should you use?

A

verapamil or diltiazem

185
Q

Why should you avoid use of digoxin and verapamil/diltiazem?

A

interference with cytochrome P450 & increased slowing of electrical conduction

186
Q

What CCB are approved for angina?

A

amlodipine, felodipine, nicardipine, nifedipine

187
Q

what is the drug of choice for variant angina?

A

CCB

188
Q

Uses of CCB other than angina?

A

HTN, arrhythmias, migrane HA prevention, raynaud’s

189
Q

MOA of b blockers in stable angina?

A 
decreased HR
decreased contractility
decreased BP
prevents reflex tachycardia
decreases work of heart
decreases O2 demand
190
Q

ADRs of beta blockers in tx of angina?

A
  • bradycardia
  • worsen peripheral vascular disease
  • CHF
  • decreased exercise tolerance
  • depression
  • sedation
  • sleep disturbances
  • block Sx of hypoglycemia
  • worsens asthma
  • withdrawal (rebound HTN)
191
Q

what beta blockers are used for management of typical angina and acute MI?

A
  • atenolol
  • metoprolol
  • nadolol
  • propanolol
192
Q

How do you know if the bblockers are working?

A

HR

193
Q

MOA of ranolazine?

A

improves cardiac diastolic fxn by manipulating Na and Ca channels that can be detrimental to cardiac performance

194
Q

indications for ranolazine?

A
  • chronic angina
195
Q

what can ranolazine be used with?

A
  • beta blockers
  • nitrates
  • CCB
  • anti-platelet therapy
  • lipid lowering therapy
  • ACEI/ARB
196
Q

SE of ranolazine?

A 
dizziness
headache
constipation
nausea
prolonged QT (arrythmias)
197
Q

What should you monitor for with ranolazine?

A

EKG - prolonged QT wave

198
Q

goals of drug therapy for angina?

A
  • relieve acute Sx
  • prevent ischemic attack
  • improve quality of life
  • reduce risk of MI
  • decrease time to symptoms
199
Q

How quickly does SL or spray NTG work? how long does it last?

A

1-3 minutes

lasts 20-30 minutes

200
Q

how should you instruct your pt to take NTG?

A

SL q5min x 3

ER if CP is not better

201
Q

it is a ____ idea to take NTG SL prior to exercise.

A

good; it prevents angina

202
Q

What is good drug choices for prophylaxis of angina?

A

isosorbide dinitrate

NTG

203
Q

NTG is volatile; after a bottle is open when should a pt discard it?

A

6 months

204
Q

first line treatment of stable angina?

A 
Need long term therapy:
#1 beta blockers
205
Q

why is beta blockers first line treatment for stable angina?

A

prolongs survival with MI, in the event angina precipitates to MI

206
Q

2nd line treatment of stable angina?

A

CCB

207
Q

Why are nitrates 3rd line treatment for stable angina?

A
  • tolerance

- less effective than CCB & BBlockers

208
Q

Pt with angina are at high risk for MI; what other drugs should be added to their therapy regimen?

A
  • aspirin or clopidogrel
  • cholesterol lowering
  • ACEI/ARB (if DM or LV dysfunction)
209
Q

what causes variant angina?

A

spasm of arterial wall muscle suddenly decreases O2 supply and increases demand on heart

210
Q

Treatment of variant angina?

A

CCB relax vessel smooth muscle
(no blockage, just spasm of smooth muscle… need to relax it)

nitrates maybe

211
Q

what is acute coronary syndrome?

A

spectrum of unstable angina to MI

212
Q

what is the most affective treatment for ACS?

A

nonpharmacologic coronary intervention

213
Q

what is the role of drugs in treatment of ACS?

A
  1. prevent recurrence of clots

2. decrease heart injury so lose as little mm as possible

214
Q

treatment of ST elevation MI?

A
  • PCI

- fibrolytics if no PCI

215
Q

treatment for MI in hospital?

A
  1. aspirin
  2. clopidogrel
  3. SL NTG
  4. beta blockers
  5. heparin
216
Q

treatment for discharge after MI?

A
  1. beta blocker
  2. ACEI
  3. Aspirin
  4. statin
  5. clopidogrel
217
Q

what prolongs survival after MI?

A

beta blocker
ACEI
aspirin

218
Q

common problems in conduction system that cause arrhythmias?

A
  1. abnormal impulse conduction (rate is slower)
  2. abnormal impulse formation (rate is faster)
  3. both of the above
219
Q

all drugs that treat arrhythmias can cause ____ arrhythmias

A

lethal

220
Q

non pharmacologic treatments for arrhythmias?

A
  • catheter ablation
  • cryoablation
  • implantable defibrillater
221
Q

when to treat arrhythmias?

A

too fast, slow, or asynchronous (when atria and ventricles don’t work together)

ones that decrease CO & BP significantly

222
Q

what affect can anti-arrhythmic medications have on normal tissue?

A

can cause drug induced arrhythmias at high doses

223
Q

anti arrhythmic drugs can have different affects at different heart rates or if situation changes; true or false?

A

true, if HR or O2 supply changes

224
Q

when do Na channel blockers work best on cardiac tissue?

A

during tachycardia because Na channels spend more time in an open state

suppress cardiac conduction more in a person with high HR than normal HR

225
Q

MOA of 1A (procainamide, quinidine, disopyramide)

A

blocks sodium channel slowing upstroke of action potential, slowing conduction of electrical impulse

226
Q

ADRs of procainamide

A 
torsade de pointes 
SLE like syndrome
nausea
diarrhea
hypotension
227
Q

Why isn’t procainamide not first line?

A

bad SE and QID (4x/d)

228
Q

ADRs of quinidine?

A

GI (N,V,D)
33% cinchonism (HA, dizziness, tinnitus)
thrombocytopenia
prolongation of QT interval

229
Q

what isn’t quinidine first line?

A

increases mortality 2 fold

230
Q

ADRs of disopyramide?

A
  • HF (has negative inotropic actions carful in old & CHF pt)
  • anticholinergic effects
231
Q

when is diopyramide used?

A

ventricular arrhythmias

232
Q

Indications for 1A?

A
  • conversion/prevention of Afib
  • A flutter
  • ventricular tachycardia
  • prevention of ventricular fibrillation
233
Q

MOA of 1B (lidocaine, mexiletine)

A

blocks Na channels (good for cells with long AP like conduction or ventricular cells, not as affective on atrial cells)

234
Q

ADRs of lidocaine

A 
hypotention
paresthesias
tremor
nervousness
nausea
light headed
slurred speech
seizures
drowsiness
235
Q

drug interactions of lidocaine?

A

amiodarone

236
Q

indications of lidocaine?

A

first line for ventricular arrhythmias (tachycardia & fibrillation) after cardiovesion or what an MI

237
Q

Lidocaine is used to treat arrhythmias after cardiovesion or MI and not prophylaxtically, why?

A

increases mortality

238
Q

how is lidocaine administered?

A

IV

239
Q

how is mexiletine administered?

A

orally

240
Q

what is mexiletine used for?

A

long term suppression of ventricular arrhythmias

241
Q

ADRs of mexiletine?

A 
tremor
gait disturbances
blurred vision
lethargy
nausea
242
Q

MOA of 1C (flecainide & propafenone)

A

block sodium & potassium channels (lesser extent)

243
Q

ADRs of 1C

A

ventricular arrhythmias, agranulocytosis, anemia, thrombocytopenia

244
Q

Drug interactions of flecainide & propafenone

A

digoxin (increases its levels)

warfarin (increases INR)

245
Q

indications of flecainide & propafenone

A
  • conversion/prevention of a fib
  • atrial flutter
  • ventricular tachycardia
  • prevention of v fib
246
Q

MOA of beta blockers as antiarrhythmics?

A
  • inhibit SNS activation of cardiac automaticity & conduction
  • slow HR
  • decrease AV node conduction
  • increase AV node refractory period
247
Q

uses of beta blockers as antiarrhythmics

A
  • rate control in a fib
  • a flutter
  • prevention of SVT
  • adjunctive ventricular antiarrhythmic therapy
248
Q

why are beta blockers (class 2) better than class 1s?

A

prevent re-infarction & sudden death after MI

249
Q

what BBlockers are used as antiarrhythmics?

A
  • metoprolol
  • esmolol
  • atenolol
250
Q

MOA of class 3 antiarrhythmics?

A

prolong ventricular AP by blocking rapid component of K channel

251
Q

when do class 3 antiarrhythmics work best?

A

at slower heart rates (not at fast ones when they are needed most)

252
Q

Class 3 antiarrhythmics work best at slow heart rates; why is it a poor idea to give someone with a slow HR class 3 antiarrhythmics?

A

increases risk for torsade de pointes

253
Q

What two class 3 antiarrhythmics has class Ib, II, & IV properties as well?

A

amiodarone & dronedarone

254
Q

in addition to potassium blocking properties what other receptor does sotalol block?

A

50%/50% beta and potassium blocking properties

255
Q

MOA of amiodarone and dronedarone?

A

prolongs AP by blocking rapid component of K channel, also blocks Na & Ca channels and beta receptors

256
Q

indications for amiodarone?

A
  • approved for serious ventricular arrhythmias
  • first line DRUG for ventricular tachycardia
  • a fib
257
Q

First line treatment, & first line drug treatment for ventricular tachycardia?

A

treatment: implantable defibrillator
Drug: amiodarone

258
Q

Why use amiodarone if first line treatment is implantable defibrillator?

A

use with defibrillator to prevent uncomfortable discharges

259
Q

ADRs of amiodarone?

A
  • bradycardia
  • heart block (prolonged QT)
  • fatal pulmonary fibrosis
  • hepatitis
  • gray-blue skin
  • retina pigment deposits (halos, optic neuritis, blindness)
  • blocks conversion of thyroid hormone (hyper/hypothyroid)
260
Q

drug interactions with amiodarone?

A
  • warfarin
  • digoxin
  • statins
261
Q

what should you monitor while on amiodarone?

A

EKG (QT prolonged)

thyroid function tests

262
Q

How does dronedarone differ from amiodarone?

A
  • shorter 1/2 life (days compared to months)
  • less thyroid toxicity
  • less lung toxicity
  • less effective in maintaining NSR
263
Q

indications for dronedarone?

A

a fib

a flutter

264
Q

ADRs of dronedarone?

A

GI (N,V,D)
abdominal pain
liver toxicities

265
Q

MOA of Sotalol?

A

AP prolonged by blocking K channel

Beta blocker activity

266
Q

indications for sotalol?

A
  • life threatening ventricular arrhythmias

- a fib (to maintain NSR)

267
Q

ADRs of sotalol?

A 
torsade de pointes
HF
bradycardia
AV block
wheezing
fatigue
268
Q

indications for dofetilide?

A
  • conversion/prevention of a fib & flutter
269
Q

ADRs of dofetilide?

A

QT prolongation, torsades de pointes, HA, dizziness

270
Q

when should you initially administer dofetilide?

A

under hospital monitoring due to ADR

271
Q

indications of ibutilide?

A

rapid conversion of recent onset of a fib/flutter

272
Q

ADRs of ibutilide?

A

hypotension
nausea
torsades de pointes

273
Q

where do class four antiarrhythmics work best

A

SA & AV node (cardiac cells dependent on Ca for upstroke)

274
Q

MOA of class 4

A

prolong conduction through AV & SA node

atria beats fast but drug blocks some of the impulses from reaching the ventricles

275
Q

indications of class 4 antiarrhythmics?

A

SVT***

276
Q

ADRs of class 4 antiarrhythmics

A

wrong arrhythmia can cause death

277
Q

MOA of adenosine

A

activates K and inhibits influx of Ca in SA node, AV node, & atrium

slows conduction through AV node and increases AV node refractory period

278
Q

which node does adenosine work best in?

A

AV node

279
Q

what is the half life of adenosine?

A

10 s

280
Q

what is adenosine 1st line for?

A

conversion of SVT to NSR

281
Q

ADRs of adenosine?

A 
flushing
SOB 
chest burning
HA
Low BP
nausea
paresthesias 
bronchospasm
282
Q

when is magnesium useful with arrhythmias?

A
  • Tx of digitalis induced ventricular arrhythmias
  • suppress drug induced torsades de points
  • treat SVT arrhythmias associated with Mg deficiency
283
Q

how does K affect the heart?

A

depresses ectopic pacemakers (tissues other than the conduction system depolarizing)

slows conduction

284
Q

what happens when K is too high or too low?

A

arrhythmias

285
Q

what increases mortality with risk of sudden death from arrhythmia?

A

implantable defibrillator

286
Q

what do we use to treat a fib

A

a lot

287
Q

major problems of a fib?

A
  1. decreased CO (atria not beating and ventricles beating too quickly)
  2. blood pools in heart and can clot
288
Q

goals of a fib treatment?

A
  1. ventricular rate control
  2. conversion to NSR
  3. prevention of embolic event
289
Q

how do we control ventricular rate in a fib?

A

slow impulses through AV node

  • CCB
  • Bblockers
  • digoxin
290
Q

how do we convert to NSR in a fib?

A

direct current cardioversion

  • electrical cardioversion
  • ibutilide
  • dofetilide
291
Q

how do you prophylactically prevent pt with Hx of Afib from leaving NSR?

A

class I or Class III

292
Q

what drugs are used to prevent embolic events after a fib suppression?

A
  • aspirin
  • warfarin
  • clopidogrel
  • dibigatran
293
Q

goal of SVT treatment?

A

slow ventricular rate

294
Q

what is first line for SVT?

A

adenosine

295
Q

what drugs can be used for acute SVT?

A
  • adenosine
  • verapamil
  • diltiazem
  • esmolol
296
Q

what drugs/treatments are used for LT SVT?

A
  • ablation
  • CCB
  • BBlockers
  • digoxin
297
Q

what is ventricular tachycardia often associated with?

A

MI

298
Q

what is first line treatment for ventricular tachycardia?

A
  • electric cardioversion (Epi & amiodarone possibly)

- implant defibrillator

299
Q

long term drug therapy for ventricular arrhythmias?

A
  • bblockers

- amiodarone

300
Q

what are torsades de pointes?

A

ventricular tachycardia induced by drugs or electrolyte abnormalities prolonging QT interval

301
Q

how to treat torsades de pointes?

A
  • stop causative agent
  • correct electrolyte abnormalities
  • IV magnesium sulfate
  • IV isoproterenol
302
Q

how to treat ventricular fibrillation?

A
  • electrical defibrillation (may add epic & amiodarone)
303
Q

long term treatment of ventricular fib?

A

implantable defibrilator

Bblocker

304
Q

how are sympathomimetics normally administered? why?

A

inhaled; more B2 stimulation

B2 receptors are on smooth mm of airways

305
Q

do sympathomimetics have anti-inflammatory activity?

A

No

306
Q

when is epinephrine used?

A 
bronchospasm of anaphylaxis
hypotensive shock (increases BP, HR, CO)
307
Q

how is epinephrine administered?

A

subQ or inhaled

308
Q

when do you see maximal effect of Epi?

A

15 minutes

309
Q

how long does Epi last?

A

60-90 minutes

310
Q

what is the downside to epic?

A

more SE than selective B2

311
Q

describe SABAs

A 
short acting
short 1/2 life
fast onset (5 minutes, peak at 30-60 minutes)
gone fast (4-6hr)
312
Q

how are SABAs usually administered?

A

inhalation by MDI or nebulizer

313
Q

why are oral and SQ SABAs less effective?

A

longer onset

more SE

314
Q

what do you prescribe for a rescue inhaler?

A

SABA

315
Q

what indicates uncontrolled asthma?

A

use of SABA >2x/week

316
Q

describe LABA

A

give 2x/d

LT tx of asthma & emphysema

317
Q

what are LABAs especially good at

A

preventing nocturnal asthmatic attacks

318
Q

black box warning of LABAs?

A

increased risk of asthma death in those using as a single agent (greatest risk in kids 4-11)

319
Q

what should be added to LABA therapy?

A

SABA

corticosteroids

320
Q

ADRs of SABAs?

A
  • Tachycardia*
  • Bronchospasms*
  • tremor*
  • anxiety
  • hyperglycemia
  • hypokalemia
  • hypomagnesemia
  • tolerance
321
Q

ADRs of LABAs

A
  • Tachycardia*
  • Bronchospasms*
  • tremor*
  • anxiety
  • hyperglycemia
  • hypokalemia
  • hypomagnesemia
  • tolerance
  • muscle cramps*
322
Q

downside of methylxanthines?

A

narrow therapeutic window

323
Q

MOA of methylxanthines?

A
  • inhibits many PDE enzymes… relaxes smooth mm & reduces inflammation
  • inhibits PDE4 inflammatory cells (decreases cytokines, immune cell migration & activation)
  • inhibition of cell surface receptors for adenosine (relaxes smooth mm & inhibits histamine release from mast cells)
324
Q

CNS ADRs of methylxanthines?

A 
HA
anxiety
restlessness
increased alertness
insomnia
dizziness
seizures

lower dose to fix

325
Q

Cardiac ADRs of methylxanthines?

A

hypotension
afib/flutter
PVCs
tachycardia

326
Q

GI ADRs of methylxanthines?

A

abdominal pain
nausea
vomitting

minimize with food, anti-acids, or full glass of liquids

327
Q

skeletal mm ADRs of methylxanthines?

A
  • strengthens contraction
  • reverses diaphragm fatigue in COPD patients
    (improves ventilator response)
328
Q

electrolyte ADRs of methylxanthines?

A

hypokalemia

hyperglycemia

329
Q

what pt should you take caution with using methylxanthines?

A

liver disease, metabolized by liver

330
Q

what is 1/2 life of methylxanthines?

A

non-smoker: 8 hours

smokers & kids (1-9): 4.5 hours

331
Q

drug interactions of methylxanthines?

A 
prevent metabolism: 
cimetidine
erythromycin
quinolone
isoniazid
verapamil
332
Q

what do you need to monitor with methylxanthines? ideal range?

A

serum blood levels 2x/yr: 10-15mcg/mL

333
Q

when do seizures and arrhythmias occur with methylxanthines?

A

25 mcg/mL

334
Q

how does ACh affect lungs?

A

bronchoconstriction & mucous secretion

335
Q

MOA of antimuscarinics/anticholinergics?

A

target M3, competitively/reversibly inhibit ACh in bronchial smooth mm causing bronchodilation

336
Q

How are antimuscarinics normally administered?

A

inhaled

337
Q

what Dx are antimuscarinic really useful for?

A

COPD

338
Q

what antimuscarinics have been approved to tx COPD? how long do they act on the body?

A

ipratropium - short acting

tiotropium - long acting

339
Q

if a pt can’t use a SABA what can you give them?

A

ipratropium

340
Q

ICS and LABAs are useful for controlling severe asthma; what other combination is useful?

A

tiotropium & ICS

341
Q

ADRs of antimuscarinics

A
  • dry mouth
  • pharyngeal irritation
  • increased IOP
  • urinary retention
342
Q

what pt should you use caution in when treating with antimuscarinics?

A

glaucoma
BPH
bladder obstruction

343
Q

what is the most effective LT treatment for asthma (all sizes and shapes)?

A

ICS

used regularly decrease # of exacerbations

344
Q

when are ICSs most effective?

A

when used daily (their efficacy does not continue after they are stopped)

345
Q

how are corticosteroids administered in urgent situations?

A

IV and orally

346
Q

T/F side effects of ICS are greater than nasal steroids.

A

T: they are given at higher doses. There is a risk of systemic effects, but less than when given systemic steroids.

347
Q

when are systemic corticosteroids used?

A

for exacerbations of asthma incompletely responsive to bronchodilators

348
Q

what is the most common oral systemic corticosteroid used for exacerbated asthma? dose?

A

prednisone (oral) 30-60mg/d in divided doses for 6-12 d

dose is tapered after airway obstruction improves

other: methylprednisolone, prednisolone

349
Q

why are IM injections of systemic corticosteroids given? what drug?

A

releases steroids over several weeks

depomedrol (methylpredinsolone)
solumedrol (methylpredinsolone)

350
Q

MOA of corticosteroids in asthma?

A

inhibit formation of inflammatory cytokines & infiltration of airways by lymphocytes, mast cells, mast cell degranulation, & eosinophils

decreases bronchial reactivity
decreases constriction of airways
reduces mucus 
decreases airway edema
decreases exacerbations
351
Q

How long does it usually take to see effects of corticosteroids?

A

4-12 hours

8 weeks for max effect

352
Q

Dosage of ICS?

A

1-2x/d for mild to moderate Sx

if severe, may need systemic steroids

353
Q

first line for asthma?

A

ICS, dosage varies have to use PC to convert

354
Q

ADRs of inhaled corticosteroids

A
  • thrush
  • dysphonia
  • reflex cough
  • bronchospasm

reduce with space & mouth rinses

355
Q

how is height affected by ICS?

A

1.2 cm or less as child, adult height unaffected

356
Q

ADRs of high dose ICS with long term use?

A
  • hypothalamic-pituitary-adrenal fxn suppression
  • osteoporosis
  • cataracts
  • glaucoma
  • edema
  • immunosuppression
  • thin skin
357
Q

MOA of cromolyn

A

inhibits cough

inhibits mast cells & eosinophils from releasing granules

358
Q

How is cromolyn dosed?

A

4x/d

MDI or nebulizer

359
Q

how long dose it take to see effects of cromolyn?

A

1-2 weeks

360
Q

how are cromolyns used?

A

poorly absorbed

only used prophylatically for Ag or exercise induced asthma, pregnancy

361
Q

ADRs of cromolyn

A
  • throat irritation
  • bad taste
  • cough
  • mouth dryness
  • chest tightness
  • wheezing
362
Q

what is leukotriene?

A

substance produced by inflammatory pathway (5-lipoxygenase enzyme) that causes bronchoconstriction, increased bronchial reactivity, mucosal edema, & hypersecretions

363
Q

MOA of leukotriene modifiers?

A

inhibit 5-lipoxygenase to prevent leukotriene production (no constriction, mucosal edema, hyper secretions)

364
Q

dosage of leukotriene modifiers?

A

1x/d

365
Q

ADRs of leukotriene modifiers?

A
  • hepatic injury (monitor LFT q6mo)***
  • Churg-Strauss
  • eosinophilia
366
Q

what is churg-strauss?

A

a syndrome of vasculitis (inflammation of blood vessels) causes by LTI

367
Q

what is eosinophilia?

A

increased eosinophils in blood caused by LTI

368
Q

drug interactions of LTI?

A

montelukast - none

zarfilukast:
- inhibits many CYP isoenzymes
- interferes with metabolism of:
phenytonin
warfarin
felodipine
lovastatin
triazolam

369
Q

leukotriene modifier clinical uses?

A
  • preventing exacerbations of asthma (ICS work better): oral useful in kids who can’t inhale
  • aspirin induced asthma
  • perennial/seasonal allergic rhinitis
370
Q

why does aspirin induce asthma?

A

causes pt to make more leukotrienes

5-10% of pt get exacerbations when exposed to NSAIDs

371
Q

MOA of omalizumab

A

prevents IgE binding to mast cells and basophils, preventing the release of inflammatory mediators after allergen exposure

372
Q

dose of omalizumab?

A

SQ q2-4weeks

373
Q

clinical use of omalizumab?

A

moderate to severe persistent asthma not well controlled on an ICS and have well documented specific desensitization to airborne allergens (mold, pollen, animal dandruff)

374
Q

how old do you need to be to take omalizumabs?

A

12

375
Q

SE of omalizumabs?

A

allergic rxn

anaphylaxis (give where you can treat anaphylaxis)

376
Q

MOA of romflumilast?

A

inhibits PDE4 in lung tissue, leading to smooth muscle relaxation & decreased inflammatory activity

377
Q

which is more selective for inhibiting PDE4: romflumilast or theophylline?

A

romflumilast

378
Q

clinical uses of romflumilast?

A

reduce COPD exacerbations

379
Q

what is romflumilast NOT used for?

A

acute episodes

NOT a bronchodilator

380
Q

SE of romflumilast?

A 
diarrhea
nausea
weight loss
anxiety
insomnia
depression
381
Q

dosage of romflumilast?

A

1x/d orally

382
Q

devices for inhaling medications?

A

MDI (metered dose inhaler)
spacers
DPI (dry powder inhaler)
nebulizer

have particles small enough they can be inhaled into lungs (aerosol)

383
Q

describe MDIs

A

drug dissolved or suspended in a liquid and placed in pressurized container

strength based on concentration

compress container to dispense medicine (metered amount released)

pt inhales

contents: propellant & medicine

384
Q

how should you inhale with MDI

A

slowly & deeply gets most drug into lung

385
Q

describe valve holding chamber & its benefits

A

better than open tube spacer

$$$

compress canister, holds med in chamber until inspiratory pressure pulls med into lungs

less coordination needed

386
Q

Describe DPI

A

micro-ionized powder goes directly to lung (not in liquid like MDI)

387
Q

How to inhale with DPI

A

deep, forceful breathe (opposite MDI)

388
Q

pros and cons of DPI

A

pros: breath actuated (don’t need hand/lung coordination) & easier to teach to use
cons: need higher inspiratory flow

389
Q

describe nebulizers

A

dissolve drug in liquid, use compressed air or vibrations to turn liquid into a fine mist, mist is inhaled

390
Q

pros & cons of nebulizers

A

pros: good last resort
cons: $$, Lg, less portable

391
Q

goals of asthma treatment

A

short term: improve fxn & decrease Sx

long term: prevent exacerbations & progressive loss of pulmonary fxn

392
Q

what should all asthma pt have?

A

SABA

393
Q

If a pt has occasional symptoms a SABA may be all they required; when should you add a corticosteroid?

A

use >2x/week
night Sx >2x/month
FEV1

394
Q

How to treat acute asthma in ER?

A
  • O2 to relieve hypoxemia
  • SABA (sometimes with ipratropium) via nebulizer with face mask

severe:
- need higher more freq. dosing
- add oral or IV steroids

395
Q

what should you NOT use during acute asthma attack?

A

DPI: requires high inspiratory flow which pt do not have during attack

396
Q

when are corticosteroids added to therapy?

A

frequent asthmatic symptoms or significant airflow obstruction despite bronchodilator

397
Q

If a pt is on low dose corticosteroids and their asthma is not controlled what can you add to improve their situation?

A
  • increased dose of inhaled steroids

- add a LABA to current dose of inhaled steroids

398
Q

If a pt is having severe asthma symptoms or has a severe obstruction what should you give them?

A

IV & inhaled corticosteroids

once better taper IV steroids

399
Q

when are antimuscarinic drugs used for acute asthma?

A
  1. if pt is intolerant to beta agonists

2. as adjunctive to SABA and steroid therapy

400
Q

what are antimuscarinics most useful for?

A

COPD

401
Q

what type of antimuscarinic should you use for acute asthma?

A

short acting

402
Q

when would you used cromolyn?

A

before event that triggers Sx

403
Q

how to use cromolyn & leukotriene modifiers in acute asthma?

A

in place of ICS if can’t use it; or in addition to it

404
Q

why are leukotriene modifiers more useful than cromolyn and less useful than ICS?

A

more useful than cromolyn because they are easier to use (often used in kids)

not as affective as inhaled steroids

405
Q

describe intermittent asthma

A

Sx >2d/w
night awakenings >2x/mo
SABA use 80%
FEV1/FVC normal

406
Q

describe mild asthma

A 
Sx >2d/week but not daily
night awakenings 3-4x/mo
SABA use >2d/week
minor inference with ADLs
FEV1 > 80%
FEV1/FVC normal
407
Q

describe moderate asthma

A 
Sx daily
night awakenings >1x/week
SABA use daily
some limitations on ADLs
FEV1 >60% but
408
Q

describe severe asthma

A 
Sx daily
night awakenings daily
SABA use daily
severe limitations on ADLs
FEV1 5%
409
Q

tx for intermittent asthma

A

SABA PRN

410
Q

tx for mild asthma

A

SABA + low dose ICS

411
Q

Tx for moderate asthma

A

SABA + low dose ICS + LABA

or

SABA + medium dose ICS

412
Q

Tx for severe asthma

A

SABA + medium dose ICS + LABA

413
Q

what to add if SABA, medium dose ICS, and LABA isn’t enough?

A

consult with asthma specialist
add high dose ICS

consider adding omalizumab if allergies

414
Q

what to add if SABA, high dose ICS, and LABA isn’t enough?

A

add oral corticosteroid

consider omalizumab if allergies

415
Q

How to treat exercise induced bronchoconstrion? (EIB)

A

SABA prior to exercise will prevent EIB for 2-4 hours

LABA prior to exercise will prevent EIB for up to 12 hours

montelukast decreases EIB in 50% of pt up to 24 hours

416
Q

when is tx of EIB with LABAs less reliable than SABAs?

A

with frequent usage

417
Q

what to give pt with asthma during pregnancy?

A

SABA - Albuterol
ICS - budesonide

maybe LABA & montelukast (not great evidence)

418
Q

teratogen asthma medication?

A

Zileuton (LTI)

419
Q

should you use DPI in kids?

A

no they can’t inhale well enough

420
Q

if parents of children refuse ICS what can you prescribe for LT treatment of asthma?

A

montelukast

421
Q

Tx for mild intermittent asthma in kids?

A

SABA PRN

422
Q

Tx for mild, moderate, severe persistent asthma in kids?

A

SABA PRN + ICS

423
Q

T/F medications for asthma are as effective for COPD?

A

False. Asthma drugs do not slow progression, are not as effective, and pathophysiology can’t be reversed in COPD.

Drugs do improve Sx and quality of life.

424
Q

Tx for acute symptoms of COPD?

A

SABA (albuterol) or short acting anticholinergic (combivent)

or both

425
Q

chronic symptoms of COPD: regular symptoms of SOB and limitations on ADLs

A

LABA or long acting anticholinergic

or both

methylxanthines (another bronchodilator) used for those intolerant or unable to used inhaled therapy

426
Q

what should you prescribe for severe & frequent exacerbations of COPD?

A

ICS

Pharm 5 (8 decks)

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