Other Flashcards

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
ADRs of dobutamine
tachycardia, angina, arrhythmias, tachyphlaxis (over compensation by body)
26
Diuretics used to relieve symptoms of CHF?
- loops | - K sparing (ALD antagonists)
27
MOA of loop diuretics
remove fluid decrease edema decrease SOB
28
ADRs of loops
``` hypotension worsened renal fxn (increased Cr) hypokalemia hypokalemic metabolic alkalosis hyperuricemia hypomagnesaemia hypocalcium ototoxicity (hearing loss) allergic rxn to sulfa Bad with NSAIDs ```
29
MOA of ALD antagonists
stop RAS reflex increase Na excretion decrease K excretion remove fluid
30
how do ALD antagonists decrease mortality in CHF?
prevent myocardial and vascular fibrosis, baroreceptor dysfunction, & renal effects
31
ADRs of ALD antagonists
- gynocomastia & menstrual irregularities (Spironolactone) - hyperkalemia - hypercholremic metabolic acidosis - kidney stones - Bad with NSAIDs & K pills
32
MOA of ACEI
``` block RAS vasodilation decrease ALD production decrease volume decrease edema decrease cardiac remodeling ``` increases symptoms in 4-12 weeks decreases incidence of hospitalization
33
ADRs of ACEI
``` dry cough rash hyperkalemia hypotension renal failure angioedema TERATOGEN bad with K pills& NSAIDS ```
34
MOA of ARBs
decrease fluid & edema & BP
35
MOA of hydralazine (aa) & isosorbide nitrate (vv) (direct vasodilators) in CHF
``` reduce preload (vv) & after load (aa) decrease cardiac remodeling ```
36
Population that benefits from direct vasodilators?
African Americans
37
S/E of direct vasodilators?
HA, nausea, anorexia, palpitations, sweating, flushing, edema, SLE, peripheral neuropathy, drug fever
38
What should all STABLE CHF pt receive?
BBlocker & ACEI (40% reduction in mortality & hospitalization)
39
MOA of Bblockers
decrease SNS activation (decrease HR & O2 demand) decrease RAS activation decreases cardiac cytokines that lead to fibrosis & ventricular wall stiffening
40
How to dose blockers?
start low & increase over 2 weeks to highest tolerated dose takes 3-6 mo to see symptom improvement in CHF
41
contraindications of BBlockers?
bradycardia asthma unstable CHF
42
MOA of ivabradine
Inhibition of (HCN) channels (f-channels) within the SA node prolongs diastolic depolarization (slows firing of SA nose & reduces HR)
43
MOA of sacubitril & valsartan
sacubitril inhibits neprilysin & increases levels of natriuretic peptides & bradykinin... decreases vasoconstriction, Na retention, & remodeling valsartan blocks ATII & ALD release
44
ARRs of sacubitril & valsartan
hypotension hyperkalemia increased Cr angioedema
45
How to treat asymptomatic CHF (structural heart changes)?
treat secondary diseases that make CHF worse (HTN, DM, obesity, & hyperlipidemia)
46
How to treat symptomatic CHF?
decrease work load of heart, restrict Na intake
47
How to treat symptomatic CHF that is worsening? (stage C & D)
First line: ACEI, bblocker, loop diuretic | ALD antagonist, vasodilators, digoxin
48
How to treat CHF when normal treatments fail?
resynchronization or transplant
49
What do you need to monitor with loop diuretics in CHF?
Weight Gain of 3-5 lbs in one week = increase dosage
50
MOA of warfarin
blocks carboxylation/inhibits synthesis of coagulation factors II, VII, IX, X, protein C & S
51
Why does warfarin often required a heparin bridge?
Warfarin has delayed onset, takes 6-50 hours to break down circulating clotting factors (max effect observed 3-5 days after therapy)
52
What do you monitor for warfarin?
PT/INR (prothrombin time)
53
What is the normal range of INR?
2 to 3
54
What is the ideal INR for mechanical prosthetic heart valves or recurrent systemic embolization?
3 to 4.5
55
Indications for warfarin?
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
56
How is heparin administered? warfarin?
Heparin - parenteral (IV or SQ) | Warfarin - oral
57
When do you start heparin and warfarin? When do you stop heparin?
Start both together... stop heparin when PT is therapeutic
58
ADRs of warfarin
``` TERATOGEN bleeding allergies (urticaria) alopecia necrosis of skin if low protein C ```
59
Absolute contraindications of warfarin?
pregnancy bleeding recent surgery
60
What drugs inhibit the metabolism of warfarin and increase risk of bleeding?
``` amiodarone cimetidine erythromycin fluconazole gemfibrozil isoniazide metronidazole ```
61
what drug inhibits warfarin absorption and increases patients risk of clots?
cholestyramine
62
How to dose warfarin?
start 2-5 mg/day check PT regularly small dose changes until reach goal PT (usually 5-7 days)
63
A high PT puts you at a risk for bleeding; what do you give to reverse high PT if no bleeding or emergent surgery?
Lower or hold dose
64
what do you give to reverse high PT in bleeding or emergent surgery situation?
subcutaneous vit K | Fresh frozen plasma
65
MOA of indirect thrombin inhibitors
Bind antithrombin and increase its function (to inhibit clotting factors IX, X, II) Inhibits clotting
66
Why is Heparin called unfractionated heparin?
It is a mixture of similar molecules with binding site for antithrombin
67
Why is heparin measured in units and not mg?
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
68
Why isn't unfractionated heparin given IM?
it is traumatic and can bleed into muscle
69
ADRs of unfractionated heparin?
bleeding alopecia (reversible) osteoporosis (LT use) Heparin induced thrombocytopenia
70
How often does heparin induced thrombocytopenia occur in pt taking unfractionated heparin? When is it usually reversible?
25% of the time It is usually mild and reversible in 4 days
71
What type of reaction is HIT?
Type I hypersensitivity rxn
72
What is the result of HIT?
Up to 4% of pt develop hypercoaguable state due to immune response
73
What are the symptoms of HIT?
decreased platelet count new blood clots in vv & aa skin necroses
74
What should you monitor frequently to avoid HIT in pt receiving unfractionated heparin?
platelet count
75
How do you treat HIT?
stop heparin | give direct thrombin inhibitor
76
contraindications for unfractionated heparin?
- 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)
77
Indications for unfractionated heparin?
- venous thrombosis - arterial thrombosis - a fib - emboli
78
How can unfractionated heparin be rapidly reversed?
protamine sulfate binds to and inactivates heparin stop drug and effect goes away in a few hours
79
Why isn't unfractionated heparin obsolete?
not cleared by kidneys | reversed by protamine
80
How is unfractionated heparin used prophylactically?
to prevent development of clot in high risk pt (venous thrombosis, afib)
81
how is unfractionated heparin used for treatment of venous thrombosis?
to prevent thrombosis from embolization & going to lungs, or from getting bigger
82
What do you monitor for unfractionated heparin?
platelet count aPTT clotting factor used to assess activity
83
what is the normal aPTT range?
1.5-2x normal
84
How does LMWH differ from unfractionate heparin?
it is fragments of heparin with antithrombin binding sites (weighs less, shorter chains)
85
MOA of LMWH
binds to antithrombin to increase its inhibition effects on IX, Xa (more than regular heparin), II (less then regular heparin)
86
How is LMWH dosed?
SQ 1-2x/day (longer 1/2 life)
87
What is the advantage of LMWH?
- greater bioavailability (more predictable response) - less frequent dosing - less thrombocytopenia - less monitoring
88
Indications for LMWH
VTE (DVT & PE)
89
Cons of LMWH?
- more expensive | - protamine sulfate does not reverse effect as well
90
what type of drug is fondaparinux?
``` Factor Xa inhibitor Synthetic heparin (made in lab): resembles heparin binding sites ```
91
Pros of fondaparinux?
SQ 1x/d | less HIT
92
cons of fondaparinux?
$$$ protamine sulfate doesn't reverse it accumulates in pt with renal impairment (bad for old ppl)
93
Indications of fondaparinux?
- acute DVT - prophylaxis of DVT after hip replair/replacement, knee replacement, or abdominal surgery - PE
94
MOA of direct thrombin inhibitors? (lepirudin, argatroban, bivalirudin, desirudin)
bind to active site on thrombin blocking effect of thrombin and preventing clotting
95
Pros of direct thrombin inhibitors?
inhibit clot- bound thrombin and circulating thrombin more predictable anticoagulation effect than heparin
96
Indications for direct thrombin inhibitors?
- HIT with thrombosis | - percutaneous transluminal coronary angioplasty
97
How are direct thrombin inhibitors administered?
parentally
98
How do you monitor effect of direct thrombin inhibitors?
PTT
99
ADRs for direct thrombin inhibitors?
bleeding | allergic rxn
100
What is the significance of dabigatran?
first oral direct thrombin inhibitor
101
indications of dabigatran?
- reduce risk of stroke - reduce risk of systemic embolism in pt with nonvalvular AF (Pt with AF with one additional risk factor for stroke)
102
Cons of dabigatran vs. warfarin?
twice a day dosing of dabigatran reduces compliance
103
Pros of dabigatran vs. warfarin?
Dabigatran does not require INR monitoring lower risk of intracranial & extra cranial bleeding in pt under 75
104
Summarize the dosing adjustments needed for dabigatran in pt with renal dysfunction.
CrCl > 30mL/min = 150 mg BID (Normal) CrCl 15-30mL/min = 75 mg BID CrCl
105
What is the stability in months of an open dabigatran bottle?
4 months
106
When converting a pt from warfarin to dabigatran what steps should be taken?
- stop warfarin | - start dabigatran when INR is below 2.0
107
Drug interactions of Dabigatran?
Don't use with pt with renal failure dronedarone ketoconazole
108
extracranial bleeding risk in patients >75 yo with dabigatran is _____ to warfarin.
similar
109
what is used to reverse effects of dabigatran? dose?
idarucizumab; give 2-2.5g IV q15minutes
110
MOA of idarucizumab?
humanized monoclonal Ab fragment that binds to dabigatran & its metabolites with higher affinity than thrombin it neutralizes dabigatran & its anticoagulation effects in minutes
111
Indications of rivaroxaban?
active factor Xa inhibitor used for prevention of - DVT, blood clots, & PE after knee or hip replacement - stroke prevention in AFib
112
What is the benefits of rivaroxaban?
no monitoring given once daily more effective than enoxaparin in preventing VTE (DVT & PE) after knee or hip replacement
113
Dose adjustments for rivaroxaban with renal dysfunction?
CrCl > 50 = 20 mg/d with dinner CrCl 15-50 = 15 mg/d with dinner CrCl
114
Steps for converting warfarin to rivaroxaban?
stop warfarin | start rivaroxaban when INR is below 3
115
Drug interactions of rivaroxaban?
``` ketoconazole itraconazole carbamazepine phenytoin rifampin ```
116
Indications for apixaban?
stroke prevention in Afib patient
117
dosing of apixaban?
5 mg 2x/d
118
When is the dose of apixaban reduced to from 5mg BID to 2.5 mg 2x/day?
> 80 yo | 1.5
119
Steps for converting from warfarin to apixaban?
stop warfarin | start apixaban when INR is below 2
120
Drug interactions of apixaban?
ketoconazole itraconazole ritonavir clarithromycin ``` Absolute contraindicated: rifampin carbamazepine phenytoin phenobarbital ```
121
What type of clots to anti platelet drugs work best at preventing?
arterial clots (MI & CVA)
122
what is the anti platelet dose of ASA?
low dose | 81-325 mg/d
123
MOA of ASA?
inhibits synethesis of thromboxane A2, permanently (for life of platelet or 10 d)... stops it from making platelets release granules that support platelet aggregation
124
How long does ASA prevent platelet aggregation?
10 days, the entire life of the platelet it bines
125
ADRs of ASA
increased bleeding allergic rxn epigastric pain heart burn
126
Contraindications of ASA?
asthma | hypersensitivity rxns
127
Indications of ASA?
- 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)
128
What is primary prevention of MI?
No Hx of MI, trying to prevent it
129
What is secondary prevention of MI?
Hx of MI, want to prevent a 2nd one
130
MOA of clopidogrel & ticlopidine?
IRREVERSIBLY blocks ADP membrane receptor on platelet needed for aggregation inhibits expression of GP IIb/IIIa receptors to prevent platelet aggregation
131
clopidogrel & ticlopidine _____ bleeding time
prolong
132
How long do clopidogrel and ticlopidine affect platelets they bind to?
life of platelet (10d)
133
ADRs of ticlopidine?
- nausea - diarrhea - bleeding - severe neutropenia (low white cell count) - TTP (thrombotic thrombocytopenic purpura)
134
What is TTP? What causes it?
Thrombotic thrombocytopenic purpura causes wide-spread coagulation and low platelet count clopidogrel & ticlopidine
135
Major ADR of clopidogrel?
bleeding TTP avoid in slow metabolizers avoid with drugs that inhibit CYP2C19 (proton pump inhibitors... omeprazole & esomeprazole)
136
What is the black box warning for clopidogrel?
Avoid in pt that have poor metabolism (CYP2C19 dysfunction) ... won't get anti platelet affect Avoid drugs that inhibit CYP2C19 (omeprazole & esomeprazole)
137
MOA of dipyridamole?
inhibits platelet uptake of adenosine & blocks ADP induced platelet aggregation
138
ADRs of dipyridamole
``` nausea diarrhea epigastic dizziness SEVERE headache rash ```
139
Dipyridamole is not strong enough to be used alone; what is it often combined with?
Aspirin & warfarin
140
What is the MOA of glycoprotein IIb/IIIa antagonists?
prevent platelet aggregation by competing with fibrinogen & vWF for platelet receptors
141
indications of glycoprotein IIb/IIIa receptor antagonists?
ST for ACS & PCI
142
ADRs of glycoprotein IIb/IIIa receptor antagonists?
bleeding | acute thrombocytopenia
143
What are anti platelet drugs used for?
arterial clots (CVA & MI)
144
What is the first line anti platelet drug?
aspirin 80-325 mg/d
145
What is second line anti-platelet drug? when is it indicated?
clopidogrel when can't use aspirin or have an event on aspirin unstable angina stroke transient ischemic attack coronary stent placement
146
what is third line anti-platelet drug?
ticlopidine use if can't take aspirin or clopidogrel
147
do you have to monitor anti platelets?
no
148
how are fibrinolytic administered?
IV
149
MOA of fibrinolytic?
convert plasminogen to plasmin plasmin degrades fibrin & fibrinogen dissolves clot
150
Cons of fibrinolytic?
will dissolve clots everywhere not just bad ones, fragile state
151
ADRs of fibrinolytic?
bleeding | allergic rxns
152
What drug can be used to stop bleeding caused by fibrinolytic?
aminocaproic acid
153
who often receives aminocapronic acid?
pt with hemophilia that take fibrinolytics
154
indications for fibinolytics?
- 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
155
What fibrinolytic should a pt with an acute ischemic stroke take within 3 hours of onset of symptoms?
alteplase
156
Contraindications of fibrinolytic?
- recent surgery - Hx of brain bleed - active internal bleed - brain cancer - suspected aortic dissection - head or facial trauma in last 3 mo
157
MOA of nitrates
release NO in vascular smooth muscle, decreases Ca & contractility venous smooth muscle relaxation, venous pooling, decreased preload, decreased CO, decreased BP
158
Do nitrates affect cardiac or skeletal muscle?
no
159
What is the order of vessel relaxation with nitrates?
veins than arteries
160
How do nitrates help angina?
decrease O2 demand, decrease work of heart = decreased angina
161
what are the indirect effects of nitrates?
tachycardia bronchi relaxation GI & GU tract relaxation
162
What removes nitrates from body?
large amounts lost during first pass effect in liver, must use large oral dose
163
How is mononitrate administered?
orally
164
how is dinitrate administered?
orally, chewable tablet or sublingual
165
how is NTG administered
sublingual, spray, buccal tablet, ointment, parenterally, orally
166
What should you use to relieve immediate chest pain?
Sublingual or spray (if dry mouth)
167
what should you use to long term treatment of angina?
buccal absorption (avoids first pass) transdermal patch tablets or capsules
168
what is the drug free period required for transdermal nitrate patches?
10 hours per day or tolerance occurs
169
ADR of nitrates?
caused be excessive vasodilation: - orthostatic hypotension - HA - dizziness - tachycardia
170
When are nitrates contraindicated?
- increased ICP
171
How can you prevent reflex tachycardia with nitrates?
BBlocker
172
If you are giving nitrates through continuous IV infusion what is the maximum amount of time you should administer it?
24 hours
173
How often should oral XL nitrates be dosed?
1-2x/d
174
Indications for Nitrates?
- chronic stable angina - variant angina (spasms) - unstable angina
175
What CCB are used in stable angina?
verapamil diltiazem dihydropyridines
176
MOA of CCB in stable angina?
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
Other than stable angina, when can CCB be used?
to prevent spasms of the aa in the brain (after subarachnoid hemorrhage or stroke)
178
ADRs of CCB?
Caused by vasodilation & hypotension: - fatigue - headache - dizziness - flushing - peripheral edema - bradycardia - CHF - conduction blocks
179
Drug interactions with CCB?
bblocker (bradycardia) | drugs metabolized by P450 (digoxin)
180
When should bepridil be used?
when pt fails to response to other abtianginal medications (may be used with nitrates & bblockers)
181
Indications for diltiazem & verapamil?
typical angina | variant angina
182
Use caution in pt with ____ when using CCB.
CHF
183
If you are pt is on a BBlocker what type of CCB should you use?
dihydropyridine (less effect on heart rate)
184
If a pt has angina, AND a Hx of atrial arrhythmias, what CCB should you use?
verapamil or diltiazem
185
Why should you avoid use of digoxin and verapamil/diltiazem?
interference with cytochrome P450 & increased slowing of electrical conduction
186
What CCB are approved for angina?
amlodipine, felodipine, nicardipine, nifedipine
187
what is the drug of choice for variant angina?
CCB
188
Uses of CCB other than angina?
HTN, arrhythmias, migrane HA prevention, raynaud's
189
MOA of b blockers in stable angina?
``` decreased HR decreased contractility decreased BP prevents reflex tachycardia decreases work of heart decreases O2 demand ```
190
ADRs of beta blockers in tx of angina?
- bradycardia - worsen peripheral vascular disease - CHF - decreased exercise tolerance - depression - sedation - sleep disturbances - block Sx of hypoglycemia - worsens asthma - withdrawal (rebound HTN)
191
what beta blockers are used for management of typical angina and acute MI?
- atenolol - metoprolol - nadolol - propanolol
192
How do you know if the bblockers are working?
HR
193
MOA of ranolazine?
improves cardiac diastolic fxn by manipulating Na and Ca channels that can be detrimental to cardiac performance
194
indications for ranolazine?
- chronic angina
195
what can ranolazine be used with?
- beta blockers - nitrates - CCB - anti-platelet therapy - lipid lowering therapy - ACEI/ARB
196
SE of ranolazine?
``` dizziness headache constipation nausea prolonged QT (arrythmias) ```
197
What should you monitor for with ranolazine?
EKG - prolonged QT wave
198
goals of drug therapy for angina?
- relieve acute Sx - prevent ischemic attack - improve quality of life - reduce risk of MI - decrease time to symptoms
199
How quickly does SL or spray NTG work? how long does it last?
1-3 minutes | lasts 20-30 minutes
200
how should you instruct your pt to take NTG?
SL q5min x 3 | ER if CP is not better
201
it is a ____ idea to take NTG SL prior to exercise.
good; it prevents angina
202
What is good drug choices for prophylaxis of angina?
isosorbide dinitrate | NTG
203
NTG is volatile; after a bottle is open when should a pt discard it?
6 months
204
first line treatment of stable angina?
``` Need long term therapy: #1 beta blockers ```
205
why is beta blockers first line treatment for stable angina?
prolongs survival with MI, in the event angina precipitates to MI
206
2nd line treatment of stable angina?
CCB
207
Why are nitrates 3rd line treatment for stable angina?
- tolerance | - less effective than CCB & BBlockers
208
Pt with angina are at high risk for MI; what other drugs should be added to their therapy regimen?
- aspirin or clopidogrel - cholesterol lowering - ACEI/ARB (if DM or LV dysfunction)
209
what causes variant angina?
spasm of arterial wall muscle suddenly decreases O2 supply and increases demand on heart
210
Treatment of variant angina?
CCB relax vessel smooth muscle (no blockage, just spasm of smooth muscle... need to relax it) nitrates maybe
211
what is acute coronary syndrome?
spectrum of unstable angina to MI
212
what is the most affective treatment for ACS?
nonpharmacologic coronary intervention
213
what is the role of drugs in treatment of ACS?
1. prevent recurrence of clots | 2. decrease heart injury so lose as little mm as possible
214
treatment of ST elevation MI?
- PCI | - fibrolytics if no PCI
215
treatment for MI in hospital?
1. aspirin 2. clopidogrel 3. SL NTG 4. beta blockers 5. heparin
216
treatment for discharge after MI?
1. beta blocker 2. ACEI 3. Aspirin 4. statin 5. clopidogrel
217
what prolongs survival after MI?
beta blocker ACEI aspirin
218
common problems in conduction system that cause arrhythmias?
1. abnormal impulse conduction (rate is slower) 2. abnormal impulse formation (rate is faster) 3. both of the above
219
all drugs that treat arrhythmias can cause ____ arrhythmias
lethal
220
non pharmacologic treatments for arrhythmias?
- catheter ablation - cryoablation - implantable defibrillater
221
when to treat arrhythmias?
too fast, slow, or asynchronous (when atria and ventricles don't work together) ones that decrease CO & BP significantly
222
what affect can anti-arrhythmic medications have on normal tissue?
can cause drug induced arrhythmias at high doses
223
anti arrhythmic drugs can have different affects at different heart rates or if situation changes; true or false?
true, if HR or O2 supply changes
224
when do Na channel blockers work best on cardiac tissue?
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
MOA of 1A (procainamide, quinidine, disopyramide)
blocks sodium channel slowing upstroke of action potential, slowing conduction of electrical impulse
226
ADRs of procainamide
``` torsade de pointes SLE like syndrome nausea diarrhea hypotension ```
227
Why isn't procainamide not first line?
bad SE and QID (4x/d)
228
ADRs of quinidine?
GI (N,V,D) 33% cinchonism (HA, dizziness, tinnitus) thrombocytopenia prolongation of QT interval
229
what isn't quinidine first line?
increases mortality 2 fold
230
ADRs of disopyramide?
- HF (has negative inotropic actions carful in old & CHF pt) - anticholinergic effects
231
when is diopyramide used?
ventricular arrhythmias
232
Indications for 1A?
- conversion/prevention of Afib - A flutter - ventricular tachycardia - prevention of ventricular fibrillation
233
MOA of 1B (lidocaine, mexiletine)
blocks Na channels (good for cells with long AP like conduction or ventricular cells, not as affective on atrial cells)
234
ADRs of lidocaine
``` hypotention paresthesias tremor nervousness nausea light headed slurred speech seizures drowsiness ```
235
drug interactions of lidocaine?
amiodarone
236
indications of lidocaine?
first line for ventricular arrhythmias (tachycardia & fibrillation) after cardiovesion or what an MI
237
Lidocaine is used to treat arrhythmias after cardiovesion or MI and not prophylaxtically, why?
increases mortality
238
how is lidocaine administered?
IV
239
how is mexiletine administered?
orally
240
what is mexiletine used for?
long term suppression of ventricular arrhythmias
241
ADRs of mexiletine?
``` tremor gait disturbances blurred vision lethargy nausea ```
242
MOA of 1C (flecainide & propafenone)
block sodium & potassium channels (lesser extent)
243
ADRs of 1C
ventricular arrhythmias, agranulocytosis, anemia, thrombocytopenia
244
Drug interactions of flecainide & propafenone
digoxin (increases its levels) | warfarin (increases INR)
245
indications of flecainide & propafenone
- conversion/prevention of a fib - atrial flutter - ventricular tachycardia - prevention of v fib
246
MOA of beta blockers as antiarrhythmics?
- inhibit SNS activation of cardiac automaticity & conduction - slow HR - decrease AV node conduction - increase AV node refractory period
247
uses of beta blockers as antiarrhythmics
- rate control in a fib - a flutter - prevention of SVT - adjunctive ventricular antiarrhythmic therapy
248
why are beta blockers (class 2) better than class 1s?
prevent re-infarction & sudden death after MI
249
what BBlockers are used as antiarrhythmics?
- metoprolol - esmolol - atenolol
250
MOA of class 3 antiarrhythmics?
prolong ventricular AP by blocking rapid component of K channel
251
when do class 3 antiarrhythmics work best?
at slower heart rates (not at fast ones when they are needed most)
252
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?
increases risk for torsade de pointes
253
What two class 3 antiarrhythmics has class Ib, II, & IV properties as well?
amiodarone & dronedarone
254
in addition to potassium blocking properties what other receptor does sotalol block?
50%/50% beta and potassium blocking properties
255
MOA of amiodarone and dronedarone?
prolongs AP by blocking rapid component of K channel, also blocks Na & Ca channels and beta receptors
256
indications for amiodarone?
- approved for serious ventricular arrhythmias - first line DRUG for ventricular tachycardia - a fib
257
First line treatment, & first line drug treatment for ventricular tachycardia?
treatment: implantable defibrillator Drug: amiodarone
258
Why use amiodarone if first line treatment is implantable defibrillator?
use with defibrillator to prevent uncomfortable discharges
259
ADRs of amiodarone?
- 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
drug interactions with amiodarone?
- warfarin - digoxin - statins
261
what should you monitor while on amiodarone?
EKG (QT prolonged) | thyroid function tests
262
How does dronedarone differ from amiodarone?
- shorter 1/2 life (days compared to months) - less thyroid toxicity - less lung toxicity - less effective in maintaining NSR
263
indications for dronedarone?
a fib | a flutter
264
ADRs of dronedarone?
GI (N,V,D) abdominal pain liver toxicities
265
MOA of Sotalol?
AP prolonged by blocking K channel | Beta blocker activity
266
indications for sotalol?
- life threatening ventricular arrhythmias | - a fib (to maintain NSR)
267
ADRs of sotalol?
``` torsade de pointes HF bradycardia AV block wheezing fatigue ```
268
indications for dofetilide?
- conversion/prevention of a fib & flutter
269
ADRs of dofetilide?
QT prolongation, torsades de pointes, HA, dizziness
270
when should you initially administer dofetilide?
under hospital monitoring due to ADR
271
indications of ibutilide?
rapid conversion of recent onset of a fib/flutter
272
ADRs of ibutilide?
hypotension nausea torsades de pointes
273
where do class four antiarrhythmics work best
SA & AV node (cardiac cells dependent on Ca for upstroke)
274
MOA of class 4
prolong conduction through AV & SA node | atria beats fast but drug blocks some of the impulses from reaching the ventricles
275
indications of class 4 antiarrhythmics?
SVT***
276
ADRs of class 4 antiarrhythmics
wrong arrhythmia can cause death
277
MOA of adenosine
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
which node does adenosine work best in?
AV node
279
what is the half life of adenosine?
10 s
280
what is adenosine 1st line for?
conversion of SVT to NSR
281
ADRs of adenosine?
``` flushing SOB chest burning HA Low BP nausea paresthesias bronchospasm ```
282
when is magnesium useful with arrhythmias?
- Tx of digitalis induced ventricular arrhythmias - suppress drug induced torsades de points - treat SVT arrhythmias associated with Mg deficiency
283
how does K affect the heart?
depresses ectopic pacemakers (tissues other than the conduction system depolarizing) slows conduction
284
what happens when K is too high or too low?
arrhythmias
285
what increases mortality with risk of sudden death from arrhythmia?
implantable defibrillator
286
what do we use to treat a fib
a lot
287
major problems of a fib?
1. decreased CO (atria not beating and ventricles beating too quickly) 2. blood pools in heart and can clot
288
goals of a fib treatment?
1. ventricular rate control 2. conversion to NSR 3. prevention of embolic event
289
how do we control ventricular rate in a fib?
slow impulses through AV node - CCB - Bblockers - digoxin
290
how do we convert to NSR in a fib?
direct current cardioversion - electrical cardioversion - ibutilide - dofetilide
291
how do you prophylactically prevent pt with Hx of Afib from leaving NSR?
class I or Class III
292
what drugs are used to prevent embolic events after a fib suppression?
- aspirin - warfarin - clopidogrel - dibigatran
293
goal of SVT treatment?
slow ventricular rate
294
what is first line for SVT?
adenosine
295
what drugs can be used for acute SVT?
- adenosine - verapamil - diltiazem - esmolol
296
what drugs/treatments are used for LT SVT?
- ablation - CCB - BBlockers - digoxin
297
what is ventricular tachycardia often associated with?
MI
298
what is first line treatment for ventricular tachycardia?
- electric cardioversion (Epi & amiodarone possibly) | - implant defibrillator
299
long term drug therapy for ventricular arrhythmias?
- bblockers | - amiodarone
300
what are torsades de pointes?
ventricular tachycardia induced by drugs or electrolyte abnormalities prolonging QT interval
301
how to treat torsades de pointes?
- stop causative agent - correct electrolyte abnormalities - IV magnesium sulfate - IV isoproterenol
302
how to treat ventricular fibrillation?
- electrical defibrillation (may add epic & amiodarone)
303
long term treatment of ventricular fib?
implantable defibrilator | Bblocker
304
how are sympathomimetics normally administered? why?
inhaled; more B2 stimulation | B2 receptors are on smooth mm of airways
305
do sympathomimetics have anti-inflammatory activity?
No
306
when is epinephrine used?
``` bronchospasm of anaphylaxis hypotensive shock (increases BP, HR, CO) ```
307
how is epinephrine administered?
subQ or inhaled
308
when do you see maximal effect of Epi?
15 minutes
309
how long does Epi last?
60-90 minutes
310
what is the downside to epic?
more SE than selective B2
311
describe SABAs
``` short acting short 1/2 life fast onset (5 minutes, peak at 30-60 minutes) gone fast (4-6hr) ```
312
how are SABAs usually administered?
inhalation by MDI or nebulizer
313
why are oral and SQ SABAs less effective?
longer onset | more SE
314
what do you prescribe for a rescue inhaler?
SABA
315
what indicates uncontrolled asthma?
use of SABA >2x/week
316
describe LABA
give 2x/d | LT tx of asthma & emphysema
317
what are LABAs especially good at
preventing nocturnal asthmatic attacks
318
black box warning of LABAs?
increased risk of asthma death in those using as a single agent (greatest risk in kids 4-11)
319
what should be added to LABA therapy?
SABA | corticosteroids
320
ADRs of SABAs?
- Tachycardia* - Bronchospasms* - tremor* - anxiety - hyperglycemia - hypokalemia - hypomagnesemia - tolerance
321
ADRs of LABAs
- Tachycardia* - Bronchospasms* - tremor* - anxiety - hyperglycemia - hypokalemia - hypomagnesemia - tolerance - muscle cramps*
322
downside of methylxanthines?
narrow therapeutic window
323
MOA of methylxanthines?
- 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
CNS ADRs of methylxanthines?
``` HA anxiety restlessness increased alertness insomnia dizziness seizures ``` lower dose to fix
325
Cardiac ADRs of methylxanthines?
hypotension afib/flutter PVCs tachycardia
326
GI ADRs of methylxanthines?
abdominal pain nausea vomitting minimize with food, anti-acids, or full glass of liquids
327
skeletal mm ADRs of methylxanthines?
- strengthens contraction - reverses diaphragm fatigue in COPD patients (improves ventilator response)
328
electrolyte ADRs of methylxanthines?
hypokalemia | hyperglycemia
329
what pt should you take caution with using methylxanthines?
liver disease, metabolized by liver
330
what is 1/2 life of methylxanthines?
non-smoker: 8 hours | smokers & kids (1-9): 4.5 hours
331
drug interactions of methylxanthines?
``` prevent metabolism: cimetidine erythromycin quinolone isoniazid verapamil ```
332
what do you need to monitor with methylxanthines? ideal range?
serum blood levels 2x/yr: 10-15mcg/mL
333
when do seizures and arrhythmias occur with methylxanthines?
25 mcg/mL
334
how does ACh affect lungs?
bronchoconstriction & mucous secretion
335
MOA of antimuscarinics/anticholinergics?
target M3, competitively/reversibly inhibit ACh in bronchial smooth mm causing bronchodilation
336
How are antimuscarinics normally administered?
inhaled
337
what Dx are antimuscarinic really useful for?
COPD
338
what antimuscarinics have been approved to tx COPD? how long do they act on the body?
ipratropium - short acting | tiotropium - long acting
339
if a pt can't use a SABA what can you give them?
ipratropium
340
ICS and LABAs are useful for controlling severe asthma; what other combination is useful?
tiotropium & ICS
341
ADRs of antimuscarinics
- dry mouth - pharyngeal irritation - increased IOP - urinary retention
342
what pt should you use caution in when treating with antimuscarinics?
glaucoma BPH bladder obstruction
343
what is the most effective LT treatment for asthma (all sizes and shapes)?
ICS used regularly decrease # of exacerbations
344
when are ICSs most effective?
when used daily (their efficacy does not continue after they are stopped)
345
how are corticosteroids administered in urgent situations?
IV and orally
346
T/F side effects of ICS are greater than nasal steroids.
T: they are given at higher doses. There is a risk of systemic effects, but less than when given systemic steroids.
347
when are systemic corticosteroids used?
for exacerbations of asthma incompletely responsive to bronchodilators
348
what is the most common oral systemic corticosteroid used for exacerbated asthma? dose?
prednisone (oral) 30-60mg/d in divided doses for 6-12 d dose is tapered after airway obstruction improves other: methylprednisolone, prednisolone
349
why are IM injections of systemic corticosteroids given? what drug?
releases steroids over several weeks depomedrol (methylpredinsolone) solumedrol (methylpredinsolone)
350
MOA of corticosteroids in asthma?
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
How long does it usually take to see effects of corticosteroids?
4-12 hours | 8 weeks for max effect
352
Dosage of ICS?
1-2x/d for mild to moderate Sx | if severe, may need systemic steroids
353
first line for asthma?
ICS, dosage varies have to use PC to convert
354
ADRs of inhaled corticosteroids
- thrush - dysphonia - reflex cough - bronchospasm reduce with space & mouth rinses
355
how is height affected by ICS?
1.2 cm or less as child, adult height unaffected
356
ADRs of high dose ICS with long term use?
- hypothalamic-pituitary-adrenal fxn suppression - osteoporosis - cataracts - glaucoma - edema - immunosuppression - thin skin
357
MOA of cromolyn
inhibits cough | inhibits mast cells & eosinophils from releasing granules
358
How is cromolyn dosed?
4x/d | MDI or nebulizer
359
how long dose it take to see effects of cromolyn?
1-2 weeks
360
how are cromolyns used?
poorly absorbed only used prophylatically for Ag or exercise induced asthma, pregnancy
361
ADRs of cromolyn
- throat irritation - bad taste - cough - mouth dryness - chest tightness - wheezing
362
what is leukotriene?
substance produced by inflammatory pathway (5-lipoxygenase enzyme) that causes bronchoconstriction, increased bronchial reactivity, mucosal edema, & hypersecretions
363
MOA of leukotriene modifiers?
inhibit 5-lipoxygenase to prevent leukotriene production (no constriction, mucosal edema, hyper secretions)
364
dosage of leukotriene modifiers?
1x/d
365
ADRs of leukotriene modifiers?
- hepatic injury (monitor LFT q6mo)*** - Churg-Strauss - eosinophilia
366
what is churg-strauss?
a syndrome of vasculitis (inflammation of blood vessels) causes by LTI
367
what is eosinophilia?
increased eosinophils in blood caused by LTI
368
drug interactions of LTI?
montelukast - none zarfilukast: - inhibits many CYP isoenzymes - interferes with metabolism of: phenytonin warfarin felodipine lovastatin triazolam
369
leukotriene modifier clinical uses?
- preventing exacerbations of asthma (ICS work better): oral useful in kids who can't inhale - aspirin induced asthma - perennial/seasonal allergic rhinitis
370
why does aspirin induce asthma?
causes pt to make more leukotrienes 5-10% of pt get exacerbations when exposed to NSAIDs
371
MOA of omalizumab
prevents IgE binding to mast cells and basophils, preventing the release of inflammatory mediators after allergen exposure
372
dose of omalizumab?
SQ q2-4weeks
373
clinical use of omalizumab?
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
how old do you need to be to take omalizumabs?
12
375
SE of omalizumabs?
allergic rxn | anaphylaxis (give where you can treat anaphylaxis)
376
MOA of romflumilast?
inhibits PDE4 in lung tissue, leading to smooth muscle relaxation & decreased inflammatory activity
377
which is more selective for inhibiting PDE4: romflumilast or theophylline?
romflumilast
378
clinical uses of romflumilast?
reduce COPD exacerbations
379
what is romflumilast NOT used for?
acute episodes | NOT a bronchodilator
380
SE of romflumilast?
``` diarrhea nausea weight loss anxiety insomnia depression ```
381
dosage of romflumilast?
1x/d orally
382
devices for inhaling medications?
MDI (metered dose inhaler) spacers DPI (dry powder inhaler) nebulizer have particles small enough they can be inhaled into lungs (aerosol)
383
describe MDIs
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
how should you inhale with MDI
slowly & deeply gets most drug into lung
385
describe valve holding chamber & its benefits
better than open tube spacer $$$ compress canister, holds med in chamber until inspiratory pressure pulls med into lungs less coordination needed
386
Describe DPI
micro-ionized powder goes directly to lung (not in liquid like MDI)
387
How to inhale with DPI
deep, forceful breathe (opposite MDI)
388
pros and cons of DPI
pros: breath actuated (don't need hand/lung coordination) & easier to teach to use cons: need higher inspiratory flow
389
describe nebulizers
dissolve drug in liquid, use compressed air or vibrations to turn liquid into a fine mist, mist is inhaled
390
pros & cons of nebulizers
pros: good last resort cons: $$, Lg, less portable
391
goals of asthma treatment
short term: improve fxn & decrease Sx long term: prevent exacerbations & progressive loss of pulmonary fxn
392
what should all asthma pt have?
SABA
393
If a pt has occasional symptoms a SABA may be all they required; when should you add a corticosteroid?
use >2x/week night Sx >2x/month FEV1
394
How to treat acute asthma in ER?
- 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
what should you NOT use during acute asthma attack?
DPI: requires high inspiratory flow which pt do not have during attack
396
when are corticosteroids added to therapy?
frequent asthmatic symptoms or significant airflow obstruction despite bronchodilator
397
If a pt is on low dose corticosteroids and their asthma is not controlled what can you add to improve their situation?
- increased dose of inhaled steroids | - add a LABA to current dose of inhaled steroids
398
If a pt is having severe asthma symptoms or has a severe obstruction what should you give them?
IV & inhaled corticosteroids once better taper IV steroids
399
when are antimuscarinic drugs used for acute asthma?
1. if pt is intolerant to beta agonists | 2. as adjunctive to SABA and steroid therapy
400
what are antimuscarinics most useful for?
COPD
401
what type of antimuscarinic should you use for acute asthma?
short acting
402
when would you used cromolyn?
before event that triggers Sx
403
how to use cromolyn & leukotriene modifiers in acute asthma?
in place of ICS if can't use it; or in addition to it
404
why are leukotriene modifiers more useful than cromolyn and less useful than ICS?
more useful than cromolyn because they are easier to use (often used in kids) not as affective as inhaled steroids
405
describe intermittent asthma
Sx >2d/w night awakenings >2x/mo SABA use 80% FEV1/FVC normal
406
describe mild asthma
``` 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
describe moderate asthma
``` Sx daily night awakenings >1x/week SABA use daily some limitations on ADLs FEV1 >60% but ```
408
describe severe asthma
``` Sx daily night awakenings daily SABA use daily severe limitations on ADLs FEV1 5% ```
409
tx for intermittent asthma
SABA PRN
410
tx for mild asthma
SABA + low dose ICS
411
Tx for moderate asthma
SABA + low dose ICS + LABA or SABA + medium dose ICS
412
Tx for severe asthma
SABA + medium dose ICS + LABA
413
what to add if SABA, medium dose ICS, and LABA isn't enough?
consult with asthma specialist add high dose ICS consider adding omalizumab if allergies
414
what to add if SABA, high dose ICS, and LABA isn't enough?
add oral corticosteroid consider omalizumab if allergies
415
How to treat exercise induced bronchoconstrion? (EIB)
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
when is tx of EIB with LABAs less reliable than SABAs?
with frequent usage
417
what to give pt with asthma during pregnancy?
SABA - Albuterol ICS - budesonide maybe LABA & montelukast (not great evidence)
418
teratogen asthma medication?
Zileuton (LTI)
419
should you use DPI in kids?
no they can't inhale well enough
420
if parents of children refuse ICS what can you prescribe for LT treatment of asthma?
montelukast
421
Tx for mild intermittent asthma in kids?
SABA PRN
422
Tx for mild, moderate, severe persistent asthma in kids?
SABA PRN + ICS
423
T/F medications for asthma are as effective for COPD?
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
Tx for acute symptoms of COPD?
SABA (albuterol) or short acting anticholinergic (combivent) or both
425
chronic symptoms of COPD: regular symptoms of SOB and limitations on ADLs
LABA or long acting anticholinergic or both methylxanthines (another bronchodilator) used for those intolerant or unable to used inhaled therapy
426
what should you prescribe for severe & frequent exacerbations of COPD?
ICS