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NURP 423 misc > Exam 1 drugs > Flashcards

Exam 1 drugs Flashcards

Solidify knowledge of drug/class/key points

1
Q

Meds used for angina, no effect on heart rate, increase smooth muscle relxation, reduce demand through vasodilation

A

Dihydropyridine Ca channel blockers: amlodipine, felodipine, nifedipine

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2
Q

Meds used for angina, minimal effect on BP, neg inotropic effect and rate control

A

Non-dihydropyridine Ca channel blockers: verapimil, diltiazem.

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3
Q

How to switch from a long acting to short acting Beta blocker

A

i.e. metoprolol succinate to tartrate: use SAME dose, dose twice daily

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4
Q

Mechanism for angina includes decreasing cathcholamine (norepi) response, decrease HR, BP, reduce workload and O2 consumption

A

Beta blockers mechanism

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5
Q

Non-selective beta blockers

A

nadolol, propanolol

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6
Q

Cardioselective beta blockers

A

atenolol, metoprolol, bisoprolol

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7
Q

alpha-beta blockers (one OK in pregnancy)

A

carvedilol (labetolol)

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8
Q

Five classes of drugs used in angina/ CAD

A

ACEi, Beta block, Ca chan block, Antiplatelet, Nitrates

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9
Q

Meds that increase blood supply, work to reduce O2 demand by interrupting renin-angiotensin system, reduce vasoconstriction (name the class and 5 meds)

A

ACE inhibitors: captopril, enalapril, lisinopril, ramipril, trandolapril

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10
Q

Benefits of ACEi for angina/CAD

A

Reduce remodeling/progression, reduce hospitalization, improve survival, as well as improve chronic stable angina Sx

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11
Q

ACEi adverse effects (one first-dose effect)

A

(hypotension), worsening renal fxn, high K, cough, angioedema, rash, ageusia, neutropenia

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12
Q

Which ACEi specifically post-MI?

A

Ramipril. Increases revascularization.

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13
Q

Monitoring with ACEi

A

If refractory HTN, need renal ultrasound - bilateral renal artery stenosis is a contraindication. Renal labs and serum K after 1-2 weeks of starting/increasing dose.

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14
Q

How long does it take 81mg ASA to have antiplatelet effect? 160-325 mg?

A

Days for 81 mg. 30 minutes for 160-325 mg.

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15
Q

What is a thienopyridine? (For CAD/ACS/unstable angina/another indication.)

A

clopidogrel (Plavix), an antiplatelet therapy, interrupts clumping same way as aspirin. (Use for 1 year in drug-eluting stents, 3 months with bare metal stents.)

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16
Q

Can someone be on both clopidogrel and aspirin?

A

Yes, the combo has no added risk of bleeding and added benefit for preventing MI

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17
Q

Aspirin for primary prevention: who and what dose?

A

Males age 45-79; females 55-79.
Doses up to 325 mg reduce risk of second MI, improve survival.
160-325 mg in acute MI (reduces death by 23% if within 24 hours) and in unstable angina.
Low dose 81-160 long term for stents, prior MI, exertional angina, DM, vascular dz.
Smokers and those with a fam hx of CAD, PVD, HTN, high LDL, DM.

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18
Q

Are anticoagulant and antiplatelet the same thing?

A

NO. ASA and thiopyridines (Plavix) affect thromboxamne/A2, but have no impact on clotting factors.

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19
Q

What med reduces preload, decreases wall tension, makes actual cell structure a little more pliable, to increase supply between coronary arteries to increase O2 availability? Name 3 drugs and 2 indications.

A

Nitrates. Isordil, Imdur, nitroglycerin.
They are endothelial vasodilators.
Used in angina/CAD and HF (stage C with hydralazine, when ACE intolerant).

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20
Q

Risk of nitrates? Contraindications?

A

Quick hypotensive effect. Avoid in head trauma, hemorrhage issues, hx of migraine (may be prone to nitrate headaches).

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21
Q

Another med besides nitrates which, at cellular level, increases supply between coronary arteries and cardiac muscle. Watch interactions due to what pathways?

A

ranolazine (Ranexa). CYP3A and sodium channels, so monitor Qtc.

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22
Q

Which drugs are OK in combo with beta blockers for CAD/angina?

A

CCB, nitrates, ACEi, ASA

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23
Q

What can NOT be combined with nitrates?

A

sildenafil

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24
Q

What can NOT be combined with CCBs?

A

Nitrates, ACEi

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25
Q

What can NOT be combined with aspirin?

A

Trick question: all are OK according to CAD/angina lecture, but of course you would use caution with anticoagulation and monitor for bleeding.

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26
Q

What 7 types of drugs are used in heart failure?

A

ACEs/ARBs, beta blockers, diuretics, digitalis, spironolactone, nitrates, and vasodilators.

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27
Q

Contraindications to ACEi

A

Renal failure (anuria, creatinine >3 mg/dl), renal artery stenosis, angioedema, pregnancy, hyperkalemia, severe hypotension, hepatic dz

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28
Q

First line drug class in heart failure. Which stages? Also used in what other indication?

A

ACE inhibitors.
Stages A, B, C, D (low dose)
Also used when LVEF <35-40% and asymptomatic.

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29
Q

ACEi may make what other class of drug less effective in setting of heart failure?

A

Diuretics

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30
Q

Are ARBs used in heart failure?

A

Only if intolerant to ACEi (cough) and 3rd (?) line after being on beta blockers, diuretics, and digoxin.

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31
Q

Name three indications for beta blockers.

A

Heart failure stages B,C, D (low dose).
Asymptomatic ventricular dysfunction.
Post MI.

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32
Q

Name three contraindications for beta blockers.

A

Asthma /reactive airway dz.
AV block (unless pacemaker).
Hypotension/bradycardia/athlete.
Note: Diabetes is NOT a contraindication!

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33
Q

Drug types NOT used as monotherapy for heart failure:

A

Beta blockers or diuretics. Diuretics would be used in HTN to prevent progression to HF, and inpatient, but wouldn’t be effective alone in HF.

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34
Q

Acute HF and decreased GFR: what do you do to the diuretic dose?

A

Increase the loop diuretic for a better response. Can titrate any diuretic down when pt is “dry” weight /euvolemic. Monitor K.

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35
Q

Besides increasing dose, what can you do if diuretics aren’t working well?

A

Consider: Dopamine to increase CO.
Reduced dose of ACEi.
Combine loop + thiazide / spironolactone / metolazone.
Dialysis.

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36
Q

Mechanisms of what medication?
Positive inotropic effect –> flood of Ca interferes with Na pump to suppress renin-angiotensin sys; reduces plasma noradrenaline, PNS activity, reduces vagal tone, aids natriuresis by normalizing arterial baroreceptors.

A

Digitalis.

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37
Q

Before using digitalis in heart failure, pt would have failed what other meds?

A

ACE, diuretics, and beta blocker. Stage C HF only.

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38
Q

When to check digitalis levels?

A

One week then every 3 months.

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39
Q

Contraindications to digitalis:

A 
AV block without pacemaker.
PVCs or Vtach.
Hypokalemia.
W-P-W with Afib.
Toxic levels.
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40
Q

Mechanisms of what medication?

Directly works on smooth muscle to dilate vessels, esp arterioles; donates nitric oxide somewhat.

A

Angiotensin II receptor antagonist.

aka vasodilator.

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41
Q

What drugs should you AVOID/consider as risk factors in heart failure, due to their potential to worsen? Name 7.

A

Long term/intermittent inotropes (beta blockers, digitalis).
Antiarrhythmics (except amiodarone).
CCBs in systolic failure (except amlodipine).
NSAIDs.
Tricyclic antidepressants.
Corticosteroids.
Lithium.

42
Q

Symptoms of digitalis toxicity.

A

Yellow halos, confusion, N/V, fatigue, HA. Fitzgerald says vision color changes are rare but anorexia is most common.

43
Q

Carvedilol for what stages of HF?

A

In stages B,C, improves BP and CO. Can use low dose beta blockers in stage D.

44
Q

Characteristics of systolic vs. diastolic HF.

A

Sys - Can’t squeeze hard enough. EF often <40%.

Dias - Stiff ventricle walls don’t adequately relax, leading to inadequate fill and stroke volume.

45
Q

WHY no CCBs in systolic HF?

A

Negative inotropic effect, would worsen.

46
Q

Difference between aspirin and clopidogrel?

A

ASA blocks prostaglandin synthesis using enzyme antagonism which inhibits platelet activation. Clopidogrel reduces ADP-induced platelet activation, and can be used in patients who have contraindications to aspirin.

47
Q

Contraindications to aspirin, name 6.

A 
Allergy to NSAIDs/ ASA.
Active ulcer.
Hx hemorrhagic bleed.
Head bleed/risk.
Kids with influenza or varicella.
Caution in renal changes.
48
Q

What are the quick relief meds for asthma?

A

Ipratropium, albuterol, prednisone, Atrovent, DuoNeb, Combivent.

49
Q

Mechanism of beta adrenergic agonists?

Includes SABA and LABA (short acting/long acting).

A

Increases cAMP, relaxes smooth airway muscle, increases bronchial ciliary activity. Considered a bronchodilator.

50
Q

AE’s of SABAs/LABAs

A

CNS stimulation, increased HR, cardiac contractility, conductivity. Increased skeletal muscle activity, hyperglycemia, hypokalemia.

51
Q

Name some SABAs.

A

albuterol (Proventil, Ventolin, ProAir), levalbuterol.

52
Q

Name some LABAs.

A

salmeterol (Advair), formoterol (Symbicort, Dulera), vilanterol. The brand names are combinations with steroids.

53
Q 
What class are these brand name asthma medications?
Symbicort, Dulera, Advair.
A

Combination inhaled corticosteroid and LABAs.

54
Q

Mechanism of inhaled corticosteroids (ICS) / systemic steroids?

A

Inhibit or induce end-effector proteins to reduce airway inflammation. (In gene promoter regions of DNA, protein transcription is stimulated or inhibited.) Affects vascular tone, permeability, and body water distribution; stimulate lipolysis, gluconeogenesis, glycogen secretion; impair leukocyte migration; inhibit production of proinflammatory proteins such as cytokines, interleukins, interferons, and chemokines.
Decrease mucous secretion and upregulation of beta receptors.

55
Q

AE’s of ICS?

A

Oral thrush, dysphonia. Rinse, gargle, spit after each dose.

56
Q

AE’s of oral/systemic steroids?

A

Short term: sodium and water retention (periph edema, increase in BP, CHF exacerbation), hyperglycemia, increased appetite and weight gain, CNS stimulation (insomnia, nightmares), peptic ulcer, leukocytosis.
Long term: adrenal suppression, muscle wasting, myopathy, bone loss, cataracts, dermal thinning/striae, peptic ulcer.

57
Q

Drug interaction with systemic steroid?

A

Contraceptive pills may decrease steroid effectiveness. Also caution in diabetes.

58
Q

What is the dose of a steroid burst for asthma?

A

Prednisone 60 mg QD or 30 mg BID, x 5 days. Or 1-2 mg/kg/day.

59
Q

What is the dose of a steroid burst for COPD?

A

Prednisone 40 mg QD x 5 days. If needed longer term, do a taper.

60
Q

Mechanism of leukotriene modifiers?

A

One kind prevents conversion of arachidonic acid to bronchoconstrictor and proinflammatory leukotrienes. Another kind blocks binding sites on eosinophils and other proinflammatory cells, with same end result.

61
Q

AE’s of leukotriene modifiers?

A

HA, a rare systemic vasculitis (Churg-Strauss), and neuropsychiatric events (sleep disturb, behavior change).

62
Q

Name some leukotriene modifiers.

A

Montelukast, zafirlukast, zileuton.

63
Q

Mechanism of mast cell stabilizers?

A

Stops mast cells from making & releasing proinflammatory mediators in response to antigens. Stops the chain of mast cells –> cytokines/chemokines recruiting additional inflammatory cells. (ALLERGY process.)

64
Q

AE’s of mast cell stabilizer?

A

Bad taste in mouth, nausea. Rare IgE allergic response, anaphylaxis within minutes; rash within hours-days.

65
Q

Name a mast cell stabilizer.

A

Cromolyn. Taken off the market due to chlorofluorocarbons and impact on ozone layer.

66
Q

Mechanism of methylxanthine?

A

These are bronchodilators, exact mech unknown. Relax smooth muscle, enhance diaphragmatic contractility, slight anti-inflamm effect. Involves inhibiting cAMP and a weak adenosine antagonism.

67
Q

Name some methylxanthines.

A

Theophylline, aminophylline.

68
Q

AE’s of methylxanthines?

A

Note, many drugs affect its metabolism and its serum concentrations must be monitored. Tachyarrhythmias, restlessness, insomnia, tremor, N/V, GER, seizure, peptic ulcer aggravation. Even life threatening cardiac effects at therapeutic levels!

69
Q

How do you use lung function tests to classify asthma severity?

A

In kids 4 and under, you don’t.
Kids 5-11, forced expiratory volume in one second (FEV1) is 80% and higher in intermittent and mild persistent asthma; 60-80% in moderate, and <60% in severe.
In age 12 and up, compare to the reference range of normal FEV1/FVC.

70
Q

How do you diagnose asthma with respect to spirometry?

A

A reduced PEF alone indicates airflow obstruction but is not diagnostic of asthma.
If FEV1/FVC is less than 0.7, airflow obstruction.
Eval for airflow obstruction REVERSIBILITY: compare baseline to 10-15 minutes following a 2-4 puff SABA treatment. FEV1 increase of 12% and absolute increase of at least 200mL.
Diagnosis requires presence of symptoms and variable airflow limitation.

71
Q

What are the 5 components other than spirometry for classifying asthma severity?

A 
Symptoms (how many days per week).  
Nighttime awakenings.  
SABA use.  
Normal activity interference.  
Exacerbations requiring steroids (per year).
72
Q

A parent calls and it sounds like kid is having a mild asthma exacerbation at home. What do you do? When would you send them to the ER?

A

Use an inhaled SABA first. Two treatments 20 minutes apart and repeat every 3-4 hours until good response with symptoms and PEF (for up to two days). Also short course of systemic steroids. But if NOT having a good response (marked wheezing, dyspnea, PEF <50% predicted) after 2 albuterol treatments, go to ER.

73
Q

So you’ve changed a patient’s asthma care plan (stepped up or down). What is appropriate monitoring timeline for visits and spirometry?

A

1-3 months after a new therapy, then each 3-12 months thereafter = GINA guidelines.
If controlled for 3+ months, then monitor every 6 months = NAEPP guidelines.
Spirometry at baseline, then 3-6 mo later, than annually.

74
Q

What are some generic and brand names of inhaled corticosteroids?

A

beclomethasone (Qvar), budesonide (Pulmicort), fluticasone (Flovent), mometasone (Asmanex)

75
Q

What class is Singulair? What about Xolair?

A 
Singulair = montelukast, a leukotriene modifier.
Xolair = omalizumab, a monoclonal antibody.
76
Q

What are key differences between asthma and COPD?

Why are inhaled corticosteroids used differently?

A

Asthma: Difficulty getting air IN. More restriction. Could resolve/reverse and be off of meds someday.
COPD: Trouble getting air OUT. More obstruction. Considered irreversible, progressive, will always need meds.
Although COPD involves an inflammatory response to particles/gases, in its CHRONIC state, inflammation isn’t necessarily part of the pathophysiology, and ICS won’t have a favorable risk/benefit profile for groups A/B. Never use ICS alone in COPD - only in combo with bronchodilator.

77
Q

Black box warning for LABAs.

A

Associated with an increased risk of asthma-related death. Must be used in combination with a “controller” med like ICS.

78
Q

Main goal of therapy in COPD?

A

Reduce exacerbations. Get them down to group B. If you can’t, they should also be seeing a specialist.

79
Q

Initial therapy/continued Sx in COPD Group B?

A

LAMA or LABA.

If cont, 2 bronchodilators (LABA + LAMA).

80
Q

Initial therapy/continued Sx in COPD Group C?

A

LAMA.

If cont. exacerbations, add LABA and maybe ICS.

81
Q

Define group C COPD (2017 guidelines).

A

Lower symptom scores (mMRC 0-1 or CAT <10), and high exacerbation history (2+ per year or 1+ with hospitalization).

82
Q

GOLD groups 1-4 refer to _________, whereas A-D refer to __________.

A

airflow limitation as percent of expected FEV1; symptom burden and risk of exacerbation

83
Q

Define group A COPD.

A

Lower symptom scores (mMRC 0-1 or CAT <10), and 0-1 exacerbations.

84
Q

Define group D COPD.

A

Higher symptom scores (mMRC 2+ or CAT 10+), and 1+ admission or 2+ exacerbations.

85
Q

Define group B COPD.

A

Higher symptom scores (mMRC 2+ or CAT 10+), but no hospitalizations or maximum 1 exacerbation.

86
Q

Define GOLD grade 1.

A

FEV1 80% of predicted or higher

87
Q

Define GOLD grade 2.

A

FEV1 50-79% of predicted.

88
Q

What would you use for a pregnant person with rhinorrhea?

A

ipratropium (Atrovent) = category B. Anticholinergic, bronchodilator.

89
Q

What would you use for a 2 year old who is already taking Claritin but still has a runny nose?

A

fluticasone (Veramyst)

90
Q

What is Afrin? Considerations?

A

phenylephrine. Use max of 3 days.

91
Q

Goals of tx of HF.

A

Prevent progression of HF. Improve Sx, improve QOL.

92
Q

Define GOLD grade 3.

A

FEV1 30-49% of predicted.

93
Q

Define GOLD grade 4.

A

FEV1 <30% of predicted.

94
Q

Class 1 anti-arrhythmic mechanism?

A

Interfere with Na channels, binding to then dissociating from them at different rates, slowing conduction in some areas. They are membrane stabilizing agents.

95
Q

Name the class I AADs: 1a, 1b, 1c.

A

1a - Quinidine, procainamide, disopyramide.
1b - Lidocaine, mexiletine.
1c - Flecainide, propafenone.

96
Q

Class II AAD mechanism? And name some.

A

Beta blockers, they slow the impulse in the AV and SA nodes, slowing ventricular rates. Atenolol, esmolol, metoprolol, propranolol

97
Q

Class III AAD mechanism? And name some.

A

They block many different channels (K, Ca, Na), treat both supraventricular and ventricular arrhythmias, and can have many side effects. Amiodarone, sotalol, others.

98
Q

Class IV AAD mechanism? And name some.

A

They slow conduction, prolong refractoriness, decrease automaticity in the nodes. They are the nondihydropyridines, also called “slow” CCBs: verapamil and diltiazem.

99
Q

Misc notes on 3 “Other” AADs:

A

Digoxin: mainly AV node slowing, doesn’t convert Afib/Aflutter to sinus, narrow therapeutic index. Low renal function predisposes to toxicity.

100
Q

What are the 3 classes of meds that you would only use as monotherapy for Afib in a sedentary patients?

A

BBs, CCBs, digoxin. They slow HR and can cause fatigue.

101
Q

Do you use NSAIDs in kids with URIs?

A

Decreasing inflammation does help relieve associated symptoms. However, caution of increased risk for inducing bronchospasm in those with asthma, chronic rhinitis, or nasal polyps.

NURP 423 misc (1 decks)

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