Exam 1 drugs Flashcards
Solidify knowledge of drug/class/key points
Meds used for angina, no effect on heart rate, increase smooth muscle relxation, reduce demand through vasodilation
Dihydropyridine Ca channel blockers: amlodipine, felodipine, nifedipine
Meds used for angina, minimal effect on BP, neg inotropic effect and rate control
Non-dihydropyridine Ca channel blockers: verapimil, diltiazem.
How to switch from a long acting to short acting Beta blocker
i.e. metoprolol succinate to tartrate: use SAME dose, dose twice daily
Mechanism for angina includes decreasing cathcholamine (norepi) response, decrease HR, BP, reduce workload and O2 consumption
Beta blockers mechanism
Non-selective beta blockers
nadolol, propanolol
Cardioselective beta blockers
atenolol, metoprolol, bisoprolol
alpha-beta blockers (one OK in pregnancy)
carvedilol (labetolol)
Five classes of drugs used in angina/ CAD
ACEi, Beta block, Ca chan block, Antiplatelet, Nitrates
Meds that increase blood supply, work to reduce O2 demand by interrupting renin-angiotensin system, reduce vasoconstriction (name the class and 5 meds)
ACE inhibitors: captopril, enalapril, lisinopril, ramipril, trandolapril
Benefits of ACEi for angina/CAD
Reduce remodeling/progression, reduce hospitalization, improve survival, as well as improve chronic stable angina Sx
ACEi adverse effects (one first-dose effect)
(hypotension), worsening renal fxn, high K, cough, angioedema, rash, ageusia, neutropenia
Which ACEi specifically post-MI?
Ramipril. Increases revascularization.
Monitoring with ACEi
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.
How long does it take 81mg ASA to have antiplatelet effect? 160-325 mg?
Days for 81 mg. 30 minutes for 160-325 mg.
What is a thienopyridine? (For CAD/ACS/unstable angina/another indication.)
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.)
Can someone be on both clopidogrel and aspirin?
Yes, the combo has no added risk of bleeding and added benefit for preventing MI
Aspirin for primary prevention: who and what dose?
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.
Are anticoagulant and antiplatelet the same thing?
NO. ASA and thiopyridines (Plavix) affect thromboxamne/A2, but have no impact on clotting factors.
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.
Nitrates. Isordil, Imdur, nitroglycerin.
They are endothelial vasodilators.
Used in angina/CAD and HF (stage C with hydralazine, when ACE intolerant).
Risk of nitrates? Contraindications?
Quick hypotensive effect. Avoid in head trauma, hemorrhage issues, hx of migraine (may be prone to nitrate headaches).
Another med besides nitrates which, at cellular level, increases supply between coronary arteries and cardiac muscle. Watch interactions due to what pathways?
ranolazine (Ranexa). CYP3A and sodium channels, so monitor Qtc.
Which drugs are OK in combo with beta blockers for CAD/angina?
CCB, nitrates, ACEi, ASA
What can NOT be combined with nitrates?
sildenafil
What can NOT be combined with CCBs?
Nitrates, ACEi
What can NOT be combined with aspirin?
Trick question: all are OK according to CAD/angina lecture, but of course you would use caution with anticoagulation and monitor for bleeding.
What 7 types of drugs are used in heart failure?
ACEs/ARBs, beta blockers, diuretics, digitalis, spironolactone, nitrates, and vasodilators.
Contraindications to ACEi
Renal failure (anuria, creatinine >3 mg/dl), renal artery stenosis, angioedema, pregnancy, hyperkalemia, severe hypotension, hepatic dz
First line drug class in heart failure. Which stages? Also used in what other indication?
ACE inhibitors.
Stages A, B, C, D (low dose)
Also used when LVEF <35-40% and asymptomatic.
ACEi may make what other class of drug less effective in setting of heart failure?
Diuretics
Are ARBs used in heart failure?
Only if intolerant to ACEi (cough) and 3rd (?) line after being on beta blockers, diuretics, and digoxin.
Name three indications for beta blockers.
Heart failure stages B,C, D (low dose).
Asymptomatic ventricular dysfunction.
Post MI.
Name three contraindications for beta blockers.
Asthma /reactive airway dz.
AV block (unless pacemaker).
Hypotension/bradycardia/athlete.
Note: Diabetes is NOT a contraindication!
Drug types NOT used as monotherapy for heart failure:
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.
Acute HF and decreased GFR: what do you do to the diuretic dose?
Increase the loop diuretic for a better response. Can titrate any diuretic down when pt is “dry” weight /euvolemic. Monitor K.
Besides increasing dose, what can you do if diuretics aren’t working well?
Consider: Dopamine to increase CO.
Reduced dose of ACEi.
Combine loop + thiazide / spironolactone / metolazone.
Dialysis.
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.
Digitalis.
Before using digitalis in heart failure, pt would have failed what other meds?
ACE, diuretics, and beta blocker. Stage C HF only.
When to check digitalis levels?
One week then every 3 months.
Contraindications to digitalis:
AV block without pacemaker. PVCs or Vtach. Hypokalemia. W-P-W with Afib. Toxic levels.
Mechanisms of what medication?
Directly works on smooth muscle to dilate vessels, esp arterioles; donates nitric oxide somewhat.
Angiotensin II receptor antagonist.
aka vasodilator.
What drugs should you AVOID/consider as risk factors in heart failure, due to their potential to worsen? Name 7.
Long term/intermittent inotropes (beta blockers, digitalis).
Antiarrhythmics (except amiodarone).
CCBs in systolic failure (except amlodipine).
NSAIDs.
Tricyclic antidepressants.
Corticosteroids.
Lithium.
Symptoms of digitalis toxicity.
Yellow halos, confusion, N/V, fatigue, HA. Fitzgerald says vision color changes are rare but anorexia is most common.
Carvedilol for what stages of HF?
In stages B,C, improves BP and CO. Can use low dose beta blockers in stage D.
Characteristics of systolic vs. diastolic HF.
Sys - Can’t squeeze hard enough. EF often <40%.
Dias - Stiff ventricle walls don’t adequately relax, leading to inadequate fill and stroke volume.
WHY no CCBs in systolic HF?
Negative inotropic effect, would worsen.
Difference between aspirin and clopidogrel?
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.
Contraindications to aspirin, name 6.
Allergy to NSAIDs/ ASA. Active ulcer. Hx hemorrhagic bleed. Head bleed/risk. Kids with influenza or varicella. Caution in renal changes.
What are the quick relief meds for asthma?
Ipratropium, albuterol, prednisone, Atrovent, DuoNeb, Combivent.
Mechanism of beta adrenergic agonists?
Includes SABA and LABA (short acting/long acting).
Increases cAMP, relaxes smooth airway muscle, increases bronchial ciliary activity. Considered a bronchodilator.
AE’s of SABAs/LABAs
CNS stimulation, increased HR, cardiac contractility, conductivity. Increased skeletal muscle activity, hyperglycemia, hypokalemia.
Name some SABAs.
albuterol (Proventil, Ventolin, ProAir), levalbuterol.
Name some LABAs.
salmeterol (Advair), formoterol (Symbicort, Dulera), vilanterol. The brand names are combinations with steroids.
What class are these brand name asthma medications? Symbicort, Dulera, Advair.
Combination inhaled corticosteroid and LABAs.
Mechanism of inhaled corticosteroids (ICS) / systemic steroids?
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.
AE’s of ICS?
Oral thrush, dysphonia. Rinse, gargle, spit after each dose.
AE’s of oral/systemic steroids?
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.
Drug interaction with systemic steroid?
Contraceptive pills may decrease steroid effectiveness. Also caution in diabetes.
What is the dose of a steroid burst for asthma?
Prednisone 60 mg QD or 30 mg BID, x 5 days. Or 1-2 mg/kg/day.
What is the dose of a steroid burst for COPD?
Prednisone 40 mg QD x 5 days. If needed longer term, do a taper.
Mechanism of leukotriene modifiers?
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.
AE’s of leukotriene modifiers?
HA, a rare systemic vasculitis (Churg-Strauss), and neuropsychiatric events (sleep disturb, behavior change).
Name some leukotriene modifiers.
Montelukast, zafirlukast, zileuton.
Mechanism of mast cell stabilizers?
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.)
AE’s of mast cell stabilizer?
Bad taste in mouth, nausea. Rare IgE allergic response, anaphylaxis within minutes; rash within hours-days.
Name a mast cell stabilizer.
Cromolyn. Taken off the market due to chlorofluorocarbons and impact on ozone layer.
Mechanism of methylxanthine?
These are bronchodilators, exact mech unknown. Relax smooth muscle, enhance diaphragmatic contractility, slight anti-inflamm effect. Involves inhibiting cAMP and a weak adenosine antagonism.
Name some methylxanthines.
Theophylline, aminophylline.
AE’s of methylxanthines?
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!
How do you use lung function tests to classify asthma severity?
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.
How do you diagnose asthma with respect to spirometry?
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.
What are the 5 components other than spirometry for classifying asthma severity?
Symptoms (how many days per week). Nighttime awakenings. SABA use. Normal activity interference. Exacerbations requiring steroids (per year).
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?
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.
So you’ve changed a patient’s asthma care plan (stepped up or down). What is appropriate monitoring timeline for visits and spirometry?
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.
What are some generic and brand names of inhaled corticosteroids?
beclomethasone (Qvar), budesonide (Pulmicort), fluticasone (Flovent), mometasone (Asmanex)
What class is Singulair? What about Xolair?
Singulair = montelukast, a leukotriene modifier. Xolair = omalizumab, a monoclonal antibody.
What are key differences between asthma and COPD?
Why are inhaled corticosteroids used differently?
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.
Black box warning for LABAs.
Associated with an increased risk of asthma-related death. Must be used in combination with a “controller” med like ICS.
Main goal of therapy in COPD?
Reduce exacerbations. Get them down to group B. If you can’t, they should also be seeing a specialist.
Initial therapy/continued Sx in COPD Group B?
LAMA or LABA.
If cont, 2 bronchodilators (LABA + LAMA).
Initial therapy/continued Sx in COPD Group C?
LAMA.
If cont. exacerbations, add LABA and maybe ICS.
Define group C COPD (2017 guidelines).
Lower symptom scores (mMRC 0-1 or CAT <10), and high exacerbation history (2+ per year or 1+ with hospitalization).
GOLD groups 1-4 refer to _________, whereas A-D refer to __________.
airflow limitation as percent of expected FEV1; symptom burden and risk of exacerbation
Define group A COPD.
Lower symptom scores (mMRC 0-1 or CAT <10), and 0-1 exacerbations.
Define group D COPD.
Higher symptom scores (mMRC 2+ or CAT 10+), and 1+ admission or 2+ exacerbations.
Define group B COPD.
Higher symptom scores (mMRC 2+ or CAT 10+), but no hospitalizations or maximum 1 exacerbation.
Define GOLD grade 1.
FEV1 80% of predicted or higher
Define GOLD grade 2.
FEV1 50-79% of predicted.
What would you use for a pregnant person with rhinorrhea?
ipratropium (Atrovent) = category B. Anticholinergic, bronchodilator.
What would you use for a 2 year old who is already taking Claritin but still has a runny nose?
fluticasone (Veramyst)
What is Afrin? Considerations?
phenylephrine. Use max of 3 days.
Goals of tx of HF.
Prevent progression of HF. Improve Sx, improve QOL.
Define GOLD grade 3.
FEV1 30-49% of predicted.
Define GOLD grade 4.
FEV1 <30% of predicted.
Class 1 anti-arrhythmic mechanism?
Interfere with Na channels, binding to then dissociating from them at different rates, slowing conduction in some areas. They are membrane stabilizing agents.
Name the class I AADs: 1a, 1b, 1c.
1a - Quinidine, procainamide, disopyramide.
1b - Lidocaine, mexiletine.
1c - Flecainide, propafenone.
Class II AAD mechanism? And name some.
Beta blockers, they slow the impulse in the AV and SA nodes, slowing ventricular rates. Atenolol, esmolol, metoprolol, propranolol
Class III AAD mechanism? And name some.
They block many different channels (K, Ca, Na), treat both supraventricular and ventricular arrhythmias, and can have many side effects. Amiodarone, sotalol, others.
Class IV AAD mechanism? And name some.
They slow conduction, prolong refractoriness, decrease automaticity in the nodes. They are the nondihydropyridines, also called “slow” CCBs: verapamil and diltiazem.
Misc notes on 3 “Other” AADs:
Digoxin: mainly AV node slowing, doesn’t convert Afib/Aflutter to sinus, narrow therapeutic index. Low renal function predisposes to toxicity.
What are the 3 classes of meds that you would only use as monotherapy for Afib in a sedentary patients?
BBs, CCBs, digoxin. They slow HR and can cause fatigue.
Do you use NSAIDs in kids with URIs?
Decreasing inflammation does help relieve associated symptoms. However, caution of increased risk for inducing bronchospasm in those with asthma, chronic rhinitis, or nasal polyps.
