Pharma Exam 2 Flashcards

1
Q

Antihistamines

A

-relieve symptoms of allergies.
-Effective for allergic rhinitis.
-Anti-pruritic (decrease itching)
-Also use for motion sickness, insomnia, Parkinson’s
-Prototype drug: diphenhydramine (Benadryl)

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2
Q

Histamine Receptors

A

-H1-your brain, skin, bronchioles, lining of the blood vessels
-H2- parietal cells located in the stomach lining, heart, uterus and vascular smooth muscle cells, surface of neutrophils
-H3- central nervous system
-H4- thymus, small intestine, spleen, the colon, bone marrow and basophils

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3
Q

Diphenhydramine (Benadryl)

A

-First generation- More sedative effects
-blocks the effects of histamine at H1-receptor sites in the respiratory tract.
-SE: Thicken respiratory secretions, No apple, grapefruit, or orange juice (decrease its absorption).
-No pts with BPH, hyperthyroidism, Caution in asthma(trap secretions down there leading to pneumonia)
-Should be discontinued 4 days before skin testing

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4
Q

Cetirizine (Zyrtec), Loratadine (Claritin), Fexofenadine (Allegra)

A

Great for seasonal allergies and can take 24 hrs to work
-Take them a month before the season starts; once the receptors already hit by the allergens; the med has to wait

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5
Q

Fluticasone (Flonase)

A
  • Intranasal Corticosteroids
    -Treats seasonal allergic rhinitis by decreasing local inflammation in nasal passages, thus reducing nasal stuffiness.
    -SE: nasal irritation, epistaxis
  • can mask signs of infection in patients with known bacterial, viral, fungal, or parasitic infections
    -NC:How to use and clean the dispenser and as directed and Not to swallow large amounts can cause palpations
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6
Q

Phenylephrine (Neo-Synephrine)

A

-Relief of congestion in the nose and Nasal Decongestants
-No pts with HTN, Hyperthyroidism, heart disease, diabetes
-*2006 Methamphetamine Abuse Act
-Monitor for: systemic effect
-Can cause rebound congestion if used more than 3 days

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7
Q

*2006 Methamphetamine Abuse Act

A

-phenylephrine (Neo-Synephrine)
-Not on store shelves anymore
-Highly regulated
-Requires ID and registration to purchase

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8
Q

Antitussive Drugs

A

-suppress cough reflex bc many resp. disorder causes non-productive cough
- Non-prod cough is a protective mechanism to force irritants out of the resp. system
-Prototype drug: dextromethorphan (Robitussin, PediaCare, Vicks 44, Benylin Pediatric).

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9
Q

Dextromethorphan (Robitussin, PediaCare, Vicks 44, Benylin Pediatric)

A

-Relief of Chronic nonproductive cough by Directly affecting the cough center in the medulla.
- NO with pts that have chronic cough resulting from emphysema and asthma bc want to them to cough up secretions. If you suppress cough with this med it can lead to pneumonia.
-SE: Drowsiness, dizziness, irritability, and restlessness
-Abusive and avoid alchy or other CNS deppressants

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10
Q

Bronchodilators

A

-Facilitate respiration by dilating the airways
-Beta-agonists (sympathomimetics)-> causes beta stimulation in the SNS-> Dilation of the bronchi and Increased rate and depth of respiration.
-Prototype drug: albuterol (Proventil, Ventolin)

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11
Q

Albuterol (Proventil, Ventolin)

A

-Bronchodilator in managing Chronic Airway Limitation (CAL) and asthma.
-“Rescue Drug.”
-SE: Tremors, insomnia, GI symp
-Don’t take with Beta-Blockers(Propranolol) which blocks beta receptor sites
- Limit caffeine intake since it has similar sympathomimetic effects which increase the risk of adverse effects

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12
Q

Respiratory Anticholinergic Agents

A

-Considered first-line treatment for patients with CAL.
-Controls the bronchoconstriction long-term.
-Prototype drug: ipratropium bromide (Atrovent)

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13
Q

Ipratropium bromide (Atrovent).

A

-Used for maintenance treatment (prophylaxis) of bronchospasm. Blocks cholinergic receptors in the lungs.
- NO Peanuts or soybean allergy
-SE: Dysgeusia (bad taste in mouth),Paradoxical acute bronchospasm
-Explain the importance of taking ipratropium daily, despite the absence of symptoms. Rinse mouth after each use to avoid fungal infections (thrush).

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14
Q

Anti-Inflammatory Agents

A

-used to manage respiratory disorders, especially asthma.
- Prophylaxis and Inhibits the production of leukotrienes and prostaglandins
-Inhaled glucocorticoid steroids=have become first-line treatment for persistent asthma.
– Can be given orally, parenterally, or by inhalation.
-Prototype drug: beclomethasone (Qvar)

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15
Q

Beclomethasone (Qvar)

A

-anti-inflammatories (steroidal)
-Maintenance treatment of asthma as prophylactic therapy.
-SE: pharyngeal and laryngeal fungal infections, Rinse mouth after inhalation and spit, Use a spacer for MDI
- No pts with Active systemic fungal infection and Suppression of immune system
-Use a beta-2 agonist inhaler before flunisolide because it dilates the bronchial tree, allowing the steroid to get
deeper into the lungs.
-NC: Take flunisolide every day, regardless of how well the patient feels; Educate pt this NOT a rescue inhaler; Monitor for toxicity- systemic toxicity, hypertension; and Long term may stunt growth in children,

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16
Q

Leukotriene Receptor Antagonist

A

-Leukotrienes are inflammatory mediators that are powerful bronchoconstrictor and vasodilators.
-Prophylaxis or treatment of chronic asthma.
-Prototype drug: Montelukast (Singulair)

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17
Q

Montelukast (Singulair)

A

-Blocks leukotriene receptor sites on cells
-SE: Rare(hallucinations, depression, sucidial ideation report immediately)
-NO pts with liver impairment
NC: Monitor ALT and educate pt its not a rescue drug so take at least 2 hrs before exercise

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18
Q

Hyperlipidemia

A

-Total cholesterol: less than 200
-LDL: 100
-HDL: 40 to 59(Good cholesterol and it can be increased with avocados and exercise)
-Triglycerides less than 150 mg/dL(come from oils and saturated fats (baked goods, processed foods)
-Always try diet & exercise before prescribing statins

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19
Q

Statins

A

-Lowers LDL cholesterol by 20-60% when given at their maximum recommended dose.
-Raise HDL levels between 5 and 10%
-Lower triglycerides between 10 and 33%.
- Discovered in Fungus
- Prototype drug: Atorvastatin (Lipitor) “Statins”

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20
Q

Atorvastatin (Lipitor)

A

-Tx: Pt. at risk for CVD( (DM, HTN, smokers, etc). Decreases inflammation in the blood vessels(Ex: Pts undergoing heart cath get high dose statins bc the procedures irritates the lining of the blood vessels)
- High 1st pass effect(Liver tries to take out a lot of it before it gets there which is why we give large does(60 or 80 mg doses)).
- Inhibit HMG-CoA reductase(enzyme used by the liver to produce cholesterol)
- No pts with acute liver disease and pregnancy( bc suppresses cholesterol which makes up the lining of cell wall which inhibits growth of child)
- SE: myopathies, rhabdmoloyisis, photosensitivity
- Most cholesterol formed between 12-3am Should be taken in the evening(take at bedtime for most effect bc stops the liver from making cholesterol). Ppl that work night shift should take it before bed in the morning.
-NC: Dietary education before medical therapy(Exerices will be more effective than diet), Monitoring CPK and Liver enzymes 3 wks to a month for adverse effects, Baseline cholesterol panel should be done and periodically thereafter(6 months), Interacts with Grape juice due to the P450 metabolism pathway may cause toxic levels( if you shut down system wont metabolize drug), Report myopathies (big AE) and Rhabdomyolysis= breakdown of muscle clogs up kidneys

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21
Q

Fibric Acid Derivatives

A

-Reduce the synthesis of triglycerides in the liver
-Decrease VLDL and LDL; Increase HDL
-Prototype: gemfibrozil (Lopid)
- Most frequently they are used in combination with statins(The combined used of a fibrate and a moderate-dose statin carries a somewhat increased risk of myopathy)
-SE: Nausea, bloating, diarrhea, liver changes

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22
Q

Bile Acid Sequestrants

A

-Prototype: colesevelam* (Welchol)

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23
Q

Colesevelam* (Welchol)

A

-Used in patients who have not responded to other drug therapy.
- Not absorbed; binds to bile acids in the GI tract-> results in increased clearance of cholesterol
-Combine with bile acids to form insoluble complex which prevents reabsorption of bile acids from small intestine
- SE: Constipation, bloating, N/V
-NC: Don’t take with other meds, Caution with warfarin, Increase fluid intake

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24
Q

Niacin (Niaspan)

A

-mega high dose Vitamin B3 (6 grams/24 hrs)
-proven to not be very effective
-Causes severe skin flushing and “hot flashes”
-Taking ASA decreases this

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25
Q

Ezetimibe (Zetia)

A

-Works in the GI tract at the small intestine to stop absorption of lipids
-Same labs, adverse effects, and precautions as the statins.
-Drug of choice for children with hypercholesterolemia

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26
Q

Role of Adrenergic Receptors

A

-When alpha-1 receptors are stimulated, they cause peripheral constriction, and blood pressure increases as a result.
-Alpha-2 receptor sites are located within the brain.
-Beta-1 receptor sites are located primarily in the heart.
-Beta-2 receptor sites are located primarily in the bronchial and vascular musculature.

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27
Q

Classification of Hypertension

A
  • Prehypertension: 120-139/80-89
  • Stage 1: 140-159/90-99
  • Stage 2: 160 and up/ 100 and up
  • HTN Crisis: 210 and up/ 120 and up
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28
Q

Drug Therapy and Hypertension

A

-Drug therapy is now recommended to be started with every patient who has been diagnosed as having hypertension, whether it is stage 1 or stage 2.
-Drug therapy is also recommended in prehypertension if the patient has compelling indications or comorbidities.
Combination therapy is indicated for stage 2 hypertension.

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29
Q

Angiotensin-Converting Enzyme Inhibitors

A

-ACE inhibitors are used as first-line antihypertensive if the patient has comorbidities.
-Prototype drug: captopril (Capoten)

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30
Q

Captopril (Capoten)

A

-Tx: HTN, CHF, diabetic nephropathy, and left ventricular dysfunction.
- Inhibits the ACE needed to change the inactive angiotensin I to the active form angiotensin II -> Thereby decreasing BP (allows the blood vessels to stay relaxed)
- No pts in 2nd or 3rd trimester of pregancy
-SE: Persistent non productive cough, angioedema- life threatening, rash and neutropenia
-Lithium- increase levels, NSAIDs- decreases effect, diuretics- first dose syncope, k+ increased K+ levels
- NC: 1st dose syncope and Monitor BUN, Cr, levels a rise may indicate renal injury, K+ may indicate intolerance to drug, Persistent dry cough should be reported to provider, Angioedema (tongue swelling, difficulty breathing) is life threating call provider immediately, and ARB’s(Losartan) are used with ACE’s are not tolerated due to cough- can still trigger andioedma

31
Q

Selective Calcium Channel Blocker

A

-Used to treat hypertension
-Block Calcium ion channels into muscles; cause vasodilation, decreasing B/P
-Some selectively target clacium channels in arterioles
-Nonselective others also affect cardiac muscle
-Prototype drug: nifedipine (Adalat CC, Procardia)

32
Q

Nifedipine (Adalat CC, Procardia)

A

-TX: HTN, Raynaud’s, angina (Prinzmetals/ variant)
- SE: headache, peripheral edema, flushing
- No pts with heart blocks and uncompensated HF
- No grapefuit juice bc it can increase the amt of med
- NC: During therapy, monitor heart rate and heart dysrhythmias regularly, Monitor Alkaline phosphatase, LDH, ALT, creatine phosphokinase (C P K), and AST, Signs of H F and reflex tachycardia

33
Q

Hydralazine (Apresoline)

A
  • Direct- Acting Vasodilators(Produces direct smooth muscle relaxation of the arteriole and reduces afterload)
  • Adjunct to other antihypertensives. (3rd or 4th drug) due to multiple side effects
  • Can be given IV for urgent decrease HTN
  • Dont take with indomethacin(NSAID)
  • SE: Arthralgia, dermatoses, splenomegaly, and glomerular nephritis
  • NC: B/P before and after administration, reflexive tachycardia, monitor for edema
34
Q

Peripherally Acting Alpha-1 Blockers

A
  • Prazosin (Minipress), terazosin (Hytrin), and doxazosin (Cardura)
    -Block postsynaptic alpha-1 adrenergic receptors, producing vasodilation of arterioles and veins and thereby decreasing blood pressure.
  • Both standing and lying blood pressures are reduced, particularly the diastolic blood pressure.
  • A substantial first-dose effect of hypotension, especially orthostatic hypotension, can occur with these drugs.
  • Terazosin and doxazosin also are used to treat benign prostatic hypertrophy.
35
Q

cardiac output

A

-The volume of blood that leaves the left ventricle in 1 minute
-SV and HR
- Stroke volume is the amount of blood that leaves the left ventricle with each contraction.
- Stroke volume is dependent on three factors: preload, contractility, and afterload.

36
Q

Pathophysiology

A

-Cardiac output decreases when the left ventricle is unable to
eject its normal volume of blood during systole
-Brain natriuretic peptide, working with atrial natriuretic peptide, regulates cardiovascular homeostasis and fluid volume.
- It is secreted primarily by the ventricular tissue in response to changes in wall tension.

37
Q

Drugs to Treat Chronic Heart Failure

A

-When the heart cannot achieve the normal cardiac output, a backlog of blood, or congestion, occurs, and heart failure develops (CHF).
-clinical benefits of ACE inhibitors and beta blockers are related to slowing the changes in the left ventricle with CHF

38
Q

Cardiac Glycosides

A

-Prototype drug: digoxin (Lanoxin)
-Digoxin does not prevent death from CHF. Improves quality of life.
- digoxin can be added to reduce hospitalizations for HF or for rate control if patients also have atrial fibrillation.
-Digoxin is not used as the primary treatment for stabilizing patients with acute episodes of non-compensated heart failure.
-Digoxin increases the force of cardiac contraction (positive inotropic effect), increasing cardiac output.

39
Q

Digoxin

A

-Tx: CHF and Afib
- Increases Cardiac conduction-> increased CO. Increases vagal tone(decrease HR). Slows AV conduction.
- No pts with Heart Block and V fib or Heart rate below 60
- SE: Dysrhtmias, Visual disturbances, Seizures, Hallucinations, neuralgia
- Antidote: Digoxin immune fab(Digibind)
- Digoxin has a narrow therapeutic index.The therapeutic dose is very close to the toxic dose. Therapeutic range 0.8-2 ng/ml
- NC: Monitor serum levels especially with the elderly, Keep K+ between 3.5 and 5.0, and Monitor for signs of dig toxicity(10-20% of pts) .

40
Q

Signs and symptoms of dig toxicity:

A

-Yellow/green halos around lights
-Visual changes
-Bradycardia
-Psychosis
-Weakness and fatigue
-Anorexia/nausea

41
Q

Beta-Adrenergic Antagonistsc( Beta Blockers)

A

-Blockage of beta-1 only (decreased heart rate, decreased
lipolysis, decreased inotropy).
- Blockage of both beta-1 and beta-2 receptors (vasodilation, decreased peripheral resistance, bronchoconstriction).
-Prototype drug: metoprolol(Lopressor)

42
Q

metoprolol(Lopressor)

A

Tx: HTN, Angina, heart failure, irregular cardiac rhythms, and migraines.
- Aspirin of cardiac
- Decreases CO and as a result decreases BP. Dec O2 demand of heart muscle
- Not for pts with asymptomatic hypoglycemia, Raynaud syndrome and antidepressant drugs
-SE: Cognitive dysfunction, asymptomatic hypoglycemia, and bronchospasms

43
Q

Phosphodiesterase Inhibitors milrinone

A

-Block enzyme phosphodiesterase type 3 which causes:
-Increases calcium for myocardial contraction in
the muscle
- Cause positive inotropic response and vasodilation
– Increase contractility and decrease afterload
– Short-term therapy only
– Palliative care infusion pumps
- Prototype Drug: milrinone (Primacor)

44
Q

Milrinone (Primacor)

A
  • Tx: HF
  • IV use only for short-term duration, onset 2-10 min
  • increased force of myocardial contraction and an increase in cardiac output by inhibiting the breakdown of cAMP phosphodiesterase 3
  • SE: ventricular dysrhythmia, hypotension, headache
  • No pts with pre-existing dysrhythmias, acute MI
  • Caution with digoxin, dobutamine, or other inotropic drugs, because their positive inotropic effects on the heart may be additive.
  • NC: Monitor Potassium levels, Monitor for hypotension, Monitor for renal impairment, Monitor for dysrhythmias and for IV use: ventricular dysrhythmias
45
Q

Why do we have a blood pressure?

A

Perfusion.(1. Volume, 2. Resistance, 3, cardiac output)

46
Q

Why do we have a blood pressure?

A

Perfusion.(1. Volume, 2. Resistance, 3, cardiac output)

47
Q

Angina

A

-The four major risk factors associated with coronary heart disease and angina are cigarette smoking, diabetes, elevated blood lipid levels, and hypertension.
-Prinzmetal or variant angina= vessels spasming that may or may not contain plaque. Occurs most often at rest.
-Microvascular Angina = Small capillary destruction of coronary arteries.Esp after stents or ballooning procedures

48
Q

Beta Blockers

A
  • prevent the beta-adrenergic receptors from being stimulated.
    -decrease the oxygen demands of the heart and thereby decrease angina.
    -Allows the heart to rest and not be stimulated by catecholamines
  • metoprolol (Lopressor)
49
Q

Calcium Channel Blockers

A

-Calcium is needed in the automatic and conducting cells of the heart to help create an action potential.
-Calcium-channel blockers inhibit calcium from moving across cell membranes.
-The effects of this inhibition on the cardiovascular system are decrease in contraction, depression of impulse formation (automaticity), and slowing of conduction velocity.
-These have the effect of decreasing the oxygen needs of the heart.
-Calcium channel blockers also cause arteriolar dilation, decreasing afterload.
-Prototype: diltiazem (Cardizem) or verapamil (See Cardiac Rhythm)

50
Q

Thrombolytic Drugs

A

-breaking down formed blood clots.
-These drugs are used for patients who are diagnosed with an evolving, acute MI; a PE; or acute ischemic stroke.
-Although these drugs are given during emergency situations and can save lives, their adverse effects can be life threatening.
-Prototype drug: alteplase (Activase)

51
Q

Nitrates

A

-Dilate vascular smooth muscle and both venous and arterial vessels (although more relaxation occurs on the venous side).
-Venous dilation decreases the returning flow of blood to the heart (preload).
-Arterial dilation reduces systemic vascular resistance and arterial pressure (afterload).
-These effects decrease the workload on the heart and its oxygen needs.
-Nitrates improve the circulation to the heart itself by redistributing blood flow to the collateral vessels.
-Prototype drug: nitroglycerin

52
Q

Nitroglycerin (Nitrostat)

A

-Prophylaxis and treatment of angina
-Vasodilator= Relaxes vascular smooth muscle and dilates both arterial and venous vessels.
-No pts with severe anemia(vasodilation decreases hemoglobin), closed-angle glaucoma (may increase IOP bc it vasodilates the whole body), head trauma or ICP
-SE: Severe Headache, tachycardia, hypotension
- No other antiHTN or r phosphodiesterase-5 inhibitors(ED medication & and it causes life-threatening hypotension; and it doesn’t respond to vasopressors but can give fluids
- NC: Assess BP every 5 min and don’t give if SBP is less than 90, Three administrations is the max, or if b/p drops to less than 90, Chest pain should be treated until 0/10, IV- glass bottles, start slow 5mcg/min titrate to pain and b/p, SL or sprays: Teach pt that three administrations is the max
- Pt Education: Sit down and take 1 if still in pain, call 911, Take 2nd after 5 min while waiting do not drive self!, and Take 3rd and last one after 5 min if pain is not a 0.

53
Q

Adjunct Drug Therapies for Angina and MI

A
  • Thrombus formation is an important concern with unstable angina, and some of these therapies specifically target this problem. (anticoagulants/antiplatelet)
  • Antihyperlipidemics often are used in conjunction with drugs to treat angina to slow the progression of coronary heart disease.
  • An ACE inhibitor is used in patients with coronary artery disease if they also have diabetes, systolic dysfunction, or both.
    -If the pain of unstable acute angina is not controlled by nitrates, morphine can be used to treat the pain.
54
Q

Antiarrhythmics work in three ways

A

-Decrease the automaticity of cardiac tissues in the ectopic sites (slows or numbs)
-Decrease the speed of conduction of electrical impulses through the heart. (slows)
-Decrease re-entry (stops)

55
Q

Class IA Antiarrhythmic Drugs

A
  • Local anesthetics or cell membrane-stabilizing drugs. Sedates the heart muscle by blocking sodium channels.
  • prototype drug: procainamide
56
Q

Procainamide

A

-Treat atrial arrhythmias and ventricular tachycardia.
-Therapeutic levels 4-8 mcg/ml.
-Depresses myocardial excitability, conduction speed, and contractility by slowing or stopping the NA+ from crossing into the cells. The effective resting (refractory) period is prolonged, increasing conduction time.
-No pts with Heart Block and HF, and myasthenia gravis
-SE: cardiotoxicity (anticholinergic- effects), confusion, N/V
-NC: May prolong QT interval and puts the patient at risk for Torsades, May interact with other antiarrhythmic and cardiac drugs

57
Q

Class II Antiarrhythmic Drugs

A

-Beta-blockers slow heart rate by suppressing the SA node, slow the speed of conduction through the AV node, and decrease the force of contraction.
-Reduce mortality in patients who have had a recent MI, those with symptomatic heart failure, and those with congenital long QT syndrome.
-Beta-blockers are the most effective drugs for controlling the ventricular rate in AFib.
- Prototype: propranolol (Inderal) or metoprolol

58
Q

Class III Antiarrhythmic Drugs

A

-Resting stage is prolonged, leading to reduction in membrane excitability of all myocardial tissue.
-Prototype drug: amiodarone (Cordarone, Pacerone).

59
Q

Amiodarone (Cordarone)

A
  • Atrial fib/flutter and in life-threatening ventricular arrhythmias.
  • ½ life of 40-55 days. Therapeutic level 0.8 - 2.8 mcg/ml
  • Blocks K+ channels during the repolarization of the cardiac muscle (resting stage). Prolongs refractory period.
  • No pts with Severe sinus-node dysfunction, 2nd and 3rd-degree AV block
  • SE: pulmonary toxicity(Black BOX Warning), liver disease, skin turns gray-blue in the sun
    -Interacts with Digoxin, flecainide (Class I C), and warfarin
  • NC: Close ICU/CVU ECG monitoring required, monitor QT intervals
60
Q

Class IV Antiarrhythmic Drugs

A

-Calcium Channel blockers
-Allows tissue to contract slower and rest longer
-Prototype drug: verapamil (Calan), Diltiazem (Cardizem)

61
Q

Verapamil (Calan)

A

-Antiarrhythmic for chronic atrial flutter or fibrillation.
-Inhibits the movement of calcium ions across the cardiac and arterial muscle cell membrane.
-No pts with Sick sinus syndrome, 2nd or 3rd-degree heart block, and hypotension
-NC: Need ECG monitoring for dysrhythmias , HR and B/P are important before and after, Electrolytes are important to monitor and keep in safe ranges (K+ & Mg+), Changes in respiratory status may indicate changes in cardiac rhythm, Weight for CCB

62
Q

What does Catopril also treat?

A

protenuira;(keep vessels open and keep pressure off kidneys)

63
Q

What should you keep at the bedside when administering Catopril?

A

Keep a trach at the bedside in case of angioedema

64
Q

Why does Captopril produce a nonproductive cough ?

A

Bradykinin, a natural inflammatory mediator, builds up bc we are stopping the body from doing what it naturally does)

65
Q

What happens if the patient develops a persistent dry cough from Captopril?

A

STOP MEDICATION AND SWITCH TO and ARB medication, which stops problems at the blood vessel instead of affecting the bradykinin in the lungs)

66
Q

What happens if the patient develops angioedema from Catptopril?

A

Call 911 don’t drive to ER

67
Q

What can hydralazine be used for?

A

Breakthrough HTN issues and it takes a while to work

68
Q

What does Digoxin slow down?

A

Slows down calcium exchange which increases calcium across the muscle

69
Q

What med should you administer a loading dose?

A

-Digoxin
- loading dose = Give high doses every 8 hours to get levels increased in their blood stream
- Push SUPER slow may cause v-tach so keep on monitor
-Stop immediately and call provider if v-tach occurs

70
Q

Why monitor Potassium with digoxin?

A

Prevent dysrhythmias

71
Q

What is a big contradiction for Metoprolol?

A

Airway diseases bc it blocks beta 2 in the lungs leading to bronchconstriction

72
Q

Why does Metoprolol cause asymptomatic hypoglycemia?

A
  • Diabetic patients will not be able to feel symptoms of hypoglycemia due to the blocking the adrenergic system.
    -Symp= Sweating, pallor, hunger, fatigue, irritability/anxiety, rapid HR, lack of concentration
73
Q

What should you monitor with Milraone?

A

Significant BP drop in 15 minutes