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PHARMA > 2nd Exam > Flashcards

2nd Exam Flashcards

1
Q

Medications that are used to treat benign prostatic hyperplasia (BPH)

A

5-alpha
reductase inhibitors and alpha1-adrenergic antagonists.

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2
Q

Medications used to treat
erectile dysfunction

A

phosphodiesterase type 5 (PDE5) inhibitors

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3
Q

needed for growth and maturation of the female reproductive
tract and secondary sex characteristics.

A

Estrogens

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4
Q

block bone resorption and reduce
low-density lipoprotein (LDL) levels.

A

Estrogens

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5
Q

suppress the release of a
follicle-stimulating hormone (FSH) needed for conception.

A

estrogens

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6
Q

a hormone secreted by the corpus luteum and adrenal glands. It is responsible for changes in uterine endometrium in the second half of the menstrual
cycle in preparation for implantation of the fertilized ovum, development of maternal
placenta after implantation, and development of mammary glands.

A

Progesterone

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7
Q

Synthetic drug that exert progesterone like activity are called

A

progestins.

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8
Q

Use to treat symptoms of menopause, prevent long-term consequences of
estrogen loss, and in some cases, to treat prostate and breast cancer

A

HORMONE REPLACEMENT THERAPY

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9
Q

stimulate uterine contractions. Use to induce labor.

A

Oxytocics

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10
Q

Oxytocics interact with several drugs including vasoconstrictors which may lead to

A

hypertension.

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11
Q

inhibit uterine contractions.
Uses to prevent preterm labor.

A

Tocolytics - Terbutaline (beta -2-adrenergic agonist)

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12
Q

Adverse effects of tocolytics

A

tachycardia in mother and fetus.

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13
Q

Nursing Considerations for Tocolytics

A

monitor heart rate of mother and fetus

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14
Q

Treatment for Male Hypogonadism

A

testosterone or other androgens

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15
Q

Use to restore normal gonadal development and secondary male sex
characteristics.

A

testosterone

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16
Q

Adverse effects of testosterone

A

water retention, edema, potential for liver damage,
acne, skin irritation.

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17
Q

provide education to client, monitor client’s
condition, monitor liver enzymes, physical assessment for signs of increased or
decreased sex hormone production

A

Nursing consideration for testosterone

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18
Q

Treatment for Erectile dysfunction

A

sildenafil (Viagra)

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19
Q

Use to treatment of erectile dysfunction. acts by relaxing smooth muscle in the corpus cavernosum,
allowing increased blood flow into the penis, resulting in a firmer and longer-lasting
erection.

A

sildenafil (Viagra)

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20
Q

Severe chest pain that is usually short (lasts 5-10mins)
- Brought on by exertion or emotional excitement

A

Angina Pectoris

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21
Q
  • Spasms of the coronary artery leads to decreased myocardial blood flow
  • Not specifically related to plaque build up
  • Pain related to vasoconstriction of artery
  • Generally, occurs in periods of rest
A

Vasospastic (Prinzmetal’s) Angina

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22
Q
  • Episodes occur suddenly, increasing intensity, and occur during periods
    of rest
  • Plaque within coronary artery ruptures
  • Medical emergency
  • Does not go away and leads to an M
A

Unstable Angina (most severe form of angina)

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23
Q

Antianginal Drugs

A

❖ Calcium Channel Blocker
❖ Nitrates (Nitroglycerin)
❖ Beta-Adrenergic Blockers (Cardioprotective - reduces the incidence of MI)

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24
Q

relax coronary artery spasm, causes negative inotropic effects,
and reduces cardiac workload and oxygen demands

A

Calcium Channel Blocker

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25
Q

what are the side effects of Calcium Channel Blocker

A

dizziness, flushing, headache, hypotension, reflex
tachycardia, peripheral edema, fatigue

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26
Q

forms nitric oxide in vascular smooth muscle, causes
vasodilation

A

Nitrates (Nitroglycerin)

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27
Q

Reduces the amount of blood returning to the heart (preload),
Reduced cardiac output, Reduced workload, Reduced
oxygen demands

A

vasodilation

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28
Q

Nitrates (Nitroglycerin) is given in what medicine route?

A

sublingually

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29
Q

decreases the cardiac workload by lowering blood pressure,
slowing heart rate and reducing contractility Also effective for HTN

A

Beta-Adrenergic Blockers (Cardioprotective - reduces the incidence of MI)

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30
Q

Preferred selective beta blockers because non-selective can
affect

A

bronchodilation

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31
Q

Occur in all age groups, in healthy and unhealthy people too, Associated conditions/diseases: HTN, cardiac valve disease, CAD, hyper/hypokalemia, MI, stroke, DM, HF

A

Dysrhythmias

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32
Q

Signs and Symptoms of Dysrhythmias

A

Dizziness, weakness, fatigue, decreased exercise tolerance,
palpitations, dyspnea, syncope (temp. Loss of consciousness due to decrease in BP)

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33
Q
  • Action potential begins when threshold potential is reached.
  • Sodium rushes in, producing rapid depolarization
  • Calcium enters at a slower rate
A

Phase 0

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34
Q
  • Brief transient phase
  • Inside of plasma membrane reverses charge, becomes positive
A

Phase 1

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35
Q
  • Plateau reached in which depolarization is maintained
  • Contraction of cardiac muscle
  • Efflux of potassium from cells
A

Phase 2

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36
Q
  • Calcium channels close
  • Additional potassium channels open
  • Repolarization returns negative resting membrane potential
A

Phase 3

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37
Q
  • Refractory Period
  • Brief period where depolarization cannot occur
  • Ensures myocardial cell finishes contracting before another
    action potential begins
A

Phase 4

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38
Q
  • HR <60 bpm
  • Common among older adults
  • Major indication for pacemakers
A

Bradydysrhythmias

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39
Q

Common bradydysrhythmias

A

Sinus bradycardia -life sustainable
Sinoatrial node dysfunction (HR in the 30s)
Atrioventricular (AV) conduction block
Arrhythmia - no rhythm (DEAD)

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40
Q
  • HR >100 bpm
  • Incidence increases in older adults and those with preexisting cardiac disease
A

Tachydysrhythmias

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41
Q

Common tachydysrhythmias:

A

Atrial tachycardia
Atrial flutter
Atrial fibrillation
Ventricular tachycardia
Ventricular fibrillation

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42
Q

Paroxysmal supraventricular tachycardia (PSVT) >200 bpm

A

Atrial tachycardia

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43
Q
  • No treatment
  • Little or no benefit to treatment with medications
A

Asymptomatic dysrhythmias

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44
Q
  • Initiated for high-risk patients
  • Avoid drug combinations that increase QT interval
A

Prophylaxis of dysrhythmias

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45
Q
  • Cardioversion or defibrillation
  • Electrical stimulation of the heart for serious dysrhythmias
  • Pacemakers
  • ICDs (implantable cardioverter defibrillators)
A

Nonpharmacologic treatment of dysrhythmias

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46
Q
  • Uses: Ventricular tachycardia during CPR, Refractory ventricular
    fibrillation during CPR, Pulseless ventricular tachycardia during CPR,
    Premature atrial tachycardia, Atrial flutter, Atrial fibrillation
  • Action:
  • Blocks sodium ion channels in myocardial cells
  • Reduces automaticity and slows velocity of action potential
  • Adverse Effects:
  • Nausea and vomiting, headache, fever, anorexia, weakness,
    confusion, psychosis at high doses
A

Class 1A: procainamide

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47
Q

Pharmacologic management of dysrhythmias

A

Sodium Channel Blockers (works in phase 0 of action potential)
Class 1A: procainamide
Class 1B:
Class 1C: Antiarrhythmics
Beta Adrenergic Antagonist: Class II
Potassium Channel Blockers: Class III
Calcium Channel Blockers: Class IV

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48
Q

Other Management of Dysrhythmias:

A

Adenosine (transient heart block)
Digoxin

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49
Q
  • Check apical and radial pulses before dose
  • Continuous ECG and BP monitoring during IV administration
  • Monitor therapeutic blood levels
A

Nursing Responsibilities for Class 1A

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50
Q
  • Shorten repolarization
  • Primary indications are ventricular dysrhythmias
A

Class 1B

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51
Q

Drugs included in Class 1B

A
  • Lidocaine (Xylocaine)
  • Mexiletine (Mexitil)
  • Phenytoin (Dilantin)
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52
Q
  • Decrease conduction velocity
  • PR, QRS, and QT intervals are often prolonged
  • Life-threatening atrial dysrhythmias
A

Class 1C: Antiarrhythmics

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53
Q
  • Reduce automaticity as well as slow conduction velocity in the heart
  • Action: block calcium channels in SA and AV nodes
  • Slows HR
A

Beta Adrenergic Antagonist: Class II

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54
Q

Drugs included in Beta Adrenergic Antagonist: Class II

A
  • Acebutolol (Sectral)
  • Esmolol (Brevibloc)
  • Propranolol (Inderal)
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55
Q
  • Block potassium ion channels in myocardial cells
  • Limited use due to serious AE such as:
  • N/V, anorexia, fatigue, dizziness, hypotension, visual
    disturbances, rashes, photosensitivity
A

Potassium Channel Blockers: Class II

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56
Q
  • Exact mechanism unknown
  • Block potassium channels but also blocks sodium ion channels
    and inhibits sympathetic activity
A

Potassium Channel Blockers: Class III

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57
Q

severe bradycardia, cardiogenic shock,
sick sinus syndrome, severe sinus node dysfunction, third-degree AV
block, hypersensitivity to iodine, lactation, COPD, electrolyte imbalances

A

Contraindications/precautions of Potassium Channel Blockers: Class III

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58
Q
  • Monitor BP during IV infusion
  • Assess for adverse effects
  • Baseline lab tests
  • Assess respiratory status
  • Supervise ambulation (could have hypotension)
  • Baseline ophthalmic exam
A

Nursing Responsibilities for Class III

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59
Q
  • Effects similar to those of beta - adrenergic antagonists
  • Monitor for bradycardia and hypotension
A

Calcium Channel Blockers: Class IV

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60
Q
  • Naturally occurring nucleoside
  • Activates potassium channels in SA and AV nodes
  • Terminates tachycardia
  • Primary indication is PSVT (very common)
  • 10-second half-life, so adverse effects are self-limiting
A

Adenosine (transient heart block)

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61
Q
  • Primarily for HF
  • Not effective against ventricular dysrhythmias
  • Patients must be carefully monitored for toxicity, drug interactions, and
    adverse effects
  • Loading dose neede
A

Digoxin

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62
Q

Prevent the formation of clots, but do not take care of current clots
- Use: venous and arterial disorders at high risk for clot formation of DVT, PE, MI, artificial heart valves, strokes

A

Anticoagulants

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63
Q

binds with antithrombin iii, inhibits the action of thrombin,
inhibits the conversion of fibrinogen to fibrin, therefore inhibiting clot
formation
- Use: prevent venous thrombosis
- Issues: Must be given IV or SC (Not PO because of first pass), monitor
laboratory (PT/INR, aPTT), side effects of bleeding and bruising

A

HEPARIN

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64
Q

Antidote of Heparin

A

Protamine sulfate

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65
Q

inactivates Xa factor
Use: prevent DVT, PE (high risk from abdominal and orthopedic
surgeries)
- Issues: ASA (aspirin), bleeding

A

Low Molecular weight heparin

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66
Q

directly inhibits thrombin, preventing fibrinogen from converting to
fibrin
- Use: treatment and prevention of DVT/PE, and thrombus prophylaxis for
unstable angina, a-fib, and stroke
- Issues: IV, SC

A

Direct Thrombin Inhibitors

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67
Q

: inhibits synthesis of vitamin K, clotting factors II, VII, IX, and X
are affected
- Use: prevents thromboembolic conditions (thrombophlebitis, PE, DVT)
- Issues: monitor labs (PT/INR)

A

WARFARIN

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68
Q

Antidote of WARFARIN

A

Vitamin K, takes 24-48 hours to be effective and may need
to give frozen plasma or platelets in the meantime

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69
Q

Prevent platelet aggregation, interrupts the cascade (the enzyme that
helps them aggregate is no longer available)

A

Antiplatelets

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70
Q

Inhibits cyclooxygenase (needed for platelet aggregation)
- Use: prevent MI and TE, prevent and treat a stroke
- Issues: bleeding and GI upset

A

ASPIRIN

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71
Q

ind to fibrin promoting conversion of plasminogen to plasmin
- Uses: DVT, PE, MI (clots)
- Issues: anaphylaxis, reperfusion dysrhythmias, hemorrhage
- Only used for treatment and not prevention
- 3-4 hours after the event occurs can you give this med

A

Thrombolytics

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72
Q
  • Used for hypertension, heart failure, renal failure, liver failure, and pulmonary edema
  • Common adverse effects: dehydration, hypotension, electrolyte imbalance
A

Diuretics

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73
Q

5 types of Diuretics

A

Thiazide and Thiazide-Like Diuretics
Loop Diuretics (Lasix)
Osmotic Diuretics
Carbonic Anhydrase Inhibitors
Potassium Sparing Diuretics

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74
Q

act on the distal convoluted renal tubule; promotes
sodium, chloride, and water excretion (may also lose K and Mg)

A

Thiazide and Thiazide-Like Diuretics

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75
Q

Use of Thiazide and Thiazide-Like Diuretics

A

HTN and peripheral edema

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76
Q

dizziness, headache, weakness, hypotension, GI
distress, constipation, hyperglycemia, electrolyte imbalance,
urticarial, hyperuricemia, blood dyscrasias, renal failure

A

Side effects of Thiazide and Thiazide-Like Diuretics

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77
Q

Contradictions of Thiazide and Thiazide-Like Diuretics

A

renal failure

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78
Q

act on the ascending loop of Henle; secretes Na, water, K, Ca, Mg

A

Loop Diuretics (Lasix)

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79
Q

dizziness, weakness, headache,
hyperglycemia, blurred vision, photosensitivity, paresthesia, othro
hypotension, hyperuricemia, electrolyte imbalance, blood
dyscrasias, elevated BUN, creatinine, lipids, and renal failure

A

Side effects/adverse effects of Loop Diuretics (Lasix)

80
Q

increase sodium reabsorption in the proximal tubule and loop of
Henle. Increase osmolality which pulls in water to excrete Na, Cl, K, and
water

A

Osmotic Diuretics

81
Q

Use of Osmotic Diuretics

A

prevent kidney failure, decrease ICP and IOP

82
Q

Action: block action of enzyme carbonic anhydrase. Excretes Na, K,
and bicarb
- Use: decrease IOP in patients with open-angle (chronic) glaucoma
- Side effects/adverse reactions: confusion, ortho hypotension, GI
distress, metabolic acidosis, fluid and electrolyte imbalance, crystalluria,
renal calculi, hemolytic anemia.

A

Carbonic Anhydrase Inhibitors

83
Q
  • Action: block action of aldosterone. Promote Na/water excretion and K
    retention
  • Use: edema due to HF, cirrhosis of the liver
  • SE/adverse reactions: dizziness, headache, weakness, hyperkalemia,
    GI distress, paresthesia, muscle cramps, hyperuricemia, blood
    dyscrasias
A

Potassium Sparing Diuretics

84
Q

DIGOXIN (prototype)

A
  • Positive Inotropic: iNcreases myocardial contractility
  • Negative chronotropic: decreases heart rate
  • Negative dromotropic: decreases conduction of the electric system
    within the heart
85
Q
  • Reduce blood volume, lower BP, reduce workload, increase CO
  • Used only for fluid overload (loop diuretics are best with thiazide added)
A

Diuretics

86
Q
  • Action: inhibits Phosphodiesterase III in cardiac and vascular smooth muscle.
    Rise in cAMP increases intracellular calcium, resulting in greater contractility
  • Increases contractility, decreased pulmonary vascular resistance
  • Vasodilator, so afterload is decreased and increased effectiveness of
    the contraction
  • Contractions/precautions: valvular heart disease, preexisting
    dysrhythmias, hypovolemia, electrolyte imbalances, renal impairment
  • Cascade: related to increased calcium reflux=increased contractility
  • Multiple toxicities with other drugs
  • Additive cardiac effects with inotropic drugs
  • Additive hypotension with antihypertensive drugs
  • For patients with HF who do not respond to ACE inhibitors, digoxin, or others.
  • Made for resistant HF (HF we cannot get a hold of)
A

Phosphodiesterase Inhibitor(PDE5): Primicor (other positive inotropic agents)

87
Q
  • Aldosterone antagonist (not a diuretic)
  • Prevents cardiac remodeling
A

Spironolactone (Aldactone)

88
Q
  • Blocks the catecholamines, slows HR, reduces contractility
  • prevents tachydysrhythmias, prevents MI damage
  • May produce remodeling of the hear
  • May worsen failure, taper dose up
A

Beta Adrenergic Antagonists

89
Q

-Regulators of BP
- kidneys via RAAS
- Baroreceptors in the aorta and carotid (feel the pressure and the need for
pressure change)
- Vasomotor center in the medulla
- Hormones: ADH, ANP, BNP

A

Antihypertensives

90
Q
  • Excess saturated fat and simple carbs, alcohol increases renin secretions,
    obesity increase CO, SV, and left ventricular filling
  • Race factors
  • African Americans have lower renin levels
  • Asian Americans tend to be more responsive to drugs
  • Native Americans are less responsive to beta blockers
  • Older adults have a higher baseline BP
A

Physiologic Risk Factors of Antihypertensives

91
Q

Antihypertensive drugs

A

Diuretics
Sympatholytic
Centrally acting alpha2 agonists
Alpha-adrenergic blockers
Adrenergic neuron blockers
Alpha1- adrenergic blockers
Direct acting arteriolar vasodilators
ACE inhibitors
Angiotensin II receptor Blockers (ARBs)
Direct Renin Inhibitor
Calcium Channel Blockers

92
Q
  • Thiazides
  • Loop diuretics
  • Combo of thiazide with K-sparing diuretics
  • Combine K-sparing with K-wasting to even out potassium
  • Combo of thiazide with other antihypertensive (ACE inhibitors,
    beta blockers, ARBs)
A

Diuretics

93
Q
  • Slows down BP by stopping sympathetic system
  • Beta-adrenergic blockers
  • SE: hypotension, dizziness, fatigue, insomnia, nightmares,
    depression, sexual dysfunction, decrease BP, decreased
    HR, bronchoconstriction (if possibly non-selective)
A

Sympatholytic

94
Q
  • Inhibit beta1 and beta2 receptors
  • Propranolol
A

Nonselective

95
Q
  • Block beta1 receptors
  • Metoprolol (prototype)
A

Cardio selective

96
Q
  • Action: stimulate alpha2 receptors, decrease CO,
    decrease epinephrine, norepinephrine, and renin release
  • Contradictions: impaired liver function
  • SE: Na and water retention, dry mouth, bradycardia
  • Rebound HTN is stopped abruptly
A

Centrally acting alpha2 agonists

97
Q
  • Action: block the alpha-adrenergic receptors results in
    vasodilation and decreased blood pressure
  • SE: ortho hypotension, headache, dizziness, drowsiness,
    nausea. Nasal congestion, edema, weight gain
A

Alpha-adrenergic blockers

98
Q
  • Action: block norepinephrine release from the sympathetic nerve
    endings, decrease in norepinephrine release, results in a lower
    BP
  • SE: ortho hypotension, tachycardia, dizziness,
    drowsiness, headache, nasal congestion, edema, weight
    gain
A

Adrenergic neuron blockers

99
Q
  • Action: blocks alpha1 receptors
  • SE: hypotension, bradycardia
A

Alpha1- adrenergic blockers

100
Q
  • Action: relax smooth muscles of blood vessels, especially
    causing vasodilation
  • SE: tachycardia, palpitations, edema, headache, dizziness,
    nasal congestion, GI bleeding, lupus like symptoms
A

Direct-acting arteriolar vasodilators

101
Q

ACE inhibitors

A
  • Action: inhibits formation of angiotensin II, interrupts cascade
  • SE: Nonproductive cough, fatigue, insomnia, N/V/D,
    hyperkalemia, dizziness, tachycardia, hypotension,
    angioedema
  • African American adults and older adults do not respond to ACEI
    monotherapy
  • Contradictions: pregnancy, k-sparing diuretics, salt substitutes
102
Q

Angiotensin II receptor Blockers (ARBs)

A
  • Action: prevent release of aldosterone, act on RAAS,
    block angiotensin II from angiotensin I receptors
  • SE: dizziness, hypotension, headache,
    hyperkalemia, hyperglycemia, GI distress, diarrhea,
    pyrosis
103
Q
  • Action: bind with renin causing a reduction of angiotensin I,
    angiotensin II, and aldosterone levels
  • Decreases BP
  • SE: Hypotension, peripheral edema, hyperkalemia, diarrhea,
    renal failure, Steven-Johnson Syndrome
A

Direct Renin Inhibitor

104
Q

Calcium Channel Blockers

A
  • Action: slow calcium channels in myocardium and vascular
    smooth muscle cells promoting vasodilation
  • SE/AE: flushing, headache, dizziness, peripheral edema,
    fatigue, GI distress, constipation, bradycardia, hypotension,
    palpitations
105
Q

Triglycerides, phospholipids, steroids (cholesterol)

A

Lipids

106
Q

arge transport from body to liver

A

Chylomicrons

107
Q
  • More than a deposit of lipids
  • Now considered primarily a chronic inflammatory process
  • Involves the infiltration of macrophages, t lymphocytes and other inflammatory
    mediators
  • Inflammatory process -> plaque formation -> causes ischemia
A

Genesis of Atherosclerosis

108
Q

Pharmacologic treatment of Genesis of Atherosclerosis

A
  • Statins (most effective)
  • Blood lipid profiles
109
Q

Drugs for Dyslipidemia

A

Statins
Bile Acid Sequestrants
Niacin (Nicotinic Acid)
Fibric Acid
Peripheral Vasodilators

110
Q
  • Can reduce LDL levels by 20-40%
  • Also, lower triglycerides and VLDL levels
  • Can raise HDL levels
  • More commonly used
  • Action: inhibits HMG CoA reductase which manufactures cholesterol
  • Basically makes cholesterol not form
  • SE: Headache, abdominal cramping, diarrhea, muscle/joint pain, heartburn
  • Serious SE: Rhabdomyolysis (breakdown of muscle fibers)
A

Statins

111
Q
  • Complex formed with bile acid and the drug
  • Binds with bile acids to inhibit cholesterol formation
  • Interacts with Warfarin
  • Has to be separately given an hour after other drugs are given
  • More adverse events than other statins
  • GI problems are the most concerning
  • Can have an increase in triglycerides
A

Bile Acid Sequestrants

112
Q
  • Action: decrease production of VLDL, lower serum triglycerides levels, also
    lowers LDL levels because it synthesis the same way as VLDLs
  • SE: warmth, flushing, itching, numbness, tingling, hypotension, dizziness,
    headache, cough
  • Can give aspirin to mediate the flushing
  • Cannot be used with diabetes patient because it can increase glucose levels
A

Niacin (Nicotinic Acid)

113
Q
  • Action: activates enzymes which increase breakdown of triglycerides
  • AE: GI problems
  • Take with food
  • Example: Gemfibrozil
  • Highly protein bound
A

Fibric Acid

114
Q
  • Used in PVD
  • Causes iNcreased ability for blood flow
  • Action: vasodilator
  • INcreases O2 in blood
  • Treat pain with activity - intermittent claudication
    Ischemia = pain
A

Peripheral Vasodilators

115
Q

block H1 receptors to decrease nasopharyngeal secretion

A

H1 blockers, Histamine1 Antagonists

116
Q

SE: drowsiness, dry mouth, decreased secretions (anticholinergic effects)

A

First Generation Antihistamines (Benadryl)

117
Q
  • Fewer anticholinergic effects, less drowsiness, longer half life
  • Ex. Claritin
A

Second Generation Antihistamines

118
Q
  • Sympathomimetics stimulate alpha and beta receptors
  • Vasoconstriction in capillaries which leads to decreased swelling
  • Issues: can cause tolerance and rebound congestion
  • Only used 3-5 days
  • Anticholinergic effect (parasympathetic but acts sympathetic): drying of mucous
    membranes
A

Nasal Decongestants

119
Q
  • Alpha-adrenergic agonists
  • Used for allergic rhinitis
  • Slower effect, but generally a longer response than nasal decongestants
  • More SE than nasal decongestants: can increase BP, and HR
  • Interactions: beta blockers (can cancel each other out), MAOIs
A

Systemic Decongestants (Ex. Sudafed)

120
Q
  • Treats allergic rhinitis
  • Anti-inflammatory actions
  • Decrease in sneezing and coughing
  • Can increase blood sugar and should caution with diabetes
A

Intranasal Glucocorticoids (Ex. Flonase)

121
Q
  • Act on cough control center in the medulla, Use it to get some sleep
  • Suppresses cough reflex
  • Problems: you want to cough out junk, if not it can cause pneumonia;
    a cough is there for a reason
  • Types: OTC, narcotic (codeine), and non-narcotic
A

Antitussives

122
Q
  • Loosen bronchial secretions to be coughed out
A

Expectorants (Robitussin)

123
Q
  • Loosen thick, viscous bronchial secretions
  • Breaks down the chemical structure of mucous molecules
  • The mucous become thin, and can be removed out by coughing
A

Mucolytics

124
Q
  • Chronic, inflammatory or obstructive
  • Mast cell lining bronchial passageways release mediators of immune
    and inflammation
  • Histamine, leukotrienes, prostaglandins, interleukins
  • Increased airway edema and secretions which
    narrows/obstructs the airway, compromising respiration
  • Sign and Symptoms: coughing, dyspnea, tightness in chest
A

Asthma

125
Q
  • Prolonged asthma attack which can lead to death
A

Status asthmaticus

126
Q

Treatment of asthma

A
  • Beta 2 Agonists (sympathetic)
  • cAMP (cyclic AMP/ cyclic adenosine monophosphate)
  • Inhaled Anticholinergic (parasympathetic acts sympathetic)
  • Inhaled Corticosteroids
  • Mast Cell Stabilizer
  • Leukotriene Modifiers
  • Methylxanthines
  • Monoclonal Antibodies
127
Q
  • relieves bronchospasm
  • Sympathetic NS- relaxes bronchial smooth muscle=dilation
  • ALBUTEROL (prototype)
A
  • Beta 2 Agonists (sympathetic)
128
Q
  • Maintains bronchodilation
  • When inhibited constriction occurs
  • Increased by sympathomimetics, bronchodilators,
    and methylxanthines
A

cAMP (cyclic AMP/ cyclic adenosine monophosphate)

129
Q
  • Prevents bronchospasm
  • Atropine- adverse effects (increase HR and BP)
  • Atrovent: short acting anticholinergic; combo with beta agonists,
    usually with first dose
  • Blocks PNS (parasympathetic NS)
A

Inhaled Anticholinergic (parasympathetic acts sympathetic)

130
Q
  • Anti-inflammatory, Most effective for asthma
  • Action: decreases inflammation of airway buy inhibiting the
    synthesis and release of inflammatory mediators (histamine,
    leukotriene, cytokines, prostaglandins)
  • Decrease mucous production and edema= decreased
    airway obstruction
  • Daily use is okay up to 4-8 weeks
  • Issues: temporary growth retardation in kids, may
    need osteoporosis drugs with adults
A

Inhaled Corticosteroids

131
Q
  • Prevents asthma attacks
  • Mast cells are large cells that release inflammatory substances
  • Action: prevents release of histamine and mediators into
    the airway
A

Mast Cell Stabilizers

132
Q
  • mediate immune/inflammatory response, from
    mast cells, and promote edema causing bronchoconstriction
  • Prophylaxis
  • Delayed onset, not for rescue
  • Action: blocks the enzyme that controls leukotriene synthesis
    or blocks the receptors
A

Leukotriene Modifiers

133
Q
  • Older med, Used when other don’t work
  • Narrow therapeutic index (HIGH RISK FOR TOXICITY)
  • Modest bronchodilators, Stimulant
  • Ex. theophylline
A

Methylxanthines

134
Q
  • Biologic therapy
  • Injected, and attached to specific receptor on target cells
    involved with IgE (releases inflammatory chemical mediators
    from mast cells and basophils)
  • Ex. Xolair: prevents inflammation and dampens the
    body’s response to allergens
A

Monoclonal Antibodies

135
Q
  • Chronic and recurrent obstruction of airflow
  • Chronic bronchitis
  • Emphysema
  • Treatment (no cure): relieve symptoms, avoid complications, treat infections, control
    cough and relieve bronchospasm
  • Pharm
  • Bronchodilators, Glucocorticoids, Leukotriene modifiers, Expectorants,
    Antibiotics, Mucolytics
A

COPD

136
Q
  • Loss of bronchiolar elasticity, destruction of alveolar walls
  • Caused by smoking, contaminants, genetics (alpha-1-antitrypsin)
  • Co2 and O2 are not exchanged well
A

Emphysema

137
Q

Decrease in total lung capacity that results in fluid accumulation and loss of elasticity
of the lung

A

Restrictive Lung Disease

138
Q

○ Holds 1-2L, emptying time is 3-4 hours
○ Chief cells: secrete pepsin
○ Parietal cells: secrete hydrochloric acid
○ Gastric producing cells: produce gastrin which helps enzymes
○ Mucus producing cells: produces mucus (protects lining from acid)
○ GMB: gastric mucosal barrier
○ Lipid soluble drugs and alcohol absorbed here

A

Stomach

139
Q

starts at pyloric sphincter, ends at ileocecal valve at the cecum, most drugs
absorbed here except for lipid soluble which are in the stomach, releases secretin,

A

Small intestine

140
Q

first 10 inches peptic ulcers= most common alteration

A

Duodenum

141
Q

first one to two meters is the most amount of drug absorption

A

Jejunum

142
Q

primary site for absorption of vitamin b12, long chain fatty acids, fat-soluble vitamins

A

Ileum

143
Q

absorbs water and electrolytes, secretes mucus, moves unabsorbed contents (fecal
matter) to rectum for elimination, contains host flora which synthesize b complex
Vitamins and vitamin k, secretes mucus, can speed or slow drug absorption,
disruption can lead to diarrhea

A

Large intestine

144
Q

Excellent and rapid absorptive surface; slower onset of action; limited by
defecation (may alter the effect of the drug); do not go through first pass

A

Lower GI/Rectal administration

145
Q

Key accessory organ; filters and processes nutrients and drugs; all drugs
pass hrough the liver (oral, not usually IV or topical)

A

Liver

146
Q

Primary functions of liver

A

■ Regulation
■ Protection (rids toxins)
■ Synthesis (bile and proteins)
■ Storage (iron and fat-soluble vitamins)

147
Q

collects blood draining from the stomach, s. Intestine, and most of the large intestine

A

Hepatic portal system

148
Q

hepatic impairment is common; usually transient
of asymptomatic; can be severe, permanent, or fatal

A

Drug-induced adverse effects

149
Q

Two physiologic areas that cause vomiting:

A

○ CTZ: chemoreceptor trigger zone (drugs, toxins)
○ VC: vomiting center (odor, smell, taste)
○ Vestibular center (motion sickness)

150
Q

Gastrointestinal System Classes & Subclasses

A
  1. Antacids (aluminum hydroxide)
  2. Histamine (H2) Receptor Antagonists (ranitidine)
  3. GI Prostaglandins (misoprostol)
  4. Proton Pump Inhibitors (omeprazole)
  5. Antiemetics
  6. Anticholinergics
  7. Laxatives
  8. Antidiarrheals
151
Q

dopamine antagonist (metoclopramide), anticholinergic
(dimenhydrinate and/or diphenhydramine)

A

Antiemetics

152
Q

dimenhydrinate

A

Anticholinergics

153
Q

stimulant (bisacodyl), saline (magnesium hydroxide), lubricant (mineral
oil), stool softeners (docusate sodium), bulk-forming (psyllium)

A

Laxatives

154
Q

locally acting (bismuth subsalicylate), systemically acting (loperamide)

A

Antidiarrheals

155
Q

Medications for GERD & PUD

A

Antacids
Histamine (H2) Receptor Antagonists
GI Prostaglandins
Proton Pump Inhibitors

156
Q

reflux of gastric acid into esophagus with
inflammation, corrosion & scarring of esophageal wall

A

Gastro-Esophageal Reflux Disease (GERD)

157
Q

ulceration in wall of stomach or duodenum

A

Peptic Ulcer Disease (PUD)

158
Q

✔ Action – buffers gastric acid from pH 1 - 2 to pH 3 – 4 → ↓ damage to tissues
✔ Uses – symptomatic relief by reducing gastric acidity for treatment of GERD,
PUD, gastritis, hiatus hernia
✔ Adverse Effects – constipation (aluminum & calcium based), diarrhea
(magnesium based)
✔ NURSING CONSIDERATIONS - give 1 hr ac or 2 hr pc other meds (↓
absorption of digoxin & antibiotics, ↑ absorption of levodopa), overuse & selfmedicating can mask underlying disease What accounts for an antacid’s
ability to interfere in absorption of other meds?

A

Antacids

159
Q

Medications Examples for Antiacid

A

o aluminum hydroxide (Amphojel, Maalox, Mylanta)
o magnesium hydroxide/oxide (Milk of Magnesia)
o calcium carbonate (Tums)

160
Q

✔ Action – ↓s hydrochloric acid secretion
✔ Uses – GERD, PUD, stress-induced ulcers
✔ Adverse Effects – diarrhea, constipation
✔ NURSING CONSIDERATIONS – usual bowel pattern, maintain hydration,
underlying infection/disease should be ruled out (eg. H. Pylori infection)

A

Histamine (H2) Receptor Antagonists

161
Q

Meds Sample for Histamine (H2) Receptor Antagonists

A

ranitidine (Zantac)

162
Q

Why is cimetidine no longer a drug of choice in GERD & PUD?

A

Nicotiana species herbs (tobacco) affect the acid-blocking effects of ranitidine

163
Q

✔ Action – inhibits gastric acid & pepsin secretion
✔ Uses – prevention & treatment of gastric ulcers caused by NSAIDs and salicylates
✔ Adverse Effects – constipation, diarrhea
✔ NURSING CONSIDERATIONS – assess for adverse effects & intervene prn – With what
NI?

A

GI Prostaglandins

164
Q

Med sample in GI Prostaglandins

A

misoprostol (Cytotec)

165
Q

✔ Action – inhibit gastric acid secretion
✔ Uses – treatment of severe GERD, esophagitis, PUD, hypersecretory disorders,
with antibiotics in treatment of H. Pylori infection
✔ Adverse Effects – diarrhea, rash

A

Proton Pump Inhibitors

166
Q

Meds example in Proton Pump Inhibitors

A

omeprazole (Losec), rabeprazole (Aciphex)

167
Q

✔ Assess for C/O esophageal or epigastric pain, reflux, blood in emesis, stool if
indicated
✔ Assess reason & pattern of use of OTC antacids
✔ Teach about adverse effects & appropriate NIs (diarrhea, constipation)
✔ Teach about taking antacids ac or pc other meds

A

nursing Interventions for Clients taking Drugs for GERD and PUD

168
Q

a reflex originating in the medulla (stimulated by cholinergic & dopaminergic fibres)

A

Vomiting

169
Q

known to have antiemetic properties and has been found helpful in
nausea and vomiting due to motion sickness, pregnancy and post-operative procedures

A

Ginger

170
Q

✔ Action – block dopamine receptors along vomit center pathways (but also at other
CNS sites)
✔ Uses – antineoplastic therapy, post-op
✔ Adverse Effects – extrapyramidal effects in larger doses (dystonia, parkinsonism,
tardive dyskinesia)
✔ Make sense of this adverse effect..

A

Dopamine Antagonist Antiemetics

171
Q

Meds Example of Dopamine Antagonist Antiemetics

A

metoclopramide (Maxeran), prochlorperazine (Stemetil)

172
Q

✔ Action – reduces Ach on vomit centre pathways & those associated with vestibular
apparatus
✔ Uses- pregnancy
✔ Adverse Effects – variable effectiveness, sedation is common, anticholinergic effects
(constipation, urinary retention, dry mouth)

A

Anticholinergic Antiemetics

173
Q

med sample of Anticholinergic Antiemetics

A

scopolamine, diphenhydramine (Benadryl), dimenhydrinate (Gravol)

174
Q

Herbs such as henbane which have anticholinergic side effects should not be taken
with _____ as the anticholinergic side effects may be increased

A

anticholinergic antiemetics

175
Q

● infrequent, incomplete or painful BMs due to ↓GI motility
● Prolonged constipation → drier stool
● Causes – low fibre and/or fluid, immobility or sedentary lifestyle, smooth muscle
weakness (from failure to go, excessive laxative use), tumors, drug effects
● Frequently → hemorrhoids & blood los

A

Constipation

176
Q

start with non-drug interventions to the client’s abilities (fibre, hydration,
exercise, teach stress management techniques)

A

treatment for constipation

177
Q

NURSING CONSIDERATIONS - Laxatives

A

✔ ABDOMINAL ASSESSMENT
✔ Assess and treat underlying cause if possible
✔ Promote physical activity within client’s limits
✔ Consult with client & dietician for added fibre and fluids of choice
✔ Assess for/teach prevention of dependency
✔ Assess for adverse effects – abdominal discomfort
✔ Teach not to strain or refrain from doing Valsalva maneuver

178
Q

✔ Action - stimulates smooth muscle to promote peristalsis
o PO act in 6 – 10 hours
o PR act in 60 – 90 minutes
✔ Adverse Effects – cramping, continuous use can cause loss of muscle tone →
dependeNcy

A

Stimulant Laxatives

179
Q

Meds Examples of Stimulant Laxatives

A

bisacodyl (Dulcolax) – do not give with milk or
antiulcer/antacids, sennosides (Colace) → dissolution of enteric coatin

180
Q

✔ Action - hypertonic fluid attracts water → distends bowel → promotes peristalsis
o PO acts in 1 – 3 hours
o continuous use can cause electrolyte imbalance & loss of muscle
tone → dependeNcy
✔ Adverse Effects – diarrhea, dependency, cramping

A

Saline Laxatives

181
Q

Meds examples of Saline Laxatives

A

magnesium citrate (Citromag), magnesium hydroxide (Milk of
Magnesia)

182
Q

✔ Action – soften stool by drawing water into bowel, PO takes up to 72 hours to act
✔ Uses – post Myocardial Infarction (MI) to prevent straining, drug of choice for active
geriatric & pregnant client with constipation

A

Stool Softening Laxatives

183
Q

Med Example of Stool Softening Laxatives

A

docusate sodium (Colace)

184
Q

✔ Action – promotes bulk (combines with water & intestinal contents), promotes
peristalsis
✔ Uses – drug of choice for immobile client requiring ongoing laxative use, irritable
bowel syndrome, control of some forms of diarrhea
✔ Adverse Effects – bowel
obstruction

A

Bulk Forming Laxatives

185
Q

Med sample Bulk Forming Laxatives

A

psyllium (Metamucil)

186
Q

frequent or watery stools, may be acute/chronic, mild/severe
✔ IS A SYMPTOM, not a disease, may be a sign of colorectal ca
✔ Causes – intestinal infection (food poisoning or clostridium difficile), fatty foods,
excessive laxative use, medication adverse effect, emotional stress, irritable bowel
syndrome, hyperthyroidism

A

Diarrhea

187
Q

✔ Nursing assessments are the same as for constipation
✔ Specimen for C&S may be ordered
✔ Skin/mucous membrane assessment
✔ Frequent peri-care & application of barrier cream
✔ Comfort measure & privacy (call bell and/or bedpan, TP and hand wipes within reach)
✔ Assess for dehydration, orthostatic BP, wt loss,
bloodwork What specifically?
✔ Tannin containing herbs such as green and black teas, black walnut, uva ursi, red
raspberry, oak and witch hazel may decrease the activity or absorption of antidiarrheals
such as Lomotil.
✔ Herbs with a laxative effect may decrease the action of antidiarrheal medications.

A

URSING CONSIDERATIONS - Diarrhea

188
Q

✔ Action – absorb excess water, irritants or bacteria → production of a soft stool
✔ Uses – diarrhea of sudden onset lasting 2-3 days with dehydration and electrolyte
losses, IBS, post GI surgery

A

Locally-acting Antidiarrheals

189
Q

Meds Examples of Locally-acting Antidiarrheals

A

bismuth subsalicylate (Pepto-Bismol, Kaopectate), psyllium
(Metamucil)

190
Q

✔ Uses – adjuNct for acute diarrhea, ileostomy, irritable bowel disease (IBD)
o Do not use in GIT infection -
o Adverse Effects – abdominal distension, constipation, worsening of diarrhea

A

Systemic Antidiarrheals

191
Q

med sample of Systemic Antidiarrheals
✔ Action – decrease autonomic stimulation of peristalsis → ↓ GIT motility → slows transit time

A

loperamide (Imodium)

192
Q

Prescription antiemetics

A

Antihistamines, anticholinergics, dopamine antagonists,
benzodiazepines, serotonin antagonists, glucocorticoids, and
cannabinoids

193
Q

Non-prescription Antiemetics

A

Antihistamines

194
Q

■ Stimulates the VC, and decrease CTZ
■ Gastric mucosa
● Action: protects, decreases irritation
○ Types:
■ Opioids (added to antiemetics): decrease stimulatio

A

Antihistamines

195
Q
A

PHARMA (3 decks)

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