2nd Exam Flashcards
(195 cards)
1
Q
Medications that are used to treat benign prostatic hyperplasia (BPH)
A
5-alpha
reductase inhibitors and alpha1-adrenergic antagonists.
2
Q
Medications used to treat
erectile dysfunction
A
phosphodiesterase type 5 (PDE5) inhibitors
3
Q
needed for growth and maturation of the female reproductive
tract and secondary sex characteristics.
A
Estrogens
4
Q
block bone resorption and reduce
low-density lipoprotein (LDL) levels.
A
Estrogens
5
Q
suppress the release of a
follicle-stimulating hormone (FSH) needed for conception.
A
estrogens
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
7
Q
Synthetic drug that exert progesterone like activity are called
A
progestins.
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
9
Q
stimulate uterine contractions. Use to induce labor.
A
Oxytocics
10
Q
Oxytocics interact with several drugs including vasoconstrictors which may lead to
A
hypertension.
11
Q
inhibit uterine contractions.
Uses to prevent preterm labor.
A
Tocolytics - Terbutaline (beta -2-adrenergic agonist)
12
Q
Adverse effects of tocolytics
A
tachycardia in mother and fetus.
13
Q
Nursing Considerations for Tocolytics
A
monitor heart rate of mother and fetus
14
Q
Treatment for Male Hypogonadism
A
testosterone or other androgens
15
Q
Use to restore normal gonadal development and secondary male sex
characteristics.
A
testosterone
16
Q
Adverse effects of testosterone
A
water retention, edema, potential for liver damage,
acne, skin irritation.
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
18
Q
Treatment for Erectile dysfunction
A
sildenafil (Viagra)
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)
20
Q
Severe chest pain that is usually short (lasts 5-10mins)
- Brought on by exertion or emotional excitement
A
Angina Pectoris
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
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)
23
Q
Antianginal Drugs
A
❖ Calcium Channel Blocker
❖ Nitrates (Nitroglycerin)
❖ Beta-Adrenergic Blockers (Cardioprotective - reduces the incidence of MI)
24
Q
relax coronary artery spasm, causes negative inotropic effects,
and reduces cardiac workload and oxygen demands
A
Calcium Channel Blocker
25
what are the side effects of Calcium Channel Blocker
dizziness, flushing, headache, hypotension, reflex
tachycardia, peripheral edema, fatigue
26
forms nitric oxide in vascular smooth muscle, causes
vasodilation
Nitrates (Nitroglycerin)
27
Reduces the amount of blood returning to the heart (preload),
Reduced cardiac output, Reduced workload, Reduced
oxygen demands
vasodilation
28
Nitrates (Nitroglycerin) is given in what medicine route?
sublingually
29
decreases the cardiac workload by lowering blood pressure,
slowing heart rate and reducing contractility Also effective for HTN
Beta-Adrenergic Blockers (Cardioprotective - reduces the incidence of MI)
30
Preferred selective beta blockers because non-selective can
affect
bronchodilation
31
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
Dysrhythmias
32
Signs and Symptoms of Dysrhythmias
Dizziness, weakness, fatigue, decreased exercise tolerance,
palpitations, dyspnea, syncope (temp. Loss of consciousness due to decrease in BP)
33
- Action potential begins when threshold potential is reached.
- Sodium rushes in, producing rapid depolarization
- Calcium enters at a slower rate
Phase 0
34
- Brief transient phase
- Inside of plasma membrane reverses charge, becomes positive
Phase 1
35
- Plateau reached in which depolarization is maintained
- Contraction of cardiac muscle
- Efflux of potassium from cells
Phase 2
36
- Calcium channels close
- Additional potassium channels open
- Repolarization returns negative resting membrane potential
Phase 3
37
- Refractory Period
- Brief period where depolarization cannot occur
- Ensures myocardial cell finishes contracting before another
action potential begins
Phase 4
38
- HR <60 bpm
- Common among older adults
- Major indication for pacemakers
Bradydysrhythmias
39
Common bradydysrhythmias
Sinus bradycardia -life sustainable
Sinoatrial node dysfunction (HR in the 30s)
Atrioventricular (AV) conduction block
Arrhythmia - no rhythm (DEAD)
40
- HR >100 bpm
- Incidence increases in older adults and those with preexisting cardiac disease
Tachydysrhythmias
41
Common tachydysrhythmias:
Atrial tachycardia
Atrial flutter
Atrial fibrillation
Ventricular tachycardia
Ventricular fibrillation
42
Paroxysmal supraventricular tachycardia (PSVT) >200 bpm
Atrial tachycardia
43
- No treatment
- Little or no benefit to treatment with medications
Asymptomatic dysrhythmias
44
- Initiated for high-risk patients
- Avoid drug combinations that increase QT interval
Prophylaxis of dysrhythmias
45
- Cardioversion or defibrillation
- Electrical stimulation of the heart for serious dysrhythmias
- Pacemakers
- ICDs (implantable cardioverter defibrillators)
Nonpharmacologic treatment of dysrhythmias
46
- 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
Class 1A: procainamide
47
Pharmacologic management of dysrhythmias
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
48
Other Management of Dysrhythmias:
Adenosine (transient heart block)
Digoxin
49
- Check apical and radial pulses before dose
- Continuous ECG and BP monitoring during IV administration
- Monitor therapeutic blood levels
Nursing Responsibilities for Class 1A
50
- Shorten repolarization
- Primary indications are ventricular dysrhythmias
Class 1B
51
Drugs included in Class 1B
- Lidocaine (Xylocaine)
- Mexiletine (Mexitil)
- Phenytoin (Dilantin)
52
- Decrease conduction velocity
- PR, QRS, and QT intervals are often prolonged
- Life-threatening atrial dysrhythmias
Class 1C: Antiarrhythmics
53
- Reduce automaticity as well as slow conduction velocity in the heart
- Action: block calcium channels in SA and AV nodes
- Slows HR
Beta Adrenergic Antagonist: Class II
54
Drugs included in Beta Adrenergic Antagonist: Class II
- Acebutolol (Sectral)
- Esmolol (Brevibloc)
- Propranolol (Inderal)
55
- 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
Potassium Channel Blockers: Class II
56
- Exact mechanism unknown
- Block potassium channels but also blocks sodium ion channels
and inhibits sympathetic activity
Potassium Channel Blockers: Class III
57
severe bradycardia, cardiogenic shock,
sick sinus syndrome, severe sinus node dysfunction, third-degree AV
block, hypersensitivity to iodine, lactation, COPD, electrolyte imbalances
Contraindications/precautions of Potassium Channel Blockers: Class III
58
- Monitor BP during IV infusion
- Assess for adverse effects
- Baseline lab tests
- Assess respiratory status
- Supervise ambulation (could have hypotension)
- Baseline ophthalmic exam
Nursing Responsibilities for Class III
59
- Effects similar to those of beta - adrenergic antagonists
- Monitor for bradycardia and hypotension
Calcium Channel Blockers: Class IV
60
- 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
Adenosine (transient heart block)
61
- Primarily for HF
- Not effective against ventricular dysrhythmias
- Patients must be carefully monitored for toxicity, drug interactions, and
adverse effects
- Loading dose neede
Digoxin
62
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
Anticoagulants
63
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
HEPARIN
64
Antidote of Heparin
Protamine sulfate
65
inactivates Xa factor
Use: prevent DVT, PE (high risk from abdominal and orthopedic
surgeries)
- Issues: ASA (aspirin), bleeding
Low Molecular weight heparin
66
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
Direct Thrombin Inhibitors
67
: 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)
WARFARIN
68
Antidote of WARFARIN
Vitamin K, takes 24-48 hours to be effective and may need
to give frozen plasma or platelets in the meantime
69
Prevent platelet aggregation, interrupts the cascade (the enzyme that
helps them aggregate is no longer available)
Antiplatelets
70
Inhibits cyclooxygenase (needed for platelet aggregation)
- Use: prevent MI and TE, prevent and treat a stroke
- Issues: bleeding and GI upset
ASPIRIN
71
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
Thrombolytics
72
- Used for hypertension, heart failure, renal failure, liver failure, and pulmonary edema
- Common adverse effects: dehydration, hypotension, electrolyte imbalance
Diuretics
73
5 types of Diuretics
Thiazide and Thiazide-Like Diuretics
Loop Diuretics (Lasix)
Osmotic Diuretics
Carbonic Anhydrase Inhibitors
Potassium Sparing Diuretics
74
act on the distal convoluted renal tubule; promotes
sodium, chloride, and water excretion (may also lose K and Mg)
Thiazide and Thiazide-Like Diuretics
75
Use of Thiazide and Thiazide-Like Diuretics
HTN and peripheral edema
76
dizziness, headache, weakness, hypotension, GI
distress, constipation, hyperglycemia, electrolyte imbalance,
urticarial, hyperuricemia, blood dyscrasias, renal failure
Side effects of Thiazide and Thiazide-Like Diuretics
77
Contradictions of Thiazide and Thiazide-Like Diuretics
renal failure
78
act on the ascending loop of Henle; secretes Na, water, K, Ca, Mg
Loop Diuretics (Lasix)
79
dizziness, weakness, headache,
hyperglycemia, blurred vision, photosensitivity, paresthesia, othro
hypotension, hyperuricemia, electrolyte imbalance, blood
dyscrasias, elevated BUN, creatinine, lipids, and renal failure
Side effects/adverse effects of Loop Diuretics (Lasix)
80
increase sodium reabsorption in the proximal tubule and loop of
Henle. Increase osmolality which pulls in water to excrete Na, Cl, K, and
water
Osmotic Diuretics
81
Use of Osmotic Diuretics
prevent kidney failure, decrease ICP and IOP
82
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.
Carbonic Anhydrase Inhibitors
83
- 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
Potassium Sparing Diuretics
84
DIGOXIN (prototype)
- Positive Inotropic: iNcreases myocardial contractility
- Negative chronotropic: decreases heart rate
- Negative dromotropic: decreases conduction of the electric system
within the heart
85
- Reduce blood volume, lower BP, reduce workload, increase CO
- Used only for fluid overload (loop diuretics are best with thiazide added)
Diuretics
86
- 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)
Phosphodiesterase Inhibitor(PDE5): Primicor (other positive inotropic agents)
87
- Aldosterone antagonist (not a diuretic)
- Prevents cardiac remodeling
Spironolactone (Aldactone)
88
- Blocks the catecholamines, slows HR, reduces contractility
- prevents tachydysrhythmias, prevents MI damage
- May produce remodeling of the hear
- May worsen failure, taper dose up
Beta Adrenergic Antagonists
89
-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
Antihypertensives
90
- 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
Physiologic Risk Factors of Antihypertensives
91
Antihypertensive drugs
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
- 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)
Diuretics
93
- 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)
Sympatholytic
94
- Inhibit beta1 and beta2 receptors
- Propranolol
Nonselective
95
- Block beta1 receptors
- Metoprolol (prototype)
Cardio selective
96
- 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
Centrally acting alpha2 agonists
97
- 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
Alpha-adrenergic blockers
98
- 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
Adrenergic neuron blockers
99
- Action: blocks alpha1 receptors
- SE: hypotension, bradycardia
Alpha1- adrenergic blockers
100
- Action: relax smooth muscles of blood vessels, especially
causing vasodilation
- SE: tachycardia, palpitations, edema, headache, dizziness,
nasal congestion, GI bleeding, lupus like symptoms
Direct-acting arteriolar vasodilators
101
ACE inhibitors
- 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
Angiotensin II receptor Blockers (ARBs)
- 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
- 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
Direct Renin Inhibitor
104
Calcium Channel Blockers
- 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
Triglycerides, phospholipids, steroids (cholesterol)
Lipids
106
arge transport from body to liver
Chylomicrons
107
- 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
Genesis of Atherosclerosis
108
Pharmacologic treatment of Genesis of Atherosclerosis
- Statins (most effective)
- Blood lipid profiles
109
Drugs for Dyslipidemia
Statins
Bile Acid Sequestrants
Niacin (Nicotinic Acid)
Fibric Acid
Peripheral Vasodilators
110
- 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)
Statins
111
- 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
Bile Acid Sequestrants
112
- 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
Niacin (Nicotinic Acid)
113
- Action: activates enzymes which increase breakdown of triglycerides
- AE: GI problems
- Take with food
- Example: Gemfibrozil
- Highly protein bound
Fibric Acid
114
- Used in PVD
- Causes iNcreased ability for blood flow
- Action: vasodilator
- INcreases O2 in blood
- Treat pain with activity - intermittent claudication
Ischemia = pain
Peripheral Vasodilators
115
block H1 receptors to decrease nasopharyngeal secretion
H1 blockers, Histamine1 Antagonists
116
SE: drowsiness, dry mouth, decreased secretions (anticholinergic effects)
First Generation Antihistamines (Benadryl)
117
- Fewer anticholinergic effects, less drowsiness, longer half life
- Ex. Claritin
Second Generation Antihistamines
118
- 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
Nasal Decongestants
119
- 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
Systemic Decongestants (Ex. Sudafed)
120
- Treats allergic rhinitis
- Anti-inflammatory actions
- Decrease in sneezing and coughing
- Can increase blood sugar and should caution with diabetes
Intranasal Glucocorticoids (Ex. Flonase)
121
- 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
Antitussives
122
- Loosen bronchial secretions to be coughed out
Expectorants (Robitussin)
123
- Loosen thick, viscous bronchial secretions
- Breaks down the chemical structure of mucous molecules
- The mucous become thin, and can be removed out by coughing
Mucolytics
124
- 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
Asthma
125
- Prolonged asthma attack which can lead to death
Status asthmaticus
126
Treatment of asthma
- 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
- relieves bronchospasm
- Sympathetic NS- relaxes bronchial smooth muscle=dilation
- ALBUTEROL (prototype)
- Beta 2 Agonists (sympathetic)
128
- Maintains bronchodilation
- When inhibited constriction occurs
- Increased by sympathomimetics, bronchodilators,
and methylxanthines
cAMP (cyclic AMP/ cyclic adenosine monophosphate)
129
- 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)
Inhaled Anticholinergic (parasympathetic acts sympathetic)
130
- 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
Inhaled Corticosteroids
131
- Prevents asthma attacks
- Mast cells are large cells that release inflammatory substances
- Action: prevents release of histamine and mediators into
the airway
Mast Cell Stabilizers
132
- 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
Leukotriene Modifiers
133
- Older med, Used when other don't work
- Narrow therapeutic index (HIGH RISK FOR TOXICITY)
- Modest bronchodilators, Stimulant
- Ex. theophylline
Methylxanthines
134
- 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
Monoclonal Antibodies
135
- 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
COPD
136
- Loss of bronchiolar elasticity, destruction of alveolar walls
- Caused by smoking, contaminants, genetics (alpha-1-antitrypsin)
- Co2 and O2 are not exchanged well
Emphysema
137
Decrease in total lung capacity that results in fluid accumulation and loss of elasticity
of the lung
Restrictive Lung Disease
138
○ 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
Stomach
139
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,
Small intestine
140
first 10 inches peptic ulcers= most common alteration
Duodenum
141
first one to two meters is the most amount of drug absorption
Jejunum
142
primary site for absorption of vitamin b12, long chain fatty acids, fat-soluble vitamins
Ileum
143
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
Large intestine
144
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
Lower GI/Rectal administration
145
Key accessory organ; filters and processes nutrients and drugs; all drugs
pass hrough the liver (oral, not usually IV or topical)
Liver
146
Primary functions of liver
■ Regulation
■ Protection (rids toxins)
■ Synthesis (bile and proteins)
■ Storage (iron and fat-soluble vitamins)
147
collects blood draining from the stomach, s. Intestine, and most of the large intestine
Hepatic portal system
148
hepatic impairment is common; usually transient
of asymptomatic; can be severe, permanent, or fatal
Drug-induced adverse effects
149
Two physiologic areas that cause vomiting:
○ CTZ: chemoreceptor trigger zone (drugs, toxins)
○ VC: vomiting center (odor, smell, taste)
○ Vestibular center (motion sickness)
150
Gastrointestinal System Classes & Subclasses
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
dopamine antagonist (metoclopramide), anticholinergic
(dimenhydrinate and/or diphenhydramine)
Antiemetics
152
dimenhydrinate
Anticholinergics
153
stimulant (bisacodyl), saline (magnesium hydroxide), lubricant (mineral
oil), stool softeners (docusate sodium), bulk-forming (psyllium)
Laxatives
154
locally acting (bismuth subsalicylate), systemically acting (loperamide)
Antidiarrheals
155
Medications for GERD & PUD
Antacids
Histamine (H2) Receptor Antagonists
GI Prostaglandins
Proton Pump Inhibitors
156
reflux of gastric acid into esophagus with
inflammation, corrosion & scarring of esophageal wall
Gastro-Esophageal Reflux Disease (GERD)
157
ulceration in wall of stomach or duodenum
Peptic Ulcer Disease (PUD)
158
✔ 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?
Antacids
159
Medications Examples for Antiacid
o aluminum hydroxide (Amphojel, Maalox, Mylanta)
o magnesium hydroxide/oxide (Milk of Magnesia)
o calcium carbonate (Tums)
160
✔ 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)
Histamine (H2) Receptor Antagonists
161
Meds Sample for Histamine (H2) Receptor Antagonists
ranitidine (Zantac)
162
Why is cimetidine no longer a drug of choice in GERD & PUD?
Nicotiana species herbs (tobacco) affect the acid-blocking effects of ranitidine
163
✔ 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?
GI Prostaglandins
164
Med sample in GI Prostaglandins
misoprostol (Cytotec)
165
✔ 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
Proton Pump Inhibitors
166
Meds example in Proton Pump Inhibitors
omeprazole (Losec), rabeprazole (Aciphex)
167
✔ 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
nursing Interventions for Clients taking Drugs for GERD and PUD
168
a reflex originating in the medulla (stimulated by cholinergic & dopaminergic fibres)
Vomiting
169
known to have antiemetic properties and has been found helpful in
nausea and vomiting due to motion sickness, pregnancy and post-operative procedures
Ginger
170
✔ 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..
Dopamine Antagonist Antiemetics
171
Meds Example of Dopamine Antagonist Antiemetics
metoclopramide (Maxeran), prochlorperazine (Stemetil)
172
✔ 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)
Anticholinergic Antiemetics
173
med sample of Anticholinergic Antiemetics
scopolamine, diphenhydramine (Benadryl), dimenhydrinate (Gravol)
174
Herbs such as henbane which have anticholinergic side effects should not be taken
with _____ as the anticholinergic side effects may be increased
anticholinergic antiemetics
175
● 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
Constipation
176
start with non-drug interventions to the client’s abilities (fibre, hydration,
exercise, teach stress management techniques)
treatment for constipation
177
NURSING CONSIDERATIONS - Laxatives
✔ 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
✔ 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
Stimulant Laxatives
179
Meds Examples of Stimulant Laxatives
bisacodyl (Dulcolax) – do not give with milk or
antiulcer/antacids, sennosides (Colace) → dissolution of enteric coatin
180
✔ 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
Saline Laxatives
181
Meds examples of Saline Laxatives
magnesium citrate (Citromag), magnesium hydroxide (Milk of
Magnesia)
182
✔ 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
Stool Softening Laxatives
183
Med Example of Stool Softening Laxatives
docusate sodium (Colace)
184
✔ 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
Bulk Forming Laxatives
185
Med sample Bulk Forming Laxatives
psyllium (Metamucil)
186
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
Diarrhea
187
✔ 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.
URSING CONSIDERATIONS - Diarrhea
188
✔ 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
Locally-acting Antidiarrheals
189
Meds Examples of Locally-acting Antidiarrheals
bismuth subsalicylate (Pepto-Bismol, Kaopectate), psyllium
(Metamucil)
190
✔ 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
Systemic Antidiarrheals
191
med sample of Systemic Antidiarrheals
✔ Action – decrease autonomic stimulation of peristalsis → ↓ GIT motility → slows transit time
loperamide (Imodium)
192
Prescription antiemetics
Antihistamines, anticholinergics, dopamine antagonists,
benzodiazepines, serotonin antagonists, glucocorticoids, and
cannabinoids
193
Non-prescription Antiemetics
Antihistamines
194
■ Stimulates the VC, and decrease CTZ
■ Gastric mucosa
● Action: protects, decreases irritation
○ Types:
■ Opioids (added to antiemetics): decrease stimulatio
Antihistamines
195
