Perfusion Clotting Pharmacology Answer Sheet

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1230 Pharmacology
Perfusion, Clotting, Fluid and Electrolyte
1. Heart failure (HF) is when the heart muscle weakens and enlarges, losing the ability to
pump blood through the heart and systemic circulation.
2. Common causes of HF include chronic HTN, myocardial infarction (MI), coronary artery
disease (CAD), heart valve disease, congenital heart disease, and arteriosclerosis.
3. In left sided HF the left ventricle does not pump blood efficiently to the peripheral system
causing blood to back up in the lungs, common symptoms include shortness of breath
(SOB) and dyspnea.
4. In right sided HF the right ventricle does not pump blood efficiently to the lungs causing
blood to back up in the peripheral system, common symptoms include peripheral edema.
5. Preload is blood flow force that stretches ventricle at the end of diastole.
6. Afterload is resistance to ventricular ejection of blood.
7. First line treatment for HF includes IV inotropes (dopamine, dobutamine),
phosphodiesterase inhibitors (milrinone), oral diuretics, beta blockers, ACE, ARB, CCB,
and vasodilators.
8. Nonpharmacological treatment of HF includes limit salt 2 g/day, 1 or less alcoholic
drinks, stop smoking, fluid intake may be restricted, loss weight if needed, decrease
saturated fat in diet, mild exercise recommended.
9. Cardiac glycosides, including digoxin, have three effects on the heart muscle inotropic
(increase myocardial contraction), chronotropic (decrease HR), dromotropic (decrease
conduction thru AV node).
10. Cardiac glycosides are also used to treat atrial fibrillation/flutter.
11. Atrial natriuretic hormone/peptide (ANH pr ANP) released during expansion and filling
of atria produce vasodilation and increased GFR resulting in increased urine production
and decreased blood volume and pressure.
12. Brain natriuretic peptide (BNP) released from atrial cardiac cells and aids in diagnosis of
HF.
Digoxin/Cardiac Glycoside
Concept/Action/Use Assessment
Patient
Nursing Interventions/Patient
Problem/Planning Teaching
Evaluation
Perfusion
Inhibits sodiumpotassium ATPase
promoting
increased force of
contraction, cardiac
output, and tissue
perfusion.
Decreases
ventricular rate.
Heart failure
atrial fibrillation
atrial flutter
Ischemia,
decreased tissue
perfusion,
decreased gas
exchange,
hypoxemia.
Patient will demo
pulse check,
range for pulse,
know high
potassium foods.
Pulse in expected
range, decreased
heart rate and lung
congestion, absence
of digoxin toxicity.
Digoxin therapeutic
range 0.8 – 2 ng/mL
Drug/herb
history
Baseline
apical pulse
Assess signs
and
symptoms
digoxin
toxicity
Apical pulse rate below 60 do
not administer.
The patient will check pulse
rate daily before taking
digoxin.
Ascertain apical pulse rate
before administering digoxin.
Assess for evidence of
digitalis toxicity.
Determine signs of peripheral
and pulmonary edema.
Monitor serum digoxin level.
Monitor serum potassium
level and report signs and
1230 Pharmacology
Perfusion, Clotting, Fluid and Electrolyte
symptoms low potassium
level weakness, fatigue,
abdominal distention,
nausea, vomiting, leg cramps.
Instruct patient to report
symptoms digoxin toxicity
loss of appetite, vomiting,
diarrhea blurred vision, green
or yellow halos, low heart
rate, palpitations, or irregular
heart rate.
13. Digitalis toxicity signs and symptoms include anorexia, vomiting, diarrhea,
blurred vision, green or yellow halos bradycardia, premature ventricular contractions,
cardiac dysrhythmias
14. Digoxin cardiotoxicity can cause ventricular dysrhythmias that can be treated with
phenytoin and lidocaine.
15. The antidote for digitalis toxicity is digoxin immune fab.
16. Hypokalemia can increase digoxin effects and result in an increased risk for digitalis
toxicity.
17. Phosphodiesterase inhibitors are a positive inotropic group of drugs that result in
myocardial contractility and vasodilation.
18. Other medications used in HF include vasodilators, ACE inhibitors, ARB’s, diuretics,
nesiritide, and some beta blockers.
19. Antianginal medications are used to treat angina pectoris.
20. Define the following:
a. Angina pectoris pain caused by inadequate blood flow to cardiac tissues.
b. Classic (stable) angina pain with predictable stress or exertion
c. Unstable angina progressively severe pain unrelated to activity, stress, exertion
d. Variant (Prinzmetal or vasospastic) angina pain at rest
21. Nonpharmacological methods of treating angina include avoid heavy meals, smoking,
extreme weather changes, strenuous exercise, emotional upset. Increase proper nutrition,
moderate exercise, adequate rest, and relaxation techniques.
22. Three types of antianginal medications are nitrates, beta blocker and CCB.
23. Nitrates cause generalized vascular and coronary vasodilation.
Nitroglycerin/Antianginal
Concept/Action/Use Assessment
Patient
Nursing Interventions/Patient
Problem/Planning Teaching
Evaluation
Perfusion
Promote
vasodilation.
Decrease preload
and afterload.
Decrease tissue
perfusion,
hypoxemia,
myocardial tissue
Decreased anginal
pain with
medications. Note
side effects dizziness,
headache, faintness
Baseline VS
Health and
drug history
Do not abruptly discontinue.
Monitor VS especially for
hypotension.
Position patient sitting or
lying for first administration.
1230 Pharmacology
Angina, AMI, HTN
emergency,
pulmonary edema,
HF
Perfusion, Clotting, Fluid and Electrolyte
injury, anxiety,
pain, dyspnea.
Patient reports
angina controlled
with medication
COP slowly.
Dry mouth could interfere
with SL absorption, sips of
water may be needed.
Gloves for ointments and
watch when defibrillating,
may cause burns.
Protect medication from
light.
If angina not subsided or
worse in 5 minutes call 911
SL tabs every 5 min X 3, seek
medical attention if pain not
relieved.
Do not ingest alcohol with
nitrates.
Do not stop BB or CCB,
withdrawal symptoms of
tachycardia and pain may be
severe.
Avoid hairy and broken skin
surfaces when applying
nitroglycerine patches.
May use acetaminophen for
headache.
24. Beta Blockers decrease the effects of the sympathetic nervous system by blocking the
action of catecholamines thereby decreasing HR and BP.
25. Calcium channel blockers (CCB) relax coronary artery spasms and peripheral arterioles
decreasing cardiac O2 demand.
26. Cardiac dysrhythmia is defined as any deviation from normal rate and pattern of
heartbeat.
27. In an ECG the P wave reflects atrial activation, the QRS reflects ventricular
depolarization, and the T wave reflects ventricular repolarization.
28. When sodium and calcium enter cardiac cells depolarization or cardiac contraction
occurs.
29. Four classes of antidysrhythmic are sodium channel blocker, beta blocker, drugs that
prolong depolarization, and calcium channel blocker.
30. Sodium channel blocker decrease sodium influx into cardiac cells resulting in decreased
conduction velocity, suppression of automaticity, and increased recovery time.
31. Beta1 blockers are cardioselective beta adrenergic blockers resulting in decreased
conduction velocity, automaticity, and recovery time.
1230 Pharmacology
Perfusion, Clotting, Fluid and Electrolyte
Acebutolol hydrochloride/Antidysrhythmias
Concept/Action/Use Assessment
Patient
Nursing Interventions/Patient
Problem/Planning Teaching
Evaluation
Perfusion
Block beta1
receptor sites
Decrease
conduction,
velocity,
automaticity, and
recovery time.
Treat premature
ventricular
contractions.
Decreased tissue
perfusion,
hypoxemia,
anxiety.
Patient will be in
normal sinus
rhythm and
comply with
medication
regimen.
Evaluate for normal
sinus rhythm, side
effects and
palpitations,
shortness of breath,
coughing and chest
pain.
Baseline VS
& ECG.
Health and
drug history.
Monitor
cardiac
enzymes
Do not abruptly discontinue.
Monitor VS especially for
hypotension.
Pt avoid alcohol increases
hypotension, caffeine
increases catecholamine
levels, and tobacco causes
vasoconstriction.
Teach patient to take as
prescribed. Teach patient to
report side effects dizziness,
faintness, nausea, and
vomiting.
Administer IV push as
recommended in drug guide.
32. Calcium channel blockers (CCB) block calcium entry decreasing excitability and
contractility.
33. Two purposes for diuretics are to decrease hypertension and edema (peripheral and
pulmonary).
34. Five categories of diuretics are thiazide and thiazide-like diuretics, loop diuretics,
osmotic diuretics, carbonic anhydrase inhibitors and potassium-sparing diuretics.
35. Thiazide diuretics act on the distal convoluted renal tubule.
Hydrochlorothiazide/Thiazides
Concept/Action/Use Assessment
Patient
Nursing Interventions/Patient
Problem/Planning Teaching
Evaluation
Elimination.
Act on distal
convoluted renal
tubule
Promote sodium,
potassium, and
water excretion and
act directly on
arterioles to
promote
vasodilation.
Elimination, fluid
overload,
abnormal
electrolyte levels.
Patient blood
pressure will
decrease and/or
patient will have
decreased
edema. Patient
will have normal
electrolyte levels.
Evaluate for
decreased blood
pressure, decreased
edema, and normal
electrolyte levels.
Assess
baseline vital
signs, urine
output,
edema,
serum
electrolytes,
glucose, and
uric acid.
Assess
history of
medications
Assess vital signs, weight,
urine output, and serum
electrolytes and glucose
values for baseline levels.
Monitor K+ levels.
Check extremities for edema.
Observe for signs and
symptoms of hypokalemia.
Monitor the patient’s daily
weight and urine output.
Suggest that the patient take
the drug early in the morning
1230 Pharmacology
Hypertension,
edema, heart
failure, ascites,
nephrotic
syndrome.
Perfusion, Clotting, Fluid and Electrolyte
and herbal
supplements.
to avoid sleep disturbance
from nocturia.
Instruct patient to slowly
change positions from lying
to standing because dizziness
may occur.
Advise patient to use
sunblock for photosensitivity.
36. Loop diuretics act on the thick ascending loop of Henle.
Furosemide/Loop Diuretic
Concept/Action/Use Assessment
Patient
Nursing
Problem/Planning Interventions/Patient
Teaching
Assess baseline Elimination, fluid Monitor urinary output and
vital signs,
overload,
weight to determine body
urine output,
abnormal
fluid gain or loss.
edema, and
electrolyte levels. Monitor vital signs and note
serum
Patient blood
decrease in BP.
electrolytes.
pressure will
Administer IV furosemide
Assess history
decrease and/or
slowly, hearing loss may
of medications patient will have
occur if it is rapidly injected.
and herbal
decreased
Observe for evidence of
supplements.
edema. Patient
hypokalemia (muscle
Assess
will have normal
weakness, abdominal
hypersensitivity electrolyte levels. distention, leg cramps
to
and/or cardiac
sulfonamides.
dysrhythmias.
Monitor potassium levels,
especially when a patient is
taking digoxin.
Suggest that the patient take
the drug early in the
morning to avoid sleep
disturbance from nocturia.
Instruct patient to slowly
change positions from lying
to standing because
dizziness may occur.
Evaluation
Elimination
Act on ascending
loop of Henle
Inhibit sodium,
water reabsorption,
increase potassium,
chloride, calcium,
magnesium
excretion.
Treat heart failure,
renal dysfunction,
HTN, nephrotic
syndrome, acute
pulmonary &
peripheral edema.
Evaluate for
decreased blood
pressure, decreased
edema, and normal
electrolyte levels.
37. Osmotic diuretics increase osmolality and sodium reabsorption and are used for kidney
failure, decreased ICP and IOP.
38. Carbonic anhydrase inhibitors block the action of carbonic anhydrase and are primarily
used for decreasing IOP with open angle glaucoma.
1230 Pharmacology
Perfusion, Clotting, Fluid and Electrolyte
39. Potassium-sparing diuretics are weaker than thiazide and loop diuretics and act primarily
in the collecting duct renal tubule.
Spironolactone/Potassium-Sparing Diuretic
Concept/Action/Use
Assessment
Patient
Problem/Planning
Nursing
Interventions/Patient
Teaching
Elimination
Assess
Elimination, fluid
Monitor urinary output.
Block action of
baseline vital overload,
Record vital signs and report
aldosterone to
signs, urine
abnormal
abnormal changes.
promote
output,
electrolyte levels. Observe for signs and
sodium/water
edema, and
Patient blood
symptoms of hyperkalemia
excretion and
serum
pressure will
(nausea, diarrhea,
potassium
electrolytes. decrease and/or
abdominal cramping, leg
retention. Treat
Assess
patient will have
cramps, numbness and
edema, HTN, heart
history of
decreased edema. tingling hands and feet,
failure,
medications
Patient will have
peaked T-wave, and
hypokalemia,
and herbal
normal
oliguria).
hyperaldosteronism. supplements. electrolyte levels. Administer spironolactone in
the morning to avoid
nocturia.
Advise patients with high
serum potassium levels to
avoid foods high in
potassium.
Evaluation
Evaluate for
decreased blood
pressure, decreased
edema, and normal
electrolyte levels.
40. Hypertension (HTN) is an increase in BP above 140/90.
41. Nonpharmacological treatment of HTN include stress-reduction techniques, exercise, salt
restriction, decreased alcohol ingestion, and smoking cessation.
42. Guidelines for HTN determination are set by joint national committee on prevention,
detection, and reduction of high blood pressure (JNC 8, 2017).
43. Six categories of antihypertensives are diuretics, sympatholytic, direct-acting arteriole
vasodilator, ACE inhibitor, ARB’s, and CCB.
44. Five categories of sympatholytic are beta adrenergic blocker, centrally acting alpha2
agonists, alpha adrenergic blocker, adrenergic neuron blocker, alpha 1 and beta1 blockers.
45. Beta-adrenergic blockers reduce cardiac output by diminishing the SNS response.
Metoprolol/Beta Blocker
Concept/Action/Use Assessment
Perfusion
Block beta1
receptor sites,
Baseline VS.
Health and
drug history.
Patient
Nursing
Problem/Planning Interventions/Patient
Teaching
Hypertension,
Monitor vital signs.
fatigue.
Monitor laboratory
results, especially BUN,
Evaluation
Evaluate for decreased
blood pressure, and
1230 Pharmacology
reduce cardiac
output by
diminishing
sympathetic
nervous system
response.
Treat heart failure,
HTN, acute
myocardial
infarction, and
angina.
Monitor
cardiac
enzymes
Perfusion, Clotting, Fluid and Electrolyte
Patient will have
decreased blood
pressure and
comply with
medication
regimen.
serum creatinine, AST,
and LDH.
Do not abruptly stop
taking beta blockers as
rebound hypertension
may result.
Advise patients to avoid
over-the-counter drugs
without first checking with
a health care provider.
Advise patient to wear a
medic alert.
adherence to medication
regimen.
46. Centrally acting alpha2 agonists decrease sympathetic activity, increase vagus activity,
decrease cardiac output, and decrease serum epinephrine, norepinephrine and renin
resulting in reduced peripheral vascular resistance and increased vasodilation.
47. Alpha-adrenergic blockers result in vasodilation and decreased blood pressure.
Prazosin hydrochloride/Alpha-Adrenergic Blocker
Concept/Action/Use Assessment
Patient
Nursing Interventions/Patient
Problem/Planning Teaching
Evaluation
Perfusion
Dilate peripheral
blood vessels by
blocking alpha1
adrenergic
receptors.
Treat hypertension.
Hypertension,
fatigue.
Patient will have
decreased blood
pressure and
comply with
medication
regimen.
Evaluate for
decreased blood
pressure, and
adherence to
medication regimen.
Baseline VS.
Health and
drug history.
Monitor vital signs.
Check daily for fluid retention
in extremities and weight
gain.
Advise patients to comply
with the drug regimen.
Advise patient not to take
OTC cough and cold
medications without first
contacting their provider.
Inform patients that
orthostatic hypotension may
occur.
Teach patient to monitor
daily weights.
48. Adrenergic neuron blockers are potent antihypertensive that block the release of
norepinephrine.
49. Alpha1 and Beta1 adrenergic blockers block both receptors and cause vasodilation which
decreases resistance to blood flow.
1230 Pharmacology
Perfusion, Clotting, Fluid and Electrolyte
50. Direct-acting arteriole vasodilators are potent antihypertensive by relax smooth muscle of
the blood vessels.
51. Angiotensin-converting enzyme inhibitor (ACE) prevent the formation of angiotensin II
and the release of aldosterone.
52. The primary SE of ACE inhibitor is constant irritated cough.
53. Angiotensin II receptor blocker (ARB) also prevent the release of aldosterone.
Valsartan/Angiotensin ll-Receptor Blocker (ARB)
Concept/Action/Use Assessment
Patient
Nursing Interventions/Patient
Problem/Planning Teaching
Evaluation
Perfusion.
Act on renin–
angiotensin–
aldosterone system
Block angiotensin II
and prevent release
of aldosterone.
Treat HTN and
heart failure.
Hypertension,
fatigue.
Patient will have
decreased blood
pressure and
comply with
medication
regimen.
Evaluate for
decreased blood
pressure, and
adherence to
medication regimen.
Baseline VS.
Health and
drug history.
Monitor vital signs.
Check daily for fluid retention
in extremities and weight
gain.
Advise patients to comply
with the drug regimen.
Inform patients that
orthostatic hypotension may
occur.
Teach patient to monitor
daily weights.
Do not abruptly stop taking as
rebound hypertension may
result.
Medication may cause harm
to fetus.
Dizziness and
lightheadedness common
during initial therapy.
Monitor for angioedema.
Teach patient to avoid foods
high in potassium.
54. Direct renin inhibitors cause a reduction both angiotensin I and II and aldosterone.
55. CCB’s promote vasodilation.
Amlodipine/Calcium Channel Blocker
Concept/Action/Use Assessment
Patient
Nursing Interventions/Patient
Problem/Planning Teaching
Evaluation
Perfusion
Inhibits influx of
calcium across
vascular smooth
muscle cell
Hypertension,
fatigue.
Patient will have
decreased blood
pressure and
Evaluate for
decreased blood
pressure, and
adherence to
medication regimen.
Baseline VS.
Health and
drug history
Monitor vital signs.
Check daily for fluid retention
in extremities and weight
gain.
1230 Pharmacology
membrane to
promote
vasodilation.
Treat HTN and
heart failure.
Perfusion, Clotting, Fluid and Electrolyte
comply with
medication
regimen.
Advise patients to comply
with the drug regimen.
Inform patients that
orthostatic hypotension may
occur.
Teach patient to monitor daily
weights.
Monitor for angioedema.
Pt avoid alcohol increases
hypotension, caffeine
increases catecholamine
levels, and tobacco causes
vasoconstriction.
56. Define the following:
a. Thrombus formation of a clot in a blood vessel
b. Embolus a blood clot moving thru the bloodstream.
c. Anticoagulants prevent formation of blood clot in circulation.
d. Antiplatelet prevents platelet aggregation.
e. Thrombolytic breaks up clots that have formed.
57. Anticoagulants help prevent venous problems deep venous thrombosis (DVT) and
pulmonary embolism (PE) as well as arterial problems coronary thrombosis, myocardial
infarction (MI), artificial cardiac valves, and cerebrovascular accident (CVA).
Heparin/Anticoagulant
Concept/Action/Use Assessment
Patient
Nursing Interventions/Patient
Problem/Planning Teaching
Evaluation
Perfusion/Clotting
Bind with
antithrombin III
Inhibit action of
thrombin.
Inhibit conversion
of fibrinogen to
fibrin.
Inhibit clot
formation.
Prevent venous
thrombosis.
Bleeding,
dehydration,
tissue injury
Patient’s PTT and
aPTT will be in
therapeutic range
and patient free of
side effects.
History of
bleeding
disorders.
Baseline VS.
Health and
drug history
PTT and
aPTT
Monitor PTT and aPTT before
administering heparin.
Examine patient’s nose,
mouth, skin (especially older
patients), urine for bleeding.
Check stool for occult blood.
Keep antidote protamine
sulfate on hand.
Teach patient to inform
dentist when taking an
anticoagulant.
Advise patient to use a soft
toothbrush to prevent
bleeding gums.
1230 Pharmacology
Perfusion, Clotting, Fluid and Electrolyte
Warfarin/Oral anticoagulant
Concept/Action/Use Assessment
Patient
Nursing Interventions/Patient
Problem/Planning Teaching
Evaluation
Perfusion/Clotting
Inhibit clot
formation.
Inhibit hepatic
synthesis of vitamin
K, thus affecting the
clotting factors II,
VII, IX, and X
Prevent venous
thrombosis.
Bleeding,
dehydration,
tissue injury
Patient’s INR will be
in therapeutic range
(2-3) and patient free
of side effects.
History of
bleeding
disorders.
Baseline VS.
Health and
drug history
INR
Monitor INR therapy.
Examine patient’s nose,
mouth, skin (especially older
patients), urine for bleeding.
Check stool for occult blood.
Keep antidote Vitamin K on
hand. May need Fresh Frozen
Plasma for hemorrhage.
Teach patient to inform
dentist when taking an
anticoagulant.
Advise patient to use a soft
toothbrush to prevent
bleeding gums.
Advise patient to use a safety
razor.
Advise patient to wear a
medic alert tag.
Advise patient to check with
provider when using OTC
medications and not to use
aspirin, it will increase
bleeding risk.
Patient should eat consistent
amounts of Vitamin K
containing foods.
Teach patient for any cut or
injury apply direct pressure
for a minimum of five to ten
minutes with clean dry
absorbent material.
58. Heparin increases clotting time by combining with antithrombin III and inactivating
thrombin.
59. Lab test to monitor heparin is PTT and a PTT and the antidote for heparin is protamine
sulfate.
60. Low molecular weight heparin (LMWH) produces more stable anticoagulant responses.
61. Oral anticoagulants inhibit hepatic synthesis of vitamin K.
1230 Pharmacology
Perfusion, Clotting, Fluid and Electrolyte
62. Lab test to monitor warfarin is PT or INR and the antidote for warfarin is vitamin K.
63. Antiplatelets are used to prevent MI, stroke, and transient ischemic attack (TIA)
Clopidogrel/Antiplatelet
Concept/Action/Use Assessment
Patient
Nursing Interventions/Patient
Problem/Planning Teaching
Evaluation
Perfusion/Clotting
Suppress platelet
aggregation.
Prevent arterial
thrombosis with
unstable angina,
AMI, stroke, TIA
Bleeding, tissue
injury
Patient will be free of
subsequent
thromboembolism
and without side
effects.
History of
bleeding
disorders.
Baseline VS.
Health and
drug history
May take with aspirin.
Stop meds 7 days before
surgery.
Do not use with hx of peptic
ulcer disorder, active
bleeding, or intracranial
hemorrhage.
Ginger, garlic, ginkgo,
feverfew, and green tea my
increase bleeding.
64. Thromboembolism is occlusion of artery or vein that results in ischemia and necrosis.
65. Thrombolytics are used for AMI, PE, DVT, noncoronary arterial occlusion, and
thrombolytic stroke.
Alteplase/Thrombolytic
Concept/Action/Use Assessment
Patient
Nursing Interventions/Patient
Problem/Planning Teaching
Evaluation
Perfusion
Bind to fibrin
promoting
conversion of
plasminogen to
plasmin which
digests fibrin in a
clot and degrades
fibrinogen,
prothrombin, and
other clotting
factors
disintegrating clots.
Disintegrate clots
and restore
perfusion due to
AMI, PE, DVT,
thrombolytic stroke
Bleeding, tissue
injury
Clot dissolved and
perfusion restored
History of
bleeding
disorders.
Baseline VS.
Health and
drug history
Monitor vital signs, increased
pulse and decreased BP may
indicate hemorrhage and
shock. VS every 15 min for
first hour, every 30 min for 8
hours and then hourly for 24
hours total.
Observe for signs and
symptoms of active bleeding.
Have antidote aminocaproic
acid on hand.
Observe for signs of allergic
reaction to thrombolytics,
itching, hives, flushing, fever,
dyspnea, bronchospasm,
hypotension, and/or
cardiovascular collapse.
Avoid administering aspirin or
NSAIDs for pain or discomfort
1230 Pharmacology
Perfusion, Clotting, Fluid and Electrolyte
when receiving a
thrombolytic.
Monitor ECG for reperfusion
or dysrhythmias.
Avoid venipuncture/arterial
sticks.
66. Define the following:
a. Hyperlipidemia excess of one or more lipids in the blood stream
b. High-density lipoprotein ‘good’ cholesterol, smallest and densest lipoprotein
removes excess cholesterol from bloodstream.
c. Low-density lipoprotein ‘bad’ cholesterol, 50-60% fat increases risk of CAD
d. Very-low-density lipoprotein mostly triglycerides
e. Chylomicrons large particles of fatty acids and cholesterol
67. Nonpharmacological cholesterol lowering methods include low fat diet, lean meat, lose
weight, exercise, smoking cessation.
68. Antihyperlipidemic include five types of bile-acid sequestrants, fibrates, nicotinic acid,
cholesterol absorption inhibitors, hepatic 3-hydroxy-3-methylglutaryl-coenzyme A
(HMG-CoA) reductase inhibitors or statins.
Atorvastatin/Antihyperlipidemic
Concept/Action/Use Assessment
Patient
Nursing Interventions/Patient
Problem/Planning Teaching
Evaluation
Perfusion
Inhibit HMG-CoA
reductase enzyme
in the liver.
Hyperlipidemia
Ischemia, nausea,
and vomiting,
decreased visual
acuity,
hyperglycemia
Patient cholesterol
level will be within
normal limits without
side effects.
Baseline VS
Health and
drug history
Liver
function.
Monitor the patient’s blood
lipid levels.
Monitor lab values for liver
function.
Observe for signs and
symptoms of GI upset.
Emphasize drug compliance
and inform patient that it may
take several weeks before
blood lipid levels decline.
Instruct patient to have
annual eye examinations and
report changes in visual
acuity.
Encourage patient to report
any unexplained muscle
tenderness or weakness that
may be caused by
rhabdomyolysis.
Do not stop abruptly, may
cause serious rebound that
1230 Pharmacology
Perfusion, Clotting, Fluid and Electrolyte
could lead to acute
myocardial infarction and
possible death.
69. Peripheral arterial disease (PAD) is a form of peripheral vascular disease (PVD)
characterized by numbness and coolness of extremities, claudication causes pain and
weakness of a limb when walking and possible leg ulcers.
Cilostazol/Vasodilator and antiplatelet
Concept/Action/Use Assessment
Patient
Nursing Interventions/Patient
Problem/Planning Teaching
Evaluation
Perfusion
Causes peripheral
vasodilation.
Inhibits platelet
aggregation.
Peripheral vascular
disease and
intermittent
claudication
Ischemia,
hypotension,
discomfort,
decreased visual
acuity,
hyperglycemia
Improved perfusion
in extremities with
decreased pain
without side effects.
Baseline VS
Health and
drug history
Signs and
symptoms
inadequate
perfusion in
extremities:
pallor, pain,
coldness in
extremities
Monitor vital signs, especially
blood pressure and heart rate.
Inform patient that a desired
therapeutic response may
take 1.5 to 3 months.
Advise patient not to smoke
(causes vasospasms) or ingest
alcohol (increases
hypotension).
Encourage patient to change
position slowly but frequently
to avoid orthostatic
hypotension.
Instruct patient not to take
aspirin or other salicylates as
they may increase antiplatelet
activity.
Patient should report flushing,
headaches, and dizziness.
May be take with food of GI
upset occurs.
70. Pentoxifylline is a hemorheological agent or blood viscosity reducer agent that improves
microcirculation and tissue perfusion in patients with intermittent claudication or
Buergers disease.
71. Intracellular fluid (ICF) is fluid inside the cells.
72. Extracellular fluid (ECF) is fluid outside the cell, interstitial, intravascular and
transcellular.
1230 Pharmacology
Perfusion, Clotting, Fluid and Electrolyte
73. The major intracellular cation is potassium.
74. The major extracellular cation is sodium.
75. Define the following:
a. Osmosis movement of water across a semipermeable membrane from low
concentration to high concentration
b. Diffusion movement of molecules from low concentration to high concentration
c. Hydrostatic pressure force of fluid within a compartment
d. Osmolality number of particles dissolved in serum.
e. Active transport needs energy to move substances across cell membrane.
f. Tonicity measurement of the concentration of IVF
g. Isotonic approximately same osmolality as ECF or plasma (fluid replacement
stays in vascular space)
h. Hypotonic less osmotic pressure than ECF (moves fluid into cells)
i. Hypertonic greater osmotic pressure than ECF (moves fluid out of cells and into
vascular system)
j. Crystalloid solution of fluid and electrolytes that move across capillary walls.
k. Colloid solution contains protein or large molecules that increase oncotic pressure
and pull fluid into vascular system.
76. Potassium is essential for electrical activity and muscle contraction.
77. Signs and symptoms of hypokalemia fatigue, muscle weakness, anorexia, N/V severe:
paresthesia, leg cramps, confusion rhabdomyolysis, myoglobinuria, ventricular
dysrhythmias, cardiac arrest, flat or inverted T-waves.
78. Signs and symptoms hyperkalemia cardiac dysrhythmias, tachycardia followed by
bradycardia, paresthesia of face tongue hands and feet, nausea, diarrhea, abdominal
cramping.
Potassium
Concept/Action/Use Assessment
Patient
Nursing Interventions/Patient
Problem/Planning Teaching
Evaluation
Electrolyte balance
Nerve conduction
and muscle
contraction
Correction of
potassium deficit
Hypokalemia
Fluid imbalance
K+ level will
normalize with
normal ECG and
without side effects.
Baseline VS
Health and
drug history
If patient is
on digoxin
check for
digoxin
toxicity (low
K+ levels
enhance the
action of
digoxin).
Signs and
symptoms
hypokalemia
Give oral K+ with at least 8 oz
water or juice.
Administer K+ containing IV
solutions via a calibrated
infusion pump. Monitor ECG
during infusions.
IV K+ must be diluted with
100 to 1000 mL and infused at
a rate of no more than 10
mEq per hour.
Never give K+ IM, IV push or
IV bolus: rapid infusion may
result in cardiac arrest.
1230 Pharmacology
Perfusion, Clotting, Fluid and Electrolyte
and
hyperkalemia
Monitor renal function and
urine output, below 25 mL per
hr may lead to hyperkalemia.
Monitor IV site closely,
infiltration may lead to tissue
necrosis.
Monitor K+ levels frequently.
Monitor and teach patient
sings and symptoms
hypokalemia nausea and
vomiting, polyuria, abdominal
distention, muscle weakness,
cardiac dysrhythmias.
Monitor and teach patient
hyperkalemia oliguria,
abdominal cramps,
tachycardia, nausea,
numbness tingling in
extremities.
Teach patient K+ in diet.
79. Sodium plays a major role in fluid volume balance and plasma osmolality.
80. Signs and symptoms hyponatremia muscle weakness, decreased DTR, headache,
lethargy, confusion, seizures, coma abdominal cramps, N/V, tachycardia pale skin
hypotension.
81. Signs and symptoms hypernatremia dry sticky mucous membranes flushed dry skin,
agitation increased body temp, dry tongue, N/V, anorexia, tachycardia, hypertension,
muscle twitching, hyperreflexia, seizures coma.
82. Calcium promotes nerve and muscle contraction.
83. Signs and symptoms of hypocalcemia anxiety irritability, tetany, hyperactive DTR,
spasms hands, wrists, feet, ankles, positive Chvostek’s and Trousseau, laryngeal spams,
cardiac dysrhythmias.
84. Signs and symptoms hypercalcemia fatigue, muscle weakness, depressed DTR,
confusion, memory impairment, anorexia, N/V constipation kidney stones.
Intravenous Calcium
Concept/Action/Use Assessment
Patient
Nursing Interventions/Patient
Problem/Planning Teaching
Evaluation
Electrolyte balance.
Weight loss,
decreased
sensation in
Calcium level will
normalize with
Baseline VS
Health and
drug history
Monitor serum total calcium
and ionized calcium levels.
1230 Pharmacology
Nerve conduction
and muscle
contraction
Calcium deficit
Perfusion, Clotting, Fluid and Electrolyte
Assess for
signs and
symptoms
hypocalcemia
and
hypercalcemia
Assess for low
albumin levels
which
decrease total
calcium levels.
If patient is on
digoxin,
elevated
calcium levels
can enhance
digoxin
action.
upper
extremities,
reduced motor
function
Monitor vital signs and report
abnormal findings.
Monitor IV closely IV
infiltration can cause tissue
necrosis.
Monitor ECG during IV
infusions.
Calcium chloride
concentrations greater than
20 mg per mL should be given
in a central line and at a rate
of no more than 1 mg per 10
minutes.
Check for IV compatible
solutions, NS, D5W and
D10W.
Oral forms need Vit D and
should be taken with meals
to reduce GI distress.
Chronic use of calcium
antacids can cause
constipation.
Monitor and teach patients
signs and symptoms
hypocalcemia tetany, muscle
cramps, numbness and
tingling hands and feet,
bleeding and cardiac
dysrhythmias.
Monitor and teach patient
signs and symptoms of
hypercalcemia flabby
muscles, pain over bony
areas, kidney stones
normal ECG and
without side effects.
85. Magnesium promotes transmission of neuromuscular impulses.
86. Signs and symptoms of hypomagnesaemia tetany like hyperexcitability ventricular
tachycardia, Vfib and hypertension.
87. Signs and symptoms hypermagnesemia lethargy, drowsiness, weakness, paralysis, loss of
DTR, hypotension, heart block.
88. Chloride is a major contributor to acid-base balance.
89. Signs and symptoms of hypochloremia tremors, twitching slow shallow breathing.
90. Signs and symptoms of hyperchloremia weakness lethargy deep rapid breathing
unconsciousness.
91. Phosphorus is essential in bone and teeth formation and neuromuscular activity.
1230 Pharmacology
Perfusion, Clotting, Fluid and Electrolyte
92. Signs and symptoms of hypophosphatemia fatigue, muscle weakness, depressed DTR,
confusion, hyperventilation, anorexia, N/V constipation
93. Signs and symptoms hyperphosphatemia tetany, hyperactive DTR, spasms hands, wrists,
feet, ankles, positive Chvostek’s and Trousseau, tachycardia nausea diarrhea abdominal
cramps.
References
McCuistion, L. E., Vuljoin-DiMaggio, K., Winton, M. B., & Yeager, J. J. (2021). Pharmacology (10th
ed.). St Louis, MO: Elsevier.
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