PHARMACOLOGY NCM 106

Pharmacology | Facilitator: Marichelle Merioles October 20, 2021

Cebu Doctors’ University College of Nursing
2F: CARDIOVASCULAR DRUGS
CARDIOVASCULAR SYSTEM - The cardiac impulse normally originates in the
Composed of: sinoatrial node located in the posterior wall of the
1. Heart right atrium
2. Blood vessels
a. Arteries Sinoatrial node
- Pacemaker
b. Veins
- Regulates the heartbeat which is approximately 60
3. Blood flow
80 beats per minute in normal adult
Chambers
Atrioventricular node
1. Right and left atria
- Located in the posterior right of the intra-atrial
2. Right and left ventricles
septum and has a continuous tract fibers called
Right atrium bundle of hees or the AV bundle
- Receives deoxygenated blood from circulation - Has an adult rate of 40 to 60 beats per minute
- If the SA node fails the av node takes over as the
Right ventricle pacemaker → slower heartrate
- Pumps blood through pulmonary artery to the
lungs for gas exchange Blood
- Blood is composed of plasma, red blood cells, white
blood cells, and platelets
Left atrium
- Function – provide nutrients including oxygen to
- Receives oxygenated blood the body cells
- Most of the oxygen is carried on the hemoglobin of
Left ventricle RBC or
- Pumps blood into the aorta for systemic circulation
White blood cells
Myocardium - Major defense mechanism of the body
- Heart muscle that surrounds ventricles an atria - Engulfs microorganisms
- Produces antibodies
Ventricles
- Thick walls, most especially the left ventricle to Platelets
produce a muscular force needed to pump blood to - Large cells
the pulmonary and syst. Circulations - Cause blood to coagulate

Atria
- Thin walls
- Less pumping action and receive blood from the
circulation and lungs

2 arteries
- Right coronary artery – supplies blood to the right
atrium on both entricles of heart
- Left coronary artery – supplies blood to the left
atrium and both ventricles of heart
Blockage to one of these arteries → myocardial infarction
or heart attack

Myocardium
- Capable of generating and conducting its own
electrical impulses
 CLASSIFICATION OF MEDICATION: CARDIAC ▪ An 80-year-old woman may have
GLYCOSIDE a BNP of 168 mg/mL
- Digitalis glycoside o BNP is higher (400 mcg/mL) in patients
- Obtained from the purple and white fox glove plant with heart failure
- Treats heart failure or congestive heart failure o A more sensitive test than ANP for
(CHF) diagnosing heart failure

HEART FAILURE 1st line of drugs for ACUTE HEART FAILURE

Inotropic agents
- When the heart muscle or myocardium weakens
(1) Dopamine
and enlarges, it loses its ability to pump blood
(2) Dobutamine
through the heart and into the systemic circulation
Phosphodiesterase inhibitors
- Called pump failure or chronic heart failure
(1) Milrinone
- When compensatory mechanisms fail and the
peripheral and lung tissues are congested → acute
Secondary drug for Heart
heart failure
Failure
Causes Digoxin
1. Chronic hypertension
2. Myocardial infarction Naturally occurring cardiac glycosides are found in a
3. Coronary artery disease number of plants including digitalis. Thus, they are also
4. Valvular heart disease called digitalis glycosides
5. Congenital heart disease
6. Arteriosclerosis
MECHANISM OF ACTION
Signs and symptoms of heart failure
Dependent on the side of the heart affected Inhibits sodium potassium pump → increase in intracellular
Left sided sodium → influx of calcium → cardiac muscle fibers
- Shortness of breath contract more efficiently
- Dyspnea
3 effects on heart muscle
Right sided
1. Positive inotropic
- Peripheral edema
a. Increases myocardia contraction stroke
volume
Laboratory tests for heart failure 2. Negative chronotropic
- Elevated Atrial Natriuretic Hormone (ANH) or a. Decreases heart rate
peptide i. Monitor heart rate of patient
o Confirms heart failure 3. Negative dromotropic
o ANH is secreted from the atria of e heart a. Decreases conduction of heart cells
and acts as an antagonist to renin and i. Increase in myocardial
aldosterone contractility strengthens cardiac
o Released during expansion of atrium then peripheral and kidney function by
it produces vasodilation and increases enhancing cardiac output,
glomerular filtration rate decreasing preload, improving
o Results: blood flow to the periphery and
▪ Large volume of urine that kidneys, decreasing edema, and
decreases blood volume and promoting fluid excretion. As a
pressure result, fluid retention in the lungs
o Normal: 20-77 pg/mL or ng/L and extremities is decreased
- Brain natriuretic peptide (BNP)
o Desired value – less than 100 pg/mL
o Positive of heart failure > 100 pg/mL Cardiac Glycoside treats the ff. conditions:
o BNP is higher than 100 microgram per ml
Atrial fibrillation
in women who are 65 years of age or older

MABALOT, BETONIO, ESCABAS 2

BSN2-E
 - Cardiac dysrhythmia with rapid uncoordinated yellow vision dizziness, weakness,
contractions of atrial myocardium confusion
Adverse Bradycardia, cardiac dysrhythmia,
Atrial flutter Effects thrombocytopenia
- Cardiac dysrhythmia with rapid contractions of S/S for Anorexia, diarrhea, nausea and
200-300 beats per minute toxicity vomiting, bradycardia (< 60 beats/min,
Oreature ventricular contraction
DIGOXIN cardiac dysrhythmia, headache,
- Cardiac glycoside malaise, blurred vision, visual illusions
- Treats heart failure and atrial fibrillation (can see white, green, or yellow halos
- Contraindicated to patients with ventricular around objects), confusion, delirium
fibrillation
- Thyroid dysfunction can alter the metabolism of
cardiac glycosides Nonpharmacologic measures for heart failure
o Pts with hypothyroidism → dose 1. Limit salt intake to 2 grams per day or 1 teaspoon
decreased per day
o Hyperthyroidism → dose increased 2. Alcohol should be decreased to 1 drink per day or
- Orally/IV completely avoided
3. Fluid intake may be restricted
Toxic effects of digoxin 4. Smoking should be avoided
- Older adults – prone to toxicity 5. Obese patients should modify their unhealthy
- Phenytoin and lidocaine – treat digoxin-induced behaviors
ventricular dysrhythmia 6. Saturated fat intake should be decreased
- Serum digoxin levels should be closely monitored 7. Mild exercise (walking or bicycling) is
and s/s of digoxin toxicity should be reported recommended
promptly to the health care provider
- Digitalis toxicity or digoxin toxicity may result in 1st ASSESSMENT
degree/2nd degree/complete heart block 1. Drug and herbal history
- ANTIDOTE: digoxin immune fab or Digifab a. Make sure that the medication the patient
o Treats severe digitalis toxicity is taking will not the decrease the
o Agent binds with digoxin to form complex potassium of the patient
molecules that can be excreted in the 2. Baseline pulse rate
urine. Thus, digoxin is unable to bind at the a. Apical pulse rate – taken for 1 full minute
cellular site of action and > 60 beats per minute
- When taken concurrently with potassium diuretic i. This is because digoxin/cardiac
(Furosemide) or Cortisone = digitalis toxicity glycoside in general has a
o What is common among furosemide or negative chronotropic effect,
cortisone = potassium loss → hypokalemia which means that it can decrease
or decreased level of potassium → heart rate
increases effects of digoxin in the ii. If patient has 58 beats/min and
myocardial cell site of action → digitalis the digoxin was still given → it will
toxicity decrease the heart rate of patient
which is fatal
Values to remember: b. How to assess?
Half-life 30-40 hours i. Use a stethoscope and place it
Therapeutic serum level 0.8-2.0 ng/mL close to the heart rate
(dysrhythmia) 3. Assess s/s if digitalis toxicity
Therapeutic serum level 0.5-1.0 ng/mL
(heart failure)
Note: monitor therapeutic level of medication
INTERVENTIONS
Side Effects Anorexia, vomiting, nausea, diarrhea, - Do not administer if pulse rate is below 60
abdominal pain, headache, blurred or beats/minute
- Monitor serum digoxin level
MABALOT, BETONIO, ESCABAS 3
BSN2-E
 o Normal therapeutic drug - Unstable (periinfarction) angina
▪ 0.8-2.0 ng/mL – cardiac o Occurs frequrntly with progressive
dysrhythmia severity unrelated to acitivty and is
▪ 0.5-1.0 ng/mL – heart failure unpredictable regarding stress/exertion
- Monitor serum potassium level and intensity
o Normal – 3.5-5.0 mE1/L - Variant (prinzmetal, vasopastic)
o Report if hypokalemia is present (can lead o Occurs during rest
to digitalis toxicity) 1. First two types are caused by narrowing or partial
- Diet food should be high it potassium occlusion of coronary arteries
o Fresh and dried fruits 2. Variant angina is caused by vessel spasm
o Fruit juices 3. It is common for a patient to have both classic and
o Vegetables – potatoes variant angina

PHOSPHIDIESTERASE INHIBITORS
Instable angina often indicates an impending MI which is
- First line med for heart failure
an emergency that needs immediate medical intervention
- Under the positive inotropic group of drugs
o treats acute heart failure
- Example – Milrinone Lactate (high alert NONPHARMACOLOGIC MEASURES (PREVENTIVE) FOR
medication) ANGINA
o can cause patient harm when they are - Avoid heavy meals, smoking, extreme weather
used in error changes, strenuous exercise, and emotional upset
- MOA: increases stroke volume and cardiac output; - Proper nutrition
promotes vasodilation - Moderate exercise – only after consulting a HCP
- IV for no longer than 48-72 hours - Adequate rest and relaxation techniques

TYPES OF ANTIANGINAL DRUGS

1. Nitrates
OTHER AGENTS FOR HEART FAILURE
2. Beta-blockers
1. Vasodilators 3. Calcium channel blockers
2. ACE inhibitors
3. Angiotensin II-receptor antagonist/blockers
4. Diuretics (thiazides, furosemide) NITRATES
5. Spironolactone - Causes generalized vascular and coronary
6. Beta blockers (some only) vasodilation → increases blood flow to the
myocardial cells
ANTIANGINAL DRUGS - Reduces myocardial ischemia but can cause
Treats angina hypotension
- Sublingual route
ANGINA PECTORIS
- A condition of acute cardiac pain caused by Medications
inadequate blood flow to the myocardium due to
(1) Nitroglycerin
o Plaque occlusions within
(2) Isosorbide dinitrate
o Spasm of coronary artery
(3) Isosorbide mononitrate
- Decreased blood flow → decreased oxygen to
- Isosorbide dinitrate: Sublingual tablet form.
myocardium → pain
Chewable tablet immediate release, and sustain
- Severe angina pectoris – tightness, pressure in the
release tablet (capsule)
center of the chest, pain radiating down to the left
- Isosorbide mononitrate – given orally in
arm
immediate and sustained release tablets
- Angina attacks → myocardial infarction

Types
- Classic (stable angina)
o Occurs with predictable stress/exertion
Indications
Controls angina, acute myocardial infarction, hypertensive
emergency, pulmonary edema, and heart failure
Mechanism of Action

MABALOT, BETONIO, ESCABAS 4

BSN2-E
 - Acts directly on the smooth muscle of blood vessels
→ relaxation and dilation
Administration of medications
- Sublingual tablet is absorbed under the tongue
(must not be swallowed)
Medication is available in these forms:
- Available in topical, transdermal and patch,
translingual, oral extended-release capsule and
tablet, aerosol spray, and IV
• Transdermal patch – duration of action is 18-
24 hours and patch must be removed nightly
to allow 8-12 nitrate-free interval
Doses and important values
- Average prescribed dose following cardiac pain –
0.4 mg
- Effect of med lasts for 30-60 minutes
- Onset of action of:
o Sublingual route – 1-3 minutes
• Transdermal – 40-60 minutes
How to keep medications safe/secured:
- Tablet decomposes when exposed to heat and light
→ must be kept in their original airtight glass
containers
- Color of the bottle is brown to protect med from
light
Effects of the medication:
- After a dose of nitroglycerin, pt. may experience
dizziness, faintness, or headache as a result of
peripheral vasodilation
- Side effects
o Headache – most common
o Hypotension, dizziness, weakness, and
faintness
! CAUTION !
- For discontinuation of ointment and patch, it has to
be tapered over several weeks to prevent rebound
the effect of severe pain
- Reflex tachycardia may occur if the nitrate is given
too rapidly
- Beta blockers, calcium channel blockers,
vasodilation, and alcohol can enhance
hypotensive effect of nitrates
o Also check on what other meds patient is
taking
- IV nitroglycerin may antagonize the effects of
heparin
MABALOT, BETONIO, ESCABAS
BSN2-E
BETA-BLOCKERS
Basic facts about the medication:
- Blocks beta 1 and beta 2 receptor sites
o When beta 1 blocked → decreased HR
o Beta 2 → bronchoconstriction
- Decrease effects of the sympathetic nervous
system by blocking the action of catecholamines –
(epinephrine, norepinephrine) → decreases HR
and bp
- Used as antianginal, antidysrhythmic, and
antihypertensive drugs
- Beta blockers effective as antianginal because by
decreasing heart rate and myocardial contractility,
they reduce the need for oxy consumption and
consequently reduce anginal pain
Indications:
- Angina (classic or stable angina), dysrhythmia, and
hypertension
Examples
- Atenolol cardio selective → blocks beta 1
- Metoprolol tartrate cardio selective → blocks beta
1 → no bronchoconstriction
- Nadolol (noncardioselective)
- Propranolol HCl (noncardioselective → decreases
heart rate → bronchoconstriction
! CAUTION !
- For discontinuation, it must be tapered over 1-2
weeks
- Pts who have decreased heart rate and blood
pressure cannot take beta blockers
Values to remember:
- Onset of action for nonselective betablockers – 30
minutes
- Cardioselective
o 60 mins (atenolol),
o 30-60 mins for metonolol
Side/Adverse Effects
o Decreased heart rate and blood pressure
o Nonselective – bronchospasm, behavioral or
psychotic response and impotence (use of Inderal)
CALCIUM CHANNEL BLOCKERS
Examples
1. Amlodipine
2. Diltiazem HCl
3. Felodipine
4. Isradipine
5. Nicardipine HCl
5
 6. Nifedipine
7. Nisoldipine
8. Verapamil HCl
Basic facts about the medication:
- Used for TREATMENT OF ANGINA
- Treats angina since calcium activates myocardial
contraction → increasing workload of heart and
the need for oxygen → thus blocking the calcium
channel will prevent in increasing the workload of
heart and need for oxy
Mechanism of Action
- MOA – relaxes coronary spasm (variant angina)
and relax peri arterioles (stable angina →
decreasing cardiac demand
- Decrease cardiac contractility, afterload, and
peripheral resistance, and reduces the workload of
the heart → decreases need for oxy demand
- Ultimate effect – decreases cardiac oxygen
demand
Medication and its specific purpose:
Nifedipine
- Most potent
- Frequently given w antianginal drugs (nitrate) to
prevent angina
- Immediate release nifedipine is usually prescribed
in hospital for acute increase in blood pressure
since it is associated with increased incidence of
sudden cardiac death
- Side effects:
o Headache, hypotension, dizziness, flushing
of skin
o Reflex tachycardia as a result of
hypotension
o Peripheral edema
o Changes in liver/kidney function
MABALOT, BETONIO, ESCABAS
BSN2-E
Assessment
- Vital signs
- Drug and health history
Interventions
- Monitor vital signs
o Check blood pressure and heart rate most
especially if patient is taking a beta
blocker)
- Position the patient sitting or lying down when
administering nitrates for 1st time since it can cause
dizziness due to peripheral vasodilation
- Offer sips of water before giving SL nitrates since
dryness may inhibit drug absorption
- Monitor effects of nitroglycerin. Report angina
that persists
- Use tongue blades or gloves when administering
nitroglycerin ointment
Patient teaching
- Administer nitroglycerin tablet if chest pain occurs
o If pain has not subsided or is worsened in
5 minutes
- Don’t take alcohol while taking nitroglycerin →
increased hypotensive effect
- Report if tolerance to nitroglycerin has developed
- Do not discontinue beta and calcium channel
blockers without approval of HCP
- Stinging or biting sensation under the tongue after
SL nitroglycerin is taken → med is fresh
o Not present with newer tablets
- Store medication bottles away from light in its
original screw cap, amber glass bottle
- Nitroglycerin patch
o Applied 1x a day, rotate skin site, avoid
hairy areas
- Place patient in supine position wit legs elevated if
hypotension results from SL nitroglycerin
6
 PHARMACOLOGY NCM 106
Pharmacology | Facilitator: Marichelle Merioles October 20, 2021
Cebu Doctors’ University College of Nursing
PART 2
- Sotalol HCl
ANTIDYSRHYTHMIC DRUGS
- People who have cardiac dysrhythmia Mechanism of Action:
- Restores cardiac dysrhythmia - Decrease conduction velocity, automacity and
recovery time or refractory blockers
CARDIAC DYSRHYTHMIA
- Arrythmia Basic facts:
- Any deviation from the normal rate or pattern of - Beta blockers – frequently prescribed for
heartbeat (bradycardia/tachycardia/irregular) dysrhythmia over sodium channel blockers
- Dysrhythmia – disturbed heart rhythm - Gradually reduced in dose upon discontinuation
- Arrythmia – absence of rhythm
- Ventricular dysrhythmia – life threatening
CLASS III: DRUGS THAT PROLONG
o There is ineffective filling of ventricles +
ineffective pumping → decreased or
REPOLARIZATION
absent cardiac output → reduced blood to Examples
the brain and other vital organs → vital 1. Adenosine
organs will be deprived of oxy and other 2. Amiodarone HCl
nutrients 3. Dofetilide
4. Ibutilide
TYPES 5. Sotalol
1. Class I – Sodium channel blockers
2. Class II – beta blockers Used in emergency treatment of ventricular dysrhythmias
3. Class III – drugs that prolong repolarization when other antidysrhythmic are ineffective
4. Class IV – calcium channel blockers
CLASS IV: CALCIUM CHANNEL BLOCKERS
SODIUM CHANNEL BLOCKERS Examples
Examples 1. Verapamil HCl
- Disopyramide phosphate 2. Diltiazem
- Procainamide HCl
- Quinidine sulfate
Mechanism of Action
- Lidocaine
- Mexiletine HCl - Blocks calcium influx
- Flecainide o Once the calcium is blocked, it can
- Propafenone HCl decrease excitability and contractility of
the myocardium
Mechanism of Action:
Side Effects/Adverse Effects
- Decrease sodium inflex into cardiac cells
- Responses to these drugs are decreased Quinidine
conduction velocity in cardiac tissues - Nausea, vomiting, diarrhea, confusion,
- Suppression of automaticity, which decreases the hypotension; heart block, neurologic and
likelihood of ectopic fossil, and increased recovery psychiatric symptoms
time or reploarizatio or refractory period
- Can serve as an important mechanism by High dose of lidocaine
suppressing tachycardias that are caused by - Cardiovascular depression, bradycardia,
abnormal conduction hypotension, seizure, blurred vision and double
vision
CLASS II: BETA BLOCKERS
Examples Beta blockers
- Acebutolol HCl - Bradycardia
- Esmolol - Hypotension
- Propranolol HCl
 Indications
Assessment - Hypertension
- Health and drug history - Peripheral edema
- Vital signs and ECG - Primarily used for pts with normal renal function

Nursing Intervention Contraindications

1. Vital signs - Renal failure, symptoms of kidney impairment or
a. Hypotension may occur shut down including oliguria, elevated BUN, and
2. Administered rug by IV push or bolus over a period elevated creatinine
of 203 minutes or as prescribed - Not used to promote fluid loss to pts with severe
3. Monitor ECG abnormal patterns renal dysfunction and creatinine clearance greater
than 30 ml per minute bec effectiveness is greatly
Patient teaching decreased
- Take drug as prescribed
- Report side/adverse effects Basic facts:
- Avoid alcohol → intensify hypotensive reaction, - Causes loss of sodium potassium, magnesium
caffeine → increases catecholamine levels, and - Promotes calcium reabsorption
tobacco → vasoconstriction - Increases serum cholesterol, LDL and triglyceride
- Should be administered in the morning
DIURETICS
TWO PURPOSES ! CAUTION !
1. Decrease hypertension or lower blood pressure - Affects glucose tolerance → hyperglycemia
2. Decrease edema (peripheral/pulmonary) o Nursing intervention – monitor blood
glucose periodically
Basic description:
- Produces increased urine flow by inhibiting sodium Side/adverse effects
and water reabsorption in the kidney tubules - Electrolyte imbalance
- Must be administer in morning to avoid nocturia o Hypokalemia, hypercalcemia,
and sleep interruption hypomagnesemia, ad bicarbonate
▪ Why does hypokalemia develop?
Types of diuretic Thiazide and thiazide-like
1. Thiazide and thiazide-like drugs diuretics also excrete potassium
2. Loop (high-ceiling) which will lead to hypokalemia
3. Osmotic diuretic ▪ Why is there hypercalcemia?
4. Carbonic anhydrase inhibitors Diuretic will promote
5. Potassium-sparing diuretics reabsorption of calc
o Hyperglycemia
THIAZIDE AND THIAZIDE-LIKE DIURETICS ▪ Monitor blood glucose level of
- Ats on the distal convoluted renal tubule beyond patient
the loop of Henle to promote sodium chloride and o Hyperuricemia and hyperlipidemia
water excretion o Dizziness, headache, nausea, vomiting,
constipation, urticaria/hives, blood
dyscrasia
Examples
1. Chlorothiazide
2. Hydrochlorothiazide
Drug-to-Drug Interactions
3. Bendroflumethiazide with nadolol
4. Methyclothiazide - Thiazide + digoxin → digitalis toxicity
5. Chlorthalidone - Thiazide + lithium → lithium toxicity
6. Indapamide
7. Metolazone
Assessment
MABALOT, BETONIO, ESCABAS 8
BSN2-E
 - Assess vital signs, weight, urine output, and serum
chem values
o For weight, take it daily when patient takes
diuretics
▪ Taken before breakfast using
same clothes to accurately
determine weight of patient
- Check for presence of peripheral edema
- Sodium and water are lost together w potassium
calc and magnesium
- Affects blood glucose and increase uric acid level
- More potent than thiazide
Contraindications
- Not be described if thiazides can alleviate body
fluid excess

Nursing interventions Side effects/side effects

- Monitor vs and serum electrolytes - Electrolyte imbalance – hypokalemia,
- Observe for signs of hypokalemia (muscle hyponatremia, hypocalcemia, hypomagnesemia,
weakness, leg cramps, and cardiac dysrhythmia) and hypochloremia
- Patient’s weight gain
o We can evaluate effectiveness of diuretic
when upon eval the patient has lost weight Drug-to-Drug interactions
not gained weight - Loop diuretic + digoxin → digitalis toxicity
o If patient is taking diuretics and still gains
weight, inform physician immediately in Assessment
order for the medication to be evaluated - Drug history (daily)
further - Vital signs, serum electrolytes, weight, and urine
o If patient has a gain weight of 2.2 pounds output
→ 1 liter of body fluids o Baseline data

Patient teaching Interventions

- Instruct patient to slowly change position from
lying down to standing
o Dizziness might occur due to orthostatic
hypotension
- Check glucose level periodically
- Suggests pts to use sunblock in direct sunlight to
prevent photosensitivity
- Encourage to eat foods rich in potassium (fruits,
fruit juices and veg)
o Thiazide and thiazide like promote
excretion of potassium
- Take drug w food to avoid GI upset
- Monitor urinary output (at least 30ml or 600ml per
24 hours)
- Weigh patient to determine fluid loss or gain
- Vital signs
o Check bp before administering med
- Administer IV furosemide slowly since hearing loss
may occur if rapidly injected
- Observe ss of hypokalemia (muscle weakness,
abdominal distension, leg cramps, cardiac
dysrhythmia)
- Monitor serum potassium level since it is
potassium wasting

LOOP (HIGH-CELING) DIURETICS Teaching

- High ceiling since more effective
- Advise to take furosemide in the morning
- Acts on thick ascending loop of Henle to inhibit
- Rise slowly from lying or sitting to standing pos
chloride transport of sodium into the circ and
- Take furosemide w food to avoid nausea
inhibit passive reabsorption of sodium

OSMOTIC DIURETIC
Examples
- Increases osmolality or concentration and sodium
- Furosemide reabsorption in the proximal tubule and the loop of
- Bumetanide Henle
- Ethacrynic acid
- Torsemide
Examples
- Mannitol
Basic facts:
MABALOT, BETONIO, ESCABAS 9
BSN2-E
 Basic facts POTASSIUM SPARING DIURETIC
- Sodium chloride and potassium and water are Examples
excreted - Spironolactone
- Eplerenone
Contraindications - Amiloride HCl
- Caution to pts with heart disease and heart failure - Triamterene

Indications Basic facts

- Prevents kidney failure, decrease intracranial - Potassium sparing – potassium will not be
pressure (in cerebral edema) and decrease excreted from body so check serum potassium of
intraocular pressure (in glaucoma) patient

Mannitol
- Potent osmotic diuretic
- Could crystalize if exposed to low temp
o Vial should be warmed to dissolve crystals
- If there are crystals, do not administer the mannitol
Side/Adverse Effects
- Fluid and electrolyte imbalance
- Pulmonary edema
- Nausea, vomiting, tachycardia, acidosis
CARBONIC ANHYDRASE INHIBITORS
Examples
- Acetazolomide
- Methazolamide
These medications block the action of enzyme carbonic
anhydrase which is needed to maintain the body’s acid-base
balance
- Inhibition of this enzyme causes increased sodium
potassium and bicarbonate excretion
Basic facts
- Used primarily to decrease intraocular pressure in
pts with chronic open-angle glaucoma
! CAUTION !
- Prolonged use → metabolic acidosis
- Hemolytic anemia and renal calculi can occur
! CAUTION !
- If serum potassium is greater than 5 mEq/L, patient
should discontinue the potassium sparing diuretic
and food high in potassium
Drug-to-Drug Interactions
- Potassium sparing diuretics + ACE inhibitor →
hyperkalemia
Side/Adverse Effets
- Hyperkalemia – main side effect
- Headache dizziness weakness anorexia nausea
vomiting diarrhea hyperuricemia muscle cramps
numbness and tingling of hands and feet
Assessment
- Drug history
- Vital signs, serum electrolyte, weight and urinary
output
Nursing interventions
- Monitor urinary output
- Observe s/s of hyperkalemia
o This type of diuretic is potassium sparing,
meaning the potassium will be retained in
the body. So, check if level of potassium is
high
- Administer in the morning

Contraindictations Patient teaching

- Patients who are in their 1st trimester of pregnancy
Side/Adverse Effects
- Acetazolamide – fluid and electro imbalance,
metabolic acidosis, nausea, vomiting, anorexia,
confusion orthostatic hypotension, crystalluria
- Take with meals to avoid nausea
- Avoid exposure to sunlight because spironolactone
can cause photosensitivity
- Patient with high serum potassium must avoid food
rich in potassium when taking potassium sparing
diuretics
RECAP

MABALOT, BETONIO, ESCABAS 10

BSN2-E
 Thiazide and thiazide-like
- Some ends with “zide” Carbonic anhydrase inhibitor
- Loss of Na, K, Mg - Decreases intraocular pressure
- Reabsorbs ca - Pota wasting; loss of na2, k and hco3
o Check if patient has already developed - Not given during 1st trimester of pregnancy
hypercalcemia - Adverse reaction – hemolytic anemia
- Cause hyperglycemia, hyperuricemia and - Renal calculi may occur in taking this medication
hyperlipidemia
- Photosensitivity Potassium sparing diuretics
- Potassium will not be excreted
Loop (high-ceiling) o Nursing intervention – closely monitor the
- More effective than other diuretic potassium level of patient
- Example – furosemide o Watch out for hyperkalemia because k is
- Pota wasting, loss of Na, K, Ca, and Mg retained inside the body
- Can affect blood glucose and increase uric acid - Example – spironolactone (common in clinical area)
level - Discontinue if k is more than 5.0 mEq/L
- Should not be prescribed if thiazides can alleviate - Side effect – hyperkalemia
body fluid excess - Causes photosensitivity
- Administer IV furosemide slowly

Osmotic diuretic
- Decreases intracranial pressure and intraocular
pressure (ICP, IOP)
- Loss of Na, Ca, and K
o Potassium wasting
▪ Check level of potassium
- Example – mannitol (crystalizes if exposed to low
temp)
o Warm container first before administering
mannitol
- Pulmonary edema – SE

MABALOT, BETONIO, ESCABAS 11

BSN2-E
 PHARMACOLOGY NCM 106
Pharmacology | Facilitator: Marichelle Merioles October 20, 2021
Cebu Doctors’ University College of Nursing
PART 3 - ANTIHYPERTENSIVES

HYPERTENSION
- Increased in blood pressure SYMPATHOLYTICS
o BP is greater than 140/90 mmHg
- Most common condition Review
- Hypertension may also lead to myocardial
infarction, stroke, renal failure, and death - Adrenergic receptors has 4 main receptors: alpha
1, alpha 2, beta 1 and beta 2
- Risk factors
o Alpha 1 – located in blood vessels,e yes,
o Diet high in saturated fat and simple
bladder, prostate
carbohydrate
o Alpha 2 – located in the post-ganglionic
o Alcohol
sympathetic nerve endings
o Obesity
o Beta 1 – located in heart and some in
kidneys
NONPHARMACOLOGIC METHODS TO TREAT
o Beta 2 – located in lungs and arteries of
HYPERTENSION:
skeletal muscles
- Stress-reduction tech
- When alpha 1 is stimulated → arterioles/venules
- Exercise
- Salt restriction constrict → increased peripheral resistance →
- Decreased alcohol increased blood pressure
- Smoking cessation - Alpha 2 stimulated → decreases sympathetic
activities, increases vagus activity, decreases
MEDICATIONS: cardiac output, decrease serum epinephrine,
1. Diuretics norepinephrine and renin → reduced peripheral
2. Sympatholytic (sympathetic depressants) vascular resistance and increased vasodilation
a. Beta adrenergic blockers - When beta 1 stimulated → increased heart rate →
b. Centrally acting alpha2 agonists increased heart strength of
c. Alpha-adrenergic blockers contraction/contractility → increased blood
d. Adrenergic neuron blockers pressure
e. Alpha1 and beta1-adrenergi blockers - Beta 2 stimulated → bronchodilation
3. Direct acting arteriolar vasodilators
4. ACE inhibitors BETA ADRENERGIC BLOCKERS
5. Angiotensin II receptor blockers
6. Calcium channel blockers Mechanism of Action
- Called such because it blocks beta receptor sites
- Blocks beta 1 → HR slows and BP decreases
DIURETICS - Blocks beta 2 → when blocked, it will cause
bronchoconstriction
- Take note which of the medications are cardio-
Basic Facts:
selective. Cardioselective means that these
- Promotes sodium depletion which decreases medications would only block beta 1. However,
extracellular fluid volume since beta blockers are nonselective, then it will
o Whenever sodium goes, water follows block beta 1 and 2.
- Expels or excretes sodium out of the body and o If beta 2 is blocked →
water follows bronchoconstriction, which is not good
- Effective as 1st line drugs for treating mild ▪ Difficulty in breathing and
hypertension dyspnea – common symptoms of
bronchoconstriction
Medications:
- Hydrochlorothiazide
o Most common frequently diuretic for
controlling mild hypertension by Basic Facts
decreasing excess fluid volume - Reduces heart rate, contractility, and renin release
 o For people with elevated serum renin level - Prazosin + nitroglycerin → syncope

Examples Side effects/adverse reactions

- Acebutolol o Orthostatic hypotension, nausea,
- Atenolol headache, drowsiness, nasal congestion,
- Bisoprolol fumarate edema, and weight gain
- Carvedilol
- Metoprolol CENTRALLY ACTING ALPHA 2 AGONISTS
- Nadolol
- Pindolol Examples
- Propranolol - Methyldopa
- Clonidine
Carvedilol and propranolol – nonselective beta blockers o Orally
o Transdermal → 7 day duration of action,
Contraindications: replaced every 7 days
- Used in caution with pts with diabetes mellitus - Guanfacine
since noncardioselective medications inhibit the
ability of the liver glycogen to glucose in response ! CAUTION !
ot hypoglycemia - Beta blockers are not given with centrally acting
alpha 2 agonists because it can accentuate the
! CAUTION ! bradycardia
- Beta blockers must not be abruptly discontinued - Methyldopa and clonidine in high doses → sodium
and water retention
Side effects/adverse effects o Always administer w diuretics since
diuretics will excrete excess body fluids
- Decreased pulse rate, decreased bp, - Not abruptly discontinued → rebound
bronchospasm (those for nonselective) hypertension, but is less likely to occur w
- Dizziness, insomnia, fatigue nightmares and sexual guanfacine
dysfunction
Side Effects and AR
ALPHA-ADRENERGIC BLOCKERS
- Drowsiness, dry mouth, dizziness, and bradycardia
Mechanism of Action: ADRENERGIC NEURON BLOCKER
- Blocks alpha 1 receptrs on the vessels and
vasodilation and decreased bp will result Mechanism of Action
- Blocks NE release from the sympathetic nerve
Examples endings
- Doxazosin, prazosin, terazosin, phenoxybenzamine - Why block norepinephrine release?
HCl o Because it is Epinephrine and
Norepinephrine will stimulate receptor
Basic Facts sites, and one of the rec will be stimulates
Treats hypertension where patients have lipid is alpha 1 receptor (example), which will
abnormalities lead to vasoconstriction → high bp
- This type of med decreases VLDL and LDL (bad - When NE is blocked → decreased in NE release →
cholesterol and responsible for fatty plaques in the lowered blood pressure
arteries or arteriosclerosis) - Potent antihypertensive drugs

- Increases HDL (good cholesterol Examples:

- Reserpine – most potent drug used to control
Drug-to-Drug interactions: severe hypertension
- Prazosin + anti-inflammatory → peripheral edema

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 ALPHA 1 AND BETA 1 ADRENERGIC BLOCKERS

Mechanism of Action
- Blocked alpha 1 → decreased resistance to blood
flow → dec bp
- Blocked beta 1 → dec heart rate and
atrioventricular contractility → lowered bp

Example
- Labetolol HCl

Basic Facts:
- Stronger on alpha receptors than beta receptors
release of aldosterone (promotes sodium retention
! CAUTION ! and potassium excretion → Sodium is excreted
- When large doses are administered → blocks beta along w h2o and potassium is retained and lowers
2 which is not good because it will lead to increased peripheral resistance
airway resistance or bronchoconstriction →
dyspnea Examples
- Benazepril
DIRECT ACTING ARTERIOLAR - Captopril
- Enalapril maleate
VASODILATORS - Perindopril
- Ramipril
Mechanism of Action: - Moexipril – cannot be taken w food
- Function by relaxing the smooth muscle of the - All meds can be taken w food
blood vessel → vasodilation → BP decrease but
sodium and water are retained → NA and H2O Contraindications
retention → peripheral edema → diuretics can be - Should not be given during pregnancy → increased
given placental bloodflow
o This is to expel excess fluid - Not be given w spironolactone or pota-sparing
diuretic → hyperkalemia since this is due excretion
Examples of sodium, retention of potassium
- Hydralazine and minoxidil – for moderate to severe - Don’t take salt substitutes which contain
hypertension potassium → since person will be at risk of
- Nitroprusside – for acute hypertensive emergency hyperkalemia
- Dizziness and lightheadedness may occur during 1st
Side Effects/Adverse Reactions week of captopril therapy
- Tachycardia, palpitation, edema, nasal congestion,
headache, dizziness, GI bleeding, lupus-like ! CAUTION !
symptoms and neurologic symptoms - Don’t discontinue captopril → rebound
o Excess hair growth (minoxidil use) hypertension

Side Effects/Adverse Reactions

ANGIOTENSIN-CONVERTING ENZYME (ACE) - Constant, irritated cough – primary effect
INHIBITORS - Nausea, vomiting, diarrhea, headache, dizziness,
REVIEW RAAS (RENIN ANGIOTENSIN SYSTEM) fatigue, insomnia, hyperkalemia, and tachycardia

ANGIOTENSIN RECEPTOR BLOCKERS (ARBS)

Mechanism of Action:
- When ACE is inhibited → inhibits the formation of Basic Facts:
angiotensin (potent vasoconstrictor_ and blocks
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 - Similar to ACE inhibitors because they prevent the Examples
release of aldosterone (sodium retaining hormone) - Verapamil – treats chronic hypertension, angina
- ACE vs ARBs pectoris, and cardiac dysrhythmia
o Arbs – block angiotensin II from - Diltiazem HCl
angiotensin I receptors found in many - Amlodipine
tissues → vasodilation and dec. peripheral - Felodipine
resistance - Nicardipine
▪ Also do not cause constant - Nifedipine – immediate release of med is only
irritated cough administered in the hospital because it could lead
o ACE – inhibit angiotensin converting to sudden death
enzyme in the formation of angiotensin II - Nisoldipine
→
- Meds used for 1st line treatment for hypertension
Side Effects/Adverse Reactions
- Flushing, headache, dizziness, ankle edema,
Mechanism of Action:
bradycardia, atrioventricular block
- Act on the renin angiotensin aldosterone system or
RAAS
ASSESSMENT FOR ANTIHYPERTENSIVE MEDICATIONS
- Drug history (for drug-to-drug interaction)
Examples
- Vital signs (most especially blood pressure and
- Losartan heart rate → used as a parameter later on to
- Valsartan evaluate if med is effective or not)
- Irbesartan - Alpha-adrenergic blockers – check urinary output
- Candesartan because drug is contraindicated if renal disease is
- Olmesartan present
- Telmisartan
INTERVENTIONS
! CAUTION !
- Monitor Vital Signs
- Not used during pregnancy - Check daily for fluid retention and weight gain (if
person is receiving alpha adrenergic blockers and
DIRECT RENIN INHIBITOR also direct acting arteriolar vasodilators since it can
cause peri edema)
Mechanism of Action
- Binds with renin → reduction in angiotensin I and PATIENT TEACHING
II and aldosterone levels - Warn patient to rise slowly to avoid ortho hyper
- When patient is taking beta blocker, alert pts with
DM for possible hypoglycemic symptoms since this
Examples: med inhibits the conversion of glycol to glucose
- Examples: aliskiren - For beta blocker, medication can cause sexual
o Effective for mild to moderate dysfunction
hypertension - Teach on non-pharmacologic method to decrease
bp
CALCIUM CHANNEL BLOCKERS Alpha Adrenergic Blockers (Health Teaching)
- Inform male pts that impotence may occur due to
Mechanism of Action: high dose
- Slow calcium channels found in the myocardial of - Tell patient to report if edema is present
heart and vascular muscles - Encourage pts to decrease salt intake
- Free calcium → increases muscle contractility and
peripheral resistance and bp ACE inhibitors (Health Teaching)
- Calcium channel blockers → block calcium channel - Warn pts to not abruptly discontinue use of
in the vascular smooth muscle → vasodilation → captopril → rebound hypertension
dec bp

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 - Don’t take salt substitutes that contain k since they
are at risk of hyperkalemia
- Warn pregnant pts not to take ace inhibitors
- Explain that dizziness and lightheadedness may
occur during 1st week of captopril therapy
- Take captopril 20 minutes to 1 hour before meals
since food decreases 35% of captopril
- Warn patient that the taste of food may diminish
during 1st month of therapy
- Advise pts to prevent foods that are high in
potassium

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 PART 4 – ANTICOAGULANTS
- other one is for warfarin the antidote for that one
ANTICOAGULANTS is vitamin k
- Are medication that prevent the formation of clot - so just remember in war there is killing again in war
- They act prophylactically to prevent formation of there is killing so w and then k which also
new clots represents for warfarin and vitamin k
- an example of an anticoagulant is heparin
Drug-to-Drug interactions:
HEPARIN - Aspirin, NSAID, sulfonamide, phenytoin,
cimetidine, allopurinol & oral hypoglycemic can
Route of Administration displace warfarin from the protein bound site and
- SubQ – prophylaxis can cause more free-circulating anticoagulant (risk
- IV – acute thrombosis for toxicity)
- When we say thrombosis this refers to clot - can displace warfarin from the protein-bound site
formation and can cause more free circulating anticoagulant
- this medication is poorly absorbed orally that is - so when there is more free drug or more warfarin
why it is given subcutaneously or intravenously that will circulate in the bloodstream the danger
for that one is that the patient is at risk for toxicity
so with this being said make sure that the antidote
Basic Facts:
which is vitamin k is always available
- Prolong clotting time- meaning it delays the
clotting of the blood
Side Effects/Adverse Reactions
- Decreased platelet count causing
thrombocytopenia - Bleeding – major side effect for warfarin
- take note when a patient experiences heparin o Nursing responsibility: patient must be
toxicity the patient is given with the antagonist or closely monitored for signs of bleeding like
the antidote protamine sulfate. petechiae, ecchymosis, and hematemesis

ASSESSMENT
Antidote
- History of abnormal clotting- because this is used
- Protamine Sulfate
to establish the need for the administration of
anticoagulants
WARFARIN
- Gather history that include complementary and
alternative therapy- so that is to check for presence
Mechanism of Action of drug to drug interaction because it could be that
- Oral anticoagulant which inhibits hepatic synthesis there are medications that are taken concurrently
of Vitamin K (by mouth) of the patient which can either increase or
- Prolonged clot time decrease the effectivity of the medication.
- Treats thrombophlebitis and embolism formation
caused by atrial fibrillation

Antidote
- Vitamin K
TAKE NOTE:
- the antidote for heparin toxicity is protamine
sulfate and the antidote for warfarin toxicity is
vitamin k
- so how are you going to remember that one easily
in heparin take note it starts with letter h and for
protamine sulfate it starts with letter p
- You just need to remember in heaven there is
peace heaven starts with h and then peace starts
with p
INTERVENTIONS
- Vital signs
- Monitor Prothrombin Time or International
Normalized Ratio for Warfarin and Activated Partial
thromboplastin Time for heparin before
administering anticoagulant
- The international normalized ratio and activated
partial thromboplastin-will help in evaluating the
ability of the blood to form clots
- Examine patient’s mouth, nose (epistaxis), urine
(hematuria), and skin (petechiae, purpura) for
bleeding- so all of these are associated to bleeding

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 - Check stools for occult blood
- make sure when heparin and warfarin administer
to the patient the antagonist or the antidotes of the
medication should be also available
PATIENT TEACHING
- Use soft toothbrush
- Warn patients to shave with electric razor
- Encourage not to smoke → increased drug
metabolism which will require the increase of the
dosage of the medication
- Teach how to control external hemorrhage like
applying pressure to certain pressure points
- Advise patients to avoid large amounts of green
leafy vegetables
- also the patient must avoid broccoli, legumes,
soybean, coffee, tea, cola, excessive alcohol and
certain herbs and nutritional supplements: such as
co-enzyme q10 fish oil, substances high in vitamin
k saint, john's worth, ginseng, and vitamin c
because these foods and substances may decrease
the effectiveness of warfarin
- further for a patient taking warfarin he must also
avoid taking garlic, ginger, kavakava, green tea,
chamomile tea, ginkgo, biloba, and acute alcohol
intoxication because also these can decrease
warfarin effectiveness
ANTIPLATELET (ANTITHROMBOTICS)
- antiplatelet or antithrombotics
Basic Facts
- this medication prevents platelet aggregation the
same with anticoagulant the objective of this
medication is also to prevent formation of blood
clot however they just differ in their mechanism of
action
- for the anticoagulant it prolongs clotting time or it
slows down your body's process of making clots but
in this type of medication which is the anti-platelet
this prevents platelet aggregation
- again they have the same objective which is to
prevent the formation of blood clot but for the
antiplatelet this acts by preventing platelet
aggregation or clumping of the platelet
- Used for prophylactic use
EXAMPLES:
- aspirin
- cilostazole
- clopidogrel
- prasaugrel
- cangrelor
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Important values
TAKE NOTE: the most common medications in the
clinical area are aspirin and clopidogrel
RECAP:
- antiplatelets are used to prevent thrombosis or
formation of blood clots in the arteries by
suppressing platelet aggregation
- antiplatelets are mainly used for prophylactic in
prevention of myocardial infarction or stroke for
patients with family history of these
- this is used for the prevention of myocardial
infarction and prevention of stroke for patients
having transient ischemic attacks
- Recommended Aspirin dose:
o 50-326 mg/day – stroke prophylaxis
o 75-126 mg/day – myocardial infarction
- Clopidogrel on the other hand is frequently used
after myocardial infarction or stroke to prevent
second event
THROMBOLYTICS
- is a clock buster meaning this classification of
medication attacks and dissolves blood clots that
have formed already
- again for anticoagulant as well as for antiplatelet
those two classifications prevent the formation of
blood clots but for thrombolytics it attacks and
dissolves the formed blood clot
Mechanism of Action
- Attacks and dissolves blood clots that have already
formed
Basic facts
- Clot buster
- Thromboembolism(which refers to the occlusion of
an artery or vein caused by a thrombose or
embolus or in other words a clot results in
ischemia that causes necrosis of a tissue distal to
the obstructed area
- it takes approximately one to two weeks for the
blood clot to disintegrate by natural fibrinolytic
mechanisms and if a new thrombus or imbulous
can be dissolved more quickly tissue necrosis is
minimized
- that is why it is essential that this thrombus or
formed clots will be dissolved immediately in order
to prevent tissue death or necrosis
Examples
- Alteplase, (Tissue Plasminogen Activator tPA),
Tenecteplase, streptokinase
18
 Side Effects and Adverse Reactions Mechanism of Action
- Allergic reaction - More effective in reducing VLDL (Very Low-Density
- Anaphylactic reaction (w/ streptokinase) Lipoprotein (levels than reducing LDL
- Hemorrhage – major complication
Drug-to-Drug Interactions
Drug-to-Drug Interactions - Fibrates + Warfarin = risk for bleeding
- take note when a patient takes thrombolytic the
use of aspirin and non-steroidal anti-inflammatory
drug must be avoided in pain management why
because these two medications also have an anti-
platelet effect and also you need to observe for 3. Nicotinic Acid (B3)
signs of active bleeding Example
- Niacin- this medication is very effective at lowering
cholesterol levels

ANTIHYPERLIPIDEMIC Mechanism of Action

- this type of medication is used to lower lipid levels
- drugs that lower lipid levels include bile acid
sequestrants, fibrates or fibric acid, nicotinic acid,
cholesterol absorption inhibitors, and hepatic 3-
hydroxy 3-methylglutaral coenzyme a reductase
inhibitors which is better known as statins now
1. Bile-acid sequestrants
Mechanism of Action
- Reduces LDL cholesterol by binding bile acids in the
intestine
- This type of medication reduces low density
lipoprotein cholesterol level by binding bile acids in
the intestine
- take note: that your ldl is considered bad
cholesterol the same also with the vldl or the very
low density lipoprotein the cholesterol which is
considered good is the hdl or the high density
lipoprotein
Examples
- Cholestyramine, colesvelam, colestipol HCl
2. Fibrates (Fibric Acid)
- an example of this medication is fenofibrate and
gemfibrozil
- commonly used in the clinical area is fenofibrate
this type of medicationnis more effective in
reducing vldlmor very low density lipoprotein
levels then for reducing ldl or low density
lipoprotein
- take note if this medication is taken with warfarin
bleeding might occur so you better assess the
medications the patient is taking
- Lowers cholesterol levels
4. Cholesterol Absorption Inhibitor
Mechanism of Action
- Acts on the cells of small intestine to inhibit
cholesterol absorption
Examples
- Ezetimibe
5. Hepatic 3-hydroxy 3-methylglutaryl-coenzyme A (HMG-
CoA) reductase inhibitor or STATINS
Mechanism of Action
- Decreases concentration of cholesterol, LDL, and
slightly increase HDL cholesterol
Basic facts:
- Serum liver enzyme should be monitored
- Eye exam is needed because of possible cataract
formation
- this type of medication can be combined with other
drugs to lower blood pressure
Examples
- Atorvastatin CA,
- Rosuvastatin
- Simvastatin
NOTE: these three medications are commonly prescribed to
patients with hyperlipidemia

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 Contraindications
- Contraindicated with liver disorder
- take note if therapy is withdrawn cholesterol and
low density lipoprotein levels will return to pre-
treatment level
Side Effects/Adverse Reactions
- Cholestyramine – constipation and peptic ulcer
- Niacin – GI disturbances, flushing of skin, abnormal
liver function, hyperglycemia, and hyperuricemia.
but with regards to flushing there are already
newer types of medications or there are already
newer niacins which does not cause skin flushing
- Statin – the medication increased liver enzymes,
rhabdomyolysis (muscle disintegration that can
become fatal)
Side Effects/Adverse Reactions
- Light headedness, dizziness, tachycardia,
palpitation & GI distress
Pentoxifylline
• Classified as Blood Viscosity reducer agent
• Improves microcirculation & tissue perfusion
• Overdose reaction → to tachycardia, areflexia
(absence of reflex) , and GI bleeding
• Must be taken w/ food and smoking avoided

PATIENT TEACHING
- Inform patient that it may take several weeks
before blood lipids decline
- Advise to have serum liver enzymes monitored
- Annual eye exam
- Take nicotinic acid w/ meal
- Flushing is common with niacin
- Not disrupt stop because rebound effect may
occur

DRUGS TO IMPROVE PERIPHERAL BLOOD FLOW

Peripheral Arterial Disease (Peripheral vascular disease)
- a common problem in older adults is
peripheral arterial disease which is also
called as peripheral vascular disease
- it is characterized by numbness in coolness
of extremities as well as claudication or the
pain and weakness of a limb when walking
but no symptoms when at rest and also
possible leg ulcers
- the primary cause is arteriosclerosis and
hyperlipidemia- resulting in atherosclerosis
and after which the arteries become
occluded

Cilostazol
Mechanism of Action
- this is an antiplatelet that has a dual purpose of
inhibiting platelet aggregation as well as causing
vasodilation to treat intermittent claudication
- when we say claudication- this refers to pain and
weakness of a limb when walking and there's no
pain and weakness when the patient is at rest

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