Baroreceptor vs RAAS

INTRODUCTION TO ANTI-HYPERTENSIVES
Renin-Angiotensin
Baroreceptor Aldosterone System
MEDICATIONS (RAAS)
1. Antihypertensives
- ACE Inhibitors Responds to short term Responds to long term
- Angiotensin II Receptor Blocker alteration in BP alteration in BP
- Calcium Channel Blocker
- Sympatholytics Acute cases Chronic cases
- Vasodilators
2. Diuretics
- Thiazide RENIN-ANGIOTENSIN ALDOSTERONE SYSTEM
- Loop
● RAAS
- Osmotic
● Compensatory mechanism when the blood
- Potassium-Sparing
pressure within the kidneys fall
3. Anti - aginal
● Primarily associated with blood pressure regulation
- Nitrates
by modulating the:
- Non-nitrates
a. Blood vessel
4. Anti-arrhythmic
- Regulated by Renin, Angiotensin,
5. Cardiac Glycosides
Aldosterone
6. Drugs Affecting the Blood
b. Sodium reabsorption
- Anticoagulants
- Reg. Aldosterone
- Thrombolytics
c. Potassium secretion
- Hemostatistics
- Reg. Aldosterone
d. Water reabsorption
- Reg. Aldosterone
BLOOD PRESSURE
e. Vascular tone
- Renin and Angiotensin
● Measurement of force applied to artery wall
● Pushing of blood against the artery IF BP DECREASES
● Every pump = blood flows 1. Aortic Depressor Nerve
● There are different factors that affects the elasticity 2. Carotid Sinus Nerve
of arterial wall 3. Vasocenter
- Increase contractility heart rate
- Increase vascular tone
DETERMINANT OF BP - Increase natriuresis/Renin release

1. Cardiac Output IF BP INCREASES

- Volume of blood pumped by a ventricle in 1 1. Brain Signals
minute - Decrease contractility heart rate
- SV * HR - Relaxed vascular tone
- Stroke volume (amt of blood @ one - Stops release of Renin
beat)
RAAS mechanism
2. Peripheral Vascular Resistance 1. Decline of BP or oxygen
- Resistance exerted in blood flow 2. Juxtaglomerular Cell (Kidney)
- Contains Pre-Renin (inactive) that binds to
3. Baroreceptors become active
- Specialized cells in the arch of the aorta 3. Renin
and carotid sinus - Active composition of angiotensin
- Mechanoreceptors 4. Angiotensinogen (Liver)
- Any change in BP is recognized on the - Renin binds to this to produce:
Arch of aorta and carotid sinus thus it will 5. Angiotensin I (inactive)
be responded - Insertion of Angiotensin Converting
Enzyme (ACE) to convert inactive to active
form
6. Angiotensin II
- Potent vasoconstrictor
- Act on site that increases BP, and perfusion
 7. A or B response ● Types of Hypertension
a. Response A
- Intense vasoconstriction
Primary Secondary
- Increase peripheral resistance
- Increase blood pressure, restores
“Essential hypertension” With comorbidity or drugs
blood flow
(medication)
- Increase kidney perfusion
- Decrease Renin
Unknown cause Due to underlying
- Then STOPS
disorders
b. Response B
- Adrenal Cortex
Obesity, genetics, etc. Types:
- Secrete Aldosterone
- Act on Nephrons
1. Isolated Hypertension
- Instruct the Sodium and Water
- Either systolic or
Retention
diastolic
- Sodium Rich Blood
abnormality
- Hypothalamus
- Ex. Sys is normal;
- Osmoreceptors
dias is abnormal
- Antidiuretic hormone release
- Signify na di magwiwii and
2. Malignant
increase Blood volume (?)
- Rapid increase in
- Further increase blood volume
BP
- Thus increase Blood pressure
- Seen on patient with
preeclampsia
Summary:
● Starts in Kidney
3. Resistant
● ACE → found in lungs and kidney
- Multiple
● Angiotensin I
Anti-hypertensive
● Angiotensin II
drugs doesn’t work
○ Sympathetic
anymore
○ Reabsorption
- Continuous increase
○ Aldosterone Secretion (response B)
of BP
○ Arterial Vasoconstriction (response A)
○ Pituitary Gland → Antidiuretic Hormone
Secretion (response B)
○ Water and salt retention → increases BV
and perfusion
○ Goes to kidney and stops renin when
desired result is acquired

HYPERTENSION

● Silent Killer
- Because manifestation varied in every
individual
● When a person’s BP is above the normal limits for a
sustained period
- One reading is not enough
- Must be consistent / sustained for days,
weeks and months STEPPED CARE APPROACH
● BP is Affected by:
○ Alcohol 1. Lifestyle Modification
○ Cigarette - Weight Reduction
○ Vigorous Activity - Decrease Sodium intake
○ Last food eaten - Moderate Alcohol intake
○ Many more - Smoking Cessation
- Increased physical exercise
2. Drug
 HEALTH TEACHING ● Adverse effects
- Reflex tachycardia
- Chest pain
P pressure (blood) monitor
- Angina
- if medication is effective
- Chronic Heart Failure
- Cardiac Arrhythmia
R rise slowly
- Ulcer
- Ensure safety
- Liver/Renal problem
- Sit on bed, dangle legs, stand up
- Photosensitivity
- Hyperkalemia
E eating must be considered
- Neutropenia
- Angioedema
S stay on medication
- Swelling underneath the skin
- Allergic response
S skipping or abrupt stopping is NO NO
- Can be life threatening if it affects
- Causes rebound hypertension
the upper airway tract
- MEC must be constant

U undesirable responses ● Drug interaction

- Side effects and adverse effects
R remind to exercise and decrease alcohol
intake
E eliminate smoking
1. + probenecid = decreased elimination
2. + potassium supplement + diuretics =
hyperkalemia (Potassium increases
normal)
3. + NSAIDS = decrease hypotensive effects
4. + Antacids = decrease absorption
5. + Tetracycline = decrease absorption of
tetracycline

● Contraindication:
ANTIHYPERTENSIVE DRUG - Renal Disease
- Sever Potassium deception
- Chronic Heart Failure
Angiotensin-Converting Enzyme Inhibitor - Pregnant and lactating women
- Category C = 1st trimester
- Category D = 2nd/3rd trimester
● “Pril”
● Mode of Action: Blocks the conversion of ● Nursing Consideration
Angiotensin I (inactive) to Angiotensin II (active 1. Encourage implementation of lifestyle
form) changes
● Uses: Hypertension and Myocardial Infarction 2. Administer on empty stomach
● E.g. 3. Alert if patient is for surgery, dialysis, or
- benazepril (Lotensin) situations which may drop the fluid volume
- captopril (Capoten) 4. Parenteral form ONLY if oral form is not
- enalapril maleate (Vasotec) available
- quinapril (Accupril) 5. Adjust dose if with renal failure
- fosinopril (Prinivil) 6. Don’t give medication when BP is below
- moexipril (Univasc) 90/70, monitor the BP especially for 2 hours
- perindopril (Aceon) after the first dose (hypotension)
- lisinopril - Increase the dose = need
- ramipril adjustment
- trandolapril - Client is not tolerable
● Side effects - Inform the doctor
- Cough 7. Avoid ambulation (dizziness)
- Hypotension 8. Report cough/ angioedema
- Headache 9. Report dysgeusia if it is already more than
- Dysgeusia (perversion of taste perception) 1 month
- Insomnia
- Nausea & Vomiting
- Diarrhea
 Used for:
Angiotensin II Receptor Antagonist - Angina
- Hypertension
● “Sartan” - Atrial fibrillation
● Selectively bind the angiotensin II receptors in the
blood vessels and adrenal cortex ● Normally, Calcium entry leads to muscular
● E.g. contraction
- telmisartan (Micardis) ● How do Dihydropyridines work?
- losartan (Diovan) 1. Binds to and blocks Calcium Channels
- irbesartan (Aprovel) 2. Calcium cannot enter muscle cells =
- candesartan (Blopress) vasodilation, decreased BP
- valsartan (Cozaar)
- eprosartan (Teveten) ● What are they used for?
● Uses: when ACE inhibitors are not tolerated, ARB’s - Conditions that lead to ↑ vascular
(Angiotensin Receptor Blocker) are the next line to resistance or ↑ vasoconstriction
be given - Hypertension
- Prinzmetal Angina
● Side effects - Raynaud's Syndrome
- Headache
- Diarrhea ● Dihydropyridines
- Dyspepsia - Effect mostly on the periphery or smooth
- Cramps muscle
- More effect on vasodilation
● Adverse effects - Less effect on heart
- Angioedema
- Can cause respiratory arrest or ● Non-Dihydropyridines
collapse due to the edema itself - Work mostly on heart or cardiac muscle
- Hyperkalemia rather than the smooth muscle
- Can alter the contractility of heart - Less effect on vasodilation
- More effect on heart
● Contraindication
- Nephro dysfunction ● Side effects and Adverse effects
- Liver disorder - Headache
- Congestive heart failure - Dizziness
- Pregnancy - Hypotension
- Category C = 1st trimester - Syncope
- Category D = 2nd/3rd trimester - Reflex tachycardia
- Constipation
● Nursing Considerations - Atrioventricular (AV) block
- Ensure that the patient is not pregnant - Bradycardia
- Take medication without regard to food - Peripheral edema

● Nursing Considerations
Calcium Channel Blockers - Monitor ECG, CR, BP
- Have “E” (emergency) cart available with IV
● “Pine” usually administration
● Mode of Action: Prevents movement of calcium ions - Position to decrease peripheral edema
in the myocardium and vascular smooth muscles - Protect drug from light and moisture
● Normally: Calcium is needed for muscle - Increase OFI and fiber in the diet
contractility, peripheral resistance, and BP - Avoid overexertion when anginal pain is
● E.g. relieved
- amlodipin (Norvasc) - May give paracetamol if with headache
- diltiazem (Cardizem) - Take medication with meals or milk
- nimodipine (Nimotop) - Do not chew or crush sustained released
- felodipine (Plendil)
Vasodilators
Potent calcium channel blocker
- nicardipine (Cardene)
- nifedipine (Procardia) MOA: Relaxes smooth muscles of blood vessels esp the
- verapamil (Calan) arteries; promotes increase blood flow to the brain &
kidney
 ● EG: Beta 1-blockers
❖ hydralazine ( Apresoline ) ● Reduce heart rate, blood pressure, myocardial
❖ Minoxidil (loniten) contractility, and myocardial oxygen consumption
❖ Diazoxide ( Hyperstat)
❖ Nitroprusside (Nitropress) Beta 2 receptors
● Mainly in the lungs, gastrointestinal tract, liver,
USES: Severe hypertension, emergencies uterus, vascular smooth muscles, and skeletal
muscle
SE/ AE: ● Serve to dilate bronchial & vascular smooth muscle
● Hydralazine: tachycardia (beta blocker),
palpitations, edema (diuretics), HA, dizziness, GI Beta 2-receptor blockade
bleed, lupus like and neurologic symptoms ● Inhibits the relaxation of smooth muscles in blood
● Minoxidil: similar effects, excess hair growth, vessels, bronchi, the gastrointestinal system, and
precipitates angina genitourinary tract
● Nitroprusside & diazoxide ( hyperglycemia) :
similar
BETA-ADRENERGIC BLOCKERS
CI: Allergy, pregnancy, lactation, cerebral insufficiency
DI: +other antihypertensive drugs = additive effect USES: hypertension, dysrhythmias, angina pectoris, heart
attacks, glaucoma, migraine, prophylaxis
NURSING CONSIDERATION
AE: rebound hypertension
D-irectly acts on vascular smooth muscle MAIN CONTRAINDICATIONS
I-ncrease renal and cerebral blood flow
L- upus like reaction (fever, facial rash, muscle, and joint ● A- sthma
pain, splenomegaly) ● B-lock (heart block)
A- assess peripheral edema ● C-OPD
T- ake with food ● D- diabetes Mellitus
O-ther side effects ( headache, dizziness, anorexia, Inc. ● E- lectrolyte Imbalance (hyperkalemia)
Cardiac, Dec. Blood pressure)
R- eview BP ( orthostatic, hypotension), blood glucose DI:

- + antacids = delayed drug absorption

- + lidocaine = increase plasma level of
Beta-Adrenergic Blocker lidocaine
- + insulin/ Oral glycosides = hypo/
MOA: hyperglycemia
● block beta 1 ( Cardiac) and / or beta 2 (lungs) - + cardiac glycosides = additive
adrenergic receptor sites; bradycardia
● Decrease the effects of the SNS by blocking the - + calcium channel blockers = increase
release of catecholamines, thereby decreasing pharmacologic and toxic effects of both
the HR, BP - + cimetidine= decrease metabolism of
beta blockers
- + theophylline = impaired bronchodilating
effect
EG:

⁃ `Nonselective Beta Blockers

◦ Carvedilol (Coreg)
◦ Nadolol ( Corgard)
◦ Propranolol ( Inderal)
◦ Timolol ( Blocadren)
◦ Pindolol (Visken)

⁃ Cadioselective Beta Blockers (B1)

◦ acebutolol (Sectral)
Beta 1 receptors ◦ atenolol ( Tenormin)
● Found in the heart and kidneys ◦ betaxolol ( Kerlone)
● When stimulated, they increase heart rate, AV ◦ bisoprolol (Zebeta)
conduction & automaticity ◦ esmolol (Brevibloc)
◦ metoprolol (Betaloc, Cardiostat)
NURSING CONSIDERATIONS:
● Lifestyle modification; Compliance (rebound
hypertension)
● Monitor blood sugar with diabetics
● Monitor triglycerides and cholesterol level (LDL)
● Monitor BP & pulse before and after
● Withhold if pulse is < 60 or SBP < 90
● Monitor any change in the rhythm or signs of CHF
Alpha-Adrenergic Blocker
● Seen in SNS
● Alpha 1
○ Found in vascular smooth muscle
● Alpha 2
○ Found in the brain specifically the brain
stem and periphery
● Blocks the alpha 1 adrenergic receptor resulting in
vasodilation of arteries and vein
● Decrease peripheral resistance; relaxes smooth
muscle of bladder / prostate
● Decrease VLDL & LDL + decrease fat deposits;
increase HDL (LDL - Low density lipoprotein; HDL -
High density lipoprotein)
● Does not affect glucose metabolism & respiratory
function
● Causes NA & H2O retention with edema; given with
diuretic
● WARNINGS: renal disease, elderly more
sensitive
EXAMPLES
● Hypertensive crisis and severe hypertension d/t
tumor (THESE DRUGS ARE POTENT)
○ Phentolamine
○ Phenoxybenzamine
○ tolazoline
● CHF (Chronic Heart Failure)
○ Prazosin (Minipress)
● Also for BPH (Benign Prostatic Hyperplasia)
○ Doxazosin (Cardura)
○ Terazosin (Hytrin)
● Side effects
○ Orthostatic hypotension (dizziness,
faintness, increase HR)
■ 1st dose syncope (hypotension
with loss of consciousness)
■ Nausea, drowsiness, nasal
congestion, weakness, loss of
libido
■ Phentolamine - reflex tachycardia
● Drug interaction
○ + other antihypertensive, alcohol, nitrates =
increase hypotensive effects
○ Prazosin + Anti inflammatory drug =
peripheral edema
○ Prazosin & nitroglycerin - syncope
● Nursing Intervention
○ Monitoring of BP more frequently
○ Protect from falling/injury
○ Assess BP and HR before each dose
○ If dose is during the day, client must remain
recumbent for 3-4
○ Assist with ambulation if client is dizzy
● Education
○ Implement safety precautions
○ Report if edema is present
○ Sugarless gum, sips of tepid H2O, etc. may
relieve dry mouth
● Mini SINS
○ Syncope and sexual dysfunction
○ Increase drowsiness, orthostatic
hypotension, HR
○ Need to be recumbent for 3-4 hours after
initial dose
○ Mini’s “SUBS” (*(minipress) are undesirable
effects of Alpha Adrenergic Blockers.
These medication end -SIN
Centrally Acting Alpha2 Agonist
● MOA:
○ Decrease sympathetic response from
brainstem to the peripheral vessels;
resulting in a decrease peripheral vascular
resistance & BP
● Stimulate the Alpha 2 receptors
○ Decrease sympathetic activity
○ Increase epinephrine, norepinephrine, renin
release
● Side effects / AE
○ Drowsiness, HA, dry mouth, dizziness,
bradycardia, constipation, hypotension,
occasional edema or weight gain
● DI
○ Paradoxical hypertension with propranolol
EXAMPLES
● Methyldopa (Aldomet)
○ Chronic hypertension / pregnancy induced
hypertension (PIH)
● Clonidine (Catapres)
*BOTH DRUGS CAUSE Na & WATER RETENTION
(USUALLY GIVEN WITH DIURETICS)*
● Nursing Consideration
○ Monitor baseline VS (q30 mins until stable
during initial therapy) & weight ( refer:wt
gain > 4lbs/week)
○ Abrupt D/C = hypertensive crisis
(restlessness, tachycardia, tremors, HA, &
increase BP), compliance
○ Taper dose gradually over more than week
○ Recommend the last dose of the day to be
taken at the bed time
○ Sugarless gum, sips of tepid water may
relieve dry mouth
Adrenergic Neuron Blockers (Peripherally
Acting Sympatholytics)
● MOA:
- inhibition of the function of norepinephrine
and its secretion from the sympathetic
nerve endings, causing a decrease of blood
pressure
● Side effects:
- Orthostatic hypotension, water and sodium
retention, vivid dreams, nightmares and
suicidal intention (common side effect of
reserpine)
Example:
- Reserpine (Serpasil)
- Guanethidine monosulfate (Ismelin)
● Nursing Considerations:
- Take the medication with meals
- Avoid alcohol
Alpha1 & Beta1 - Adrenergic Blockers
● MOA:
- Alpha1 adrenergic blocker blocks alpha1
receptor sites
● Can be found and seen in vascular
smooth muscles
- Beta1 adrenergic blocker blocks beta1
receptor sites
● Can be found and seen in cardiac
muscles
- The blockage of both receptor sites result
to decrease in BP and moderate
decrease in PR
● Side effect:
- Orthostatic hypotension
- GI disturbances
- Nervousness
- Dry mouth
- Fatigue
● Adverse effect:
- Heart block
● Contraindications:
- Large doses of the medicine could block
beta2 receptors (located in the lungs),
leading to increase in airway resistance in
patients with asthma
- E.g. Labetalol (normodyne), Carteolol
(cartrol)
CARDIAC GLYCOSIDES
● Originally derived from poisonous fox- glove or
digitalis plant
● Used by William Withering of England to alleviate “
dropsy”
- edema of extremities caused by cardiac
and kidney insufficiency secondary to CHF
Ex. digoxin (Lanoxin, Lanoxicaps) = PO, IV
● MOA: inhibits Na- K pump which increases
intracellular calcium and allow more calcium to
enter myocardial cells during depolarization
causing:
- (+) inotropic action ( inc myocardial
contraction)
- (-) chronotropic action ( dec heart rate)
- (-) dromotropic action ( dec conduction
velocity)
- ✓ Increase cardiac output and
renal perfusion
● Uses: CHF, AF, A flutter,
- rapid onset, excreted thru kidney, has a
narrow margin of safety
● Digitalis toxicity: anorexia, diarrhea, N/V, ● Sodium Rich Foods: buttermilk, margarine,
bradycardia, cardiac dysrhythmias, HA, malaise, canned goods, processed foods, fast foods,
blurred vision, visual illusions ( white, green, yellow preserved foods, tomato ketchup
halos around objects), confusion and delirium
● Antidote: digoxin immune Fab (intoxication with
serum level of > 10ng/mL) ANTI-ANGINAL
- Binds with digoxin to form complex
molecules that can be excreted in the urine
Coronary Artery Disease lumen of blood vessels
(CAD) become narrow, thus
● CI: hypersensitivity, ventricular tachycardia and blood is no longer able to
fibrillation, heart block, MI, renal insufficiency, flow freely to the muscles
electrolyte imbalance (increased Calcium,
decreased K & Mg) “ suffocation of the chest”,
occurs when myocardial
demand for oxygen
● DI:
cannot be met by
- + verapamil, quinidine, quinine, narrowed blood vessels
erythromycin, tetracycline,
cyclosporine = increase toxic effect Angina Pectoris ANGINA PAIN:
- + loop diuretics/ hydrochlorothiazide = - chest tightness
HYPOKALEMIA ( increase the effect at its - pressure in the
myocardial cell action site) center of the chest
- pain radiating
- + cortisone preparations = sodium
down the neck and
retention & potassium excretion left arm
- + thyroid hormones, metoclopramide = less
effective Myocardial Infarction (MI) occurs when coronary
- + antacids = decrease digitalis absorption vessels are completely
occluded and the cells that
depend on the vessels
● NURSING CONSIDERATIONS
for oxygen become
○ Consult prescriber about loading dose ischemic, then necrotic
○ Monitor apical pulse in one full minute, and die.
monitor for quality and rhythm
○ Check dosage & preparation carefully
● TYPE OF ANGINA
○ Check pediatric dose with extreme care
1. Classic (stable)
○ Follow dilution carefully for IV preparation - occurs with stress exertion
○ Administer IV dose very slow over at least 5 2. Unstable (preinfarction)
minutes - occurs frequently over the course
○ Weigh patient of a day with progressive severity
○ Avoid administering oral drug with food or 3. Variant (Prinzmetal, vasospastic)
antacid - occurs during rest
○ Maintain emergency equipment on standby
● TYPES OF ANTI-ANGINA
■ lidocaine (arrhythmias)
1. Non-nitrates
■ phenytoin (seizure)
- Non- nitrates (beta blockers)
■ atropine SO4 ( to inc cardiac rate)
- Calcium channel blockers)
■ cardiac monitor
2. Nitrates
○ Monitor therapeutic level of digoxin (0.5 – 2
- isosorbide mononitrate (Imdur,
ng/ mL) , digoxin toxicity
isoket, isordil)
- nitroglycerin (Deponit, Nitrostat)
● Potassium Rich foods: banana, avocado,
broccoli, dried fruits, oranges, nuts , potato, prunes,
NITRATES
tomato
● MOA:
- dilation of the veins = less blood return to
the heart (decrease preload)
 - dilation of arteries = less vasoconstriction
Spray - lift tongue then spray, avoid
and resistance (decrease afterload) inhaling the drug

● USES: treatment & prevention of angina, dec BP General: (withhold or dili maghatag when)
- BP < 90/60
● SE: HA ( most common), dizziness, hypotension, - HR <60
reflex tachycardia, decrease CR, GI distress, - Acetaminophen for HA
- Reassess chest pain after 2-5 minutes (SL,
flushing
spray, except PO)

● AE: some degree of hepato / nephrotoxicity

DIURETICS
● Nursing Consideration:
Assess Chest Pain Nephrons are the functional unit of the kidneys
P - reciprocating factors
Q - uality Three Basic Processes to produce urine :
R - adiation ● Filtration
S - everity/ symptoms, and ● Re-absorption
T - time ● Secretion

- take on empty stomach; Diuretics produce increases in urine flow by inhibiting

PO undergoes hepatic first pass
sodium and water reabsorption from kidney tubules.
effect

- every 5 min X 3 doses; effect 2 main purpose

lasts for 10 minutes ● To decrease hypertension
- store in dry & dark bottle ● To decrease edema
- check expiration date ( up to six
SL months only)
Indications:
- take sips of water BEFORE
administration ● Congestive Heart failure
- allow drug to dissolve before ● Pulmonary edema
taking anything PO ● Liver failure & cirrhosis
- burning / stinging sensation ● Renal diseases
means the drug is potent ● Hypertension
● Glaucoma
Buccal - place drug between upper lip and
gum or between cheek and gum
Contraindication
IV Infusion - dilute drug in glass IVF bottles ● Allergy
via infusion pump, onset 1-3 ● Fluid & electrolyte imbalance
minutes same with SL ● Severe renal disease
● Systemic Lupus Erythematosus
Tropical - remove previous application
● DM
Ointment - spread drug over a 6x6 in area
on chest, back, upper arm, and
cover with a plastic wrap
- rotate site, avoid touching the
ointment

Patch - patch is waterproof

- apply wearing gloves at ACW,
non hairy portion
- remove previous patch, rotate
sites
- remove after 12 hours to prevent
tolerance
- do not apply defibrillator paddles
over the drug, may cause burn

Thiazide Diuretics
● Mode of Action
- increase NA & water excretion by inhibiting NA
reabsorption in the distal tubule of the kidney
*not effective for immediate diuresis*
● Eg
- chlorothiazide (Diuril)
- chlorthalidone (Thalitone)
- hydrochlorothiazide (Hydrodiuril)
- indapamide (Lozol)
- metolazone (Zaroxolyn)
● Uses
- mild-moderate hypertension, edema associated
with CHF, cirrhosis with ascites
● Contraindications
- decrease in serum K, renal/hepatic
dysfunction, gout
● Drug Interactions
- + lithium = lithium toxicity
- + digoxin = digoxin toxicity (bradycardia, N/V,
visual changes)
- + corticosteroids, amphotericin, ticarcillin =
hypokalemia
- + sulfonamides = cross sensitivity
● Side effects / Adverse effects
- Hypokalemia, hyponatremia, hypomagnesemia,
hypotension, bicarbonate loss, hypercalcemia,
hyperglycemia, hyperuricemia, N/V, constipation,
rashes, dizziness, weakness, increase LDL,
photosensitivity (common), H/A, dehydration
(common), blood dyscrasias
● Nursing Responsibilities
- Monitor BP (since diuretics can decrease
the circulating blood volume, thus can
cause hypotension), weight once a day,
urine output, edema
- Monitor K, Na, Ca, blood glucose, LDL,
triglycerides (since diuretics can cause
electrolyte imbalance)
- Change position slowly (for patient safety;
orthostatic hypotension because of
diuresis)
- No alcohol
- Take with meals preferably in AM (applies
to all diuretics)
- Eat foods high in K (banana, avocado,
broccoli, dried fruits, oranges, nuts, potato,
prunes, tomato)
- Manage photosensitivity (wearing of dark
glasses, wearing sunscreen/sun protection)
- Signs of hypokalemia [muscle weakness,
cardiac dysrhythmias, cramps, dizziness,
N/V, tingling sensation, “U” wave on the
ECG (3.5 - 5.1 mEq/L)]
● Education
T - ake time to check VS
H - yperglycemia, hypokalemia, hyperuricemia
monitoring
I - nstruct to weigh in daily
A - void sudden position changes
Z - ugar monitoring
I - &O (intake & output) monitoring
D - iuresis is expected: I&O
E - at potassium rich foods
Loop Diuretics
● Mode of Action
- inhibits Na & Cl absorption from the loop of henle
and distal tubules, causes rapid diuresis, little
effect on glucose
● Eg
- furosemide (Lasix) = common medication given
- torsemide (Demadex)
- ethacrynic acid (Edecrin)
- bumetanide (Bumex) = can cause ototoxicity
● Uses
- HPN, edema associated with CHF, cirrhosis with
ascites, hypercalcemia
● Drug Interactions
- + lithium = lithium toxicity
- + digoxin = digoxin toxicity (bradycardia, N/V,
visual changes)
- + corticosteroids, amphotericin, ticarcillin =
hypokalemia
- + sulfonamides = cross sensitivity
● Side effects / Adverse effects
- Hypokalemia, hyponatremia, hypocalcemia,
hypomagnesemia, hypochloremia, hyperuricemia,
orthostatic hypotension, constipation, N/V,
decrease platelet, ototoxicity (IV bumetanide),
dehydration, photosensitivity, thiamine deficiency,
hyperglycemia (glycogenolysis), elevated BUN &
creatinine
● Nursing Responsibilities
- Monitor VS, edema, urine output, serum K, Na,
Ca, Cl, thiamine, blood glucose & platelet levels,
Mx of digoxin & lithium toxicity
- Potassium rich foods
- Give slow IVTT (2 mins) to prevent hearing loss
- Take with meals, in AM
● Education
C - heck for weight gain
E - nsure VS prior to administration
I - &O monitoring
L - laboratory values assessment ( pertaining to
electrolyte imbalance)
I - nstruct to rise slowly
N - cturia prevention: AM only (promotes rest)
G - ive it with meals
 ● Eg
Osmotic Diuretics - spironolactone (Aldactone)
- amiloride (Midamor)
● Mode of Action - triamterene (Dyrenium) = causes blue urine
- increase osmotic pressure in the glomerular
filtrate, preventing reabsorption of water & ● Uses
electrolytes - HPN, edema = CHF, nephrotic syndrome to
counteract hypokalemia caused by other diuretics
● Eg
- mannitol (Osmitrol) = for ICP ● Contraindication
- urea (Ureaphil) - severe renal disease, severe hyperkalemia
- glycerin (Osmoglyn) = to decrease intraocular
pressure (IOP) ● Drug Interactions
- isosorbide (Ismotic) - + lithium = lithium toxicity
- + ACE inhibitor = hyperkalemia
● Uses - + digoxin = digoxin toxicity
- increased intracranial pressure (ICP), edema, - + K supplements (eg. kalium durule) =
prevention of renal failure, oliguria, inducing hyperkalemia
diuresis during chemotherapy
● Side effects / Adverse effects
● Contraindication - Hyperkalemia, N/V, diarrhea, dry mouth, rash,
- anuria dizziness, weakness, bluish colored urine
(triamterene) = it is normal, hypotension, increase
● Drug Interactions potassium level result in peaked T wave on ECG
- increase hypokalemia which may increase digoxin - Headache, photosensitivity, anemia, decrease
toxicity platelet

● Side effects / Adverse effects ● Nursing Responsibilities

- pulmonary edema d/t rapid fluid shifting, N/V, - Monitor VS, urine output, serum K level
tachycardia, decrease Na, K, Cl, Ca, dehydration - Inform client that hypotensive effects may not be
seen for 2 weeks
● Nursing Responsibilities - Avoid potassium rich foods
- Monitor VS, weight, urine output, serum K, Na, Cl, - Manage photosensitivity (avoid sunlight, wearing
Ca of dark glasses, wearing sunscreen/sun protection)
- Watch for rapid increase in BP & rapid sympathetic - Avoid salt substitutes
overactivity (increase HR, tremor, agitation) - Take with meals
- Assess lung and heart sounds - Bluish colored urine is harmless
- Check skin turgor, LOC, Mx of dec ICP - Administer in AM
- Mannitol: check bottle or vial for crystallization,
warm bottle & shake vigorously to dissolve ● Interventions
crystals, if it doesn’t dissolve = DO NOT administer D - iet: decrease sodium intake
: use IV line with filter I - ntake & output monitoring
: infuse for 30-60 minutes U - undesirable effects
R - eduction of edema
● Education E - electrolytes review
O - liguria, edema, inc. ICP (indication) T - ake early in the da; with meals
S - tops reabsorption of water I - nteractions: digoxin
M - annitol C - ause/aggravate diabetes
O - output of urine, electrolytes - monitor S - ensitivity to sunlight
T - issue dehydration UE
I - ncreased frequency/volume of urination
C - irculatory overload UE ANTI-ARRHYTHMICS

Potassium Sparing Diuretics Conduction System

● Mode of Action 1. Sinoatrial Node

- acts on the distal tubule to promote Na and water
excretion & prevent potassium excretion; AKA: - Made up of pacemaker cells “Natural
aldosterone antagonist pacemakers”
 - Start of the conduction system which ● P to R interval
gives electrical impulse to atrial bundle - If shortened/ long = abnormality in the
- Produce action potential and electrical conduction system
impulses traveling done to the heart, ● AV Conduction
● PR Segment
manifest in steps
● ST Segment
- Contraction of the atria
● Problem in P wave
2. Atrioventricular Node
- Tachycardia, atrial fibrillation, atrial flutter
3. AV bundle or “Bundle of His”
4. Right & Left Bundle Branch
5. Purkinje Fiber The ECG Waves
- Act on ventricular cells
- Signals ventricles to start to contract atrium 1. P waves
then the ventricular (separately) - Atrial depolarization
- Which is formed as the impulse originating
in the SA node.
2. QRS complex
- Depolarization of Bundle of His (Q)
- Depolarization (RS)
3. T-wave
- Represents the repolarization of ventricles
4. PR-interval
- Indicates AV conduction time
5. QT Interval
- Reflects ventricular action potential duration
6. U
- Repolarization of purkinje fibers in ventricle

Abnormalities in ECG Waves

ELECTROCARDIOGRAM (ECG)
- trace where the transfer or conductivity
● NORMAL CONDUCTION
happens
- Effective conduction
- Clear sinus rhythm
PQRST & U
- Each letter corresponds to a specific step in the
● ATRIAL FIBRILLATION
conductivity of the heart
- Rapid signal of SA node
QRS
- Disorganized
- Crosses or reached the AV Node
- Atrium = grabe contract
T
- Ventricle = calm
- Repolarization
- Restart of the cycle
U
- Repolarization (but it is not clear where this
conductivity came from)
● PREMATURE VENTRICULAR CONTRACTION
- Contraction at QRS complex
- Not properly defined P because qrs entered
● ATRIAL FLUTTER
- Saw like tooth tracing
- P wave
- Small QRS but a lot of P
- Rapid firing of SA node
● VENTRICULAR TACHYCARDIA
- P wave cannot be distinguished
Automaticity of Heart
● AUTOMATICITY
- The ability of the pale or P cells to:
- generate action potentials or
electrical impulse without being
excited to do so by the external
stimuli.
- Brain does not govern the heart
- Heart is dependent
- Continuously beating due to
automaticity
- Does not need outside stimuli to
contract
5 Phases of Action Potential
1. PHASE 0
- Occurs when the cell reaches the point of
stimulation.
- The sodium gates are open along the cell
membrane sodium rushes into the cell then
causing: DEPOLARIZATION
(contraction)
- Sodium = extracellular
- Potassium = intracellular
2. PHASE 1
- Is a very short period during which the
sodium ion concentration equalizes
inside and outside the cell.
3. PHASE 2
- Plateau stage
- Occurs as the cell membrane becomes
less permeable to sodium, calcium
slowly enters the cell causing
potassium to leave the cell.
 - The cell membrane is trying to return to its Phase 4
resting phase called: REPOLARIZATION - Extracellular: Sodium
(relaxation) - Intracellular: Potassium

4. PHASE 3
Cardiac Dysrhythmia
- Is a time of rapid repolarization as the
sodium gates are closed and potassium
● Aka: cardiac arrhythmia
flows out the cell.
● Defined as deviation from the normal rate or pattern
of heartbeat.
5. PHASE 4
● Bradycardia/Tachycardia
- Occurs when the cell comes to rest.
- The sodium-potassium pump returns to
the membrane to its resting potential ANTI-ARRHYTHMIC DRUGS/MEDICATION
(sodium outside the cell-potassium inside
the cell). ● Affects the action potential of the cardiac cells,
- Spontaneous depolarization begins again. altering their automaticity, conductivity or both.
● Are used in emergency situations.
HOW OFTEN WILL THIS CYCLE OCCUR? ● Can also produce new arrhythmias
- Every heartbeat (60-100 bpm in 1 minute) (PROARRHYTHMIC)
● 5 classification
● Will affect the conduction of the heart

CONDUCTION SYSTEM
1. Sinoatrial node (SA)
a. Caridiomyocytes or Pacemaker cells is the
specialized cell in the SA node
b. Pacemaker of the heart
c. Will send electrical impulses
d. Will send impulses to atrial bundle then it
connects to atrioventricular node or AV
node
2. Atrioventricular Node
a. Will send impulses to bundle of his
3. AV bundle or bundle of his
a. Sends electrical impulses to the right and
left bundle branch
4. Purkinje fiber
a. Action potential will act to ventricular cells
SUMMARY (in order):
causing contraction of ventricles.
Phase 4
- Extracellular: Sodium
- Intracellular: Potassium CLASS I ANTI-ARRHYTHMICS

Phase 0 - Are the drugs that blocks the sodium channels in

- Extracellular: Sodium the cell membrane during action potential
- Intracellular: Potassium & Sodium (since Na enters - Depressing phase 0 action potential
the cell)
SUBTYPES:
1. Class 1a
Phase 1/2 2. Class 1b
- Equal Sodium inside and outside the cell 3. Class 1c
- Intracellular: Ca, K, Na (gibira nya sad ang calcium
pasulod) ● Class 1A
MOA:
- Depress the phase 0 action potential and
Phase 3
prolong the action potential duration.
- Extracellular: Potassium - Slows down conduction and prolongs
- Intracellular: Sodium & Calcium repolarization
 - Example: NURSING CONSIDERATIONS:
1. DISOPYRAMIDE (Norpace) ● Monitor ECG, VS, serum electrolytes, CBC kidney
2. MORICIZINE (Ethmozine) & liver function
3. PROCAINAMIDE (Pronestyl ● Maintain life support equipment
4. QUINIDINE (Cardioquin) ● Give parenteral form only if oral form is not feasible
● Titrate dose to achieve control of arrhrythmia
● Class 1B ● Establish safety precaution
MOA: ● Lifestyle modification
- Slows conduction and shortens
repolarization
- Depresses the phase 0 somewhat and CLASS II ANTI-ARRHYTHMICS
actually shorten the duration of action
potential. - Are Beta-adrenergic blockers
- EXAMPLES: MOA:
1. LIDOCAINE (Xylocaine) - Reduces calcium entry, decreases
a. Used for acute ventricular conduction velocity; automacity, and
arrhythmias in MI patients, recovery period.
cardiac surgery, - Blocks beta receptors, causing depression
emergency treatment when of phase 4 of action potential.
diagnostic test are not EXAMPLES:
available 1. Acebutolol (Sectral)
b. Therapeutic level: 1.5-5 2. Esmolol (Brevibloc)
mcg/mL 3. Propranolol (Inderal)
c. Administer in 2-3 minutes 4. Sotalol (Betapace)
2. MEXILETINE (Mexitil) THERAPUETICS INDICATIONS:
3. TOCAINIDE (Tonocard) - Supraventricular tachycardia
- PVC’s
● Class 1C CONTRAINDICATIONS:
MOA: ● Sinus bradycardia (<45bpm)
- Prlolongs conduction with little or no effect ● AV blocks
on repolarization. ● Cardiogenic shock
- Markedly depresses phase 0, with resultant ● CHF
extreme slowing of conduction ● Asthma
- Example: ● Respiratory depression
1. FLECAINIDE (Tambocor) DRUG INTERACTION:
2. PROPAFENOME (Rhythmol) 1. Verapamil = synergestic
2. Insulin = hypoglycemia
THERAPUETIC INDICATIONS: UNDESIRABLE EFFECTS:
● Ventricular arrhythmias ● Same with Class 1
● Loss of libido
UNDESIRABLE EFFECTS:
1. CNS
- Dizziness, drowsiness, fatigue, twitching, CLASS III ANTI-ARRHYTHMICS
mouth numbness - AKA: potassium channel blockers
- Slurred speech, vision changes, tremors
2. GIT MOA:
- Altered taste, nausea, vomiting - Prolongs repolarization during ventricular
3. CVD dysrythmias, prolongs action potential duration.
- Arrythmias, hypotension, cardiac arrest - BLocks potassium channel ad slow the outward
4. Others movement of potassium during phase 3 of the
- Respiratory arrest action potential.
EXAMPLES:
DRUG INTERACTION: 1. Amiodrone (Cordarone)
● Digoxin& beta blockers = Arrhythmias 2. Bretylium
● Quinidine + Digoxin = Toxicity 3. Ibutilide (Corvert)
● Cimetidine + class1 = Toxicity 4. Dofetilide (Tikosyn)
● Anticoagulants = bleeding increase 5. Sotalol (Betapace)
THERAPUETIC INDICATION:
● Ventricular arrhythmias
● Atrial fibrillation
● Atrial Flutter
CONTRAINDICATIONS:
● No Contraindications
● AV block: Ibutilide & Dofetilide

UNDESIRABLE EFFECTS:
● Liver toxicity - amiodarone

DRUG INTERATION:
● Digoxin & Quindine = toxicity

CLASS IV ANTI-ARRHYTHMICS
- Calcium channel blockers
MOA:
- Blocks the movement of calcium ions across the
cell membrane, depressing the generation of action
potentials, delaying phase 1 and 2 replorization,
and slowing conduction thru the AV node.
THERAPUETIC INDICATION:
● Supraventricular tachycardia
EXAMPLES:
1. Diltiazem (Cardizem)
2. Verapamil (Calan)
CONTRAINDICATIONS:
● Allergy
● Heart blocks
● Pregnancy & lactation
● CHF/hypotension
DRUG INTERACTION:
● Beta-blockers
○ Cardiac depression
● Digoxin
○ Additive AV slowing
● digoxin , Prazosin, Quinidine
○ Toxicity
OTHER DRUGS:
1. Adenosine (Adenogard)
- Slows conduction through AV node, IV
- Used for supraventricular tachycardia
(SVT)
2. Digoxin
- CHF/HF
- Used for Atrial fibrillation
3. Mg SO4
- Given for pregnancy induce hypertension or
preeclampsia
ANTICOAGULANTS

DRUGS AFFECTING BLOOD COAGULATION 1. WARFARIN (COUMADIN)

ANTICOAGULANTS - drugs that interfere with the normal
coagulation process
ANTIPLATELET- alter the formation of platelet plug
THROMBOLYTICS - break down the thrombus that has
been formed by stimulating the plasmin system
-works by interfering the formation of vitamin K -
dependent clotting factors and prolongation of
clotting times
-PO, onset 3 days, duration 4-5 days
Uses: AF, artificial heart valves, prevent thrombus
and embolization affecting MI and pulmonary
embolism
 Antidote: phytonadione (Aquamephyton)- a form of
vitamin K (responsible for promoting the liver
synthesis of clotting factors)
LAB: Prothrombin time (PT) - maintained at 1.25 -
2.5 times the laboratory control value
INTERNATIONAL NORMALIZED RATIO (INR) =
2-3
2. HEPARIN
-Naturally occurring substance that inhibits the
conversion of prothrombin to thrombin, thus
blocking the conversion of fibrinogen to fibrin which
is the final step of clot formation
Uses: treatment and prevention of venous thrombosis and
pulmonary embolism, AF with embolization, prevent clotting
of blood samples in dialysis and venous tubing.
Antidote:
Overdose:
IV - protamine sulfate
PO - vitamin K; coumadin
Lab:
● Whole blood clotting time (WBCT) 2.5 - 3 X control
● Activated Partial Thromboplastin Time (aPTT) upto
40s
● Partial Thromboplastin time (PTT) 1.5 - 2.5 X
control in secs
CI: hypersensitivity, bleeding tendencies, psychosis,
diarrhea (loss of vitamin K or plasminogen)
AE: bleeding, warfarin = alopecia, dermatitis, prolonged &
painful erections (less frequent)
DI:
● Heparin +( aspirin, NSAID, thrombolytics) =
increase effect
● Heparin + (nitroglycerine, protamine) = decrease
effect
● Warfarin + (aspirin, NSAIDs, sulfonamides) =
increase effect
● warfarin + (oral contraceptives, phenytoin, rifampin
= decrease effect
● warfarin + alcohol = increase bleeding
NURSING CONSIDERATIONS:
● Avoid large amount of green leafy vegetables, fish,
liver, coffee and tea; NO alcohol
● Evaluate therapeutic levels
● Signs of bleeding
● Safety precautions (electric razor, avoid contact
sports, use pressure dressing, NO IM injection,
inform dentist, soft bristled toothbrush)
● Maintain antidote standby
● Medic alert card, do not smoke, NO aspirin
ANTIPLATELETS
Uses: adjunct to thrombolytic therapy in the treatment of MI
& prevention of re- infarct, prevention of MI and stroke
Eg:
● abciximab (ReoPro), IV
● clopidogrel (Plavix), PO
● anagrelide (Agrylin), PO
● sulfinpyrazone (Anturane), PO
● dipyridamole (Persantine), PO
ticlopidine (Ticlid), PO
● eptifibatide (Integrilin) , IV
● tirofiban (Aggrastat), IV
● aspirin (generic), PO : cilostazol (Pletaal), PO
CI: hypersensitivity, pregnancy, lactation, bleeding disorder,
recent surgery
AE: bleeding, Gi discomfort, HA
NURSING CONSIDERATIONS: (same with
anticoagulants)
THROMBOLYTIC AGENTS
MOA: converts plasminogen to plasmin to dissolve clot
Uses: pulmonary embolism, DVT, MI, acute ischemic CVA
CI: severe hypertension, active bleeding, hemophilia,
thrombocytopenia, GI bleed, hypersensitivity
DI: inc bleeding with NSAIDs, antiplatelet, anticoagulant
SE: bleeding, rash (streptokinase), febrile reaction, N/V,
flushing, hypotension
EG:
● streptokinase ( Kabikinase, Streptase)
● urokinase ( Abbokinase)
● anistreplase
● anisoylated plasminogen streptokinase activator
complex (APSAC)
● reteplase
● Alteplase (t- PA) -> CVA
● tenecteplase
NURSING CONSIDERATIONS:
● Check BP prior (defer if < / = 90/60)
● Monitor bleeding time, hgb, platelet count, APTT
● Monitor signs of bleeding up to 24 hours post the
last dose Check for allergic reactions esp to
streptokinase (Benadryl may be given prior)
 ● IV drugs that are mixed should be used within 24
hours, infusion pump
ANTI-INFECTIVES PART 2
● Avoid invasive procedure
● Apply pressure for 5-10 mins on all discontinued IV Tetracyclines
sites
● Prevent bleeding
- Isolated from STREPTOMYCES AUREOFACIENS
in 1948
ANTIDOTE: aminocaproic acid (Amicar) - 1st broad spectrum antibiotics effective against
gram (+) bacteria & many organisms
HEMOSTATIC AGENTS [mycobacterium, rickettsiae, spirochetes,
chlamydiae]
- Not effective against S. aureus, Pseudomonas or
MOA: hasten clotting of blood by inhibiting the substance Proteus
that activate plasminogen - Can be used against Mycoplasma pneumoniae
- Combined with:
- Metronidazole and bismuth subsalicylate
Uses: to stop bleeding
== useful in treating Helicobacter pylori
CI: elevated BP, clotting disorders (peptic ulcer)
- ORAL and TOPICAL tetracycline – used to treat
SE: increase BP ( most common), HA, N/V, abdominal - severe acne vulgaris
cramps diarrhea, fatigue, muscle pain
● Mode of Action
- INHIBIT BACTERIAL PROTEIN SYNTHESIS
AE: intrarenal obstruction d/t clot formation, anaphylaxis
[Bacteriostatic]
(esp with aprotinin) - continuous use of tetra – resulted in bacterial
resistance; increased resistance in the treatment
DI: aminocaproic acid + oral contraceptives = increase of pneumococci & gonococci infections
coagulation
● Classifications
Eg: ● SHORT ACTING
- tetracycline {Tetracyn, Panmycin} for gram (+),
Systemic hemostatic:
gram (-), RT & skin disorders, chlamydial,
o Aprotinin gonorrhea, syphilis, rickettsial
o Vitamin K [t ½ = 6-12 hrs]
o Aminocaproic acid - oxytetracycline Hcl {terramycin} for UTI
o Carbazochrome NA
o Tranexamic acid o somatostatin ● INTERMEDIATE
- demeclocycline HCl (Declomycin) for broad
spectrum [t ½ = 10-17 hrs]
Topical
-Gelfilm / gelfoam ● LONG-ACTING (to be taken with food)
-Microfibrillar collagen - doxycycline hyclate (Vibramycin) for bacterial
-Thrombin infection & acne
-Oxidized cellulose - minocycline HCl (Minocin)
[t ½ = 11-20 hrs]

- Frequently prescribed for ORAL use, available also

for IM [cause pain on injection & tissue irritation];
IV route – treat severe infections
- newer ORAL drugs: DOXYCYCLINE,
MINOCYCLINE, METHACYCLINE: rapidly &
complete absorbed,
- not to be taken with MAGNESIUM and ALUMINUM
preparation (antacids), MILK-PRODUCTS
containing calcium or Iron-containing drugs ==
prevent absorption of the drug
- TAKEN on EMPTY STOMACH – 1 hr before meals
(ac) or 2 hrs after meals (pc)
[except doxycycline & minocycline]
● Side effects and Adverse Effects
- GI - NVD {mgt: SFF, ice chips, replace fluids}
- PHOTOSENSITIVITY - sunburn reaction
{sunblock, clothing}
- TERATOGENIC EFFECT - not taken 1st trimester
– PC: D
- Discolors teeth (irreversible) == not taken last
trimester & children < 8yrs
- Balance difficulty – damage to vestibular part of
the inner ear (minocycline) {safety}
- NEPHROTOXICITY - if given in high doses
- SUPERINFECTION - disrupt microbial flora {oral
hygiene}
● Amikacin (1970) [IM/IV] - effective against
Pseudo esp. if resistant to gentamicin &
tobramycin
● Netilmicin (1980) [IM/IV] - less toxic compared
to other aminoglycosides
● Pharmacokinetics
- Gentamicin Netilmicin (latest)
PC: C (can’t rule out) PC: D (+ risk)
{A} : IM, IV
{M} : T½ short (SHL) - 3-4x a day, PB - low (with
pharma response
{E} : unchanged in URINE

● Education ● Pharmacodynamics
S - unlight sensitivity - Gentamicin Netilmicin (latest)
[decomposes in light/heat = TOXIC- store out of ONSET
light & extreme heat] IM/IV: RAPID IM: RAPID, IV - immediate
T - ake full glass of H20 PEAK
O - antacid, IRON & MILK 1-2 hrs 0.5-1.5 hr
P - ut drug into empty stomach DURATION
6-8 hrs unknown
● Drug Interactions
- ANTACIDS, IRON containing drugs, MILK – ● Side effects
prevent absorption of Tetra {take 2 hrs apart} - GI- NAV; rash, numbness, tremors, visual
- ORAL CONTRACEPTIVES – lessened effect of disturbances, tinnitus, muscle cramps or
OCP weakness, photosensitivity
- PENICILLIN – decreased activity of Penicillin
- AMINOGLYCOSIDES – increased risk ● Adverse effects
Nephrotoxicity - URTICARIA, PALPITATIONS
- Thrombocytopenia
- Superinfections
Aminoglycosides - Liver damage
More serious:
- Act by inhibiting bacterial protein synthesis - OTOTOXICITY - 8th cranial nerve damage
(Bactericidal) - NEPHROTOXICITY - oliguria {slowly
- Used against serious infection caused by gram (-) administered}
bacteria [E. coli, Proteus, Pseudomonas & Serratia] - NEUROTOXICITY - neuromuscular blockade,
- Cannot be absorbed in the GIT, cannot cross CSF numbness
(in adults only)
- Primarily administered IV ● Drug Interactions
- Drug of Choice: Tularemia & Bubonic Plague - Penicillin – less effective aminoglycoside
- Anticoagulant (Warfarin) – increased its activity =
● 1st aminoglycosides == STREPTOMYCIN BLEEDING
SULFATE - used in treatment of TB; derived
from bacterium Streptomyces griseus in 1944, ● Nursing Interventions
administered IV - Monitor periodical audiograms, BUN/creatinine &
- ORAL PREPARATIONS: given to decrease vestibule function studies over 10 days therapy
bacteria in the bowel - Adjust renal insufficiency
Examples: - Monitor VS, peak and serum levels
1) paromomycin - useful in treating intestinal - For IV admin., dilute and administer slowly to
amebiasis & tapeworm prevent toxicity
2) neomycin - used as preoperative bowel - Monitor I & O, hydrate well before and during
antiseptic therapy (flush in between)
- Others: (treat pseudomonas) - If anorexia or nausea occurs, SFF meals
● Gentamicin (1963) [IM/IV] - against gram (-) - Establish plan for safely if vestibular nerve effects
esp. pseudomonas occur
● Kanamycin [PO/IM/IV] - for hepatic coma - Administer other antibiotics 1 hour before/after
● Tobramycin (1970) [IM/IV] - kill Pseudomonas amino
- Recommend using sunblock & protective clothing
when exposed to the sun
“THE AMINO MICE” (toxic mice!!!)
- “ONE CAN’T HEAR” - OTOTOXICITY
- “ONE CAN’T PEE” - NEPHROTOXICITY
- “ONE CAN’T FEEL” - NEUROTOXICITY
Macrolides
- {Macrolides, Vancomycin, Lincosamides, Ketolides}
similar spectrum although differ in structure
- Used fr Mild to moderate infections of the RT
(sinuses, GIT, skin, soft tissues; diphtheriae,
impetigo, STD)
● ERYTHROMYCIN (1950s) (Erythrocin, Erymax)
- derived from Streptomyces erythreus
- most commonly prescribed if with allergy to
penicillin
- effective against gram (+) and some gram (-)
except S. aureus
- Drug of Choice: Mycoplasma P., Legionnaires’
disease
- Prevention of Rheumatic Fever
- PC: B (no risk evident)
● Mode of Action
- inhibits CHON synthesis, BACTERIOSTATIC (low
dose) / BACTERICIDAL (high dose)
● Contraindications
- Hepatic disease, Lactation
● Pharmacokinetics
- PO form is well-absorbed in the duodenum; ACID
resistant salts (ETHYLSUCCINATE STEARATE,
ESTOLATE) are added to decrease dissolution,
increase absorption in the intestines; FOOD does
not hamper absorption of ACID resistant
macrolides
- NO IM, IV - give slowly to prevent PHLEBITIS
- PB: 65%
- T½ : PO (1-2 hr), IV (35 hrs)
- Excreted : through the BILE, FECES & small
amount through the urine
● Pharmacodynamics
- PO
- Onset : 1 hr
- Peak : 4 hrs
- Duration : 6 hrs
● Side effects
- NAVIDA is common, PRURITUS, RASH,
TINNITUS
● Adverse effects
- Superinfections, urticaria, hearing loss,
hepatotoxicity [“yellow sclera”], jaundice,
anaphylaxis
● Drug Interactions
- Acetaminophen, Phenothiazine, Sulfonamide -----
↑ HEPATOTOXICITY (reversible)
- ↑ Effect of DIGOXIN, CARBAMAZEPINE,
THEOPHYLLINE, CYCLOSPORINE, WARFARIN,
TRIAZOLAM
- ↓ Effect of PCN, CLINDAMYCIN
- ↓ absorption if taken with ANTACIDS
- Erythromycin + Verapamil, Diltiazem,
Clarithromycin, Fluconazole = elevate Erythro
concentration = cardiac death
● EXTENDED MACROLIDE GROUP
● azithromycin (ZITHROMAX)
- Indications: mild-moderate streptomycin
infection, RTI, gonorrhea, chancroid {STD}, H.
influenzae, Strep., S. aureus
- PC: C (can’t be ruled out)
- A: PO - once a day x 5 days - incompletely
absorbed in GIT
- D: T ½ : 40-50 hrs; only 37% reaches in the
systemic circulation
- E: bile, feces & urine
- Side effects:
NAVDA is uncommon, give AC / 1 hr before
meals or 2 hrs after meals + 1 glass of water
not FRUIT JUICE
- IV PREP - must be diluted in NSS or D5W - to
prevent phlebitis
● Clarithromycin (KLARICID)
- Indications: RTI, gram (-) & (+), tissue
infections, H. pylori
- PC: C
- A: PO
- D: T ½ : 3-6 hrs ==== 2 x a day
- M: PB = 65-75%
- E: bile
- Side Effects:
NAVDA is common, TAKE with MILK/MEAL
● dirithromycin (DYNABAC)
- Indications: CHRONIC BRONCHITIS, URTI,
CAP, Skin Infections, H. pylori, Legionnaires’
disease, Chlamydia
- PC: C
- A: PO x 5 days
- D: T ½ : 20-50 hrs
- M: protein bound
- E: bile, feces
- Side Effects:
NAVDA is common, TAKE with FOOD, or
within 1 hr of eating
● Nursing Care
- Do not refrigerate suspension form of
Clarithromycin
- Monitor liver enzymes – signs & symptoms of
hepatotoxicity
- Administer IV slowly
 - Give IM into deep muscle
- Avoid fruit juices
- Manage NAVDA
- Check for superinfections. Give
YOGURT/BUTTERMILK
- Check drug interactions
- Evaluate effectiveness: WBC level, temperature,
cultures
● The Macrolide Girl
G - GI disturbances (undesirable effects)
I - IV site (check irritation)
R - reduces activity of med if given with acids (fruit
juices) or food
L - liver function test
Lincosamides
- Similar to macrolides but more toxic
- Change CHON function & prevent cell division or
cause cell death (both)
● CLINDAMYCIN (Cleocin)
- widely prescribed against most gram (+)
organism; absorbed better, more effective,
fewer toxic for severe infections caused by
same strains of bacteria that are susceptible
to macrolides
- A: rapidly absorbed from GIT or from IM
injections
- D: T ½ : 2-3 hrs – PB: 94%; crosses the
placenta & enters breastmilk
- M: liver – caution – HEPATIC & RENAL
impairment
- E: urine & feces
- Side Effects:
GI reaction - pseudomembranous
colitis; GI irritation
● LINCOMYCIN (Lincocin)
- to treat severe infections when penicillin
cannot be given
- A: rapidly absorb in GIT or from IM injections
- D: T ½ : 5 hrs
- M: liver – caution – hepatic & renal impairment
- E: urine & feces
- Toxic Effects:
GI reaction, Pain, Skin infection, BM
depression
● Nursing Care (same with macrolides)
- CAREFUL MONITORING
- GI activity & fluid balance
- STOP if with bloody diarrhea
VANCOMYCIN HCl (Vancocin)
- ALMOST abandoned = nephrotoxicity & ototoxicity
(damage auditory or vestibular [CN 8])
- Glycopeptide bactericidal antibiotic (1950s); against
staphylococcal infxns
- used against drug-resistant S. aureus and in
cardiac surgical prophylaxis with PEN allergies;
potentially life-threatening infections not responding
to other less toxic antibiotics
● Mode of Action: Bactericidal
- Inhibits bacterial cell wall synthesis
● Pharmacokinetics
- ORAL - not absorbed systemically; excrete in the
feces
- IV - for severe infections due to MRSA,
septicemia, bone, skin and lower respiratory tract
infections that are resistant to other antibiotics;
excreted in urine
- PB: 30% Half-life: 6 hrs
● Drug Interactions
- Drug-drug
- = if with amphotericin B, polymycin, furosemide,
cisplatin - ↑ NEPHROTOXICITY
- = if with methotrexate - ↑ methotrexate toxicity
● Side effects and Adverse effects
- chills, dizziness, fever, rashes, nausea, vomiting,
thrombophlebitis @ injection site
● Dose Related Toxicity
- tinnitus, high tone deafness, hearing loss &
nephrotoxicity
RAPID IV INFUSION:
- “RED-NECK or RED MAN SYNDROME” resulting
in Histamine release & chills, fever, tachycardia,
profound fall in BP, pruritus or red
nose/neck/arms/back
● Nursing Care
- Refrigerate IV solution after reconstruction, use
within 96 hrs
- Flush IV line in between antibacterials. Evaluate IV
site for phlebitis, avoid extravasation
- Ensure safety
- Check baseline hearing. Refer to EENT. Report
ringing in ears or hearing loss, fever and sore
throat.
- Monitor blood pressure during administration
- Monitor renal function tests - Creatinine, BUN and
urine output; and Liver enzymes
- Yogurt for superinfection
- Check for pregnancy & lactation
● Rudolf the Red - Neck reindeer - Check signs & symptoms of SUPERINFECTIONS
Rudolf the red - neck reindeer (stomatitis, furry black tongue, genital discharge,
Had an adverse side effect itching)
From the drug Vancomycin - Check symptoms of CNS stimulation =
Must keep all labs in check nervousness, insomnia, anxiety & tachycardia >>>
Caution with renal failure, avoid hazardous machinery
Hearing Loss and allergies,
Take a temp and blood cultures,
‘Specially a CBC!!! Sulfonamides

Fluoroquinolones
● Mode of Action
- interfere with the enzyme DNA gyrase (needed to
synthesize bacterial DNA) = Broad spectrum
bactericidal
I. NALIDIXIC ACID (Negram) / CINOXACIN
(Cinobac)
- Prescribed primarily for UTI by gram (-)
E.coli, LRTI, skin, soft tissue, bone & joint
infxns
II. CIPROFLOXACIN (Cipro) / NORFLOXACIN
(Noroxin)
- Broad spectrum including P. aeruginosa
III. LEVOFLOXACIN (Levaquin) /
SPARFLOXACIN (Zagam) /
TROVAFLOXACIN (Trovan) = new
- Treat respiratory problems (CAP), chronic
bronchitis, acute sinusitis, UTI & skin
infections
- Absorbed from GIT, low PB, moderately
short half-life, 75% excreted in the urine
IV. GATIFLOXACIN (Tequin) / MOXIFLOXACIN
(Avelox) = 1999
- OD dosing is more active than
Levofloxacin against S. pneumoniae
● Side effects
- Photosensitivity >>> use sunglasses, sunblock,
protective clothing
- Dizziness, N/V, diarrhea, flatulence, abdominal
cramps, tinnitus, rash
● Nursing Management
- Assess RENAL function
- Drug & diet history:
- Avoid caffeine
- Antacids & Iron prep = decreases absorption
of Fluoroquinolones
- Monitor serum theophylline & blood glucose
levels - with Theo, caffeine, Oral
hypoglycemics = INCREASE their effects
- With NSAIDS = CNS reactions = seizure
- Administer 2 hrs ac or after antacids
- With IRON preparation = give with full glass of
water
- IV – infuse over 30 mins, dilute with
approximate amount
- “Sulfa drugs”
- One of the oldest antibacterial agents; when PCN
(miracle drug) was initially marketed, sulfa was not
prescribed
- First isolated from a COAL TAR derivative
compound in early 1900; produced for clinical use
against coccal infections in 1935
- First group of drugs used against bacteria
- Not classified as an antibiotic because they were
not obtained from biological substances.
● Mode of Action
- Inhibit bacterial synthesis of FOLIC ACID,
essential for bacterial growth, necessary for
synthesis of PURINE & PYRIMIDINES, which are
precursors of RNA & DNA
- For cells to grow and reproduce, they require Folic
acid; human cannot synthesize FA but depend on
folate from the diet. Bacteria are impermeable to
FA & must synthesize it inside the cell
- Remain inexpensive & effective against UTI,
trachoma, ear infection, newborn eye prophylaxis
- 90% effective against E. coli; useful in treatment of
meningococcal meningitis & against organisms
Chlamydia & Toxoplasma gondii; not effective
against viruses & fungi
● Pharmacokinetics
- A: well absorbed by the GIT
- D: well distributed to body tissues and brain
- M: liver
- E: urine
● Pharmacodynamics
- Many for ORAL administration
- Also in solution & ointment for ophthalmic use and
in cream form = SILVER SULFADIAZINE
(silvadene) and MAFENIDE ACETATE
(Sulfamylon)
- Most – highly protein bound & displaced other
drugs by competing for CHON sites
● 2 Classifications
I. SHORT ACTING
A. SULFADIAZINE - ORAL AGENT W/ BROAD
SPECTRUM USE
- slowly absorbed from GIT, peak 3-6 hr
- poorly soluble in urine, cause
crystallization; can damage kidneys if
less H20 intake
 B. SULFISOXAZOLE (Gantrisin) - broad
spectrum; recommended by CDC for
treatment of STD
- useful with Sulfadiazine in prophylactic
treatment of streptococcal infection -
Rheumatic fever; hypersensitive to
Penicillin
- rapidly absorbed from GIT, peak 2 hrs
- excreted in urine, T ½ = 4.5 - 7.8 hrs
II. INTERMEDIATE
A. SULFAMETHOXAZOLE (Gantanol)
- poorer water solubility than Sulfisoxazole
B. SULFASALAZINE (Azulfidine)
- Used to treat ULCERATIVE COLITIS and
CROHN’s disease
- Carried by AMINOSALICYLIC ACID
(Aspirin)
- rapidly absorbed from GIT
- peak levels 2-6 hrs
- metabolized in the liver
- excreted - urine: T ½ 5-10 hrs
C. COTRIMOXAZOLE (Septra, Bactrim)
- combination drug of Sulfamethoxazole &
trimethoprim (synergistic effect)
- effective in treating otitis media,
bronchitis, UTI and pneumonitis by
Penumocystis Carinii
- DOC: Pneumocystis Carinii Pneumonia
(PCP)
- infused over 60-90 minutes; no IM
- A: rapidly from the GIT; peak 2hrs
- M: liver
- E: urine; T ½ : 7-12 hrs
- PC: Teratogenic - birth defects -
Kernicterus
- distributed into Breast Milk = diarrhea &
rash on infant
● Therapeutic Action
- Competitively block
PARA-AMINOBENZOIC ACID
(PABA) to prevent synthesis of Folic
acid in susceptible bacteria that
synthesize their own folates for
production of DNA & RNA
● Adverse effects/Side effects
- rash, itching
- BLOOD : hemolytic anemia, aplastic anemia,
pancytopenia (prolonged and high dosages) - due
to BM depression
- GI : anorexia, N/V {SFF}
- CRYSTALLURIA (crystals in urine); hematuria
(sulfonamides are insoluble in acid urine)
{Increase OFI – dilutes the drug}
Adverse effects…
- Photosensitivity {AVOID sunbathing & excess UV
light}
- Cross-sensitivity - with different sulfonamides
- Hepatotoxicity & nephrotoxicity
- Superinfections {frequent oral care, ice chips,
sugarless candy - to relieve discomfort}
- Hypersensitivity reaction = STEVEN’S
JOHNSONS SYNDROME {D/C drug}
- CNS effects: HA, dizziness, vertigo, ataxia,
convulsions, depressions
● Drug Interactions
- Increase effects of Warfarin
- Decrease absorption if taken with antacids
- Increase hypoglycemic effect of sulfonylureas
- Decrease effectiveness of contraceptives
● Drug Interactions
- Baseline S. crea, BUN, urine output (should be
1,200 ml/day)
- Increase OFI- 2,000 ml/day or administer with full
glass of H20
- Baseline CBC, liver enzymes (AST, ALT, alkaline
phosphatase); monitor for jaundice, icteric sclera
- Monitor VS, check for fever & bleeding
- Observe for hematologic reaction that may lead to
life-threatening anemias; monitor signs of sore
throat, purpura
- Check for signs of superinfections
- Administer 1 hr ac or 2 hrs pc with 1 glass of water
- Avoid/limit sun exposure, use sunblock
- Use clinistix to monitor urine sugar & ketones in
diabetic patients (not clinitest tab)
- Not to be taken with antacids
- Avoid during last trimester of pregnancy
● Education
S - unlight sensitivity
U - undesirable effects - RASH, RENAL TOXICITY
L - ook for urine output, fever, sore throat & bleeding
F - luids galore
A - norexia, anemia
Unclassified Antibacterial Drugs
● CHLORAMPHENICOL (Chloromycetin)
- Discovered in 1947
- MOA: BACTERIOSTATIC - inhibits bacterial
protein synthesis
- SPECTRUM: BROAD - especially against
rickettsiae, mycoplasma, H. influenzae
- USES: serious infections of skin, soft tissue, CNS
infections - including meningitis, ophthalmic
infections — when less toxic drugs cannot be
used; T ½ : 1.5-4 hrs
- PC: C
- PB: 50-60%
- SIDE EFFECTS:
- BM depression - blood dyscrasias
- NEURO - confusion, peripheral neuritis,
depression
- GRAY SYNDROME - in newborn
characterized by: abdominal distention,
vomiting, pallor, cyanosis; NB may die due to
immature liver function
 - NURSING CARE:
- Monitor infection, bleeding
- Monitor for anemia, CBC
- Monitor LOC
● SPECTINOMYCIN HYDROCHLORIDE (Trobicin)
- introduced in 1971 against Neisseria gonorrhoeae
(GONORRHEA)
- allergic to PCN, Cephalosporins, Tetracycline
- administered IM single dose - BACTERIOSTATICS
- PC: B; PROTEIN BOUND - 10%; T ½ : 1-3 hrs
ANTI-VIRAL
- Most difficult to treat than bacterial infections
because virus depends on biochemical processor of
the host cells for its replication
- Drugs that interfere with virus may also damage
cells
MOA: inhibit viral replication by interfering viral nucleic acid
synthesis in the cell

● QUINUPRISTIN / DALFOPRISTIN (Synercid)

- Treat VREF – Vancomycin-resistant Enterococcus AGENTS FOR INFLUENZA AND RESPIRATORY
faecium bacteremia & skin infected by S.aureus & VIRUSES
S. pyogenes
Eg.:
- Disrupts CHON synthesis of the organismWhen
● amantadine (Symmetrel) - PO
administered through peripheral IV line = PAIN,
● oseltamivir (Tamiflu) - PO
EDEMA & phlebitis
● ribavirin (Virazole) - aerosol inhalation
- SE: N/V, diarrhea, pseudomembranous colitis,
● rimantadine (Flumadine) - PO
headache, anaphylaxis, elevated AST & ALT
● zanamivir (Relenza) - inhaler
● Nursing Care
CI: allergy, pregnancy & lactation, renal & liver disease
- Check for DHN, monitor stools
- Check for patency of IV line; infuse over 1 hr in
AE: lightheadedness, dizziness, insomnia, nausea,
D5W
orthostatic hypotension, & urinary retention
- Check for S/S of anaphylaxis
- Monitor ALT, AST, jaundice, icteric eyes
DI: with anticholinergic drugs = increase atropine like effect
- Give ice chips, SFF
NURSING CONSIDERATIONS:
Peptides ● Start regimen as soon after the exposure to the
virus as possible (achieve best effectiveness
and decrease the risk of complications)
- derived from cultures of bacillus subtilis ● Administer the full course of drug
● Provide safety measures (protect patient from
● POLYMYXIN injury)
- Interferes with cellular membrane
- Bactericidal
- Affects gram (-) like E. coli, P. aeruginosa, AGENTS FOR HERPES
klebsiella, shigella
- Not absorbed orally
● Herpesviruses
- IM causes pain; best given slow IV
● Herpes simplex virus type 1
- SE: dizziness
● HSV2
- AE: nephrotoxicity / neurotoxicity
● HSV3: Varicella - zoster (chicken pox or
shingles)
● BACITRACIN
● HSV4: Epstein - Barr virus
- Inhibits cell wall synthesis
● CMV: cytomegalovirus
- Bactericidal / Bacteriostatic
- Most gram (+), some gram (-), can treat meningitis
- Not absorbed by GIT
- Given IM/IV
- SE: N/V
- AE: nephrotoxicity, respiratory paralysis, blood
- dyscrasia, anaphylaxis
EG.:
● acyclovir (Zorivax), famciclovir (Famvir),
valacyclovir (Valtrex) = herpes; PO
● cidofovir (Vistide) = CMV in AIDS; IV
● foscarnet (Foscavir) = both; IV
● ganciclovir (Cytovene) = long term treatment &
prevention of CMV; IV
CI: CNS disorders, allergy, pregnancy & lactation, renal
disease
SE: N/V, HA, depression, rash, hair loss, inflammation &
burning sensation at the site of injection and topical
AE: renal dysfunction
DI:
● + other nephrotoxic meds = inc toxicity
● + zidovudine = inc drowsiness
TOPICAL ANTIVIRALS (HSV)
● idoxuridine
● Penciclovir
● trifluridine
NURSING CONSIDERATIONS:
● Extreme caution to children (carcinogenic);
foscarnet (affect bone growth & development)
● Good hydration (decrease toxic effects to the
kidney)
● Administer as soon as possible, compliance
● Wear protective gloves when applying the drug
topically (decrease risk of exposure to the drug
and inadvertent absorption)
● Safety precautions = CNS effects (orientation,
side rails, lighting, assistance)
● Warn that GI upset, N/V can occur (prevent
undue anxiety, increase awareness of the
importance of nutrition)
● Monitor renal function
● Avoid sexual intercourse if with genital herpes
● Avoid driving and hazardous tasks if with
dizziness & drowsiness
NURSING CONSIDERATIONS:
• Monitor clotting time, urine output, signs of anaphylaxis
• Leave gelfoam until bleeding stops, remove immediately
after bleeding is controlled & wash the site to decrease risk
for infection
• Check BP prior ( defer if > 140/90)
AGENTS FOR HIV & AIDS
● Enzymes needed by viruses:
- Reverse transcriptase
- helps uncoat the virus; single
stranded viral RNA is converted
into DNA
- Integrase
- helps viral DNA migrates into the
nucleus of the cell, where I is
spliced into the host DNA (provirus)
=> duplicated together with the cell
genes every time the cell divides
- Protease
- assists in the assembly of newly
formed viral particles
Nucleoside/ Nucleotide Reverse Transcriptase
Inhibitors (NRTIs)
● MOA: blocks the reverse transcriptase enzyme
needed for viral replication
● E.g.
- zidovudine (Retrovir)
- didanosine (Videx)
- stavudine (Zerit)
- lamivudine (Epivir)
- abacavir (Ziagen)
- tenofovir (Viread)
- emtricitabine (Emtrive
● Fixed dose:
- lamivudine/zidovudine (Combivir)
- abacavir/ lamivudine/ zidovudine (Trizivir)
- abacavir/ lamivudine (Epzicom)
- efavirenz/ emtricitabine/ tenofovir (Atripla)
- emtricitabine/ tenofovir (Truvasa)
● Side Effects
- Less tenofovir - renal toxicity
- GI: nausea, diarrhea, abdominal pain
(transient – 2 weeks)
- Mitochondrial toxicity: lactic acidosis,
peripheral neuropathy, myopathy,
pacreatitis, lipoatrophy (wasting of fats in
face, buttocks and extremities)
● Nursing Considerations:
- Should be taken with food except
didanosine (60 min AC or 2 hours PC)
- Requires dosage adjustment except
abacavir (creatinine clearance <
50mL/min)
- Fixed dose avoided if with renal
insufficiency
Non- nucleoside Reverse Transcriptase
Inhibitors (NNRTIs)
● MOA: prevent viral replication by competing with
binding of the revere transcriptase enzyme at the
active site
- Used to reserve protease inhibitors
(resistance)
● E.g.
1. efavirenz (Sustiva)
- First-choice drug
- PC: D
- CNS toxicities: dizziness, sedation,
nightmares, euphoria, loss of
concentration
- Administered as a component of
Atripla
- OD @ HS
- Empty stomach / low fat meal
(prevent excessive drug
absorption)
2. nevirapine ( Viramune) - alternative
- Pregnancy (1st tri)
- Planning to conceive
- Not using effective/ consistent
contraception
- < risk: rash hepatotoxicity
Entry Inhibitors
● MOA: prevents HIV cell entry (fusion of HIV and
CD4)
● E.g.
1. enfuvirtide
- the only agent approved
- Indicated in combination with 3-5
other anti- retroviral agents (for
clients with limited treatment
option)
- Expensive. 90 mg Sub-Q. BID
- Injection site reaction:
- Subcutaneous nodules,
redness
- Others: rash. Diarrhea,
serious allergic reaction
(anaphylaxis)

3. delavirdine (Rescriptor)
- Least potent antiviral activity
- Not recommended as part of
regimen

Protease Inhibitors

● MOA: act at the end of the HIV cycle to inhibit the

production of infectious HIV virus
● E.g.
- lopinavir/ ritonavir (first line)
- atazanivir
- fosamprenavir (second either boosted with
retonavir or not)
- amprenavir
- tipranavir
- darunavir
- saquinavir
- indinavir
- ritonavir
- nelfinavir

● NOTE:
- Ritonavir boosting
- mainstay of PI therapy (potent
inhibitory effect)
- Take with food
- + didanosine
- one hr before or two hours after
ritonavir