degree of constriction or dilation in

arterioles and arteries.

LESSON 1 - DRUGS THAT AFFECT THE
- Baroreceptors (pressure
CARDIOVASCULAR SYSTEM
receptors) specialized cell on the
arch of the aorta.
A. ANTIHYPERTENSIVES - Renin - Angiotensin Aldosterone
1. ACE inhibitors system (RAAS) compensatory
2. Angiotensin ii receptor blocker mechanism when blood pressure
3. Calcium Channel Blocker within the kidney fall
4. Sympatholytics
5. Vasodilators

B. DIURETICS
1. Thiazide
2. Loop
3. Potassium-Sparing
4. Osmotic

C. ANTI-ANGINAL
1. Nitrates
2. Non-nitrates

D. ANTIARRHYTHMIC 1. Dehydration, Na+ deficiency, or

hemorrhage (Initial stimulus: decrease
E. CARDIAC GLYCOSIDES Blood volume, decrease BP)
2. decrease in blood volume
F. DRUGS AFFECTING THE BLOOD 3. decrease in blood pressure
1. Anticoagulants 4. JG cells or juxtaglomerular cells of
2. Hemostatics kidneys
3. Thrombolytics 5. increased renin
6. angiotensinogen from the liver
BRIEF REVIEW ANATOMY / PHYSIOLOGY 7. increased angiotensin I
a. Cardiac Output - equals the product of 8. Lungs ACE (angiotensin converting
heart rate and stroke volume enzyme)
b. Peripheral Vascular Resistance - 9. increased angiotensin II
determined by local blood flow & the 10. adrenal cortex
degree of constriction or dilation in 11. increased aldosterone
arterioles and arteries. 12. in kidneys, increased Na+ and water
- Baroreceptors (pressure reabsorption and increased secretion of
receptors) specialized cells in the K+ and H+ into urine
arch of the aorta 13. increased blood volume
14. blood pressure increases until it returns
Renin-Angiotensin Aldosterone System to normal
(RAAS) 15. vasoconstriction of arterioles
- Compensatory mechanism when blood 16. increased K+ in extracellular fluid
pressure within the kidneys fall
–––––––HYPERTENSION––––––
DETERMINANTS OF BP: - silent killer
a. Cardiac output - equals the product of - When a person’s blood pressure is
heart rate and stroke volume above the normal limits for a sustained
b. Peripheral vascular resistance - period
determined by local blood flow and the
Types:
1. Primary or essential - No known cause
2. Secondary - With co-morbidities
–––––STEPPED CARE APPROACH:–––––
Step 1: Lifestyle modification
- With reduction
- Decrease sodium intake
- Moderate alcohol intake
- Smoking cessation
- Increase physical exercise
- Take medication as prescribed
Step 2: Inadequate response
- Continue lifestyle modifications. if
measures in step 1 are not sufficient to
lower blood pressure to an acceptable
level, then drug therapy is added:
● Diuretic (decreases serum sodium
levels and blood volume)
● Beta-blocker (leads to a decrease in
heart rate and strength of contraction,
as well as
● vasodilation)
● ACE inhibitor (blocks the conversion of
angiotensin 1 to angiotensin 2)
● Calcium channel blocker {which relaxes
muscle contraction) or other autonomic
blockers
● Angiotensin ll-receptor blocker (blocks
the effects of angiotensin on the blood
vessel)
Step 3:
- Inadequate response consider change
in drug dose or class, or addition of
another drug for combined effects.
● aliskiren with hydrochlorothiazide (Tekturna
HCT)
● atenolol with chlorthalidone (Tenoretic)
● amiodipine with benazepril (Lotrel)
● amlodipine with valsartan (Enforce)
● bisoprolol with hydrochiorothiazide (Ziac)
● candesartarn with hydrachlorothiazide (Atacand
HCT)
● chiorthatidone with clonidine (Combipres)
● enalapril with hydrochlorothiazide (Vaseretic)
● eprosartan with hydrochlorothiagide (Teveten
HCT)
● fosinopril with hydrochlorothiazide (Monopril
HCT)
● hydrochlorothiazide with benazepril (Lotensin
HCT)
Step 4: Inadequate response
- All of the above measures are continued
- A second or third agent or diuretic is
added if not already prescribed
HEALTH TEACHING: PRESSURE
● P - pressure (blood) monitoring
● R - rise slowly
● E - eating must be considered
● S - stay on medication
● S - slipping or abrupt stopping is No-No
● U - undesirable responses
● R - remind to exercise, decrease alcohol
● E - elimination smoking
Three basic processes to produce urine.
A. Filtration - the movement of water and
solutes from the plasma in the
glomerulus, across the glomerular
capsule membrane and into the
capsular space of the Bowman’s
capsule.
B. Reabsorption - movement of molecules
out of the tubule and into the peritubular
blood; 80% water, sodium, potassium,
chloride, and most other substances is
reabsorbed.
20% of the glomerular filtrate enters the
loop of henle.
- Ascending limb - Sodium is
reabsorbed
- Distal tubule - sodium is
reabsorbed
- Final reabsorption of water -
distal tubule and small tubules
The remaining water and solutes are now
appropriately called urine
C. Secretion - movement of molecules out
of the peritubular blood and into the
tubule for excretion
 Proximal tubule - uric acid, creatinine,
hydrogen ions, and ammonia are
secreted
Distal tubule - potassium ions, hydrogen
ions, and ammonia are secrete
● ACE inhibitors - block formation of
angiotensin II, causing vasodilation and
block aldosterone secretion, decreasing
fluid volume
● beta blockers - decrease the heart rate
and myocardial contractility, reducing
cardiac output
● alpha 2 agonists - decrease sympathetic
impulses from the CNS to the heart and
arteries, causing vasodilation
● alpha 1 blockers - inhibit sympathetic
activation in arterioles, causing
vasodilation
● direct vasodilators - act on smooth
muscle of arterioles, causing
vasodilation
● calcium channel blockers - black
calcium ion channels in arterial smooth
muscle, causing vasodilation
● angiotensin receptor blockers - prevent
angiotensin II from reaching its
receptors, causing vasodilation
● diuretics - increase urine output and
decrease fluid volume
–––––ANTIHYPERTENSIVE–––––
a. Angiotensin - Converting enzyme (ACE)
inhibitors (“pril”)
MOA (Mechanism of Action): blocks the
conversion of angiotensin 1 to angiotensin 2
Uses: Hypertension, MI
Eg.
- Benazepril (lotesin)
- Moexipril (Univasc)
- Captoril (capoten)
- Perindopril (Aceon)
- Enalapril maleate (Vasitec)
- Lisinopril
- Quinapril (Accupril)
- Ramipril
- Fosinopril (Prinivil)
- Trandora
SE (Side effects): cough, hypotension, HA,
dysgeusia (any perversion of taste perception)
insomnia. N/V, diarrhea.
AE (Adverse effects): reflex tachycardia, chest
pain, angina, CHF, cardiac arrhythmias, ulcers,
liver and renal problem, photosensitivity,
hyperkalemia, neutropenia, angioedema
DI (Drug interactions): + probenecid =
decrease elimination
+ K supplement and diuretics =
hyperkalemia
+ NSAIDS = decrease hypotensive effect
+ Antacids = decrease absorption of the
drug
+ Tetracycline = decrease absorption of
tetra
CI (Contraindications): renal disease, severe
NA depletion, CHF, pregnant and lactating
women
Nursing Consideration
● Encourage implement lifestyle changes
● Administer on an empty stomach
● Alert if patient is for surgery/
dialysis/situations which may drop the
fluid volume
● Parenteral form only if oral form is not
available
● Adjust dose if with renal failure
● Do not give if BP is below 90/70,
monitor BP esp for 2 hours after the first
dose (hypotension)
● Avoid ambulation (dizziness)
● Report cough / angioedema
● Report dysgeusia if more than 1month
B. Angiotensin 2 receptor antagonist SE/AD: HA, dizziness, hypotension, syncope,
(“sartan”) reflex tachycardia, constipation, AV block,
- Selectively bind the angiotensin 2 bradycardia, peripheral
receptors in the blood vessels and
adrenal cortex. NURSING CONSIDERATION
- Monitor ECG, CR, BP
Eg. - Have “E” cart available with IV
telmisartan (micardis) administration
losartan (diovan) - Position to decrease peripheral edema
- Protect drug from light and moisture
irbesartan (aprovel)
- Increase OFI and fiber in the diet
candesartan (blopress) - Avoid overexertion when anginal pain is
valsartan (cozaar) relieved
eprosartan (teveten) - may give paracetamol if with HA
- Take with meals or milk
USES: when ACE inhibitors are not tolerated - No not chew or crush sustained release
-
SE: HA, diarrhea, dyspepsia, cramps –––––SYMPATHOLYTIC DRUGS–––––
The sympatholytics comprise 5 five groups of
AE: angioedema, hyperkalemia drugs:
1. beta adrenergic blockers
CI: nephro dysfuction, CHF, pregnancy 2. centrally acting alpha 2 agonists
3. alpha- adrenergic blocker
Nursing considerations: 4. adrenergic neuron blocker
- unsure female patients is not pregnant (peripherally acting sympatholytics)
- Take without regard to food 5. alpha 1 and beta 1 adrenergic
blockers
Effects of ARBs
- lower (angiotensin 2 effects, 1. Beta-adrenergic blockers
aldosterone, and ADH) - Beta blockers “OLOL”/ beta - adrenergic
- Lower (resistance) blocking agents/ beta-adrenergic
- Lower (blood volume) antagonists/ beta antagonists

C. Calcium channel blocker MOA: block beta 1 (cardiac) and / or beta 2 (lung)
adrenergic receptor sites; decrease the effects of
MOA: the SNS by blocking the release of catecholamines,
thereby decreasing the HR and BP.
- prevent movement of calcium ions in the
● *Beta-one receptors Are found in the heart
myocardium and vascular smooth and kidneys. When stimulated, they
muscles. increase heart rate, AV conduction, &
- Normally: Calcium increase muscle automaticity
contractability, peripheral resistance and ● Beta1-blockers reduce heart rate, blood
BP pressure, myocardial contractility, and
myocardial oxygen consumption.
Eg. ● *Beta-two receptors Mainly in the lungs,
Amlodipine (Norvasc) gastrointestinal tract. liver, uterus, vascular
nimodipine (nimotopp) smooth muscle, and skeletal muscle. Serve
diltiazem (cardizem) to dilate bronchial and vascular smooth
muscle.
felondipine (plendil)
● Beta2-receptor blockade Inhibits relaxation
nicardipine (cardene) of smooth muscle in blood vessels, bronchi,
nifedipine (procardia) the gastrointestinal system, and the
verapamil (calan) genitourinary tract

USES: angina, hypertension, atrial fibrillation

USES: hypertension, dyshythmias, angina BLOCKER
pectoris. ● B bradycardia
● L lipidemia increase, libido decrease
AE: rebound hypertension ● O bronchospasm
● C CHRonduction abnormalities
CI: (ABCDE) ● K Contriction peripheral vascular
● A asthma ● E Exhaustion motional depression
● B block (heart block) ● R reduces recognition of hypoglycemia
● C COPD - “Blocker” outlines undesirable
● D diabetes Mellitus effects of Beta Blockers
● E electrolyte imbalance (hyperkalemia)
2. ALPHA - ADRENERGIC BLOCKER
DI: ➔ MOA: blocks alpha 1 adrenergic
+ antacids = delayed drug absorption receptors resulting in vasodilation of
+ lidocaine = increase plasma level of arteries and veins
lidocaine ◆ Decrease peripheral resistance;
+ insulin/ OHA = hypoglycemia relaxes smooth muscle of bladder
+ cardiac glycosides = addictive / prostate
bradycardia ● Enlargement prostate
+ calcium channel blockers = increase gland
pharmacologic and toxic effects of both ● BPH, benign prostatic
+ cimetidine = decrease metabolism of hypertrophy, relax smooth
beta blockers mm of bladder, so no more
+ theophylline = impaired difficulty in urination d/t
bronchodilating effects improved flow
◆ Decrease VLDL & LDL =
EG: decrease fat deposits ; increase
❖ Nonselective beta blockers HDL
- carvedilol (coreg) ● Decrease serum
- propranolol (inderal) cholesterol
- pindolol (visken) ● Hyperlipidemia
- nadolol (corgard) ◆ Does not affect glucose
- timolol (blocadren) metabolism & respiratory function
❖ Cardioselective beta blockers (B1) ● Can be given to DM
- acebutolol (sectral) patients
- betaxolol (kerlone) ◆ Causes Na & H2O retention with
- esmolol (brevibloc) edema; given with diuretics
- atenolol (tenormin) ◆ WARNINGS: renal disease,
- bisoprolol (zebeta) elderly more sensitive
- metoprolol (betaloc, cardiosta) ❖ Potent Alpha Blockers: hypertensive
crisis & severe hypertension from
Nursing Considerations: catecholamine secreting tumors of the
- Lifestyle modification adrenal medulla (pheochromocytoma)
- Compliance (rebound hypertension) ➢ Eg.
- Monitor blood sugar and diabetics ■ Phentolamine
- Monitor triglycerides and cholesterol ■ Phenoxybenzamine
level (LDL) ■ tolazoline
- Monitor BP and pulse before and after ■ Prazosin (Minipress) =
- Withhold if pulse is <60 or SBP <90 CHF
- Monitor any change in the rhythm or ● Congestive heart
signs of CHF failure
 ■ Doxazosin (Cardura) = ➢ Sugarless gum, sips of tepid H20,
also for BPH etc. may relieve dry mouth
■ Terazosin (Hytrin) = also ■ Not cold water
for BPH ➔ Mini's SINS
➢ Hypertensive crises ◆ S - yncope or sexual dysfunction
■ Very high BP, shoots up, ◆ I - ncreased drowsiness,
■ Alpha 1 blocker orthostatic hypotension, HR
➔ SE: orthostatic hypotension ( dizziness, ◆ N - eed to be recumbent for 3-4
faintness, increase HR) 1st dose hours after initial dose
syncope (hypotension with loss of ◆ Mini's “SINS” (minipress) are
consciousness) Nausea, drowsiness, undesirable effects of Alpha
nasal congestion, weakness, loss of Adrenergic Blockers. These
libido medications end in “SIN”
◆ Phentolamine - reflex tachycardia
● Increase apical PR 3. CENTRALLY ACTING ALPHA2 AGONIST
● cause heart to work harder ➔ MOA:
via baroreceptors ◆ decrease sympathetic response
◆ Orthostatic hypotension from brainstem to the peripheral
● Fowler's position, dangle vessels; resulting in a decrease
legs, if no dizziness, then peripheral vascular resistance &
ambulate BP
● Do not sit up and ambulate - ✓ Stimulate the alpha2
● Do not immediately receptors:
ambulate - Decrease sympathetic
➔ DI: activity
◆ + other antihypertensive, alcohol, - Increase vagus
nitrates = increase hypotensive nerve
effects - Exert function in the brain
◆ Prazosin + anti inflammatory drug - Suppress sympathetic
= peripheral edema blood to heart
◆ Prazosin & nitroglycerin = - ✓ Decrease epinephrine,
syncope norepinephrine, renin release
➔ SE/AE:
❖ NURSING INTERVENTIONS: ◆ drowsiness, HA, dry mouth,
➢ Monitor BP frequently dizziness, bradycardia,
■ Always monitor BP and constipation, hypotension,
PR occasional edema or weight gain
■ Withhold medication and ➔ Dl: paradoxical hypertension with
inform prescriber propranol
➢ Protect from falling / injury
➢ Assess BP and HR before each
dose ➔ EG:
➢ If dose is during the day, client ◆ Methyldopa (Aldomet) (for
must remain recumbent for 3-4 ° chronic/PIH)
■ 3 - 4 hours, lie on bed ● DOC for women with PIH
■ Assist to prevent fall ● No other drugs taken by
related injuries client
➢ Assist with ambulation if client is ◆ Clonidine (Catapres) cause Na &
dizzy water retention (given with
➔ Education: diuretics)
➢ Implement safety precautions
➢ Report if edema is present
 ❖ NURSING CONSIDERATIONS:
➢ Monitor baseline VS ( q30 mins
until stable during initial
➢ Abrupt discontinuation =
hypertensive crisis (restlessness,
tachycardia, tremors, HA, &
increase BP)
➢ Taper dose gradually over more
than one week
➢ Sugarless gum, sips of tepid
water may relieve dry mouth
➢ Weight gain
■ Measured in pounds
4. ADRENERGIC NEURON BLOCKERS
(PERIPHERALLY ACTING SYMPATHOLYTIC)
- Potent antihypertensive drugs
- Psychological effect
❖ MOA:
➢ block norepinephrine release
from the sympathetic nerve
endings that results in decrease
BP
❖ SE:
➢ orthostatic hypotension, Na &
water retention, vivid dreams,
nightmares & suicidal intention
(reserpine)
❖ EG:
➢ reserpine (Serpasil) and
guanethidine
❖ NURSING CONSIDERATIONS:
➢ Take with meals, no alcohol
➢ Last drug of treatment of chronic
hypertension (Last resort)
5. ALPHA1 & BETA1 - ADRENERGIC
BLOCKERS
➔ MOA:
◆ blocks both alpha1 and beta1
receptor sites; decrease BP &
moderately decrease PR.
● Check BP and apical pulse
➔ SE:
◆ orthostatic hypotension, GI
disturbances, nervousness, dry
mouth, fatigue
➔ AE: heart block
➔ Cl:
◆ large doses could block beta 2
receptors = increase airway
resistance in patients with asthma
➔ Eg:
◆ labetalol (Normodyne)
◆ carteolol (Cartrol)
–––––––E. VASODILATORS–––––––
➔ MOA:
◆ relaxes smooth muscles of blood
vessels esp the arteries; promotes
increase blood flow to the brain &
kidney
◆ Direct acting arterial vasodilators
● Smooth mm of arteries
● Direct relaxation of vascular
smooth mm
◆ Not effect on the heart
● Purely
● Dilate or relaxes artery
➔ USES: severe hypertension, emergencies
➔ EG:
◆ hydralazine (Apresoline)
◆ diazoxide ( Hyperstat)
◆ minoxidil (Loniten)
◆ nitroprusside ( Nitropress)
➔ SE/ AE:
◆ hydralazine: tachycardia (beta
blockers), palpitations, edema
(diuretics), HA, dizziness, Gl bleed,
lupus like and neurologic symptoms
minoxidil: similar effects, excess hair
growth, precipitates angina
● Lupus like, autoimmune,
antibodies attack own cells of
the body
◆ Nitroprusside & diazoxide
(hyperglycemia)
➔ Cl: allergy, pregnancy, lactation, cerebral
insufficiency
➔ DI: + other antihypertensive drugs =
additive effect
❖ NURSING CONSIDERATIONS
DILATOR:
➢ D - irectly acts on vascular smooth
muscle
➢ I - ncrease renal and cerebral blood
flow
➢ L - upus like reaction ( fever, facial
rash, muscle and joint pain,
splenomegaly)
➢ A - ssess peripheral edema
➢ T - ake with food
➢ O - ther side effects (headache,
dizziness, anorexia, Inc. Cardiac,
Dec. Blood pressure)
➢ R - eview BP (orthostatic
hypotension), blood glucose
 –––––––DIURETICS–––––––
➔ Produces increased urine flow by
inhibiting sodium and water reabsorption
from the kidney tubules.
➔ 2 main purposes:
◆ To decrease hypertension
● Lowers down
decrease fluid peripheral
or primary
◆ To decrease edema
● Increases urine flow
● Promote diuresis
● Increase urine output
● Na and H2O, Excreted in
large amount, since
inhibited reabsorption
● I&O monitoring
➔ INDICATIONS:
◆ ✓ Congestive heart failure
◆ ✓ Pulmonary edema
◆ ✓ Liver failure & cirrhosis
◆ ✓ Renal diseases
◆ ✓ Hypertension
◆ ✓ Glaucom
➔ CONTRAINDICATIONS:
◆ Allergy Fluid & electrolyte
imbalances
◆ Severe renal diseases SLE DM
(Systemic lupus erythematosus)
➔ 1kg or 2.2 lbs wt gain = 1 liter of fluid
➔ 1st line drugs for treating Hypertension
◆ Fewer SE
◆ Given in combination with anti
HPN agents
➔ *glomerulus → PCT → descending loop
of Henle → ascending loop of Henle →
DCT → collecting duct
Types:
1. Thiazide Diuretics
➔ MOA:
◆ increase Na & water excretion by
inhibiting Na reabsorption in the
distal tubule of the kidney .
◆ ** not effective for immediate
diuresis
➔ Uses:
◆ mild- moderate HPN, edema
associated with CHF, cirrhosis
with ascites Warning: decrease
K, renal/ hepatic dysfunction,
gout
➔ DI:
◆ + lithium = lithium toxicity
● Lithium, bipolar disorder
◆ + digoxin = digoxin toxicity (
bradycardia, N/, visual changes)
● Hypokalemia
● Digitalis toxicity
BP, ● Antidote: digoxin immune fab
(Digibind)
◆ + corticosteroids, amphotericin,
ticarcillin = hypokalemia
◆ + sulfonamides = cross sensitivity
➔ SE/ AE:
◆ hypokalemia, hyponatremia,
hypomagnesemia, hypotension,
bicarbonate loss, hypercalcemia,
hyperglycemia, hyperuricemia, N/N,
constipation, rashes, dizziness,
weakness, increase LDL,
photosensitivity, H/A, dehydration,
blood dyscrasias
➔ Eg:
◆ chlorothiazide (Diuril)
◆ hydrochlorothiazide (Hydrodiuril)
◆ metolazone (Zaroxolyn)
◆ chlorthalidone (Thalitone)
◆ indapamide ( Lozol)
➔ Nursing Responsibilities:
◆ Monitor BP, wt OD, urine output,
edema
◆ Monitor K, Na, Ca, blood glucose,
LDL, triglycerides
◆ Change position slowly
◆ No alcohol
◆ Take with meals preferably in AM
◆ Eat foods high in K ( banana,
avocado, broccoli, dried fruits,
oranges, nuts ,potato, prunes,
tomato)
◆ Manage photosensitivity
◆ Signs of hypokalemia (muscle
weakness, cardiac dysrhythmias,
cramps, dizziness, N/V, tingling
sensation, "U" wave on the ECG
(3.5 - 5.1 mEq/L)
➔ Nursing Responsibilities THIAZIDE
◆ 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 monitoring
◆ D - iuresis is expected: I&O
◆ E - at potassium rich food
II. Loop Diuretics ● Promote diuresis through
➔ AKA high ceiling or K wasting diuretics osmosis
➔ Ascending and descending loop of ● Given as IV solution, when
Henle filtered by glomerulus,
➔ MOA: does not undergo
◆ inhibits Na & Cl absorption from reabsorption
the loop of henle and distal ● Osmosis, fluids move low
tubules , causes rapid diuresis, solute concentration to
little effect on glucose high solute concentration
➔ USES: ○ Solutes are not
◆ HPN, edema associated with reabsorbed
CHF, cirrhosis with ascites, ○ Osmotic force,
hypercalcemia inhibit passive
➔ DI: same with thiazide reabsorption
◆ + lithium = lithium toxicity ○ Urine flow
◆ + digoxin = digoxin toxicity ( increases
bradycardia, N/, visual changes) ● Taken as IV route
◆ + corticosteroids, amphotericin, ● Narrow angle glaucoma
ticarcillin = hypokalemia ○ Decrease
◆ + sulfonamides = cross sensitivity intraocular
➔ Eg: pressure, or lead to
◆ furosemide (Lasix) blindness
◆ torsemide ( Demadex) ➔ USES:
◆ ethacrynic acid (Edecrin) ◆ increase ICP, edema, prevention
◆ bumetanide (Bumex) of renal failure, oliguria, inducing
➔ Nursing Responsibilities: diuresis during chemotherapy
◆ Monitor VS, edema, urine output, ➔ Cl: anuria
serum K. Na, Ca, Cl, thiamine, ➔ DI:
blood glucose & platelet levels, ◆ increase hypokalemia which may
Mx of digoxin & lithium toxicity increase digoxin toxicity
● Check serum K 3.5 – 5 ml
➔ SE/ AE:
◆ Potassium rich foods
◆ Give slow IVTT (2 mins) to prevent ◆ pulmonary edema d/T rapid fluid
hearing loss shifting, NV, tachycarida,
● IV give w/in 2 mins to prevent decrease Na, K, Cl, Ca,
ototoxicity dehydration
◆ With food, in AM ➔ Eg
➔ Nursing Responsibilities CEILING ◆ mannitol (Osmitrol)
◆ C - heck for weight gain ◆ urea (Ureaphil)
◆ E - nsure VS prior to ◆ glycerin (Osmoglyn) = dec IOP
administration ◆ isosorbide (Ismotic)
◆ I - & O monitoring ➔ Nursing Responsibilities:
◆ L - aboratory values assessment ◆ Monitor VS, wt, urine output,
◆ I - nstruct to rise slowly serum NA, K, CI,
◆ N - octuria prevention: ◆ Watch for rapid increase in BP &
◆ G - ive it with meals rapid sympathetic over-activity
(increase HR, tremor, agitation) -
III. Osmotic Diuretics ◆ Assess lung and heart sounds
➔ MOA: ◆ Check skin turgor, Level of
◆ increase osmotic pressure in the consciousness, manifestations of
glomerular filtrate, preventing decrease ICP
reabsorption of water & ◆ Mannitol: check bottle or vial for
electrolytes crystallization, warm bottle &
 shake vigorously to dissolve ➔ Nursing Responsibilities:
crystals, if it doesn't dissolve = ◆ Monitor VS, urine output, serum
DO NOT administer - use IV line K level
with filter - infuse for 30-60 mins. ◆ Inform client that hypotensive
● do not administer if effects may not be seen for 2
crystallized, if bottle exposed weeks
to cold env, warm not boil, IV ◆ Avoid potassium rich foods
line or needle has filter ◆ Manage photosensitivity
➔ Nursing Responsibilities OSMOTIC ◆ Avoid salt substitutes Take with
◆ O - liguria, edema, inc. meals
ICP(indication) ◆ Bluish colored urine is harmless
◆ S - tops reabsorption of water ◆ Administer in AM
◆ M - annitol
◆ O - utput of urine, electrolytes - ––––––Interventions for DIURETICS:––––––
monitor ● D - iet: decrease sodium intake
◆ T - issue dehydration ● I - ntake & output monitoring
◆ I - ncreased frequency/volume of ● U - ndesirable effects
urination ● R - eduction of edema
◆ C - irculatory overload ● E - lectrolytes review
● T - ake early in the day; with meals
IV. Potassium Sparing Diuretics ● I - nteractions:digoxin
➔ MOA: ● C - ause/aggravate diabetes
◆ acts on the distal tubule to ● S - ensitivity to sunlight
promote Na and water excretion
& prevent potassium excretion;
● Not excreting
● Preventing K excretion
➔ AKA: Aldosterone antagonist
➔ USES: HPN, edema = CHF, nephrotic
syndrome to counteract hypokalemia
caused by other diuretics
➔ Cl: severe renal disease, severe
hyperkalemia
➔ DI:
◆ + lithium = lithium toxicity
◆ + ACE inhibitor = hyperkalemia
◆ + digoxin = digoxin toxicity
◆ + K supplements (eg kalium
durule) = hyperkalemia
➔ SE/AE:
◆ hyperkalemia, N/V, diarrhea, dry
mouth, rash, dizziness,
weakness, bluish colored urine
(triamterene) hypotension,
increase potassium level result in
peaked I wave on ECG
➔ AE:
◆ HA (headache), photosensitivity,
anemia, decrease platelet Eg:
amiloride (Midamor)
spironolactone (Aldactone)
triamterene (Dyrenium)
 –––––––ANTIANGINAL–––––––
- *Coronary Artery Disease (CAD)
- lumen of blood vessels become
narrow, thus blood is no longer
able to flow freely to the muscles
- *Angina pectoris
- "suffocation of the chest”, occurs
when myocardial demand for
oxygen cannot be met by
narrowed blood vessels
- ***anginal pain:
- chest tightness, pressure in the
center of the chest, and pain
radiating down the neck and left
arm.
- *Myocardial Infarction (MI)
- occurs when coronary vessels is
completely occluded and the cells
that depend on the vessels for
oxygen become ischemic, then
necrotic and death
- Ischemic → necrotic → cell death
- Angina Pectoris- sudden pain due to drop of
oxygen
- Ischemic - reduced blood flow
- Necrotic - cells of the heart die due to
ischemia
Types of Angina:
1. Classic (stable)
a. occurs with stress exertion
2. Unstable (pre-infarction)
a. occurs frequently over the course of
a day with a progressive severity
3. Variant (Prinzmetal, vasospastic)
a. occurs during rest caused by
coronary artery spasm
Types of Anti-Anginals:
1. Non-nitrates (beta blockers, calcium
channel blockers)
2. Nitrates: Isosorbide mononitrate (Imdur,
isoket, isordil); nitroglycerin (Deponit,
Nitrostat)
Nitroglycerin
- improve blood flow to the heart, nitroglycerin
opens up (dilates) the arteries in the heart
(coronary arteries), which improves
symptoms and reduces how hard the heart
has to work.
● Side effect:
○ headache (commonly solved with
paracetamol per doctor’s order)
○ Radiation (of pain), can the pain be
felt in places far from the origin
○ The more muscles affected by low
oxygen, more cell death
Nitrates
➔ MOA
◆ SA : Dilation of the veins =
Decrease oxygen demand by
dilating veins, which decreases
preload (less blood return)
◆ VA : Increase oxygen supply by
relaxing coronary vasospasm
◆ CCB: dilation of arteries = Less
vasoconstriction and resistance
(decrease afterload)
◆ BB: Decrease oxygen demand by
decreasing heart rate and
contractility
➔ Uses: treatment & prevention of angina,
decrease BP
➔ SE: HA (most common) , dizziness,
hypotension, reflex tachycardia, decreased
CR, GI distress, flushing.
➔ AE: Some degree of hepato / nephrotoxicity.
NURSING CONSIDERATIONS:
● Assess chest pain: Precipitating factors,
Quality, Radiation, Severity/ Symptoms and
Time.
● PO: take on empty stomach; undergoes
hepatic first pass effect
- Sustained release if taken per orem
● SL: every 5 min X 3 doses; effect lasts for
10minutes
○ Store in dry & dark bottle
○ Check expiration date (Up to six
months only)
○ Take sips of water BEFORE
administration
○ Allow drug to dissolve before taking
anything PO
○ Burning/ Stinging sensation means
the drug is potent
- Sublingual every 5 mins, if after 5
mins the previous med is still
present, replace with new
● Buccal : Place drug between upper lip and
gum or between cheek and gum
● IV infusion : dilute drug in glass IVF bottles
via infusion pump, onset 1-3 minutes same
with SL
- Use nitroglycerin in glass IVF bottles
because if plastic (polyvinyl), the
plastic will absorb the medication
● Topical Ointment : remove previous
application: spread drug over 6x6 in are 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
- Anterior Chest Wall and also
Thigh
○ Removes previous, rotate sites
○ Remove after 12 hours to prevent
tolerance
○ do not apply defibrillator paddles
over the drug may cause burn.
- Using defibrillator over drug
can cause arrhythmia
● Spray: lift tongue then spray, avoid inhaling
the drug
● General: withhold
- Assume Myocardial Infarction (MI) if
not relieved of symptoms
––––––CARDIAC GLYCOSIDES––––––
● Congestive Heart Failure (CHF) - condition
in which the heart fails to effectively pump
blood around the body due to damaged or
overworked heart muscle (myocardium).
○ Can be left sided or right sided:
○ Left side- Towards lungs affected
○ Right side- Towards systemic
circulation affected (backflow)
● Causes: Coronary artery disease,
Cardiomyopathy, Hypertension, Valvular
heart disease.
● 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
★ ICF(K) & ECF(Na)
➔ MOA:
◆ INHIBITS NA- K pump which
increases intracellular calcium and
allow more calcium to enter
myocardial cells during
depolarization causing:
◆ (+) inotropic action - increase
myocardial contraction
◆ (-) Chronotropic action - decrease
heart rate
◆ (-) dromotropic action - decrease
conduction velocity
◆ > Increase cardiac output and renal
perfusion.
➔ Digitalis Toxicity:
◆ anorexia, diarrhea, N/V, bradycardia,
cardiac dysrhythmias, HA, malaise,
blurred vision, visual illusions (white,
green, yellow halos around objects),
confusion and delirium
◆ Antidote:
● Digoxin immune Fab
(intoxication with serum level
of. 10ng/ml)
● Bind with digoxin to form
complex molecules that can
be excreted.
➔ CI:
◆ Hypersensitivity, ventricular
tachycardia and fibrillation, heart
block,MI, renal insufficiency,
electrolyte imbalance (increased
calcium, decreased K &Mg)
➔ DI:
◆ +Verapamil, quindine, quinine,
erythromycin, tetramycin,
cyclosporine = increase toxic effect
◆ CONTINUATION
NURSING CONSIDERATIONS
❖ Consult prescriber about loading dose
❖ Monitor Apical pulse in one full minute,
monitor for quality and rhythm
❖ Check dosage & preparation carefully
❖ Check pediatric dose with extreme care
❖ Follow dilution carefully for IV preparation
❖ Administer Iv dose very slow over at least 5
minutes
❖ Weight patient
❖ Avoid administering oral drug with food or
antacid.
❖ Maintain emergency equipment on standby
= Lidocaine (arrythmias), Phenoytoin
(seizure), atropine( give if tachycardia exist
) SO4
❖ Monitor therapeutic level of digoxin
(0.5-2ng/ml), digoxin toxicity.
❖ Potassium rich foods
➢ Banana, avocado, broccoli, dried
fruits, oranges, nuts, potato, prunes,
tomato
❖ Sodium rich foods
➢ Buttermilk, margarine, canned
goods, processed foods, fast foods,
preserved foods, tomato ketchup
––––DRUGS AFFECTING THE BLOOD––––
● Works at various steps in the clotting ang
clot dissolving process in order to restore
the balance that is needed to maintain the
cardiovascular system
◆ Prevent or promote clots
❖ ANTICOAGULANTS - drugs that interfere
with the normal coagulation process
❖ ANTIPLATELET - alter the formation of
platelet plug
❖ THROMBOLYTICS - breakdown the
thrombus that has been formed by
stimulating the plasmin system
❖ HEMOSTASIS AGENTS
★ Hemostasis, physiologic process by w/ch
bleeding is stopped
★ Many diff ways of preventing bleeding
★ Platelet aggregation, Formation of a plug to stop
bleeding
★ Reinforcement with fibrin in clotting
★ Activation of plasminogen to dissolve clot
formed
Mechanisms of Blood coagulation
1. Vascular Response
a. Platelets release serotonin causing
vasoconstriction
b. If part in the body is injured, there
will be a vascular response first
2. Platelet Aggregation
a. Platelets form a mechanical barrier
or wall to close off the break in the
capillary
b. Fibrin causes long lasting protection
3. Chemical clotting
a. Release of clotting factors :
i. Clots - prevent blood loss
ii. Clotting - chain of reaction
stimulated by the release of a
chemical called
thromboplastin from injured
cells
★ We need to block prothrombin
● Injury or damage
○ Injury/ rupture to blood vessel
● Vessel contracts
○ Blood vessels around the wound
constrict - reduce blood flow to the
damaged area. Activated Platelets stick
to injury site
● Platelet plug
○ Platelets become sticky and clump
together to form platelet plug.
○ Platelets & damaged tissue release
clotting factors (eg. Factor VIII)
● Fibrin clot
○ Blood clotting mechanism to form Fibrin
which acts like a mesh to stop the
bleeding.
THROMBOPLASTIN
↓
Acts on PROTHROMBIN & causes it to be converted into its
active form THROMBIN
↓
Acts on another blood protein FIBRINOGEN
↓
When activated, it is converted to FIBRIN
↓
Fibrin web forms a plug that stops flow of blood to tissues
↓
Platelet thromboplastin ( reinforcing fibrin network)
↓
CLOT
↓
Dissolved by a blood - borne enzyme (PLASMIN)
↓
Plasmin digests the thread of fibrin by first making them
soluble & break them into small fragments
★ Thrombus
○ Artery; Arterial thrombosis
○ Occlude artery, coagulation cascade is
initiated
★ Embolus
○ Thrombus that goes into the circulation
○ Travels in vascular system; Localized
1. ANTICOAGULANTS
a. WARFARIN (COUMADIN)
● 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 factor
● LAB:
○ prothrombin time (PT) - maintained at
1.25 - 2.5 times the laboratory control
value
○ International Normalized Ratio (INR)=
2-3
b. 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
● SQ, IV, immediate onset, does NOT cross
the placenta and NOT enter the breast milk
● Uses: treatment and prevention of venous
thrombosis and pulmonary embolism, AF
with embolization, prevent clotting of blood
samples in dialysis and venous tubing
● LAB:
○ ✓ whole blood clotting time (WBCT)
2.5-3 X control
○ ✓ Activated Partial Thromboplastin
Time (aPTT) upto 40 sec
○ ✓ Partial Thromboplastin time (PTT)
1.5-2.5 X control in sec
● Cl: 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,phenitoin, 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
○ Check for 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
2. ANTIPLATELETS
● Uses: adjunct to thrombolytic therapy in the
treatment of MI & prevention of re-infarct,
prevention of MI and stroke
● Eg:
○ abciximab (ReoPro), IV
○ anagrelide (Agralyn), PO
○ dipyridamole (Persantine), PO
○ eptifibatide (Integrilin), IV
○ aspirin (generic), PO
○ cilostazol (Pletaal), PO
○ clopidogrel (Plavix), PO
○ sulfinpyrazone (Anturane), PO
○ ticlopidine (Ticlid), PO
○ tirofiban (Aggrastat)
● Cl: hypersensitivity, pregnancy, lactation,
bleeding disorder, recent surgery
● AE: bleeding, Gi discomfort, HA
● NURSING CONSIDERATIONS:
○ same with Anticoagulants
3. THROMBOLYTIC AGENTS
● MOA: converts plasminogen to plasmin to
dissolve clot
● Uses: pulmonary embolism, DVT, MI, acute
ischemic CVA
● Cl: severe hypertension, active bleeding,
hemophilia, thrombocytopenia, GI bleed,
hypersensitivity
● DI: increase bleeding with NSAIDs,
antiplatelet, anticoagulant
● SE: bleeding, rash (streptokinase), febrile
reaction, N/V, flushing, hypotension
● AE: hemorrhage
● EG:
○ streptokinase (Kabikinase,
Streptase)
○ urokinase ( Abbokinase)
○ anistreplase anisoylated
plasminogen streptokinase activator
complex (APSAC)
○ reteplase
○ Alteplase (t- PA)
○ 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
○ Avoid invasive procedure
○ Apply pressure for 5-10 mins on all
discontinued IV sites
○ Prevent bleeding
● ANTIDOTE: aminocaproic acid (Amicar)
4. HEMOSTATIC AGENTS
● MOA: hasten clotting of blood by inhibiting
the substance that activate plasminogen
● Uses: to stop bleeding
● Cl: elevated BP, clotting disorders
● SE: increase BP (most common), HA, N/V,
abdominal cramps diarrhea, fatigue, muscle
pain
● AE: intrarenal obstruction d/t clot formation,
anaphylaxis
● Dl: aminocaproic acid + oral contraceptives
= increase coagulation
● Eg:
○ Systemic hemostatic:
■ Aprotinin
■ Aminocaproic acid
■ Tranexamic acid
■ Vitamin K
■ Cabazochrome NA
■ somatostatin
○ Topical:
■ Gelfilm/gelfoam
■ Thrombin
■ Microfibrillar collagen
■ Oxidized cellulose
● 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)
 ● Frequently prescribed for ORAL use,
available also for IM [cause pain on
LESSON 2 - ANTIBACTERIAL DRUGS
injection & tissue irritation]; IV route –
PART 2
treat severe infections
–––––––––TETRACYCLINES––––––––– ● Newer ORAL : DOXYCYCLINE,
● Isolated from STREPTOMYCES MINOCYCLINE, METHACYCLINE :
AUREOFACIENS in 1948. rapidly & complete absorbed
● 1st broad spectrum antibiotics effective ● Not to be taken with MAGNESIUM and
against gram (+) bacteria & many ALUMINUM preparation (antacids)
organisms [mycobacterium, rickettsiae, ● MILK-PRODUCTS containing calcium or
spirochetes, chlamydiae] Iron containing drugs == prevent
● Not effective against S. aureus, absorption of the drug
Pseudomonas or Proteus ● TAKEN on EMPTY STOMACH – 1 hr ac
● Can be used against Mycoplasma or 2 hrs pc (except doxycycline &
pneumoniae. minocycline)
● + Metronidazole and bismuth
subsalicylate == useful in treating SIDE EFFECTS and ADVERSE REACTIONS:
Helicobacter pylori (peptic Ulcer) 1. GI - NVD {mgt: SFF, ice chips,
● ORAL and TOPICAL tetracycline – used replace fluids}
to treat severe acne vulgaris 2. PHOTOSENSITIVITY – sunburn
reaction {sunblock, clothing}
MOA: 3. TERATOGENIC EFFECT – not taken
- INHIBIT BACTERIAL PROTEIN 1st trimester – PC (pregnancy
SYNTHESIS {Bacteriostatic} category): D
- Continuous use of tetracyclines – 4. Discolors teeth (irreversible) == not
resulted in bacterial resistance; taken last trimester & children < 8yrs
increased resistance in the treatment of 5. Balance difficulty – damage to
pneumococci & gonococci infections vestibular part of the inner ear
(minocycline) {safety}
CLASSIFICATIONS: 6. NEPHROTOXICITY – if given in high
● SHORT ACTING doses
○ a.) Tetracycline {Tetracyn, 7. SUPERINFECTION – disrupt
Panmycin} microbial flora {oral hygiene}
■ >gram (+), gram (-), RT,
skin disorders, chlamydial, NURSING EDUCATION: STOP
gonorrhea, syphilis, *S - unlight sensitivity-[decomposes in
ricketssial light/heat = TOXIC- store out of light &
■ >[t ½ = 6-12 hrs] extreme heat]
○ b.) Oxytetracycline Hcl * T - ake full glass of H20
{terramycin} * NO - antacid, IRON & MILK
■ > UTI * P - ut drug into empty stomach
● INTERMEDIATE
○ Demeclocycline HCl DRUG INTERACTIONS:
(Declomycin) ● ANTACIDS, IRON containing drugs,
■ > broad spectrum MILK – prevent absorption of Tetra {take
■ >[t ½ = 10-17 hrs] 2 hrs apart}
● LONG-ACTING (to be taken with food) ● ORAL CONTRACEPTIVES (OCP) –
○ a.) doxycycline hyclate lessened effect of OCP
(Vibramycin) ● PENICILLIN – decreased activity of
■ bacterial infection & acne Penicillin
○ b.) minocycline HCl (Minocin); [t ● AMINOGLYCOSIDES – increased risk
½ = 11-20 hrs] Nephrotoxicity
 –––––––––AMINOGLYCOSIDES––––––––– SIDE EFFECTS:
● ACT by inhibiting bacterial protein - GI - NAV; rash, numbness, tremors,
synthesis (Bactericidal) visual disturbances, tinnitus, muscle
● Used against serious infections caused cramps or weakness, photosensitivity
by gram (-) bacteria [E. coli, Proteus,
Pseudomonas & Serratia] ADVERSE REACTIONS:
● Cannot be absorbed in the GIT, cannot - URTICARIA, PALPITATIONS;
cross CSF (in adults only) Thrombocytopenia; Superinfections-
● Primarily administered IV agranulocytosis; Liver damage
● DOC: Tularemia & Bubonic Plague Most serious:
● 1st aminoglycosides - STREPTOMYCIN ● OTOXICITY – 8 th cranial nerve
SULFATE – used in treatment of TB; damage {safety}
derived from bacterium Streptomyces ● NEPHROTOXICITY – oliguria {slowly
griseus in 1944, administered administered}
● NEUROTOXICITY- neuromuscular
IV ORAL PREPARATIONS: blockade, numbness
- given to decrease bacteria in the bowel
1) paromomycin- useful in treating DRUG INTERACTIONS:
intestinal amebiasis & tapeworm ● Penicillin – less effective aminoglycoside
2) neomycin- used as preoperative ● Anticoagulant (Warfarin)– increased its
bowel antiseptic activity
- OTHERS: (treat pseudomonas)
● Gentamycin (1963) [IM/IV] = against NURSING INTERVENTIONS
gram (-) pseudomonas ● Monitor periodical audiograms,
● Kanamycin [PO/IM/IV] = for hepatic BUN/creatinine & vestibule function
coma • Tobramycin (1970) [IM/IV] = kill studies over 10 days therapy
Pseudomonas ● Adjust renal insufficiency
● Amikacin (1970) [IM/IV] = effective ● Monitor VS, peak and serum levels
against Pseudo esp. if resistant to ● For IV admin., dilute and administer
gentamicin & tobramycin slowly to prevent toxicity
● Netilmicin (1980) [IM/IV] = less toxic ● Monitor I & O, hydrate well before and
compared to other aminoglycosides during therapy (flush in between)
● If anorexia or nausea occurs, SFF
PHARMACOKINETICS: Gentamycin meals
● Establish plan for safely if vestibular
PREGNANCY CATEGORY: C (can’t rule out) nerve effects occur.
● Netilmicin: D (+) Risk ● Administer other antibiotics 1 hour
● [A or absorbtion}: IM,IV before/after amino
● [M or metabolism]: T ½ short (SHL) - ● Recommend using sunblock &
3-4X a day, CHON bound-low protective clothing when exposed to the
● [E or excretion)]: unchanged in URINE sun.

PHARMACODYNAMICS: –––––––––MACROLIDES–––––––––
● Macrolides, Vancomycin, Lincosamides,
Ketolides - similar spectrum although
differ in structure
● Mild to moderate infections of the
respiratory tract, sinuses, GIT, skin, soft
tissues; diphtheriae, impetigo, STD
● ERYTHROMYCIN (1950s) (Erythrocin,
Erymax)
 ● Derived from Streptomyces erytheus • ● ↑ Effect of DIGOXIN,
Most commonly prescribed if with CARBAMAZEPINE, THEOPHYLLINE,
allergy to penicillin CYCLOSPORINE, WARFARIN,
● Effective against gram (+) and some TRIAZOLAM
gram (-) except S. aureus ● ↓ Effect of PCN, CLINDAMYCIN
● DRUG OF CHOICE: Mycoplasma P., ● ↓ absorption if taken with ANTACIDS
Leggionaire’s disease ● Erythromycin + Verapami, Diltiazem,
● Prevention of Rheumatic Fever Clarithromycin, Fluconazole = elevate
Erythro concentration = leading to
Pregnancy Category: B (no risk evident) cardiac death

MOA: inhibits CHON synthesis, EXTENDED MACROLIDE GROUP:

BACTERIOSTATIC (low dose)/BACTERICIDAL 1. Azithromycin (ZITHROMAX)
(high dose) a. Indications: mild-moderate
streptomycin infection, RTI,
Contraindications: Hepatic disease, Lactation gonorrhea, chancroid {STD}, H.
influenzae, Strep. , S. aureus
PHARMACOKINETICS: b. Pregnancy Category (PC):C
- PO form is well-absorbed in the (can’t be ruled out)
duodenum; ACID resistant salts c. A: PO – once a day x 5 days –
- (ETHYLSUCCINATE STEARATE, incompletely absorbed in the GIT
ESTOLATE) are added to decrease d. D (distribution): t ½: 40-50 hrs;
dissolution, increase absorption in the only 37% reaches in the systemic
intestines; FOOD does not hamper circulation
absorption of ACID resistant macrolides. e. E: bile, feces & urine (less)
- NO IM, IV (too painful) – if ever, give f. Side Effects:
slowly to prevent PHLEBITIS i. NAVDA is uncommon, give
- Protein Bound : 65% AC./ 1 hr ac or 2 hr pc + 1
- t½: PO (1-2 hr), IV (35 hr) glass of water not FRUIT
- Excreted: through the BILE, FECES & JUICE
small amounts through the urine. g. IV PREP – must be diluted in
NSS or D5W – to prevent
PHARMACODYNAMICS: phlebitis
➔ PO 2. Clarithromycin (KLARICID)
➔ Onset : 1 hr a. Indications: RTI, gram (-) & (+),
➔ Peak : 4 hrs tissue infections, H. pylori
➔ Duration : 6 hrs b. PC: C
c. A: PO
SIDE EFFECTS: NAVDA (nausea, vomiting, d. D: t ½ : 3-6 hrs ==== 2 x a day
diarrhea), pruritus, rash, tinnitus e. M: PB = 65-75%
f. E: bile
g. Side Effects:
ADVERSE EFFECTS: i. NAVDA is common, TAKE
- Superinfections, Urticaria, Hearing loss, with MILK/MEAL
Hepatotoxicity [“yellow sclera”], 3. dirithromycin (DYNABAC)
Anaphylaxis a. Indications: CHRONIC
BRONCHITIS, URTI, CAP, Skin
DRUG INTERACTIONS: Infections, H. pylori, Legionnaire’s
● Acetaminophen, Phenothiazine, disease, Chlamydia
Sulfonamide -----↑ HEPATOTOXICITY b. PC: C
(reversible) c. A: PO x 5 days
d. D: t ½ : 20-50 hrs
 e. M: PB = uk LINCOMYCIN (Lincocin)
f. E: bile, feces To treat severe infections when penicillin cannot be
g. Side Effects: given
i. NAVDA is common, TAKE ● [A] rapidly absorb in GIT or from IM
injections
with FOOD, or within 1 hr
● [D] t ½ = 5 hrs
of eating ● [M] liver – caution – hepatic & renal
impairment
NURSING CARE: ● [E] urine & feces
● Do not refrigerate suspension form of
Klarithromycin TOXIC EFFECTS: GI reaction, Pain, Skin infection,
● Monitor liver enymes – signs & BM depression
symptoms of hepatotoxicity
● Administer IV slowly NSG CARE:
● Give IM into deep muscle ● SAME WITH MACROLIDES – CAREFUL
● Avoid fruit juices MONITORING
● GI activity & fluid balance
● Manage NAVDA
● STOP if with bloody diarrhea
● Check for superinfections. Give
YOGURT/BUTTERMILK
––––––VANCOMYCIN HC1 (Vancocin)–––––
● Check drug interactions. ● ALMOST abandoned = nephrotoxicity &
● Evaluate effectiveness: WBC level , ototoxicity (damage auditory or vestibular
temperature, cultures [CN 8])
● Glycopeptide bactericidal antibiotic (1950s);
THE MACROLIDE GIRL against staphylococcal infxns used against
● G - GI disturbances ( undesirable drug-resistant S. aureus and in cardiac
effects) surgical prophylaxis with PEN allergies;
● I - V site ( check irritation) potentially life threatening infections not
● R - reduces activity of med if given with responding to other less toxic antibiotics.
acids (fruit juices) or food
MODE OF ACTION: BACTERICIDAL: inhibits
● L - liver function test
bacterial cell wall synthesis
–––––––––LINCOSAMIDES––––––––– PHARMACOKINETICS:
● Similar to macrolides but more toxic
- ORAL – not absorbed systemically,
● Change CHON function & prevent cell
excreted in the feces
division or cause cell death (both)
- IV – for severe infections due to MRSA,
● CLINDAMYCIN [Cleocin]
septicemia, bone, skin and lower respiratory
● Widely prescribed against most gram (+)
tract infections that are resistant to other
organism; absorbed better, more effective
antibiotics
fewer toxic
- excreted in the urine
● For severe infections caused by same
- PB: 30%
strains of bacteria that are susceptible to
- Half-life : 6 hours
macrolides
DRUG INTERACTIONS:
● Drug-drug = if with amphotericin B,
PHARMACOKINETICS: polymycin, furosemide, cisplatin -
● [A] rapidly absorbed from GIT or from IM ● ↑ NEPHROTOXICITY = if with methotrexate
injections - ↑ methotrexate toxicity
● [D] t ½ = 2-3 hrs – PB: 94%; crosses the
placenta & enters breastmilk PC : B; only if SIDE EFFECTS AND ADVERSE REACTIONS:
benefit clearly outweighs risk - chills, dizziness, fever, rashes, nausea,
● [M] liver – caution – HEPATIC & RENAL vomiting, thrombophlebitis @ injection site
impairment
● [E] urine & feces DOSE RELATED TOXICITY: tinnitus, high tone
deafness, hearing loss & nephrotoxicity.
SIDE EFFECTS: GI reaction - pseudomembranous
colitis; GI irritation
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
Rudolf the red – neck reindeer
Had an adverse side effect From the Drug
Vancomycin Must keep all labs in check
Caution with renal failure, Hearing Loss and
allergies, Take a temp and blood cultures,
‘Specially a CBC!!!
––––––FLUOROQUINOLONES––––––
MODE OF ACTION: interfere with the enzyme
DNA gyrase (needed to synthesize bacterial
DNA) = Broad spectrum bactericidal
Types:
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 targeting P. aeruginosa
6 infections in 1935.
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 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 : I/O, BUN,
Creatinine • 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 • Check S/S of
SUPERINFECTIONS (stomatitis, furry
black tongue, genital discharge, itching)
● Check symptoms of CNS stimulation =
nervousness, insomnia, anxiety &
tachycardia >>> avoid hazardous
machinery
–––––SULFONAMIDES–––––
- “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
- First group of drugs used against
bacteria
- Not classified as an antibiotic because
they were not obtained from biologic
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 (FA); 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;
● [M] liver
● [D] well distributed to body tissues and
brain [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 <
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 hrl;
excreted in urine, t ½ = 4.5 -7.8 hrs 7 II.
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 2 hrs
- [M] liver
- [E] urine; t ½ 7-12 hrs
- PC: Teratogenic- birth defects -
Kernicterus ; distributed into breastmilk
= 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);
hemturia (sulfonamides are insoluble in
acid urine) {Increase OFI – dilutes the
drug}
● 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 (d/t
effect to nerves)
DRUG INTERACTIONS:
● Increase effects of Warfarin
● Decrease absorption if taken with
antacids
● Increase hypoglycemic effect of
sulfonylureas
● Decrease effectiveness of
contraceptives
NURSING CARE:
● 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 sorethroat, 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
SULFA:
● S - unlight sensitivity
● U - ndesirable 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 level of consciousness
(LOC)
SPECTINOMYCIN HYDROCHLORIDE
(Trobicin)
● Introduced in 1971 against Neisseria
gonorrhea (GONORRHEA)
● For allergic to PCN, Cephalosporins,
Tetracycline
● Administered IM single dose
–BACTERIOSTATICS
● PC : B
● PROTEIN BOUND – 10%; t ½ = 1-3 hrs
QUINUPRISTIN / DALFOPRISTIN (Synercid)
● Treat VREF – Vancomycin-resistant
Enterococcus faecium bacteremia &
skin infected by S. eus & S. pyrogenes
● Disrupts CHON synthesis of the
organism
● When administered through peripheral
IV line = PAIN, EDEMA & phlebitis
● SE: N/V, diarrhea, pseudomembranous
colitis, Headache, anaphylaxis, elevated
AST & ALT
● NURSING CARE:
○ Check for DHN, monitor stools •
Check for patency of IV line;
 infuse over 1 hr in D5W
○ Check for S/S of anaphylaxis
○ Monitor ALT, AST, jaundice,
icteric sclerae
○ Give ice chips, SFF

PEPTIDES
● derived from cultures of bacillus subtilis
● Eg: POLYMYXIN
● Interferes with cellular membrane
● Bactericidal
● Affects gram (-) like E. coli, P.
auruginosa, klebsiella, shigella
● Not absorbed orally
● IM causes pain
● Best given slow IV
● SE: dizziness
● AE: nephrotoxicity/ neurotoxicity

BACITRACIN
● Inhibits cell wall synthesis
● 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.

LESSON 3 - ANTIVIRAL AGENTS
➢ More 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
AGENTS FOR INFLUENZA AND
RESPIRATORY VIRUSES
● Amantadine (Symmetrel) - PO
● Oseltamivir (Tamiflu) - PO
● Ribavirin (Virazole) - aerosol inhalation
● Rimantadine (Flumadine) - PO
CI: allergy, pregnancy & lactation, renal and
liver disease
AE: lightheadedness, dizziness, insomnia,
nausea, orthostatic hypotension, & urinary
retention
DI: with anticholinergic drugs = increases
atropine like effect
Nursing Considerations:
- Start regimen as soon after the
exposure to the virus as possible
(achieve best effectiveness and
decrease the risk of complications)
- Administer the full course of drug
- Provide safety measures (protect patient
from injury)
–––––AGENTS FOR HERPES––––
Herpes viruses
- Herpes simplex virus type 1
- HSV2
- HSV3: Varicella-zpster (chickenpox or
shingles)
- HSV4: Epstein - Barr virus
- CMV: cytomegalovirus
Herpes lesion: found on the shaft of penis
(male), vagina, vulva, cervix, (female), and
around anus.
● Acyclovir (Zovirax), Famciclovir
(Famvir), Valacyclovir (Valtrex) - herpes;
PO
● Cidofovir (Vistide) - IV = CMV in AIDS
● Foscarnet (Foscavir) = both; IV
● Ganciclovir (Cytovene) = long term
treatment and prevention of CMV; IV
CI: CNS disorders, allergy, pregnancy and
lactation, renal diseases
SE: N/V, HA, depression, rash, hair loss.
Inflammation and 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
of the kidney)
➢ Administer as soon as possible,
compliance
➢ Wear protective gloves when applying
the dug 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 and drowsiness
 AGENTS for HIV & AIDS Nursing Considerations:
- Should be taken with food except
didanosine (60 min AC or 2 hours PC)
- Requires dosage adjustment except
abacavir (creatinine clearance < 50 mL/min)
- Fixed dose avoided if with renal
insufficiency

PROTEASE INHIBITORS

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

production of infectious HIV virus
● Lopinavir / ritonavir (first line)
● Atazanavir
● Fosamprenavir (second either boosted with
ritonavir or not)
● Amprenavir
Enzymes needed by viruses:
● Tipranavir
● Reverse transcriptase - helps uncoat the
● Darunavir
virus; single stranded viral RNA is converted
● Saquinavir
into DNA
● Indinavir
● Integrase - helps viral DNA migrates into the
● Ritonavir
nucleus of the cell, where is spliced into the
● Nelfinavir
host DNA (provirus) => duplicated together
with the cell genes every time the cell
Note:
divides
- Ritonavir boosting - mainstay of PI therapy
● Protease - assists in the assembly of newly
(potent inhibitory effect)
formed viral particles
- Take with food
- + didanosine = one hour before or two
Nucleoside / Nucleotide Reverse
hours after ritonavir
Transcriptase Inhibitors (NRTIs)
ENTRY INHIBITORS
MOA: blocks the reverse transcriptase enzyme
MOA: prevents HIV cell entry (fusion of HIV and
needed for viral replication
CD4)
➔ Zidovudine (Retrovir)
● Enfuvirtide - the only agent approved
➔ Didanosine (Videx)
- Indicated with 3-5 other ant-retroviral agents
➔ Stavudine (Zerit)
(for clients with limited tx option)
➔ Lamivudine (Epivir)
- Expensive. 90 mg Sub-Q. BID.
➔ Abacavir (Ziagen)
● Injection site reaction:
➔ Tenofovir (Viread)
- Subcutaneous nodules, redness
➔ Emtricitabine (emtriva)
- Others: rash, diarrhea, serious allergic
reaction (anaphylaxis)
Fixed Dose:
- lamivudine/zidovudine (Combivir)
- Abacavir / lamivudine / zidovudine (Trizivir)
- Abacavir / lamivudine (Epzicom)
- Efavirenz / emtricitabine / tenofovir (Atripla)
- Emtricitabine / tenofovir (Truvasa)

SE (less tenofovir - renal toxicity):

- GI: nausea, diarrhea, abdominal pain
(transient - 2 weeks)
- Mitochondrial toxicity; lactic acidosis,
peripheral neuropathy, myopathy,
pancreatitis, lipoatrophy (wasting of fats in
face, buttocks, and extremities)