Antibacterials 1st two DOC are type of pneumonia

considered as atypical pneumonia

Eryth tonsitilitis, wounds
(sudden onset)
Clindamycin post partum – STDs, GI infection, skin & soft tissue
Azith/clarith common prescriptions infection (includes tonsillitis)
o Side/Adverse Effects:
▪ N/V, diarrhea, abdominal cramps (GI
MACROLIDE discomfort-gastric irritating; common)
▪ Hepatotoxicity (liver: organ)
- MOA: inhibits bacterial CHON synthesis
(common MOA) EXTENDED MACROLIDE GROUP
- Example: (broad spectrum) 1. Azithromycin (ZITHROMAX)
Alternative for patients allergic to PCN 80 pesos 1 dose (estimated)
➢ Erythromycin - Indications: mild-moderate streptococci
➢ Azithromycin infection, RTI, gonorrhea, chancroid (STD), H.
➢ Clarithromycin influenzae, Strep. PNA, S. aureus
Erythromycin - PC: C (can’t be ruled out)
- A: PO – once a day x 3-5 days – incompletely
o Derived from fungus-like bacterium
absorbed in the GIT
(Streptomyces erythreus)
- D: t 1⁄2: 40-50 hrs; only 37% reaches in the
o First macrolide developed, good alternative for
systemic circulation
patients allergic to penicillin
- E: bile, feces & urine (less)
o Bacteriostatic @ lower doses
- S/E: NAVDA is uncommon, give AC./ 1 hr ac or
o Bactericidal @ higher doses
2 hr pc + 1 glass of water not fruit juice taken in
o Preparations:
an empty stomach
IM – too painful; not preferred; irritating soln
- IV PREP – must be diluted in NSS or D5W – to
PO – added with the ff:
prevent phlebitis (inflammation of vein)
▪ + ethylsuccinate
o Means that drug is irritating that is why
▪ + striate
must be diluted
▪ + estolate
2. Clarithromycin (KLARICID) – 2nd developed
= readily absorbed (GI)
- Indications: RTI, MAC, gram (-) & (+), tissue
R: gastric acid destroys therefore acid infections, H. pylori
resistant salts are added to decrease - PC: C
dissolution in the stomach allowing the drug - A: PO
to be absorbed in the duodenum - D: t 1⁄2: 3-6 hrs - 2x a day
o Metabolized in the liver - M: PB = 65-75%
o Excretion in the bile to feces - E: bile
o Cross the breastmilk and placenta - S/E: NAVDA is common, take with milk/meal
o IV COMPOUNDS: 3. Dirithromycin (DYNABAC)
▪ + lactobimate - Indications: Chronic Bronchitis, URTI, CAP, skin
▪ + gluceptate infections, H. pylori, Legionnaire’s disease,
Chlamydia
= increase absorption - PC: C
o Indications: - A: PO once a day x 5days
▪ Most active gram (+); moderate gram (-) - D: t1/2: 20-50hrs
▪ DOC: drug of choice - M: PB = uk
– Mycoplasma pneumonias - E: bile, feces
– Legionnaires disease - S/E: NAVDA is common, take with food, or
within 1 hr of eating
THE MACROLIDE GIRL
G - GI disturbances (undesirable effects)
I - IV site (check irritation; check signs of phlebitis)
R - reduces activity of med if given with acids (fruit
juices) or food
L - liver function test bc known to be hepatotoxic
LINCOSAMIDES
- Similar to macrolides but more toxic
- Inhibit bacterial CHON synthesis
- Bacteriostatic & bactericidal
- Reserve for infections = bacteria is
susceptible to macrolides
- Preparation: rapidly absorb from GIT or IM
injection; parenteral, topical, vaginal
- Metabolized in the liver; excreted thru feces
& urine; crosses the placenta and enters
breast milk
- Example:
➢ clindamycin (Cleocin) – added to
astringents such as eskinol (treat
acne/pimples)
➢ lincomycin (Lincocin)
CLINDAMYCIN
- Most prescribed
- Active against gram (+) (eg. staph,
anaerobic)
- Not effective against gram (-)
- Absorbed better, higher serum drug
concentration
- Fewer toxic effects
- S/E:
➢ N/V, stomatitis, rash
- A/E:
➢ PSEUDOMEMBRANOUS COLITIS –
inflammation of colon/intestines (started
to develop bloody diarrhea)
➢ anaphylactic shock
- D/I:
➢ Incompatible with aminophylline,
phenytoin, barbiturates & ampicillin
Clostridium difficile – normally found in intestines
but may increase in number especially after intake
of antimicrobial agents; common
- Considerations:
o Same with macrolides with additional
precautions:
➢ GI activity
➢ Fluid balance
➢ Severe bloody diarrhea due to
pseudomembranous colitis
VANCOMYCIN (vancocin)
- A glycopeptide bactericidal antibiotic for
severe infections
- MOA: inhibits bacterial cell wall synthesis by
binding to the cell wall precursor
- Indications:
➢ IV: used extensively to treat methicillin-
resistant Staph Aureus (MRSA) &
methicillin-resistant staph species non-
aureus (SSNA) and endocarditis
➢ PO: staph endocarditis (affected organ-
heart particularly sa endocardium; signs
complication especially if frequent ang
tonsillitis) & pseudomembranous colitis
- C/I: renal failure, hearing loss (cochlear),
loss of balance (vestibular) concurrent use
of other nephrotoxic/ototoxic drugs
o Cranial nerve VIII vestibulocochlear-
responsible for balance&hearing
- S/E: N/V, taste alterations
- A/E:
➢ Dose related toxicity (tinnitus, high tone
deafness, hearing loss, loss of balance)
- Control dose
 ➢ Nephrotoxicity
➢ Rapid infusion can produce “red neck
syndrome/red man syndrome” (resulting
from histamine release and chills, fever,
tachycardia, profound fall in BP-
hypotensive, pruritus or red
face/neck/arms/back)
➢ Eosinophilia (inc. eosinophils),
neutropenia (dec. neutrophils), Stevens-
Johnson syndrome
Red neck syndrome
SJS- common drug reaxn; develop
profound rashes & blistering; itchiness;
can happen to any drug
- D/I: may increase toxicity with
aminoglycosides, amphotericin B, aspirin &
furosemide
- Considerations:
➢ Baseline hearing – before start drug,
dpat alam ang capacity sa hearing
➢ Blood pressure during administration –
rapid infusion may cause hypotension
➢ Renal function
➢ Peak & trough levels
➢ “red neck syndrome”
➢ IV site: phlebitis, extravasation (seeping
out of fluid from IV line; fluid
accumulation sa tissues bc of
extravasation of fluid)
➢ Refrigerate IV solution after
reconstitution (naadd nan gg water); use
within 96 hours
- Education:
➢ Report ringing of ears or hearing loss,
fever & sore throat
➢ Lab reports are necessary part of the
treatment
CHLORAMPHENICOL
- Frequently prescribed antimicrobial drug
- MOA: inhibits bacterial synthesis by
interfering with mRNA activity
- Eg: chloromycetin- sweet and milky taste;
pedias usually prescribe this
- Indications:
➢ Active against Gram (+) bacteria
(including most strains of MRSA)
➢ Gram (-) bacteria & anaerobes
➢ Not active against pseudomonas
aeruginosa & enterobacter species
➢ First choice of treatment for
staphylococcal brain abscess, mixed
organisms, meningitis
o Brain infections
➢ Original indication: treatment of typhoid
“tipos”
- S/E: fever
- A/E:
➢ Blood dyscrasias (bone marrow
depression)
Can lower all blood cells; adverse effect
suppress the bone marrow – cannot
produce blood cells
Low WBC leukopenia – prone to
infection
Low platelets – thrombocytopenia –
prone to bleeding
➢ Aplastic anemia – low RBC
➢ Jaundice (direct toxic liver effects)
Sign that there is a toxic effect to liver;
can result to: gbs
➢ Gray baby syndrome: usually seen in
newborn infants because of immaturity
of liver
- Considerations:
➢ Assess blood work before & during
therapy
 Determine blood cell levels
➢ Assess for potentiation (increase effect)
for clients receiving phenytoin (anti-
seizure/anticonvulsant), oral
antidiabetics, oral anticoagulants
FLUOROQUINOLONES
- MOA: interfere topoisomerase II (DNA
gyrase) and topoisomerase IV = enzymes
that are required for synthesis of bacterial
DNA and therefore, are required for
bacterial growth and replication
- Bactericidal
- Example:
➢ Ciprofloxacin – 1st line of suspected
anthrax
o Anthrax does not spread directly
from one infected animal or person
to another; it is spread by spores
(parang powder)
o Bioterrorism- pag nainhale – severe
infection
o cutaneous anthrax
➢ Gatifloxacin – OD dose
➢ Gemifloxacin
➢ Levofloxacin
➢ Lomefloxacin
➢ Moxifloxacin
➢ Norfloxacin
➢ Ofloxacin
➢ Nalidixic acid – UTI
- Indication:
➢ Both gram (+) and gram (-)
➢ UTI, gonorrhea, gastroenteritis
➢ Bone & joint infection
➢ Bronchitis, pneumonia
- C/I:
➢ Hypersensitivity in children < 18 yo
➢ Pregnancy & lactation
➢ Hepatic & renal impairment
➢ CNS disorder & seizure
- S/E: N/V, diarrhea, HA, dizziness, dry
mouth, photosensitivity
o Photosensitivity- drug chemical itself
is photosensitive (must not be
exposed to direct sunlight or else
may cause degradation of drug); pag
ang drug can cause photosensitivity
reaxn (pt must not be exposed
sunlight- may develop extreme
sunburn light reaxn)
- A/E: seizure
- D/I:
➢ Antacids, iron, sucralfate(anti-ulcer drug)
may decrease absorption of drug up to
98%
o Kremil-S (antacid)
➢ May increase effects of theophylline &
warfarin
o Theophylline (anti-asthma drug;
danger-cause toxicity)
o Warfarin (anticoagulant; danger-
can cause severe bleeding)
➢ Increase risk of photosensitivity
reactions with St. John’s Wort (herb;
tipton weed) therapy (anti-depressant)
- Considerations:
➢ Monitor s/s of infection, WBC, culture,
BUN, creatinine
➢ Maintain urine output = 1200-1500
mL/day
➢ Slowly infuse IV ciprofloxacin and
ofloxacin into large vein over 1 hour to
minimize vein irritation
- Education:
➢ Instruct to take 1 hr/2 hrs after meal or 2
hrs before/after antacids of iron
➢ Take with food if GI distress occurs
➢ Administer with full glass of water
➢ Drink 6-8 glasses of fluid/day
➢ Avoid exposure to sunlight during &
several days after drinking
➢ Avoid hazardous activities that require
alertness until the CNS response has
been determined. Depresses CNS that’s
why it may cause dizziness &
lightheadedness.
 ➢ 30-60% of oral dose excreted through
the urine unchanged; highly nephrotoxic;
increase oral fluid intake
SULFONAMIDES
- Isolated from coal tar (uling) derivative
compound in 1900’s (not antibiotic)
- MOA: inhibits bacterial synthesis of folic
acid (essential for biosynthesis of RNA,
DNA and CHON) which is essential for
bacterial growth
- Bacteriostatic, alternative drug to PCN
(penicillin)
- Example:
• Short Acting - rapid absorption and
excretion
1. Sulfadiazine – poorly soluble in urine,
can cause crystallization; tx systemic
infection
2. Sulfamethizole (SMZ) – tx UTI
3. Sulfisoxazole
With sulfadiazine treatment of
streptococcal infection = DOC: otitis
media, UTI
• Intermediate-acting – moderately slow
absorption & excretion
1. Sulfamethoxazole - poorer water
solubility
2. Sulfasalazine - tx: ulcerative colitis,
crohn’s disease, rheumatoid arthritis
3. Trimethoprim-sulfamethoxazole (co-
trimoxazole; TMP) – DOC for
pneumocystis carinii pneumonia
(opportunistic infection); bactericidal
Encounter pneumonia in what
condition: common with
HIV/AIDS
• Long – acting
1. Sulfamethoxypyridazine
2. Sulfameter
- Indications:
➢ New born eye prophylaxis (part of
newborn care; lagay ng topical tx)
➢ Meningococcal meningitis
➢ Chlamydia (STD) & toxoplasma gondii –
t. gondii-protozoan results from
ingesting contaminated raw meat or soil
or careless handling of the contents of
an infected cat’s litter box; an infected
pregnant woman can transmit the
infection for her fetus causing congenital
toxoplasmosis
➢ Prostatitis- inflammation of prostate
gland
➢ GI infection (shigellosis, diarrhea)
➢ Ophthalmic and topical use
(sulfacetamide sodium), skin wound
➢ Burns (silver sulfadiazine & mafenide
acetate)
- S/E: GI disturbances: anorexia, n/v
- A/E: photosensitivity, hypersensitivity, bone
marrow depression esp in elderly,
hepato/nephrotoxicity (crystalluria), Steven-
Johnson syndrome (blistering and peeling of
skin, arthralgia), cross sensitivity with other
sulfonamides
- D/I:
➢ May increase effects of warfarin
➢ Antacids decrease absorption
- Considerations:
➢ Baseline hepatic, renal, hematologic
studies
➢ I&O, adjust fluid intake to maintain
output of 1500mL/24 hours
➢ Administer 1hour before or 2hours after
meals, with food if GI distress occurs
➢ Avoid direct skin exposure to sun
➢ May result in false – positive urine sugar
and ketone test with diabetics
➢ Early signs of blood dyscrasia
SULFA
S - unlight sensitivity
U - ndesirable effects (toxicity)
L - ook for urine output & early signs of blood
dyscrasia
F - luids galore!!!!!
A - norexia, anemia

TETRACYCLINES
- Isolated from Streptomyces Aureofaciens
(1948)
- 1st broad spectrum antibiotics (gram + & - ;
mycobacteria, rickettsiae, spirochetes,
chlamydiae)
- Act by inhibiting bacterial CHON synthesis
- Not effective against Staph, Pseudo, or
Proteus
- Indications:
➢ Mycoplasma pneumoniae
➢ Treatment for helicobacter pylori-cause
gastric ulcer (in combination with
metronidazole and bismuth
subsalicylate)
➢ Pneumococcal & gonococcal infections
(increased resistance)
- Oral & topical: treat severe acne vulgaris
- IM: cause pain & tissue irritation
- IV: use to treat severe infection
- • Short Acting: (t1⁄2 = 6-12 hrs) empty
stomach
1. Tetracycline
2. Oxytetracycline HCL
• Intermediate Acting: (t1⁄2 = 10-17 hrs)
empty stomach
1. demeclocycline HCL
2. methacycline HCL
• Long Acting: (t1⁄2 = 11-20 hrs)
1. doxycycline hyclate
2. minocycline HCL
(to be taken with food)
- S/E: N/V & diarrhea
- A/E:
➢ Photosensitivity - excessive reaction to
direct sunlight or ultraviolet light leading
to redness of burning of the skin =
demeclocycline
➢ Teratogenic effect (1st trimester)
➢ Irreversible teeth discoloration (children
< 8 y.o.(nagdevelop pa ang permanent
teeth), pregnant last trimester-
development of tooth bud)
➢ Nephrotoxicity
➢ Superinfection (mouth ulcers, anal &
genital discharge)
➢ Damage to vestibular (loss of balance)
part of inner ear = taken w/ minocycline
- Considerations:
➢ Should not be given with magnesium &
aluminum preparations (antacid); milk
products containing Ca; iron containing
drugs
➢ Lipid soluble tetracycline (better absorb
when taken with milk products & food)
= doxycycline & minocycline
➢ Monitor liver enzymes, BUN and serum
creatinine
➢ Monitor VS and Urine output
➢ Assess for rash and pattern of bowel
activity
➢ Store medication out of light and heat
➢ Avoid excessive exposure to sunlight,
photosensitivity persists after D/C drug
(sun block, protective clothing)
➢ Take on empty stomach, drink with full
glass of water and avoid bedtime dose
➢ Stools may be green or yellow
➢ Topical application may cause skin to
turn yellow
➢ Recommend additional contraceptives
(other) and not rely on oral
contraceptives (lessen effectivity)
Tetra the cycler needs to STOP & go protect
himself from the sun.
S – unlight sensitivity
T – ake with full glass of water
- antacid, iron, milk
P – ut drug into empty stomach except
minocycline & doxycycline
TMS: NO SUNLIGHT – Tetra, Macrolides, Sulfa
TMF: NO FOOD – Tetra, Macrolides, Fluoro
AMINOGLYCOSIDES
- BACTERIOSTATIC examples:
➢ Chloramphenicol
➢ Erythromycin
➢ Clindamycin
➢ Sulfonamides
➢ Trimethoprim
➢ Tetracyclines
- BACTERICIDAL examples:
➢ Aminoglycosides
➢ Beta-lactams
➢ Vancomycin
➢ Rifampin
➢ Metronidazole
- MOA: bacteria cannot synthesize the
CHONs necessary for their function and
replication
- Highly toxic drug; hindi bastabasta binibigay
- Indication:
➢ Reserved for infections that did not
respond to less toxic drugs
➢ Gram (-) bacteria – E. Coli, Proteus,
Pseudomonas
➢ Some gram (+) are resistant
- DOC: tularemia & bubonic forms of plagues
o Tularemia- also called rabbit fever or
deer fly fever-is caused by bacterium
Francisella tularensis
o Bubonic plage caused by bacterium
Yersinia pestis. 1-7 days after
exposure to the bacteria, flu-like
symptoms develop. These
symptoms include fever, headaches,
and vomiting. Swollen and painful
lymph nodes occur in the area
closest to where the bacteria
entered the skin.
- Streptomycin Sulfate
o First aminoglycoside
o Used in treatment of TB
o Derived from bacterium
Streptomyces griseus in 1944
o Ototoxicity (CN VIII) and bacterial
resistant can develop
- Medicines:
➢ Amikacin - has a broader spectrum; it
resists degradation by most enzymes
that inactivate gentamycin and
tobramycin
➢ Gentamycin - gm (-) esp pseudomonas
➢ Netilmicin - less toxic
➢ Tobramycin sulfate - burn
wounds/ocular infection; inhaled to treat
cystic fibrosis
➢ Streptomycin sulfate
➢ Kanamycin – for hepatic coma
➢ Neomycin sulfate - pre-op bowel
antiseptic
➢ Paromomycin - amebiasis/tapeworm
- Cannot be absorbed from GIT; cannot cross
CSF (BBB of adults)
- Prep: IM & IV except neomycin &
paromomycin
Oral preparation – given to decrease
bacteria in the bowel
- S/E: Anorexia, nausea, vomiting,
photosensitivity
- A/E:
➢ Nephrotoxicity (cast, albumin, RBC,
WBC in urine, decrease creatinine
clearance, increased serum creatinine
and BUN)
➢ Ototoxicity (due to damage of 8th cranial
nerve: deafness or decreased hearing,
tinnitus, dizziness, ataxia)
➢ Neurotoxicity (visual disturbances,
respiratory paralysis, apnea)
➢ Hypersensitivity
- Interactions:
➢ Increase action of anticoagulants
➢ Loop diuretics may increase ototoxicity
& nephrotoxicity
➢ Penicillins, vancomycin, & amphotericin
B may increase nephrotoxicity
➢ Decrease if with penicillin (administer 1
hour before/after aminoglycosides)
- Considerations:
➢ Monitor audiograms, BUN, creatinine, &
vestibular studies over 10 days therapy
➢ Adjust for renal insufficiency
➢ Monitor VS, peak serum levels
➢ For IV administration: dilute & administer
slowly to prevent toxicity
 ➢ Monitor I&O, hydrate well before &
during therapy
➢ Manage S/E (anorexia, N/V,
photosensitivity)
➢ Establish plan safety if vestibular nerve
effects occur
“THE AMINO MICE” (toxic mice)
“I CAN’T HEAR”
“I CAN’T FEEL”
“I CAN’T PEE..”
“ONE CAN’T HEAR” – OTOTOXICITY
Damages CN VIII
“ONE CAN’T PEE” – NEPHROTOXICITY
Damages kidneys
“ONE CAN’T FEEL” – NEUROTOXICITY
Damage CNS – leading to neuritis,
numbness, tingling sensation
ANTI-FUNGALS
(ANTI-MYCOTICS)
“mycosis” – an infection caused by fungus
Fungus has a rigid cell wall that is made up of chitin
and various polysaccharides and a membrane that
contains ergosterol (makes them resistant to
antibiotics)
Treatment for systemic (candidiasis,
histoplasmosis) and superficial (tinea
pedis/athlete’s foot

I. POLYENES
a) Amphotericin B (Fungizone)
• MOA: binding to the fungal cell
membrane: forming open channels >>
increase cell permeability and leakage
of intracellular components.
• Very potent but with many unpleasant
side effects (renal failure)
• DOC: severe systemic infection; IV
• SE/AD: fever, N/V, dec BP, paresthesia,
thrombophlebitis, nephrotoxicity,
hypersensitivity, electrolyte imbalance
(hypokalemia & hypomagnesemia)
b) Nystatin (Mycostatin)
 • MOA: increases permeability of fungal a) Flucytosine (Ancoban)
cell membrane • combination therapy with other
• Oral preparation – intestinal candidiasis, antifungal drugs (Amphotericin B)
poorly absorb in GIT • well absorbed in GIT
• Suspension – mouth or throat fungal
infection
o swish>gargle>swallow
• Ointment, suppository, cream – vaginal
• SE: fever, N/V, rash, diarrhea (large
dose)

II. AZOLE GROUP IV. ANTIPROTOZOAL

MOA: interfere with the a) Atovaquone (Mepron)

formation of ergosterol (major • Used to treat mild to moderate
sterol in fungal cell Pneumocystis carinii pneumonia.
membrane)
a) Ketoconazole (Nizoral)
• First effective antifungal –orally
absorbed
• Used to treat some mycoses with
amphotericin B (give with food; no
antacid)
• Shampoo = dandruff
• SE: dizziness, blurred vision CONSIDERATIONS
• AE: hepatomegaly; photosensitivity ▪ GSCS
b) Itraconazole (Sporanox) ▪ Monitor IV sites
• PO ▪ Check liver enzymes, creatinine, BUN, I/O
• Systemic fungal infection ▪ Take with meals – oral forms (NAVDA)
c) Miconazole (Monistat) ▪ Check for hypersensitivity reaction (rash)
• Ointment – vaginitis; IV-fungal bladder ▪ For topical: wash hands before & after
infection application
d) Fluconazole (Diflucan) ▪ For athlete’s foot: wear cotton socks, change 2-
• PO 3 times daily
• Oropharyngeal and systemic; ▪ Jock itch worm or ring worm: wear well fitting,
hepatotoxic non-constrictive, ventilated clothing
e) Voriconazole ▪ Intravaginal
f) Posaconazole o Read instructions carefully
NOTE: vaginal tablet, cream, ointment and solution o Insert high into the vagina
(topical preparation to treat candidiasis and tinea o Continue use through menstruation
infections) o Wear a minipad to avoid staining
clothing, do not use tampon
o Wash applicator with mild soap and
III. ANTIMETABOLITE rinse thoroughly after each use
o Avoid sexual intercourse while using the
MOA: disrupts fungal DNA and RNA synthesis
drug
ZOLE
Z OLE – many drug interactions can occur
O bserve hygiene measures to control infections
L iver Function Tests – monitor
E ducate to take with food
- Meet “ZOLE” the toad who destroys fungal
infections, such as ringworm. “ZOLE” will
help you remember some key points with
these drugs. It will also help you remember
the medication used for these infections,
since they have the letters zole in them.

AMPHOTERRIBLE
- Amphoterrible is a monster. He treats
monster infections such as histoplasmosis
and other life-threatening fungal infections.
He has a terrible habit of creating
irregularities in the heart (arrhythmias). The
X marks the spot of the kidney since 80% of
clients receiving this drug may develop
some nephrotoxicity.
ANTI-TUBERCULAR DRUGS

Tuberculosis
- Caused by acid-fast bacillus
- Mycobacterium tuberculosis; transmitted
through droplets dispersed in the air through
coughing/sneezing;
- Have an outer coat of mycolic acid that
protects them from many disinfectants
allows them to survive.

1st line drugs Mechanism of Action Side Effects

(RIPES)
• Alters DNA & RNA activity in the Orange colored urine/body
bacterium (bacteriostatic) fluids; hepatotoxic
RIFAMPICIN • Best taken on empty stomach
(gastric irritation)
• Protect from light
• Inhibits cell wall synthesis Peripheral neuropathy – tingling
(bactericidal) sensation/numbess
• Blocks pyridoxine (B6-needed for Pyridoxine 10-50mg
ISONIAZID
nerves) which is used for
intracellular enzyme production Also prescribed to avoid
• Take before meals peripheral neuropathy

• Both; rapidly bacteriostatic & Hepatotoxic, ototoxic

slowly bactericidal Photosensitivity
PYRAZINAMIDE • NAVDA GI upset w/ food
• Protect from light Hyperuricemia-increase uric
acid in blood
Inhibits cellular metabolism Nephrotoxicity/visual
(bacteriostatic) disturbance (optic neuritis –
ETHAMBUTOL affects red & green
not be given to children 6 yrs or less
discrimination)
(can’t reliably monitor vision)
First drug to treat TB Ototoxicity – tinnitus (ringing
STREPTOMYCIN sensation in ear) & hearing
impairment

• Para-aminosalycylic acid, kanamycin,

2nd line drugs: cyclosserine, capreomycin

Drug Combination:
1. MYRIN-P = Etham + Rifam + INH + PZA
(RIPE)
2. COMBIPAK = Rifam + INH + PZA (RIP; can
be given to children since no etham)
3. RAMBUTOL = Rifam + Etham (REM)
Minimum of 6 mos max of 1 yr, orally daily
Why combine? To prevent development of resistant
strain to any drug; MDT (Multi Drug Therapy)
Considerations:
L iver enzymes – must be monitored
U se cautiously with renal dysfunction
N o alcohol because hepatotoxic
G ive pyridoxine
S hould take on empty stomach/screen vision
ANTI-LEPROSY (anti-Hansen’s disease)
• Leprosy – caused by Mycobacterium leprae;
characterized by disfiguring skin lesions and
destructive effects on the RT

• Determine history, exposure, PPD Treatment

tuberculin test & reaction, CXR and any • DAPSONE (similar to Sulfa) – inhibits folate
allergies synthesis
• Medical history-CI = severe hepatic • CLOFAZIMINE (Lamprene) –binds to
diseases: check liver enzyme values, bacterial DNA sites = cell death
bilirubin, BUN, S. crea
• Evaluate S/S of peripheral neuropathy
• Assess hearing chages – Ototoxicity
(adverse effect to streptomycin)
ANTI-HELMINTHICS
• INH – 1 hr ac or 2 hrs pc – food decreases
absorption rate
• Give pyridoxine (Vit B6) prevent p.
neuropathy
• Collect sputum specimens for AFB, 3
consecutive AM specimen
• Eye exam (INH & Ethambutol) – visual
disturbances
• Take drugs as prescribed
• Not to take with antacids – decreases
absorption
• Avoid alcohol – increased risk of
hepatotoxicity
• Avoid direct sunlight & decreased risk of
photosensitivity
• RIFAMPICIN – urine, feces, saliva, sputum,
sweat, tears – harmless red-orange color 4 GROUPS OF HELMINTHS
• Contact lens – may be permanently stained
1. Cestodes (tapeworms - segmented w/head &
• Take lots of fluids
hooks or suckers) – beef, pork, fish
• Use barrier contraceptives – OCP may not
be effective

LUNGS – interventions for the undesirable effects

of INH
 SE: HA, dizziness, fever, chills and malaise, rash,
pruritus, loss of hair

NURSING CONSIDERATIONS:
• assess history, food eaten
• collect stool specimen
• Take drug with food, small frequent feeding
2. Trematodes (flukes - flat) – intestinal, liver, lung, • Avoid driving, change position slowly
blood
• Take drug as prescribed
• Inform health care provider about OTC meds
taking
• For intestinal infection, some measures that
help prevent worm reinfection or help prevent
spread to other family members.
3. Intestinal nematodes (roundworms) – giant, • Vigorous use of soap and water after use of
ascaris, hookworm, pinworm, threadworm, toilet
whipworm • Showering in the morning to wash away any
4. Tissue-invading nematodes – tissue/pork ova deposited in the anal area during the night
roundworm • Changing and laundering undergarments, bed
linens and pajama daily
• Disinfecting toilet & toilet seats, bathroom and
bedroom floors periodically
• Proper handling of food and food preparation
(Nematodes)
• Control flies
• Avoid sexual intercourse or use condom in with
ANTIHELMINTHICS vaginal infection

1. Pyrantel pamoate Paralyze the intestinal

tract of the worm
Uses: giant roundworm, ANTI-MALARIAL
(Combantrin) SD
hookworm, pinworm
Malaria
2. Mebendazole Inhibits glucose and
- caused by protozoan parasites (plasmodium
other nutrients of
falciparum, malariae, vivax, ovale)
helminths
(Antiox) x 3 days - Causes RBC deformity and increase fragility
Uses: giant roundworm, and decrease oxygen transport
hookworm, pinworm - CM: fever, chills, sweating, anemia,
spleenomegaly, hepatomegaly, malaise
3. Thiabendazole Interferes with parasitic
metabolism

(Minzotel) x 2 days Uses: roundworm & Chloroquine HCL (Aralen)

pinworm
• The mainstay of anti-malarial therapy
4. Praziquantrel paralyzes the worm • MOA: enters human RBC and changes the
metabolic pathways necessary for the
Uses: TAPEWORM;
reproduction of plasmodium
(Biltricide) SD flukes
• SE: GI upset, fatigue
• AE: blurring of vision, blindness, ototoxicity
 • Other drugs:
o Quinine sulfate – chloroquine
resistant malaria
o Primaquine, mefloquine
Aralen Series
▪ Prevention: 500 mg (300 mg base) PO
once/week
▪ Non-chloroquine-resistant
- 1 g (600 mg base) PO, then
- 500 mg (300 mg base) PO 6-8 hours later,
then
- 500 mg (300 mg base) PO at 24 hours & 48
hours after initial dose
ANTI-PARASITIC (DERMA)
Pediculosis - lice infection (head,
body, pubic)
Scabies –caused by sarcopte scabie, characterized
by: eruptive lesion from burrowing of the female
parasite, transmitted through direct contact with
skin, clothing and bedding
Lindane (Kwell)
• MOA: unknown, thought to stimulate the
parasite’s CNS leading to seizure and death
• SE: local skin irritation
• AE: hypersensitivity
Considerations:
• Administer twice (1st immediately after dx;
2nd one week after the initial)
• Administer to all household members
• Wear gloves to remove nits by using fine-
tooth combed with vinegar
• Apply to all body area except face
ANTI-PROTOZOAL
Used to treat:
Amebiasis (E. histolytica) – N/V, diarrhea,
abdominal cramping and weakness
Trichomoniasis (T. vaginalis) – reddened inflamed
vaginal mucosa, burning itching and yellowish-
green discharge
Metronidazole (Flagyl)
• MOA: inhibits DNA synthesis, bactericidal
• USES: DOC for intestinal and systemic
amebiasis; prophylaxis from abdominal and
colorectal surgery, H. pylori and
trichomoniasis
• SE: N/V, diarrhea, unpleasant taste
• AE: HA, dizziness, ataxia, superinfection
Nursing Considerations:
• Avoid alcohol (disulfiram like reaction) =
nausea, flushing, tachycardia, increase
vomiting
• Protected sex, proper hygiene, proper food
preparation
ANTI-VIRAL
- 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
I. Agents for Influenza and Respiratory Viruses
a) Amantadine (Symmetrel) – PO
b) Oseltamivir (Tamiflu) – PO
c) Ribavirin (Virazole) – aerosol inhalation
d) Rimantadine (Flumadine) – PO
 e) Zanamivir (Relenza) – inhaler
CI: allergy, pregnancy & lactation, renal & liver
disease
AE: light-headedness, dizziness, insomnia, nausea,
orthostatic hypotension, & urinary retention
DI: with anti-cholinergic drugs = increase atropine
like effect
Considerations:
a) Acyclovir (Zovirax), Famciclovir (Famvir),
• Start regimen as soon after the exposure to Valacyclovir (Valtrex) = herpes; PO
the virus as possible (achieve best b) Cidofovir (Vistide) – IV = CMV in AIDS
effectiveness and decrease the risk of c) Foscarnet (Foscavir) = both; IV
complications) d) Ganciclovir (Cytovene) = long term
• Administer the full course of drug treatment & prevention of CMV; IV
• Provide safety measures (protect patient
from injury) CI: CNS disorders, allergy, pregnancy & lactation,
renal disease
SE: N/V, HA, depression, rash, hair loss,
II. Agents for Herpes inflammation & burning sensation at the site of
Herpes viruses injection and topical

▪ Herpes simplex virus type 1 AE: renal dysfunction

▪ HSV2 DI:
▪ HSV3: Varicella-zoster (chickenpox or
shingles) + other nephrotoxic meds = inc toxicity
▪ HSV 4: Epstein–Barr virus + zidovudine = inc drowsiness
▪ CMV: cytomegalovirus

TOPICAL ANTIVIRALS (HSV)

• Idoxuridine
• Penciclovir
• Trifluridine
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, siderails, 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

III. Agents for HIV & AIDS

Enzymes needed by viruses:
• Reverse transcriptase – helps uncoat the
virus; single stranded viral RNA is converted Med. Mgt: AIDS
into DNA HAART (Highly Aggressive or Active Anti-Retroviral
• Integrase – helps viral DNA migrates into Therapy)
the nucleus of the cell, where it is spliced
- is believed to effective that decreases up to
into the host DNA (provirus) => duplicated
66% mortality rate in HIV AIDS client.
together with the cell genes every time the
- used to suppress HIV viral replication and the
cell divides
progression of HIV disease
• Protease – assists in the assemble of newly
formed viral particles 2 Categories of Drug:
1. Reverse Transcriptase Inhibitors
a. Nucleoside RTI (NRTI)
Entry Inhibitors
b. Non-nucleoside RTI (NNRTI)
MOA: prevents HIV cell entry (fusion of HIV and 2. Protease Inhibitors
CD4)
▪ Enfuvirtide – the only agent approved
o Indicated in combination with 3-5 other
anti-retroviral agents (for clients with
limited tx option)
o Expensive. 90 mg Sub-Q. BID
▪ Injection site reaction:
o Subcutaneous nodules, redness
o Others: rash, diarrhea, serous allergic
reaction (anaphylaxis)

2 NRTIs + NNRTI or Protease Inhibitors

Fusion Inhibitor

1. Reverse Transcriptase Inhibitors

- It interferes w/ the action of the reverse
transcriptase enzyme that the virus uses to
covert its RNA into a DNA
 • Mitochondrial toxicity: lactic acidosis,
peripheral neuropathy, myopathy,
pancreatitis, lipoatrophy (wasting of fats in
face, buttocks and extremities)
NC:
• Should be taken with food except
didanosine (60 min AC or 2 hours PC)
a. Nucleoside/Nucleotide Reverse Transcriptase
• Requires dosage adjustment except
Inhibitors (NRTI) / nucleoside analogs
abacavir (creatinine clearance < 50mL/min)
• Eg: zidovudine, didanosine, dideoxycytidine
• Fixed dose avoided if with renal
& stavudine
insufficiency
• MOA: blocks the reverse transcriptase
enzyme needed for viral replication Non-nucleoside Reverse Transcriptase Inhibitors
• Zidovudine (Retrovir) (NNRTIs)
• Lamivudine (Epivir) - MOA: prevent viral replication by competing
• Abacavir (Ziagen) with binding of the reverse transcriptase
• Didanosine (Videx) enzyme at the active site
• Stavudine (Zerit) - Used to reserve protease inhibitors
• Tenofovir (Viread) (resistance)
• Emtricitabine (Emtriva) • Efavirenz (Sustiva)
b. Non-nucleoside Reverse Transcriptase - First-choice drug
Inhibitors (NNRTI) - PC: D
- CNS toxicities: dizziness, sedation,
nightmares, euphoria, loss of concentration
- Administered as a component of Atripla
o OD @ HS
o Empty stomach / low fat meal
(prevent excessive drug absorption)
• Nevirapine (Viramune)
- Alternative
o Pregnancy (1st tri)
o Planning to conceive
o Not using effective/consistent
contraception
- < risk: rash hepatotoxicity
• Eg: Nevirapine (viramine), delavirdine • Delavirdine (Rescriptor)
(rescriptor) - Least potent antiviral activity
Fixed dose: - Not recommended as part of regimen

• Lamivudine/Zidovudine (Combivir)
• Abacavir/Lamivudine/Zidovudine (Trizivir) 2. Protease Inhibitors
• Abacavir/Lamivudine (Epzicom)
- Interferes w/ the action of protease, a viral
• Efavirenz/Emtricitabine/Tenofovir (Atripla)
enzyme that cuts CHONs into pieces that
• Emtricitabine/Tenofovir (Truvasa)
are assembled into the coat or newly
SE (less tenofovir–renal toxicity) produced HIV particles
• GI: nausea, diarrhea, abdominal pain
(transient–2 weeks)
• Eg: Nelfinavir, Saquinavir, Ritonavir,&
Indinavir
• 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
retonaviror 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
DRUGS AFFECTING THE CARDIOVASCULAR - Compensatory mechanism when blood
SYSTEM pressure within the kidneys fall
ANTIHYPERTENSIVES
BARORECEPTORS
• ACE inhibitors
• Vasodilators
• Angiotensin II receptor blocker
• Calcium Channel Blocker
• Sympatholytics
DIURETICS

• Thiazide
• Osmotic
• Loop
• Potassium-Sparing

BLOOD PRESSURE – is the measurement of force

applied to artery walls
RENIN-ANGIOTENSIN SYSTEM
Normal BP: 120/80
Systolic (during heart’s contraction)/Diastolic
(relaxation)
Systolic – expected to be higher
Diastolic – should be below 80
BRIEF REVIEW ANAPHYSIO
• Determinants of BP
- Cardiac output – amt of blood ejected by left
ventricle to the circulatory system every
minute; stroke volume x heart rate; high CO
– high BP; blood volume low, low BP – if 20/25?% of that cardiac output goes to the kidney
there is blood loss
Mababa ang BP – juxta cells release renin
- Peripheral vascular resistance – resistance
(hormone that cause angiotensinogen from the liver
to the vessels; vessels constricted –
to be converted into angiotensin I) – angio. I
diameter is small (high resistance-pressure
pagdaan sa lungs upon circulation; with the
would also be high); if diameter is big (low
presence of an enzyme ACE – ACE converts
resistance; low BP)
angio. I to angio. II
• Baroreceptors (pressure receptors) specialized
cells in the arch of the aorta
So sensitive to the pressure of blood; as blood pass
through, if there is a sufficient pressure, it will be
send by the baroreceptors and they send info to the
brain but if the blood volume is low, the pressure is
insufficient, as the baroreceptors send info to brain,
the brain would initiate a compensatory mechanism
that will help improve the pressure
• Renin-Angiotensin Aldosterone system
 • TYPES:
- Primary – no other disease; no known
cause; possible: obese pt, diet is high Na,
lifestyle-stressful, take alcohol, severe
smoker
- Secondary – associated with a disease
condition; ex. Presence of a tumor in
kidney/adrenal gland > release abnormal
hormones > inc. BP
• Stepped Care Approach/Laddered Care
Approach
1. Lifestyle modification
Angiotensin II – potent vasoconstrictor 1. Weight reduction
2. Dec sodium intake
Dietary Approaches to Stop
Hypertension (DASH)
3. Moderate alcohol intake
4. Smoking cessation
5. Increase physical exercise
2. + drug

HEALTH TEACHINGS
P-ressure (blood) monitor
R-ise slowly – change positions gradually; abrupt
stopping result to rebound hypertension
Will also stimulate the adrenal cortex of the adrenal
gland to release aldosterone; aldosterone will E-ating must be considered
cause nephrons (where water is filtered) to retain
S-tay on medication
(wala naeliminate si sodium) Na & water; where
salt goes, water follows S-kipping or abrupt stopping is NO-NO (result to
rebound hypertension)
When blood is filtered in the glomerulus, it will try to
remove electrolytes, removes excess fluid para U-ndesirable responses
maihi. Since madaming water nakaattach sa
sodium, nagincrease ang blood volume > increase R-emind to exercise, decrease alcohol
BP E-liminate smoking
(Other effect) too much Na in the blood, masense
ng hypothalamus through its osmoreceptors >
release anti diuretic hormone – hormone will ANTIHYPERTENSIVES
prevent diuresis; (try to compensate-kailangan
I. Angiotensin-Converting Enzyme
madungagan ug water; para madilute ang Na) >
Inhibitors (‘pril’)
with anti-diuresis, di magihi ang pt, maretain more
MOA: blocks the conversion of angiotensin I to
ang sodium in water, thus increases blood volume
angiotensin II - by inhibiting the enzyme (ACE), no
> inc. BP
conversion
Uses: hypertension, MI
HYPERTENSION
Ex:
• “silent killer” – most are asymptomatic
- benazepril (Lotesin)
• When a person’s blood pressure is above the
- captopril (capoten)
normal limits for a sustained period
 - enalapril maleate (Vasotec)
- quinapril (Accupril)
- fosinopril (Prinivil)
- moexipril (Univasc)
- perindopril (Aceon)
- lisinopril
- ramipril
- trandorapril
S/E: cough (common s/e; usually dry cough),
hypotension, HA, dysgeusia (any perversion of
taste perception), insomnia, N/V, diarrhea
Cough – inhibition of metabolism of bradykinin
(inflammatory mediator); if severe na ang coughing
(not the recommended drug)
A/E: reflex tachycardia (inc. HR), chest pain,
angina, CHF (congestive heart failure), cardiac
arrythmias, ulcers, liver & renal problem,
photosensitivity, hyperkalemia (potassium retained
in blood; electrolyte imbalance), neutropenia,
angioedema (fluid accumulation sa face)
Potassium known to cause cellular excitability –
hyperkalemia- twitching, convulsion, seizure
Hypokalemia- excessive loss of K – paralysis; body
weakness
DI:
+ probenecid = decrease elimination
+ potassium supplement & diuretics = hyperkalemia
+ NSAIDS = decrease hypotensive effect
+ Antacids = decrease absorption
+ tetracycline = decrease absorption of tetra
CI: renal disease, severe Na depletion, CHF,
pregnant and lactating women
CONSIDERATIONS:
• 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; strenuous activities
(dizziness)
• Report cough/angioedema
• Report dysgeusia if more than 1 month
II. Angiotensin II Receptor Antagonist
(‘sartan’)
Selectively bind the angiotensin II receptors in the
blood vessels and adrenal cortex; makes the
angiotensin II inactive
Also called Angiotensin II Receptor Blockers
(ARBs)
Ex:
- telmisartan (Micardis)
- losartan (Diovan)
- irbesartan (Aprovel)
- candesartan (Blopress)
- valsartan (Cozaar)
- eprosartan (Teveten)
USES: when ACE inhibitors are not tolerated
S/E: HA, diarrhea, dyspepsia, cramps
A/E: angioedema, hyperkalemia
CI: nephro dysfunction, CHF, pregnancy
CONSIDERATIONS:
• +++ ensure female patient not pregnant
• Take without regard to food
III. Calcium Channel Blockers (‘dipine’)
MOA: prevents movement of calcium ions in the
myocardium and vascular smooth muscles.
Normally: Ca inc muscle contractility, peripheral
resistance and BP
Ca essential for muscular contraction
Ex:
- amlodipine (Norvasc)
- diltiazem (Cardizem)
- nicardipine (Cardene) } potent
- nifedipine (Procardia) } potent
- verapamil (Calan)
- nimodipine (Nimotopp)
- felondipine (Plendil)
USES: Angina, hypertension, atrial fibrillation
SE/AD: HA, dizziness, hypotension, syncope (loss
of consciousness), reflex tachycardia, constipation,
AV block, bradycardia, peripheral edema
CONSIDERATIONS:
• Monitor ECG (cardiac rhythm), CR, BP
• Have “E” cart available with IV administration (diuretics), HA, dizziness, GI bleed, lupus
(Emergency cart w/ emergency drugs) like and neurologic symptoms
• Position to decrease peripheral edema - minoxidil: similar effects, excess hair
• Protect drug from light and moisture growth, precipitates angina
• Increase OFI and fiber in the diet because one o Minoxidil – same drug available in
side effect is constipation topical applied to scalp used to
• Avoid overexertion when anginal pain is promote hair growth (usually used
relieved by men)
• May give paracetamol if with HA o (Liquid) minoxidil – do not apply with
• Take with meals or milk bare hands; wear gloves
- Nitroprusside & diazoxide (hyperglycemia):
• No not chew or crush (tablet form) sustained
similar
released
CI: allergy, pregnancy, lactation, cerebral
insufficiency
DI: + other antihypertensive drugs = additive effect
CONSIDERATIONS:
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, spleenomegaly)
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

V. Sympatholytic Drugs
IV. Vasodilators Agents that decrease the activity of the sympathetic
MOA: relaxes smooth muscles of blood vessels nervous system (SNS).
(dilates blood vessels) esp the arteries; promotes
increase blood flow to the brain & kidney
Ex:
- hydralazine (Apresoline)
- minoxidil (Loniten) } potent
- diazoxide (Hyperstat) } potent
- nitroprusside (Nitropress)
USES: severe hypertension, emergencies Sympathetic – fight or flight; the more body need
Not to be taken as a maintenance drug oxygen, promote hypertension
Parasympathetic – rest and digest, save more
SE/AE:
energy
- hydralazine: can cause tachycardia (taken
with beta blockers), palpitations, edema
4 MAIN RECEPTORS:
Alpha 1 – increase force of contraction,
vasoconstriction = HPN, mydriasis (pupil dilation),
decreased salivary secretions
Alpha 2 – inhibits release of norepinephrine =
dilates BV, decrease GI motility & tone
Beta 1 – increase HR & force of contraction,
increase renin = HPN
Beta 2 – dilates bronchioles, GI and uterine
relaxation, increase blood sugar, increase blood
flow in the skeletal muscles
BETA-BLOCKERS “OLOL grp”
• beta-adrenergic blocking agents,
• beta-adrenergic antagonists,
• beta antagonists.
A. BETA-ADRENERGIC BLOCKERS
MOA: block beta 1 (Cardiac) and / or beta 2 (lungs)
adrenergic receptor sites; decrease the effects of
the SNS by blocking the release of catecholamines,
thereby decreasing the HR and BP
Nonselective (both beta 1&2)
Cardioselective (beta 1)
Beta-2 blockers (beta 2)
Beta-one receptors
- are found in the heart and kidneys.
- When stimulated, they increase heart rate,
AV conduction, & automaticity.
Beta1-blockers
- reduce heart rate, blood pressure,
myocardial contractility, and myocardial
oxygen consumption.
Beta-two receptors
- mainly in the lungs, gastrointestinal tract,
liver, uterus, vascular smooth muscle, and
skeletal muscle.
- serve to dilate bronchial & vascular smooth
muscle.
Beta2-receptor blockade
- inhibits relaxation of smooth muscle in blood
vessels, bronchi, the gastrointestinal
system, and the genitourinary tract.
USES: hypertension, dysrhythmias, angina pectoris
A/E: rebound hypertension (would happen if
magstop sa maintenance drugs)
Main contraindications (ABCDE)
A-sthma (the more it can cause
bronchoconstriction; effect sa beta 2)
B-lock (heart block-condition where in there is an
alteration in the electrical activity of the heart that
may cause heart to have a slow contraction)
C-OPD chronic obstructive pulmonary disease
D-iabetes Mellitus (nonselective have an effect to
the blood glucose)
E-lectrolyte Imbalance (hyperkalemia)
DI:
+ antacids = delayed drug absorption
+ lidocaine = increase plasma level of lidocaine
(cause toxicity); lidocaine – anti-arhythmic drug
given to patients having dysrhythmia/altered heart
rhythm
+ insulin/OHA = hypo/hyperglycemia
+ cardiac glycosides (drug given to pts having heart
failure) = additive bradycardia
+ calcium channel blockers = increase E-xhaustion
pharmacologic and toxic effects of both
-motional depression
+ cimetidine (drug given to ulcer) = decrease
R-educes recognition of hypoglycemia
metabolism of beta blockers
+ theophylline (drug for asthma) = impaired
bronchodilating effect B. ALPHA-ADRENERGENIC BLOCKERS
“sin”
Ex:
MOA: blocks alpha 1 adrenergic receptors resulting
Nonselective Beta Blockers
in vasodilation of arteries and veins
- Carvedilol (Coreg)
Decrease peripheral resistance; relaxes smooth
- Nadolol (Corgard)
muscle of bladder/prostate
- Propranolol (Inderal)
- Timolol (Blocadren) - These drugs are also given to patients
- Pindolol (Visken) having BPH (Benign prostatic hypertrophy)

Cardioselective Beta Blockers (B1)
- Acebutolol (Sectral)
- atenolol (Tenormin)
- betaxolol (Kerlone)
- bisoprolol (Zebeta)
- esmolol (Brevibloc)
- metoprolol (Betaloc, Cardiostat)
CONSIDERATIONS:
• Lifestyle modification; Compliance (rebound
hypertension)
• Monitor blood sugar with diabetics
• Monitor triglycerides and cholesterol level (LDL
which may be increased d/t intake of drug)
• Monitor BP & pulse before and after
• Withhold if pulse is < 60 or SBP < 90
• Monitor any change in the rhythm or signs of
CHF
Decrease VLDL & LDL = decrease fat deposits;
increase HDL
Does not affect glucose metabolism & respiratory
function bc it has only effect to alpha 1 receptor
Causes Na & H2O retention with edema; given with
diuretics
WARNINGS: renal disease, elderly more sensitive
Ex:
- Potent Alpha Blockers: hypertensive crisis &
severe hypertension from catecholamine
secreting tumors of the adrenal medulla
(pheochromocytoma)
o Phentolamine
o Phenoxybenzamine
o Tolazoline
- Prazosin (Minipress) = CHF
- Doxazosin (Cardura) = also for BPH
- Terazosin (Hytrin) = also for BPH

BLOCKER S/E:

- outlines undesirable effects of Beta Blockers. - orthostatic hypotension (dizziness,

faintness, increase HR)
B-radycardia
- 1st dose syncope (hypotension with loss of
L-ipidemia (LDL) increases consciousness)
-libido decreases - Nausea, drowsiness, nasal congestion,
weakness, loss of libido
bronchospasm (effect on beta 2 receptors) - Phentolamine – reflex tachycardia
C-HF DI:
-onduction abnormalities + other antihypertensive, alcohol, nitrates =
K-onstriction peripheral vascular increase hypotensive effects
Prazosin + anti-inflammatory drug = the more it can
cause Na & water retention resulting to peripheral
edema
Prazosin & nitroglycerin = syncope
CONSIDERATIONS:
• Monitor BP frequently
• Protect from falling/injury bc of syncope
• Assess BP and HR before each dose
• If dose is during the day, client must remain
recumbent for 3-4° prevent injury
• Assist with ambulating 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’s SINS
- Mini’s “SINS” (minipress) are undesirable effects
of Alpha Adrenergic Blockers. These medications
end in SIN.
S-yncope
-exual dysfunction
I-ncreased drowsiness, orthostatic hypotension, HR
N-eed to be recumbent for 3-4 hrs after initial dose
C. CENTRALLY ACTING ALPHA-2 AGONIST
MOA: decrease sympathetic response from
brainstem to the peripheral vessels; resulting in a
decrease peripheral vascular resistance & BP
Stimulate the alpha-2 receptors:
o Decrease sympathetic activity
o Increase vagus nerve
o Decrease epinephrine, norepinephrine,
renin release
SE/AE: drowsiness, HA, dry mouth, dizziness,
bradycardia, constipation, hypotension, occasional
edema or weight gain
DI: paradoxical hypertension with propranolol
Ex:
- Methyldopa (Aldomet) (used for chronic/PIH
pregnancy induced hypertension) ***
- Clonidine (Catapres) ***
*** cause Na & water retention (given with
diuretics to eliminate excess fluid retention)
NURSING CONSIDERATIONS:
• Monitor baseline VS (q30 mins until stable
during initial therapy) & weight (refer: wt gain >
4 lbs/week)
• Abrupt D/C = hypertensive crisis (restlessness,
tachycardia, tremors, HA, & increase BP),
compliance
• Taper dose gradually over more than one week
• Recommend the last dose of the day to be
taken at bed time
• Sugarless gum, sips of tepid water may relieve
dry mouth
D. ADRENERGIC NEURON BLOCKERS
(PERIPHERALLY ACTING
SYMPATHOLYTICS)
MOA: block norepinephrine release from the
sympathetic nerve endings that results in decrease
BP
S/E: orthostatic hypotension, Na & water retention,
vivid dreams, nightmares & suicidal intention
(reserpine)
Ex:
- Reserpine (Serpasil)
- Guanethidine monosulfate (Ismelin)
These drugs are reserved for chronic
hypertension
NURSING CONSIDERATIONS:
• Take with meals, no alcohol
E. ALPHA-1 & BETA-1 – ADRENERGIC
BLOCKERS
MOA: blocks both alpha-1 and beta-1 receptor
sites; decrease BP & moderately decrease
peripheral resistance
S/E: orthostatic hypotension, GI disturbances,
nervousness, dry mouth, fatigue
A/E: heart block
CI: large doses could block beta-2 receptors =
increase airway resistance in patients with asthma
Ex:
- Labetalol (Normodyne)
- Carteolol (Cartrol)

DIURETICS

3 BASIC PROCESSES TO PRODUCE URINE:

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.
REVIEW ON FUNCTION OF THE KIDNEY
Reabsorption – movement of molecules out of the
tubule and into the peritubular blood
▪ About 80% of water, sodium, potassium,
chloride, and most other substances is
reabsorbed.
▪ About 20% of the glomerular filtrate enters
the loop of Henle.
▪ Descending limb of the loop of Henle > area
where water is reabsorbed
▪ Ascending limb > sodium is reabsorbed
Kidney Function
▪ Distal tubule > sodium is reabsorbed
- Eliminates waste ▪ Final reabsorption of water > distal tubule
- Regulates fluid balance and small collecting tubules
- Regulates blood pressure ▪ The remaining water and solutes are now
- Regulates RBC production thru release of appropriately called urine as it is being
erythropoietin collected in the collecting tubule
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 secreted

END OF MIDTERMS
DIURETICS
- Also known as water pills
- Produces increased urine flow by inhibiting
sodium and water reabsorption from the
kidney tubules back to the peritubular
capillaries
- Sodium and water increase the blood
volume, causes hypertension
2 main purposes:
- To decrease hypertension (increases urine
output)
- To decrease edema (accumulation of fluid
in the interstitial spaces; manas)
Indications:
- Congestive heart failure
- Pulmonary edema
- Liver failure & cirrhosis can promote ascites
- Renal diseases
- Hypertension
- Glaucoma – increased intraocular pressure
Contraindications:
- Allergy
- Fluid & electrolyte imbalances
- Severe renal diseases
- SLE Systemic lupus erythematosus
- DM
Glomerulus (filtration) > tubules – proximal –
descending – loop of Henle – ascending – distal –
collecting tubule
Peritubular capillaries (reabsorption and secretion)
I. 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: pts having decreased K, renal/hepatic
dysfunction, gout
DI:
+ lithium = lithium toxicity
+ digoxin = digoxin toxicity (bradycardia, N/V, visual
changes)
+ corticosteroids, amphotericin, ticarcillin =
hypokalemia
+ sulfonamides = cross sensitivity
SE/AE: hypokalemia, hyponatremia,
hypomagnesemia, hypotension (blood volume
decreased), bicarbonate loss, hypercalcemia,
hyperglycemia (dec glucose uptake/inc insulin
resistance), hyperuricemia (lessen elimination of
uric acid > accumulates), N/V, constipation (effect
of dehydrating pt), rashes, dizziness, weakness,
increase LDL, photosensitivity, H/A, dehydration,
blood dyscrasias (lowering the platelets)
Electrolytes are being secreted (potassium,
sodium, magnesium) causes hypokalemia,
hyponatremia, hypomagnesemia (s/e); on the other
hand, calcium is spared > hypercalcemia
Ex:
- Chlorothiazide (Diuril)
- Chlorthalidone (Thalitone)
- Hydrochlorothiazide (Hydrodiuril)
- Indapamide (Lozol)
- Metolazone (Zaroxolyn)
NURSING RESPONSIBILITIES:
• Monitor BP, wt OD (everyday; same time, same
clothing), urine output, edema
• Monitor K, Na, Ca, blood glucose, LDL,
triglycerides
• Change position slowly to prevent orthostatic
hypotension
• No alcohol
• Take with meals preferably in AM if night,
madalas na pagihi, interrupt sleep
• Eat foods high in K (banana, avocado, broccoli, - Ethacrynic acid (Edecrin)
dried fruits, oranges, nuts, potato, prunes, - Bumetanide (Bumex)
tomato) NURSING RESPONSIBILITIES:
• Manage photosensitivity
• Monitor VS, edema, urine output, serum K, Na,
Signs of hypokalemia (muscle weakness, cardiac
Ca, Cl, thiamine, blood glucose & platelet
dysrhythmias, cramps, dizziness, N/V, tingling
levels, Mx (manifestation) of digoxin (cardiac
sensation, “U” wave on the ECG (3.5-5.1 mEq/L) glycoside which can cause lower HR) & lithium
T-ake time to check VS (mood stabilizer toxicity
• Potassium rich foods
H-yperglycemia, hypokalemia, hyperuricemia
monitoring • Give slow IVTT (2 mins) to prevent hearing loss
• With food, in AM
I-nstruct to weigh in daily
C-heck for weight gain
A-void sudden position changes
E-nsure VS prior to administration
Z-ugar monitoring
I-&O monitoring
I-&O monitoring
L-aboratory values assessment
D-iuresis is expected: I&O
I-nstruct to rise slowly
E-at potassium rich foods
N-octuria prevention:
G-ive it with meals
II. Loop Diuretics
MOA: inhibits Na & Cl absorption from the loop of
henle and distal tubules, causes rapid diuresis, little III. Osmotic Diuretics
effect on glucose MOA: increase osmotic pressure in the glomerular
filtrate, preventing reabsorption of water &
electrolytes (high osmotic pressure, attracts the
fluid to stay within the glomerular filtrate so that it is
not reabsorbed back into the peritubular capillaries)
USES: increase ICP, edema, prevention of renal
failure, oliguria, inducing diuresis during
chemotherapy
CI: anuria
USES: HPN, edema associated with CHF, cirrhosis
with ascites, hypercalcemia DI: increase hypokalemia which may increase
digoxin toxicity
DI: same with thiazides
SE/AE: pulmonary edema d/t rapid fluid shifting,
SE/AE: hypokalemia, hyponatremia, hypocalcemia,
NV, tachycardia, decrease Na, K, Cl, Ca,
hypomagnesemia, hypochloremia, hyperuricemia,
dehydration
orthostatic hypotension, constipation, N/V,
decrease platelet, ototoxicity (IV bumetanide), Ex:
dehydration, photosensitivity, thiamine deficiency, - Mannitol (Osmitrol) given per IV
hyperglycemia (glycogenolysis), elevated BUN & - Urea (Ureaphil)
creatinine - Glycerin (Osmoglyn) = dec IOP
Ex: - Isosorbide (Ismotic)
- Furosemide (Lasix) common NURSING RESPONSIBILITIES:
- Torsemide (Demadex)
• Monitor VS, wt, urine output, serum Na, K, Cl,
Ca
• Watch for rapid inc in BP & rapid sympathetic
overactivity (inc HR, tremor, agitation)
compensatory mechanism
• Assess lung and heart sounds check for
pulmonary edema
• Check skin turgor, LOC, Mx of dec ICP
• Mannitol: check bottle or vial for crystallization,
warm bottle & shake vigorously to dissolve
crystals, if it doesn’t dissolve = do not
administer
o Use IV line with filter
o Infuse for 30-60mins
O-liguria, edema, inc ICP (indication)
S-tops reabsorption of water(MOA)
+ 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 T wave on ECG
AE: HA, photosensitivity, anemia, decrease platelet
Ex:
- Spironolactone (Aldactone) common
- Amiloride (Midamor)
- Triamterene (Dyrenium)

M-annitol (common example) NURSING RESPONSIBILITIES:

O-utput of urine, electrolytes – monitor • Monitor VS, urine output, serum K level
• Inform client that hypotensive effects may not
T-issue dehydration UE
be seen for 2 weeks
I-ncreased frequency/volume of urination (expect); • Avoid potassium rich foods
w/ foley cath • Manage photosensitivity
C-irculatory overload UE • Avoid salt substitutes
• Take with meals
• Bluish colored urine is harmless
IV. Potassium Sparing Diuretics • Administer in Am
MOA: acts on the distal tubule to promote Na and
water excretion & prevent potassium excretion
AKA: aldosterone antagonist
Aldosterone released > production of ADH –
prevent diuresis

INTERVENTIONS FOR DIURETICS

D-iet: decrease sodium intake
I-ntake & output monitoring
U-ndesirable effects
R-eduction of edema
USES: HPN, edema = CHF, nephrotic syndrome to
counteract hypokalemia caused by other diuretics E-lectrolytes review

CI: severe renal disease, severe hyperkalemia T-ake early in the day; with meals

DI: I-nteractions: digoxin lower further HR

C-ause/aggravate diabetes
S-ensitivity to sunlight
COMPARISON OF DIURETICS
CARDIAC GLYCOSIDES / ANTI-ANGINA
Manages condition that affects CVD
Congestive Heart Failure (CHF)
- Condition in which the heart fails to
effectively pump blood around the body due
to damaged or overworked heart muscle.
- Usually, the left ventricle fails bc mas
mabigat ang trabaho (pumps blood to
systemic circulation); if mapuno si left
ventricle magcongest > same sa left atrium
> flow back sa pulmonary circulation;
congestion of pulmonary circulation
(coughing, orthopnea-when lying down) >
back flow ang blood to venous circulation
Causes:
- Coronary artery disease
- Cardiomyopathy affect muscles of heart
- Hypertension
- Valvular heart disease affects heart valves
RAAS – Renin angiotensin aldosterone system
Baroreceptor – specialized cells sa aortic arch
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 (increased myocardial
contraction)
– (-) chronotropic action (dec heart rate)
– (-) dromotropic action (dec electrical
conduction velocity)
– Increase cardiac output and renal perfusion
(bld flow to kidneys)
Uses: CHF, AF atrial fibrillation, A flutter,
*** rapid onset, excreted thru kidney, has a narrow
margin of safety
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 for digitalis toxicity: digoxin immune Fab
(intoxication with serum level of > 10ng/mL)
▪ Binds with digoxin to form complex
molecules that can be excreted in the urine
CI: Hypersensitivity, ventricular tachycardia and
fibrillation, heart block, MI, renal insufficiency,
electrolyte imbalance (inc. Ca, dec K & Mg)
DI:
+ verapamil, quinidine, quinine, erythromycin,
tetracycline, cyclosporine = increase toxic effect
+ loop diuretics/hydrochlorothiazide =
HYPOKALEMIA (increase the effect at its
myocardial cell action site)
+ cortisone preparations = sodium retention &
potassium excretion
+ thyroid hormones, metoclopramide = less
effective
+ antacids = dec digitalis absorption
NURSING CONSIDERATIONS
• Consult prescriber about loading dose
• Monitor apical pulse in one full minute, monitor Anti-Anginals
for quality and rhythm Coronary Artery Disease (CAD) – lumen of blood
• Check dosage & preparation carefully (oral/IV vessels become narrow; thus, blood is no longer
form) able to flow freely to the muscles.
• Check pediatric dose with extreme care
Angina Pectoris – “suffocation of the chest”, occurs
• Follow dilution carefully for IV preparation
when myocardial demand for oxygen cannot be
• Administer IV dose very slow over at least 5
met by narrowed blood vessels
minutes
• Weigh patient bc it can cause systemic *** anginal pain: chest tightness, pressure in the
congestion > generalized edema “anasarca” > center of the chest, and pain radiating down the
inc. body wt (fluid retention) neck and left arm.
• Avoid administering oral drug with food or Myocardial Infarction (MI) – occurs when coronary
antacid vessels is completely occluded and the cells that
• Maintain emergency equipment on standby = depend on the vessels for oxygen become
lidocaine (arrhythmias), phenytoin (anti- ischemic, then necrotic and die.
seizure), atropine SO4 sulfate (to inc. cardiac
rate), cardiac monitor Types of Angina:
• Monitor therapeutic level of digoxin (0.5 – 2 1. Classic (stable) – occurs with stress exertion
ng/mL), digoxin toxicity
2. Unstable (preinfarction) - occurs frequently over
• Potassium Rich foods: banana, avocado, the course of a day with progressive severity
broccoli, dried fruits, oranges, nuts, potato,
prunes, tomato 3. Variant (Prinzmetal, vasospastic) - occurs
• Sodium Rich Foods: buttermilk, margarine, during rest
canned goods, processed foods, fast foods, Types of Anti-Anginals:
preserved foods, tomato ketchup
1. Non- nitrates (beta blockers, calcium channel
blockers)
Angina – a type of temporary chest pain, pressure 2. Nitrates:
or discomfort
o isosorbide mononitrate (Imdur, isoket,
Heart muscle is not receiving enough oxygen due isordil)
to a narrowed coronary artery. o nitroglycerin (Deponit, Nitrostat)

NITRATES
MOA: vasodilators
 - dilation of the veins = less blood return to
the heart (decrease preload)
- dilation of arteries = less vasoconstriction
and resistance (decrease afterload)
Uses: treatment & prevention of angina, dec BP
SE: HA (most common), dizziness, hypotension,
reflex tachycardia, decrease CR, GI distress,
flushing of skin
AE: some degree of hepato/nephrotoxicity
NURSING CONSIDERATIONS:
• Assess chest pain: (PQRST) Precipitating
factors, Quality, Radiation, Severity/symptoms,
and Time
• PO: take on empty stomach; undergoes hepatic
first pass effect which can lessen bioavailability
• SL sublingual: every 5 min X 3 doses; effect
lasts for 10 minutes; pag di pa narelieve within
3 doses, not anginal pain anymore
o store in dry & dark bottle • Spray: lift tongue then spray, avoid inhaling the
o check expiration date (up to six months drug; like sublingual but mist
only) General NC:
o take sips of water BEFORE administration
o allow drug to dissolve before taking • withhold: BP < 90/60, HR <60, acetaminophen
anything PO for HA, reassess chest pain after 2-5 minutes
o burning/stinging sensation means the drug (SL, spray, except PO)
is potent sign that it is effective
• 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
• Topical Ointment: toothpaste-like container
o remove previous application
o spread drug over a 6x6 in area on chest,
back, upper arm, and cover with a plastic
wrap
o rotate site, avoid touching the ointment can
be absorbed by the skin and can experience
side effects
• Patch:
o patch is water proof
o apply wearing gloves at ACW anterior chest
wall, non-hairy portion
o remove previous patch, rotate sites
o remove after 12 hours to prevent tolerance
o do not apply defibrillator paddles over the
drug, may cause burn
DRUGS AFFECTING BLOOD COAGULATION • Clotting – chain of reaction stimulated by
the release of a chemical called
thromboplastin from injured cells
- Works at various steps in the clotting and clot
dissolving process in order to restore the balance
that is needed to maintain the cardiovascular
system
• 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
Mechanisms of Blood Coagulation
1. Vascular Response
- Platelets release serotonin causing
vasoconstriction
2. Platelet Aggregation
- Platelets form a mechanical barrier or
wall to close off the break in the capillary
3. Chemical Clotting ANTICOAGULANTS
- Release of clotting factors 1. WARFARIN (COUMADIN)
CLOTTING FACTORS - works by interfering the formation of
I. Fibrinogen vitamin K – dependent clotting
factors and prolongation of clotting
II. Prothrombin times
III. Tissue factor - PO, onset 3 days, duration 4-5 days
IV. Calcium ions - Uses: AF, artificial heart valves,
V. Proaccelerin prevent thrombus and embolization
affecting MI and pulmonary
VI. Serum prothrombin conversion accelerator
embolism
VII. Anti-hemophilic factor A
- ANTIDOTE: phytonadione
VIII. Christmas factor; antihemophilic factor B (Aquamephyton)- a form of vitamin K
(responsible for promoting the liver
IX. Stuart factor; thrombokinase
synthesis of clotting factors)
X. Plasma Thromboplastin/antihemophilic
- LAB: prothrombin time (PT) -
factor C
maintained at 1.25 – 2.5 times the
XI. Hogeman factor; antihemophilic D laboratory control value
XII. Fibrin stabilizing factor : International Normalized Ratio (INR)= 2-3
2. HEPARIN
• Clots – prevent blood loss
 - 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.
Antidote: overdose: protamine sulfate
– strongly basic CHON drug forms stable
salts with heparin as soon as the two drugs
come in contact immediately reversing the
effect of heparin (paradoxically:
anticoagulant effect if not with heparin)
LAB:
• whole blood clotting time (WBCT) 2.5- 3
X control
• Activated Partial Thromboplastin Time
(aPTT) up to 40 sec
• Partial Thromboplastin time (PTT) 1.5-
2.5 X control in secs.
3. ANTITHROMBIN (THROMBATE III)
- Naturally occurring anticoagulant;
treatment of antithrombin III
deficiency.
4. ARGATROBAN (ACOVA)
- IV treatment of heparin induced
thrombocytopenia.
5. BIVALIRUDIN (ANGIOMAX)
- Inhibits thrombin, used with ASA to
prevent ischemic event to patient
undergoing transluminal coronary
angioplasty
• 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,
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
- Sigs 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 reinfarct,
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), IV
• CI: hypersensitivity, pregnancy, lactation,
bleeding disorder, recent surgery
• AE: bleeding, Gi discomfort, HA
• NURSING CONSIDERATIONS: (same)
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
• 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
- ANTIDOTE: aminocaproic acid
(Amicar)
- Prevent bleeding
HEMOSTATIC AGENTS
• MOA: hasten clotting of blood by inhibiting
the substance that activate plasminogen
• Uses: to stop bleeding
• CI: 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 (esp with aprotinin)
• DI: aminocaproic acid + oral contraceptives
= increase coagulation
• EG:
- Systemic hemostatic:
• Aprotinin
• Vitamin K
• Aminocaproic acid
• Cabazochrome NA
• Tranexamic acid
• Somatostatin
- Topical:
• Gelfilm/gelfoam
• Microfibrillar collagen
 • Thrombin
• 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)