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Exam 2 Review

Anti-Infective Drug Therapy


Anti-infective agents target foreign organisms infecting the body and do NOT
possess selective toxicity.
No anti-infective drug exists that does not affect the host.
Resistance Mechanisms:

Produce enzyme to deactivate the antimicrobial drug


Change cellular permeability to prevent drug entering cell
Alter transport systems to exclude drug from active transport into cell
Alter binding sites on membrane or ribosomes to no longer accept drug
Produce antagonist chemical to the drug

Side Effects

Renal failure
Gastro toxicity: ie. Diarrhea
Hypersensitivity
Neurotoxicity: can damage or interfere with function of nerve tissue
o Ex. aminoglycoside can collect in 8th cranial nerve and cause dizziness,
vertigo, and hearing loss.
Superinfections: infection by one type of bacteria that may be resistant and
is allowed to proliferate. Can also be secondary infection such as a yeast
infection.

Bacteriostatic: prevent growth of bacteria


Bactericidal: kill bacteria directly
Broad spectrum antibiotics: effect a wide range of organisms
Narrow Spectrum: self-explanatory
3 Principle Factors for antibiotic selection
1. ID the infecting organism, match the drug with the bug
2. Drug sensitivity of offending organism, narrow ultimately better
3. Host factors: site of infection; status of host immune system
Classifications

Aminoglycosides

Used to treat serious infections caused by gram-negative aerobic bacilli


Ex. gentamicin, neomycin, streptomycin, tobramycin
They inhibit protein synthesis in susceptible strains of Gram neg. bacteria
They irreversibly bind to bacterial ribosomes stopping protein synthesis
needed for the cell to survive. Kills the cell (bactericidal)
Gram negative bacteria: pseudomonas aeruginosa, E. Coli, staph aureus
Absorption: Well absorbed after IM administration. IV administration results in
complete bioavailability. Some absorption follows administration by other
routes.
Distribution: Widely distributed throughout extracellular fluid; crosses the
placenta; small amounts enter breast milk. Poor penetration into CSF.
Metabolism and Excretion: >90% excreted unchanged by kidneys.
Evaluate eighth cranial nerve function by audiometry before and throughout
therapy. Hearing loss is usually in the high-frequency range. Ototoxicity.
Renal function tests as well, nephrotoxicity. Encourage lots of fluid intake to
avoid.
G: gentamicin
B: Garamycin; G-Mycin; Jenamicin
Classification:
Ther. Class: anti-infectives
Pharm. Class: aminoglycosides
Mechanism of Action:
Inhibits protein synthesis in bacteria at level of 30S ribosome.

Carbapenems

New class of broad spectrum antibiotics


Effective against gram + and -.
Can be very toxic to GI
Bactericidal by inhibiting cell membrane synthesis.
Ex. s. pneumonia, h. influenza, s. aureus, e. coli, c. diff
Common side effects are GI related, c. diff, diarrhea, nausea, vomiting
leading to dehydration and electrolyte imbalance. Metabolic alkalosis
Valproic acid(taken for anti-seizure) use in combination with Carbapenems
can cause serum valproic acid to fall and increase seizure risk.
Again, drink fluids to reduce renal toxicity

Cephalosporins

Similar to penicillins in structure. 2nd and 3rd generations mostly used now.
Bactericidal action by inhibiting cell membrane synthesis. The affected
bacteria cells weakened cell walls swell and burst by osmotic pressure.
Cross sensitivity with penicillins is common (if allergic to one good chance
allergic to other).

Apparently well absorbed by GI, but drug book says IM and IV is best.
Toxic to kidney and liver, monitor liver enzymes and kidney function.
Common Side Effects:
CNS: SEIZURES (HIGH DOSES) .
GI: PSEUDOMEMBRANOUS COLITIS, diarrhea, nausea, vomiting.
Derm: rashes, pruritis, urticaria.
Hemat: agranulocytosis, bleeding, eosinophilia, hemolytic anemia,
neutropenia, thrombocytopenia.
Local: pain at IM site, phlebitis at IV site.
Misc: ALLERGIC REACTIONS INCLUDING ANAPHYLAXIS , superinfection.
Drug to Drug: cephalosporin and aminoglycoside concurrent use can increase
nephrotoxicity. Also, anticoagulant (Coumadin) use with cephalosporin can
increase bleeding risk.
Teach symptoms of blood loss, no alcohol up to 72 hours after discontinuation
of drugs.
Name:
G: cefotaxime
B: Claforan
Classification:
Ther. Class: anti-infective
Pharm. Class: third generation cephalosporin

Fluoroquinolones

Newer class of synthetic antibiotics with broad spectrum


Gram negative, treats: e. coli; gonorrhea; group D streptococci, UTI and skin
infections
Cipro used for prevention of anthrax in event of germ warfare
Enter cell by passive diffusion and interfere with action of DNA enzymes
required for growth and reproduction of bacteria.
Inhibits bacterial DNA synthesis by inhibiting DNA gyrase enzyme.
Absorption: 70% absorbed after oral administration; IV administration results
in complete bioavailability.
Need to do renal function tests to avoid toxicity
Common Side Effects:
CNS: ELEVATED INTRACRANIAL PRESSURE (INCLUDING PSEUDOTUMOR
CEREBRI) , SEIZURES, agitation, confusion, depression, dizziness, drowsiness,
hallucinations, headache, insomnia, nightmares, paranoia, tremor.
GI: PSEUDOMEMBRANOUS COLITIS, abdominal pain, diarrhea, nausea, liver
enzymes .
GU: vaginitis.
Derm: photosensitivity, rash.
Endo: hyperglycemia, hypoglycemia.
Hemat: eosinophilia.
Local: phlebitis at IV site.

MS: tendinitis, tendon rupture.


Neuro: peripheral neuropathy.
Misc: hypersensitivity reactions including ANAPHYLAXIS .
Antacid use with fluoroquinolones reduces its effect, take at least 4 hours
apart.
Drugs that shorten QT interval taken with these can cause cardiac reaction
Taken with NSAIDs can cause seizures
Taken with corticosteroids can increase risk of tendon rupture or tendinitis
Teaching: Avoid UV light exposure and report any tendon pain or weakness

Penicillins and Penicillinase-resistant antibiotics

Mechanism of action is interrupting the bacterial cell wall synthesis. Human


cells use different mechanism making this effect selective toxicity
Rapidly absorbed from GI, peak levels within 1 hour. Sensitive to gastric acid
so empty stomach best to improve absorbtion. Excreted unchanged in urine,
so renal function important for safe use.
Monitor renal function, contraindicated in pt with either penicillin or
cephalosporin allergy.
Common Side effects: N/V, diarrhea, ab pain, glossitis, stomatitis, gastritis,
sore mouth, furry tongue(yeast infection). Primarily due to related to loss of
bacteria in normal flora and from super-infections including yeast infections.
It inactivates aminoglycosides.
Take on empty stomach for proper absorbtion

Sulfonamides

They inhibit folic acid synthesis


Used for UTIs, STDs, ulcerative colitis.
Mechanism of action: cells are impermeable to folic acid and therefore by
inhibiting folic acid synthesis bacteria cannot produce RNA/DNA. It
competitively blocks PABA to prevent folic acid production.
Can effect gram + and -.
Teratogenic (think folic acid)
Monitor: renal BUN, creatinine; heme CBC, allergic reactions
N/V, diarrhea, etc; renal effects, CNS: headache, dizzy, vertigo;
photosensitive, anaphylaxis
Drug to Drug: with cyclosporine risk of nephrotoxicity rises

Macrolides (Erythromycins)

Often used for infections resistant to penicillin


Similar spectrum as penicillin. Depending on dose and target can be
bactericidal or bacteriostatic
Used for whooping cough, legionnaires dx, haemophilus influenza,
mycoplasma pneumonia, strep

Newer types have longer half lifes. Ex Z pack 3-5 days but will stay in system
for 10 or more days.
Broad spectrum, mostly gram +.
SE: GI, take with food
Azithromycin (Zithromax)- PO or IV, long half life; less GI effects,
bacteriostatic, used commonly for resp infection (bronchitis)
Clindamycin (Cleocin)- PO, IM, IV, topical- inhibits bacterial protein synthesis;
often given with other drugs for broader spectrum.
Vancomycin (Vancocin)- IV- bactericidal for gram +; used for MRSA, C. diff,
cardiac surgery prophylaxis for clients with penicillin allergy
o SE: ototoxicity and nephrotoxicity
o Frequent peak trough numbers to avoid toxicity
Linezolid(Zyvox)- new antibiotic for MRSA and VRE

TB

Caused by bacillus mycobacterium tuberculosis, kills more people than any


other major health problem. Approx 1.5 billion have it worldwide.
Mycobacterium have resistant cell wall to penetration so treatment continues
for 6-12 months. 2-4 antibiotics used together because resistance is common
and mycobacteria grow slowly.
Common in HIV
Rifampin, pyrazinamide, and ethambutol used in combination with isoniazid.

Antivirals

Used against influenza A, herpes, CMV(cytomegalovirus, aka herpes), HIV,


and hep B and C.
Drugs for herpes and CMV include: acyclovir, foscarnet, ganciclovir,
valacyclovir (Valtrex)
Herpes drugs inhibit viral DNA replication
Absorbed in GI, out in urine
Monitor: renal: BUN and creatinine, drugs for herpes/CMV are highly toxic (no
pregnancy or lactation)
SE: N/V, headache, depression (dopamine levels), paresthesias, neuropathy,
rash, hair loss.

Anti Fungals

Azoles is large group on antifungals to treat topical and systemic fungal


infections
o Fluconazole(Diflucan) and ketoconazole(Nizoral)
o Considered less toxic but not as effective against severe infection
Mechanism of action: binds to sterols and cause cell death or interfere with
replication depending on fungus.
CYP450 system-READ about it and drug interactions

Other Agents

Antiprotozoal agents inhibit DNA synthesis in susceptible protozoa.


Flagyl used for amoebas and trichimonas
Absorbed in GI, monitor renal for toxicity, BUN/creatinine
SE: CNS:headache, dizzy, ataxia, peripheral neuropathy ; GI: N/V, diarrhea;
Superinfections
Combination with anticoagulants can increase bleeding up to 8 days after
stopping therapy.
Teaching: avoid alcohol

Respiratory Drugs

Antitussives

Drugs to suppress cough reflex


Mechanism of action: works directly on medullary cough center of brain to
depress cough reflex.
Other antitussives effect the respiratory tract directly, all of which are used in
situation of non-productive cough.
Rapid oral absorbtion.
Monitor: Dont give to pt that needs cough to maintain airway (post op pt).
Also be careful of asthma and emphysema pt because it can lead to
accumulation of secretions.
SE: drying effect on membranes, drowsiness/sedation, nausea, constipation,
dry mouth
Pt education: dont drive, dont take if pregnant/lactating

Decongestants

Decrease overproduction of secretions by causing vasoconstriction of upper


respiratory tract. Helps promote drainage and improved airflow.
Monitor: avoid giving to people that would not want sympathetic activity, ie
HTN pt.
Topical agents: ephedrine, oxymetazoline, or phenylephrine.
o Mech of action: sympathetic action of vasoconstriction leading to
decreased edema open airways.
o Pharmacokinetics: onset almost immediate, not usually absorbed
systematically

Oral agents: pseudoephedrine, stimulates alpha-adrenergic receptors in nasal


mucus membranes, shrinking them. Reaches peak level in 20-45 min.
SE: Rebound congestion: adverse side effect, can lead to prolonged overuse
of decongestants.

Antihistamines

Block the release of histamine during inflammation that would normally


increase secretions and narrow airways.
1st gen=Benadryl ; 2nd gen= zyrtec, allegra, Claritin
Mech of action: selectively block histamine-1 receptor sites
Absorption: Well absorbed after oral or IM administration but 4060% of an
oral dose reaches systemic circulation due to first-pass metabolism.
Distribution: Widely distributed. Crosses the placenta; enters breast milk.
Metabolism and Excretion: 95% metabolized by the liver.
Monitor: history of arrhythmias or prolonged QT interval (fatal cardiac
arrhythmias)
SE:
CNS: drowsiness, dizziness, headache, paradoxical excitation (increased in
children)
EENT: blurred vision, tinnitus
CV: hypotension, palpitations
GI: anorexia, dry mouth, constipation, nausea
GU: dysuria, frequency, urinary retention
Derm: photosensitivity
Resp: chest tightness, thickened bronchial secretions, wheezing

Expectorant

Increase productive cough to clear airways by liquefying lower resp tract


secretions, reducing viscosity.
Guaifenesin is only currently available
Pharmacokinetics: rapidly absorbed in stomach, onset 30 min and duration 46 hrs.
SE: GI=N/V and anorexia
CNS=headache, dizzy
Education: do not use more than 7 days, seek medical care

Mucolytics

Increase or liquefy resp secretions in pt with thick tenacious secretions.


Used in COPD, cystic fibrosis, pneumonia, or TB.
Acetylcysteine and dornase alfa
Mech of action: breaks apart mucoproteins in resp secretions, resulting in
decrease in tenacity and viscosity.

Pharmacokinetics: nebulization or direct through trachea via endotracheal


tube.
Monitor: caution in broncho-spasms , peptic ulcer, and esophageal varicesincreased secretion could aggravate condition.
SE: GI upset, stomatitis(inflammation of mucous lining of mouth),
rhinorrhea(runny nose), bronchospasm, and rash.

Bronchodilators/Antiasthmatics

Facilitate breathing by dilating the airways


Include: xanthines, sympathomimetics, and anticholinergics
Xanthines= naturally occurring, includes caffeine and theophylline. Not first
choice bronchodilators.
Mech of action:
o Xanthines directly affect smooth muscle of resp tract. Also, thought to
inhibit the release slow-reacting anaphylaxis substance and histamine,
decreasing swelling/narrowing.
Rapidly absorbed from GI, reach peak in 2 hours. IV reaches peak in minutes.
Monitor: caution in GI problems, coronary dx, resp disfunction, renal/hepatic
dx.
SE: GI upset, nausea, irritability, arrhythmias, tachycardia, seizures, brain
damage, death.
Drug interaction: nicotine increases metabolism of xanthines, so dose must
be increased if pt continues to smoke. If quit smoking dose must go down or
toxicity occurs.

Beta-Specific Adrenergic Agonists(mimic sympathetic NS)

Used to manage and treat bronchial spasm, asthma, and other obstructive
pulmonary conditions. Ex. albuterol
Sympathomimetics: drugs that mimic sympathetic NS, ie. Dilation of bronchi
and increased rate/depth of breathing.
Mech of action: most are beta 2 found in bronchi. They also increase BP, HR,
vasoconstriction, decrease renal and GI BF. This can limit usefulness in some
pts(ex. HTN)
Pharmacokinetics: inhaled or oral. Rapid if inhaled.
Monitor: dont give if it would aggravate with sympathetic stimulation
SE: Things attributed to sympathetic stimulation; sweating, pallor, HTN, etc
Education: Use 30 to 60 min before exercise to unsure peak effect when
needed.

Anticholinergics

For pt who cant tolerate sympathetic stimulation, however not as effective as


those drugs.

Mech of action: bronchodilator effecting vagus nerve, blocks action of


neurotransmitter Ach.
Normally this stimulation would cause smooth muscle constriction; results in
a relaxation of smooth in bronchi, leading to bronchodilation.
Pharmacokinetics: inhaled, action in 15 min, peak 1-2 hrs, 3-4 effects.
Monitor: soy/peanut allergy
SE: dizzy, headache, fatigue, nervousness, dry mouth, sore throat,
palpitations, increase BP, urine retention.

Drugs Affecting Inflamation

Used in treatment of asthma and COPD where inflammation could further


narrow airways.
Uses inhaled steroids, leukotriene receptors, and mast cell stabilizer.

Inhaled Steroids

Effective against bronchospasm


Mech of action: when inhaled, reduces effectiveness of inflammatory cells.
This helps decrease swelling and promotes beta-adrenergic receptor activity,
that relaxes smooth muscle and inhibits bronchoconstriction.
Pharmacokinetics: can take 2-3 weeks to reach effective levels.
Monitor: DO NOT use for acute attack. Taper carefully during transfer to
inhaled steroids, can cause adrenal insufficiency.
SE: sore throat, horse, cough, dry mouth, fungal infection(mouth/throat)
Education: decongestant drops can aid before use of inhaled steroid if
congestion an issue. Rinse mouth after use to limit GI upset.

Leukotriene Receptor Agonists