N319 Anti-Infectives – Exam I
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Inhibition (slows down) vs. inducing (speeds up)
Antibacterial = antibiotics
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Bacteria
o Prokaryotes = one cell (bacilli or cocci)
o Gram positive (membrane more permeable) vs gram negative à harder to treat
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Antiseptic = on outside of body to kill bacteria (hand sanitizer)
Antimicrobial = inhibits bacterial growth
Antibiotics (match the bug to the drug)
o Bacteriostatic = inhibit growth à body able to catch up and fight
o Bactericidal = kill bacteria
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Body defenses
o Age, nutrition, immunoglobulins, circulation, WBC, organ function
o Natural resistance: no previous exposure to antibacterial drug
o Nosocomial infections: infection when pt. is in hospital (drug resistant)
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Resistance to Antibacterial
o Inherent resistance = bacteria is resistant to medication
o Acquired resistance = other bacteria can pass its resistance
o Antibiotic misuse = viral infections, no infection, incorrectly taking
o Cross – resistance = can occur between antibacterial drugs
o Ex: MRSA (vancomycin à led to more strains), VREF, VRSA
Antibiotic Combination Effects
o Additive = effect is doubled
o Potentiative = one makes another better
o Antagonistic = desired effect reduced
General Adverse
o Allergic reaction
o Superinfection à secondary infection = normal flora is killed (C. diff), only antibiotic use causes
 the broader the spectrum = the more likely to cause a superinfection
 narrow spectrum only hit a specific bacteria
o Organ toxicity
Antibacterial Spectrum
o Narrow = one bacteria type (penicillin, erythromycin)
o Broad = gram positive & negative (tetracycline & cephalosporins), organism isn’t identified
Common terms
o Infectious – how easy is it to get into the body?
o Contagious – how easy is it spread?
o Virulent – how sick does it make you?
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o Vector – living organism which delivers disease (mosquitos)
o Reservoir – where the disease lives
o Fomites – objects that carry or hold disease
The older the antibiotic = the more resistance there is
FOCUS ON YOUR CLASSES! AND WHAT MAKES THEM DIFFERENT!!
Penicillin (-cillin)
N319 Anti-Infectives – Exam I
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Structure: beta-lactam ring structure
Action:
o inhibit cell wall synthesis
o bacteriostatic or bactericidal (depends on drug and dose)
Side effects/adverse reactions:
o Hypersensitivity, anaphylaxis
o Superinfection
o Tongue discoloration, stomatitis
o GI distress
o Clostridium difficile-associated diarrhea
Nursing process
o Interventions:
 Obtain a sample for lab culture and antibiotic sensitivity to discern the ineffective
organism
 Monitor for superinfection, especially in patients taking high doses for a long time
types:
o basic
 narrow spectrum
 use – gram + and few –
 Streptococcus and Clostridium species
 Anthrax, tetanus, diphtheria, endocarditis, respiratory infection, syphilis
o broad-spectrum
 gram + and –
 Proteus mirabilis and Salmonella species
 Treats respiratory, skin, intraabdominal, urinary tract, and gynecologic infections,
Otitis media, sinusitis
o penicillinase- resistant
 narrow spectrum
 gram +
 Penicillinase-producing Staphylococcus aureus
 Other Staphylococcus species
 Treats endocarditis, meningitis, bacteremia, skin, and respiratory infections
o extended spectrum
 gram –
 Proteus and Serratia species
 Enterobacter and Acinetobacter species
 Treats respiratory, intraabdominal, and skin infections
o Beta-lactamase inhibitors
 Inhibits bacterial beta-lactamases extending their antimicrobial spectrum
 In combination with penicillinase-sensitive penicillin to prevent from being destroyed
Cephalosporins (-ceph)– resistance to penicillin = resistance to cephalosporin version too
o Beta-lactam structure
o Action:
o Inhibits cell wall synthesis
o Bactericidal
o Treat
o Respiratory, urinary, skin, bone, joint, and genital infections
o Side effects/adverse reactions
o Headache, dysgeusia, GI distress
N319 Anti-Infectives – Exam I
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o Clostridium difficile-associated diarrhea
o Increased bleeding, seizures
o Nephrotoxicity
o Stevens-Johnson syndrome – skin sloughs off
o Elevated hepatic enzymes
Generations:
o 1st = gram + and some –
 Staphylococci, Streptococci
 E. coli, Klebsiella, Proteus, Salmonella and Shigella species
o 2nd = gram + and –
 Staphylococci, Streptococci, E. coli
o 3rd = gram + and –
 E. coli
 Pseudomonas aeruginosa
 Serratia and Acinetobacter species
 Has increased resistance to destruction by beta-lactamases
o 4th = gram + and –
 Staphylococci, Streptococci
 E. coli
 Highly resistant to destruction by beta-lactamases
o 5th gram + and – (newest)
 Staphylococci, MRSA, Streptococci, E. coli
 Klebsiella and Proteus species, Pseudomonas aeruginosa
 Highly resistant to destruction by beta-lactamases
Drug interactions
o Alcohol = disulfiram-like reaction (flushing, dizzy, headache, nausea, vomiting, cramps)
 Includes alcohol in sugars and mouth wash
o Uricosurics = decrease cephalosporin excretion
o Don’t need extra contraceptives if on birth controls
Macrolides: Erythromycin (-mycin)
o Binds to 50S ribosomal subunits and inhibits protein synthesis
o Broad spectrum à gram + and some –
o Bacteriostatic with low to moderate doses, bactericidal with high
o Use:
o Mild to moderate respiratory, sinuses, skin, soft tissue, GI tract infections, diphtheria,
impetigo, STIs
o Side effects/adverse reactions
o Anaphylaxis, superinfection
o PHOTOSENSITIVITY
o Tinnitus, ototoxicity, headache, seizures
o Dysgeusia, tooth discoloration, GI distress
o Clostridium difficile-associated diarrhea
o Nephrotoxicity, hepatotoxicity
o Stevens-Johnson syndrome
o Drug interactions
o Levels of warfarin, theophylline, and carbamazepine increase.
o Erythromycin levels increase with fluconazole, ketoconazole, itraconazole, verapamil,
diltiazem, and clarithromycin.
o Risk of sudden cardiac death.
N319 Anti-Infectives – Exam I
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Azithromycin levels may be reduced by antacids à changes GI absorption
Oxazolidinones – newer drug class
o Action:
o Inhibit protein synthesis on 50s ribosomal subunit
o Gram +
o Bacteriostatic and bactericidal
o Use:
o Bacteremia, sepsis, MRSA, VREF
o Respiratory and skin infections
o Side effects/adverse reactions
o Anaphylaxis, seizure
o Tongue and tooth discoloration, GI distress
o Peripheral neuropathy, headache
o Anemia, thrombocytopenia, neutropenia
o Clostridium difficile-associated diarrhea
o Stevens-Johnson syndrome
Lincosamides – related to macrolides
o Action:
o Inhibit bacterial protein synthesis
o Gram +
o S. aureus and anaerobic organisms
o Bacteriostatic and bactericidal
o Use
o Treats acne, bacteremia, septicemia, MRSA, respiratory, intraabdominal, skin, gynecologic,
and bone/joint infections (harder to treat due to less blood supply)
o Side effects/adverse reactions
o Anaphylaxis, superinfection
o Xerosis, dysgeusia, glossitis, stomatitis, GI distress
o Clostridium difficile-associated diarrhea
o Pancytopenia, Stevens-Johnson syndrome
o Drug interactions
o Clindamycin and lincomycin are incompatible with aminophylline, phenytoin, barbiturates,
and ampicillin. (Cannot be in the same IV line)
Glycopeptides – primary weapon against MRSA
o Action:
o Inhibit cell wall synthesis
o Gram + MRSA
o Bactericidal
o Use:
o Respiratory, skin, and bone/joint infections
o Bacteremia, septicemia, and endocarditis
o MRSA, Clostridium difficile-associated diarrhea
o Vancomycin = IV only for systemic use, but orally for C. diff
o Adverse:
o Red neck or red man syndrome à TOXIC not ALLERGIC REACTION
 Occurs when IV too rapid**
 Severe hypotension
N319 Anti-Infectives – Exam I
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 Red blotching of face, neck, chest, and extremities
 Watch the rate, different for everyone
Disulfiram-like reaction to alcohol
Ketolides – 18+ years, no kids
o Structurally related to macrolides
o Blocks bacterial protein synthesis
o Use
o Treats community-acquired pneumonia, MRSA
o Effective against Streptococcus pneumoniae, Haemophilus influenzae
o Side effects:
o Exacerbation of myasthenia gravis
o Visual disturbances
Tetracyclines -older behind penicillin
o Action:
o inhibit protein synthesis
o broad spectrum, bacteriostatic
o bacterial resistance
o gram + and –
o Use:
o Helicobacter pylori, MRSA
o Treats acne, anthrax, plague, gingivitis, cholera, STIs, skin, and urinary and respiratory
infections
o Side effects:
o PHOTOSENSITIVITY
o Do not give to children younger than 8 years
o Can cause discoloration of permanent teeth
o Drug–food interactions – metabolized on the p450 thing
o Milk products
o Antacids
o Oral contraceptives
o Penicillin – antagonistic effect
o Aminoglycosides – antagonistic effects
**KNOW HOW PEAK AND TROUGH WORK (Trough = drawn before giving med, peak = max amout of med)
Glycylcyline
o Action:
o Block protein synthesis
o Bacteriostatic
o Use:
o Complicated skin and intraabdominal infections, community-acquired pneumonia
o Side effects:
o PHOTOSENSIVITY
Aminoglycosides – strong weapon, serious infections only, p450
o Action:
o Inhibit protein synthesis, bactericidal
N319 Anti-Infectives – Exam I
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Use:
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Easily crosses the blood-barrier for kids
Effective against gram-negative E. coli, Proteus, Pseudomonas species
Treats serious respiratory, skin, urinary, bone/joint, intraabdominal infections, plague,
bacteremia, septicemia, endocarditis, meningitis, and hepatic encephalopathy
o Bowel preparation
Side effects/adverse reactions
o Anaphylaxis, superinfection, seizures
o Photosensitivity, anemia, stomatitis, GI distress
o Ototoxicity, nephrotoxicity, neurotoxicity – increase fluids
o Clostridium difficile–associated diarrhea
o Stevens-Johnson syndrome
Drug interactions
o Penicillins decrease aminoglycoside effectiveness.
o Increased action of oral anticoagulants
o Ethacrynic acid with aminoglycosides may lead to ototoxicity.
Fluoroquinolones
o Action:
o Interfere with enzyme DNA gyrase needed to make bacterial DNA
o Gram + and gram –
o Bactericidal
o Use:
o UTI, skin infections, OB issues, Anthrax
o Good alternative if allergic to penicillin, cephalosporins, and other antibiotics
o CAN CAUSE SPONTANEOUS TENDON RUPTURE, NERVE DAMAGE causing them to remove from the
market
o Side effects:
o Superinfections – due to broad spectrum
o Know if pain in the heel or leg precursors are to ruptured tendons
Lipopeptides
o Action:
o Inhibit bacterial protein, DNA, and RNA synthesis
o Effective against gram + Staphylococcus aureus, MRSA
o Bactericidal
o Use:
o Skin infections, septicemia, endocarditis
o Side effects:
o Anemia, bleeding, interactions with rhabdomyolysis and inhibits metabolism of warfarin =
increase of bleeding times
Unclassified Antibacterial Drugs
Chloramphenicol
o Action:
o inhibit bacterial protein synthesis, bacteriostatic
o use:
o gram + and –
o serious infections: bacteremia, septicemia, meningitis, typhoid fever, micro plasm pneumonia
N319 Anti-Infectives – Exam I
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side effects:
o optic neuritis, glossitis, stomatitis, pancytopenia
Quinupristin/Dalfopristin
o Action:
o Disrupt bacterial protein synthesis
o S. aureus and S. pyogenes
o Use:
o Treats VREF, skin infections
o Side effects:
o C. diff, hyperbilirubinemia, arthralgia
Obiltoxaximab
o Action:
o Inhibit binding of protective antigen of bacterial toxin to cellular receptors preventing lethal
factor of anthrax from intracellular entry
o Bacillus anthracis
o Treats:
o Anthrax
Sulfonamides – one of the oldest antibiotics
o Inhibit bacterial synthesis of folic acid à inhibit bacterial growth
o Bacteriostatic
o Gram negative
o Use – otitis media, meningitis, malaria, respiratory and UTI
o Good choice if allergic to penicillins
Nitroimidazoles
o Disrupts DNA and protein syntheses in bacteria and protozoa
o Flagyl belongs in this class à go to for protozoal, H-pylori infections, and C.diff
o Alcohol and flagyl = make people sick
Tuberculosis (acid-fast bacillus)
o Droplets (coughing, sneezing, talking)
o At risk = immunocompromised, living or working in high risk, illegal drugs, healthcare
o 1/3 of world could be infected à most of US isn’t vaccinated bc not prevalent
o Mycobacteria are small and thick waxy covering to make hard to get rid of
o Can go dormant à true airborne illness à can stay suspended indefinitely
o if you are healthy, TB should not be an issue because your body covers it and hides it à shows up in
Xray à can cause bad damage to the lungs
o TB put HIV on radar à looking for unseen illnesses
o Symptoms look like other illnesses
o MAKE SURE YOU KNOW CAVATATIONS = holes in lungs from TB
o Antitubercular Drugs
o Single – drug therapy is ineffective (2 years)
o Multi-drug therapy is what is used (6-9 months)
o Drug selection
 First line: Isoniazid, rifampin, rifabutin, rifapentine, pyrazinamide, ethambutol
o Combination therapy (minimum of 3-5 drugs)
 Initial 2 months à continuation = 4-7 months
N319 Anti-Infectives – Exam I
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 They must finish regimen à has to be reported
Side effects
 Rifampin = turns body fluids orange à soft contact lenses may be permanently
discolored
 Meds not easy to take
Isoniazid (INH)
 Route: Oral, IM
 Inhibits bacterial cell wall synthesis
Special populations:
 Pregnancy, HIV, pediatrics
Fungal infections (candidiasis)
o Local = mucous membranes, hair, nails, moist areas (Mild)
o Systemic = lungs, abdomen CNS (severe) à ring worm
o Hard to treat because they are complex organisms à opportunistic
o Antifungals
o Polyenes
 Amphotericin B - Treats severe, systemic fungal infections (IV only) à high risk for
toxicity
 Binds to fungal cell membranes, causing cell permeability, and leakage of
cellular contents
 Nystatin (Mycostatin)- Oral, topical
 Binds to sterols causing loss of intracellular potassium and other cell
contents
o Azoles
 Azoles- Oral, IV, vaginal, topical
 Increases permeability of fungal cell membrane by inhibiting ergosterol
synthesis
 Side effect: hypokalemia and hepatotoxicity
o Antimetabolites
 Selectively penetrating the fungal cell which disrupts fungal DNA and RNA synthesis
 Well-absorbed from the GI tract
 Used in combination with other antifungals such as amphotericin
o Echinocandins- IV
 Inhibits biosynthesis of essential components of fungal cell wall which interferes with
growth and reproduction of Candida and Aspergillus species
 Side effects- Injection site reaction, Elevated hepatic enzymes
WHEN YOU SEE A MEDICATION THAT IS IV ONLY LOOK FOR INFILTRATION AND STUFF
 Viruses
 Method of transmission à Droplets: coughing, sneezing, talking
 Process of replication of itself
 Common viral infections
• Influenza, herpes, hepatitis
 Influenza (flu) – ANTIVIRALS = SHORTEN THE DURATION & LESSEN SEVERITY & DECREASE
INFECTION RATE
• Highly contagious, Affects nose, throat, lungs
• Seasonal, more prevalent from fall to spring
• Can be deadly to populations that are more at risk
N319 Anti-Infectives – Exam I
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 Herpes
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Antigen types
 Influenza A - Moderate to severe viral infection
 Influenza B - Mild viral infection
 Influenza C - Mild respiratory, viral infection
Tamiflu – needs to be give within 24-48 for effectiveness
Herpes simplex virus type 1 (HSV-1) à Causes with cold sores
Herpes simplex virus type 2 (HSV-2)à Causes lesions on genitalia
Varicella-zoster viruses (HSV-3 or VZV)à Causes chickenpox and shingles
Epstein-Barr virus (HHV-4 or EBV)à Causes mononucleosis
Cytomegalovirus (HHV-5 or CMV) à Causes eye pain vision disturbances in those w/
weakened immune system
 Hepatitis virus
• Serious liver infection
• Needlestick, intimate sexual contact, or childbirth
• Bloodborne pathogens spread via blood and body fluids
• Hepatitis B à always fatal, C à almost able to cure
 Non-HIV antivirals - Prevent or delay spread of viral infection
• Inhibits viral replication
• Influenza antivirals
• Decrease viral spread
• Shorten duration of signs and symptoms
• Side effects- Dizziness, headache, insomnia, fatigue
• GI distress, abnormal behavior
 Herpes simplex antivirals
• Interferes with DNA synthesis
 Cytomegalovirus antivirals
• Use—CMV retinitis in people with AIDS
• Inhibits DNA polymerase to suppress viral replication
• Side effects- Headache, dizziness, GI distress
 Hepatitis antivirals
• Delay progression of liver disease.
• Do not discontinue abruptly or exacerbations can occur.
• Inhibit viral replication
• Side effects—Mild to life-threatening
 Fatigue, flu-like symptoms, depression
 Alopecia, anorexia, dysgeusia, arthralgia, myalgia
 Thyroid and ophthalmic dysfunction
 Hepatotoxicity, renal impairment, infection
 Malaria
• Vector is mosquitos and reservoir is water
• Antimalarial à try to prevent malaria
 anorexia
Helminths – parasitic worms
o Four groups of helminths
 Cestodes (tapeworms)
 Trematodes (flukes)
 Intestinal nematodes (roundworms)
 Tissue-invading nematodes (tissue roundworms)
o Transmission
N319 Anti-Infectives – Exam I
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 Entry from infected soil to humans
 Intestines, blood vessels, and liver
Anthelmintic drugs – destroy parasitic worms
 1-3 days
Peptides
 Interferes with the bacterial cell wall causing cell death
 Classifications
 Antiviral, antimicrobial, antifungal, antiparasitic
 Peptides
 Colistimethate
 Polymyxins
 Bacitracin
 Metronidazole
STUDY NOTES:
24 hours after lecture is the best time to study
Focus on: Classes of drugs, TB, HIV (replication and growth process)
Even number of questions from each chapter
Straight multiple choice (fill in the blank once in a while)
Chapter 29 – HIV and AIDS – related Drugs
o HIV
o RNA retrovirus – unable to survive and replicate unless in a human
 Uses a piece of genetic material and enzymes to hijack host to replicate its own DNA
o Destroys CD4+ T cells, immune deficiency
o How is it transmitted?  prevent through lowering viral load
 Sexually transmitted  tied to gays and promiscuous behavior
 Sharing needles, body fluids
o HIV is the virus  develops into AIDS = immune system is no longer functioning
o HIV life cycle
 Infects the host which requires specific CD4+ T receptors
 Attachment = GB120 to inject into the host cell membrane into CD4
 Enters the host and releases RNA and enzymes of the virus
 Puts the new viral DNA into host DNA where it will continue to replicate
 The virus matures and will be ready to infect others
o Symptoms occur 2-12 weeks after exposure  by this time it is too late
o Labs
 CD4 = you want this to be high
 HIV RNA quantative assay (viral load) = you want this to be low
 HIV resistance = determine resistances
o Enzymes:
 Reverse transcriptase = HIV to make copy of DNA “reading backwards”
 Integrase = new DNA to be integrated into the host DNA
 Protease = cuts HIV into specific infectious molecules
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Classes of antiretrovirals
 Nucleoside/ nucleotide reverse transcriptase  blocks reverse transcriptase
interferes
 Didanosine taken 30 – 2 hours pc
 Side effects  lipoatrophy = destroy fat cells
 Nonnucleoside reverse transcriptase  blocks reverse transcriptase directly
N319 Anti-Infectives – Exam I
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Protease inhibitor  release of immature, defective, and noninfectious viral particles
 Strong P450 inhibitors too
 Fusion (entry) inhibitor + CCR5 antagonists  blocks the attachment phase to not
allow binding
 Integrase strand transfer inhibitors  prevents new viral DNA from being integrated
into the host DNA
Immune Reconstitution Inflammatory Syndrome (IRIS)  basically treating and when immune
system is better it will begin to fight diseases it couldn’t before
 Paradoxical = exacerbation of treated opportunistic infection
 Unmasking = response to undiagnosed or subclinical opportunistic infection
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Opportunistic infections  treat as indicated
o TB – affects lungs, may affect other organs
o Kaposi sarcoma – cancer! dark blue lesions, mucous membrane, GI tract, lymph nodes
o Pneumocystis jiroveci pneumonia – fungal infection in the lungs
o Toxoplasmosis – uncooked meat and cat poop  brain
o Cryptosporidiosis – bowel mucosa  common during flooding
o Mycobacterium avium complex – blood infection  related to TB
o Cytomegalovirus – virus in whole body  may lead to blindness
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Antiretroviral in pregnancy
o Treatment early to suppress viral load and transmission
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Occupational exposure – get help immediately
Chapter 31 – Vaccines
o Active – body produces antibodies & natural immunity
o Passive – antibodies from another source
o Community – exposed to antigen
o Vaccines
o Adjuvant – additives to increase shelf-life and effectiveness
o HPV must be administered before sexual activity
Chapter 48 – Urinary Disorders
Lower – cystitis (bladder and urethra)  more in females, usually E. coli, dysuria
Upper – pyelonephritis (kidneys)  chills, fever, flank pain
Nitrofurantoin – good with e. coli, good for uncomplicated UTI’s, broad spectrum
Methenamine – NOT AN ANTIBIOTIC, URINARY ANTISEPTIC, changes pH of urine slightly acidic to kill
bacteria – LOWER UTI only
Trimethoprim – sulfamethoxazole
Fluoroquinolones – CAUTION USE ONLY IN UNCOMPLICATED UTI IF NO OTHER TREATMENT OPTION –
due to possible spontaneous rupture of tendons
Urinary analgesics – Phenazopyridine – relieve pain, no antiseptic  URINE WILL BE BRIGHT ORANGE
Urinary stimulants – Bethanechol – increase bladder tone, make them go
Urinary antispasmodic – oxybutynin – relieves urges
N319 Anti-Infectives – Exam I