🦠 Module 2 · Anti-Infectives

🧵 Exam traps ⭐ HIGH YIELD

• Draw the culture BEFORE the first antibiotic dose — but do not delay antibiotics in sepsis. The correct action is 'obtain cultures, then administer.'
• Trough is drawn about 30 minutes before the next dose and is the toxicity value; peak is drawn after. Students reverse them constantly.
• 'Finish the whole prescription even though you feel better' is a resistance-prevention answer, not a comfort answer.
• Not every '-mycin' is an aminoglycoside. Gentamicin, tobramycin, and amikacin are. Vancomycin, clindamycin, and erythromycin are NOT.
• Phenazopyridine turns urine orange but is only a bladder analgesic — it does not treat the infection. Nitrofurantoin (which turns urine brown) does.
• Nystatin for thrush is swished and then swallowed or spit per the order; it is not simply drunk like a liquid antibiotic.

What is the difference between a bactericidal & bacteriostatic antibiotic?⭐ HIGH YIELD

BACTERICIDAL antibiotics KILL the bacteria. BACTERIOSTATIC antibiotics only stop them from reproducing and leave the existing bacteria for the immune system to clear.

• That distinction only matters when the patient's immune system cannot finish the job. A healthy patient does fine with either.
• Bactericidal is REQUIRED for immunocompromised patients (neutropenia, chemotherapy, HIV, transplant) and for life-threatening infections such as acute bacterial endocarditis, meningitis, and sepsis.
• Bacteriostatic drugs can fail in those patients because there is no functioning immune system to kill what is left behind.
• Some drugs are bacteriostatic at low concentration and bactericidal at high concentration, which is why dose and level matter.
• Combining a bacteriostatic drug with a bactericidal drug can be antagonistic, because the cidal drug needs actively dividing bacteria to work.

-CIDAL = homiCIDAL, it kills. -STATIC = it just holds them STATIONARY.

Give examples of bactericidal & bactericidal antibiotics.⭐ HIGH YIELD

BACTERICIDAL: penicillins, cephalosporins, carbapenems, aztreonam, vancomycin, aminoglycosides, fluoroquinolones, metronidazole, daptomycin, isoniazid, rifampin. BACTERIOSTATIC: tetracyclines, macrolides, sulfonamides, trimethoprim, clindamycin, linezolid, chloramphenicol, nitrofurantoin.

• Easy rule: if it wrecks the CELL WALL or DNA, it kills. If it blocks the RIBOSOME (protein synthesis), it usually only stalls.
• THE EXCEPTION EXAMS LOVE: aminoglycosides (gentamicin, tobramycin, amikacin) block protein synthesis but are BACTERICIDAL.
• Trimethoprim and sulfamethoxazole are each bacteriostatic alone, but TOGETHER as Bactrim they are bactericidal. That is the textbook's example of a synergistic combination.
• Vancomycin is bactericidal against most organisms but only bacteriostatic against enterococci.
• All beta-lactams (anything with a beta-lactam ring: penicillins, cephalosporins, carbapenems, monobactams) are bactericidal.

Wall and DNA drugs KILL. Ribosome drugs STALL. Aminoglycosides cheat and kill anyway.

Broad-Spectrum vs Narrow-Spectrum Antibiotics⭐ HIGH YIELD

BROAD-spectrum antibiotics cover a wide variety of organisms, both gram-positive AND gram-negative. NARROW-spectrum antibiotics target only a specific subset, either gram-positive or gram-negative.

• Broad-spectrum is started EMPIRICALLY while culture results are pending, then narrowed once the organism and sensitivities are known (de-escalation).
• Broad-spectrum is also used for polymicrobial infections, for surgical and procedural prophylaxis, and when a narrow agent has already failed.
• The price of broad-spectrum is damage to the patient's MICROBIOME, which causes SUPERINFECTION: C. difficile pseudomembranous colitis (can be fatal) and Candida yeast infections.
• Probiotics such as lactobacillus may be recommended to help restore normal flora.
• Nurse's role: watch culture results, make sure the provider sees them, and advocate for narrowing the antibiotic when the sensitivities come back.

Broad = shotgun while you wait. Narrow = sniper once you know the target.

How can antimicrobial resistance be prevented?⭐ HIGH YIELD

Prevent resistance by (1) taking the FULL prescribed course even after symptoms resolve, (2) not prescribing antibiotics for viral illnesses like the common cold, and (3) using directly observed therapy (DOT) for long regimens such as tuberculosis.

• Stopping early is the classic patient behavior that breeds resistance: it fails to kill the target organisms and selects for resistant variants.
• Overprescribing is the classic provider behavior. Patients often DEMAND antibiotics for viral upper respiratory infections; teaching is the nursing intervention.
• Longer courses mean worse adherence. TB treatment lasts 6 to 12 months, which is exactly why multidrug-resistant TB emerged.
• Other strategies: culture BEFORE the first dose, narrow the spectrum once sensitivities return, antimicrobial stewardship programs, hand hygiene and infection control, no leftover or shared antibiotics, and vaccination.
• Scale of the problem per the CDC: at least 2 million antibiotic-resistant infections and 23,000 deaths per year in the US. MRSA and VRSA are the named resistant organisms.

Finish the bottle, skip it for viruses, and watch them swallow it.

What are the common adverse effects associated with antibiotics as a group?⭐ HIGH YIELD

As a class, antibiotics cause GI upset (nausea, vomiting, diarrhea), allergic and hypersensitivity reactions up to anaphylaxis, and SUPERINFECTION, meaning C. difficile diarrhea and candidiasis (oral thrush, vaginal yeast).

• GI distress is the most common complaint and is the reason patients stop early. Teach that food may ease it, but check whether the specific drug requires an empty stomach.
• Superinfection: new diarrhea (especially foul, watery, 3 or more stools a day), white patches in the mouth, or vaginal itching and discharge during or after antibiotics. C. diff colitis can be fatal.
• Allergy ranges from a mild rash to urticaria, laryngeal edema, and anaphylaxis. Always check allergies before the first dose and keep epinephrine available.
• Organ toxicities to know: NEPHROTOXICITY and OTOTOXICITY (aminoglycosides, vancomycin), hepatotoxicity (isoniazid, rifampin), photosensitivity (tetracyclines, sulfonamides, fluoroquinolones, macrolides), and QT prolongation (macrolides, fluoroquinolones).
• Antibiotics also reduce the effectiveness of ORAL CONTRACEPTIVES (the textbook flags this with amoxicillin and tetracyclines), so teach a backup method.

Every antibiotic: gut upset, allergy, and a yeast or C. diff surprise.

What is culture and sensitivity?⭐ HIGH YIELD

A CULTURE grows a sample from blood, urine, sputum, or a wound to identify the organism. The SENSITIVITY tells you which antibiotics that specific organism will respond to (and which it is resistant to). Always collect the culture BEFORE the first antibiotic dose.

• Giving the antibiotic first invalidates the result and can delay effective treatment. This is the single most tested nursing point on this topic.
• Results take about 1 to 5 days, so treatment usually starts empirically with a broad-spectrum drug and is narrowed later.
• A gram stain is the fast screen: violet = gram-positive (Staphylococcus, Streptococcus), red/pink = gram-negative (E. coli, Neisseria). It guides an initial choice in minutes rather than days.
• The nurse is responsible for collecting an accurate specimen, monitoring the results, making sure the provider sees them, and questioning the order if the prescribed drug does not cover the organism.
• 'Resistant' on the report means that drug will NOT work no matter the dose.

Culture BEFORE the cure. Draw it, then hang it.

Which drugs cause photosensitivity?⭐ HIGH YIELD

The four antibiotic classes your textbook names are TETRACYCLINES, SULFONAMIDES, FLUOROQUINOLONES, and MACROLIDES. Outside antibiotics, the big ones are amiodarone, thiazide and loop diuretics, phenothiazines (promethazine, chlorpromazine), retinoids, and St John's wort.

• Teaching for ALL of them: broad-spectrum sunscreen, hat and long sleeves, avoid peak sun (10 a.m. to 4 p.m.), and no tanning beds. The reaction looks like an exaggerated sunburn that appears fast.
• Doxycycline is the one you will actually see this with in practice, because it is prescribed so often for acne, Lyme disease, and respiratory infections.
• Amiodarone causes a distinctive slate-gray or blue-gray skin discoloration with sun exposure, on top of ordinary photosensitivity.
• Also on the list: TMP-SMX (a sulfonamide), sulfonylureas, NSAIDs (especially piroxicam), TCAs and some SSRIs, isotretinoin and tazarotene, voriconazole, hydrochlorothiazide, and furosemide.
• Photosensitivity is not an allergy. It does not mean stop the drug, but it does mean the patient must protect their skin for the whole course.

SAT-M burns: Sulfonamides, Amiodarone, Tetracyclines, Macrolides plus fluoroquinolones. Sunscreen for all of them.

What are the causes and treatments of oral candidiasis (thrush)?⭐ HIGH YIELD

Oral candidiasis (thrush) is a Candida albicans overgrowth caused by anything that disrupts normal flora or immunity: BROAD-SPECTRUM ANTIBIOTICS and INHALED CORTICOSTEROIDS without rinsing are the top two. Treat with NYSTATIN swish and swallow, clotrimazole troches, or oral fluconazole for moderate to severe cases.

• Nystatin technique (tested): swish for 30 seconds or as long as tolerated, then swallow (or spit if ordered), and DO NOT eat or drink for 10 to 30 minutes afterward so the drug stays in contact with the tissue.
• Prevention with inhaled steroids: use a spacer and RINSE AND SPIT after every dose.
• Other causes: immunosuppression (HIV/AIDS, chemotherapy, transplant, corticosteroids), uncontrolled diabetes, dentures, xerostomia, infancy, and old age.
• Looks like: white curd-like plaques on the tongue, palate, and buccal mucosa that SCRAPE OFF and leave a red, raw, sometimes bleeding base. Patients report burning, altered taste, and pain with swallowing.
• Thrush in a healthy adult with no obvious cause is a red flag: screen for HIV and diabetes. Extension into the esophagus (odynophagia) is an AIDS-defining condition and needs systemic fluconazole.

White patches that wipe off = thrush. Swish, swallow, then nothing by mouth for 30 minutes.

What are the different pharmacological classes of HIV antiretrovirals? Give an example of a drug in each class.⭐ HIGH YIELD

Five classes: NRTIs (tenofovir), NNRTIs (efavirenz), PROTEASE INHIBITORS (darunavir or atazanavir), INTEGRASE INHIBITORS/INSTIs (dolutegravir), and ENTRY INHIBITORS (maraviroc, a CCR5 antagonist; enfuvirtide, a fusion inhibitor).

• Suffix clues do most of the work: -navir is a protease inhibitor, -tegravir is an integrase inhibitor, -virine is an NNRTI.
• Standard first-line regimen today is 2 NRTIs plus an INSTI, for example tenofovir + emtricitabine + dolutegravir, often as a single combination tablet.
• Class effects worth knowing: NRTIs cause LACTIC ACIDOSIS with hepatomegaly and steatosis (the textbook names this plus pancreatitis, and says to stop the drug immediately if pancreatitis occurs). Zidovudine causes bone marrow suppression. Abacavir requires HLA-B*5701 testing first.
• Protease inhibitors cause metabolic problems (hyperlipidemia, insulin resistance, fat redistribution) and enormous CYP450 interactions. Ritonavir and cobicistat are used deliberately as 'boosters' because they inhibit CYP3A4.
• Many antiretrovirals affect the KIDNEYS. Monitor urine output and renal labs, per the textbook.
• St John's wort and rifampin induce CYP3A4 and can make antiretrovirals fail completely.

-navir NAVigates protease. -tegravir inTEGRates. -virine is the NNRTI.

Why are multiple antiretroviral drugs given simultaneously?⭐ HIGH YIELD

Because HIV mutates constantly. Attacking several DIFFERENT STAGES of the viral life cycle at once suppresses replication far more completely and makes it nearly impossible for the virus to develop resistance to all the drugs at the same time. This is combination antiretroviral therapy (ART).

• A single drug would be defeated within weeks by a single mutation. Three drugs from two or more classes require multiple simultaneous mutations, which is statistically very unlikely.
• Standard regimen is at least 3 active drugs from 2 or more classes, usually 2 NRTIs plus an integrase inhibitor.
• The goal is an UNDETECTABLE viral load, which both preserves the CD4 count and makes sexual transmission effectively zero (U=U, undetectable equals untransmittable).
• ADHERENCE is the whole ballgame. Missed doses let the virus replicate in the presence of partial drug levels, which is the exact condition that selects for resistance. The textbook stresses compliance teaching.
• Single-tablet combination products exist specifically to support adherence.
• Never stop or hold antiretrovirals without provider direction, even for a hospital admission or NPO status.

One drug, one mutation, game over. Three drugs at three steps and the virus can't keep up.

phenazopyridine⭐ HIGH YIELD

Phenazopyridine (Pyridium, Azo) is a urinary tract ANALGESIC dye, NOT an antibiotic. It numbs the bladder and urethra to relieve burning, urgency, and frequency while an actual antibiotic treats the infection.

• It turns urine BRIGHT ORANGE-RED. Warn the patient in advance, because it looks alarming and it permanently STAINS clothing, undergarments, and soft contact lenses. Remove contacts while taking it.
• It treats only the SYMPTOM. Teach explicitly that they must still take the full antibiotic course. Feeling better is not being cured.
• Limit use to 2 DAYS when taken with an antibiotic. Longer use masks whether the infection is actually resolving.
• Take with or after food to reduce GI upset.
• Contraindicated or used with caution in renal impairment. Can cause hemolytic anemia and METHEMOGLOBINEMIA, especially in G6PD deficiency; report yellowing of the skin or eyes, blue-tinged skin, or shortness of breath.
• It can also interfere with urine dipstick tests (glucose, ketones, urinalysis), so note it on the lab requisition.

Pyridium numbs, it does not cure. Orange urine, ruined underwear, 2 days max.

ketoconazole & fluconazole⭐ HIGH YIELD

Both are AZOLE antifungals that block ergosterol synthesis and destabilize the fungal cell membrane. KETOCONAZOLE is an imidazole, now used mainly TOPICALLY for skin infections because oral use carries severe HEPATOTOXICITY and QT risk. FLUCONAZOLE is a triazole, better tolerated and the workhorse ORAL/IV agent for systemic yeast infections.

• The textbook's split: imidazoles (miconazole, ketoconazole, clotrimazole) treat fungal SKIN infections such as athlete's foot, jock itch, and ringworm. Triazoles (fluconazole) treat systemic yeast infections including oral thrush and cryptococcal meningitis, both common in AIDS, and triazoles are more selectively toxic with fewer side effects.
• Fluconazole penetrates CSF and urine well, which is why it is used for cryptococcal meningitis. A single 150 mg oral dose treats uncomplicated vaginal candidiasis.
• BOTH are potent CYP450 inhibitors, so both raise levels of warfarin, phenytoin, statins, and many other drugs. Fluconazole plus warfarin is a bleeding risk; azoles plus simvastatin risks rhabdomyolysis. Oral ketoconazole is contraindicated with drugs that prolong QT.
• Monitor LIVER FUNCTION with either one. Teach the patient to report unexplained bruising or bleeding, abdominal pain, dark urine, jaundice, fever, or rash.
• Oral ketoconazole absorption requires an ACIDIC stomach, so PPIs, H2 blockers, and antacids block it. Fluconazole absorption is unaffected by gastric pH.
• Both may cause fetal harm; fluconazole at high dose is teratogenic. Finish the full course even after symptoms clear.

Ketoconazole stayed on the skin because it wrecked the liver. Fluconazole got to stay systemic.

acyclovir & valacyclovir⭐ HIGH YIELD

Both are antiherpes antivirals that terminate the viral DNA chain during replication. VALACYCLOVIR is a PRODRUG of acyclovir with much better oral absorption, so it is dosed far less often. Used for genital herpes, cold sores, chickenpox, and shingles.

• Neither one CURES herpes. They shorten and reduce outbreaks, and lower doses can be taken long-term for suppression. Say this plainly to patients.
• START AS EARLY AS POSSIBLE after symptoms appear, ideally within 24 to 72 hours or at the first tingling/prodrome. Started late, they do very little.
• PUSH FLUIDS. Both are NEPHROTOXIC because the drug can crystallize in the renal tubules. IV acyclovir must be infused over at least ONE HOUR to prevent renal tubular damage, never IV push.
• Route rules from the textbook: acyclovir is PO, IV, or topical. Never give it IM or subcutaneously. Give with food if GI upset occurs.
• Both LOWER THE SEIZURE THRESHOLD and can cause neurotoxicity (confusion, tremor, hallucinations), especially in older adults and in renal impairment. Doses must be reduced for reduced kidney function.
• Teach: avoid sexual contact while lesions are present, herpes is still transmissible without visible lesions, and expect fatigue so plan rest.

Valacyclovir is acyclovir that learned to be absorbed. Start early, drink water, never IV push.