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ID test 1
Bugs n drugs
| Question | Answer |
|---|---|
| Adhesion | Pathogens ability to attach to a host |
| Invasions | Ability to enter a host |
| Evasions | ability to escape host defenses Abscess formation, capsule formation, biofilm production Doubling time |
| Nerds | Gram Positive: Enterococcus (VRE)and staph epi Gram Negative:Acinetobactor |
| Jocks | Gram Positive: Streptococcus pyogenes Toxin production, adhesion, fast doubling time Streptococcus pneumoniae Encapsulated Gram Negative:Legionella pneumophila Pleomorphic, grows in water |
| Sterile areas of the body | Lungs, liver, bile, pancreas, kidneys, uterus and CSF |
| Host defense mechanisms | First line - Natural Physical Barriers Skin Mucous membranes Respiratory tract Intestinal tract Genitourinary tract Eye Second line - Immune system |
| What results on the skin from the breakdown or lipids into fatty acids? | The acid mantle, ph 5-6 which is an inhospitable environment for bacteria |
| What immunoglobulins are contained in body cavity secrections? | IGG and IGA |
| What antimicrobial defenses are contained in tears? | IGA and lysozymes |
| What level of leukocytes found on a cbc indicates infection? (leukocytosis) | >10- 12 k = leukocytosis |
| What is left shift? | an increase in immature neutrophils (bands) |
| WHat temperatures are considered fever? | >100.4 F > 38 C |
| Stain used to detect fungus and molds? | Lactophenol cotton blue |
| Stain used to detect parasites | trichrome |
| Stain used to detect cryptococcal only fungal infections | India ink |
| what bacteria is an acid fast stain typically used to detect | mycobacterium and nocardia |
| why do we need an acid fast attain? | the cell wall is a thin layer of peptidoglycan but is mostly mycolic acid. the process makes the bacterial cell wal retain the red colored carbol fuschin |
| Which culture and sensibility test is measured with a zone of inhibition? | Kirby Bauer test. |
| if the zone of inhibition is large is the good or bad for resistance and how is it measured? | it is a good indicator of low resistance and is measure in millimeters |
| Which test uses two fold serial dilutions to determine the MIC of an organism? | Broth dilution method. |
| The higher the number on a serial broth dilution means what with reference to resistance? | The higher the number the more resistant the organism is to the antibiotic. |
| What increments do broth dilutions follow? | 0.125, 0.25, 0.5, 1.0,2.0, 4.0, 8.0 ... |
| What testing method uses zone of inhibition to measure the MIC of an antibiotic? | E-Test |
| What does MIC represent? | The relationship between one bug and one drug. |
| Define pharmacodynamics | The relationship between an antibiotic and a specific bug. |
| Why do we use pharmacodynamics? | To determine specific drug potency or the differences in potency between drugs in the same class of antibiotics. |
| What is drug drug additivism? | When one drug compliments another drug enhancing the effect from 1-2 IE 1+1=2 |
| What is drug synergy? | multiplicative increase in efficacy, I.E. 1+1=5 |
| What is a static antibiotic? | <3 log kill in 24 hours |
| What is a cidal drug? | > 3 log kill in 24 hours |
| Gram Positive cocci in clusters | Staph auer and staph epi |
| Gram positive in pairs or chains | Step Pneumo, strep pyogenes (GAS), Strep agalactacie (GBS) Entero face, Enteor facalus |
| Gram positive bacilli | Lysteria monocytogenes |
| Gram negative cocci in pairs and chains | Neisseria and M. catt |
| Gram negative bacilli or rods (enterobactericiae) | E coli and klebsiela serraatia, proteus, enterobacter, morganella |
| atypicals | legionella, chlymadia and mycoplasma pneumo |
| anaerobes | clostridium and bacteroides |
| staph A is resistant due to what? | the MecA gene which produces the betalactamase penicillinase |
| two types of Strep MRSA? | CA and HA |
| primary locations for HA MRSA | skin 37%, respiratory 22%, UTI, 20 % |
| Primary locations for CA MRSA | SKIN 70% |
| Agents used to treat MRSA | Reliable – active against almost all MRSA – 100% Vancomycin, telavancin Linezolid Daptomycin Tigecycline Ceftaroline TMP/SMX Less reliable Doxycycline – 70% Clindamycin – 60% |
| aka for staph epi | NERD coag neg strep or staph not epi |
| how to treat staph epi infections | Reliable MRSA agents |
| common infections caused by staph epi? | Catheter-related bloodstream infections Catheter-related urinary tract infections Skin/skin structure infections – cellulitis Prosthetic joint infections Prosthetic valve endocarditis |
| strep pneumo aka pneumococcus locations | sinuses and skin |
| strep pneumo infections? | Most Common Cause of: Community-acquired pneumonia Bacterial meningitis Can cause Sinusitis Otitis media Skin/skin structure infections Much much more |
| strep pneumo virulence level? | Highly virulent JOCK |
| Strep pneumo defenxe system | Encapsulation |
| Strep pyogenes is AKA as what? | Group A strep (GAS) Flesh eating bacteria |
| Why is GAS both virulent and pathogenic? | it is a toxin producer and casuse tissue necrosis |
| what is the primary t/Tx for GAS? | Still sensitive to penicillin |
| Gas is the common cause of what infections? | Strep throat Skin/skin structure infections Toxic Shock Syndrome |
| Common AKA for strep agalactiae? | GBS |
| location for GBS | normal vaginal flora in 40 % of women |
| when do we typically test for GBS | During pregnancy |
| GBS is the most common cause of what? | neonatal sepsis |
| E. Faece and E. facalis normal locations | Gi tract, mouth and skin |
| which is more resistant, e faece or e. faecalis? | In your Faeceium |
| common infections caused by E face twins? | Nosocomial (hospital-acquired) Blood stream infections Endocarditis UTI Wound infections |
| How to treat AMP S and vanc S enterococcus infections? | 1st line – penicillins Amp/amox/pen ± BLI, pip/taz, ticar/clav 2nd line – carbapenems |
| How to treat AMP R and Vanc S enterococcus infections | Vancomycin |
| How to treat amd R and Vanc R enterococcus infections | Linezolid Daptomycin Tigecycline |
| common carrier for listeria | Food stuffs like queso fresco, hot dogs, raw unpasteurized foods, refrigerated patte's and smoked foods |
| who should avoid the foods that can carry listeria? | Pregnant and imunocomprimised |
| two Neisseria species | Meningitis and gonorrhoeae |
| Is Neisseria gonorrhoeae normal flora and what does is cause? | NO, and gonorrhea |
| What does M catt commonly cause | URTI'S: ottis media, laryngitis, sinusitis and pneumonia |
| Gram negative rod general rules | Common bacteria in GI tract Just about any antibiotic with Gram-negative activity will have intrinsic activity Exceptions: Pseudomonas, Acinetobacter Antibiotic susceptibilities vary widely dependent upon resistance mechanisms |
| Gram negative rod treatment | Empiric therapy:1st line = anti-pseudomonal beta-lactam if Pseudomonas or other resistant GN rods are suspected De-escalation (ASAP)with: 1st line = “narrowest spectrum” beta-lactam that is sensitive 2nd line = Amino, fq,severe allergy |
| two most common producers of ESBL (extended spectrum beta lactamase prodcuers) | E-coli and klebsiela |
| Common producers of AmpC beta lactamase | S-Serratia P-Proteus P-Pseudomonas A-Acinetobactor C-Citrobactor E-Enterobactor M- Morganella |
| What does AMP-C do? | Makes the bacteria resistant to all beta lactams except Cefepime and carbapenems |
| What is the most common gram positive cause of HCAP? | MRSA |
| What is the most common gram negative casue of HCAP? | Pseudomonas |
| What types of HCA infections besides Pneumonia can pseudomonas cause? | Blood stream infections, wound infections, post-op infections, UTI |
| Antibiotics active against pseudomonas | Pip/tazo, Ticar/Clav, cefepime, ceftazadime, Imi, mero, dori, aztreonam, Aminoglycosides(AGT, FQ's (Cipro and levo), colistin |
| Where is acinetobactor typically found | on hospital equipment |
| how long can acinetobactor live on inanimate objects | 1 day to 2 weeks |
| why does acinetobactor have a high mortality rate? | not due to virulence rather the severity of the illness the patient already has. |
| What infections does h flu cause? | CAP Meningitis Sinusitis Otitis media Conjunctivitis |
| Why is h flu a JOCK? and how do we treat it? | It is encapsulated and we vaccinate for it primarily. |
| Name all three encapsulated organisms | N. meningitidis, S. pneumoniae, H. influenzae |
| What is associated with clostridium botulinum and what does it cause? | Honey and home canned foods, paralysis due to toxin production |
| how do we treat clostridium botulinum? | no abx must get antitoxin from cdc. |
| What is associated with clostridium tetani? | Puncture wounds especially from a metal object |
| what happens when you get clostridium tetani infection? | muscle spasms, spasma and nyperflexia due to toxin production |
| How do we treat clostridium tetani? | penicillin, surgery and muscle relaxants and we vaccinate every ten years |
| What is caused by clostridium perfringens? | Gas gangrene |
| how do we treat clostridium perfringens? | antitoxins, surgery and hyperbaric chamber |
| what is associated with a clostridium difficile infection? | CDAD, cdif associated DIARRHEA |
| Treatment for C-DIFF infection | oral metronidazole or oral Vancomycin |
| Anti MRSA beta lactam | ceftaroline |
| anti enterococcal beta lactams | penicillin, amoxicillin, ampicillin, pip/tazo, ticar/clav and carbepenems |
| antipseudomonal beta lactams | pip/tazo, ticar/clav, cefepime, ceftazadime, imi, meor, dori and aztreonam |
| anti anaerobic beta lactams | amox/ clav, amp/sulbactam, pip/taz, ticar/clav, cefotetin, cefoxitin and carbapenems |
| volume of distribution of beta lactams? | 0.7 l/kg, water is 0.6 L/Kg, they go everywhere water goes. |
| where do beta lactams fail to go? | Bone and Variable to CSF |
| what pharmacodynamics parameters do beta lactams have? | Time>mic: Penicillins= 50% Cephalosporins = 60-70% Carbepenems= 40% |
| When can we use cephalosporins and carbapenems when a patient has an allergy to penicillin? | When the reaction is not anaphylactic |
| options if patient has a severe penicillin allergy? | aztreonam and other non beta lactams |
| Penicillin ROA? | V=po G= IV IM |
| PCN monitoring parameters | Electrolytes and renal function, renal adjustment required |
| what is PCN unstable against? | betalactamase and penicillinase producers |
| what does PCN treat? | GAS, GBS and syphilis are the most common places in therapy for PCN. |
| ROA for naf and OXacillin | IV |
| ROA for Dicloxcillin | PO |
| monitoring parameters for NAF/OX and dicloxacillins? | Hepatic enzymes, excreted hepatically, electrolytes: high NA |
| Are NAF, OX and diclox stable against penicillinase producers? | Yes! |
| What is the place in therapy for NAF, OX and Diclox? | DOC FOR MSSA INFECTIONS!!!!! |
| ROA for PIP/tazo and Ticar Clav? | IV for both |
| Activity for Pip/tazo and ticar/clav? | penicillinase producers, anaerobes, enterococcus and pseudomonas. |
| general rules about cephalosporin's | increasing gram negative coverage with generations, no enterococcal or listeria activity, stable against penicillinase, not anaerobic activity except cefotetan and cefoxitin |
| 1st gen cephs | Cephalexin (Keflex)PO Cephazolin (Ancef) IV |
| 1st gen cephs place in T/Tx? | skin and skin stricture infections |
| 1st gen excretion method | Renal, monitor renal function |
| 2nd gen cephalosporin's IV options? | cefoxitin(Mefoxin)IV cefotetan (Cefotan)no longer produced |
| 2nd gen spectrum | GP, Gn anaerobes |
| 2nd gen excretion method | Renal, monitor renal fxn |
| 2nd gen ceph PO option | cefuroxime (Ceftin, Zinacef) |
| 3rd gen cephalosporin's IV option | Ceftriaxone (Rocephin) |
| 3rd gen Ceph Po option | cefixime (Suprax) |
| 3rd gen monitoring parameters? | excreted both renal and hepatic, only need dose adjustment if both are comprimised |
| 3rd gen adverse rxns | biliary sludging in pediatric patients |
| place in therapy for 3rd gen cpehs | DOC for CAP with azithromycin |
| 3rd generation ceph that is only excreted renally | ceftazadime (Fortaz) |
| ceftazadime ( Fortaz) activity | pseudomonal, gn and weak gp |
| what inactivates ceftazadime? | ampC and betalactamase |
| 4th gen ceph | cefepime (Maxipime) |
| cefepime (maxipime) roa and monitoring parameters? | IV and monitor renal fxn as excreted renally |
| cefepime (Maxipime) activity | pseudomonal and active against ampc and betalactamase |
| cefepime (Maxipime) place in therapy | Option for impiric T/Tx in HC associated infections |
| 5th gen ceph | ceftaroline (Teflaro) |
| ceftaroline (Teflaro) ROA and monitoring parameters | IV and renal as it is excreted renally |
| Ceftaroline activity | Resistant Gram-pos MRSA and MDR-S. pneumoniae, VRSA and linezolid-resistant SA, common gram negative organisms |
| what degrades ceftaroline (Teflaro)? | Amp C and ESBL |
| Carbepenem activity (except ertapenem) | Active against Pseudomonas sp. Active against Enterococcus sp. Active against anaerobes Stable against penicillinase Stable against ampC beta-lactamase Stable against ESBLs extended-spectrum beta-lactamases |
| Imipenem/cilastin brand name | Primaxin |
| meropenem brand name | Merem |
| doripenem brand name | Doribax |
| imi/mero/ dori ROA and monitoring parameters | IV and monitor renal fxn |
| Imi/mero and dori adverse rxn | Seizures that are dosage based Pts with prior neurological issues at higher risk Stroke, epilepsy Risk of seizure: imipenem > meropenem > doripenem |
| What is the difference between ertapenem and the other three car | Ertapenem does not cover pseudomonas so is not used for hospital patients. typically used for diabetic foot infections |
| what patients are more likely to have seizures when given carbapenems? | people with past stroke, epilepsy and patients on dialysis |
| monobactam | aztreonam (Azactam) |
| aztreonam (Azactam) roa and monitoring parameters | IV and monitor renal rxn as excreted renally |
| Aztreonam activity | stable against penicillinase and gram negatives |
| when do we use aztreonam? | in the event of a severe bata lactam allergy and if desperate. |
| what cross reactivity does aztreonam (Azactam) have? | if allergic to ceftazadime also allergic to aztreonam, same side chain |
| Concentration dependent antibiotics | aminoglycosides, Daptomycin and bactrim |
| time dependent antibiotics | all beta lactams and monobactams |
| auc/mic dependent antibiotics | FQ's, macrolides, tetracyclines, linezolid, glycopeptides |
| amino glycosides | gentamycin, tobramycin, amikacin |
| aminoglycoside spectrum | gram negative and antipseudomonal, used in combo with beta lactams for gram positive infections for staph A, coag neg staph and enterococcus |
| aminoglycoside MOA? | inhibit protein synthesis, binds 30 s subunit. has post antibiotic effect. cidal |
| aminoglycoside VD? | Low, low tissue concentration, mostly stays in vasculature 0.2-0.3 l/kg, low abscess conc. |
| aminoglycoside PD's? | Peak/concentration dependent killing |
| PD goal for AG's with gram negative infections? | > or equal to 16 times the MIC |
| dosing for gent and tobramycin for gram negative infections? | 5-7 mg /kg (IBW) q 24h |
| synergistic dosing for gent and tobramycin for gram positive infections? | 1 mg/kg (IBW) q8h |
| aminoglycoside adverse reactions | ototoxicity, nephrotoxicity, neuromuscular block and rash |
| aminoglycoside ROA | all IV |
| gentamycin and tobramycin monitoring parameters | renal dosage adjustment required troughs for traditional dosing <1-2 mcg/ml once daily dosing <1 mcg/ml gram negative peak >16x MIC |
| amikacin dosing? | 15-20 mg/kg (IBW)q24 |
| amikacin mooitoring parameters | renal fxn, dosage adjustment required trough goal < 8 mcg/ml |
| levofloxacin spectrum | GP, GN, Pseudomonas, anaerobe and atypical |
| moxifloxicin spectrum | GP, GN, anaerobe and atypical |
| ciprofloxacin spectrum | GN and pseudomonas |
| FQ MOA | binds dna gyrase topoisomerase II stopping replication= gn ACTIVITY BINDS DNA GYRASE TOPOISOMERASE IV interferes with separation of dna molecules= GP activity |
| FQ VD | High VD high concentrations found in kidneys, liver, bile and lungs serum> site in bone and csf |
| FQ PD's | AUC/MIC |
| PD goals for FQ's | GP pathogens MIC> 35 GN pathogens MIC> 125 |
| FQ common adverse reactions? | N/V/D, dizziness/ confusion (mostly in the elderly), dose related CNS with levo >750 mg dose, cations bind in stomach (oral only) |
| FQ uncommon adverse rxns with BBW? | Joint symptoms BBW for arthralgias (swelling, tendon rupture)Risk factors: Age >60, BMI <30 kg/m2, concurrent use of glucocorticoids, women significantly more likely than men to develop rupture |
| Fq uncommon rxn non BBW | photosensitivity and LFT elevation |
| cipro ROA and monitoring parameters? | IV and PO and monitor renal fxn, dosage adjustment required |
| cipro place in therapy | best po option for anti-pseudomonal T/Tx, used for UTI, 90% bioavailable |
| levo ROA and monitoring parameters | IV and PO, monitor renal fxn dosage adjustment required, QT wave prolongation, glucose abnormalities |
| levo place in therapy | CAP for patients with beta lactam allergy, antipseudomonal agent (secondary and a bad choice) |
| Moxifloxacin (Avelox) ROA and monitoring parameters | IV and PO, QT wave prolongation and glucose abnormalities, excreted HEPATICALLY! |
| can moxi treat pseudomonas? | NO, no antipseudomonal activity |
| Place in therapy for moxi | CAP patients with beta lactam allergy |
| Macrolides | Azithromycin, Clarithromycin and erythromycin |
| Macrolide spectrum | GP, GN (non- rods) and atypical. Erythromycin has activity against 50% of CA-MRSA but azith and clarith have none |
| Macrolide MOA | Binds 23s subunit of the 50 s subunit block exit of the growing chain inhibiting protein synthesis |
| Macrolide VD | Serum < site: lymph and CSF |
| Macrolide PK | AUC/MIC |
| Macrolide adverse rxn | N/V/D and metallic taste |
| Macrolide drug interactions | azith< eryht< clarith all interact with anything metabolized by the liver. most commonly aan inhibitor of the cyp450 system. most noteably with all is warfarin, theophylline, digoxin and cyclosporine |
| macrolide uncommon adverse reaxtions? | Hearing loss – dose related Eosinophilia Transaminase elevation QT prolongation |
| eryth ROA and monitoring parameters | IV and PO, Monitor LFT's, qt wave prolongation and drug interactions |
| place in therapy | prokinetic gent, GBS prophylaxis in pregnant patients allergic to PCN |
| Azithromycin (Zithromax) ROA and monitoring parameters | IV and PO. LFT's |
| Azithromycin (Zithromax)) place in therapy | DOC for Chlamydia trichomonas DOC for CAP for out pts DOC for CAP for in pts + beta-lactam Common option for all upper respiratory tract bacterial infections (beta-lactams preferred) Sinusitis, otitis media, bronchitis |
| Clarithromycin ROA and monitoring parameters | PO only and LFT's and drug interactions |
| tetracyclines | doxycycline, tetracycline, minocycline and kinda tigecycline |
| TCN spectrum | ALL have GP, gram negative non rods and atypical. Tigecycline has GN rods and anaerobes also |
| TCN MOA | inhibits protein synthesis by binding the 30 s subunit blocking the attachment of trna to mrna |
| TCN VD | High VD serum >site: Lung Sinus Gynecological tissue Bone Bile Periodontal tissue Serum>site: CSF |
| TCN PD | AUC/MIC |
| TCN adverserxn's | N/V/D, photosensitivity and tooth staining (contraindicated in children<12 |
| TCn drug interactions | Cations bind in the stomach |
| tetracycline ROA and monitoring parameters | IV and PO. renal and hepatic fxn, decrease frequency with CrCl <50 and avoid altogether in patients with severe hepatic dysfunction |
| tetracycline place in therapy | treatment of h-pylori and acne |
| doxycycline (Vibramycin)and minocycline (Minocin)roa and monitoring parameters | IV and PO and no adjustment for renal or hepatic dysfunction |
| place in therapy for doxy and mino | Doxy - oral MRSA treatment option Mino – tx of MDR ancinetobacter infections Odd infections Anthrax Chlamydia Tick borne diseases |
| tigecycline (Tygacil) ROA and monitoring parameters | IV and hepatic fxn, dose adjust if severe, pancreatic enzymes and N&V occurs in 33% of people |
| tigecycline (tygacil) place in therapy | MRSA treatment alternative MDR S. pneumoniae treatment alternative VRE treatment alternative Pt with multiple antibiotic allergies Carbapenemase producing pathogens |
| Lincosamides | clindamycin (Cleocin) |
| Glycopeptides | Vancomycin, televancin (Vibativ) |
| Oxazolidinones | Linezolid (Zyvox) |
| Lipopeptides | Daptomycin (Cubicin) |
| clindamycin (Cleocin Spectrum | GP: MRSA/ staph, strep no entero. anaerobes:Bacteroides sp. Peptostreptococcus sp. Fusobacterium sp. NO clostridium activity |
| clindamycin MOA | Binds 50 s subunit inhibiting protein synthesis |
| clindamycin VD | Medium 0.6-1.2 l/kg can be found in Bone (osteomyoletis), sputum (can be used for pneumonia), tissue and sinus tract Not good in CSF |
| clindamycin PD? | Unknown |
| clindamycin adverse effects | N/V/D which is dose limiting, considered the major cause of CDAD, |
| clindamycin max dosing? | max oral dose is 450 mg q6h max IV dose 600-900 mg q6-8h |
| clindamycin ROA | IV and Po |
| clindamycin place in therapy | DOC for GAS infection with PCN patients with PCN allergy and anaerobic infections |
| Bactrim spectrum | GP, MRSA, GN no GAS or enterococcus |
| Bactrim MOA | Dna inhibition through PABA (sulfameth) and dihydrofolic acid (trimetho) |
| Bactrim VD? | medium, limited data, UTI, pneumonia, joint infections and skin/stricture infections |
| Bactrim PD | Concentration dependent both static and cidal |
| Bactrim common adverse reactions | Dermatologic: Rash Urticaria Gastrointestinal Loss of appetite N/V Renal Elevation in SrCr w/o ↓ in GFR Interstitial nephritis Crystalluria Hyperkalemia |
| Bactrim serious adverse reactions | Hematologic: Agranulocytosis Aplastic anemia Hepatic Hepatic necrosis Fulminant liver failure Immune hypersensitivity reaction Rash Erythema Multiforme Stevens-Johnson syndrome Toxic epidermal necrolysis |
| Bactrim ROA and monitoring parameters | IV and PO, Renal dose adjustment if renal dysfunction, K+ and LFT's |
| Bactrim place in therapy | UTI's, PCP prophylaxis in HIV patients with a cd4 count <50, MRSA skin infections |
| Linezolid (Zyvox) spectrum | GP, MRSA and enterococcus, including resistant strep pneumo and VRE. Also mycobacterium avium, TB and nocardium |
| Linezolid (ZYvox) MOA | prevent the formation of 30s and 50 s subunits into the 70s subunits |
| linezolid (ZYvox) VD | Medium 0.5-1.0 l/kg. serum , sites: lung phagocytes and tissues serum> site: CSF |
| linezolid PD | AUC/MIC |
| linezolid (ZYvox) common adverse rxn's | thrombocytopenia >14 days of therapy neutropenia >28 days of therapy |
| linezolid serious adverse reactions | Lactic acidosis, peripheral neuropathy > 28 days of T/Tx, optic neuropathy > 28 days of T/Tx, serotonin syndrome |
| linezolid (Zyvox) ROA and monitoring parameters | IV and PO 100% bioavailability. Monitor CBC |
| linezolid (Zyvox) place in therapy | MRSA pneumonia MRSA skin infections Vancomycin resistant Enterococcus (VRE) infections Alternative therapy for Mycobacterium and Nocardia infections |
| Vancomycin and televancin spectrum | All GP, MRSA and enterococcus |
| Vanco and televancin MOA | cell wall inhibitor, binds d-ala d-ala blocking cross linking process |
| vanco tissue VD | medium VD 0.6-0.7, serum < site, none Serum > site Lung, Tissue and CSF |
| vanco and televancin PD | AUC/MIC maybe time/mic still being debated |
| vanco trough goals | 15-20 mcg/ ml |
| vanco dosing | 15 mg/kg q 8-12 often dose 1g q12 |
| vanco adverse common adverse reactions | infusion reaction (redman syndrome) slow th rate of infusion Nephrotoxicity: trough and duration related |
| vanco rare adverse reactions | ototoxicity related to peak dose, neutropenia and thrombocytopenia |
| televancin common adverse reactions | Hematologic: Thrombocytopenia Nephrotoxic CNS: Insomnia, psychiatric disorder, headache GI: Metallic/soapy taste, N/V/D GU: Foamy urine |
| televancin rare adverse reactions | transient hearing loss and qt wave prolongation |
| Vanco ROA and monitoring parameters | IV nd PO (Po only for CDAD infections Monitor: serum trough concentrations and SCr levels |
| vanco place in therapy | first line option for all MRSA infections with a possible exception for Pneumonia. Tied with metronidazole for CDAD infections |
| televancin ROA and monitoring parameters | IV monitor SCr, platlets and K+ |
| Daptomycin (Cubicin) spectrum | GP, MRSA and enterococcus |
| Daptomycin (Cubicin) MOA | cell wall inhibitor |
| Daptomycin (Cubicin) VD | Low, 0.1-0.2 l/kg minimal data, not appropriate for CSF infections Distributes to the lugs but is bound by surfactant so is useless in pneumonia. |
| Daptomycin (Cubicin) PD | Peak dependent killing, rapidly cidal peak dependent to prevent regrowth |
| Daptomycin common adverse reactions | myalgias and myocitis |
| Daptomycin rare adverse reactions | rhabdo and renal failure secondary to rhabdo |
| Daptomycin (Cubicin) ROA and monitoring parameters | IV Monitoring parameters: Creatinine kinase – prior to start then weekly SrCr – dose adjustments in renal failure |
| Daptomycin (Cubicin) place in therapy | Secondary therapy for: MRSA bacteremia, endocarditis and skin and skin stricture infections |
| Rifampin spectrum | GP, MRSA and enterococcus and mycobacterium like TB and avium... |
| Rifampin MOA | DNA damage, inhibits transcription of dna to rna |
| interesting kinda unique parts of Rifampin MOA | Intracellular Penetrates biofilms Able to kill bacteria in stationary phase All intra-cellular antibiotics should share this attribute |
| rifampin VD | HIGH 1.5-2.0l/kg: Concentrates in: [serum] ≤ [site] Abscess Bile Stomach wall Ascites Liver Other sites of distribution: [serum] > [site] Bone CSF Lung |
| Rifampin PD | AUC/MIC |
| Rifampin common adverse reactions | abnormal skin, sweat saliva, tear and urine colors, range from orange to brown, Increased LFT's |
| Rifampin ROA and monitoring parameters? | IV and PO Monitoring parameters:Renal function – dose change in renal failure Hepatic function Q 2 weeks DRUG INTERACTIONS – potent inducer of 3A4 |
| Rifampin place in therapy | First line for mycobacterium like TB, used in combination for treatment of staphylococcal and enterococcal infections Foreign material – hip, catheter, heart valve |
| Drugs Rifampin is CI with? | Fosamprenavir Lopinavir Saquinavir Tipranavir Voriconazole |
| Is Rifampin an inducer or inhibitor of the cyp 450 system? | Potent inducer, always check for interactions before giving Rifampin |
| Colistin spectrum | strictly gram negative activity against pseudomonas |
| which gram negatives is Colistin not active against? | Proteus sp. Serratia marcescens Moganella morganii Neisseria sp. Moraxella catarrhalis Providentia sp. Helicobacter pylori |
| Colistin MOA | electrostatic displacement of CA and Mg from membrane lipids causing cell membrane degredation |
| Colistin VD | Low, 0.3- 0.5 l/kg tissue= serum binds to liver kidneys, brain, heart, muscle, lungs and placenta for up to 5 days. CSF 25% of serum level |
| Colistin PD | Peak dependent killing |
| Colistin adverse reactions | Nephrotoxicity, dizziness, seizures, tingling, Inhalation route: Bronchospasms Acute respiratory failure Respiratory tract paralysis |
| Colistin ROA and monitoring parameters | IV monitor SCr and mental status changes |
| Colistin place in therapy | MDR pseudomonas and acinetobactor infections...the only drug that is succeseptable inhalation used for PNA and colonization in intubated patients |
| Nitrofurantoin spectrum | GP, GN, MRSA and enterococcus |
| Nitrofurantoin MOA | DNA damage, attacks ribosomal proteins, DNA, respiration, pyruvate metabolism and other intracellular components |
| Nitrofurntoin VD | Unknown, 50% excreted in urine (25% unchanged) and 50 % in bile, if kidney gfr low then less in urine. CrCl between 30-60 = CI |
| Nitrofurantoin PD | Peak dependent killing |
| Nitrofurantoin adverse reactions | Hematologic: Hemolytic anemia Eosinophilia Hepatic: Cholestatic jaundice syndrome Hepatic necrosis Immune hypersensitivity reaction Neurologic: Neuropathy Respiratory: Interstitial lung disease Pulmonary fibrosis |
| Nitrofurantoin ROA and monitoring parameters | PO monitor SCr to determine appropriate patients |
| Nitrofurantoin place in therapy | UTI's only, especially in pregnant patients (DOC) |
| Metronidazole spectrum | Anaerobes only |
| Metronidazole MOA | DNA damage systemic: Reduced metronidazole interacts with DNA to cause a loss of helical structure, strand breakage, and resultant inhibition of nucleic acid synthesis and cell death |
| Metronidazole VD (tissue) | medium 0.5-1 l/kg [Tissue] ≈ [Serum] Female GU tract – pelvic tissue, uterus, etc. Peritoneal fluid Bone Pancreas Colorectal tissue [CSF] = 50-75% of serum |
| Metronidazole PD | Peak dependent killing |
| Metronidazole adverse reactions | gastro, some neurological like seizures, Leukopenia and disulfiram like reactions avoid ETOH during and for 48 H post T\Tx |
| Metronidazole ROA and monitoring parameters | IV, PO, topical and vaginal monitoring parameters...none listed |
| Metronidazole place in therapy? | DOC for CDAD infections, bacterial vaginitis, vaginal protozoal infections, other protozoal infections like giardia |
| quinupristin/dalfopristin spectrum | GP, MRSA, enterococcus, GN rods and atypicals |
| Quinupristin/dalfopristin MOA | binds 50 s subunit inhibiting protein synthesis |
| Quinupristin/dalfopristin VD | LOW 0.45 for q and 0.25 for D, [Tissue] > [Serum] Kidney Liver Spleen Salivary glands WBC [Tissue] < [Serum] Skin/soft tissue Does not cross BBB or placenta |
| Quinupristin/dalfopristin PD | AUC/MIC |
| Quinupristin/dalfopristin adverse reactions | thrombophlebitis, injection site rxns, Conjugated hyperbilirubinemia, Arthralgia Myalgia |
| Quinupristin/dalfopristin ROA and monitoring parameters | iv Hepatic transaminase elevation Dose adjustment in severe hepatic dysfunction Bilirubin increases |
| chloramphenicol spectrum | GP, MRSA, enterococcus, GN rods and atypicals |
| Chloramphenicol MOA | Inhibits transpeptidation prohibiting protein synthesis on 70s subunit |
| Chloramphenicol VD | Medium: Concentrates in: [serum] ≤ [site] Kidney Liver Other sites of distribution: [serum] > [site] CSF – 50% of serum |
| Chloramphenicol adverse reactions | Grey baby syndrome, fatal in newborns and toddlers, neurotoxicity, aplastic anemia (usually fatal occurring months post therapy), |
| Chloramphenicol ROA and monitoring parameters | IV, OT and OP, rarely used, baseline cbc q 2 days during therapy |
| Selective pressure | Survival of the fittest bugs |
| Mechanisms of antibiotic resistance | Intrinsic (lack of drug target)or Acquired resistance |
| alteration of the antimicrobial agent | ESBL, AMP-c beta lactamase alters the drug before it can reach the target |
| Acquired antibiotic resistance: Mutation in the target site | Changes in the target molecule occur as a result of spontaneous mutation, resulting in decreased affinity of the target for the antimicrobial Ex: PBP alteration to PBP2a |
| Acquired antibiotic resistance: Decreased accumulation | Decreased uptake Ex: Porin channel modifications Porin channels only in Gram-negative bacteria Increased efflux Ex: Efflux pumps – may be nonspecific, effluxing multiple antimicrobials and/or other cellular ingredients |
| how is staph A resistant to penicillin? | >95 % resistant by producing beta lactamase |
| Define MRSA and why it is resistant | Presence of the mecA gene, encodes penicillin-binding protein 2a (instead of PBP 2) Alteration of binding site confers resistance to ALL beta-lactams (except ceftaroline) 50/50 MSSA to MRSA |
| How are VISA (vanc intermediate SA) and GISA (glycopeptide SA) resistant? | Thickened cell wall increasing the number of D-ala-D-ala targets, preventing adequate drug concentration from reaching binding sites at cell wall |
| How is VRSA resistant | Resistant mechanism: Plasmid mediated transfer of vanA gene vanA gene codes for D-ala-D-lactate leaving no binding site for vancomycin |
| How is VRE (vanc resistant enterococcus) resistant? | vanA gene vanA codes for D-ala-D-lactate leaving no binding site for vancomycin |
| gram negative amp C Beta-lactamase MOA? | Chromosomally mediated (mostly), can be spread to other bacteria via plasmids Confers clinical resistance to most beta-lactams Exceptions: cefepime and carbapenems Beta-lactamase inhibitors (tazobactam, sulbactam, clavulanate) NOT effective |
| What are the common amp-C beta -lactamse producers? | S;serratia P; proteus, pseudomonas A; Acinetobactor C; Citrobactor E; Enterobactoer M; Morganella |
| Define ESBL | -lactamases capable of hydrolyzing penicillins, cephalosporins, monobactams Inhibited by clavulanic acid in vitro – NOT CLINCIALLY RELEVANT |
| Common ESBL producers? | Klebsiella pneumoniae Escherichia coli Less common ESBL producers Pseudomonas aeruginosa Proteus mirabilis |
| ESBL MOA | Plasmid mediated so can be easily transferred between bacteria species Plasmids often contain genes coding for other resistance mechanisms against AG, chloramphenicol, sulfonamides, trimethoprim, TCN, FQs End result: multi-drug resistant pathogen |
| Treatment of choice for ESBL's? | Carbepenems and Non--lactams – ONLY if susceptible AND non-life threatening infections (UTI or pyelonephritis) |
| Define KP carbepenemase | First associated with Klebsiella, but all Enterobacteriaceae and Pseudomonas have been associated with carbapenmase production KPC is plasmid mediated Bacteria with KPC enzymes inactivate all beta-lactams |
| Agents most likely to be active against carbepenemase producers? | Colistin, amikacin, rarely tigecycline |
| In what patients do mold infections most commonly occur? | imunocomprimised patients |
| What are the most common mold infections? | aspergillus and mucorales both have very high mortality rates |
| most common site of aspergillus infection? | Pulmonary |
| most common site of mucorales infections? | nose, mouth, sinus – invade up into brain |
| Where and whom do Fusarium mold infection effect | Immunocompetent – superficial Nail infections Kertitis Immunosuppressed – invasive Nose/mouth/sinus Pulmonary Skin |
| where do candida yeast infections occur? | Normal flora of GI tract Superficial infections Skin, mouth (thrush), esophagitis, UTI, genital Invasive infections (systemic) Intra-abdominal, bloodstream infections |
| How are dimorphic endemic fungi unique? | Ability to cause disease in a healthy host Association with a specific ecologic niche in the environment Demonstration of temperature dimorphism (mold in the environment at a temperature of 25°–30° C and yeast at body temperature |
| how do dimorphic endemic enter the body and what do they cause? | Enter host via respiratory system, initially causes pulm infections, can spread systemically |
| Name the polyenes | Amphotericin B Nystatin |
| Name the triazoles | Fluconazole Itraconazole Voriconazole Posaconazole |
| Name the Echinocandins | Caspofungin Micafungin Anidulafungin |
| Name the "other" antifungal | 5-FC (flucytosine) |
| Amphotericin spectrum and ROA | Mold – not as good as vori or posa Yeast – not as good as azoles Dimorphic |
| Nystatin ROA and spectrum | Yeast – cutaneous or mucocutaneous infections aka superficial infections |
| Polyene MOA | Cell membrane inhibitor Binds to ergosterol in the fungal cell membrane, forms pores, leaking Na, K, and Ca, depolarizing cell |
| Ampho B adverse rxns | Infusion related – chills/rigors, fever, tachypnea Nephrotoxicity Electrolyte depletion |
| Ampho B PD | Peak dependent killing |
| Ampho B Lipid-associated formulations created to decrease ADRs | AmBisome – liposomal – tolerated best - $$$ Amphotec Abelcet |
| Ampho B place in therapy | First line for Cryptococcus neoformans meningitis Systemic candida infections - back up option when azoles or echinocandins fail |
| Nystatin place in therapy | Topical powder for mild skin infections Swish and spit for thrush and mild esophagitis |
| Fluconazole ROA and spectrum | IV, PO All yeast except C. krusei Dimorphic |
| Itraconazole ROA and spectrum | PO Yeast Mold – itra < vori < posa Dimorphic |
| Voriconazole ROA and spectrum | IV and PO Yeast Mold – itra < vori < posa Dimorphic |
| Posaconazole ROA and spectrum | PO Yeast Mold – itra < vori < posa Dimorphic |
| Azole MOA | Cell membrane inhibitor Inhibit the fungal cytochrome P-450 inhibiting synthesis of ergosterol. Depletion of ergosterol in the cell membrane and accumulation of toxic intermediate sterols, causing increased membrane permeability |
| Azole PD? | AUC/MIC |
| Itraconazole PK problems | unpredictable concentrations Solution – best absorbed on empty stomach Capsules – best absorbed with food (soda/cola best) |
| Voricanazole PK issues | IV formulation in sulfobutylether-beta-cyclodextrin (SBECD) – renally cleared Used to be contraindicated in CrCl < 50 ml/min – SBECD can cause renal vacuoles at high doses (really high doses) |
| Posaconazole PK issues | unpredictable concentrations High fat food will double absorption Taken 4 xs daily to maximize absorption – even though 35 hr t ½ |
| Azole ADR's | Hepatic – transaminase elevation, GI – N/V DI – CYP 3A4 inhibitors Voriconazole – vision changes – blurred, color changes (blue), photophobia |
| Fluconazole place in therapy | First line for systemic Candidal infections First line for moderate/severe skin infections |
| Itraconazole place in therapy | Oral option for dimorphic/endemic fungi |
| Voriconazole place in therapy | First line for Aspergillus and other mold infections |
| Posaconazole place in therapy | Option for Aspergillus First line for Mucormycosis infections |
| Echinocandin ROA and spectrum | IV Yeast – all Candida sp. NO Cryptococcus Mold – Aspergillus sp. only |
| Echinocandin Mechanism of Action | Cell wall inhibitor, Inhibits 1,3-beta glucan synthase resulting in an weak cell wall |
| Echinocandin ADR's and PD | Almost none Some histamine release during infusion No hepatic or renal issues PD= Peak dependent killing |
| Echinocandin place in therapy | Candidal systemic infections First line tx option – tied with fluconazole Aspergillus Combination tx with voriconazole |
| 5-fluorocytosine (5-FC) ROA and spectrum | PO Yeast Only used in combo with ampho B for Cryptococcus infections |
| 5-fluorocytosine (5-FC) MOA | DNA/ RNA inhibitor, 5-FU is phosphorylated and incorporated into RNA where it causes miscoding and halts protein synthesis. |
| 5-fluorocytosine (5-FC):PD ADR and monitoring parameters | PD - % T > MIC ADRs In pts with renal dysfuntion: Heme: leukopenia, thrombocytopenia GI: enterocolitis Death Monitor serum concentrations – goal < 100 mcg/ml |
| Cyclovir PO only options | Valacyclovir, famciclovir and valganciclovir |
| Cylovir iv and po options | acyclovir and ganciclovir |
| topical cyclovir option | penciclovir |
| when a cyclovir has VAL in the front what does that mean? | an increase in bioavailability |
| Cyclovir MOA | inhibit dna synthesis |
| cyclovir PD | AUC/MIC |
| Acyclovir, valacyclovir, famciclovir adverse reactions | Malaise, HA Nephrotox, crystaluria at high IV doses |
| Ganciclovir, valganciclovir adverse reactions | Neutropenia Dose limiting side effect – causes early discontinuation of treatment often Occurs > 7 days of tx Thrombocytopenia Nephtrotox |
| cyclovir monitoring parameters | SCR for all and CBC for val and ganciclovir |
| Acyclovir and valacyclovir place in therapy | First line treatment for HSV and VZV Oral acyclovir dosed 4 xs daily Valacyclovir dosed BID – better compliance |
| Famciclovir place in therapy | Oral option for HSV |
| Penciclovir place in therapy | Topical option for HSV 1 ***no topical treatments have shown dramatic impact on duration of blisters/ulcers (Abreva – docosanol, Zovirax – acyclovir |
| Ganciclovir and valganciclovir place in therapy | First line for CMV or resistant HSV and VZV |
| Foscarnet MOA, PK/PD | MOA: DNA inhibitor PK D – medium E – renal |
| Foscarnet Adverse Reactions | Narrow therapeutic range Nephrotoxicity Azotemia, protenuria, ATN ATN – acute tubular necrosis Dose limiting ADR Occurs > 7 days of treatment Electrolyte chelator of divalent cations Mg, K, Ca, P CNS – HA, seizure, hallucinations |
| Foscarnet Monitoring | SrCr CBC Chem 7, BMP, renal panel Electrolytes – Ca, Mg, P |
| Foscarnet Place in Tx | CMV infections when: Ganciclovir resistant Ganciclovir induced-neutropenia Treatment of resistant herpes viruses HHV 6, 7 |
| Cidofovir MOA, PK | Inhibits DNA synthesis PK D – medium E – renal |
| Cidofovir Adverse Reactions | Nephrotoxicity Proteinuria, azotemia, glycosuria, metabolic acidosis Contraindicated in CrCl < 55 ml/min Neutronpenia |
| Cidofovir monitoring | SrCr CBC |
| Cidofovir Place in Tx | CMV infections when: Resistant to ganciclovir Ganciclovir induced-neutropenia Treatment of resistant herpes viruses HHV 6, 7 |
Created by:
btrain67
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