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Clinical Medicine > Pharm Disease/Pulm > Flashcards

Pharm Disease/Pulm Flashcards

1
Q

what are the steps to approaching antimicrobial tx?

A

determine the presence of infection, determine the pathogen, select presumptive therapy based on host and drug factors, therapeutic steps

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2
Q

what are the ways to confirm the presence of infection?

A

H&P, predisposing factors (immunosuppressed, chemo, corticosteroid use, HIV), signs and symptoms

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3
Q

what are some of the signs and symptoms of an infection?

A

Fever >100.4, WBC with differential with left shift or elevated white cells, ESR, CRP, procalcitonin, pain and inflammation, disease specific signs and symptoms

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4
Q

what can cause a false + fever?

A

drugs that induce fever like beta lactase (penciling, cephalosporins, salicylates, phenytoin

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5
Q

what can cause a false - fever?

A

drugs that tx fever: aspirin, APAP, NSAIDS, corticosteroids

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6
Q

what does a left shift indicate?

A

that the BM is producing more neutrophils to fight off the infection

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7
Q

what percent of bands indicates infection?

A

> 10%

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8
Q

what does an elevated ESR (erythrocyte sedimentation rate) tell you?

A

that there is an inflammatory process, it cannot tell you for certain there is an infection

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9
Q

what does CRP tell you?

A

that there is an inflammatory process, it cannot tell you for certain there is an infection

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10
Q

what is PCT biomarker for?

A

if elevated: bacterial infection. the higher the PCT, the worse the infection.

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11
Q

what are 3 ways to identify/classify a pathogen?

A

stains, serologies, culture and sensitivity

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12
Q

which kind of bacteria will show up purple on a gram stain?

A

gram positive

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13
Q

what is the difference between the cell walls of gram+ and - bacteria?

A

gram + have more peptidoglycan, gram - have more lipids which lets more stuff in and out (why the purple stain sticks in gram +)

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14
Q

besides the gram stain, what are two other stains to identify other microbes/

A

acid fast stain for mycobacteria and nocardia; the india ink stain for cryptococcus

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15
Q

Which kind of bacteria have cocci and bacilli?

A

both gram - and gram +

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16
Q

T or F: infections can arise from endogenous (native) bacteria if an antimicrobial is used

A

T: the antimicrobial can kill off other things, allowing the native flora to take over

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17
Q

which lab step would you take first before you treat someone empiracally?

A

a gram stain to determine which organism to go after

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18
Q

what are 3 examples of illnesses/fluids you would do a gram stain on?

A

CSF for meningitis, urtethral smears for STIs, abscesses or effusions

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19
Q

what kind of test would you use to determine the specimen of a respiratory tract infection? how do you know if you got a good sample?

A

sputum; got a good sample if

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20
Q

what is the most definitive method for dx and tx of an infection?

A

cultures

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21
Q

detection and quantification of antibodies directed against a specific pathogen or its components

A

antibody and antibody detection

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22
Q

what are the some examples of antibody tests and what can you use them for?

A

immunofluoresence: CMV, RSV, varicella, borrelia burgdorferi; latex aglutination: meningococcus antigens in CSF, legionella pneumophelia; enzyme linked immunoassay (ELISa) HIV, herpes, RSV, pneumococcus, N. gonorrhea

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23
Q

what are 2 different molecular techniques to determine a unique pathogen?

A

hybridization DNA probes; PCR

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24
Q

what are some of the host factors to keep in mind when tx an infection?

A

drug allergies, age, pregnancy, renal and hepatic function, concomitant drug therapy, underlying disease states

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25
Q

what are some of the drug factors to keep in mind when tx an infection?

A

antimicrobial activity, spectrum of activity, pharmacokinetics and dynamics, tissue penetration, adverse effects, cost and convenience

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26
Q

what 2 things are req’d for bacterial cell growth?

A

cell wall division and protein synthesis

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27
Q

for which kind of condition would you want to use a really broad antibiotic?

A

if they are really sick and you don’t have time to figure out what it is and you want to tackle everything you can get right away

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28
Q

what is the MIC? what is the importance of it?

A

the lowest antimicrobial concentration that prevents visible growth of an organism after 24 hours of incubation; the MIC is used to determine dosing of abx

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29
Q

what are 5 ways to test microbial sensitivity?

A

macrodilution methods, microdilution methods, kirby bauer disk diffusion, e-test, automated methods

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30
Q

what are 2 examples of automated susceptibility testing of microbes?

A

vitek system: growth measured by assessment of turbidity q hr for 15 hrs; microscan system: fluorogenic substrate hydrolysis as an indicator of bacterial grwoth

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31
Q

what are the 3 ways bacteria are categorized according to their abs sensitivity or resistance?

A

resistant, intermediate, susceptible

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32
Q

how high should the peak of the abx in the blood be above the MIC in order to classify a microbe as susceptible?

A

the peak of the serum abx should be 2-4 times the MIC of the microbe

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33
Q

what factors influence abx resistance?

A

not high enough dose, prolonged exposure, daycare/sharing germs, inappropriate abx, overuse

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34
Q

what is the general trend of abx resistance in the USA?

A

its getting higher…

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35
Q

what do you want to check frequently to stay up to date on which microbes are resistant in your are?

A

antibiogram or your states health department report

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36
Q

what are the 3 requirements for abx to work?

A

penetrate cell, reach target, kill organism

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37
Q

what are a microbes mechanisms of resistance against a abx?

A

efflux, altered target, less permeable membrane, drug inactivation

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38
Q

what is a protein in a bacteria that is an example of an altered target?

A

penicillin bindig protein (PBP) alters its shape so that B-lactam abx (like penicillin) can’t bind it=they are ineffective

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39
Q

what is the concentration dependent killing rate? example?

A

more is better: some bacteria are killed at higher concentrations; example=aminoglycosides and fluoroquinolone.

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40
Q

which type of abx generally exhibit a post antibiotic effect? what’s a benefit of the PAE?

A

bactericidal; don’t have to dose as often

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41
Q

what is the goal of PAE?

A

to be above the MIC for 50% of the time

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42
Q

what is the pharmacokinetic/dyanmic goal of CKDR?

A

area under the curve/MIC should equal at least 25; 100 is ideal.

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43
Q

What are the different classes of penicillins/

A

narrow spectrum (“the originals”), penicillin’s-resistant penicillins, and extended spectrum penicilllins

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44
Q

Narrow spectrum penicillins: 2 examples and routes and which is most commonly used, spectrum of activity, common uses

A

Penicillin G (IV, IM, PO) and penicillin V (PO). V is most commonly used.
Spectrum:
G+: strep (A, B, pneumonia), enterococcus (limited)
G- Neisseria meningitidis (G)
Anaerobes: Peptostreptococcus, clostridium (not difficile)
Other: Treponema pallidum, Listeria (G), Borrelia Burgdorferi
Uses:
Strep pharyngitis (DOC) [strep pyogenes]
Strep pneumoniae infections (if sensitive)
Endocarditis from Strep viridian’s
Endocarditis prophylaxis
Meningitis due to Neisseria meningitis
Syphilis (treponema pallidum) DOC
Lyme disease (Borrelia burgdorferi) carditis, meningitis, arthritis, high dose

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45
Q

what’s the drug of choice for strep pharyngitis? (strep pyogenes)

A

Narrow spectrum Penicillin

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46
Q

what’s the drug of choice for syphilis? (treponema palladium)

A

narrow spectrum penicillin

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47
Q

Penicillinase-resistant penicillin: What are 2 examples and routes and which is most commonly used, spectrum of activity, common uses

A

Nafcillin (IV), Dicloxacillin (PO)
G+ MSSA, Strep (A, B, pneumoniae), MSSE
anaerobes: peptostreptococcus
Uses: skin infections due to MSSA, MSSE, osteomyelitis due to staph aureus, infection of prostethic joint due to MSSA, MSSE, line infections due to staff

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48
Q

Extended spectrum penicillins (amino penicillins) What are 2 examples and routes and which is most commonly used, spectrum of activity, common uses

A

amoxicillin (PO), ampicillin (IV, IM, PO);
G+ Strep (A, B, pneumoniae), enterococcus,
G- H. flu, Neisseria, Proteus, Anaerobes: peptostreptococcus, clostridium (non difficile),
Other: Listeria, H.pylori, borrelia burgdorferi
better coverage than narrow spectrum penicillin. better enterococcus coverage and added a few other microgs but no coverage for treponema palladium (syphilis)
Uses: strep pharyngitis (S. pyogenes), Otitis media, URI, enterococcus infection (with ahminoglycosides), UTI (proteus), meningitis from listeria monocytogenes, H. pylori (with 2nd abx+proton pump inhb), Lyme

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49
Q

amino-penicillins + beta lactamase inhibitor example and route , spectrum of activity, common uses

A

amoxicillin/clavulanate;
G+ Staph, strep, enterococcus (with amino glycoside)
G-H. Flu, Neisseria, Proteus, M. cat, E. coli, Klebsiella
Anaerobes: peptostreptococcus, clostridium (non difficile), Bacteriodes fragilis
Uses: otitis media, sinusitis, aspiration pneumonia, bites (dog, cat, human), UTI, anaerobic infections (abscess)

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50
Q

what’s the drug of choice for otitis media?

A

amoxicillin

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51
Q

what is preferred to anti pseudomonas antibiotics?

A

antipseudomonal penicillins + beta lactamase inhibitor

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52
Q

anti pseudomonas penicillins + beta lactamase inhibitor example and route , spectrum of activity, common uses

A

piperacillin +tazobactam
G+ staph, strep , enterococcus
G- H. flu, neisseria, M. cat, E. coli, Klebsiella, proteus, pseudomonas, serratia, enterobacter
Anaerobes: peptostreptococcus, clostridium (non difficile), B. fragilis
use: ruptured appendix, GI surgery, diverticulitis, nosocomial pneumonia (tend to be more gram - and this med covers a lot of gram -s), pseudomonas infections, febrile neutropenia

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53
Q

what are penicillins adverse effects and CI?

A

generally well tolerated; diarrhea (disrupts normal flora if PO, esp clavulanate), allergic rxn: rash MC, anaphylaxis, increased LFTs, interstitial nephritis, Amox/amp specific: maculopapular rash with mono infections (65-90%), CLL (90%), and allopurinol (15-20%) do not mistake for true allgx rxn. seizures with high doses. neutropenia, thombocytopenia. thrombophlebitis (irritating to veins).
CI: hypersensitivity to any PCN

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54
Q

What is the general trend of activity of cephalosporins against microbes from 1st generation to 3rd generation?

A

the 1st generation has great activity against gram +, less against gram -; and the 3rd has less activity against gram + and great against gram -. the 2nd generation is in between.

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55
Q

1st generation cephalosporins example and route , spectrum of activity, common uses

A 
cephalexin (pO), cefazolin (IV) 
G+ Staph, strep
G- EKP
uses:
skin and skin structure infections
bone infections
surgical prophylaxis
uncomplicated UTI (EKP)
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56
Q

2nd generation cephalosporins example and route , spectrum of activity, common uses

A

Cefuroxime (ceftin), Cefoxitin (mefoxin)
G+Staph, Strep (weaker)
G- H. flu, Neisseria, M. cat, E. coli, Klebsiella, Proteus
Anaerobes: (cefoxitin is best, cefotetan next best) B. fragile, clostridium (non diff), peptostreptococcus
uses: respiratory tract infection like community acquired pneumonia, sinusitis, AECB, otitis media
UTI, cystitis, pyelonephritis
specifically for cefoxitin and cefotetan (anaerobic activity) surgical prophylaxis: GI, GU, GYN, tx pelvic inflammatory diseases with doxycycline

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57
Q

3rd/4th generation cephalosporins 3 examples and route , spectrum of activity, common uses

A

cefpodoxime (vantin) PO, ceftriaxone (rocephin) IV, ceftazidime (fortaz) (antipseudomonal)
G+ staph, strep (weaker than 1st and 2nd), MRSA (ceftaroline only)
G- H. flu, Neisseria, M. cat, EKP, ES (no P). Pseudomonas (only ceftazidime, cefipime)
uses: PO for respiratory tract infections
UTI: cystitis, pyelonephritis
IV: empiric for serious infections, meningitis (DOC + vancomycin)
w/amino glycoside for pseudomonas, febrile neutropena

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58
Q

which 4th generation cephalosporin paradoxically has activity against MRSA?

A

ceftaroline (teflaro)

59
Q

what is the DOC for meningitis?

A

3rd/4th generation cephalosporins + vancomycin

60
Q

what’s the difference in coverage between 3rd/4th generation cephalosporins and 3rd/4th with BLI?

A

same as above but may improve coverage of resistant enterobacteriaceae, Klebsiella, and Pseudomonas; ceftolozane/Tazobactam primarily do gram -, including pseudomonas and resistant enterobacteriacaea

61
Q

what are the adverse effects of cephalosporins? CIs?

A

AE: generally well tolerated, hypersensitivity, cross rxn with penicillin (=rash in 2%), diarrhea, neutropenia, thrombocytopenia, platelet dysfunction
CI: hypersensitivity to cephalosporin, pt with anaphylaxis or hives (type 1 allgx) to PCN. Don’t use ceftriaxone in neonates with increased bilirubin secondary kernicterus risk

62
Q

which 3rd/4th gens. cephalosporin is helpful in those with otitis media and N/V?

A

IM CEFTRIAXONE useful in pts with otitis media and severe N/V

63
Q

carbapenems examples and route , spectrum of activity, common uses

A

imipenem+cilastatin
broad spectrum
G+ staph, strep
G- good + pseudomonas
Anaerobes Good except C. diff
Doesn’t cover resistant microbes, enterococcus or atypical pneumonia pathogens
use: serious nosocomial infections like pneumonia, bacteremia, urosepsis, serious polymicrobial infections, nosocomial intra abdominal infections, pseudomonas, febrile neutropenia

64
Q

which drug is similar to imipenem but has less activity against pseudomonas and enterococcus?

A

ertapenem

65
Q

what are the adverse effects and CIs for ertapenem

A

AE: allergy: rash, anaphylaxis; cross sensitivity with beta lactam anaphylaxis, GI problems
CI: those with seizures or on seizure meds (it can cause more of them), meningitis

66
Q

which class of drugs is a G- specialist, working against pseudomonas; serious gram - stuff: sepsis, UTI, osteomyelitis, pneumonia, intra abdominal infections, CF with adverse effects of N/V, rash, rare cross sensitivity to PCNs and cephalosporins

A

monolactams

67
Q

what is the DOC for N. gonorrhea?

A

ceftriaxone

68
Q

what kinds of tx should you use for pseudomonas?

A

double tx with a 3rd/4th gen cephalosporin like ceftazidime or cefipime + an amino glycoside

69
Q

which drug inhibits bacterial cell wall synthesis at earlier step than B lactams

A

vancomycin

70
Q

which drug is DOC for MRSA, MRSE

A

vancomycin

71
Q

vancomycin examples and route , spectrum of activity, common uses

A

think gram + and C. diff: very good against staph, MRSA (HCA), MRSE, strep (all strains of strep pneumonia), enterococcus (with ahminoglycosides)
No gram - coverage
anearboes: C. diff, (oNLY PO use for it)peptrostreptococcus
uses: serious infections by HCA-MRSA, MRSE, and enterococcus (good alt to PCN allergies), serious infections by S. aureus, enterococcus, or Strep in pts intolerant of B lactase, infections caused by resistant gm + organisms, C. diff colitis (alternative to metronidazole) Endocarditis prophylaxis for selected GU, GI procedures in PCN intolerant pts

72
Q

what’s a good alternative to PCN for enterococcus infections?

A

vancomycin

73
Q

what drug is an alternative to metronidazole for C. diff colitis

A

vancomycin

74
Q

vancomycin AE, monitoring, pharmacokinetics, resistance,

A

ae: Think kidneys and ears: nephrotoxicity (though less common with newer preparations), ototoxicity (MC when combo with aminoglycosides), more common with sustained trough levels of >20 ug/mL, Red neck/man syndrome: rash on neck, face, back due to rapid infusions
monitoring: Need to obtain trough level at 4th dose. Recommended level: 10-15 ug/Ml (15-20 for osteomyelitis or MRSA) after steady state before next dose
pharmacokinetics: not absorbed from GI tract, diffuses into pleural, pericardial, synovial, and ascitis fluids. Thearpeutic levels in CSF only occur if meninges are inflamed and with high doses to penetrate it. ADJUST FOR RENAL.
resistance in VRE, MRSA from overuse

75
Q

what’s the only po indication for vancomycin?

A

C. diff because we want it in the GI tract

76
Q

what are some DISCOURAGED uses of vancomycin?

A

Use is DISCOURAGEd if using for prophylaxis for infection or colonization of vascular catheters, eradication of MRSA colonization or CA-MRSA, primary tx for C. diff colitis, routein prophylaxis for very low birth weight infants, routine prophylaxis for peritoneal dialysis

77
Q

what are the different alternatives to tx ing both HCA MRSA and CA MRSA if vancomycin can’t b used?

A

HCA MRSA alternatives: TMP/SMX, linezolid, daptomycin, televancin, ceftaroline. CA MRSA: mild/moderate infections: TMP/SMX, doxycycline or minocycline, (alternative clindamycin). severe infections: vancomycin (alternatives linezolid, daptomycin)

78
Q

fluoroquinolones moa and mechanisms of resistance and common overuses

A

inhibits DNA replication via inhibiting topoisomerases II (conrols supercoiling) and IV (separates daughter from parent dna)
mor: resistance: efflux, gene mutations, permeability
Overuse in AECB, chronic sinusiits, and prophylaxis for travelers diarrhea (e. coli)

79
Q

fluoroquinolone examples of each gen and common uses

A

1st gen: ciprofloxacin; 2nd gen: levofloxacin; 3rd gen: moxifloxacin
uses: UTI (pyelonephritis (cipro>levo, moxi), uncomplicated cystitis (alt if e. coli resistant to TMP/SMX), prosatitis
osteomyelitis from gram- bacteria (pseudomonas), cap (moxi>levo»cipro), M. tuberculosis (alternative), complicated gram - and anaerobic abdominal and gynecological infections (chipper +metronidazole)

80
Q

How effective are the 3 classes of fluoroquinolone against gram - bacteria? against gram +? which can fight b. frag? can they fight pseudomonas?

A

They are all pretty good at gram - bacteria, 4th gen slightly worse. The 3rd and 4th gen are better at gram +, 2nd gen doesn’t fight them very well. only 4th gen can fight b. frag and only 1st gen can fight pseudomonas

81
Q

what are the adverse effects of fluoroquinolone? drug intx?

A

limit in kids

82
Q

Trimethoprim-sulfamethoxazole: MOA, spectrum and uses, kinetics (adjust for renal pt?), adverse effects, CI, monitoring, drug intx

A

MOA: inhibit DNA, RNA and protein production by blocking the folate pathway; SMX is a structural analog of PABA which is used to make dihydrofolic acid. TMP inhbiits dihydrofolate reductase and the production of cofactors used to synthesize purines, thymidine, and DNA.
spectrum and uses: G+: S. pneumoniae (50% resistance), Staph (MSSA, MRSA, CA-MRSA); G-: H. Flu, Mcat, E. coli, Klebsiella, Serratia (variably susceptible) Other: GI anaerobes: enterotoxigenic e. coli, salmonella, shigella, vibrio cholerae, yersinia enterocoliticia. listeria, nocardia, mycobacterium marinum. pneumocystis (carini) jiroveci. Uses: RTIs: pneumocystis pneumonia DOC, AECB, acute sinusitis, UTIs: uncomplicated cystitis DOC (if e. coli is sensitive), prostatitis, orchitis, epididymitis; GI: traveler’s diarrhea from enterotoxigenic E. coli, shigellosis, Others: b. cepacia, s. maltophelia, serratia, nocardia, typhoid fever
kinetics (adjust for renal pt?) yes- CHANGE FOR RENAL DYSFCN. Single strenght vs. double strength oral and IV.
adverse effects: 15% with sulfa allgx, N/V, anorexia, rash, photosensiitivty. Rare serious stuff: SJS, TEN, blood dyscrasia (leukopenia, neutropneia), hepatoxic stuff, rare crystalluria,renal toxicity, hyperkalemia (beware with ACEI, ARB, k sparing diuretics, K supplements or less renal clearing.
ci: hypersensitivity to any sulfa or TMP, folate deficiency, infants 5 days

83
Q

what’s the DOC for pneumocystis pneumonioa?

A

TMP/SMX

84
Q

what’s the DOC for uncomplicated cystitis?

A

TMP/SMX

85
Q 
aminoglycosides: 
MOA
spectrum and uses
 kinetics (adjust for renal pt?)
adverse effects
CI
monitoring
drug intx
A

MOA: bind irreversibly to 30s bacterial ribosome, thus inhibiting protein synthesis
spectrum and uses: most gm-: including pseudomonas (tobramycin is best) and serratia (gentamicin is best and also used most often b/c less expensive). Use: serious hospital acquired infections caused by pseudomonas aeruginosa and enterobacteriacaea, enterococcus endocarditis (in combo with amp, pen, or vanco), serious staph infections (synergy with B lactams because the G+ agent lets aminoglycoside in cell)
kinetics (adjust for renal pt?): IV only, small Vd, doesn’t penetrate CSF, renal elminiation. ADJUST FOR RENAL. Dose based on severity of infection, body wt, and renal fcn. Has both PAE and CDKR.
adverse effects: irreversible ototoxicity: dizziness, impaired vision, nystagmus, vertigo, N/V, balance and walking problems; cochlear: tinnitus, hearing impairment; nephrotoxicity: reversible acute tubular necrosis
CI: hypersensitivity to any amino glycoside
monitoring: need baseline serum drug peak 30-60 min after infusion and trough level 30 min before infusion
drug intx: none
preg cat: D: potential for renal dysfcn in developing fetus

86
Q

which drug is paradoxically a good synergist with beta lactase in staph infections?

A

aminoglycosides like gentamicin, which are normally only gm - agents

87
Q 
tetracyclines
MOA: 
spectrum and uses:
 kinetics (adjust for renal pt?):
adverse effects:
CI:
monitoring:
drug intx:
A

MOA: inhibit protein synth at 30s
spectrum and uses: Strep, staph, H. flu, Neisseria, M. cat, E. coli +/- Kleb, +/- B. frag, Clostridium (non diff) listeria, rickettsia, spirochetes, myocplasmas, chlamydiae, borrelia burgdoreferi. Uses: Resp infections: CAP, atypical pneumonia pathogens like mycoplasma and chlamydia) AECB, legionella (alt to ery), genital infections (chlamydia trachomatis, NGU, PID, epididymitis, prostatitis, lymphogramuloma venerum, granuloma inguinale, syphilis (alt to PCN), systemic infections: rickettsia (rocky mountain spotted fever), brucellosis, lyme (doxy DOC), vibrio cholera, tularemia, other: pasteurella multocida (alt to amox/clav), helicobacer pylori (with bismuth, metronidazole, or clari) propionibacterium acnes
kinetics (adjust for renal pt?): bacteriostatic. Decrease absorption with milk, antacids, iron supplements, and other substances with calcium,aluminum or iron (doxy and mino less affected). Eliminaed renally except doxy and mino. adjust for renal
adverse effects: gray-brown or yellow permanent discoloratino of teeth in kids

88
Q

what’s the DOC for diphtheria?

A

erythromycin

89
Q 
macrolides: erythromycin
MOA: 
spectrum and uses:
 kinetics (adjust for renal pt?):
adverse effects:
CI:
monitoring:
drug intx:
A

macrolides: erythromycin
MOA: induce dissociation of tRNA from 50s subunit and prevent protein synthesis
spectrum and uses: g+ staph (not great), Strep: GABHS +/-, S. pneumo (pen S) good, alt to PCN, s.pneumo (pen R) poor; g- H. flu +/-neisseria, M. cat, c. (non diff); OTHERS: m. pneumo, Legionella pneumo, Chlamydia, treponema pallidum, ueaplasma urealyticum, bordetella pertussis, camphylobacter jejuni, some rickettsia. USES: diphtheria DOC, bordatella pertussis, CAP
kinetics (adjust for renal pt?): low bioavailability, destroyed by gastric acid, food decreases absorption. Not in CNS or CSF. Crosses placenta and breast milk. Excreted in bile mostly 1/2 life is 1.4 hours. don’t need to adjust for renal
adverse effects: safe. N/V/D. cramps. Rare transient hearing loss, vtach, QT prolong.
CI: none
monitoring: none
drug intx:inhibits metabolism (thus increasing): theophylline, warfarin, triazolam, bromocriptine, carbamazepine, cyclosporine

90
Q

what’s the DOC for bordatella pertussis?

A

clarithryomycin and azithromycin

91
Q 
macrolides: clarithromycin
MOA: 
spectrum and uses:
 kinetics (adjust for renal pt?):
adverse effects:
CI:
monitoring:
drug intx:
A

MOA:
spectrum and uses: g+ staph (not great), Strep: GABHS +/-, S. pneumo (pen S) good, alt to PCN, s.pneumo (pen R) poor; g- better H. flu than ery +/-neisseria, M. cat, c. (non diff); OTHERS: m. pneumo, Legionella pneumo, Chlamydia, bordetella pertussis DOC, camphylobacter jejuni, some rickettsia, h. pylori (with tinidazole in sequential tx), mycobacterium avium intracellulare complex (MAC), toxoplasma gondii, borrelia burddorgeri (deer tick vector), babesia microti (Ixodes tick vector). USES: diphtheria, bordatella pertussis, CAP
kinetics (adjust for renal pt?): 50% bioavailability, penetrates alveolar macrophages and PMNs, metabolized to an active metabolite, parent and metabolite renally eliminated. ADJUST FOR crcl

92
Q 
macrolides: azithromycin
MOA: 
spectrum and uses:
 kinetics (adjust for renal pt?):
adverse effects:
CI:
monitoring:
drug intx:
A

MOA: g+ staph (not great), Strep: GABHS +/-, S. pneumo (pen S) good, alt to PCN, s.pneumo (pen R) poor; g- better H. flu than ery and clari neisseria, M. cat, c. (non diff) peptostreptococcus; OTHERS: m. pneumo,, Chlamydia trachomatis, treponema pallidum, ueaplasma urealyticum, bordetella pertussis DOC, ureaplasma urealyticum, N. gonorrhea
spectrum and uses: g+ staph (not great), Strep: GABHS +/-, S. pneumo (pen S) good, alt to PCN, s.pneumo (pen R) poor; g- better H. flu than ery and clari (but recent bacteriologic failures with AOM) neisseria, M. cat, c. (non diff) peptostreptococcus; OTHERS: m. pneumo,, Chlamydia trachomatis, treponema pallidum, ueaplasma urealyticum, bordetella pertussis DOC, ureaplasma urealyticum, N. gonorrhea. common uses in kids: pharyngitis/tonsillitis (alt to PCN or ery if allgx), acute otitis media, common uses in adults: STIs: urethritis, cervicitis, proctitis (need to evaluate and tx partners), URIs: sinusitis, pharyngitis, LTIs community acquired pneumonia
kinetics (adjust for renal pt?): 40% bioavailability, high intracellular uptake in PMNs and intracellular pathogens (like mycoplasma, chlamydia, legionella, ureaplasma, neisseria), high tissue levels. Hepatic metabolism. Half life 68 hrs. eliminated unchanged in feces. No need to change for renal failure or class a or b liver cirrhosis
adverse effects: GI: diarrhea, nausea, vomiting, abdominal pain
CI: hypersens to any macrolide
monitoring: none
drug intx:, none

93
Q

what’s the DOC for B. fragile?

A

clinadmycin or metronidazole

94
Q 
clindamycin
MOA: 
spectrum and uses:
 kinetics (adjust for renal pt?):
adverse effects:
CI:
monitoring:
drug intx:
A

MOA: inhibit 50s ribosome
spectrum and uses: anaerobes and gram +: stpah, strep, some PenR s. pneumo; B. frag DOC, other bacteroides: clostridia, peptostreptococcus, propionobacterium acnes, fusobacterium. Parasites: gardnerella, toxopalsmosis, pneumocystis (carini) jiroveci. Uses: tx staff and strep in PCN allgx pts in pharyngitis, retropharyngeal abscess, staph osteomyelitis, anaerobic infections: often in triple therapy for intrabadominal infections (with amp, gent,clinda), acne, vaginal tx of gardnerella vaginalis, toxoplasmosis in pts with AIDS (alt to sulfa), PID (chlamyida in combo with genatmicin)
kinetics (adjust for renal pt?): well abosrbed (90%), but extensive 1st pass.wide distribution except CNS, accumulates in CNS and abscesses. Hepatic metabolism. Elimination in bile. No adjust for renal.
adverse effects: diarrhea in 20%, pseudomembranous colitis, rare hepatotoxicity and hypersensitivity
CI: hypersensitivity to clindamycin or other lincosamine (lincomycin)
monitoring: none
drug intx:none

95
Q 
metronidazole
MOA: 
spectrum and uses:
 kinetics (adjust for renal pt?):
adverse effects:
CI:
monitoring:
drug intx:
important piece of pt ed
A

MOA: reactive metabolites damage DNA and other macromolecules
spectrum and uses: anaerobes and parasites: gm- and bacteroides and some g+ clostridium. Other: protozoa like trichomonas, giardia, entamoeba, H. pylori. Uses: tx serious anaerboci infections in peritoneum, liver, skin, CNS, bones, joints, lower respiratory tract (caused by bacteroides); prophylaxis prior to abdominal, gyne or colorrectal surgery. C difficile colitis DOC, bacterial vaginosis, hepatic encephalopathy, crohn’s disease–rectal disease only, PUD due to h. pylori
kinetics (adjust for renal pt?): well abosrbed, large Vd, penetrates tissues including CSF, metabolized extensively, eliminated 20% unchanged, may accumulate with renal and hepatic dysfcn
adverse effects: neuro effects like seizures at high dosese and peripheral neuropathy. Disulfiram like effect in persons drinking ETOH (the substance used to deter alcoholics). GI upset, metallic taste, darkened urine
CI: hypersensitiivty to metronidazole or other nitroimidazole derivatives
monitoring:
drug intx:CYP3A/4 3A5-7 inhibitor. Increases concentrations of warfarin.
pt ed: don’t have alcohol during tx or after for 3 days, it can make you feel really crummy

96
Q

what factors do you consider when thing someone with pneumonia? what tests can you use to decide?

A

Tx low risk pts at home, tx high risk pts in hospital. Identifying RFs: comorbidites, Patient Outcomes Research Team PORT OR CURB-65 confusion, uremia, RR>30, BP with SBP65 and presence of MDR pathogens.

97
Q

what are the pharm ways to tx pneumonia (not the algorithm here) for pharm tx: will you treat empiracally or get a specimen?

A

NON PHARM: fluids (more than normal), rest. Pharm: abx, sx: NSAIDS, tylenol to reduce fever, honey, cough suppressants. treat empirically, need to take care of it ASAP.

98
Q 
what txs are indicated for these pts with pneumonia:
outpt healthy, no abx in last 3 months
outpt comorbidites, immunosuppressed or abx in last 3 months
outpt MDR area
inpt, non ICU
inpt, iCU no r/o pseudomonas
inpt ICU r/o pseudomonas
inpt ICU mrsa
A

std tx for outpt (previously healthy no recent abx) is macrolides (or doxy). std tx for 1) outpt with comorbidities, immunosuppressing conditions, or use of abx within 3 months or 2) regions with >25% macrolide resistant s. pneuo or 3) inpt non ICU is respiratory FQ (moxi, levo, gemi) OR macrolide+ beta lactam. std tx for ICU w/ out pseudomoans is beta lactam + resp FQ or azithro, or if pseudo + beta lactam + pseudo.

99
Q

what duration of tx is indicated for pts with pneumonia?

A

duration: minimum of 5 days. must be afebrile for 2-3 days, no signs of clinical instability before d/c tx. see sanford guide for duraiton for specific pathogens.

100
Q

when should you see improvements in pts with pneumonia if started on the right abx? what if you don’t see improvements?

A

should see improvements in 2-3 days. if not responding consider infectious and non infectious txs. If on IV, switch to oral as soon as hemodyamically stable, improvement in sx, can ingest orally, and functioing GI

101
Q

SARS: pathogen, transmission, incubation, sx, case detection, tx

A

pathogen:SARS assoc corona virus
transmission: spread via droplets.
sx: early systemic sx then after 2-7 days local sx of dry cough and/or SOB, +/- URI sx., pneumonia in CXR by day 7-10. often lymphopenia.
incubation:Avg inc time is 6.4 days.
case detection: documented exposure risk or radiographically confirmed pneumonia or acute respiratory distresss syndrome of unknown etiology AND rfs of travel to china, hong kong or tawiwan or close contact will ill person in these areas or recent travel to these areas or employment in a lab that works with it or in healthcare setting with direct patient contact or part of a cluster of cases of atypical pneumonia.
tx: supportive, tx for pneumonia until confirmed otherwise

102
Q

what are the indications for giving antivirals for influenza?

A

Those at high risk that should get antiviral to reduce complications: 65, american indians/alaska native, chronic diseases, immunosuppression or drugs that cause this, pregnancy of 40 or liviing in LTC facility

103
Q

what are some of the antivirals for influenza? when should they be given? which can be given to the youngest pts?

A

within 48 hrs if possible and after if high risk. oseltamivir (tamiflu) can be given to youngest >2 wks, zanamivir (inhaled), peramivir (IV)

104
Q

what are the typical signs and hx of someone with asbestosis? what other category is it a part of?

A

high res CT: sub pleural linear densities parallel to the pleura, parenchymal fibrosis, bands in parenchyma, honeycombing if advanced, pleural plaques

+hx of asbestos exposure or pipe fitting, navy worker, etc

it is an interstitial lung disease

105
Q

what are the benefits of pulm rehab?

A

improvements in dyspnea, exercise capacity, health status and healthcare utilization

106
Q

how can o2 help with copd?

A

improves intellectual fcning, memory, better sleep, decreased night time arousals, improves daytime performance

107
Q

how is COPD classified according to GOLD?

A

GOLD classifications of severity: all have FEV1/FVC 80, moderate 50

108
Q

which disease is the 3rd leading cause of death, 15-20%of smokers get it, and 2nd leading cause of disability

A

COPD

109
Q

what are RFs for COPD?

A

smoking and environmental exposures like indoor biomass fuel or burning coal. Occupational vapors when intense or prolonged exposure. Outdoor air pollution, factors that affect lung growth during gestation, genetics

110
Q

what is needed for a dx of copd?

A

consider RFs and need pulmonary function testing/spirometry. Confirmed if post bronchodilator FEV1/FVC is still

111
Q

what are the goals of tx for copd? what are the possible txs?

A

smoking cessation, reduce sx, improve exercise tolerance, minimize rate of decline in lung fcn, maintain or improve QOL, preventing and txing exacerbations, limit complications; non pharm: all attempt smoking cessation (only thing that slows progression) , pulm rehab, (for sx with FEV1 15 hrs reduces mortality in those with severe hypoxemia (

112
Q

what drug: peak 1.5-3hr lasts for 24 hours, watch for crcl

A

tiotropium, spiriva handihaler

113
Q

what’s an important piece of pt ed for someone taking tiotropium?

A

usually need to inhale x2 to get all powder out, don’t swallow the capsule

114
Q

anticholinergic bronchodilators:MOA and adverse effects

A

decrease cyclic GMP which increases bronchial smooth muscle relaxation; dry mouth, metallic taste, r/o systemic anticholergic effects like blurred vision, constipation, urinary retention

115
Q

what is a short acting and long acting bronchodilator? what are the common side effects? what is a good piece of pt ed?

A

SA: albuterol (proventil) and LA salmeterol (servent); tachycardia, tremor, hypokalemia; always check proper inhaler technique with spacer so it doesn’t get on back of throat

116
Q

how does methylxanthine bronchodilators work? AE and signs of toxicity, indications, dose adjust for who?

A

MOA: blocks phosphodiesterase which increases CAMP and causes relaxation of smooth muscle of bronchi and pulmonary blood vessels. Also stimulatesrespiratory center and enhances ADLs in pt with severe COPD; (think of how you feel aftera bunch of caffeine) restlessness, insomnia, GERD drnig sleep,palpitations, potentition of diuresis signs of toxicity CAMP: >20mg/L NVD, HA, insomnia,irritability; >30 mg/L:hyperglycemia, hypotensino, atrial tach, vtach, refractory seizures, indication: severe COPD, esp if nocturnal dyspnea; dose adjust: metabol by liver, excreted by kidney. Shorter t1/2 in smokers, decreased clearance in elderly, slow onset not for acute sx

117
Q

which drugs when combined with LA bronchodilators are best at managing COPD sx? adverse effects, who should get them?

A

inhaled corticosteroids. r/o of pneumonia, withdrawal can lead to sx so taper, LT tx not recommended b/c of systemic effects;oral candidiasis and hoarse voice; people with fever

118
Q

what drug should be considered for those with severe COPD and h/o exacerbations? how does it work and what are side effects?

A

phophdiesterase 4 inhibitor: roflumilast (daliresp) selectively inhibits PDE4 which metabolizes CAMP which leads to more cAMP around and bronchodilation?. AE N/D, depression, suicide, wt loss, abdominal pain, increased cancer risk, don’t use in mod-severe hepatic impairment

119
Q

what and how often should you monitor copd?

A

mild: annually; moderate: q 3-6 months; severe 2-4 months, spirometry every year, Qx q 2-3 months,sx, smoking status, and exposure at each visit. Meds at each visit along with technice and adherence. Exacerbation hx.

120
Q

what are the 5rs if someone doesn’t want to quit smoking yet?

A

relevance, risks, reward, roadblocks, repetition

121
Q

what are the diff ways to tx smoking?

A

interventions by physicians work! 5 As and 5 Rs. Behavioral tx, nicotine replacement tx, bupropion, varenicline, 2nd line: clonidine, nortiptyline

122
Q

what are the diff types of nicotine replacement tx? who shouldn’t take them?

A

patch, gum, nasal spray; active smokers (nicotine overdose), pregnancy, lactation, active peptic ulcer disease

123
Q

what should every smoker who wants to quit be on?

A

support program, behavioral tx

124
Q

what are the side effects of the patch? imp pt ed? who shouldn’t take it?

A

erythema, burning or pruritis at application site; apply to non hair, clean, dry skin on upper body or arm, rotate site to prevent irritation. Nicotine continues to be deliverd hours after patch removed–can’t light up right away

125
Q

pt ed for nicotine gum

A

chew until feel tingling, park it in gums, then start chewing again when tingling gone

126
Q

nicotine nasal spray indications, ae, dosing

A

nicotine delivered more rapidly: for those who need a quick fix; nasal and throat irritation, rhiniits, sneezing, coughing, water eyes; 1-2 sprays per hour for 3 months

127
Q

nicotine inhaler dosing

A

each cartidge delivers 4 mg of nicotine, inhale prn most pts use 6-16 cartiges per day for 3 months then taper over 6-12 weeks

128
Q

nicotine lozenge dosing, pt ed

A

based on time to first cigarette: one lozenge every 1-2 hrs for 6 weeks then every 2-4 hours for wks 7-9 then one lozengge every 4-8 hours 10-12 ; allow it to dissolve slowly over 20-30 min; avoid eating or drinking acidic bevs 15 prior to and during lozenge use

129
Q

bupropion for smoking cessation moa, ae, ci, drug intx

A

moa: unknown but seems to be related to inhibitnig reuptake of noradrendergic (norepinephrine) or dopamingeric
initiate while still smoking, ae: seizures with high doses, insomnia, irritability, dry mouth, headache, wt gain or loss decrease dose in renal and hepatic pts; ci: hx of seizure, coadmin with MAOI, current or prior dx of anorexia or bulimina nervosa
drug intx: with cabamazepine (decreases it) or cimetidine (increases it) and MAO inhibitors increases toxicity

130
Q

varenicline (chantix) MOA, drug intx, ae, preg,

A

moa: selectively blocks nicotine binding to alpha 4 beta 2 nicotinic acetylcholine receptors and at the same time stimulates the receptor mediated activity at a lower level than nicotine which reduces severity of cravings and withdrawal sx, smoking cigarrettes while on it may also decrease the sense of satisfaction
drug intx: no established safety of using vareniciline with other smoking cessation aids, combined with patch can cause side effects of N/V, HA, dizziness, dyspepsia and fatigue. Adjust dose for renal.
ae: N(more common)/V (less common), sleep disturbance, HA, abnormal dreams, constipation, flatulence, change in taste perception, may cause bizarre behavior, suicidal ideation, suiicde. May be linked to MI, seizure, DM, dizziness, confusion. Etoh may increase intoxication, aggresive behavior and amnesia.
preg C
as effective as zyban, but has more side effects. Perhaps try zyban first.

131
Q

what are the only meds that can prevent and treat inflammation for asthma/

A

corticosteroids

132
Q

can inhaled corticosteroids alter progression or underlying severity of disease in asthmatics?

A

NO. they cannot cause the person to move down in severity.

133
Q

how do inhaled corticosteroids work in asthma?

A

reduce inflammation by decreasing airway hyperresponsiveness, thus decreasing PRN albuterol use

134
Q

how long does it take for ICS to take effect?

A

max effect in days to weeks, not for resuce purposes.

135
Q

what are some of the short term local and LT systemic risks associated with ICS?

A

r/o of pneumonia, withdrawal can lead to sx so taper if used for a long time. LT tx not recommended b/c of systemic effects:can cause dose related stunted growth in kids (1.2 cm) which can persist into adulthood.other systemic effects: fluid retention, muscle weakness, ulcers, malaise, impaired wound healing, N/V, HA, osteoporosis (adults), cataracts (adults), glaucome (adults). local effects: oral candidiasis, hoarse voice (dysphonia), cough/throat irritation. High dose ICS + multiple oral bursts of steroids can cause posterior subcapsular cataracts or reduced bone density.

136
Q

what are the benefits of a long acting bronchodilator for asthma?

A

daily long term control and bronchodilator. Blunts exercise induced sx for longer time, decrease nocturnal sx, improve quality of life

137
Q

what is the onset and peak of salmaterol?

A

onset of effect in 30 min, peak effect in 1-2 hours

138
Q

what are the benefits of combo ICS + LABA?

A

May decrease the need to increase the ICS, good for nocturnal sx, useful for exercise induced asthma when taken 30 minutes before exercise

139
Q

what are the indications for other asthma meds that can prevent inflammation like singulair?

A

prevents inflammation but cannot treat inflammation. Not as good as ICS. Improves lung fcn, decreases the need for SABA. Prevents exacerbations. But the preferred combo therapy is LABA.

140
Q

when and what are systemic corticosteroids indicated?

A

for severe, acute exacerbations: quick relief of inflammation when SABAs are uneffective or with a gradual deterioration with or without prior tx or to establish control in an existing or newly dx’d pt

141
Q

what is the proper technique for MDIs?

A

. Need to prime and clean inhaler.wash out weekly to get the gunk out and set out to dry. Patient instructions: take off cap and hold inhaler upright, shake the inhaler, tilt head back slightly and breathe out. position the inhaler either in mouth, or with spacer or 1-2 inches away (hard to do this). press down on the inhaler to release the meds as you start to breathe in slowly for 3-5 seconds. hold breath for 10 seconds to allow the meds to reach deeply into the lungs. repeat puffs as directed, waiting 1 minute between puffs to penetrate lungs better.

142
Q

what is the proper technique for using a DPI?

A

DPI pt instructions: no need to shake or turn upside down, no need for spacer, can inhale deeply and rapidly over 1-2 seconds, wash out mouth afterwards

143
Q

what is the advantage of a spacer?

A

it allows evaporation of propellant prior to inhalation and enhanced clinical effect in those with poor hand lung coordination. decreases oropharyngeal deposition

Clinical Medicine (19 decks)

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