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PHARMACOLOGY > Block 2 Harris > Flashcards

Block 2 Harris Flashcards

0
Q

the MBC for most bactericidal drugs is…

A

4-5x the MIC

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1
Q

define MIC and MBC

A

MIC=minimum inhibitory growth= lowest [antibiotic} that inhibits bacterial growth after 24 hrs in a specific medium

MBC= minimum bactericidal concentration= lowest [antibiotic} that prevents growth on antibiotic-free subculture (aka kills 99.9% of bacteria with antibiotic then replate on antibiotic free plate)

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2
Q

microbiostatic drugs are rarer… name them

A 
antibacterial
1. chloroamphenical
2. clindamycin
3. macrolides
4. tetracycline
	antifolates
1. Trimethoprim= TMP
2. Sulfonamides

Antifungal

  1. fluconazole
  2. ketoconazole
  3. Itraconazolew
  4. terbafine
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3
Q

why would you not give chloramphenical (=other protein syn -) to a premature infant

A

you need to glucaronate the drug which is a phase 2 rxn, which babies cant do therefore you get
1. flaccid baby
2. cardiovascular collapse
GRAY BABY SYNDROME

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4
Q

what are the aminoglycosides and what is a classic side effect of them

A
  1. gentamicin
  2. amikacin
  3. streptomycin

SIDE EFFECTS= NO

  1. Nephrotoxicity
  2. Ototoxicity–> if taken more than 5 days–> can cause permanent hearing loss
  3. NM paralysis–> seen with patients with Myastenia gravis
    - at high doses–>-ACh release like myasthenia gravis
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5
Q

clindamycin is another protein syn - which causes….

A

SUPERINFECTIONS FROM CLOSTRIDIUM DIFFICILE
–> pseudomembranous colitis (= inflammation of colon which causes antibiotic associated diarrhea)–> treat with metronidazole

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6
Q

vancomycin (non-B lactam penicillin) if administered in less than 1 hrs (rapid infusion) causes

A

red man syndrome

1. hypotension and flushing

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7
Q

tetrecyclines (which are protein syn - of 30s) can cause

A
  1. photosensitivity
  2. discoloration of tooth and bone (bc it deposits here)
    - -> = reason you dont give tetracyclines to kids
  3. liver toxicity–> if given in high doses during pregnancy
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8
Q

if you taking tetracycline (30s -) you should not take it with

A

dairy food–> will cause gastric discomfort

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9
Q

chloroamphenical (50s -) is…

A
  1. too toxic for minor use and can cause
  2. gray baby syndrome–> if given to infants because they can do phase 2 rxns and the drug must be glucuronated
  3. anemia–> reversible and dose related
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10
Q

sulfonamides which are anti-folates can cause

A
  1. hypersensitivity if given orally for long periods
    - -> can cause steven-johnson syndrome= epidermis separates from dermis–> crust around lips and oral mucosa
  2. kernicterus= bilirubin induced brain dysfunction
    - -> increased amount of unbound drug in neonate is problem
    - neonates have a premature liver and cant conjugate bilirubin
    - sulfonamides displace bilirubin from the protein–> excess unconjugated bilirubin= highly neurotoxic
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11
Q

fluroquinolines (FQ) are normally well tolerated but can cause

A
  1. cartilage toxicity–> reason you dont give FQ to kids or preg women
  2. musculoskeletal issues–> tendon ruptures
  3. photosensitivity
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12
Q

metronidazole a misc. DNA antibiotics thats is metabolized to its active form by ferrodoxin can cause

A
  1. Gi issues–>metallic taste in mouth

2. if drinking alcohol–> it can cause disulfiram like effects

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13
Q

define synergy and give an example

A

when 2 antibiotics work at 2 different sites in either the same or different metabolic pathways
EX:
1. ampicillin + gentamicin–> ampicillin facilitates entry of gentamicin
2. TMP+SMX= trimethoprim+ sulfamethoazole
–>both - folate metabolism but affect different steps of the pathway
-TMP–> - dihydrofolate reductase which takes folate and makes tetrahydro folic acids
-sulfamethoazole–> - dihydropteroate synthetase which takes PABA and makes folic acid

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14
Q

which drug is good for aerobic infections

A

aminoglycosides

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15
Q

which drug is good for anaerobic infections

A

metronidazole

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16
Q

what are the B lactam drugs

A
  1. penicillins
  2. cephalosporins
  3. other
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17
Q

what are the penicillins

A
  1. natural pens
  2. anti staph pens
  3. amino-pens
  4. anti pseudomonal
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18
Q

what are the natural pens

A
  1. penicillin V

2. procaine or benzathine + penicillin G

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19
Q

what are the anti-staph penicillins

A 
anti staph=coNDOM
Nafcillin
Dicloxacillin
Oxacillin
Methicillin
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20
Q

what are the amino penicillins

A
  1. ampicillin

2. amoxicillin

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21
Q

what are the antipseudomonal penicillins

A
  1. pipercillin

2. ticarcillin

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22
Q

what do Beta lactamase - do

A

they bind to the beta-lactam ring and protect it–> preventing B-lactamase from cleaving the B-lactam ring

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23
Q

which penicillins are B lactamase susceptible

A

mostly natural penicillins

  • cephalosporins are more B-lactamase resistant
  • carbapenems are resistent to most B-lactamases
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24
Q

what are the 3 MOA for all the B-lactam drugs (penicillins, cephalosporins, monobactams, and carbapenems)

A
    • PBP (penicllin binding proteins) on cell membranes
      PBP–> synthesis of the cell wall
  2. block transpeptidase rxn of some PBPs that catalyze cross-linkage of peptidoglycan chains–> decreases cell wall integrity
  3. gram + cocci–> produce autolysins
    –> block cell wall formation of gram + cocci= unopposed autolysin activity which degrades cell wall
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25
Q

gram - bacteria have

A

porins in their outer membrane–> antibiotic must you this to get into the periplasmic space where PBP are found

therefore–> change the porin and drug cant get in

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26
Q

how B-lactamase - work (AKA MOA)

A

B-lactamase - bind to conserved region or B-lactamase and changes the B-lactamases structure–> this prevents the lactamase from binding to the B-lactam ring

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27
Q

name the B-lactamase - combinations

A
  1. clavulanic acid +
    - amoxicillin= amino
    - ticaricillin= anti-pseudo
  2. tazobactam+
    - pipercillin= anti-pseudo
  3. sulbactam +
    - ampicillin= amino
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28
Q

How is resistance to B-lactam drugs developed

A
  1. natural= organism has no cell wall
  2. acquired
    - due to acquiring plasmid of B-lactamase to bacteria
    - decreased penetration of the drug intro outer membrane
    • -> cant reach PBP
      - modify PBPs so drug cant bind
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29
Q

what is the only oral combination of penicillin drugs

A

clavulanic acid + amoxicillin= duh amoxicillin= bubble gum medicine

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30
Q

which other penicillins are give IV or IM only

A
  1. anti-pseudomonals

and all the other combinations

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31
Q

which penicillins do you give slow release over time

A

pen. G + procaine or benzathine

benzathine+ pen G–> DOC for syphillis

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32
Q

generally how is the absorption of penicillins

A

most penicillins are incompletely absorbed

EXCEPTION= amoxicillin= almost completely absorbed

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33
Q

all penicillins…

A

gross the placenta BUT ARE NOT TERATOGENIC= safe in pregnancy

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34
Q

what is the only penicillin excreted by the biliary and renal route?

A

ANTI-STAPH

most penicillins excreted just by the kidneys= must adjust dose in renal failure

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35
Q

penicillins cause hypersensitivity–> why?

A

bc their metabolite PENICILLOIC ACID triggers an immune rxn

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36
Q

which penicillin kills gram + cocci (strept) the best

A

natural penicillin

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37
Q

which penicillin has the narrowest spectrum

A

anti-staph–> use for staph inf

1. MSSA=methicillin sensitive staph. aureus

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38
Q

if you want to use a broad penicillin–> good gram + coverage with decent gram- coverage, you would use

A

amino pens

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39
Q

which pen has the broadest spectrum and why

A

anti-pseudomonal, bc it kills more gram -s

often need to add aminoglycerides (gentamicin) with anti-pseudomonals if you are treating serious infections

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40
Q

when are cephalosporins used

A

in hospital setting for prophylaxis vs. surgical wound infections due to their broad spectrum

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41
Q

what are the 1st gen cephalosporins

A
  1. cef-azolin

2. ceph-alexin

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42
Q

what are the 2nd gen cephalosporins and the saying

A
  1. ce-fac-lor
  2. ce-fox-itin
  3. ce-furo-xime
  4. ce-faman-dole

its a FACt I love FOXy FURry FAMAN

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43
Q

what are the 3rd gen cephalosporins

A
  1. cefo-peraz-one
  2. cefo-tax-ime
  3. ceft-azid-ime
  4. ceft-riax-one
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44
Q

what is the only 4th gen cephalosporin

A

cefe-pime

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45
Q

what is the new cephalosporin and what is it used for?

A

ceft-arol-ine

for

  1. acute bacterial SKIN AND SKIN STRUCTURE INFECTIONS (ABSSSI)–> think MSSA and MRSA
  2. community acquired bacterial pneumonia
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46
Q

how are most cephalosporins administered?

A

IV–> due to poor oral absorption

EXCEPTIONS= those given orally

  1. ceph-alexin= 1st gen
  2. ce-fac-lor= 2nd gen
  3. ce-furo-xime= 2nd gen
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47
Q

which cephalosporins can adequately get into the CSF

A
  1. ce-furo-zime= 2nd gen

2. all 3rd gens

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48
Q

most cephalosporins are only excreted via the kidney but what is the exception

A

ceft-riax-one= 3rd gen

–> excreted through the bile into feces–> use in pts with renal insufficiency

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49
Q

which 2 cephalosporins produce disulfiram like effects like metronidazole

A
  1. ce-faman-dole= 2nd gen
  2. cefo-peraz-one= 3rd gene
  • aldehyde dehydrogenase which cause the accumulation of acetaldehyde
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50
Q

which cephalosporins can cause bleeding and why

A

same ones that produce disulfiram like effects

  1. ce-faman-dole= 2nd gen
  2. ceft-peraz-one= 3rd gen

they cause anti- vit K effects–> NEED TO GIVE THEM VIT K TO CORRECT

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51
Q

what is the only narrow spectrum cephalosporin and what does it kill

A

1st gen cephalosporins

kill gram + cocci
some gram - rods
	1. E. coli
	2. Klebsiella
	3. Proteus
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52
Q

what is the only broad spectrum cephalosporin and what is it good at killing

A

2nd gen cephalosporins–> BEST CEPH FOR KILLING ANAEROBES

  1. non difficile clostridium
  2. bacteroides–> ce-fox-itin
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53
Q

if you think its a gram - infection and your thinking about using a cephalosporin you would use

A

3rd gen cephalosporin

gram - cocci–> Neisseria

  1. N. meningitidis
    - -> ceft-riax-one or cefo-tax-ime
  2. gonorrhea–> ceft-riax-one

gram - rods–> enterics

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54
Q

if you want to use a cephalosporin in neonates but are afraid bc you know neonates can do phase 2 rxns (glucuronidation), you might give

A

cefo-tax-ime= 3rd gen

bc its only eliminated by the kidney

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55
Q

2nd gen cephalosporins are good for treating

A
  1. otitis media
  2. UTIs

DONT USE FOR MENINGITIS–> you dont achieve sufficient levels in CSF
EXCEPTION:
1. ce-furo-xime= 2nd gen
2. 3rd gens= more effective in penetrating CSF

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56
Q

when do you use 3rd gen cephalosporins

A
  1. aerobic gram - bacteria
  2. best agents for
    - -> aerobic gram - meningitis
    - -> biliary tract infections

alt to 2nd gen cephalosporin

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57
Q

characteristics of 4th gen cephalosporins

A

cephalosporin with greatest stability vs. B-lactamase

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58
Q

what are the other B-lactam drugs

A
  1. carbapenems

2. Monobactams

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59
Q

what are the carbapenems (other B-lactam drugs)

A
  1. imi-penem + cilastatin–> which protects imipenem from being cleaved into a NEPHROTOXIC METABOLITE
  2. mero-penem
  3. erta-penem
  4. dori-penem
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60
Q

which carbapenem do you have to combine with another drug and why

A

imipenem +cilastatin

cilastatin protects imipenem from being cleaved into a NEPHROTOXIC METABOLITE

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61
Q

what is the broadest spectrum B-lactam antibiotic prep available

A

imipenem + cilastatin

carbapenems= broadest spectrum drug we have–> kill almost anything

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62
Q

what is a side effect commonly associated with imipenem

A

seizures in ppl with renal problems

–> they cant clear the drug

63
Q

monobactams (other B-lactam) have…

A

no gram + or anaerobic coverage!!

64
Q

monobactams are good against

A

aerobic gram - rods

65
Q

what B-lactam drug has no cross-reactivity in pts allergic to penicillin

A

monobactams

66
Q

what is the main non- B lactam cell wall drug

A

VANCOMYCIN

67
Q

what are the other non B-lactam cell wall drugs

A
  1. bacitracin
  2. polymyxins
  3. teicoplanin
68
Q

what is the MOA of vancomycin

A

prevents peptidoglycan elongation by binding to the D-ala-D-ala terminal

69
Q

how do bacteria get resistance to vancomycin

A

change the D-ala to a D-lactate which prevents binding of vancomycin

VR-SA
VR-EF

70
Q

vancomycin is the DOC for

A
  1. hospital acquired MRSA

life threatening gram +!!

71
Q

if vancomycin which is administered via IV is given to quickly you get…

A

red man syndrome

-histamine mediated (due to mast cell degranulation) flushing of the upper torso and hypotension

72
Q

what are the protein synthesis inhibitors

A
  1. tetracyclines
  2. aminoglycosides
  3. macrolides
    4 others
73
Q

what are the 2 main tetracyclines

A
  1. tetracycline

2. doxycycline

74
Q

what are the aminglycosides

A
  1. gentamicin
  2. amikacin
  3. streptomycin
75
Q

what are the macrolides

A
  1. ery-thromycin
  2. azi-thromycin
  3. clari-thromycin
76
Q

MOA for tetracyclines

A

bind to the 30s ribosomal subunit
–> blocks access of the acyl tRNA to the mRNA-ribosome complex at the acceptor site
therefore if the tRNA never binds you cannot add on AA to the growing peptide chain

77
Q

tetracyclines are

A

broad spectrum but their use is limited by resistance

78
Q

resistance mechanism for tetracyline

A

naturally occuring R factor–> confers inability of the organism to accumulate the drug
–> due to a Mg2+ dependent active efflux of drug by the protein TetA!!

79
Q

what drug has a mechanism similar to tetracycline and how is it different

A

tige-cycline

it binds with 5x greater affinity for the 30s subunit

80
Q

spectrum of tige-cycline

A

most gram + including

  1. MRSA
  2. VREF

used for complicated skin and intra-abdominal infections

81
Q

how is tigecycline different from tetracycline

A

tigecycline is not affected by efflux pumps (TetA)

82
Q

tetracyclines should not be taken with

A
  1. dairy foods–> tetracyclines chelate with Ca2+–> form NONABSORBABLE PRODUCTS
    not as big of a problem with doxycycline
  2. antacids–> tetracyclines chelate with Mg2+ and Al3+

if pt takes tetracycline tell them it can cause GI upset but to not take antacids bc it will make it worse

83
Q

basically tetracylines can…

A

chelate with dairy products and antacids–> will reduce [plasma] of tetracycline

  1. Ca
  2. Mg
  3. Al
84
Q

tetracyclines can…

A
  1. bind to tissues undergoing calcification like teeth and bones–> deposit here causing discoloration
  2. cross the placenta and concentrate in fetal bones and dental area
85
Q

tetracyclines are metabolized by…

A

glucuronidation (phase 2) in the liver

86
Q

___________________ is the exception and is excreted in bile

A

doxycycline

87
Q

tetracyclines can cause

A
  1. upset GI–> dont take with dairy
  2. deposit in bones and teeth–> discoloration
  3. lover and renal toxicity esp in preg women
  4. PHOTOTOXICITY
88
Q

aminoglycosides are the mainstay treatment for

A

aerobic gram - rods

synergistic with ampicillin

89
Q

how do aminoglycosides get into bacteria

A
  1. passive diffusion
  2. active O2 transport
    - ->low pH or anaerobic conditions–> inhibit entry
90
Q

MOA for aminoglycosides

A

bind to 30s ribosomal subunit–> interfering with initiation complex of peptide formation
–> induces misreadings of mRNA–> incorporation of incorrect AA into growing peptide chain–> NON-FUNCTIONAL OR TOXIC

91
Q

aminoglycosides are good vs.

A

gram - organisms–> bc they cant get through thick peptidoglycan wall

92
Q

aminoglycosides are…

A

for 2 drug bugs (gentimicin + ampicillin)–> ampicillin helps break down peptidoglycan wall

  1. enterococcus faecalis–> endocarditis
  2. listeria–> meningitis
93
Q

side effects of aminoglycosides

A

NO
1. nephrotoxicity–> due to drug accumulating in the kidneys
2. ototoxicity–> due to high peak plasma levels and using aminoglycosides for longer than 5 days
3. NM paralysis at very high doses–> - Ach release
can cause resp paralysis

94
Q

since aminoglycosides have long lasting effects you dose…

A

once a day even though they have a short half life

95
Q

MOA of macrolides= protein syn -

A

bind to 50s subunit–> - aminoacyl translocation reaction

96
Q

spectrum for macrolides

A

broad spectrum–> atypical bacteria

gram - rods

  1. Haemophilus
  2. Legionella
  3. chlamydia, chlamydophila
  4. mycobacterium avium

ACs for MAC

97
Q

when do you use macrolides

A

as an alt. to B-lactams in pts allergic to penicillin that require treatment for NON-LIFE THREATENING GRAM + INFECTIONS

98
Q

macrolides are also specifically used for

A
  1. mycoplasma pneumonia

2. legionella pneumonia

99
Q

combo used to eradicate H. pylori

A
  1. clari-thromycin
  2. amoxicillin
  3. lansoprazole
100
Q

macrolides=

A

Macrolides
methylation of binding site= resistance
motilin +–> increased gastric motility= side effect

101
Q

how does bacteria develop resistance to macrolides

A
  1. decrease antibiotic uptake
  2. methylation of the binding site–> this decreased affinity of the 50s subunit for the antibiotic
  3. bacteria produces esterases which cleave the antibiotic
102
Q

what is the new drug similar to macrolides and what are its properties

A

Teli-thromycin

binds 10x tighter to 2 different sites on the ribosome
has less resistance compared to macrolides

103
Q

what is the only fluid macrolides dont distribute

104
Q

whats abnormal about macrolides

A

ery-thromycin penetrates prostatic fluid well

105
Q

macrolides from least to greatest p450 -

A

Azi-thromycin
Clari-thromycin
Ery-thromycin–> interacts with alot of drugs

C and E–> inhibit theophylline and warfarin

106
Q

macrolides as a group…

A

dont need to be adjusted in renal failure

clari-thromycin only needs to be adjusted in severe renal failure

107
Q

side effects of macrolides

A
  1. increase Gi motility due to + motilin receptors
    - -> good for diabetic patients with peripheral neuropathy to vagus nerve which causes decrease in gastric emptying
  2. teratogen–> some ery-thromycin and clari-thromycin
108
Q

what are the other protein synthesis inhibitors

A
  1. chlor-amphenical
  2. clindamycin
  3. strepto-gramins
  4. line-zolid
109
Q

what is the MOA of all the other protein synthesis -

A

similar to macrolides

bind to 50s subunit and - peptidyl transferase
= - transfer of the peptide chain

110
Q

when would you use chlor-amphenicol

A

as an alt when you have a pt with a rickettsial infection like typhus or rocky mt spotted fever who can not have tetracycline

CHLORAMPHENICOL IS TO TOXIC TO USE FOR MINOR INFECTIONS

111
Q

SE of chloramphenicol

A

neonates cant glucuronidate the drug (which is needed for metabolism)–> phase 2
–> results in gray baby syndrome

112
Q

what is the main use of clindamycin

A

anaerobes–> severe infection due to bacteroides

113
Q

clindamycin is only cleared by the…

A

liver–> must adjust in liver failure

114
Q

clindamycin can cause

A

a C. dif superinfection= pseudomembranous colitis= inflamm of colon–> antibiotic induced diarrhea

treat with metronidazole or give vancomycin if its resistant

115
Q

streptogramins is used for

A

gram + cocci

life threatening infections due to
VREF= enterococcus faecium
VRSA

for complicated skin or skin structure infections due to MSSA

116
Q

linezolid is

A

back up to back up

for gram + cocci

for
VREF
VRSA

117
Q

what are the antifolates

A
  1. sulfonamides

2. TMP/SMX= trimethoprim-sulfamethoazole

118
Q

MOA of sulfonamides (sulfa-metho-azole)

A

competes with PABA for dihydro-pteroate synthetase, preventing PABA from being converted to folic acid

bacteria must synthesize folic acid
humans cant and have to get from diet

119
Q

how is resistance to sulfonamides developed

A
  1. change dihydro-pteroate synthase by mutation or plasmid transfer
  2. decrease the uptake of sulfonamides
  3. increase PABA synthesis–> can outcompete the drug
120
Q

sulfonamides can be used for

A

conjunctivitis

121
Q

sulfonamides if given orally for a long time can cause

A

Stevens-Johnson syndrome

122
Q

MOA of TMP= trimethoprim

A

competitively inhibits dihydrofolate reductase

prevents folic acid–> tetrahydrofolic acid–> AA, purines, pyrimidine synthesis

123
Q

TMP/SMX works synergistically to prevent the formation

A

of tetrahydrofolic acid

124
Q

uses of TMP/SMX

A
  1. back up for listeria= gram + rod
  2. gram - cocci= neisseria meningitidis

DOC for Pneumocystis jiroveci pneumonia–> give IV

125
Q

what is common to antifolates

A

bone marrow suppression

  1. megaloblastic anemia
  2. leukopenia= low # leukocytes
  3. thrombocytopenia
126
Q

what are the miscellaneous DNA antibiotics

A
  1. metronidazole

2. daptomycin

127
Q

MOA of metronidazole

A

bacteria has ferrodoxin–> which metabolizes metronidazole to its active form which interacts with DNA

128
Q

metronidazole is used for

A

Giardia lamblia
Entamoeba histolytica
Trichomonas vaginalis

Bacteroides
Clostridium

on the

METRO

Garderella= bacterial vaginosis

129
Q

metronidazole is generally considered the DOC for

A

susceptible anaerobic infections

130
Q

metronidazole causes

A
  1. metallic taste in mouth

2. disulfiram like effects if taken with alcohol

131
Q

what drugs do you not have to adjust for in a pt with renal failure

A
  1. anti-staph
  2. 3rd gen cephalosporin
  3. doxycycline
  4. macrolides
  5. metronidazole
132
Q

MOA for daptomycin

A

binds to bacterial cell membrane–> rapid depolarization–> loss of membrane potential–> - protein, DNA, RNA synthesis

133
Q

use daptomycin= miscellaneous DNA antibiotic

A

susceptible complicated skin and skin structure infections–> think MRSA

good for gram + cocci

134
Q

FQ are limited to

A

gram - organisms

135
Q

MOA of fluoroquinolines

A
  • bacterial DNA gyrase/topoisomerase 2

topoisomerase 2–> relaxes positive supercoils in DNA= required for normal transcription and replication

+ supercoiling=tension=inhibited replication

136
Q

name the fluoroquinolines

A

2nd gen

  1. cipro-floxacin
  2. o-floxacin

3rd gen

  1. levo-floaxacin
  2. moxi-floxacin

4th gen= gemi-floxacin

137
Q

which generations of FQ are very broad

A

3rd and 4th gen

138
Q

FQ are active against practically

A

all aerobic gram - rods–> except pseudomonas (use cipro to kill)

139
Q

3rd and 4th gen FQ kill

A

anaerobes

  1. bacteroides
  2. clostridium–> but not difficile

referred to as resp RQ some active vs penicillin/macrolide resistant Strept. pneumoniae
levofloxacin= candy

140
Q

resistance to FQ

A
  1. mutation of bacterial DNA gyrase/topoisomerase 2

2. decreased FQ accumulation in bacteria

141
Q

FQ can cause

A
  1. problems with collagen metabolism and cartilage development
  2. tendonitis and tendon ruptures
  3. phototoxicity
142
Q

like tetracyclines, when on FQ you should avoid

A

antacids or iron and zinc supplements

143
Q

ciprofloxacin…

A
  • p 450 enzymes

interfers with metabolism of theophylline

144
Q

see phototoxicity with…

A
  1. tetracyclines
  2. sulfonamides
  3. fluoroquinolines
145
Q

drug for urinary tract antiseptic

A

Nitro-furan-toin

146
Q

MOA of nitrofurantoin= UTI

A

bacteria metabolize drug to active form

active form–> inhibits enzymes and damages DNA

147
Q

use of nitrofurantoin

A

uncomplicated UTI

148
Q

nitrofurantoin

A

turns urine brown

149
Q

pathphys of UTIs

A

ascend to urinary tract due to the short proximity of the peri-rectal area to the female urethra
–> migration to the bladder–> ascend the ureters to the kidneys

150
Q

use of what may promote colonization of urinary tract

A

use of spermicides and diaphragms as method of contraception

151
Q

if you have an uncomplicated UTI treatment is…

A

1st–> TMP-SMX

if that doesnt work then you use fluroquinolines

152
Q

if you have a complicated UTI you use

A

anti-pseudomonal penicillin + gentamicin

153
Q

if preg and you get a UTI use

A

nitrofurantoin

154
Q

what is pro-bene-cid and what is its MOA

A

probenecid is an antigout drug

MOA= inhibits tubular reabsorption of uric acid –> which increases the urinary excretion of uric acid

155
Q

purpose of learning about probenecid

A

it inhibits the tubular secretion of acids, such as

  1. penicillins
  2. cephalosporins
  3. fluroquinolines

aka, if pt is on antigout med (probenecid) it will increase the half life of penicillins, cephalosporins and FQ by preventing their secretion

PHARMACOLOGY (5 decks)

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