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Pharmacology > Exam1Lec8/9/10Antimicrobials > Flashcards

Exam1Lec8/9/10Antimicrobials Flashcards

1
Q

What are antibotics

A

Chemicals produced by microorganisms to inhibit the growth of, or, kill other microorganisms

NATURAL

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2
Q

We want antibiotics to have selective toxicity, why?

A
  • Kill or damage a microbe without damage to the host
  • Therefore, the ideal antibiotic would kill pathogenic microbes without side effects for the patient, e.g., penicillin G comes the closest
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3
Q

How do we obtain selectivity toxicity?

A

Antibiotics target cellular differences between the host & the pathogenic microbe, e.g., penicillin inhibits the cell wall which is not in the mammalian cells

Target differences

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4
Q

What is the therapetic ratio (index)

A
  • Therapeutic ratio (index), Ratio of the toxic dose to the effective dose of the drug, e.g., TI = LD50/ED50 (want LD to be high and ED to be low so TI to be a big number)
  • Differs for each antimicrobial agent, i.e., some more toxic than others
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5
Q

What are the human body defenses against infection?

A

(1) Barriers: e.g., skin & mucous membranes
(2) Responses: antibodies, complement system, etc.

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6
Q

When do we use antimicrobials?

A
  • Human body naturally kills pathogenic microbes
  • However antimicrobials used when those natural defenses, Overwhelmed or damaged
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7
Q

Antimicrobials can be either _ or _

A

Either bactericidal or bacteriostatic

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8
Q

What is bacteriostatic and what are examples?

A
  • inhibit bacterial cell replication but do not kill the organism at clinically achieved concentrations (we need to be careful with doses)
  • e.g. chloramphenicol, erythromycin, & tetracyclines (TEC)
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9
Q

What are bactericidal and examples?

A
  • Bactericidal: causes microbial cell death & lysis at clinically achieved concentrations
  • e.g. penicillins, cephalosporins, & aminoglycosides (PAC)
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10
Q

What is either cidal or static based on the composition of enviroment

A

sulfonamides

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11
Q

Label and give example for each

A
  1. Bacteriostatic-eg. erythromycin
  2. Bacteriocidial-eg. pencillin G
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12
Q

What drugs attack cell wall

A
  • Penicillin
  • Cephalosporins
  • Monobactams
  • Carbapenems
  • Vancomyic

PEN hit a VAN, so her CErtification for her CAR was MONO

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13
Q

What is used to stop transcription

A
  • Quinolones- DNA gyrase
  • Rifampin-RNA polyerase
  • Metronidazole-DNA

MET the Royal QUeen

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14
Q

What is used to stop protein synthesis

A
  • Aminoglycosides
  • Tetracyclines
  • Macrolides
  • Chloramphenicol

MAC and Tarte has an AMazing CHecking account

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15
Q

What is used for the cell membrane

A
  • Polymyxins
  • Daptomycin

POLY DAPed the membrane

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16
Q

What is used against folic acid

A
  • Trimethoprime
  • Sulfonamides

TRi SUrFing on ACID

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17
Q

What are the 4 reasons why a patient may not respond to therapy with antibacterials

A
  1. misdiagnosis (fungal/viral v bacterial)
  2. No infection (increase temp becasue of non microbial cause)
  3. Do not complete full length of therapy
  4. Patient self treatment of infection with antimicrobials that were not prescribed for them
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18
Q

What are the five factors to consider when treating an infection? (host determinants)

A
  1. Sensitivity of organism to drug (drug resistance)
  2. Appropiate dosage (adult v neonatal- might have immature enzymes)
  3. Route of administration (PO vs. IV)
  4. Duration of therapy (days, weeks, months)
  5. Special patent features (immune systam, age, renal fxn)
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19
Q

What might distrub the microflora and what might it cause?

A
  • use of an antimicrobial agent might disturb the ecologically balance leading to the overgrowth of pathogenic microbes which are inherently resistant to the antimicrobial agent
  • This phenomenon is known as superinfection
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20
Q

Empiric therapy?

A

clinician will start txt instead of waiting for results. They will take a history and get as much info to make a decision and sollow treatment guidelines

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21
Q

What microorganisms in burns would cause an acute infection

A

S. aureus, S. pyogenes, P. aeruginosa

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22
Q

What microorganism is most likely to cause an acute infection with skin infections

A

S. aureus, S. pyogenes, Herpes zoster

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23
Q

What microorganisms would most likely cause acute infections with decubitus wound infections (bed sore)

A

S. aureus, E. coli, Bacteroides fragilis

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24
Q

What microorganism will most likely cause acute infection in tranumatic and surgical wounds

A

S. aureus, S. pyogenes, P. aeruginosa

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25
Q

What should we do for optimal therapy (anitmicrobial susceptibility)

A

Obtain cultures in order to identify the pathogenic microbe(s) & then do drug sensitivity testing (e.g., Disk-diffusion test, Broth dilution susceptibility test, etc.) to determine the MIC (minimum inhibitory concentration) or MBC (minimum bactericidal concentration)

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26
Q

What is used for first choice of antibodic in treponema pallidum, syphilis

A
  • Benezathine Penicillin G
  • Given IM
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27
Q

What is used for first choice Antibiotic in TB

A

Rifampin + Isoniazid + Pyrazinamide + Ethambutol

RIPE

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28
Q

What is used for first choice antibodic in P. aeruginosa, Pneumonia

A

Piperacillin/Tazobactam+ Tobramycine

PIPER TAZed TOBY

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29
Q

Most antimicrobial drugs & their metabolites excreted primarily by the kidneys, might have to have their dosage modified with what type of patient

A

impaired renal function

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30
Q

In order to ensure the drug hits the site of infection, what should we do?

A

At least 3-5 times the MIC to ensure optimal therapeutic response

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31
Q

What are some areas of the body that are difficult to penetrate by some antimicrobial drugs?

A

Meninges, joint spaces or eye

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32
Q

What can serve as a guide to adjust the dose of drug in renal

A

Creatinine clearance rate, Surrogate measure of renal function, GFR

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33
Q

Where favorable penetration for drugs

A

sites with inflammation

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34
Q

If we have decrease in renal fxn, how is the AUC affect?

A

Area under curve (plasma cont): it will be higher due to a higher cont.

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35
Q

What two drugs should be careful with hepatic fxn impairment

A
  • Chloramphenicol
  • Clindamycin- becasue of increase in half life
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36
Q

What is used to measure heptatic function

A

Sound clinical judgment used to guide therapy, Child-Pugh score

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37
Q

What do neonates have low cont of?
Why do we need to be careful with drugs in neonates

A
  • UDP-glucuronosyl transferase which conjugates chloramphenicol
  • The transferase is not present to make drug more water solube so it can cause CV collapse, gray baby syndrome
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38
Q

What drug do we increase to infacts and young children? Why?

A
  • Gentamicin becasue volume of distribution
  • As we age, we increase lipid profile and younger pts are more aqueous
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39
Q

What does sulfonamides do and what population is contriaindicated?

A
  • Displace bilrubin from alumin in the blood which can then deposit in the brain, kernicterus or toxic encephalopathy
  • Contraindicated in neonates
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40
Q

What does tetracycline cause

A
  • permanent discoloration of growing teeth of children
  • casue intracranial hyertension infants and children
  • Bind to calcium
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41
Q

What does isoniazid cause?

A

increase hepatitis

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42
Q

What drug do we need to be careful with in CHF patients? Why?

A

Ticarcillin disodium/Clavulanate potassium-> 2g of Na and 0.1 of K+ per day
Pts already has problem with cardiac output and the Na+K will cause more issues (ex. decrease HR)

43
Q

What an example of synergy

A
  • Cell wall synthesis inhibitor (penicillin) + protein synthesis inhibitor (aminoglycoside)
  • Sequential pathway, B-lactamase inhibitor
44
Q

For synergy, what do we not do?

A

Do not use two drugs of same class or have the same mechanism of action

45
Q

What are five drugs that are issues in preganacy and nursing? explain why

A
  1. Metronidazole
    * Mutagentic
  2. Dulfonamides
    * Breast milk
    * Kernicterus: increase bilirubin, displaced from albumin
  3. Antifolate drugs
    * decrease of conts. of folic acid in pregnant women
  4. Fluoroquinolones
    * Affect cartilage growth

5.Tetracyclines
* inhibit bone growth, tooth enamel dysplasia

46
Q
A
  1. additive (indifference)
  2. Synergism
  3. Antagonism
47
Q

What is drug resistance

A

Condition in which there is insensitivity or decreased sensitivity to drugs that ordinarily cause inhibition of cell growth or cell dealth

48
Q

What are mechanisms of antimicrobial resistance in pathogenic microbes:

A
  • decrease drug uptake -> cannot get to site
  • increase drug efflux -> bacteria can create a pumps and pump the drugs out
  • Enzymatic inactivation -> B lactases
  • decrease affinity for site of action
49
Q

What are the gram postivity bacteria and what is used

A

Staphylococcus aureus, Streptococcus pneumoniae, Enterococcus faecalis, Listeria monocytogenes

Use Vanco

50
Q

What are the gram negative bacteria and what do you use?

A

Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, Haemophilus influenzae

Aminoglycosides

51
Q

What are the anaerobes

A

Clostridioides (Clostridium, Peptoclostridium) difficile, Bacteroides fragilis

52
Q

Where are B lactamases located in gram neg and pos?

A

Neg: inside
Pos: outside

53
Q

What are some key difference of gram - and +

A

-: porins, outer membrane and less peptidogylcan
+: thicker peptidoglycan layer

54
Q

What is a target for vanco?

A

glucosyltransferese and peptidoglycan synthase

55
Q

What are all the penicillins?

A
  • Pen G
  • Amoxicillin
  • Dicloxacilin
  • Ticarcillin
  • Piperacillin
56
Q

What is the mech of action and resistance of penicillins?

A

MOA:
* inhibit peptidoglycan transpeptidase (prevent corss linking)
* PBP
* Autolysins

Resist:
* Change in PMP
* tolerance, deficiency in autoytic enxymes
* change in porin
* b-lactamase

57
Q

What is the pharmcokinetics of pen?

A

inflammation, treat meningitis, arthritis and endophtalmitis

58
Q

Side effects of pen?

A
  • Gastric distress
  • IV pain
  • C. Diff
  • Pen allery
  • Na+
  • Neuroxitity because it inhibit GABA ⭐️
59
Q

What is the MOA and resistance of cephaloporins

A

same as pen

60
Q

What does the first gen of cephalosporins treat?

A

PECS
* Proteus miralilis
* E.coli
* Klebisella pneum
* Staph or strep

61
Q

What does second gen cephalosporins treat

A

HEN PEK
* Haempphilius influ
* Enterobacter aerogenes
* Neisseria gon

62
Q

What does 3rd gen of cephalosporins treat?

A

ACES
* acinetobacter cal.
* Citrobacter div.
* Enterobacter c.
* Serratia mar.
* serious G-

63
Q

What does 4th gen of cephalosporins treat?

A
  • Pseud. aeruginos
  • Citrobacter freundii
  • gram +
64
Q

waht does 5th gen of cephalosporins treat

A

MRSA and not pseudomonas

65
Q

What is the mechanisms of action and resistance in imipenem?

A

Same as pen

66
Q

What is imipenem used for to treat?

A

G- rods, Pseudo artuinosa and listeria mono.

67
Q

What is special about carbapenems and their pharmacokinetics?

A

formualted with dipeptidase inhibitor, cilastatin

68
Q

What is the SE of carbapenems

A

Seizures and hypersensitivity rxns

69
Q

What is the MOA and resistance of monobactam?

A

same as pen

70
Q

What is aztrenonam used for to treat

A

Gr - rods
P.aerg

71
Q

When do we use a monobactam

A

when pt has pen allergy

72
Q

What is the MOA and resistance of vancomycin

A

MOA: inhibitor of pepidoglycan synthase, binds to D-ala-D-ala. Inhibitor of pentapeptide precursor and membrane carrier

Resistance: D-ala-D lactate

73
Q

What is vanco used for?

A

G+, MRSA and C.diff

74
Q

What is something unique about vanco’s Pharmacokin?

A

Can enter CSF with inglamed meninges

75
Q

What is the SE of vanco

A

ototoxicity
nephrotoxicity

76
Q

What the MOA and resistance of daptomycin?

A

Bind to cell membrane and fromas pores
increase MIC

77
Q

What is daptomycin used for ? when can we not use it?

A
  • G+, MRSA and VRE
  • Cannot use for lung ingection because pulmonary surfactants inactivate it
78
Q

What is the SE of cyclic lipopeptide

A

myppathy
rhabdomyolysis

79
Q

What binds to the target A site?

A

Tectracycline and aminoglycosides

80
Q

What is the MOA and resistance of tetracyclines

A

MOA: binds to 30s (STATIC)
resist: Ribosomal change

81
Q

What is tetracycines used for?

A

Myco pneum
Cutibacterium acnes

82
Q

What is imp with tetracylines pharmacokin

A

Chelation
Dox is fecally eliminated

83
Q

What are the SE of tetracyclines?

A
  • Contraindicated in preg
  • Discoloar of teeth and inhibit bone
  • photsensitivity
  • superinfection: c.diff and c. albicans
84
Q

What is the MOA for tigecyclines, used for what/

A

Bind to 30s and static
usef for MRSA, VRE and PRSP

85
Q

What are macrolides MOA and MOR?

A

MOA: 50s (p site) STATIC
resist: meth of 23

86
Q

What are macrolides used for?

A
  • Chalmy pneum
  • H. influ
  • M. car
  • URTI
  • Pneumonia
  • Otitis media
87
Q

What is the SE of macrolides and the drug interactions?

A

SE: prolong the QTc interval
Inter: inhibit CYP3A4

88
Q

What is the MOA and SE of chloramphenicol

A

MOA: 50s STATIC (cidal for meningitis)
MOR
SE: gray baby syndrome (premature infacnts, decr in UGT)

89
Q

What is the MOA and MOR in Clindamycin

A

MOA: 50s STATIC
MOR: meth of 23

90
Q

What are the uses and SE of lincosamides

A

Uses: CA-MRSA and BLA
Side: CDAD

91
Q

What is the MOA AND MOR in streptogramins

A
  • 50s and cidial
  • ribosomal methylas and actyltransferase
92
Q

What are streptogramins used for and their SE

A

USED; osteomyelitis and endocarditis
SE: arthralgias and myalgias

93
Q

What is the MOA AND MOR in aminoglycosides

A

MOA: 30s (CIDIAL)
MOR:decr porin perm, decrease ribosomal binding

USED WITH B-LAC

94
Q

WHat is teh MOA and the usage of fidaxomicin?

A

binds to RNA polymerase
C.DIFF and CDAD

vanco also for C.diff

95
Q

What is teh MOA and MOR of sulfonamides

A

MOA: inhibit dihydropteroate synthase

MOR: do not biosysnthsize folic acid, increase PABA profuction, dihydropterote synthase. decrease sulfa permeability

96
Q

Whart are sulfonamides used for and SE?

A

Broad spectrum and for UTIs
SE: RASH: SULFA ALLERGY, SJS,TEN, kernicterus (newborn encephalopathy)

97
Q

What is something special about sulfonamides and their pharmocokin

A

inhibit CYP2C9 so increase warfarin

98
Q

What is the useage of trimethoprim and sulfamethozaole

A

MRSA, E.coli, UTI and prostatitis

99
Q

What is the SE of Trimethoprim/sulfamethozaole

A

hemolytic anemia

100
Q

What is teh MOR of trimethoprim and sulf

A

Tri: decrease DHFR affinity, decrease cell pemeation and over production of DHFR

101
Q

What is the MOA of quinolones

A
  • Inhibit toposimerase II (DNA gyrase, Supercoli)
  • Inhibit DNA REPLICATION
102
Q

Under Fluroquinolone, what do we used to treat UTIs and inhalation anthrax

A

Cipofloxin for UTI and inhalation anthrax
Levofloxacin for UTI and UTRI

103
Q

What is the SE for quinolones?

A

Tendonitis and Myasthenia gravis

104
Q

What is the drug interaction and what does quinolones inhibit?

A

Chelation
Inhibt CYP1A2, increase caffeine

Pharmacology (26 decks)

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