Exam1Lec8/9/10Antimicrobials Flashcards
(104 cards)
1
Q
What are antibotics
A
Chemicals produced by microorganisms to inhibit the growth of, or, kill other microorganisms
NATURAL
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
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
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
5
Q
What are the human body defenses against infection?
A
(1) Barriers: e.g., skin & mucous membranes
(2) Responses: antibodies, complement system, etc.
6
Q
When do we use antimicrobials?
A
- Human body naturally kills pathogenic microbes
- However antimicrobials used when those natural defenses, Overwhelmed or damaged
7
Q
Antimicrobials can be either _ or _
A
Either bactericidal or bacteriostatic
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)
9
Q
What are bactericidal and examples?
A
- Bactericidal: causes microbial cell death & lysis at clinically achieved concentrations
- e.g. penicillins, cephalosporins, & aminoglycosides (PAC)
10
Q
What is either cidal or static based on the composition of enviroment
A
sulfonamides
11
Q
Label and give example for each
A
- Bacteriostatic-eg. erythromycin
- Bacteriocidial-eg. pencillin G
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
13
Q
What is used to stop transcription
A
- Quinolones- DNA gyrase
- Rifampin-RNA polyerase
- Metronidazole-DNA
MET the Royal QUeen
14
Q
What is used to stop protein synthesis
A
- Aminoglycosides
- Tetracyclines
- Macrolides
- Chloramphenicol
MAC and Tarte has an AMazing CHecking account
15
Q
What is used for the cell membrane
A
- Polymyxins
- Daptomycin
POLY DAPed the membrane
16
Q
What is used against folic acid
A
- Trimethoprime
- Sulfonamides
TRi SUrFing on ACID
17
Q
What are the 4 reasons why a patient may not respond to therapy with antibacterials
A
- misdiagnosis (fungal/viral v bacterial)
- No infection (increase temp becasue of non microbial cause)
- Do not complete full length of therapy
- Patient self treatment of infection with antimicrobials that were not prescribed for them
18
Q
What are the five factors to consider when treating an infection? (host determinants)
A
- Sensitivity of organism to drug (drug resistance)
- Appropiate dosage (adult v neonatal- might have immature enzymes)
- Route of administration (PO vs. IV)
- Duration of therapy (days, weeks, months)
- Special patent features (immune systam, age, renal fxn)
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
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
21
Q
What microorganisms in burns would cause an acute infection
A
S. aureus, S. pyogenes, P. aeruginosa
22
Q
What microorganism is most likely to cause an acute infection with skin infections
A
S. aureus, S. pyogenes, Herpes zoster
23
Q
What microorganisms would most likely cause acute infections with decubitus wound infections (bed sore)
A
S. aureus, E. coli, Bacteroides fragilis
24
Q
What microorganism will most likely cause acute infection in tranumatic and surgical wounds
A
S. aureus, S. pyogenes, P. aeruginosa
25
What should we do for optimal therapy (anitmicrobial susceptibility)
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)
26
What is used for first choice of antibodic in *treponema pallidum*, syphilis
* Benezathine Penicillin G
* Given IM
27
What is used for first choice Antibiotic in TB
Rifampin + Isoniazid + Pyrazinamide + Ethambutol
| RIPE
28
What is used for first choice antibodic in P. aeruginosa, Pneumonia
Piperacillin/Tazobactam+ Tobramycine
| PIPER TAZed TOBY
29
Most antimicrobial drugs & their metabolites excreted primarily by the kidneys, might have to have their dosage modified with what type of patient
impaired renal function
30
In order to ensure the drug hits the site of infection, what should we do?
At least 3-5 times the MIC to ensure optimal therapeutic response
31
What are some areas of the body that are difficult to penetrate by some antimicrobial drugs?
Meninges, joint spaces or eye
32
What can serve as a guide to adjust the dose of drug in renal
Creatinine clearance rate, Surrogate measure of renal function, GFR
33
Where favorable penetration for drugs
sites with inflammation
34
If we have decrease in renal fxn, how is the AUC affect?
Area under curve (plasma cont): it will be higher due to a higher cont.
35
What two drugs should be careful with hepatic fxn impairment
* Chloramphenicol
* Clindamycin- becasue of increase in half life
36
What is used to measure heptatic function
Sound clinical judgment used to guide therapy, Child-Pugh score
37
What do neonates have low cont of?
Why do we need to be careful with drugs in neonates
* 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
38
What drug do we increase to infacts and young children? Why?
* **Gentamicin** becasue volume of distribution
* As we age, we increase lipid profile and younger pts are more aqueous
39
What does sulfonamides do and what population is contriaindicated?
* Displace bilrubin from alumin in the blood which can then deposit in the brain, kernicterus or toxic encephalopathy
* Contraindicated in neonates
40
What does tetracycline cause
* permanent discoloration of growing teeth of children
* casue intracranial hyertension infants and children
* Bind to calcium
41
What does isoniazid cause?
increase hepatitis
42
What drug do we need to be careful with in CHF patients? Why?
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
What an example of synergy
* Cell wall synthesis inhibitor (penicillin) + protein synthesis inhibitor (aminoglycoside)
* Sequential pathway, B-lactamase inhibitor
44
For synergy, what do we not do?
Do not use two drugs of same class or have the same mechanism of action
45
What are five drugs that are issues in preganacy and nursing? explain why
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
1. additive (indifference)
2. Synergism
3. Antagonism
47
What is drug resistance
Condition in which there is insensitivity or decreased sensitivity to drugs that ordinarily cause inhibition of cell growth or cell dealth
48
What are mechanisms of antimicrobial resistance in pathogenic microbes:
* 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
What are the gram postivity bacteria and what is used
Staphylococcus aureus, Streptococcus pneumoniae, Enterococcus faecalis, Listeria monocytogenes
Use Vanco
50
What are the gram negative bacteria and what do you use?
Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, Haemophilus influenzae
Aminoglycosides
51
What are the anaerobes
Clostridioides (Clostridium, Peptoclostridium) difficile, Bacteroides fragilis
52
Where are B lactamases located in gram neg and pos?
Neg: inside
Pos: outside
53
What are some key difference of gram - and +
-: porins, outer membrane and less peptidogylcan
+: thicker peptidoglycan layer
54
What is a target for vanco?
glucosyltransferese and peptidoglycan synthase
55
What are all the penicillins?
* Pen G
* Amoxicillin
* Dicloxacilin
* Ticarcillin
* Piperacillin
56
What is the mech of action and resistance of penicillins?
MOA:
* inhibit peptidoglycan transpeptidase (prevent corss linking)
* PBP
* Autolysins
Resist:
* Change in PMP
* tolerance, deficiency in autoytic enxymes
* change in porin
* b-lactamase
57
What is the pharmcokinetics of pen?
inflammation, treat meningitis, arthritis and endophtalmitis
58
Side effects of pen?
* Gastric distress
* IV pain
* C. Diff
* Pen allery
* Na+
* Neuroxitity because it inhibit GABA ⭐️
59
What is the MOA and resistance of cephaloporins
same as pen
60
What does the first gen of cephalosporins treat?
PECS
* Proteus miralilis
* E.coli
* Klebisella pneum
* Staph or strep
61
What does second gen cephalosporins treat
HEN PEK
* Haempphilius influ
* Enterobacter aerogenes
* Neisseria gon
62
What does 3rd gen of cephalosporins treat?
ACES
* acinetobacter cal.
* Citrobacter div.
* Enterobacter c.
* Serratia mar.
* serious G-
63
What does 4th gen of cephalosporins treat?
* Pseud. aeruginos
* Citrobacter freundii
* gram +
64
waht does 5th gen of cephalosporins treat
MRSA and not pseudomonas
65
What is the mechanisms of action and resistance in imipenem?
Same as pen
66
What is imipenem used for to treat?
G- rods, Pseudo artuinosa and listeria mono.
67
What is special about carbapenems and their pharmacokinetics?
formualted with dipeptidase inhibitor, cilastatin
68
What is the SE of carbapenems
Seizures and hypersensitivity rxns
69
What is the MOA and resistance of monobactam?
same as pen
70
What is aztrenonam used for to treat
Gr - rods
P.aerg
71
When do we use a monobactam
when pt has pen allergy
72
What is the MOA and resistance of vancomycin
MOA: inhibitor of pepidoglycan synthase, binds to D-ala-D-ala. Inhibitor of pentapeptide precursor and membrane carrier
Resistance: D-ala-D lactate
73
What is vanco used for?
G+, MRSA and C.diff
74
What is something unique about vanco's Pharmacokin?
Can enter CSF with inglamed meninges
75
What is the SE of vanco
ototoxicity
nephrotoxicity
76
What the MOA and resistance of daptomycin?
Bind to cell membrane and fromas pores
increase MIC
77
What is daptomycin used for ? when can we not use it?
* G+, MRSA and VRE
* Cannot use for lung ingection because pulmonary surfactants inactivate it
78
What is the SE of cyclic lipopeptide
myppathy
rhabdomyolysis
79
What binds to the target A site?
Tectracycline and aminoglycosides
80
What is the MOA and resistance of tetracyclines
MOA: binds to 30s (STATIC)
resist: Ribosomal change
81
What is tetracycines used for?
Myco pneum
Cutibacterium acnes
82
What is imp with tetracylines pharmacokin
Chelation
Dox is fecally eliminated
83
What are the SE of tetracyclines?
* Contraindicated in preg
* Discoloar of teeth and inhibit bone
* photsensitivity
* superinfection: c.diff and c. albicans
84
What is the MOA for tigecyclines, used for what/
Bind to 30s and static
usef for MRSA, VRE and PRSP
85
What are macrolides MOA and MOR?
MOA: 50s (p site) STATIC
resist: meth of 23
86
What are macrolides used for?
* Chalmy pneum
* H. influ
* M. car
* URTI
* Pneumonia
* Otitis media
87
What is the SE of macrolides and the drug interactions?
SE: prolong the QTc interval
Inter: inhibit CYP3A4
88
What is the MOA and SE of chloramphenicol
MOA: 50s STATIC (cidal for meningitis)
MOR
SE: gray baby syndrome (premature infacnts, decr in UGT)
89
What is the MOA and MOR in Clindamycin
MOA: 50s STATIC
MOR: meth of 23
90
What are the uses and SE of lincosamides
Uses: CA-MRSA and BLA
Side: CDAD
91
What is the MOA AND MOR in streptogramins
* 50s and cidial
* ribosomal methylas and actyltransferase
92
What are streptogramins used for and their SE
USED; osteomyelitis and endocarditis
SE: arthralgias and myalgias
93
What is the MOA AND MOR in aminoglycosides
MOA: 30s (CIDIAL)
MOR:decr porin perm, decrease ribosomal binding
| USED WITH B-LAC
94
WHat is teh MOA and the usage of fidaxomicin?
binds to RNA polymerase
C.DIFF and CDAD
| vanco also for C.diff
95
What is teh MOA and MOR of sulfonamides
MOA: inhibit dihydropteroate synthase
MOR: do not biosysnthsize folic acid, increase PABA profuction, dihydropterote synthase. decrease sulfa permeability
96
Whart are sulfonamides used for and SE?
Broad spectrum and for UTIs
SE: RASH: SULFA ALLERGY, SJS,TEN, kernicterus (newborn encephalopathy)
97
What is something special about sulfonamides and their pharmocokin
inhibit CYP2C9 so increase warfarin
98
What is the useage of trimethoprim and sulfamethozaole
MRSA, E.coli, UTI and prostatitis
99
What is the SE of Trimethoprim/sulfamethozaole
hemolytic anemia
100
What is teh MOR of trimethoprim and sulf
Tri: decrease DHFR affinity, decrease cell pemeation and over production of DHFR
101
What is the MOA of quinolones
* Inhibit toposimerase II (DNA gyrase, Supercoli)
* Inhibit DNA REPLICATION
102
Under Fluroquinolone, what do we used to treat UTIs and inhalation anthrax
Cipofloxin for UTI and inhalation anthrax
Levofloxacin for UTI and UTRI
103
What is the SE for quinolones?
Tendonitis and Myasthenia gravis
104
What is the drug interaction and what does quinolones inhibit?
Chelation
Inhibt CYP1A2, increase caffeine
