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EXAM 2 - LAM > Antimicrobials - UGHHHHH > Flashcards

Antimicrobials - UGHHHHH Flashcards

1
Q

what do Beta Lactams do?

A

destroy cell wall via interfering with transpeptidase enzymes (responsible for cross-links between peptidoglycan strange)

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2
Q

what are some restrictions of beta-lactams (the MUST haves?)

A

MUST have cell walls and/r growing (most effective during log phase of growth)

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3
Q

What organisms may persist with beta lactase?

A

static

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4
Q

leta-lactams have synergism with ________ thus help prevent relapse and failures in serious infections with tolerant microorganisms

A

Aminglycosides

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5
Q

what is penicillin effective against?

A

many G+ (FEW G- [inactive at normal dose])

BOTH anaerobic and aerobic bacteria

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6
Q

What is the exception of anaerobic and aerobic penicillin efficacy?

A

Bacteroides

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7
Q

3rd generation cephalosporins are a class of _______?

A

B-lactams

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8
Q

How are 3rd generation cephalosporins different than normal?

A

WIDER spectrum f activity (tx resistant G- infections in very compromised cases)

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9
Q

3rd generation cephalosporins have properties like _________?

A

penicillins (BUT are more stable and temp changes)

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10
Q

T/F 3rd generation cephalosporins are toxic?

A

FALSE/NOPE, relatively non-toxic (BUT repeated IV administration may cause local phlebitis)

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11
Q

T/F 3rd generation cephalosporins HURT when they are injected.

A

T

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12
Q

Carbapenems are a class of what?

A

New class of 3rd generation cephalosporins

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13
Q

______ & ______ are among the most active drugs against a wide variety of bacteria (resistant to B-lactamase destruction) - What are they effective against?

A

imipenem and meropenem

anaerobic and aerobic microorganisms

Anaerbes are highly susceptible (Bacteroides fragilis)

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14
Q

T/F toxicity is common with B-lactams?

What are some effects?

A

F (toxicity is rare)

Hypersensitivity reactions = skin reactions, angioedema, drug fever, serum sickness, vasculitis, eosinophilic, anaphylaxis

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15
Q

What should be administered IV with caution esp. if hyperkalemia is present?

A

Potassium Penicillin

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16
Q

What are 3 common examples of aminoglycosides?

A

Gentamycin, toramycin, amikacin

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17
Q

what do aminglycosides interfere with? Are they most effective against G+ or G-

A

membrane associated bacterial ribosomes

susceptible aerobic bacteria
Mostly G- (bacilli) - ex. pseudomonas

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18
Q

What facilitates the movement of Aminoglycosides across cell wall?

What decreases the movement?

A

passive movement facilitated by ALKALINE ph!

low PH increases resistance more >100x

decreased passage also with low O2 tension (hypoxic tissues) - caution with treating anaerobes in low O2 environments (NOT effective against obligate anaerobes & fungi)

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19
Q

What is hella important to remember with regards to administering Beta-lactams and any drugs given after?

A

Cell wall injury from B-lactams will increase uptake of aminoglycosides

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20
Q

Are aminoglycosides effective against streptococci?

A

NOT really (moderately sensitive - quite resistant)

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21
Q

What is a major negative effect of animoglycosides?

what are 2 others?

A

filtered and absorbed into brush border of proximal tubule & LOH via ionization = transported into cells= sequestered in lysosomes = lysosomes rupture = accessive accumulation (mainly in renal cortex) = tubular necrosis = MONITOR renal function (evidence in 3-5d)

ototoxicity, NM blockage

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22
Q

what is an example of fluoroquinolone?

A

enrofloxacin

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23
Q

What does fluoroquinolone do?

A

inhibits DNA/RNA enzyme synthesis

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24
Q

what is fluoroquinolone effective against?

A

aerobic G- (genitourinary, GI tract, bone inf, soft tissues/skin infections) & G+

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25
Q

What are fluoroquinolone not effective against?

A

anaerobic

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26
Q

what are examples of macrlids?

A

Erythromycin, azithromycin, clarithromycin

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27
Q

What do macrolids do?

What is is confined to?

A

interfere with protein synthesis (reversibly bind to 50s subunit of ribosome) - confined to rapidly dividing bacteria and mycoplasmas

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28
Q

What are macrolids affective against?

A

G+ > G-

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29
Q

Are macrolids bacteriostatic r bacteriocydal?

A

static

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30
Q

T/F macrolides are concentration dependent?

A

F (they are time dependent)

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31
Q

What are macrolids syngergicstic with?

A

rifampin (Rhodococcus equi)

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32
Q

macrolids can be used to tx _______ infections.

A

respiratory

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33
Q

_____ are sensitive to macrolid-indiced GI disturbances.

A

Horses (can be fatal)

34
Q

what do sulfonamides do?

A

blocks several enzymes needed for biogenesis and other metabolic reactions necessary for formation of RNa

35
Q

______ is great against external auditory canal infections.

A

fluoroquinolone

36
Q

are sulfonamides static or cidal?

A

static

37
Q

high concentrations of sulfonamides are found in the _____.

A

urine

38
Q

what are some potentiated sulfonamides? What do they do?

A

trimethoprim, pyrimethamine

inhibit dihydrofolate reductase in bacteria and protozoa (not effective if used alone)

39
Q

what is critical in defense mechanism for bacteriostatic Abs?

A

adequate cellular and humoral defense mechanisms

40
Q

When are sulfonamides most effective?

A

early stages of acute infections (when organisms are rapidly multiplying)

41
Q

What do sulfonamides effective against?

A

G+, G-, some protozoa

42
Q

what is combined to tx protozoal disease

A

sulfonamides + pyrimethamine

43
Q

what is used to tx burns to prevent gram + & G- organisms?

A

SSD

44
Q

Concentrations of sulfonamides in _______ exceed concentrations in _________..

A

kidneys, plasma

skin, liver, lungs, are slightly less than corresponding plasma concentrations

45
Q

how are sulfonamides excreted?

A

urine primarily; also in feces, milk (1-3.5x higher than plasma)

46
Q

what do tetracyclines do?

A

reversible binding of 30s subunit (prevention ribosomal translation)

47
Q

How are tetracyclines further classified (include examples)

A

short acting - oxytetracycline,
intermediate acting - de-methyl-choro-tetracycline
long acting = doxy

48
Q

Are tetracyclines static or cidal?

Are they concentration or time dependent?

A

static

time

49
Q

Where are tetracyclines found in high concentrations in the body?

A

kidneys, liver, bile, spleen, lungs, bone

50
Q

tetracyclines are the drug of choice to tx ____ & ____.

A

rickettsia & mycoplasma

51
Q

what are tetracyclines effective against?

A

G +, G-, anaerobe, aerob., even some protozoa

52
Q

What is a SE of tetracyclines?

A

D in horses (esp, of animal is critically ill or stressed)

chelate Ca in teeth & bones (yellow-brownish discoloration, impairs healing)

rapid Iv injection = hypotension

nephrotocic

WBC chemotactic/phagocytosisi

53
Q

What is an examples of a phenol?

A

chloremphenicol

54
Q

What are phenols effective against?

A

G+, G-, anaerobes (bactericides fragilis)

55
Q

phenols are known to be…

A

highly effective well tolerated broad spec Abs

56
Q

what do phenols do?

A

inhibit microbial protein synthesis by binding to 50s bubonic of 70s ribosome (IMPAIRS peptide transferred activity)

57
Q

are phenols static or cidal?

A

static (can be Cidal in high concentrations)

58
Q

Where are phenols absorbed?

A

upper GI

59
Q

T/F chloramphenicol doesn’t undergo hepatic metabolism?

A

FALSE - it undergoes extensive haptic metabolism (liver dz prevents normal metabolic degradation and active Ab accumulates in body)

60
Q

What is an example of glycopeptide?

A

vancomycin

61
Q

what do glycopeptides do?

A

prevents cell wall synthesis and produces rapid bactericidal effect in DIVIDING bacteria

62
Q

What are glycopeptides effective against?

A

G+ (NOT against G-)

63
Q

where are glycopeptide excreted?

A

kidneys (in ACTIVE form)

64
Q

what are some hypersensitivity reactions related to glycopeptides?

A

ototoxicity

nephrotoxicity

65
Q

what are Nitroimidazles used to tx?

A

protozoa ABs

anaerobic

66
Q

what is an examples of Nitroimidazle?

A

metronidazole

67
Q

T/F Nitroimidazles can be used off label in feed animals?

A

FUCK NO!

this is prohibited

68
Q

metronidazole is effective against what?

A

ptotozoa + obligate anaerobic bacteria (Bacteriodes fragilis, B. melanogenicus, Fusobacterium, C. perfringens, other clostridial inf)

69
Q

metronidazole is NOT effective against what?

A

facultative anaerobes, obligate aerobes, microaerophilic bacteria

70
Q

how is metronidazole absorbed?

A

in GI (bioavailability = 60=100%)

- serum concentrations in 1-2h (widely distributed to all tissues)
- penetrates BBB
 - attains tx concentrations in abscesses & empyema fluid
71
Q

What is a weird thing that metronidazole is also effective against?

A

adjunct to tx solid tumors (radiosensitizors)

72
Q

How do NSAIDS work?

A

reduce biosynthesis of Prostaglandins via inhibiting COX (converts arachidonic acid into prostaglandins) = impairs inflammatory process

73
Q

where is Cox 1 found?

what is it classified as?

A

all tissues

constitutive

74
Q

Where is cox 2 found?

what is it classified as?

A

damaged or inflamed tissues

non-constitutive (also involved in thermoregulation and pain response)

75
Q

What are the bodies NORMAL protective mechanisms?

A 
D
ulcers
colic
protein less
right dorsal colitis
renal papillary necrosis
toxicity
76
Q

What do most NSAIDS on the market tx?

A

cox 1 & cox 2

77
Q

what is the cox 2 inhibitor on the market?

A

firocoxib

78
Q

what is flunixin meglamine commonly used to tx?

A

pain & enodtoxemia associated with colic (helps with arterial hypoxemia, vasdilation, CV shock, D)

79
Q

what can be used with lameness exams?

A

lidocaine (30-45 mins), bupivicane (90-120mins), mepivicaine HCL (4-6hrs)

80
Q

complications of nerve blocks

A

broken needle shaft
SC infection
synovial infection

EXAM 2 - LAM (4 decks)

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