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Phase 1 > Boothe Antibiotics and GI drugs > Flashcards

Boothe Antibiotics and GI drugs Flashcards

1
Q

stimulating neurotransmitters of the GI

A

dopamine
GABA
norepinephrine

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2
Q

inhibitory neurotransmitters of the GI tract

A

serotonin
calcitonin
cholecystekinin
corticotropin releasing factor

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3
Q

Leptin role

A

communicates about fat reserves
induces satiety and inhibits NPY
Increases alpha MSH

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4
Q

adiponectin role

A

influences lipid and carb metabolism necessary for insulin action
necessary for insulin’s actions - increases tissue glucose use, decreases hepatic glucose formation

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5
Q

What are the two orexigenic (appetite stimulating) peptides?

A

NPY - neuropeptide Y

AgRP - Agouti related protein

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6
Q

What are the anorexigenic peptides (appetite suppressing)

A

POMC - pro opiomelanocortin

alpha MSH - alpha melanocyte hormone

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7
Q

ASP role

A

increases glucose uptake, triglyceride synthesis and storage
decreases in periods of fasting
may stimulate insulin secretion
produced by complement factor C

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8
Q

What is the role of Ghrelin

A

opposes leptin
increases food intake
decreases energy expenditure

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9
Q

Mirtazapine

A

piperazino-azeprine anti depressant
5-HT (serotonin) agonist
inhibits serotonin reuptake

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10
Q

Benzodiazepine as an appetite stimulant

A

gabaminergic and inhibits satiety at the hypothalamus

remember that diazepam can cause an idiosyncratic hepatic toxicity in cats

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11
Q

cyproheptadine

A

anti histamine
inhibits serotonergic receptors
don’t understand why but it is a serotonin antagonist that increases appetite in cats (so opposite of mirtazapine that agonizes serotonin but serotonin is considered an inhibitory NT so who knows)

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12
Q

megestrol

A

the only treatment for human cachexia
stimulates appetite by antagonizes TNF alpha, IL1, IL6, INT-gamma
thromboembolic - it is a synthetic progesterone

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13
Q

Listat

A

pancreatic lipase inhibitor

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14
Q

dirlotapide

A

brand name silentrol
microsomal triglyceride transfer protein that blocks the assembly and release of lipoprotein particles into blood
appetite is suppressed locally at the GI and less fat is absorbed

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15
Q

differences between the emetic center and the chemoreceptor trigger zone? BBB, proximity to neuro tracts, stimulants

A
  • emetic center is protected by the BBB, near the nucleus tractus solitarius of the vagus nerve and stimulated with afferent peripheral and central signals
  • the chemoreceptor triger zone (CRTZ) is close to the emetic center but is NOT protected by the BBB, stimulated mainly by blood borne chemicals
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16
Q

what neurotransmitters does the nucleus solitarius respond to?

A

enkephalin
histamine (that is how you vomit from motion sickness, histamine release from CN VIII)
serotinin
Ach

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17
Q

how does Ach influence emesis?

A

Ach is the main agent mediating afferent limb of emesis from peripheral causes
muscarinic receptors initiate impulses through the vagus
dopamine receptors inhibit stomach motility

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18
Q

where does apomorphine act to induce emesis

A

acts on D2 dopamine receptors at the CRTZ

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19
Q

where and how does maropitant inhibit emesis

A

acts at the emesis center with NK receptor antagonism blocking the action of substance P
effective and safe for peripheral and central stimulated causes of vomiting (because it works at the emesis center so the highest you can go and it is specific)
can cause bone marrow hypoplasia in patients less than 11 weeks

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20
Q

how do anti histamines inhibit vomiting

A

blocks histamine release in the vestibular apparatus

may be able to penetrate the BBB and then will act on the emesis center too

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21
Q

how does phenothiazine (like acepromazine) act as an anti emetic

A

acts in the CRTZ

antidopaminergic

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22
Q

how does metoclopramide inhibit emesis

A

acts at the CRTZ
5HT3 antagonist, 5HT4 agonist
increases lower esophageal sphincter tone
anti dopaminergic

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23
Q

how does ondansetron act as an anti emetic

A

acts at the CRTZ
serotonin antagonist
specific and safe

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24
Q

how does cyproheptadine act as an anti emetic?

A

anti histamine, anti serotonin

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25
Q

how does metoclopramide act as a pro motility drug

A

central and peripheral anti dopaminergic effect
increases LES tone
increases the force and frequency of gastric antral contraction
relaxes pyloric sphincter
promotes peristalsis in duodenum and jejunum
affects other drugs’ bioavailability

26
Q

how does domperidone act as a promotility agent?

A

dopamine antagonist
similar to metoclopramide but does not cross BBB
activity at the CRTZ
coordinates antrodudodenal contractions

27
Q

how does cisapride act as a promotility drug

A

activity at all GI sites stimulates 5HT4 receptros

can cause blockage of K+ and prolong QT interval then lead to Torsade de pointes

28
Q

what is the clinical relevance of the MIC being close to Cmax?

A

the closer the MIC or MIC 90 is to Cmax, the greater the risk of therapeutic failure. Cmax is the very maximum concentration the antibiotic can achieve

29
Q

what is the difference between alpha and beta hemolytic strep

A

in alpha strep, the Hb of RBC is reduced

in beta strep, the RBC are markedly disrupted and that makes beta strep more pathogenic

30
Q

What does it mean for a MIC to be less than the breakpoint made by CLSI for a parent antibiotic?

A

if the MIC is less than the breakpoint, the bacteria is susceptible

31
Q

what is the difference between the MIC and the MBC?

A

minimum inhibitory vs minimum bactericidal. MBC is the concentration that kills whereas MIC is the concentration that stops growth. if the MBC and MIC are pretty similar, that antibiotic is bactericidal

32
Q

name five broad classes of cidal antibiotics

A 
beta lactams
glycopeptides
polymyxin B
colistin
fluoroquinolones

abx that target cell walls or membranes, DNA = usually cidal

33
Q

name four families of bacteriostatic drugs

A

tetracyclines
macrolides
lincosamides
sulfonamides

Usually drugs that target single ribosomal subunit

34
Q

what defines the PAE in vivo?

A

PAE is the post antibiotic effect
in vivo, it is the time it takes for the number of CFU’s to increase 10 times following a concentration drop below the MIC

35
Q

what is the MPC

A

mutant prevention concentration
if the MPC is achieved instead of MIC, resistance is minimized
if a population of bacteria reaches more than 10^8, more likely to mutate

36
Q

How does the Cmax relate to MIC for concentration dependent drug efficacy?

A

Cmax must be 10-12x greater than MIC

37
Q

how does the plasma drug concentration relate to the MIC for time dependent drugs to be effective?

A

plasma drug concentration (PDC) needs to be 2-4x the MIC for the majority of the dosing interval

38
Q

what are the three D’s to reduce resistance

A

de-escalate
design a treatment plan to minimize use
decontaminate

39
Q

characteristics of beta lactams - MOA, time vs concentration dependent, spectrum, subclasses

A
  • MOA - incorporates into actively growing cell wall –> osmotic lysis of cell, inhibits the transpeptidase enzyme - the penicillin binding protein
  • time dependent
  • good gram positive, some anaerobes, weak gram negative
  • does not work well in hypertonic environments
  • penicillins, carbapenems, cephalosporins
  • weak acids
  • eliminated by the kidneys only - will accumulate in urine
  • cannot cross BBB except for imipenem, cannot cross mammary or prostatic tissue
40
Q

characteristics of penicillins

A

beta lactam with good G+ and anaerobe coverage, not great G-

extended spectrum has activity against pseudomonas

41
Q

characteristics of carbapenems

A

beta lactam that is pretty resistan to beta lactamases
although beta lactams are time dependent, carbapenem is effective enough that the PDC only needs to be 2-4x higher than MIC for 25% of the time

42
Q

generations of cephalosporins

A

all are ineffective against enterococcus

  1. good G+ and G-, okay anaerobe - cephalexin (best for staph), cefazolin (good for G-)
  2. more G- but a little less G+, good anaerobe - cefoxitin, cefaclor, cefamandole
  3. longer half lives, good against Pseudomonas, enterobacter and serratia - ceftiofur, cefotaxime, ceftazadime, cefpodoxime,
43
Q

What are ways that bacteria can be resistant to beta lactams

A
  • many staph have beta lactamases
  • efflux pumps
  • pseudomonas changes porins
  • enterococcus and MRSA (via the mecA gene) have changes in their penicillin-binding protein
44
Q

characteristics of glycopeptides: main example, MOA, time or concentration dependent, spectrum, excretion, adverse effects

A
  • vancomycin is the main example
  • time dependent and cidal
  • inhibits cell wall elongation
  • effective against staph, strep, anaerobes, some enterococcus, clostridium, corynebacterium
  • renal excretion
  • potential for nephrotoxicity, hypersensitivity, ototoxicity
45
Q

characteristics of phosphoric acid derivative: main example, MOA, time or concentration dependent, spectrum, excretion, adverse effects

A
  • fosfomycin
  • inhibits phosphopenolpyruvate transferase, which is needed for peptidoglycan cell wall synthesis
  • concentratoin dependent
  • has negligible protein binding
46
Q

characteristics fo aminoglycosides: main example, MOA, time or concentration dependent, spectrum, excretion, adverse effects

A
  • amkicacin, gentamycin, neomycin (most nephrotoxic), streptomycin (least nephrotoxic)
  • one of the few abx that targets ribsosome and is cidal - targets 30s ribosome to inhibit protein synthesis
  • concentration-dependent - because it causes an irreversible binding of the drug to the 30s ribosome subunit
  • great for aerobic gram - like E coli, klebsiella, pseudomonas, serratia
  • activity will decrease if combined with another ribosomal binder, synergistic with cell wall antibiotics
  • decreased efficacy in acidic environments but in basic pH gets reabsorbed
  • renal tubular cells sequester in lysosomes, you can see increased gamma glutamyl transferase levels with renal tubular damage
47
Q

characteristics of fluorinated quinolones: main example, MOA, time or concentration dependent, spectrum, excretion, adverse effects

A
  • enrofloxacin, ciprofloxacin
  • directly inhibits DNA synthesis by targeting DNA gyrase (topoisomerase II and IV)
  • irreversibly binds to topoisomerase so concentration dependent
  • second generation includes cipro - broad G- and some G+
  • third generation includes levofloxacin - increased spectrum to include some anaerobes
  • fourth generation includes trovafloxacin and has the broadest spectrum - really just human use
  • effective agains a number of G- bugs
  • resistance is mediated by a mutation in target topoisomerase, decreased porin expression increased efflux, decreased lipids in LPS, plasmid mediated horizontal transmission of qnr gene
  • anatagonistic with ribosomal inhibitors
  • inhibits GABA receptor binding
  • can impair hepatic metabolism and prolong the effect of some drugs
  • chelates with Mg and Ca which leads to cartilage deformity and delay in tendon/ligament repair
  • dose dependent retinal degeneration
  • streptococcal TSS in necrotizing fasciitis
48
Q

characteristics of macrocyclic: main example, MOA, time or concentration dependent, spectrum, excretion, adverse effects

A
  • rimfampin
  • MOA: inhibits beta subunit of DNA dependent RNA polymerase –> suppress RNA synthesis
  • mostly bactericidal
  • mostly considered concentration dependent
  • highly protein bound, lipid soluble
  • induces microsomal enzymes that affect metabolism of other drugs - increased risk of toxicity with MDR1 dogs
  • resistance easily occurs so use with other antibioitcs
  • turns urine, plasma, tears all orange
  • excreted in bile
49
Q

characteristics of metronidazole: MOA, time or concentration dependent, spectrum, excretion, adverse effects

A
  • secreted by a streptomycete
  • MOA: impairs microbial RNA and DNA synthesis
  • prodrug - needs to undergo nitrous reduction inside the organism
  • cidal
  • concentration dependent
  • can penetrate BBB
  • good against anaerobes like clostridium, okay against G+ anaerobes, no aerobe actitivy because they don’s have the electron transport necessary to convert it from the pro drug form
  • eliminated by the liver
  • can discolor urine red/brown
  • can cause drug interactions by inhibiting the metabolism of cimetidine and inducing the metabolism of prednisone, rifampin, phenobarb
50
Q

characteristics of sulfonamide/trimethoprim: MOA, time or concentration dependent, spectrum, excretion, adverse effects

A
  • MOA of sulfonamide - competitive inhibitor of synthetase enzyme (PABA) = inhibition of folic acid synthesis
  • MOA of trimethoprim (a diaminopyrimadine) - inhibit reductase enzyme = decreased folic acid precursor
  • together, they are cidal but alone they are static
  • time dependent
  • good against most G+, G- and anaerobes but not good against pseudomonas
  • resistance is mostly plasmid mediated
  • eliminated in urine
  • dogs have decreased N acetylation which makes them more susceptible to toxicity
  • two drug reactions: type A is dose dependent and will cause thyroid suppression, aplastic anemia, and crystalluria. Type B is immune mediated and will cause KCS, thrombocytopenia, arthropathy, hepatopathy
  • Doberman arthropathy is most at risk breed
51
Q

characteristics of tetracyclines: main example, MOA, time or concentration dependent, spectrum, excretion, adverse effects

A
  • doxycycline, minocycline (these have high liposolubility and can cross BBB)
  • bacteriostatic
  • MOA - bind to 16s portion on 30S ribosomal subunit = can’t add amino acids
  • time dependent
  • accumulates in reticuloendothelial cells
  • can become incorporated in enamel and discolor teeth
  • minocycline is excreted in bile only
  • doxycycline in the GI and kidneys
  • all others in kidneys, GI, and bile
  • can chelate cations
  • rarely can cause hepatotoxicity, Fanconi syndrome, esophageal erosion in cats
52
Q

characteristics of phenicols: main example, MOA, time or concentration dependent, spectrum, excretion, adverse effects

A
  • chloramphenicol
  • MOA - binds at 50s ribosomal subunit and inhibits peptidyl transferase
  • effective against G+, G-, anaerobes
    resistance is from bacteria causing acetylation
  • bacteriostatic
  • time dependent
  • can cause bone marrow suppression (dose-dependent and independent), particularly in cats
  • hepatic metabolism, needs to be glucoronidated but will inihibit hepatic metabolism of other drugs
  • don’t use with macrolides or they will compete for 50s subunit
  • synergistic with beta lactams because chloramphenicol will inhibit beta lactamases
53
Q

characteristics of lincosamides: main example, MOA, time or concentration dependent, spectrum, excretion, adverse effects

A
  • clindamycin
  • static
  • time dependent
  • MOA: inhibit 50S ribosomal subunit to stop peptidyl transferase
  • aerobic G+, nocardia, anaerobes, mycoplasma
  • accumulates in WBC so decent biofilm penetration
  • eliminated in bile
  • okay penetration in CSF and brain
  • can lead to clostridial overgrowth when combined with chloramphenicol or erythromycin
54
Q

characteristics of macrolides/azalides: main example, MOA, time or concentration dependent, spectrum, excretion, adverse effects

A
  • mostly static but it is cidal for strep
  • time and concentration-dependent - depends on the species
  • MOA - bind 50s ribosomal subunit - binds in 2 placse
  • erythromycin covers G+, Pasteurella, bordetella, mycoplasma
  • azithromycin covers less G+ more G-
  • resistance is caused by efflux pumps, altered ribosomal target, enterobacter producing esterase that hydrolyzes the antibiotic
  • inhibits cytochrome P450
  • eliminated in bile, except for clarithro that is metabolized in liver
  • tylosin and ketolide are also examples
55
Q

characteristics of oxazolidinones: main example, MOA, time or concentration dependent, spectrum, excretion, adverse effects

A
  • linezolid
  • binds to P site of 50s and 70s ribosomal subunits
  • cidal
  • enterohepatic recycling and renal excretion
  • can cause myelosuppression and neurotoxicity
  • spectrum includes G+, enterococci, anaerobes, nocardia, actinomyces
56
Q

characteristics of daptomycin: main example, MOA, time or concentration dependent, spectrum, excretion, adverse effects

A
  • MOA - bind to cell membrane
  • good for G+ and anaerobes
  • cidal
  • concentration dependent
  • renal excretion
57
Q

characteristics of fusidic acid

A
  • MOA - interferes with ribosomal translocation
  • good G+ coverage
  • cidal
  • rapid resistance if used alone
58
Q

characteristics of bacitracin

A
  • inhibits peptidoglycan synthesis
  • G+ and a few G -
  • for topical use only! nephrotoxic systemically
59
Q

characteristics of Polymyxin

A
  • cidal
  • gets mostly G-
  • eliminated by the kidneys
  • systemically would be nephrotoxic
  • associated with pemphigus vulgaris
60
Q

characteristics of novobiocin

A
  • G+ and G-
  • MOA: cell membrane and wall synthesis disruption
  • if given systemically, will cause bone marrow suppression, nausea, vomiting, diarrhea
61
Q

characteristics of mupirocin

A
  • inhibits protein synthesis
  • aerobic G+ and some G-
  • no much resistance yet
62
Q

characteristics of nitrofurans

A
  • static
  • 50% eliminated in urine in active form
  • inhibits oxidative reactions necessary for formation of bacterial acetyl coenzyme A
  • can cause GI toxicity, peripheral neuropathy

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