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MEP2 Pharmacology Midterm > Lecture 5 -2nd half > Flashcards

Lecture 5 -2nd half Flashcards

1
Q

slide 38

A
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2
Q

slide 39

A
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3
Q

What to know to select correct treatment:

A

-identify organism
-susceptibility of organisms to a give mobile agent
-client factors (regnanct, allergies, breastfeeding)
-safety of drugs
-cost of drug

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4
Q

Gram negative:

A

-thin peptidoglycan layer
-has outer lipid layer that has LPS: harder for antibiotics to penetrate LPS layer
-gram stain pink

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5
Q

Gram Positive:

A

-thick layer of peptidoglycan
-no outer lipid layer
-gram stain purple

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6
Q

Gram variable Bacteria:

A

-not clearly pink or purple gram stain (both)
-mobiluncus spp, and gardnerella vaginalis which are typical associated with bacterial vaginosis are gram variable
-it’s likely BV if not yeast

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7
Q

slide 44 labelling gram + vs -

A
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8
Q

mobiluncus and gerdnerella

A

mobiluncus = gram - with thin peptidoglycan cell wall and an outer membrane

gernerella = gram + with thick cell wall and absence of external membrane

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9
Q

Susceptibility to Antimicrobial Agents:

A

-antibiotic resistance rapidly increased (superbugs, MRSA as examples)
-how to avoid:
1.Use antibiotics properly and avoid when possible
2.Start with narrow-spectrum (narrow treats single group of microbes, extended/medium treat more globally, broad spectrum is a wide range)
3.Culture and sensitivity tests (helpful with drug allergies)
4.Counsel clients appropriately (complete entire course of treatment)

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10
Q

-**slide 47 = white circles are different antibiotics, yellow is bacteria. Circles with big green circles are effective antibiotics for that specific bacteria

A
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11
Q

Antibiotic Resistance:

A

-occurs when antibiotics that have historically killed a given strain of bacteria no longer work
-arises from alteration sin bacterial DNA (mutations or takes on DNA from another strain)

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12
Q

Antibiotic Resistance Mechanisms:

A

-microbes can become antibiotic resistant by take DNA from another drug resistant strain (horizontal gene transfer)
-drug resistance genes often coded on plasmid dna

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13
Q

horizontal gene transfer occurs in 3 ways:

A
  1. transformation
    -pieces of dna are taken up from the external environment
  2. conjugation
    -transfer of plasmid dna via direct cell to cell contact (via a pilus)
  3. transduction
    -a bacteriophage (virus that infects bacteria) performs the gene transfer
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14
Q

slide 50 antibiotic resistance mechanisms

A
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15
Q

Antibiotic Resistance Types:

A
  1. Enzymatic inactivation of antibiotic
    -most common mechanism
    -bacteria make enzymes that metabolize antibiotics
    -ex beta-lactamases
  2. Decreased antibiotic uptake
    -gram - organisms can be resistant to some antibitoics as drug cannot pentrate outer cell membrane
    -decrease number of porins
    -ex cephalopsporins
  3. increased antibiotic efflux
    -energy dependent pumps transport the drug out of cells
    -ex quinolones
  4. modification of antibiotic targets
    -receptors for drugs, target molecules, enzymes are modified
    -ex. s. aureus became resistant to methicillin because the penicllin-binding protein changed shape
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16
Q

slide 52 antibiotic resistance - types

A
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17
Q

Antibiotics:

A

-anti life - inhibit growth of bacteria without hammering host

-bacteriocidal = kill directly, ex penicillins make holes in bacteria, bacteria die, immune system clears up the cellular fragments

-bacteriostatic = stop growth or division of bacteria
-need an actively fighting immune system to resolve the infection

18
Q

slide 54 modes of antibiotic action

A
19
Q

cell wall synthesis inhibitors

A

-peptidoglycan cell wall is in bacteria is made of a carbohydrate backbone linked together by amino acid side chains and cross bridges

-the beta-lactam antibtioics (ex peniciilins and cephalosporins) inhibit the formaion of the peptide cross-bridges

-the peptidoglycan cell wall is thus incomplete and weakened, and the cell may undergo autolysis

20
Q

slide 56 cell wall synthesis inhibitors

A
21
Q

slide 57 protein synthesis inhibitors

A
22
Q

Protein synthesis inhibitors - 50s subunit

A

50s subunit
-clindamycin
-macrolide class - azithromycin and erythromycin

23
Q

Protein synthesis inhibitors - 30s subunit

A

30s subunit:
-aminoglycoside class - gentamicin
-tetracycline class - doxycycline

-trna interference:
-mupirocin (part of apno)

24
Q

dna synthesis inhibitors

A

fluroquinolones inhbit dna synthesis:
-most common is cirprofloxacin
-gets inside bacteria via porins and inhibits DNA gyrase
-dna gyrase is the enzyme responsible for relaxing/uncoilin DNA so it can be replicated

nitrofurantoin is a prodrug:
-activated by susceptible bacteria when excreted into urine
-reactive intermediates have many functions, including inhibit bacterial DNA synthesis but also:
inhibit protein synthesis, inhibit aerobic energy metabolism, inhibit RNA synthesis, inhibit cell wall synthesis

25
Q

bacterial dna synthesis slide 60

A
26
Q

folate synthesis inhibitors slide 61

A
27
Q

why do we care about folic acid in humans

A

-need dietary folic acid to make bases for DNA (we dont make our own folic acid)
-without proper bases, dna cant divide
-if dna cant divide then cells cant divide
-since the neural tube is formed very early in development and requires tons of cell division, deficiency in folic acid leads to nerual tube defects (aren’t enough cells to close the neural tube properly)

28
Q

folic acid in bacteria

A

-principle is the same as in humans except that bacteria make their own folic acid
-use p-aminobenzoic acid (PABA) for de novo synthesis

29
Q

fungal anatomy

A

-usually multicallular eukaryotic organsims
-cells have cell walls containting chitin (as oposed to cellulose or peptidoglycan)
-cannot make their own food (heterotrophic) and obtain nutrients from organic material
-most infections (actually more of a dysbiosis) in the midwifery context are caused by candida albicans
-this is a yeast that lives in the resp., gi and repro tracts
-member of the family ascomycota, part of the normal human microbiome

30
Q

antifungals

A

-inhibit growth of fungi without harmin host
5 classes: azoles, polyenes, echinocandins, allylamines, pyrimidine analogs
-effective against candida species

31
Q

antifungals on 188/24

A

azoles:
-clotrimazole (cannesten)
-fluconazole
-miconazole (monistat)

polyenes:
-nyastatin

32
Q

Azoles

A

-are an antifungal
-inhibit sterol 14alpha-demethalase
-essential enzyme in sterol biosynthesis
-prevents the formation of ergosterol - a vital component in fungal cell membranes

33
Q

polyenes

A

-an antifungal
-acts on the fungal cell membrane through hydrophobic interactions
-sequester membrane sterols, creating membrane pores - cell death

34
Q

slide 65

A
35
Q

slide 66

A
36
Q

nipple pain

A

-all purpose nipple ointment APNO
-mupirocin-betamethasone valerat-miconazole
-mupirocin = a topical antibiotic
-betamethasone valerate = a steroidal anti-inflammatory
-miconazole = antifungal, effective against yeasts and also some gram + bacteria
-ibuprofen can be added for pain relief PRN
-made at compounding pharmacy

37
Q

slide 70 APNO prescription

A
38
Q

APNO - mupirocin (topical)

A

-mupirocin inhibits protein production in cell (inhibits trna production)
-can be absorbed by the infant PO but majroty sticks to nipple
-often suspended in polyehtylene glycol (PEG) - some people have allergies to PEG

39
Q

APNO - betamethasone valerate (topical)

A

-high potency steroidal anti-inflammatory
-purpose in apno is to decrease pain caused by tissue inflammation
-side effects from long-term use, not in short term topical use

40
Q

APNO - miconazole

A

-antimycotic/antifungal - inhibits formation of ergosterol which is necessary for fungal cell walls
protection against thrush
-effective against some gram + bacteria - useful as staphylococcus may lead to mastits in an inflammed cracked areola/nipple
-side effects (unlikely as less than 1% absorbed into maternal cicrualtion)
-on skin - stinging, eryhtmea and local irritaion, contact dermatitis is rare
-unclear how much reaches baby when breastfeeding

41
Q

APNO - ibuprofen

A

-and dont forget ibuprogen can be added
-practioners vary on their managment regarding when they add to the prescription
-ibuprofen is an NSAID
-inhibits inflammation by inhibiting the cox enzymes in the prostaglandin pathway

MEP2 Pharmacology Midterm (12 decks)

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