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NUNP 532 Pharmacology > ANTIMICROBIALS from lecture slides > Flashcards

ANTIMICROBIALS from lecture slides Flashcards

1
Q

Why are nitrites relevant to urinalysis for UTI?

What is the other main identifier in a urinalysis for UTI?

A

Formed when gram neg bacteria in urine break down nitrates

Leuks

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2
Q

Which drugs are beta-lactams?

A

Penicillins
Cephalosporins
Carbapenems
Monobactam

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3
Q

Common glycopeptide?

A

Vancomycin

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4
Q

Name 2 tetracyclines

A

tetracycline, doxycycline

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5
Q

Name 2 macrolides

A

erythromycin, clarithromycin

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6
Q

Name 3 aminoglycosides

A

gentamicin, streptomycin, neomycin

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7
Q

Bacteriostatic vs bacteriocidal?

A

Bacteriostatic antibiotics work by stopping replication/proliferation of
bacterial cells. Bactericidal antibiotics kill bacteria.

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8
Q

Gram positive bacteria AKA?
Describe the outer layers of these bacteria

A

Monoderm bacteria

bound by a single-unit lipid
membrane, and, in general, they contain a thick layer (20–80 nm) of peptidoglycan responsible for
retaining the Gram stain

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9
Q

Describe the composition of gram negative bacteria

AKA?

A

Diderm bacteria

Bounded by a cytoplasmic membrane and an outer cell membrane. They contain only a thin layer of peptidoglycan (2–3 nm) between these
membranes. The presence of inner and outer cell membranes defines a new compartment in these
cells: the periplasmic space (periplasmic compartment).

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10
Q

WHat happens when you try to gram stain atypical bacteria?

A

Atypical bacteria do not have a peptidoglycan layer at all and therefore do not retain the violet
colour with Gram staining

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11
Q

Staphylococcus & streptococcus - are they gram pos or negative?

A

Both gram positive cocci

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12
Q

Clostridium and Listeria - are these gram pos or neg?

A

Positive bacilli

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13
Q

Neisseria meningitidis and Neisseria Gonorrhoeae - gram pos or neg?

A

Negative (cocci)

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14
Q

H influenzae and B. Pertussis - pos or neg?

A

Negative

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15
Q

Kiebsiella
E. Coli

Pos or neg?

A

Neg

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16
Q

Pseudomonas
Shigella
Salmonella
Proteus

Pos or neg?

A

Negative

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17
Q

What is the #1 cause of atypical pneumonia?

A

Mycoplasma pneumoniae

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18
Q

2 other illnesses that result from atypical bacteria?

A

Chlamydia & Rickets

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19
Q

Bacteria (whether inherent in a human or, introduced) must reproduce/replicate or
proliferate in order to become problematic in the body.

Growth of bacteria is defined as the increase in _______

A

cell number.

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20
Q

Process by which bacteria replicate?

A

Binary fusion (fission)

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21
Q

3 processes by which bacteria proliferate?

A

Conjugation, transformation & transduction

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22
Q

What kind of infection typically causes eruptions of fluid or pus filled pustules

A

bacterial

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23
Q

What kind of infection is this: bright red, may be darker around the
border of the affected area, may be scaly and may also have pustules (esp. around
the edges of the affected area;

A

Fungal

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24
Q

Describe typical presentations of parasitic infection

A

typically have a defined edge and scaley, dry. Some parasites
however, are living and can be seen moving whilst their eggs are laid in the skin
and appear as pustules or are attached to hair.

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25
Q

WHere do fungi like to live in the body?

A

Warm, moist areas :)

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26
Q

Where in the body are bacteria more prevalent?

A

Areas exposed to the environment

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27
Q

What areas of the body are parasites more prevalent?

A

areas where there is hair growth and, exposed to the environment

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28
Q

MOA of β-lactam abx?
Describe how it alters bacterial structure (in gram pos bacteria)

A

All β-lactam antibiotics inhibit bacterial growth by interfering with the transpeptidation
reaction of bacterial cell wall synthesis, killing the cell.

The cell wall of the bacteria has a rigid outer layer that completely surrounds the
cytoplasmic membrane, maintains cell integrity, and prevents cell lysis (death) from
high osmotic pressure.
● The rigidity of the cell is maintained by a binding protein that allows a cross-link to
be formed with nearby peptides.
● β-lactam antibiotics work by covalently binding to the site of the binding enzyme
and stopping the cross-linking reaction and thereby weakening the cell wall
(eventually causing its death).

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29
Q

Are beta-lactam abx effective against gram neg, pos, or botg?

A

BOTH

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30
Q

Describe how beta-lactam abx kill gram neg cells?

A

; they enter the
periplasmic space via a porin (opening) in the
outer cell membrane to interrupt the
Peptidoglycan reaction and disrupt cell wall
integrity.

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31
Q

4 major classes of beta lactams?

A

1) Penecillins
2) Cephalosporins
3) Carbapenems
4) Monobactams

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32
Q

Beta lactams: The kinetics of this class of antibiotics is influenced by each drug’s _____ and ______

A

acid
stability and protein binding.

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33
Q

Are tetracyclines bacteriostatic or cidal?

A

Mostly static, few are bacteriocidal

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34
Q

MOA of tetracyclines?

A

t-RNA inhibitors

work by
binding to 50S subunits and blocking
peptide bond formation or, to the 30S
subunit and preventing binding of the
incoming tRNA unit stopping replication.

From internet: exert their bacteriostatic effect by inhibiting protein synthesis in bacteria. This antibiotic prevents transfer- RNA (tRNA) molecules (a type of nucleic acids which transport amino acids) from binding to the 30S subunit of bacterial ribosomes

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35
Q

Are tetracyclines effective against gram pos, neg or both

A

both

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36
Q

How is tetrcycline different in terms of how it interacts with the GI tract?

A

A portion of an orally administered dose of tetracycline remains in the gut lumen alters
intestinal flora and is excreted in the feces

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37
Q

Where does absorption of most of a tetracycline occur?

A

upper small intestine

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38
Q

How is absorption of tetracyclines affected by food and other changes in pH?

A

Absorption impaired by food, antacids and
alkaline pH

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39
Q

Are tetracyclines safe for pregnant women and newborns?

A

NO
Tetracyclines are distributed widely to tissues in the body fluids, they cross the placenta and are
also excreted in breast milk.

Tetracyline exposure in
utero puts the child at risk of hypomineralization (affects enamel) and
yellow staining

Tetracycline binds calcium during mineralization

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40
Q

MOA of macrolides

A

Cidal & static

inhibits protein synthesis via binding to the bacteria’s 50S ribosomal
RNA.

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41
Q

Macrolides - effective against gram neg, pos, or both?

A

BOTH

42
Q

Name of macrolide drugs?

A

Erythromycin, clarithromycin

43
Q

GI considerations for taking erythromycin?

A

Erythromycin (and its derivatives) must be administered for oral use with an enteric coating;
much of the erythromycin base is destroyed by stomach acid. Food also interferes with
absorption.

44
Q

Does erythromycin have many side effects? How does it affect other drugs?

A

Side effects are common with oral and intravenous use. Erythromycin in particular inhibits
cytochrome P450 enzymes thus increasing the concentrations of other drugs

45
Q

MOA of aminoglycosides

A

Aminoglycosides are bactericidal drugs that work by inhibiting protein synthesis and
interfere with ribosomal function

46
Q

List some aminoglycosides

A

streptomycin, neomycin, kanamycin, amikacin, gentamicin,
tobramycin, sisomicin, netilmicin etc.

47
Q

Aminoglycosides - gram neg, pos or both?

A

GRAM NEGATIVE

48
Q

Aminoglycosides are almost always used in combination with what other antibiotics?

A

they are
almost always used in combination with a B-lactam antibiotic to extend empiric
coverage and to take advantage of the potential synergism between these two classes
of drugs. In fact, penicillin-aminoglycoside combinations are quite effective for critically
ill patients.

49
Q

Are aminoglycosides effective PO meds?
Stable at alkaline or acidic pH?

A

The drugs are water-soluble, stable in
solution and more active at alkaline
than acid pH.

Unfortunately, aminoglycosides are
absorbed very poorly from the intact GI
tract and almost the entire oral dose is
excreted in feces after oral
administration hence, aminoglycosides
are usually administered IV as a 30-60
minute infusion.

50
Q

What are our 3 classifications of antifolate drugs?

A

1) Sulfonamides 2)trimethoprim 3) Quinolones

51
Q

MOA of antifolate drugs?

A

Folate is essential in bacteria for the production of purines and nucleic acid synthesis. Bacteria cannot use exogenous folate and must synthesize it from PABA

Sulfonamides (and other antifolate drugs) inhibit bacteria and some protozoa by inhibiting folate production
within the organism making it unable to replicate.

52
Q

Antifolates - gram neg, pos or both?

A

BOTH

53
Q

What happens when you give Rickettsiae sulfonamides?

A

They are stimulated & grow more!

54
Q

Sulfonamides come in 3 forms with regard to pharmacokinetics. What are they?

A

a) Oral absorbable (absorbed in the stomach and small intestine and distributed
widely to tissues and body fluids, placenta, and fetus).
i) Sulfamethoxazole
ii) Sulfadiazine
iii) sulfadoxine

a) Oral non-absorbable
i) Sulfasalazine

a) Topical
i) Sulfacetamide
ii) Mafenide acetate
iii) Silver sulfadiazine

55
Q

Describe metabolism/excretion of sulfonamides. What’s an important consideration in this regard?

A

A portion of absorbed drug is acetylated or glucuronidated in the liver

Sulfonamides and inactive metabolites are excreted in the urine mainly by glomerular filtration hence, those patient with significant kidney disease will require adjusted (reduced) doses.

56
Q

TRIMETHOPRIM - MOA

A

Antifolate drug
These drugs selectively inhibit the
process leading to synthesis of purines
and ultimately DNA in bacteria.

In combination with sulfamethoxazole,
these drugs are often bactericidal.

57
Q

By what route do we administer trimethoprim? How is it excreted?

A

Trimethoprim can be given orally or IV
either alone, or in combination with
sulfamethoxazole. Trimethoprim is excreted in the urine
within 24hrs. For patient with reduced
kidney function, dosage should be
reduced.

58
Q

The half life of quinolones is highly variable (3-10 hours). What does this mean for dosing?

A

consideration is required
with dosing to avoid toxicity or under
dosing.

59
Q

Quinolones MOA

A

Quinolones are effective against a
variety of gram negative and gram
positive bacteria by way of blocking DNA
synthesis and inhibiting DNA
transcription and replication of bacteria.

60
Q

Trimethoprim is often combined with what drug?

A

Sulfamethoxazole

61
Q

What is Metronidazole? MOA?

A

antiprotozoal drug that has potent antibacterial activity against
ANAEROBES

Once taken up by anaerobes, it is reduced by reacting with ferredoxin with results in
products that accumulate in and are toxic to anaerobic cells.
The metabolites of metronidazole are taken up into bacterial DNA forming unstable molecules.

(Summary of this on the table she posted is “inhibits DNA synthesis, breaks down DNA”)

62
Q

Is metronidazole bacteriostatic or cidal?

A

cidal

63
Q

What particularly nasty bacteria is killed by metronizadole?

A

C Diff

64
Q

Is metronidazole also effective against aerobic bacteria

A

No, only anaerobic

65
Q

How do we administer metronidazole?
What kind of organ dysfunction might lead to toxicity for this drug?

A

Metronidazole is well absorbed after oral administration, widely
distributed in tissues and raches serum levels after one 250 mg oral dose.

It is metabolized in the liver and may accumulate in hepatic insufficiency.

66
Q

What kind of drug is benzoyl peroxide?

A

Antibiotic and keratolytic

67
Q

MOA of benzoyl peroxide

A

● Suppresses the growth of P.acnes through release of active oxygen
● Can also reduce inflammation and promote keratolysis (peeling of the
horny layer of the epidermis)
● Metabolized at the skin - converted to benzoic acid

68
Q

2 major classes of antifungals?

A

azole drugs and the echinocandins

69
Q

MOA of azoles?

A

Inhibit the biosynthesis of ergosterol, an essential component of the fungal cytoplastic membrane

70
Q

Are the azoles topical or systemic treatments?

A

There are 12 members of the azole family and most are topical (3 can be
used systemically for mycoses).

71
Q

What are the azoles active against? Broad or narrow spectrum?

A

Active against a broad spectrum of fungi including dermatophytes and Candida species

72
Q

How is azole absorption affected by food? Should meals be eaten with these meds when taken PO?

A

best taken with a fatty meal which enhances absorption

73
Q

MOA of echinocandins?

A

Newest class of antifungal drugs
● Disrupt the fungal cell wall.

74
Q

Can the echinocandins be given orally?

A

No, topically of IV

75
Q

Echinocandins - broad or narrow spectrum? Active against what?

A

Antifungal spectrum is narrow; Aspergillus and Candida species only

76
Q

3 members of the echinocandin family?

A

1) caspofungin (approved for IV therapy and is better tolerated than Amphotericin B)
2) micafungin
3) anidulafungin

77
Q

What is Amphotericin B? MOA?
Absorption from GI tract?

A

polyene macrolide (a drug containing many double bonds and a
large lactone ring of 12 or more atoms).

This drug is selective in its
fungicidal effect; it binds with
fungal cell membrane sterol,
Ergosterol ( not human
cholesterol)…and alters the cell
permeability by forming pores in
the cell membrane. The pore then
allows leakage of intracellular ions
and macromolecules eventually
leading to cell death.

78
Q

What organ dysfunction needs to be considered for amphotericin B?

A

renal and hepatic impairment have little impact on drug concentrations so NO dosing changes need be considered for those patients.
(trick question!)

79
Q

Absorption of Amphotericin B via GI tract…good or bad?

A

This drug is poorly absorbed from the GI tract so is effective only on fungi within the
lumen of the tract. Only utilized for severe fungal infections that are systemic

80
Q

Amphotericin B - broad or narrow spectrum?

A

Amphotericin B has the broadest
spectrum of action of all antifungal
agents.

81
Q

What are pediculicides? MOA?

A

Neurotoxins used to treat scabies and lice infestations
● Work by paralyzing and killing lice and mites by acting on nerve cell
membranes of the parasite, disrupting the sodium channel transport.
● Can also have ovicidal effects (killing eggs

82
Q

What is the difference in effect of administering low dose vs high dose steroids? Is toxicity an issue in low doses?

A

Glucocorticoid drugs can be used to maintain physiologic function when provided in low doses; when
given in high doses, these drugs produce pharmacologic effects and are used to treat inflammatory
disorders (asthma, rheumatoid arthritis) and certain cancers.

○ When used in low (physiologic) doses, glucocorticoids are devoid of toxicity (this is how they are
used for the skin

83
Q

Does topical therapy with steroids typically require weaning?

A

No, generally not doses high enough to require weaning

84
Q

Describe MOA of steroids on skin?

A

Glucocorticoid receptors are located inside the cell so glucocorticoids must penetrate the cell
membrane and then bind with receptors in the cytoplasm;

○ Binding with the receptor causes the conversion of the receptor from an inactive to active form;

○ The receptor-steroid complex migrates to the cell nucleus where it binds to chromatin in the
DNA and alters the activity of target genes;

○ Activity of the target gene (in general) is increased causing increased transcription of mRNA
molecules that code for regulatory proteins (which in effect ‘normalize’ the skin environment)

85
Q

which preparation (vehicle) of steroids provides the highest medical absorption?

A

Ointment

86
Q

When is ointment an appropriate choice for steroid preparation? What skin characteristics would be less appropriate for this application?

A

thick, greasy preparation with an oil or petroleum jelly base and little water if any

Provides an occlusive film that retains moisture so is a good choice for dry skin or thickened skin (e.g.,
lichenification) but poor choice for weeping or oozing skin conditions

87
Q

When to use a cream for steroids?

A

Cream: an emulsion of oil and water
* Not as thick as ointment but thicker than lotion
* Good for inflamed skin and dry, sensitive skin and more appropriate for intertriginous areas than
ointment

88
Q

When to use lotion for steroid application?

A

Lotion: are water based – some contain alcohol or acids which can cause a burning sensation
* Have a lighter feel than cream as little or no oil
* Easy to spread so good for large or hairy areas (e.g., intertriginous areas)

89
Q

T/F topical application of steroids won’t cause systemic side effects

A

False - it CAN

90
Q

What will affect the level of systemic absorption of topical steroids?

A

Site of application, and surface area covered, as well as solubility, also effects duration of effect and systemic effect

○ Absorption is higher in regions where the skin is especially permeable and lower in regions where penetrability is poor

91
Q

We probably don’t need to memorize this…but can you recall which steroids are highest potency vs lower potency?

A

I Clobetasol Proprionate 0.05% cream, ong, solution, foam
II Betamethasone dipropionate 0.05% cream, ong. lotion
III Betamethasone dipropionate 0.05% cream, ong, lotion
IV Mometasone furoate 0.1% cream, lotion
V Betamethasone valerate 0.1% cream, ong, lotion
VI Triamcinolone acetonide 0.025% cream, lotion
VII Hydrocortisone 0.5%-2.5% cream, solution, on

92
Q

Prescribing decision for steroid topical treatment type and vehicles depends on…

A

● Diagnosis/lesion type
● Anatomic region
● Integrity of the skin
● Total surface area involved
● Frequency and duration of treatment
● Use of aides (e.g. occlusive dressing)

93
Q

T/F If you’re using a potent steriod, it will likely be necessary to apply more than once a day. A less potent steroid only requires OD application

A

False - if potent, won’t be applying more than once a day

94
Q

What kinds of skin lesions would require high potency steroids (category I and II)?

A

High Potency (1-III): Severe dermatoses, thick plaques (non-facial/non-intertriginous)
○ Psoriasis
○ Severe and/or resistant atopic dermatitis
○ Severe poison ivy
○ Nummular eczema
○ Severe hand eczema
○ Lichen sclerosus of skin
○ Lichen planus
○ Allopecia
○ Palms/soles

95
Q

What kind of skin lesions/diagnoses would you expect to prescribe a lower potency (category V, VI, VII) steroid?

A

V Mild or moderately severe acute eczema, seborrheic dermatitis

VI Chronic eczema on thin or vascularized tissue or scalp, seborrheic dermatitis

VII Chronic eczema on thin or vascularized tissue (lids), seborrheic dermatititis

Low to Medium Potency: large areas requiring treatment
○ Diaper dermatitis
○ Eyelid dermatitis
○ Facial dermatitis
○ Perianal inflammation
○ Genital dermatitis

96
Q

What body parts would you expect to prescribe a ointment (Ong) of steroids?

A

Soles, palms, forearm flexural (extensor surface)

97
Q

What are “intertriginous areas”?

A

Areas where 2 areas of skin touch/rub on one another. Includes groin folds, axillae, and gluteal cleft…probably any skin folds?

98
Q

What body parts would you expect to prescribe a cream, lotion or paste?

A

Intertriginous areas
Eyelinds & genitalia
Face (says cream, lotion or gel)

99
Q

What is Tretinoin (Retinoids)? MOA?

A

Derivative of Vitamin A;
● Work to unplug existing comedones and prevent development of new
ones;
● Can reduce inflammation, causes thinning of stratum corneum and can
therefore improve penetration of other topical agents;
● May be used alone or in combination with other drugs including topical or
oral antimicrobial (see guideline).

100
Q

According to the Canadian guidelines, should an NP be the first to prescribe Isotretinoin (accutane) to a patient?

A

No, done by derm

101
Q

What is Isotretinoin (accutane)? What is it used for? MOA?

A

Derivative of Vitamin A
● Used to treat severe. Nodulocystic acne vulgaris
● Decreases sebum production, sebaceous gland size, inflammation and
keratinization
● Decreases ability of sebum (a nutrient for P.acnes)

102
Q

Key considerations/safety concenrs for accutane use?

A

Metabolized in liver
● Half life 21 hr
● Eliminated in urine and feces
● Requires monitoring of liver function!
● Extremely teratogenic
**Should be on contraceptive

NUNP 532 Pharmacology (26 decks)

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