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PHRM-1058 > Principles of Antimicrobial Therapy > Flashcards

Principles of Antimicrobial Therapy Flashcards

1
Q

What is the simplest and most common way to identify a pathogen?

A

gram stain

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2
Q

Why does bacteria stain differently? Gram positive will stain what color? Gram negative will stain what color?

A

structural components of the cell wall
+ : purple
- : pink/red

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3
Q

Describe acid-fast staining.

A

mycobacterium class, presumptive results, requires confirmation with cultures

stains every cell, non-acid fast bacteria become de-stained, counter stain applied (non-acid fast become blue, acid-fast become pink/red)

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4
Q

Describe India ink staining.

A

KOH, identifies fungi, cannot identify organism involved (need body fluids)

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5
Q

Describe ELISA.

A

used to identify antigens + antibodies and proteins + glycoproteins

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6
Q

Describe latex agglutination.

A

identification of antibodies of blood groups, can be used to respond to patient’s refractory to treatment

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7
Q

Name some drug factors that narrow antimicrobial agent choice.

A

availability, dosage form, cost

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8
Q

Name some host factors that narrow antimicrobial agent choice.

A

allergies, organ function, infection site, concomitant disease/therapies

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9
Q

What type of information on susceptibility is gathered using Kirby-Bauer disk diffusion?

A

qualitative

diameter of disk determines if bacteria is susceptible to resistant to antibiotic

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10
Q

Describe the E-test (MIC).

A

helps determine concentration of drug needed, minimal concentration of antibiotic needed to inhibit growth

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11
Q

Describe serial dilution of antimicrobial drugs.

A

multiple test tubes each containing a higher concentration of antibiotic, determines minimal bactericidal concentration or minimal inhibitory concentration

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12
Q

Describe drug resistance.

A

adaptive response in which microbes begin to tolerate an amount of drug that would ordinarily by inhibitory or harmful, due to genetic versatility, more virulent, can be intrinsic or acquired

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13
Q

Define intrinsic drug resistance.

A

bacteria must be resistant to any antibiotic that they produce

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14
Q

Define acquired drug resistance.

A

The adaptive response by a microbe that was previously sensitive to a drug

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15
Q

List some mechanisms of bacterial resistance.

A

enzymes that degrade antibiotics, alteration of bacterial cell walls/membranes

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16
Q

How is antimicrobial therapy achieved without harming the host cell?

A

disrupting the cellular processes or structures of bacteria, fungi, protozoa or to inhibit the virus multiplication cycle

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17
Q

List some characteristics of the ideal drug.

A

maintain potency, compliments host defences, does not negatively affect the host’s health, reasonably priced/readily available, can be quickly delivered to site of infection, remains active in tissue and body fluids, and does not contribute to microbial resistance

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18
Q

Define antimicrobials.

A

all-inclusive term for any antimicrobial drug, regardless of its origin

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19
Q

Define prophylaxis.

A

use of a drug to prevent the potential for infection of a person at risk

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20
Q

Define chemotherapeutic drug.

A

any chemical used in the treatment, relief, or prophylaxis of a disease

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21
Q

Define antimicrobial chemotherapy.

A

use of chemotherapeutic drugs to control infection (will have effect on actual organism)

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22
Q

Define synergism.

A

coordinated/correlated action by 2 microbes that results in a heightened response or greater activity

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23
Q

Define microbial antagonism.

A

microbes compete for survival in a common environment by taking actions that inhibit or destroy another organism

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24
Q

Antimicrobials can be divided into 3 different groups, what are they?

A

natural antibiotics, synthetic drugs, and semi-synthetic drugs

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25
Q

Describe broad-spectrum range of activity.

A

greatest range of activity, exert effects on cellular components which are found in most pathogens

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26
Q

Describe medium-spectrum range of activity.

A

effective on a wider range of cell types

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27
Q

Describe narrow-spectrum range of activity.

A

effective on a small range of cell types, goal of antibiotic stewardship is to prescribe this type (lower antibiotic resistance)

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28
Q

List the 5 mechanisms of drug action.

A

inhibition of cell wall synthesis, breakdown of the cell membrane structure/function, inhibition of DNA and RNA structure/function, inhibition of protein synthesis, blocking key metabolic pathways

29
Q

How do drugs affect cell wall synthesis?

A

interfere with enzymes (peptidases) that aid in the production of PG, makes the cell osmotically fragile and more susceptible to outside water/pressure

*cells unable to produce PG will not be affected

30
Q

B lactams led to the development of what class of antibiotics?

A

broad

31
Q

Chemical alterations of B-lactam ring led to development of new antibiotics, name them. (4)``

A

penicillins, cephalosporins, carbapenems, monobactams

32
Q

Describe the B lactase and B lactase inhibitor combination. What type of infection is this useful for?

A

B lactase producing bacteria inhibit the activity of penicillins
B lactase inhibitors overcome this resistance
useful for polymicrobial infections

33
Q

Natural penicillin is effective against what?

A

gram + bacteria and anaerobes

34
Q

List some adverse effects of penicillin.

A

hypersensitivity, thrombocytopenia, GI disturbances, interstitial nephritis, CNS toxicities

35
Q

List some adverse reactions so cephalosporins.

A

hypersensitivity, minor GI complaints. hypoprothrominemia flushing (nausea, thirst, palpitations, chest pain, vertigo, death)

36
Q

List some clinical uses of carbapenems.

A

broad spec: gram - bacilli, most anaerobes, gram +, MSSA, strep

37
Q

List clinical uses and adverse reaction for Monobactams (Aztreonam).

A

uses - gram - aerobic bacilli

rxn - rare rash, anaphylaxis

38
Q

Describe the action of Vancomycin.

A

prevents formation of rigid cell wall by inhibiting PG

bactericidal against gram +, bacteriostatic against enterococci

39
Q

List the clinical uses and adverse reactions of vancomycin.

A

uses - MRSA, C. diff, when treatment with other antibiotics has failed

rxn - red man syndrome, ototoxicity, nephrotoxicity

40
Q

How do drugs effect cell membrane function?

A

damage membrane which disrupts metabolic functions or cell lysis, membrane loses selective permeability and death occurs by osmosis

41
Q

What type of specificity do drugs that affect cell membrane function exhibit?

A

particular microbial groups based on differences in membrane composition

42
Q

Do drugs that affect cell membrane function inhibit PG synthesis?

A

no, may affect human cell membranes

43
Q

List the clinical uses and adverse reactions of Colistin (Colistmethate).

A

uses - systemic infections by gram - bacteria, nebulizer against multi drug-resistance P. aeruginosa and acinetobacter

rxn - reversible nephrotoxicity, dose-dependent neuromuscular blockade
surface active agent that causes disruptions in cell membranes

44
Q

How do drugs affect nucleic acid synthesis?

A

block synthesis of structural nucleotides, 3 different stages: inhibition of replication, inhibition of helicases, or stopping transcription, can cause damage to host cell

45
Q

Describe the clinical uses and adverse reactions of Quinolones (Fluoroquinolones).

A

uses - upper/lower respiratory infections, GI infections, skin infections

rxn - nausea, vomiting, diarrhea, prolonged Q-T interval

46
Q

How do Quinolones act?

A

block nucleic acid synthesis by inhibiting an enzyme that bacteria use to coil DNA into a double helix for translation/replication, stops bacterial growth

47
Q

Rifampin and Rifabutin are active against what type of microorganisms? How do these drugs act?

A

mycobacteria

inhibits RNA polymerase

48
Q

List some adverse reactions of Rifampin and Rifabutin.

A

hepatotoxicity, fever, chills, nausea, vomiting, orange bodily fluids

49
Q

Drugs that block protein synthesis DO or DO NOT have selective action against bacteria?

A

do

*can cause damage to eukaryotic mitochondria

50
Q

How do drugs that block protein synthesis act?

A

blocks formation of bacterial ribosomes to block synthesis of bacterial proteins (critical enzymes involved in translation/multiplication)

51
Q

Describe the mechanism of action of aminoglycosides.

A

bind irreversibly to bacterial ribosomes, inhibit RNA translation into proteins (production of non-functional proteins), destabilize cell wall, cell lysis

52
Q

List some clinical uses and adverse reactions of aminoglycosides.

A

uses - nosocomial gram -

rxn - nephrotoxicity, ototoxicity, NM blockade (with rapid high dose, rare)

53
Q

List the mechanism of action and the adverse reactions of Streptomycin Antimycobacterial.

A

MOA - block protein synthesis

rxn - nephro/ototoxicity

54
Q

Describe the mechanism of action and adverse reactions of Isoniazid.

A

*used against TB
MOA - inhibits cell wall synthesis by blocking protein synthesis, bactericidal

rxn - hepato/neurotoxicity

55
Q

List the clinical uses and mechanism of action of tetracyclines. (7)

A

gram + and gram -, Rickettsiae, Chlamydiae, Mycoplasmas, Spirochetes, Protozoa, Mycobacteria

MOA - prevents formation of polypeptide chain of the protein being synthesized, no function for cell

56
Q

List some adverse reactions of tetracyclines.

A

nausea, vomiting, diarrhea, inhibit bone growth/Ca/Mg/Al/Fe absorption

57
Q

List the clinical uses and adverse reactions of Tigecycline.

A

uses - complicated skin and intraabdominal infections

rxn - nausea, vomiting, diarrhea, abdominal pain

*mostly bacteriostatic, can be bactericidal

58
Q

List the clinical uses and adverse reactions of chloramphenicol.

A

uses - gastroenteritis/sepsis, salmonella, rickettsial diseases

rxn - bone marrow suppression, optic neuritis

59
Q

Describe the MOA of chloramphenicol.

A

Prevents binding of new AA to polypeptide chain that results from transcription/translation phase

60
Q

List the clinical uses and adverse reactions/precautions of macrolides.

A

uses - atypical/community-acquired pneumonia

rxn - GI complaints, can increase concentration of other drugs (theophylline, warfarin, triazolam)

*bacteriostatic

61
Q

Describe the competitive inhibition that occurs with drugs that affect metabolic pathways.

A

act like false substrates to disrupt the central pathways in susceptible microbes, increased concentrations of the drug ensure that the enzyme needed in a metabolic pathway is constantly occupied by the metabolic analog rather than the true substrate, cellular metabolism is slowed/stopped

62
Q

Describe the mechanism of action and clinical use of TMP-SMX.

A

MOA - blocks enzymes needed for bacteria to produce folic acid

uses - PCP prophylaxis, acute bronchitis, otitis media, shigellosis, good activity against MRSA

63
Q

List some adverse reactions of TMP-SMX.

A

nausea, vomiting, diarrhea, hypersensitivity, neutropenia, thrombocytopenia, hemolytic anemia, jaundice, hepatic necrosis, drug-induced lupus (autoimmune)

64
Q

Oseltamivir and Zanamavir fall under what category?

A

neuraminidase inhibitors

65
Q

List the clinical uses and adverse reactions/precautions of Oseltamivir and Zanamavir.

A

uses - influenza A/B

rxn - nausea and vomiting for first 2 days

66
Q 
Ribavirin:
AKA?
variable results in treatment of what?
how to deliver aerosolized dosage?
side effects?
A

virazole, severe RSV, SPAG, teratogenic effect

67
Q

Why are antifungals a difficult therapy?

A

may harm human cells, airborne/GI/skin entry

68
Q

Describe the clinical uses and adverse reactions of Polyenes (amphotericin B and nystatin)

A

uses - aspergillosis, blastomycosis, histoplasmosis, coccidioidomycosis, and cryptococcosis

rxn - flushing, fever, chills, renal impairment

PHRM-1058 (7 decks)

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