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Block 1: Pharmacology > Lecture 8, 9, and 10 > Flashcards

Lecture 8, 9, and 10 Flashcards

1
Q

Antibiotics?

A

(Chemicals produced by microorganisms)
-Inhibit growth of or kill other microorganisms
-Can be natural products as well as synthetic drugs
-Selective toxicity

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2
Q

Selective Toxicity?

A

Kill or damage a microbe without damage to the host

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3
Q

How to Achieve Selective Toxicity?

A

Antibiotics target cellular differences between host and pathogenic microbe

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3
Q

How to Achieve Selective Toxicity?

A

Antibiotics target cellular differences between host and pathogenic microbe

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4
Q

Therapeutic Index?

A

Ratio of the toxic dose to the effective dose of the drug

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5
Q

TI?

A

(Therapeutic Index)

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6
Q

Cidal?

A

KILL (lysis of cell wall to cause death)

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7
Q

Static?

A

INHIBIT (stop bacteria from growing (does not kill))

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8
Q

Human Body have natural defense to Bacteria?

A

1) Barriers: ex. skin and mucous membranes
2) Responses: antibodies, complement system, etc.

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9
Q

Human body naturally kills?

A

Pathogenic Microbes

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10
Q

Antimicrobials are used when?

A

Natural Defenses are overwhelmed or damaged

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11
Q

Bacteriostatic?

A

Inhibit bacterial cell replication but do not kill the organism at clinically achieved concentrations

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12
Q

Bacteriostatic Drugs?

A

(STATEC)
-Tetracyclines
-Erythromycin
-Chloramphenicol

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13
Q

Bactericidal?

A

Causes microbial cell death and lysis at clinically achieved concentrations

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14
Q

Bactericidal Drugs?

A

(PACS A PUNCH)
-Penicillins
-Aminoglycosides (Gentamycin, Tobramycin)
-Cephalosporins

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15
Q

Sulfonamides?

A

Either -cidal or -static according to composition of the environment

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16
Q

Sulfonamides Examples?

A

-Blood
-Pus
-Urine

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17
Q

Bactericidal drugs at low concentrations can behave as?

A

Bacteriostatic

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18
Q

Bacteriostasis if continued long enough will?

A

Decrease bacterial viability

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19
Q

Distinction between -cidal and -static antimicrobials can be important in?

A

Selection of therapy, especially in patients with a compromised immune system

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20
Q

Cell Wall Synthesis?

A

-Penicillin (G, Ampicillin)
-Cephalosporin (Ceftriaxone, Ceftaroline)
-Carbapenems (Imipenam)
-Monobactams (Aztreonam)
-Vancomycin (Tricyclic Glycopeptide)

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21
Q

DNA –> RNA?

A

-Quinolones (DNA gyros, Replication (Ciprofloxacin, Levofloxacin))
-Rifampin (RNA Polymerase)
-Metronidazole (Damage DNA)

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22
Q

Protein Synthesis?

A

-Tetracyclines (Doxycycline)
-Aminoglycosides (Gentamycin, Tobramycin)
-Chloramphenicol
-Macrolides: Azithromycin, Erythromycin

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23
Q

Cell Membrane?

A

-Polymyxins
-Daptomycin

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24
Q

Folic Acid?

A

-Trimethoprim
-Sulfonamides (Sulfamethoxazole)

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25
Q

“Please Come C My Vehicle”?

A

(Cell Wall Synthesis)
-Penicillin (G, Ampicillin)
-Cephalosporin (Ceftriaxone, Ceftaroline)
-Carbapenems (Imipenam)
-Monobactams (Aztreonam)
-Vancomycin (Tricyclic Glycopeptide)

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26
Q

“MR. Q”?

A

(DNA –> RNA)
-Quinolones (DNA gyros, Replication (Ciprofloxacin, Levofloxacin))
-Rifampin (RNA Polymerase)
-Metronidazole (Damage DNA)

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27
Q

“MCAT”?

A

-Tetracyclines (Doxycycline)
-Aminoglycosides (Gentamycin, Tobramycin)
-Chloramphenicol
-Macrolides: Azithromycin, Erythromycin

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28
Q

Determinants of Bacterial Response to Therapy?

A

(Reasons why a patient may NOT respond to therapy with antibacterials)
1) Misdiagnosis
2) No Infection
3) Do not complete full length of therapy
4) Patient self-treatment of infections with antimicrobials that were not prescribed for them

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29
Q

A virus is not?

A

A bacteria

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30
Q

Factors to consider when treating an infection?

A

1) Sensitivity of organism to drug (drug resistance)
2) Appropriate dosage (adult vs. neonatal)
3) Route of administration (PO vs. IV)
4) Duration of therapy (7 days vs. 14 days)
5) Special patient features (ex. immune system, age, renal function)

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31
Q

All drugs are excreted through the kidneys except?

A

Doxycycline

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32
Q

Indigenous Microbial Flora serve to?

A

Control growth of potentially pathogenic microbes

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33
Q

Use of an antimicrobial agent might disturb?

A

Ecologically balance leading to overgrowth of pathogenic microbes which are inherently resistant to antimicrobial agent (Superinfection)

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34
Q

Examples of IMF?

A

-C. Diff
-C. Albicans
(Use Vancomycin)

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35
Q

Vancomycin is used for?

A

C. Diff

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36
Q

Burns?

A

(SSP)
-Staph
-Strep
-Pseudo aeru

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37
Q

Skin Infections?

A

(SSH)
-Staph
-Strep
-Herpes

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38
Q

Decubitus Wound Infections?

A

(SEB)
-Staph
-E. Coli
-Bact fragilis

39
Q

Traumatic and Surgical Wounds?

A

(SSP)
-Staph
-Strep
-Pseudo aeru

40
Q

Burns and Traumatic and Surgical Wounds?

A

(SSP)
-Staph
-Strep
-Pseudo aeru

41
Q

For Optimal Therapy?

A

-Obtain cultures in order to identify the pathogenic microbe(s)
-Then do drug sensitivity testing

42
Q

MIC?

A

Minimum Inhibitory Concentration (used more)

43
Q

MBC?

A

Minimum Bactericidal Concentration (can be toxic)

44
Q

Goal of Drug Sensitivity Testing?

A

3-5x MIC to get rid of infection

45
Q

Most important consideration for appropriate therapy?

A

Susceptibility of pathogenic microbe (Will drug inhibit/kill)

46
Q

For Syphilis?

A

(Treponema pallidum)
Use Benzathine (salt) + Penicillin G

47
Q

For Tuberculosis?

A

(Mycobacterium)
(RIPE)
-Rifampin + Isoniazid + Pyrazinamide + Ethambutol

48
Q

RIPE?

A

Rifampin + Isoniazid + Pyrazinamide + Ethambutol

49
Q

For Pneumonia?

A

(Pseudomonas aeruginosa)
(PTT)
-Piperacillin/Tazobactam + Tobramycin (B-lactam/B-lactam inhibitor)

50
Q

PTT?

A

Piperacillin/Tazobactam + Tobramycin (B-lactam/B-lactam inhibitor)

51
Q

Host factors that modify the choice, dose, or route of administration of antimicrobial drugs?

A

-Patient
-History of a previous adverse drug reaction (ex. penicillin allergy)

52
Q

More favorable penetration can occur in?

A

These sites with inflammation

53
Q

Desirable drug concentrations at the site of infection that are?

A

At least 3 to 5 times the MIC (to at least inhibit) to ensure optimal therapeutic response

54
Q

Some area are difficult to penetrate by some antimicrobial drugs?

A

Ex. meninges, joint spaces, or eyes

55
Q

Most antimicrobial drugs and their metabolite are excreted primarily by?

A

Kidneys and their dosage may have to be modified with impaired renal function

56
Q

Dose adjustments based on?

A

Patients’ renal function

57
Q

Hepatic Function?

A

-More difficult to measure
-Chloramphenicol, IV
-Clindamycin, IV

58
Q

Chloramphenicol, IV?

A

-Hepatic function impairment (use with caution)
-Reduced dosage and monitor serum concentration

59
Q

Clindamycin, IV?

A

-Hepatic function impairment, NO dosage adjustment recommendations
-Use with caution with severe liver disease

60
Q

Increase Gentamicin dose for?

A

Infants/Young Children

61
Q

Isoniazid?

A

Increase hepatitis risk, Increase age

62
Q

CHF Patients?

A

Ticarcillin disodium/ Clavulanate potassium –> Na+ and K (can cause edema and arrhythmis)

63
Q

Children (Tetracycline)?

A

-Permanent discoloration of growing teeth of children
-Can cause intracranial hypertension in infants and children

64
Q

Neonates (Chloramphenicol)?

A

-Low concentrations of (UGT) which conjugates chloramphenicol, then cleared the kidneys
-Infants died from cardiovascular collapse, Gray Baby Syndrome
-Give lower dose

65
Q

Neonates (Sulfonamides)?

A

-Displace bilirubin from albumin in the blood which can then deposit in the brain, Kernicterus or toxic encephalopathy
-Contraindicated in neonates

66
Q

Pregnancy and Nursing Contradictions?

A
  • Metronidazole (Mutagenic)
    -Sulfonamides (Breast Milk) (Kernicterus: Increase bilirubin, displaced from albumin)
    -Antifolate drugs (lower concentrations of folic acid in pregnant women (can lead to spina bifida))
    -Fluoroquinolones (affect cartilage growth)
    -Tetracyclines (inhibit bone growth, tooth enamel dysplasia)
67
Q

Metronidazole?

A

Mutagenic

68
Q

Sulfonamides?

A

-Breast Milk
-Kernicterus: Increase bilirubin, displaced from albumin

69
Q

Antifolate drugs?

A

Lower concentrations of folic acid in pregnant women (can lead to spina bifida)

70
Q

Fluoroquinolones?

A

Affect cartilage growth

71
Q

Tetracyclines?

A

Inhibit bone growth, Tooth enamel dysplasia

72
Q

Tetracyclines?

A

Inhibit bone growth, Tooth enamel dysplasia

73
Q

Prophylactic use of Antimicrobial Drugs?

A

1/4 to 1/2 of antimicrobial drugs used in hospitals for infection prevention

74
Q

Drug Combinations (Tuberculosis)?

A

Use 4 drugs (RIPE)

75
Q

Do NOT use 2 Drugs of the?

A

Same Class or Have the Same Mechanism of Action (with combined therapy want to attack at different sites) (wouldn’t want 2 B-Lactams)

76
Q

Insensitivity of decreased sensitivity to drugs?

A

Drug Resistance

77
Q

Mechanisms of antimicrobial resistance in pathogenic microbes?

A

-Decrease Drug uptake (porins)
-Increase Drug efflux (gets rid of drug by pumping it out)
-Enzymatic inactivation (B-lactamase) (This is why we have B-lactamase inhibitors)
-Decrease affinity for site of action (change site of action, can’t bind)

78
Q

Types of Bacteria?

A

-Gram-Positive
-Gram-Negative
-Anaerobes
-Miscellaneous

79
Q

Gram-Positive?

A

(Vancomycin)
-Staph
-Strep
-E. Faecalis
-Mono

80
Q

Gram-Negative?

A

(Aminoglycosides)
-E. Coli
-Kleb
-Pseudo
-H. Influenzae

81
Q

Anaerobes?

A

-C. Diff
-Bacterio Fraglis

82
Q

Miscellaneous?

A

-Trep
-Myco
-Rickett

83
Q

Gram +?

A

-Lactamase Outside
-Thicker Peptidoglycan Wall

84
Q

Gram -?

A

-Outer Membrane with Porin Channel
-Thin Peptidoglycan Layer
-Lactamase Inside

85
Q

NAMs and NAGs cross-link with?

A

Each Other

86
Q

Penicillin targets?

A

Transpeptidase (Penicillin Binding Protein (PBP)) this enzyme is important from cross-linking

87
Q

Penicillin also causes cell lysis in?

A

Hypotonic Solution water wants to flow in to make less concentrated and reach equilibrium

88
Q

Fosphomycin inhibits?

A

Pyruvyl Transferase (enzyme used in formation of NAM)

89
Q

Peptidoglycan Synthase is major target for?
Another target is?

A

Vancomycin, Pentapeptide (both enzymes are used to produce peptidoglycan)

90
Q

Incorporates penicillin when trying to cross-link?

A

Transpeptidase

91
Q

Preserve B-Lactams needed due to drug resistance?

A

B-Lactamase Inhibitors

91
Q

Preserve B-Lactams needed due to drug resistance?

A

B-Lactamase Inhibitors

92
Q

Penicillins?

A

-Penicillin G (Natural)
-Amoxicillin, Ampicillin (Amino group added)
-Dicloxacilin (Narrow, staph)
-Ticarcillin + Piperacillin (Pseudo)
-Mechanisms of action

93
Q

PBP required for?

A

Maintenance of rod shape

94
Q

B-Lactam?

A

Cell Wall Synthesis Inhibitor

95
Q

Mechanisms of Action (Penicillins)?

A

-Inhibit peptidoglycan transpeptidase, Prevents cross-linking of glycopeptide polymers
-Penicillin binding proteins (PBP) –> lethal effects
-Trigger autolysins –> cellular rupture

Block 1: Pharmacology (9 decks)

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