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Pharmacology 2 > Test 4 > Flashcards

Test 4 Flashcards

1
Q

Selective Toxicity

A

***the ability of a drug to inquire a target cell or organism without injuring other cells or organisms that are non-targeted.

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2
Q

Disruption of the bacterial cell wall:

A

bacteria are encased in a rigid cell wall that encases a very hypertonic solute. If not for the rigid cell wall, water would follow the osmotic gradient, causing bacterial swelling and ultimate bursting. Several antibiotics work to weaken the cell wall.

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3
Q

Inhibition of enzymes unique to the bacteria:

A

inhibiting specific enzymes that are critical to bacterial survival.

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4
Q

Disruption of protein synthesis:

A

we can impair protein synthesis in bacterial cells. Selective because bacterial ribosomes are different than mammalian ribosomes.

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5
Q

Narrow spectrum Antibiotics:

A

active against only a few bacteria

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6
Q

Broad Spectrum Antibiotics:

A

active against a wide variety of bacteria

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7
Q

Bactericidal:

A

Bacterial Killers

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8
Q

Bacteriostatic:

A

Suppress Growth, but do not kill

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9
Q

Normal Flora:

A

Body’s normal bacterial and fungal community

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10
Q

Pathogen:

A

overgrowth or introduction of new bacteria that causes an infectious response to the host

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11
Q

Aerobes vs Anaerobes:

A

Aerobes require oxygen to survive and Anaerobes do not.

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12
Q

Superinfection:

A

Secondary infection with resistant bacteria

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13
Q

Nosocomial Infections:

A

Infections acquired in hospitals and nursing homes. Typically very drug resistant.

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14
Q

MIC

A

.

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15
Q

MBC

A

.

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16
Q

Resistance:

A

organisms that were highly responsive to an antibiotic that becomes less susceptible over time (ex staph, strep, Pneumo, Klebsiella, Enterococcus)

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17
Q

Mechanisms of Bacterial Resistance-

A
  1. Production of drug-metabolizing enzymes (ex Penicillinase)
  2. Cease active uptake of the drug
  3. Altered receptor sites- example penicillin binding proteins.
  4. Synthesis of compounds that antagonize actions of the antibiotic (ex bacteria develop ability to synthesize PABA, which leads to Sulfonamide resistance)
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18
Q

Acquiring resistance-

A
  1. Spontaneous Mutation- Random changes in a bacterial DNA. Leads to very Low level resistance. Additional mutations leads to greater resistance.
  2. Conjunction- where bacteria “Communicate” to one another and share/transfer DNA that leads to resistance (sometimes multi-drug resistance.
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19
Q

Antibiotics and the Emergence of Resistance

A

** ABX can promote overgrowth of bacteria that have acquired mechanisms of resistance***

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20
Q

NORMAL BACTERIAL FLORA

A

Under drug free cond., bacteria keep eachother under check. They secrete toxic compounds that are toxic to other bacterias well as compete for nutrients.

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21
Q

SUPERINFECTIONS-

A

new infection that develops during the course of treatment of a primary infection. Normal Flora is altered allowing for resistant organism to flourish.

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22
Q

NARROW SPECTRUM VS. BROAD SPECTRUM-

A

Broad spectrum kill off more of the normal flora, thus the more broad spectrum, it can more than likely facilitate the emergence of superinfections.

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23
Q

INDISCRIMINATE USE OF ABX-

A

he more bacteria SEE an antibiotic, the more opportunity to delelop resistance. Much of our resistance issues today are secondary to improper abx use.

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24
Q

CDC CAMPAIN TO PREVENT ANTIMICROBIAL RESISTANCE.

A
  1. VACCINATE- especially flu and Pna
  2. GET THE CATHETERS OUT- IV,ART,URINARY,ET, ETC…
  3. TARGET THE PATHOGEN** CULTURES AND SENSITIVITY** Always obtain prior to initial ABX use.
  4. ACCESS THE EXPERTS- input from infectious disease experts.
  5. PRACTICE ANTIMICROBIAL CONTROL- ABX SURVILLANCE PROGRAMS, order sets, education, feedback.
  6. USE LOCAL DATA.- ANTIBIOGRAM-assista in guiding initial drug selection
  7. TREAT INFECTION- NOT CONTAMINATION ** obtain samples correctly, decontaminate skin, etc,,,**
  8. TREAT INFECTION, NOT COLONIZATION- ex Sputum samples, skin swabs
  9. JUDICIOUS USE OF VANC.- Drug of last resort for MRSA and multi-drug resistant strep pneumo
  10. STOP ABX AT THE PROPER TIME
  11. ISOLATE THE PATHOGEN- proper isolation of PTs, disposal of body fluids, proper cleaning of hospital rooms
  12. WASH YOUR HANDS! AT LEAST 50%FAILURE
    RATE
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25
Q

ANTIBIOTIC SELECTION: EMPERIC THERAPY:

A

in severe infections, you may have to initiate ABX therapy before test results are available

  1. BROAD SPECTRUM- INITIAL
  2. NARROW THE SPECTRUM: AFTER THE BACTERIA IS ISOLATED AND CULTURE ANS SENSITIVITY RESULTS RETURN
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26
Q

ANTIBIOTIC SELECTION: IDENTIFYING THE ORGANISM

A
  1. GRAM STAIN- Quick analysis through gram staining – tells if gram+ cocci, gram- cocci, gram neg rod, or gram + rods. This can narrow the choices of empiric treatment.
  2. culture-place sample on medium conducive to bacterial growth.
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27
Q

ANTIBIOTIC SELECTION: DRUG SUSCEPTIBILITY-

A

mainly used for organisms that have high incidence of resistance. To guide appropriate ABX useage.

DISK DIFFUSION-

Broth Dilution Test-

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28
Q

DISK DIFFUSION-

A

inoculating an agar plate, then place discs that contain different ABX on the agar plate. The degree of sensitivity is proportional to the size of the bacteria free zone around the disk.

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29
Q

Broth Dilution Test-

A

Bacteria are grown in a series of tubes containing different concentrations of different antibiotics. We can establish:

  1. Minimum Inhibitory Concentration (MIC)- Lowest concentration of an antibiotic that produces complete inhibition of bacterial growth.
  2. Minimum Bactericidal Concentration (MCB)- lowest concentration of drug that produces a 99.9% decline in the number of bacterial colonies.
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30
Q

Host Defenses-

A

Immune system. Without an intact immune system, antibiotics are rarely successful. (Ex AIDS). Goal typically is to suppress bacteria enough to tip the scale back in the direction of the host immune defenses. If poor immune function, need to be VERY aggressive with CIDAL antibiotics. Cannot afford to miss.

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31
Q

Site of Infection-

A

Antibiotics must be able to get to the site of infection in sufficient concentrations (typically 4-8 times the MIC)

  1. CNS Infections - BBB
    2 . Pneumonia
  2. Abscesses
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32
Q

Doses and Duration:

  1. Dosage:
A 
Success resides in obtaining adequate concentrations of 
effective antibiotics (typically 4-8 times the MIC) for sufficient periods of time. Must keep in mind pharmacokinetic variables such as ADME- Absorption, Elimination, Metabolism, and Distribution. Things important such as kidney functions, body weight, volume of distribution, site of infection, MIC ect..
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33
Q

Doses and Duration:

  1. Duration:
A

Differ depending on variables such as:

A. Site of infection - (ex. Simple UTI, vs. Endocarditis vs Prostatitis)
B. Host Defenses
C. Bug Being Treated

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34
Q

***** IMPORTANT TO TREAT LONG ENOUGH.

A

Important to tell patients to continue their medication for the full length of time, even though they may feel better (Even Normal). Early Antibiotics withdrawal is a big cause of recurrent infection and drug resistance. **

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35
Q

Combination Therapy:

  1. Effects:
A

a. Additive - 1 + 1 = 2 (Clarithromycin Plus Amoxicillin For H.Pylori)
b. Synergistic - 1 + 1 = 5 (Trimethoprim + Sulfamethoxazole / Piperacillin + Gentamycin. )
c. Antagonistic- 1 + 1 = 0 (Tetracycline plus Penicillin)

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36
Q

Combination Therapy:

  1. Indicated:
A

a. Severe infection- Until the pathogen has been identified. Broad Empiric coverage
b. Mixed Infections- perforated bowel, diabetic foot, dog bite
c. Prevention of resistance- TB
d. Enhanced Antibiotic Activity.- Penicillin plus Aminoglycoside

(PCN weakens the cell wall and allows for great penetration of the AMG)

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37
Q

Prophylactic Antibiotic Use- ALMOST NEVER INDICATED EXCEPT

A
  1. Surgery- ex Cefazolin pre surgery
  2. Bacterial Endocarditis- individuals with congenital, valvular heart disease, or prothetic valves take antibiotics before dental procedures and surgery
  3. Neutropenia- ex Bactrim DS in AIDS Patients to prevent Pneumonia
  4. Influenza Outbreaks- Amantadine/ Ramantadine
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38
Q

Monitoring Clinical Response

A
  1. Fever Curves
  2. WBC: Bands
  3. Regression of Erythema (For Tissue Infections)
  4. Improvement in Chest Xray for Pneumona
  5. General Improvement in health Status
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39
Q

GRAM POSITIVE COCCI- Stain little, round, and blue

A
  1. STAPH AUREUS- skin bug Can be very aggressive. Micro-abcesses.
  2. STAPH-EPI- skin bug Normally do not cause infection unless immunocompromised. Often a contaminant. Sometimes associated with line infections.
  3. STREP A- Strep throat
  4. STREP B- post partum infections
  5. STREP PNEUMO- aggressive. Upper resp. #1 pathogen for pneumonia, sinusitis, ear infections.
  6. ENTEROCOCCUS- from mouth to gut. Used to be called group D strep. Becoming extremely resistant (VRE)
    Pepto and peptostrepto-
  7. ANAEROBES. Grow in mouth, Typically not a problem unless very poor hygiene.
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40
Q

GRAM POSITIVE COCCI- Stain little, round, and blue

STAPH AUREUS

A

skin bug Can be very aggressive. Micro-abcesses.

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41
Q

GRAM POSITIVE COCCI- Stain little, round, and blue

STAPH-EPI-

A

skin bug Normally do not cause infection unless immunocompromised. Often a contaminant. Sometimes associated with line infections.

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42
Q

GRAM POSITIVE COCCI- Stain little, round, and blue

STREP A-

A

Strep throat

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43
Q

GRAM POSITIVE COCCI- Stain little, round, and blue

STREP B

A

post-pardom infections

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44
Q

GRAM POSITIVE COCCI- Stain little, round, and blue

STREP PNEUMO

A

aggressive. Upper resp. #1 pathogen for pneumonia, sinusitis, ear infections.

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45
Q

GRAM POSITIVE COCCI- Stain little, round, and blue

ENTEROCOCCUS-

A

from mouth to gut. Used to be called group D strep. Becoming extremely resistant (VRE)

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46
Q

GRAM POSITIVE COCCI- Stain little, round, and blue

Pepto and peptostrepto- ANAEROBES.

A

Grow in mouth, Typically not a problem unless very poor hygiene.

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47
Q

GRAM POSITIVE RODS: STAIN BIG, BLUE, RODS

A
  1. LISTERIA- May be in the very old, or very young. Can cause meningitis or pulmonary infection
  2. C.DIFF- GI bug. Very resistant to bacteria Can be a superinfection that causes PSEUDOMEMBRANOUS COLITIS.
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48
Q

GRAM POSITIVE RODS: STAIN BIG, BLUE, RODS

  1. LISTERIA-
A

May be in the very old, or very young. Can cause meningitis or pulmonary infection

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49
Q

GRAM POSITIVE RODS: STAIN BIG, BLUE, RODS

  1. C.DIFF-
A

GI bug. Very resistant to bacteria Can be a superinfection that causes PSEUDOMEMBRANOUS COLITIS.

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50
Q

GRAM NEGATIVE COCCI: STAIN LITTLE ROUND AND RED.

A
  1. Neisseria meningococcus- Can cause drastic infection. Very quick and aggressive. Eppidemics.
  2. NEISSERIA GONOCOCCUS- Gonorrhea
  3. MORAXELLA- upper respiratory (sinusitis, ear, Pneumonia).
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51
Q

GRAM NEGATIVE COCCI: STAIN LITTLE ROUND AND RED.

  1. Neisseria meningococcus-
A

Can cause drastic infection. Very quick and aggressive. Eppidemics.

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52
Q

GRAM NEGATIVE COCCI: STAIN LITTLE ROUND AND RED.

  1. NEISSERIA GONOCOCCUS-
A

GONOCOCCUS- Gonorrhea

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53
Q

GRAM NEGATIVE COCCI: STAIN LITTLE ROUND AND RED.

  1. MORAXELLA-
A

upper respiratory (sinusitis, ear, Pneumonia).

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54
Q

GRAM NEGATIVE RODS: STANI BIG, ROD SHAPED, AND RED

A
  1. PSEUDOMONAS- usually nonpathogenic. Very resistant. TWO BUG DRUG.
  2. B. FRAG- ANAEROBIC Resistant to beta lactams AND cephalosporins due to beta lactamase prodx. (WONT WORK).
  3. SALMONELLA/ SHIGELLA- GI BUGS (DIARRHEA). Travellers diarrhea. (esp salmonella)
  4. E. COLI- # 1 PATHOGEN IN UTIs (esp in women)
  5. H. FLU - UPPER RESP TRACT INFECTIONS
  6. ACINETOBACTER- major resistance problems in hospitals/ nursing homes
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55
Q

GRAM NEGATIVE RODS: STANI BIG, ROD SHAPED, AND RED

PSEUDOMONAS-

A

usually nonpathogenic. Very resistant. TWO BUG DRUG.

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56
Q

GRAM NEGATIVE RODS: STANI BIG, ROD SHAPED, AND RED

B. FRAG-

A

ANAEROBIC Resistant to beta lactams AND cephalosporins due to beta lactamase prodx. (WONT WORK).

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57
Q

GRAM NEGATIVE RODS: STANI BIG, ROD SHAPED, AND RED

SALMONELLA/ SHIGELLA- GI BUGS (DIARRHEA).

A

Travellers diarrhea. (esp salmonella)

58
Q

GRAM NEGATIVE RODS: STANI BIG, ROD SHAPED, AND RED

E. COLI-

A

1 PATHOGEN IN UTIs (esp in women)

59
Q

GRAM NEGATIVE RODS: STANI BIG, ROD SHAPED, AND RED

. H. FLU

A

UPPER RESP TRACT INFECTIONS

60
Q

GRAM NEGATIVE RODS: STANI BIG, ROD SHAPED, AND RED

ACINETOBACTER-

A

major resistance problems in hospitals/ nursing homes

61
Q

ATYPICALS-

A

Cause infections that look like other infections. Don’t gram stain! Hard to ID!

  1. mycoplasma- not typically that severe. Walking man’s PNA
  2. LEGIONELLA- Can be severe
  3. CHLAMYDIA- upper resp and GYN
62
Q

PENICILLIN MOA-

A

Weakens cell wall causing lysis and death (bactericidal). Rigid cell wall with high osmotic pressure.

63
Q

PENICILLIN RESISTANCE-

A

GRAM POSITIVE have 2 layer cell membranes that PCN can easily penetrate, however, GRAM NEGATIVE have 3 layer cell membranes. Difficult for PCN to penetrate and bind to PBP’s. (Penicillin binding proteins).

  1. PBP’s- PENICILLIN BINDING PROTEINS ** TARGET FOR PCN ON THE CELL WALL.*** Expressed only when actively growing. Bacteria are altering the PBPs making it harder for PCN to bind.
  2. BETA LACTAMASES- enzymes which cleave beta lactam rings EX- STAPH in the 1940’s 100% sensitive, in 1960’s 80% resistance. Many G+ and G- produce.
64
Q

CLASSIFICATION-
NARROW SPECTRUM-

(Penicillinase sensitive) (ex PENICILLIN G)

A
  1. SPECTRUM: GRAM POSITIVE COCCI, (non penicillinase producing), GRAM NEGATIVE COCCI, GRAM POSITIVE ANAEROBES, SPIROCHETES
  2. MAIN USE STREP THROAT AND SYPHILIS***MULTIPLE FORMS Pen-G PO, depot forms for IM injection, IV.
  3. DISTRIBUTION- In the abcense of inflammation, poor CNS penetration
  4. PK- RENALLY ELIMINATED
  5. ALLERGIES: MOST COMMON DRUG ALLERGY!!! From rash to anaphylaxis. Allergic to one, allergic to all. 1st dose, stay in office for 30 min. Epi on hand. Alternatives: ERY, VANC, POSSIBLY CEPHALOSPORINS
65
Q

What is the most common drug allergy?

A

Pennicillin

ALLERGIES: MOST COMMON DRUG ALLERGY!!! From rash to anaphylaxis. Allergic to one, allergic to all. 1st dose, stay in office for 30 min. Epi on hand. Alternatives: ERY, VANC, POSSIBLY CEPHALOSPORINS

66
Q

NARROW SPECTRUM (Penicillinase resistant antistaphlococcal penicillin) (ex. Methicillin)

A

DRUGS- METHICILLIN (obsolete), NAFCILLIN (IV), OXACILLIN, DICLOXACILLIN

SPECTRUM: INDICATED for PCNase producing staph (staph aureus and staph epi)

2, MRSA- altered PBPs. VANCOMYCIN IS DOC

67
Q

BROAD SPECTRUM:

A

AMOXICILLIN AND AMPICILLIN

SPECTRUM: PCN( gram + cocci (non pcnase producing), gram – cocci, gram + anaerobes, spirochetes, plus some G- rods (H flu, E COLI, Salmonella, Shigella) PLUS strep throat and syphilis.

PCNase- still inactivated by PCNase, so poor for staph and other PCNase producing G-

68
Q

EXTENDED SPECTRUM PENICILLINS

A

DRUGS: PIPERACILLIN, TICARCILLIN

SPECTRUM: AMOXICILLIN (gram + cocci (non pcnase producing), gram – cocci, gram + anaerobes, spirochetes, plus some G- rods (H flu, E COLI, Salmonella, Shigella) PLUS strep throat and syphilis.) ( PLUS PSEUDO, PROTEUS, SOME KLEBSIELLA

USES: MOSTLY FOR PSEUD (IN COMBO WITH AMG)

TICARCILLIN- VERY LARGE Na+ loads. Caution with CHF and Renal failure pts.

69
Q

E.BETA LACTAMASE INHIBITORS (not ABX)

A
  1. CLAVULANIC ACID, TAZOBACTAM, AND SULBACTAM
  2. MOA: Inhibits beta lactamase. Combined with PCNs to extend their spectrum to some beta lactamase bacteria (staph aureas, Staph Epi, B. Frag, Proteus, H.Flu).
70
Q

What is the MOA of CEPHALOSPORINS

A

MOA: BETA lactams (bacterialcidal) **similar to PCN but more stable against beta lactamase producing bacteria ** Bind to PBPs and disrupt cell wall synthesis.

71
Q

What is the Spectrum of activity of CEPHALOSPORINS

A

SPECTRUM OF ACTIVITY: AS one progresses from 1st generation to 4th generation

  1. Increased activity against G- rods
  2. Increased resistance to beta lactamase
  3. Increased ability to penetrate the CNS (Meningitis).
72
Q

1ST GENERATION CEPHALOSPORINS

A

(cefazolin/cephalexin)

gram postitve (staph,strep). If MRSA, resistant however. Essentially no G- coverage

73
Q

2nd GENERATION CEPHALOSPORINS

A

( cefuroxime and cefotetan)

GRAM +( STAPH,STREP,ENTEROCOCCUS,PEPTOCOCCUS, PEPTOSTREPTOCOCCUS,C DIFF, TETANI,PERF, LISTERIA PLUS SOME GRAM –(E.COLI,H.FLU,PROTEUS, MORAXELLA)

74
Q

3RD GENERATION CEPHALOSPORINS

A

(Cephtazidime and Ceftriaxone) KEEPS BUGS-

CEFTAZIDIME IS THE ONLY ONE THAT HAS EXCELLENT PSEUD COVERAGE, AND EXCELLENT CNS PENETRATION.

75
Q

4TH generation CEPHALOSPORINS

A

(CEFIPINE) Resistant to Beta Lactamases and Pseudomonas. VERY BROAD

76
Q

CEPHALOSPORINS P’KINETICS

A
  1. CSF PENETRATION. Best with 3rd and 4th generation Cephs.

2. Renal adjustment not necessary for cefoperazone and ceftriaxone

77
Q

CEPHALOSPORINS ADVERSE DRUG REACTIONS

A
  1. HYPERSENSITIVITY- 5-10% CROSS REACTIVITY TO pcn ALLERGIES
  2. BLEEDING- cefmetazole, cefoperazone, cefotetan interferes with vit k metabolism. Prolongs PT (LIKE COUMADIN). Monitor INR and can treat with Vit K!*
  3. DISULFIRAM- CEFMETAZOLE, CEFOPERAZONE, CEFOTETAN
78
Q

CARBAPENEMS- used with CILASTATIN, AN enzyme inhibitor.

A

DRUGS—IMIPENEM, MEROPENEM, ERTAPENEM

79
Q

What is the spectrum of activity for IMIPENEM, MEROPENEM, ERTAPENEM?

A

SPECTRUM GRAM + AND GRAM –( esp. pseudomonas) and Anaerobes (Extremely broad spectrum). Broadcast single ABX we have. ***resistant to PCNases and great penetration into the G- cell walls.

80
Q

What is the Pharmacokinetics of IMIPENEM, MEROPENEM, ERTAPENEM?

A

P’kinetics- Combined with CILASTATIN to improve urine concentrations. IMIPENEM is metabolized by dipeptidase at the renal brush border. CILASTATIN Inhibits dipeptidase.

81
Q

What are the ADEs of IMIPENEM, MEROPENEM, ERTAPENEM?

A

ADEs hypersensitivity, superinfections, seizures, allergic cross reactivity with PCN

82
Q

What are the uses of IMIPENEM, MEROPENEM, ERTAPENEM?

A

USES- SERIOUS INFECTIONS, PSEUDOMONAS, MIXED INFECTIONS

83
Q

MONOBACTAMS: AZTREONAM
MOA:

A

Binds to PBPs, but only Gram – cocci and rods (NEISSERIA GONOCOCCUS, NEISSERIA MENINGOCOCCUS, MORAXELLA CATHARRALIS, KLEBSIELLA,E.COLI, ENTEROBACTER, PROTEUS, PROVIDENTIA, SERRATIA, SALMONELLA, SHIGELLA, H. FLU, ACINETOBACTER, PSEUDOMONAS, B.FRAGELLA, CITROBACTER).

84
Q

MONOBACTAMS: AZTREONAM SPECTRUM-

A

SPECTRUM- GRAM – AEROBES, NEISSERIA, H.FLU, PSEUDOMONAS, ENTEROBACTERIACIAE (E.COLI, KLEBSIELLA, PROTEUS,SERRATIA, SALMONELLA, SHIGELLA)

Parenteral only

Appears safe in pts with PCN allergies

Expensive

85
Q

VANCOMYCIN

MOA:

A

DISRUTS CELL WALL SYNTHESIS BUT DOES NOT DO SO VIA PBPS. Binds to precursor molecules for cell wall synthesis.

86
Q

VANCOMYCIN SPECTRUM-

A

GRAM +COCCI AND GRAM +RODS DOC FOR MRSA (AND USED TO BE FOR C.DIFF) Also used for gram + infections when PCN allergic.

87
Q

VANCOMYCIN P’KINETICS-

A

NOT ABSORBED WELL ORALLY (THIS IS A GOOD THING FOR TREATING c-Diff because it sits in the gut and does its job.

Used IV for systemic infections

88
Q

VANCOMYCIN ADE:

A

RED MAN SYNDROME- Give over 60 min or more. Massive release of histamine

NEPHROTOXICITY- not as much as once thought. Must check trough levels to ensure adequate clearance (typically <15-20 mcg/ml)

89
Q

What are the BACTERIOSTATIC INHIBITORS OF PROTEIN SYNTHESIS

A

TETRACYCLINES, MACROLIDES, AND OTHERS

90
Q

TETRACYCLINEs: Extensive use has resulted in resistance. Use hs declined
Drugs- TETRACYCLINE, MINOCYCLINE, DOXYCYCLINE

MOA:

A

Inhibits protein synthesis in the cell, preventing reproduction. Binds to the 30s subunit of the ribosome

91
Q

TETRACYCLINE, MINOCYCLINE, DOXYCYCLINE SPECTRUM:

A

SPECTRUM: ATYPICALS (LEGIONELLA, MYCOPLASMA, CHLAMYDIA), AND H.PYLORI MOSTLY

92
Q

TETRACYCLINE, MINOCYCLINE, DOXYCYCLINE THERAPEUTIC USES:

A

ROCKY MOUNTAIN SPOTTED FEVER, CHLAMYDIA, BRUCELLOSIS, CHOLERA, MYCOPLASMA, LYME DISEASE, H.PYLORI, ACNE, UNCOMPLICATED UPPER RESP TRACT INFECTIONS.

93
Q

TETRACYCLINE, MINOCYCLINE, DOXYCYCLINE P’KINETICS:

A

DO NOT administer with milk or other high calcium products, iron, magnesium antacids (interferes with absorbtions) Administer 2 hr. before or 2 hrs. after.

94
Q

TETRACYCLINE, MINOCYCLINE, DOXYCYCLINE ADEs

A

GI: Irritant-can cause esophageal ulceration. Avoid HS dosing. Take with full glass of water.

BONES AND TEETH- binds to calcium, causing a yellow/brown discoloration to teeth

Photosensitivity- use sunscreen

95
Q

Macrolides- Erythromycin, Azythromysin, Clarithromycin

MOA:

A

inhibition of protein synthesis. Binds to the 50S subunit of the ribosome.

96
Q

Macrolides- Erythromycin, Azythromysin, Clarithromycin Spectrum/ Therapeutic uses-

A

Gram-positive cocci, Atypicals. Alternative in PCN allergic patients. Azithromycin, Clarithromycin have reasonable H. Flu and Moraxella coverage.

97
Q

Macrolides- Erythromycin, Azythromysin, Clarithromycin Pharmacokinetics:

A

central nervous system penetration is poor.

Enzyme inhibitor- caution with the open Theophylline, carbamazepine, and Warfarin. (Erythromycin primary, but watch for all. )

98
Q

Macrolides- Erythromycin, Azythromysin, Clarithromycin Adverse drug reactions.

A

Adverse drug reactions.
Gastrointestinal upset pain with nausea and vomiting.

QT prolongation and torsades avoid with other CYP three A4 inhibitors.

Phlebitis- IV. Must dilute Heavily.

99
Q

Clindamycin-

MOA-

A

Inhibition of protein synthesis by binding to 50S subunit of the ribosome.

100
Q

Clindamycin-

Spectrum:

A

Spectrum: Gram + aerobes and anaerobes. Utilization mainly for anaerobic coverage.

101
Q

Clindamycin- ADE-

A

ADE- Pseudomembraneous Colitis -> superinfection of the bowel with C- Diff (Anaerobic G+ rod). Treatment is PO Vancamycin or PO Metronidazole.

102
Q

Linezolid (Zyvox)

MOA-

A

MOA- Bind to the 23S portion of the 50S ribosomal subunit. Very Unique, thus cross resistance is rare.

103
Q

Linezolid (Zyvox) Spectrum:

A

Spectrum: MRSA, VRE, Should only be used for these infections. No activity for Gram Negative.

104
Q

Linezolid (Zyvox) ADR:

A

Myelosuppression ( Check CBC every week )

Drug Interactions- Weak inhibitor of MAO, do not use with sympathomimetics or foods containing tyramine.

105
Q

Quinupristin / Dalflopristin (Synercid)

MOA-

A

2 drugs which inhibit protein synthesis **(synergy).

106
Q

Quinupristin / Dalflopristin (Synercid)

Use:

A

Vancomyocin resistant E. Faecium, MRSA, Multi-Drug resistant strep pneumo.

107
Q

Quinupristin / Dalflopristin (Synercid)

Drug Interactions-

A

CYP450 Inhibitor
ADE-

  1. Hepatoxicity- check LFT’s twice during 1st week then weekly thereafter,

Thrombophlebitis- 50% incidence. Often needs central line administration.

Safe in PCN allergic patients.

108
Q

name the Aminoglycosides:

A

Gentamicin, Tobramycin, Amikacin

Narrow spectrum, bactericidal, given parenterally.

109
Q

Gentamicin, Tobramycin, Amikacin

MOA-

A

Binds to 30S Ribosomal subunit and inhibits protein synthesis. Drugs that work through this mechanism are generally static. However, the AMG cidal activity occurs from the production of abnormal proteins that insert themselves into the cell membrane, causing weakness and leaking to occur.

110
Q

Gentamicin, Tobramycin, Amikacin

Resistance-

A

via bacterial production of enzymes capable of inactivating the AMG.

Amikacin is resistant to these enzymes.

111
Q

Gentamicin, Tobramycin, Amikacin Spectrum:

A

Spectrum: Especially Gram Negative rods and some G+ cocci (Staph and Enterococcus). No Anaerobic Activity.

112
Q

Gentamicin, Tobramycin, Amikacin

Use:

A

Treatment of severe nosocomial infections, esp. Psudomonas and KEEPS bacteria.

113
Q

Gentamicin, Tobramycin, Amikacin

Pharmacokinetics:

A

Postantibiotic Effect= bactericidal activity persists several hours after serum levels have dropped below MBC.

Interpatient Variability- Must individualize the dosing and sometimes levels are unpredictable. Must take into account wt, RFx, site of infection, peak goal. ect.

Concentration dependent killers.

Pharmacokinetics: Highly polar compounds. Thus IV only and very poor CNS penetration. Highly concentrated in the inner ear and kidneys ->

Toxicity. Drugs are eliminated in the kidneys.

Peaks must be high enough for efficacy, but with troughs low enough to limit toxicity.

Conventional dosing of
Gentamicin and Tobramycin:

Peaks: 0.5 - 1 hour after end of infusion (Range 4-10 ug/ml)

Trough: Just before the next dose (Range 0.5 - 2 ug/ml)

Recording timing of doses and timing of blood sample (Levels) VERY IMPORTANT!

114
Q

Gentamicin, Tobramycin, Amikacin ADE:

A

Ototoxicity- via accumulation, can cause cochlear damage (hearing) and vestibular damage (balance). Early cochlear damage is initiated by tinnitus (ringing). Early vestibular damage is manifested by HA/ Nausea/ Dizziness. Damage is dependent on elevated trough levels. Need time to wash out. Prolonged exposure equals toxicity. Largely irreversible.

Nephrotoxicity- related to accumulative doses as well as elevated trough levels. Can manifest early on as proteinuria, elevated BUN, and elevated serum creatinine.

Neuromuscular blockade- can inhibit neuromuscular transmission. Patient is at highest risk are those with myasthenia gravis.

115
Q

Gentamicin, Tobramycin, Amikacin Dosing schedule-

A

QDAY vs. Q8. Since concentration deptendent killer and post antibiotic effect, potentially greater kill and less toxicity with QDAY vs Q8. Less laborious (peaks, troughs, pharmacokinetic specialists ect) Much higher peaks with QDAY and greater wash out period.

116
Q

Drug differences:

Gentamicin-

A

Cost: Cheapest

Combo Therapy: Typically combined with another antibiotic. (PCN / CEPH / or VANC)

Administration: IV, IM, Intrathecal

117
Q

Drug differences:

Tobramycin:

A

Psudomonas: Slightly better for Pseudomonas as compared to Gentamycin, but slightly less activity for G+ cocci.

Cost: significantly more expensive than Gentamycin.

Resistance: Generally if resistant to Gentamycin, probably resistant to Tobramycin

Administration: IV / IM / Nebulized (CF)

118
Q

Drug differences:

Amikacin:

A 
Spectrum: Broad Spectrum for Gram Negative Rods. Klebsiella, 
    E-coli, 
    Enterobacter, 
    Proteus, 
    Providentia, 
    Serratia, 
    Salmonella, 
    Shigella. 
    H.Flu , 
    Acinetobacter, 
    Psudomonas, 
    B.Fragilis, 
    Citrobacter

Resistance: Least vulnerable to inactivation by bacterial enzymes.

Cost: Very Expensive

Use: Typically reserved for infections that are resistant to Gentamicin and Tobramycin.

119
Q

Sulfonamides :

A

** Sulfonamides were the 1st drugs available for systemic bacterial infections. They preceded PCN.

Overview Sulfonamides: structural analogs of PABA (Para-aminobenzotic acid) **–Vit B Family and is part of the folic acid structure.

120
Q

Sulfonamides : MOA-

A

MOA- Folic acid is a compound required for the synthesis of DNA, RNA, proteins (All Cells). However, bacteria are unable to take up folate from their surroundings. Must synthesize their own. Sulfonamides inhibit the synthesis of folic acid in bacteria. They will utilize the sulfonamide instead of PABA ant try to synthesize the folic acid.

121
Q

Sulfonamides:

Spectrum:

A 
Spectrum: Gram Positive Cocci   
Staph
Strep
Enterococcus
Peptococcus
Peptostreptococus
(sometimes even MRSA), 
Clamydia, 
P.Carinii, 
G.Bactilli (Esp H.Flu/E.Coli)
122
Q

Sulfonamides :

Therapeutic Uses:

A
  1. Therapeutic Uses: UTI, URTI, Sometimes PO therapy for Resolving MRSA if sensitivity data supports.
123
Q

Sulfonamides : Side Effects:

A

Side Effects:
Hematologic:
Hemolytic Anemia: G6PD Deficiency Anemia. (AA, Mediterranean Decent , Greek, Italian, Spanish, Portugese) ** Interesting that malaria does not survive as well in G6PD deficient patients. Thus it is believed that this was an acquired protective mechanism against malaria.

Agranulocytosis
Thrombocytopenia
Aplastic Anemia

Skin Reactions:
Photosensitivity
Mild Rashes

Stevens Johnsons. Mortality approx 25% ** Watch for cross sensitivity with loops, thiazides, sulfonylureas, celecoxib**

Kernicterus: In Newborns. Displaces billirubin from Albumin. Can Deposit into the brain and cause neurologic side effects. Don’t give to less than 2 months old, pregnancy, or breastfeeding.

Crystalluria- crystalizes out in the urine. Can cause renal toxicity. Uncommon in today’s generation of sulfonimides as the have enhanced solubility. It is still a goood idea to drink 8-10 glasses of water a day while taking it.

124
Q

Sulfonamides :

ADME:

A

ADME:
Absorption: Well absorbed. (IV- PO)

Distribution: Well distributed (lungs/prostate/ high concentrations in urine)

Elimination: Renally

Drug interactions: CY450 Inhibitor (CYP2C9)
**Warfarin
Phenytoin
Some oral hypoglycemics
Fluoxetine (Prozac)
125
Q

Combination: Trimethoprim:SMX (Bactrim/Cotrim)

MOA-

A

MOA- Inhibits consecutive steps in folic acid synthesis.

**Synergistic Combo!!!

126
Q

Combination: Trimethoprim:SMX (Bactrim/Cotrim)

Spectrum-

A 
Spectrum- Enhanced when compared to wither agent alone. 
    E.Coli
    Proteus
    Salmonella / Shigella
    H.Flu
    P.Carinii
    Some Gram Positive (Even MRSA)
127
Q

Combination: Trimethoprim:SMX (Bactrim/Cotrim)

Uses:

A

UTIs, Otitis, Bronchitis, Pneumonia, PCP

128
Q

Name the Fluroquinolones

A

Drugs: Ciprofloxacin, LevoFloxacin, Moxifloxacin (And others)

129
Q

Ciprofloxacin, LevoFloxacin, Moxifloxacin

MOA-

A

MOA- Inhibits DNA gyrase which converts circular DNA into supercoil structure. If we prevent the supercoil, replication cannot take place.

130
Q

Ciprofloxacin, LevoFloxacin, Moxifloxacin

Spectrum- Bactericidal:

A 
Spectrum- Bactericidal:
Most Gram Negative Rods
E.Coli
Klebs
Salmonella
Shigella
H.Flu
Pseudomonas
Gram Negative Cocci- Gonococcus, meningococcus
Gram Positive Pneumococcus
131
Q

Ciprofloxacin, LevoFloxacin, Moxifloxacin

Pharmacokinetics:

A

Excellent Absorption rivals IV (IV ->PO)

Excellent Distribution aside from CSF

132
Q

Ciprofloxacin, LevoFloxacin, Moxifloxacin

Uses:

A

URI, UTI, Bones, Joints, and soft tissue.

133
Q

Ciprofloxacin, LevoFloxacin, Moxifloxacin

ADE-

A

ADE-
CNS: Dizziness, confusion, psychosis, rarely seizures.

Tendon Rupture: Typically in the Achilles tendon. Disrupts cartilage stabilization. Generally CI in children less than 18 years old.

Photosensitivity

Drug Interactions -
Absorption impaired by cations (antacids, iron, calcium, and zinc) Administer quinolones 6 hours prior or 2 hours after.

Theophylline- increased levels due to CYP450 inhibition (Especially Cipro)

Warfarin- Increased Levels.

134
Q

Metronidazole-

MOA-:

A

MOA-: Bactericidal to Anaerobes. Anaerobes take up the drug wich ultimately precipitates DNA strand Breakage.

135
Q

Metronidazole-

therapeutic Uses:

A

Therapeutic Uses: Anaerobes

 H.Pylori Surgical Procedures (Belly Bugs)

 C-Diff Colitis (PO)
136
Q

Metronidazole- Side Effects:

A

Side Effects: Disulfiram Reaction

Drug Interactions: Warfarin

137
Q

Rifampin-

MOA-

A

MOA- Inhibits RNA polymerase which inhibits protein synthesis

138
Q

Rifampin- Spectrum-

A

Spectrum- Most Gram Positive Cocci and Gram Positive Rods like H.Flu. ** DO NOT USE as Mono Treatment due to development of rapid resistance.

139
Q

Rifampin-

Pharmacokinetics-

A

Pharmacokinetics- potent inducer of CPY450 (Warfarin / Phenytoin / Carbamazepine / oral contraceptives, Protease inhibitors, ect. )

140
Q

Rifampin-

Uses:

A

Uses:
Tuberculosis- in combo with other drugs
Meningococcus- highly effective for add on therapy with meningitis
Infections caused by staph epi and staph aureas- endocarditis, osteomylitis

141
Q

Rifampin- ADE-

A

ADE-
Hepatoxicity- transaminase elevation approximately 14% of the time. Typically harmless.

Dislocation of body fluids- red orange dislocation of the urine, sweat, tears, can permanently stain contact lenses.

142
Q

What are the Antibiotics that interfere with warfarin

A 
Sulfonamides
Trimethoprim
Ciprofloxacin
Moxifloxacin
Metronidazole
Erythromycin
Azythromycin
Clarithromycin
Rifampin

Pharmacology 2 (7 decks)

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