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Patho Fall 2023 Block 1 > Test 1A > Flashcards

Test 1A Flashcards

1
Q

What are the 4 classes of antibiotics that INHIBIT CELL WALL SYNTHESIS?

A
  1. Penicillin
  2. Cephalosporin
  3. Carbapenem
  4. Vancomycin (Glycopeptide is the class)
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2
Q

What does “inhibit cell wall synthesis” mean?

A

These antibiotics inhibit transpeptidase to weaken the cell wall…Letting fluid into the cell.

Antibiotic does not let the cell wall be what it is supposed to be: when bacteria don’t have a stable cell wall–> they DIE!

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3
Q

MOA of penicillins:

A

Disrupt cell wall synthesis, inhibit transpeptidases, activate autolysis (kill themselves).

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4
Q

Penicillin typically treats:

A

UTI, STI (gonorrhea), URI/pneumonia, peritonitis, septicemia.

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5
Q

Adverse reactions of penicillin:

A

Pruritis (itching), rash, GI upset, yeast, anaphylaxis.

Get a good medicine history: lots of drug interactions!

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6
Q

The 4 types of penicillin:

A
  1. Natural PCN
  2. Penicillinase resistant PCNs
  3. Aminopenicillins
  4. Extended spectrum
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7
Q

Fun Facts about Natural PCN: PCN G&V:

A

-Usually IM/IV, but PO is a thing.
-LEAST toxic.
-Works on gram -/+, cocci, anaerobic bacteria, spirochetes.
-1/2 life is 30 min (unless kidney dysf)
-CAN be used with aminoglycosides (gets in cell & disrupts protein synthesis).
-USED IM A LOT to treat SDIs.

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8
Q

Fun Facts about Penicillinase Resistant PCNs: NAFCILLIN (IV):

A

-IV ONLY
-Resist breakdown by penicillinase enzyme.
-Sometimes called “ANTI-STAPH PCN”

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8
Q

Fun Facts about Aminopencillins: AMPICILLIN:

A

-1st broad spectrum
-SE: diarrhea and rash.
-PO/IV–> if giving a PO Aminopenicillin, give Amoxicillin.
-Renal sensitive (monitor kidneys).
-Lots of drug resistance.

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8
Q

What are the 2 types of aminopenicillins?

A

Ampicillin and Amoxicillin

*Structure allows these to work better against GRAM - than other PCNs.

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9
Q

Fun Facts about Aminopenicillins: AMOXICILLIN:

A

-Less side effects than ampicillin.
-Common PEDS med: ear, nose, throat, genitourinary and skin. STREP A
-PO only.

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10
Q

Fun Facts about Extended Spectrum PCN: PIPERACILLIN:

A

-WIDER spectrum: MOST intense!
-Always given with beta lactamase inhibitor.
-ANTI-pseudomonal–>good for pseudomonas infections.
-SE: Affects platelet function and watch patient’s with renal dysfunction.

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11
Q

MOA of Cephalosporins:

A

Inhibit cells wall synthesis (inhibit transpeptidases); activate autolysis (they kill themselves).
-Often resistant to beta-lactamase.

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12
Q

SE of Cephalosporins:

A

-Some cross-sensitivity with PCN allergy (don’t give if patient has PCN anaphylaxis).
-Mild diarrhea, abdominal cramps, RASH, pruritis, redness, edema.
-Pregnancy B category.

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13
Q

1st generation Cephalosporins:

A

Cefazolin & Cephalexin

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14
Q

Fun Facts: 1st generation Cephalosporins: CEFAZOLIN & CEPHALEXIN:

A

“Fazolis LEX”
-works well for Gram (+) bacteria: Staph and non-enterococcal strep infections.
-Given PO and IV (Cefazolin is IV ONLY).
-Treats: UTIs (keflex) and skin infections.
-CEFAZOLIN: common for surgical prophylaxis.
-NO BBB.

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15
Q

Fun Facts: 2nd generation Cephalosporins: CEFUROXIME & CEFOTETAN:

A

“FUR FOX TAN”
-NOT common
-More gram (-), but does have gram (+) coverage.
-IV & PO
-CEFUROXIME: does not kill anerobic bacteria (bac that don’t need O2); BUT IS USED for some intestinal infections.
-NO BBB & NO pseudomonas.

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16
Q

Fun Facts: 3rd generation Cephalosporins: CEFTRIAXONE, CEFTAZIDIME, & CEFOTAXINE:

A

“ONE DIME TAX$$$”
-Most potent in fighting Gram (-).
-IV and IM only.
-CEFTRIAXONE:
-Extremely long-acting (long 1/2 life) so
only 1x/day.
-CROSSES BBB.
-DO NOT give to pts with liver failure.
-CEFTAZIDIME:
-Works well for pseudomonas (although
becoming more resistant.

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17
Q

Fun Facts: 4th generation: Cephalosporins: CEFEPIME:

A

“4th Pie”
-VERY broad spectrum (gram+/-).
-NOT SURE OF what kind of infection??? A lot of time will start pt on Cefepime b/c it works against A LOT!
-Treats: skin infections, UTIs, pneumonias and DOES CROSS BBB and work against pseudomonas.

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18
Q

Fun Facts: 5th generation: Cephalosporins: CEFTAROLINE:

A

“end of the LINE”
-Good for multi-drug resistant staph: MRSA, MSSA, VRSA/VISA.
-NOT good for enterobacteria, pseudomonas, ESBL or Klebsiella.
-IV only.
-Renally dosed–>monitor kidneys.

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19
Q

What are the Carbapenems?

A

Imipenem/Cilastin & Meropenem

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20
Q

MOA of Carbapenems:

A

Inhibits cell wall synthesis.

-VERY BROAD SPECTRUM

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21
Q

AE of Carbapenems:

A

Drug-induced seizure.
-All IV & must be infused over 60 MIN b/c of seizure

-Typically used as a last resort med so that resistance does not develop (BROADEST SPECTRUM OF ALL ABX).

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22
Q

Fun Facts about Carbapenems: IMIPENEM/CILASTIN:

A

-USED FOR COMPLICATED infections.
-Imipenem is combo’d with Cilastin–> which inhibits enzyme in kidneys (dehydropeptidase) so imipenem is not broken down and stays in system longer/more effective.
-Very resistant to beta-lactamase.
-AE: nephrotoxicity (monitor kidneys) and seizures (especially in elderly).
-CAN CROSS BBB
-IV only.

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23
Q

Fun Facts: Carbapenems: MEROPENEM:

A

-Little less coverage than imipenem, but still gram (-/+) and broad spectrum.
-Does NOT degrade kidneys & LESS seizure activity.
-SE: rash/diarrhea/GI distress.
-IV only.

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24
Q

SE of Imipenem/Cilastin:

A

Nephrotoxicity: monitor kidneys
Seizure (esp. elderly).

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25
Q

MOA of Glycopeptide: VANCOMYCIN:

A

Inhibits cells wall synthesis: destroys by binding to bacterial cell wall, producing immediate inhibition of cell wall synthesis and death.

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26
Q

Vancomycin is used to treat:

A

-Gram (+) infections (including MRSA & PCN resistant pneumococcus).
-ORAL VANC–> given to treat C-DIFF & pseudomembranous colitis.
-DOES NOT cross BBB.

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27
Q

LOTS of SE for Vancomycin:

A

-Monitor kidneys: kidneys eliminate Vanc; decrease dose for renal dysfunction.
-OTOTOXICITY: with high levels (reversible)
-Immune-mediated thrombocytopenia: damage to platelets–> monitor platelets.
-Monitor neuromuscular blockades (paralytics)–>respiratory
-RED MAN syndrome: from rapid infusion: flush, rash, itchy, tachycardia, hypotension.
-1/2 the dose (slower, over longer time)
-Pre-medicate with Benadryl.
-Draw peak and trough levels.

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28
Q

Classes that INHIBIT PROTEIN SYNTHESIS:

A
  1. Aminoglycosides
  2. Lincosamides
  3. Macrolides
  4. Tetracyclines
  5. Fluoroquinolones
  6. Sulfonamides
  7. Metronidazole
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29
Q

How does inhibition of protein synthesis work?

A

By targeting:
-Transcription: nucleus, messenger RNA or cytoplasm. OR
-Translation: cytoplasm, ribosomes, add amino acids, protein synthesis (damage).

-STOPS the bacteria from making competent protein–> which then kills the,/stops them from reproducing.

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30
Q

MOA of Aminoglycosides:

A

Inhibits/alters protein synthesis–> binds to bacterial ribosomes and prevents protein synthesis.

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31
Q

Fun Facts about Aminoglycosides: GENTAMYCIN, AMIKACIN & TOBRAMYCIN:

A

-Potent ABX that work well on Gram (-)… also work on gram (+), but need other ABX for synergistic effect.
- Used to treat COMPLICATED infections: complicated UTIs, gynecological infections, peritonitis, endocarditis, PNS, osteomyelitis (related to DM).

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32
Q

SE of Aminoglycosides: GENTAMYCIN, AMIKACIN & TOBRAMYCIN:

A

SE: nephrotoxicity (monitor BUN/Cr), Ototoxicity.

Gentamycin: be careful giving with paralytics (PROFOUND respiratory dysfunction); myasthenia gravis; CNS–> confusion, depression, numb/tingling; cochlear damage (permanent).

-Therapeutic monitoring: peak and trough levels–>dose accordingly to renal function.

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33
Q

SE of Gentamycin:

A

Gentamycin: be careful giving with paralytics (PROFOUND respiratory dysfunction); myasthenia gravis; CNS–> confusion, depression, numb/tingling; cochlear damage (permanent).

34
Q

MOA of Sulfonamides: SULFAMETHOXALE & TRIMETHOPRIM: (Bactrum)

A

Don’t destroy, but inhibit bacteria growth by preventing the synthesis of FOLIC ACID needed for DNA synthesis.

35
Q

Sulfonamides: SULFAMETHOXALE & TRIMETHOPRIM Treats:

A

uncomplicated UTIs, respiratory infections, salmonella, shigellosis.
-Often given to HIV patients.

36
Q

SE of Sulfonamides: SULFAMETHOXALE & TRIMETHOPRIM:

A

-Don’t give to patients with sulfa allergies.
-Photosensitivity.

37
Q

MOA of Metronidazole:

& Treats:

A

Inhibits DNA synthesis: Anerobic only.
Antiprotozoal and antibacterial

-Crohn’s disease
-antibiotic associated diarrhea (c-diff)…flagyl + PO vanc.
-“flagyl”

38
Q

SE of Metronidazole:

A

-DO NOT TAKE WITH ALCOHOL (24 hours before or 36 hours after)–> toxic metabolite.
-AE: N/V, xerostomia (dry mouth), vaginal candidiasis.
-Lots of drug-drug interactions.
-(Flagyl)

39
Q

MOA of Fluroquinolones: CIPROFLOXACIN & LEVOFLOXACIN:

A

Destroys bacteria by altering their DNA.
-Mostly Gram (-) and some gram (+) coverage. VERY POTENT- Broad spectrum.
-Very good oral absorption: good for home use!

40
Q

Fun Facts about Fluroquinolones: CIPROFLOXACIN:

A

-PO, IV, topical.
-treats: UTIs, STIs (gonorrhea), U/L RTIs, ANTHRAX. (RAPID GROWING ORGANISMS)
-NO BBB

SE: prolonges post-ABX effects: concentrated in neutrophils:
-stays in bone, joints.
-DONT give to under 18 and over 60
(arthropathy effect).
-If there is bone pain—> STOP!

41
Q

SE of CIPROFLOXACIN:

A

SE: prolonges post-ABX effects: concentrated in neutrophils:
-stays in bone, joints.
-DONT give to under 18 and over 60
(arthropathy effect).
-If there is bone pain—> STOP!

42
Q

Fun Facts about Fluroquinolones: LEVOFLOXACIN:

A

-Broad spectrum of activity (like CIPRO), but advantage of only taking 1X/day.
-PO or IV–> 100% bioavailability orally.
-Less resistance.
USES: more activity against pneumococcal and other ‘atypical’ respiratory inf (acute sinus inf, bronchiolitis, comm-acquired PNA).

SE: seizures, kidney failure, heart rhythm, photosensitivity.

43
Q

SE of Levofloxacin:

A

SE: seizures, kidney failure, heart rhythm, photosensitivity.

44
Q

What are the 3 Tetracyclines:

A
  1. Tetracycline
  2. Doxycycline
  3. Minocycline
45
Q

What are the 2 Fluroquinolones?

A
  1. Ciprofloxacin
  2. Levofloxacin
46
Q

MOA of Tetracyclines:

A

Bacteriostatic drugs that inhibit protein synthesis by binding to ribosomes.
-Broad spectrum–> major resistance has developed.

47
Q

Uses of Tetracyclines:

A

Rocky mountain spotted fever, chlamydia & trichomonas, Lyme disease, cholera, PID, mycoplasma PNA, acne.

48
Q

SE of Tetracyclines:

A

-NO pregnant women/nursing women or children under 8: enamel hypoplasia, discoloration of teeth.
-photosensitivity, yeast inf and thrombocytopenia.

49
Q

Fun Facts about Tetracycline: TETRACYCLINE:

A

-Bacteriostatic.
-PO: give fasting, giving more decreased % of absorption.
-NO IV.
-concentrates in bone, liver, spleen and TEETH.
-SE: N/V/D, H/A, photosensitivity, dizziness, angioedema and anaphylaxis.

50
Q

Fun Facts about Tetracycline: DOXYCYCLINE:

A

-Treats: Chlamydia and mycoplasma infections.
-Prophylaxis for STIs
-Acne and other non-dangerous skin infections.

51
Q

Fun Facts about Tetracycline: MINOCYCLINE:

A

-Neisseria meningitides.
-Decreases symptoms of RA
-USES: meningitis, RA, acne, rosacea.

52
Q

What are the Macrolides?

A
  1. Erythromycin
  2. Azithromycin
53
Q

MOA of Macrolides:

A

Inhibit protein synthesis by binding to ribosomes.
-Bacteriostatic in general, bactericidal in high concentrations.

54
Q

USES of Macrolides:

A

“YUCK DRUGS”
- upper/lower resp inf, skin inf, soft tissue inf, STIs (gonorrhea) & unique infections: Legionnaire’s, Listeria, mycoplasma PNA.

-Works well against bacteria that get into a host cell and reproduce.

55
Q

Fun Facts about Macrolides: ERYTHROMYCIN:

A

-Has hypomotility benefits for DM gastroparesis & increased gastric motility & emptying.
NO BBB
-PO & IV (IV very painful) & oral absorption isn’t great.
-DO NOT TAKE ON AN EMPTY STOMACH! (GI upset)

56
Q

Fun Facts about Macrolides: AZITHROMYCIN:

A

(ZPACK)
-Less GI upset
-DONT TAKE WITH FOOD–> decreases absorption.
-Very good tissue penetration and long duration of action.

57
Q

MOA of LINCOSAMIDES: CLINDAMYCIN:

A

Binds to ribosomes and inhibits protein synthesis (stops the bacteria from reproducing).

58
Q

USES for Lincosamides: CLINDAMYCIN:

A

-Chronic bone infections, GU tract infection, intra-abdominal infection, anaerobic PNA, septicemia, serious skin infections, prophylaxis for endocarditis.

-ALL enterobacteria (VRE/CRE) are resistant to Clindamycin.

59
Q

SE of CLINDAMYCIN:

A

-GIVES C-DIFF
-Monitor use of paralytics for respiratory distress.
-VERY TOXIC–> monitor peak and trough levels

60
Q

MOA of ACYCLOVIR:

A

3 ways: 1. INTERFERES with viral nucleic acid synthesis (stop DNA/RNA synthesis); 2. PREVENTS virus from binding to cells (can’t get in = can’t replicate; 3. STIMULATES body’s immune system to kill virus.

61
Q

USES of ACYCLOVIR:

A

HSV1 (oral)
HSV2 (genital)
VZV (varicella/chicken pox)

-Decreases symptom severity & frequency- NOT a CURE! (the “gift” that keeps on giving”)
-Used for initial and recurrent treatment
-Routes: PO, IC, topical

62
Q

SE of ACYCLOVIR:

A

GI distress, renal impairment, seizures, ITP (careful with patients with low platelets).
IV: tissue necrosis.

63
Q

MOA of OSELTAMIVIR:

A

Inhibit neuraminidases in flu virus. (TAMIFLU)

64
Q

USES of OSELTAMIVIR:

A

Prophylaxis and treat ACTIVE FLU
-Before/within 48 hours of symptom
onset.
-Mostly elderly/immunocompromised
after known exposure to FLU A or B.

65
Q

SE of OSELTAMIVIR:

A

N/V; seizures; renal impairments.

66
Q

MOA of GANCICLOVIR:

A

Inhibits DNA polymerases–> chain termination (stops replication).

67
Q

USES of GANCICLOVIR:

A

Cytomegalovirus (CMV): immunocompromised pts (AIDS/transplant).
-Controls–> DOES NOT CURE!

-IV and PO

68
Q

SE of GLANCICLOVIR:

A

4 BLACK BOX warnings:
1. hematologic toxicity (low blood ct)
2. Fertility
3. Fetal toxicity
4. Carcinogenesis

-Don’t give with Imipenem/Cilastin (seizure)
-Watch kidneys
-If you as a RN crush it and it gets on your skin–> wash with soap and water

69
Q

Bacteriostatic

A

Medications that slow or inhibit bacterial growth.

70
Q

Bactericidal

A

Medications that KILL the bacteria.

71
Q

Narrow spectrum

A

Effective against a “few” species of organisms.
-Using a BB gun
-Know the organism and what the drug s sensitive to.

72
Q

Resistance

A

Ability of an organism to survive against an antimicrobial or render the antimicrobial ineffective.
-Innate: always been that way.
-Acquired: mutated to resist.

73
Q

Selective toxicity

A

Toxic to a specific cell while sparing other cells around it: so normal cells in close proximity don’t also get killed.

74
Q

Example of a super infection:

A

C-Diff…
Giving the patient antibiotics for one thing/primary infection in the process give them C-Diff.

75
Q

Ceftriaxone:

A

1of3 3rd generation Cephalosporins:
-EXTREMELY long-acting: long 1/2 life–> 1X/day.
-DOES cross BBB
-IV/IM only.
-DO NOT give to patients with liver failure.

76
Q

Ceftaroline

A

5th generation cephalosporin:
-Give for NASTY STAPH or MULTI DRUG resistant bacteria (MRSA/VRSA).
-Therefore, watch kidneys! STONG broad spectrum drug–> monitor kidney function!
-IV only.

77
Q

Peak

A

Draw a peak when theoretically the drug would be at the highest level in the patient’s system–> 15-30 min AFTER the drug is started/its in the patient’s system.

78
Q

Trough

A

Lowest level of the drug in patient’s system. Measured immediately before the next dose is given. (30 minutes prior to next dose due).

79
Q

What are some drug interactions of penicillin?

A

Oral contraceptives, warfarin & NSAIDs

80
Q

Biggest worry with Carbapenems:

A

SEIZURES
-infuse over 60 min

81
Q

What ABX causes red man?

A

Vanc

82
Q

What are the cephalosporins? Name them.

A

1st: Cefazolin & Cephalexin
2nd: Cefuroxime & Cefotetan
3rd: Ceftriaxone, Ceftazidime & Cefotaxine
4th: Cefepime
5th: Ceftaroline

83
Q

Penicillin G & V is used in combo with:

A

aminoglycosides.

84
Q

ABX that are good against pseudomonas?

A

-Piperacillin
-Ceftazidime
-Cefepime
-Vanc (pseudomembranous colitis)

Patho Fall 2023 Block 1 (3 decks)

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