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Pharm > Antibiotics, Antiviral, and Antifungal > Flashcards

Antibiotics, Antiviral, and Antifungal Flashcards

1
Q

How do bacteria harm the host?

A

 Divert nutrition away from host, depriving cells of O2 and food
 Elaborate toxic chemicals
 Activate a harmful immune response

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2
Q

Not all bacteria are harmful…

A

 Source of vitamins (K) & essential fatty acids
 Prevent over-growth of harmful bacteria

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3
Q

How the body defends against bugs

A

 Infections are typically “partially controlled” by the
body’s own immune system
 The invading organism gets a “foot hold”, but
can’t flourish, except in overt infections

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4
Q

How do antibiotics works with the body’s immune system

A

 Most antibiotics “tip the scales” in favor of the
immune system
 “slow” bacterial spread and reproduction so immune system can kill it of

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5
Q

Bactericidal

A

kills bacterial D E A D
* Penicillins and Vancomycin

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6
Q

Bacteriostatic

A

Blocks replication of bacteria
* Tetracycline
* Chloramphenicol

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7
Q

In an “immunocompramized patient”, which is the preferred type of antibiotic, a bacteriosidal or a bacteriostatic agent?

A

Bactericidal

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8
Q

Bacteria - Prokaryotes

A
  • Cell wall
  • Cell membrane (unique phospholipids)
  • 60s (larger) ribosome
  • No nuclear membrane
  • Unique mechanism of RNA/DNA synthesis
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9
Q

Human Hosts (Eukaryotes)

A
  • No cell wall
  • Cell membrane (but different phospholipids compared to bacteria)
  • 50s (larger) ribosome
  • Nuclear membrane
  • standard eukaryotic RNA/DNA synthesis
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10
Q

What is selective toxicity

A

 Degree to which the drug impairs/kills invading
organism’s cells compared to the host’s cells –> similar to therapeutic window

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11
Q

When to use Broad spectrum antibiotics:

A

Useful when infection is caused by “unknown”
organism

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12
Q

Broad spectrum antibiotics side effects

A

 Kill off “good” bacteria”
 Predispose to resistance
 Typically strong medications with toxic side effects (except penicillins)

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13
Q

Narrow Spectrum Antibiotics

A

 Specifically target one type of bacteria
 May have better side effect profile
 Less resistance
 Less effect on normal bacteria in and on body

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14
Q

Mechanisms of antibiotic drugs

A

 Cell wall synthesis inhibitors
 Cell membrane inhibitors
 Protein synthesis inhibitors
 Metabolic and nucleic acid (RNA and/or DNA) synthesis inhibitors

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15
Q

Inhibition of Cell wall synthesis and function

A
  • bacteria have a rigid cell wall
  • Drugs targeting the synthesis of bacterial cell wall typically have good selective toxicity
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16
Q

Bacteria have a rigid cell wall -

A

 Key constituent is peptidoglycans
 Peptidoglycans are cross-linked in a way that
provides strength
 Any compromise of bacterial cell architecture
activates a suicide/autolysis pathway

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17
Q

One new antibiotic targets…..

A

bacterial lipid II and III, important precursor molecules for forming the cell wall

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18
Q

Bacterial Cell Wall Inhibitors

A

Beta-Lactam antibiotics
Cephalosporins & Penicillins

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19
Q

What is the first known antibiotic

A

Penicillins

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20
Q

How do penicillins work

A

Binds to a special bacterial cell wall enzyme (penicillin binding protein) used in peptidoglycan synthesis
 Bacteria develop a special enzyme that degrades penicillins (penicillinase)

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21
Q

Naturally occurring penicillins

A

Penicillin G & V
Narrow

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22
Q

Synthetic penicillins

A

Ampicillin & Amoxicillin
Broader

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23
Q

What penicillins have been developed that are resistant to breakdown or are combined with penicillinase-blocker

A

 Augmenten (Amoxicillin plus Clavulate, inhibits breakdown)

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24
Q

Imipenem

A

Relatively narrow spectrum penicillin

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25
Q

Cilastatin

A

a compound that prevents the excretion of impenem from the kidney, thus trapping it

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26
Q

Primaxin

A
  • a combination of Imipenem and Cilastatin that has very broad spectrum antibiotic activity
     Active against > 90% of all clinically important
    bacterial infectious agents
     Overcomes resistance in many infectious agents  Acts synergistically with aminoglycside antibiotics
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27
Q

Uses of Penicillins

A

 Still one of the most useful classes of antibiotics
 Mainstay of therapy for skin, respiratory, GI
infections
 Generally well tolerated
 Very high therapeutic window

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28
Q

Limitations of Penicillins

A

 Methicillin-resistant S. aureus (MRSA) –> Other beta-lactam resistant strains have also developed
 Allergic reactions –> Type II hypersensitivity reactions; Potential for anaphylactic shock and bronchospasm
 Prolonged use: CNS & hematological side effects

29
Q

Cephalosporins

A

Different class, but similar mechanism as
penicillins

30
Q

3 generations of drugs within cephalosporins

A

 1st- narrow, mainly gram +
 2nd-broader,gram + & -
 3rd-broad against gram -, but no effect on gram +  4th generation, but mainly used in Europe

31
Q

Uses of Cephalosporins

A

 Drug of choice for UTIs, prophylaxis post-surgery  Alternative or “second line” of defense if penicillin
fails

32
Q

1st Generation Cephalosporin

A

Cefazolin

33
Q

Limitations of Cephalosporins

A

 Most cephalosporins are well tolerated
 Produce type-II hypersensitivity reaction, similar to penicillins
 Often there is “Cross-reaction” with penicillins
(i.e. if patients is allergic to one, greater chance
they are allergic to the other)
 Susceptible to resistance if infection is resistant to penicillin (Methicillin)

34
Q

Polymixins

A
  • Bacterial Cell Membrane Inhibitors
  • Cationic compounds attracted to the bacterial cell
    phospholipid membrane (more than the host’s cell membrane)
  • Directly “Punch holes” in the cell membrane layer
  • Results in connection between inside and outside:
    creates a “leak” that is fatal
  • Rapidly lethal to bacteria
  • Not very selectively toxic (i.e. many adverse/side
    effects)
35
Q

Vancomycin

A
  • Bacterial Cell Membrane Inhibitors
  • Reserved for serious life-threatening infections (C-diff, staph, endocarditis)
  • Ototoxic and nephrotoxic
36
Q

Bacitracin

A
  • Bacterial Cell membranes inhibitors
  • Useful for STDs and a wife variety of infections, but limited by side effects when given systemically
  • Used topically for burns and skin infections
37
Q

How to bacterial protein synthesis inhibitors work

A

 Most bind to bacterial ribosomes
 Inhibit polypeptide synthesis or leads to misreading of mRNA
 May be bacteriostatic or bactericidal

38
Q

Largest subclass of bacterial protein synthesis inhibitors

A

Aminoglycosides
- very broad spectrum
- toxicity problems, monitors liver enzymes

39
Q

Macrolides/Erythromycins

A
  • Bacterial Protein Synthesis Inhibitors
  • good for gram +’s, but side effects include hepatitis
  • Bacteriostatic at low dose, bactericidal at high dose
40
Q

Azithromycin

A
  • Macrolides/Erythromycin
  • ear & respiratory tract infections
  • Has added benefit of being packaged as a “Z-pack” allowing short duration of Rx
41
Q

Tetracyclines

A
  • Bacterial Protein Synthesis Inhibitors
  • broad spectrum, in general can’t be taken with Ca
    foods
  • Doxycycline (Vibramycin)- broad spectrum bacteriostatic agent
42
Q

Chloramphenicol

A
  • Bacterial Protein Synthesis Inhibitors
  • Broad spectrum, severe infections
43
Q

Uses and Limitations of Tetracycline

A

 Useful for hard to Rx infections like Chlamydial and Rickettsia and spirochetes
 Limited by development of tetracycline- resistant bacteria strains

44
Q

Ethionamide

A
  • inhibits bacteria protein synthesis
  • used as a second line of defense to treat tuberculosis or Hansen’s disease
45
Q

How do Bacterial RNA/DNA Synthesis Inhibitors work?

A

 May bind bacterial DNA directly preventing replication or bind to and inhibit enzymes
used in replication or transcription
 Mainly as “back up” antibiotics (when there
is resistance or reaction) or for severe infections

46
Q

Are Bacterial RNA/DNA Synthesis Inhibitors bacteriostatic or bactericidal?

A

Most are bacteriostatic

47
Q

Characteristics of Bacterial RNA/DNA Synthesis Inhibitors

A
  • low selective toxicity/many side effects
  • very diverse family
  • Mainly as “back up” antibiotics (when there is resistance or reaction) or for severe infections
48
Q

RNA/DNA Synthesis Inhibitor Drug

A

Ciprofloxacin (Cipro): useful for a variety of infections including UTI
Class: Floroquinolene: inhibits DNA gyrase, blocking DNA coiling

49
Q

Antibiotic Resistance

A
  • Antimicrobial Resistance is accelerating: MRSA, VRE, MDRSA, MDRTB
  • New drug development is not keeping pace
50
Q

Solutions to antibiotic resistance

A

 Eliminating antibiotics from livestock feed
 Decreasing use of antibiotics for self-limiting
infections
 Eliminating use of antibiotics for viral infections

51
Q

Do the matching the antibiotic with the correct cellular mechanism thing

A
52
Q

Virus mechanisms

A

 Work by being incorporated into host’s cell
DNA and directing their self replication and dispersal
 Can be either DNA or RNA based
 Usually have a protein coat, but can also
have a lipid/glycoprotein envelope

53
Q

How to anti-viral drugs work

A

by inhibiting the DNA polymerase enzyme

54
Q

Acyclovir (Zovirax)

A
  • Anti-viral
  • Treats Herpes infection
  • In infected cell converted to acyclovir triphosphate
    (ATP) by viral thymidine kinase enzyme
  • ATP inhibits the DNA polymerase enzyme
  • ATP is also incorporated into viral DNA strands, further inhibiting function
  • Only effective in preventing or “limiting” infection… does not kill off dormant virally infected cells
55
Q

Side effects of Acyclovir

A

impaired renal function
hematological
GI and CNS disturbances

56
Q

Antivirals to treat AIDS

A
  • Zidovudine
  • Inhibits the reverse transcriptase enzyme used to convert viral RNA to DNA
57
Q

Saquinavir Mesylate

A

 Anti-retroviral, protease inhibitor used to Rx AIDS  Prevents cleavage of viral polypeptide such
that mature viruses cannot be formed
 Used exclusively in advanced HIV infection with
low CD4 count
 Many side effects including CNS disturbances
 N&V and GI problems common
 Pancytopenia- may be lethal

58
Q

Terminology for AIDS therapies

A

 cART = combination antiretroviral therapy
 HART = highly active antiretroviral therapy These are synonymous and the specific combination of antiviral drugs differs
** These are synonymous and the specific combination of antiviral drugs differs

59
Q

How many Hepatitis-B medications are out there

A

7 approved anti-viral drugs for chronic hepatitis B infection

60
Q

Standard therapy for hepatitis B

A

Interferon - 2b (interferon A)

61
Q

Side effects of hepatitis medications

A

 Flu-like symptoms: pyrexia, myalgia and headache
 Adverse effects Rx with NSAIDS
Other AE: dizziness, fatigue, arthralgia, diarrhea,
anorexia, neutropenia and leukemia, irritability & depression

62
Q

What does hepatitis b medication result in

A

clearance of serum HBV DNA in 25% and
63% of patients with HBeAg+ and HBeAg- hepatitis B, respectively

63
Q

Remdesivir

A

 In October 2020, FDA approved remdesivir to Rx
COVID-19 in adults and children > 12 y/o.
 Clinical trials suggest remdesivir may modestly
speed recovery
 Mechanism: nucleoside analog and inhibits the
RNA-dependent RNA polymerase of SARS-CoV-2

64
Q

Adverse Effects of Remdesivir

A

pain, bleeding, bruising of the skin, soreness, or swelling near the place where the medication was injected

65
Q

Fungi

A
  • ubiquitous throughout the soil, water and air… about 100,000 species
  • normally harmless, but when immune fx is impaired, they may cause pathology
66
Q

Primary fungi infections in humans

A

Aspergillosis, Blastomycosis, Cryptococcosis and
Histoplasmosis

67
Q

What is Mycosis

A

infections caused by fungi

68
Q

minor fungal infections are typically controlled by…

A

immune system

69
Q

Amphotericin B

A

 Most common antifungal agent prescribed
(Amphocin)
 Useful for Candida and Cryptococcus
 Administered by slow IV infusion or by local or topical
administration
 Binds to fungal cell membrane lipid leading to increased permeability and death
 Many side effects including HA, fever, muscle & joint pain, weakness, N&V, nephrotoxicity

Pharm (12 decks)

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