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PATHO/PHARM I > Week 4: Infection for real this time > Flashcards

Week 4: Infection for real this time Flashcards

1
Q

What is the PROCESS of infection?

A
  1. Encounter
  2. Transmission
  3. Colonization
  4. Invasion or Penetration
  5. Dissemination
  6. Cellular or tissue damage
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2
Q

Two ways that an individual can ENCOUNTER or come in contact with microorganisms

A
  1. Endogenous microorganisms
  2. Exogenous microorganisms
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3
Q

Endogenous microorganisms

A

Organisms already present in the body and part of the normal microbiome

Naturally on us

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4
Q

Exogenous microorganisms

A

Are transmitted from an external environment.

Not naturally on us

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5
Q

Two ways transmission of microorganisms can occur:

A
  1. Direct Transmission/Contact
  2. Indirect Transmission
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6
Q

Direct Transmission/Contact Two Types

A
  1. Vertical Transmission
  2. Horizontal Transmission
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7
Q

Vertical Transmission

A

From mother to child across placenta, during delivery from birth canal or breast milk

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8
Q

Horizontal Transmission

A

From one person to another through exposure to blood and body fluids

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9
Q

Indirect Transmission

A

Occurs from contact with:

infected materials,

inhalation or droplet infection,

ingestion of contaminated food or water

or inoculation

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10
Q

Colonization

A

Colonization is the ability of a pathogenic microorganism to survive and multiply on or within the human environment.

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11
Q

Invasion or Penetration

A

Invasion or penetration is the ability of pathogens to cross surface barriers including the skin and mucous membranes.

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12
Q

What does Invasion or Penetration require?

A

Requires penetration or break in the integrity of the barrier

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13
Q

Dissemination

A

Dissemination or spread of infection can occur by direct extension through surrounding tissue or through the blood or lymphatic vessels.

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14
Q

Two ways Tissue damage can occur?

A
  1. Directly
  2. Indirectly
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15
Q

Direct Tissue Damage

A

Production of toxins

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16
Q

Indirect Tissue Damage

A

Indirect as a result of an immune response with inflammation, swelling, scarring or necrosis

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17
Q

What are the STAGES of infection?

A
  1. Incubation Period
  2. Prodromal Stage
  3. Invasion or Acute Illness Period
  4. Convalescence
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18
Q

Incubation Period- what is it?

A

The period from initial exposure of infectious agent and the onset of symptoms.

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19
Q

Incubation period- what happens?

A

The microorganisms have:

entered the individual,

undergone initial colonization

and begun multiplying but are insufficient numbers to cause symptoms

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20
Q

How long does incubation period typically last?

A

Several hours to years

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21
Q

Prodromal Stage

A

The occurrence of initial symptoms, which are often very mild

Pathogens continue to multiply during this stage

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22
Q

Invasion or acute illness period

A

The pathogen is multiplying rapidly, invading farther and affecting the tissues at the site of initial colonization as well as other areas

the immune and inflammatory responses have been triggered; symptoms may be specifically related to the pathogen or to the inflammatory response

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23
Q

Convalescence: most cases what happens?

A

In most instances, the individual’s immune and inflammatory systems successfully remove the infectious agent and symptoms decline

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24
Q

Convalescence: less cases what happens?

A

the disease may be fatal or enter a latency phase with resolution of symptoms until pathogen reactivation at a later time

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25
Q

When can an infectious disease be contagious?

A

During all stages of infection

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26
Q

What are a common cause of disease?

A

Bacteria

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27
Q

How does gram staining differentiate microorganisms?

A

Gram staining differentiates the microorganisms as gram-positive or gram-negative bacteria

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28
Q

Gram positive bacteria

A

Gram-positive bacteria have teichoic acid and peptidoglycan in their outer membranes causing them to appear dark purple on Gram stain.

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29
Q

Gram- negative bacteria

A

Gram-negative bacteria have a lipopolysaccharide (LPS) in the outer membrane causing them to appear light pink on Gram staining.

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30
Q

Viruses

A

Are obligatory intracellular microbes consisting of nucleic acid protected from the environment by a protein shell, the capsid

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31
Q

The viral life cycle is completely intracellular and involves what steps

A
  1. Attachment/binding
  2. Penetration
  3. Uncoating
  4. Replication
  5. Assembly
  6. Release
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32
Q

Attachment during viral life cycle

A

Attachment to a specific receptor on the target cell

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33
Q

Penetration phase during viral life cycle

A

(entrance into the cell by endocytosis or membrane fusion)

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34
Q

Uncoating Phase during viral life cycle

A

is the release of viral nucleic acid from the viral capsid by viral or host enzymes

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35
Q

Replication phase during the viral life cycle

A

Replication is the synthesis of viral proteins and messenger RNA (mRNA).

The viruses inject their DNA or RNA into the host nucleus and use host resources for viral reproduction.

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36
Q

Assembly phase during viral life cycle

A

Assembly is the formation of new virions.

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37
Q

Release phase in viral life cycle

A

Release or shedding of new virions is by lysis or budding from the cell membrane.

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38
Q

Two basic Fungi Structures

A
  1. Single celled yeasts
  2. Multicellular molds
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39
Q

Infections caused by Fungi

A

Mycoses

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40
Q

Mycoses characteristics

A

Can be superficial, deep or opportunistic

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41
Q

Superficial mycoses

A

Occur on or near skin or mucous membranes and usually produce mild and superficial disease

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42
Q

Dermatophytes

A

Fungi that invade the skin, hair, or nails

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43
Q

Diseases that dermatophytes produce

A

The diseases they produce are called tineas (ringworm)

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44
Q

Examples of tineas

A
  1. Tinea pedis
  2. Tinea cruris
  3. Tinea capitis
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45
Q

Tinea pedis

A

feet ringworm

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46
Q

Tinea cruris

A

groin ringworm

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47
Q

Tinea capitis

A

scalp ringworm

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48
Q

What is the most common cause of fungal infections in humans?

A

Candida albicans

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49
Q

Candida albicans

A

Opportunistic yeast that is a commensal inhabitant in the normal microbiome of many healthy individuals.

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50
Q

Where does C. albicans reside in healthy individuals?

A

residing in the skin, gastrointestinal tract, mouth, and vagina.

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51
Q

When healthy people take antibiotic therapy, what can happen with their naturally occurring C. albicans?

A

Candida overgrowth may occur, resulting in localized infection, such as vaginitis or oropharyngeal infection (thrush)

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52
Q

In immunocompromised people (especially those with diminished neutrophil levels) what happens with the Candida?

A

disseminated infection may occur

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53
Q

What does disseminated candidiasis involve?

A

Disseminated candidiasis may involve deep infections of several internal organs

The mortality rate among individuals with septic or disseminated candidiasis is about 30%

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54
Q

Parasitic microorganisms

A

Establish a relationship in which the parasite benefits at the expense of the other species.

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55
Q

Examples of unicellular protozoa

A

Malaria

Amoeba

Flagellaes

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56
Q

Name for parasitic worms

A

Helminths

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57
Q

Example of Helminths

A

Flukes

Nematodes

Tapeworms

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58
Q

How are most protozoan parasites transmitted?

A

Many protozoan parasites are transmitted through vectors or ingested.

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59
Q

Two possible traits of Antibacterial antibiotics?

A
  1. Bactericidal
  2. Bacteriostatic
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60
Q

Bactericidal

A

bactericidal (kill the microorganism)

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61
Q

Bacteriostatic

A

inhibit growth until the microorganism is destroyed by the individual’s own protective mechanisms

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62
Q

Mechanisms of Action of Most Antibiotics

A
  1. Inhibition of the function or production of the cell wall/membrane
  2. Prevention of protein synthesis
  3. Blockage of DNA replication
  4. Interference with folic acid metabolism
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63
Q

Four Basic Actions of Antibiotic Resistance:

A
  1. Decrease the concentration of the drug at its site of action
  2. Inactivate the drug
  3. Alter the structure of drug target molecules
  4. Produce a drug antagonist
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64
Q

Beta-Lactamase

A

Produced by most S.aureus species

Prevents the action of penicillin on the microorganismal cell wall

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65
Q

Selective toxicity of a drug

A

is defined as the ability of a drug to injure a target cell or target organism without injuring other cells or organisms that are in intimate contact with the target.

selective toxicity indicates the ability of an antibiotic to kill or suppress microbial pathogens without causing injury to the host.

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66
Q

Three examples of how we achieve selective toxicity:

A
  1. Disruption of the Bacterial Cell Wall
  2. Inhibition of an Enzyme Unique to Bacteria
  3. Disruption of Bacterial Protein Synthesis
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67
Q

Two schemes to classify Antimicrobial Drugs:

A
  1. Narrow Spectrum Antibiotics
  2. Broad Spectrum Antibiotics
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68
Q

Narrow Spectrum Antibiotics

A

Narrow-spectrum antibiotics, are active against only a few species of microorganisms.

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69
Q

Broad Spectrum Antibiotics

A

Broad-spectrum antibiotics are active against a wide variety of microbes.

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70
Q

Which type of drugs are generally preferred? Narrow or broad spectrum?

A

Narrow spectrum

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71
Q

Classification of Antimicrobial Drugs by Susceptible Organisms

A
  1. Antibacterial Drugs
  2. Antifungal Drugs
  3. Antiviral Drugs
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72
Q

Classification by Mechanism of Action: Antimicrobial drugs fall into seven major groups based on mechanism of action.

Drugs that:

A
  1. Drugs that inhibit bacterial cell wall synthesis/ activate enzymes that disrupt cell wall
  2. Drugs that increase cell permeability
  3. Drugs that cause lethal inhibition of bacterial protein synthesis
  4. Drugs that cause nonlethal inhibition of protein synthesis
  5. Drugs that inhibit bacterial synthesis of DNA and RNA or disrupt DNA function
  6. Antimetabolites
  7. Drugs that suppress viral replication
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73
Q

Drugs that inhibit bacterial cell wall synthesis/ activate enzymes that disrupt cell wall- -How?

A

These drugs weaken the cell wall and promote bacterial lysis and death

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74
Q

Drugs that increase cell permeability- Why and effect?

A

Drugs increase the permeability of cell membranes, causing leakage of intracellular material

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75
Q

Drugs that cause lethal inhibition of bacterial protein synthesis- How?

A

We don’t know why inhibition = cell death

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76
Q

Drugs that cause nonlethal inhibition of protein synthesis-HOW

A

Inhibit bacterial protein synthesis.

These agents only slow microbial growth- not kill

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77
Q

Drugs that inhibit bacterial synthesis of DNA and RNA or disrupt DNA function- How?

A

These drugs inhibit synthesis of DNA or RNA by binding directly to nucleic acids or by interacting with enzymes required for nucleic acid synthesis.

They may also bind with DNA and disrupt its function.

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78
Q

Antimetabolites- how do they work on harming microbes?

A

These drugs disrupt specific biochemical reactions.

The result is either a decrease in the synthesis of essential cell constituents or synthesis of nonfunctional analogs of normal metabolites.

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79
Q

Drugs that suppress viral replication- how?

A

Most of these drugs inhibit specific enzymes

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80
Q

Microbes have four basic mechanisms for resisting drugs

A
  1. Decrease the concentration of a drug at its site of action
  2. Alter the structure of drug target molecules
  3. Produce a drug antagonist
  4. Cause drug inactivation
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81
Q

How do microbes acquire mechanisms of resistance?

A
  1. Spontaneous Mutation
  2. Conjugation
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82
Q

Spontaneous Mutation

A

Spontaneous mutations produce random changes in a microbe’s DNA.

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83
Q

How many drugs does spontaneous mutation confer resistance?

A

Spontaneous mutations confer resistance to only one drug.

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84
Q

Conjugation

A

Conjugation is a process by which extrachromosomal DNA is transferred from one bacterium to another.

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85
Q

Where does conjugation primarily occur?

A

Conjugation takes place primarily among gram-negative bacteria.

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86
Q

Difference between Spontaneous Mutation and Conjugation?

A

In contrast to spontaneous mutation, conjugation frequently confers multiple drug resistance.

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87
Q

Causes of Antibiotic Resistance?

A
  1. Lack of compliance with drug regimen
  2. Overuse of antibiotics
88
Q

Superinfection/Suprainfection

A

A superinfection is defined as a new infection that appears during the course of treatment for a primary infection.

89
Q

When do new infections (or superinfections) develop?

A

New infections develop when antibiotics eliminate the inhibitory influence of normal flora, thereby allowing a second infectious agent to flourish.

90
Q

Common example of suprainfection?

A

Development of vaginal Candida infection in a female treated with a broad spectrum antibiotic for a UTI

91
Q

Priniciple Adverse Effects of Penicillins:

A

Allergic reactions

92
Q

The penicillins have what in their structure and are therefore known as what?

A

Penicillins have beta- lactam ring in their structures and are known as beta-lactam antibiotics

93
Q

What is included in the beta-lactam family?

A
  1. Cephalosporins
  2. Carbapenems
  3. Azetreonam
94
Q

All the beta-lactam antibiotics share the same mechanism of action which is?

A

Disruption of the bacterial cell wall

95
Q

Penicillins weaken cell wall by two actions:

A
  1. Inhibition of transpeptidases
  2. disinhibition (activation) of autolysins
96
Q

The molecular targets of the penicillins (transpeptidases, autolysins, other bacterial enzymes) are collectively known as?

A

Penicillin-binding proteins (PBPs)

These molecules are names because penicillins must bind to them to produce antibacterial effects

97
Q

Penicillinase (Beta-Lactamases)

A

Beta-lactamases are enzymes that cleave the beta-lactam ring and thereby render penicillins and other beta-lactam antibiotics inactive

98
Q

Classification of Penicillins: Four major categories

A
  1. Narrow spectrum penicillins that are penicillinase sensitive (will be inactivated by penicillinase)
  2. Narrow spectrum penicillins that are penicillinase resistant
  3. Broad spectrum penicillins
  4. Extended spectrum penicillins
99
Q

Examples of Narrow Spectrum Penicillins: Penicillinase sensitive

A
  1. Penicillin G
  2. Penicillin V
100
Q

Example of Narrow-spectrum Penicillins: penicillinase resistant

A
  1. Nafcillin
  2. Oxacillin
  3. Dicloxacillin
101
Q

Examples of Broad-spectrum penicillins (aminopenicillins)

A
  1. Ampicillin
  2. Amoxicillin
102
Q

Examples of Extended-spectrum penicillin

A

Piperacillin

103
Q

How is Penicillin G (Benzylpenicillin) administered?

A

IV or IM

104
Q

Types of Allergic Reactions of Penicillins:

A
  1. Immediate
  2. Accelerated
  3. Delayed
105
Q

Immediate Penicillin Allergic Reaction occur when?

A

Immediate Reactions occur within 2 to 30 minutes after drug administration

106
Q

Accelerated Penicillin Allergic Reaction occur when?

A

Accelerated reactions occur within 1 to 72hours

107
Q

Delayed Penicillin Reactions occur when?

A

Delayed reactions occur within days to weeks.

108
Q

Immediate and Accelerated Allergic Reactions to Penicillin are mediated by what?

A

Immunoglobulin E (IgE) antibodies

109
Q

Anaphylaxis when taking penicillin leads to what?

A
  1. Laryngeal edema
  2. Bronchoconstriction
  3. Severe Hypotension
110
Q

Anaphylactic reactions occur more frequently with what drug?

A

penicillins

111
Q

Difference between Penicillin G and Penicillin V:

A

Penicillin V is stable in stomach acid, whereas penicillin G is not.

112
Q

Which Penicillin can be taken orally? G or V?

A

Because of its acid stability, penicillin V has replaced penicillin G for oral therapy.

113
Q

Beta-Lactamase Inhibitor

A

Beta-lactamase inhibitors are drugs that inhibit bacterial beta-lactamases.

114
Q

How to extend the antimicrobial spectrum of the penicillin?

A

By combining a beta-lactamase inhibitor with a penicillinase-sensitive penicillin, we can extend the antimicrobial spectrum of the penicillin.

115
Q

What are the combo of penicillins and beta-lactamase inhibitors that are available? There are three

A
  1. Ampicillin/sulbactam [Unasyn]
  2. Amoxicillin/clavulanate [Augmentin]
  3. Piperacillin/tazobactam [Zosyn]
116
Q

What is the most widely used group of antibiotics?

A

Cephalosporins

117
Q

Common Cephalosporin characteristics:

A

Are Beta-lactam antibiotics

Similar in structure and function to penicillins

Bactericidal

Low toxicity

118
Q

How are cephalosporins grouped?

A

The cephalosporins can be grouped into five “generations” based on the order of their introduction to clinical use.

119
Q

When progressing from first generation agents to fifth generation agents, what should we know about the cephalosporins?

A

As we progress from first-generation agents to fifth-generation agents, there is

(1) increasing activity against gram-negative bacteria and anaerobes,

(2) increasing resistance to destruction by beta lactamases, and

(3) increasing ability to reach the cerebrospinal fluid (CSF).

120
Q

Because of poor absorption, how should Cephalosporins be administered?

A

Because of poor absorption from the gastrointestinal (GI) tract, many cephalosporins must be administered parenterally (intramuscularly [IM] or intravenously [IV]).

121
Q

Adverse Effects to Cephalosporins:

A
  1. Allergic reactions
  2. Bleeding
122
Q

Drug interactions with Cephalosporin:

A

Alcohol + Cephalosporin

Drugs that promote bleed + Cephalosporin

Calcium + Ceftriaxone (3rd gen)

123
Q

Alcohol + Cephalosporin what happens?

A

induces a state of alcohol intolerance.

If a patient taking these drugs were to ingest alcohol, a disulfiram-like reaction could occur.

124
Q

Drugs that promote bleed + Cephalosporin

A

more bleeding!

125
Q

Characteristics about Carbapenems

A
  • are beta lactam antibiotics

-very broad antimicrobial spectrum

  • not active against MRSA
126
Q

Four drugs in Carbapenems:

A
  1. Imipenem,
  2. Meropenem
  3. Ertapenem.
  4. Doripenem
127
Q

Prototype Carbapenem

A

Imipenem

128
Q

Imipenem- what spectrum; route of administration?

A

Extremely broad spectrum

IV only

129
Q

Principle indications for Vancomycin

A

C.diff infection

MRSA infection

Treatment of serious infections with suspectible organisms in pts allergic to penicillins

130
Q

Major toxicity of Vancomycin and adverse effects:

A

Renal failure

Ototoxicity- usually reversible and is rare

131
Q

How to minimize risk of adverse effects of vancomycin?

A

Monitor drug serum level- peaks and troughs

infuse vancomycin slowly

132
Q

What drug is a cell wall synthesis inhibitor and does not contain a beta-lactam ring?

A

Vancomycin

133
Q

What happens when vancomycin is rapidly infused?

A

Rapid infusion of vancomycin can cause flushing, rash, pruritus, urticaria, tachycardia, and hypotension.

134
Q

How to avoid rapid infusion effects of vancomycin?

A

infusing slowly, over 60 minutes or more

135
Q

Azetreon belongs to a class of beta-lactam antibiotics known as?

A

Monobactams

136
Q

Mechanism of action for Aztreonam

A

Aztreonam binds to PBP3.

Drug inhibits cell wall synthesis and thereby promotes cell lysis and death

137
Q

Antimicrobial Spectrum and Therapeutic Use of Aztreonam a (Monobactam):

A

Narrow antimicrobial spectrum

Only active against gram negative aerobic bacteria

138
Q

How is Aztreonam administered and why?

A

It is not absorbed by the GI tract so must be administered parenterally (IM or IV)

139
Q

Adverse effect of Aztreonam

A

Similar to other beta-lactam antibiotics

140
Q

Drugs that are Bacteriostatic Inhibitors of Protein Synthesis:

A
  1. Tetracycline
  2. Macrolides
  3. Clindamycin
  4. Linezolid
141
Q

What spectrum type of drug are Tetracyclines?

A

The tetracyclines are broad-spectrum antibiotics.

142
Q

Four types of Tetracyclines:

A
  1. tetracycline,
  2. demeclocycline,
  3. doxycycline
  4. minocycline
143
Q

Disorders that Tetracyclines are first line drugs are:

A
  1. Treatments of infectious disease
  2. Treatment of acne
  3. Treatment of Peptic Ulcer Disease
  4. Mycoplasma pneumoniae
  5. Lyme Disease
  6. Anthrax
144
Q

How is Tetracylines effected by food intake?

A

Absorption of three agents (tetracycline, demeclocycline, and doxycycline) is reduced by food, whereas absorption of minocycline is not.

145
Q

Why should tetracylines NOT be given with calcium, iron, magnesium, aluminum and zinc?

A

The tetracyclines form insoluble chelates with calcium, iron, magnesium, aluminum, and zinc. The result is decreased absorption.

146
Q

Tetracyclines should NOT be given with what?

A

Tetracyclines should not be administered together with:

(1) calcium supplements,
(2) milk products (because they contain calcium),
(3) iron supplements,
(4) magnesium-containing laxatives, and
(5) most antacids (because they contain magnesium, aluminum, or both).

147
Q

Adverse Effects of Tetracyclines:

A
  1. Tetracyclines irritate the GI tract.
  2. Diarrhea may result from superinfection of the bowel (in addition to nonspecific irritation), it is important that the cause of diarrhea be determined.
  3. Tetracyclines bind to calcium in developing teeth, resulting in yellow or brown discoloration;
  4. When taken after the fourth month of gestation, tetracyclines can cause staining of deciduous teeth of the infant.
  5. Photosensitivity
148
Q

Are Macrolides narrow or broad spectrum?

A

Macrolides are broad spectrum antibiotics that inhibit bacterial protein synthesis.

149
Q

What is the oldest member of the Macrolide family?

A

Erythromycin

150
Q

What are the members of the macrolide family?

A
  1. Erthyromycin
  2. Clairithromycin
  3. Azithromycin
151
Q

What kind of bacteria are Erythromycin used for?

A

The drug is active against most gram positive and gram negative

152
Q

What is a treatment of choice for people allergic to Penicillin G?

A

Erythromycin

153
Q

What illnesses specifically is Erythromycin used for?

A

Whooping cough

acute diphtheria

Corynebacterium diphtheria

chlamydial infections

M. pneumoniae.

Streptococcus pyogenes

154
Q

Adverse Effects of Erythromycin (a Macrolide)

A

Erythromycin is generally free of serious toxicity and is considered one of our safest antibiotics.

  1. the drug does carry a very small risk of sudden cardiac death from QT prolongation.
  2. Gastrointestinal disturbances (epigastric pain, nausea, vomiting, diarrhea) are the most common side effects.
  3. Superinfections, thrombophlebitis, transient hearing loss
155
Q

Drug interactions of Erythromycin

A

Erythromycin can increase the plasma levels and half-lives of several drugs, thereby posing a risk of toxicity.

156
Q

Mechanism of action of Clindamycin

A

Inhibits protein synthesis

157
Q

Antimicrobial Spectrum of Clindamycin

A

Clindamycin is active against most anaerobic bacteria (gram positive and gram negative) and most gram-positive aerobes.

158
Q

Uses for Clindamycins:

A
  1. Because of its efficacy against gram-positive cocci, clindamycin has been used widely as an alternative to penicillin.
  2. The drug is employed primarily for anaerobic infections outside the CNS (it does not cross the blood-brain barrier).
159
Q

Adverse Effects of Clindamycin

A
  1. Clostridioides difficile–Associated Diarrhea
  2. Hepatic toxicity
  3. Blood dyscrasis
  4. Diarrhea
  5. Hypersensitivity
160
Q

Linezolid- why is it important?

A

The drug is important because it has activity against multidrug-resistant gram-positive pathogens, including vancomycin-resistant enterococci (VRE) and methicillin-resistant Staphylococcus aureus (MRSA)

to delay the emergence of resistance, linezolid should generally be reserved for infections caused by VRE or MRSA, even though it has other approved uses

161
Q

Linezolid is primarily used against what kind of bacteria?

A

Active against aerobic and facultative gram positive bacteria

It is a bacteriostatic inhibitor of protein synthesis

162
Q

What drug inhibits bacteria by inhibiting protein synthesis and causing cell death?

A

Aminoglycosides- they are bacteriocidal

163
Q

Aminoglycosides: narrow or broad spectrum? What kind of bacteria are they used for?

A

The aminoglycosides are antibiotics used primarily against aerobic gram-negative bacilli.

Narrow spectrum

164
Q

Most commonly employed Aminoglycosides

A
  1. Gentamicin
  2. Tobramycin
  3. Amikacin
165
Q

How are Aminoglycosides administered and why?

A

Not absorbed in the GI so must be administered parenterally to treat systemic infections

166
Q

Adverse Effects of Aminoglycosides:

A

Nephrotoxicity

Ototoxicity

Hypersensitivity reactions

Neuromuscular blockade

167
Q

How does ototoxicity occur with use of Aminoglycosides?

A

The risk of ototoxicity is related primarily to excessive trough levels of drug rather than to excessive peak levels.

When trough levels remain persistently elevated, aminoglycosides are unable to diffuse out of inner ear cells, and hence the cells are exposed to the drug continuously for an extended time. It is this prolonged exposure, rather than brief exposure to high levels, that underlies cellular injury.

168
Q

Aminoglycoside-Induced Neuromuscular Blockade:

A

Aminoglycosides can inhibit neuromuscular transmission, causing flaccid paralysis and potentially fatal respiratory depression.

169
Q

How to treat neuromuscular blockade caused by Aminoglycosides?

A

Reversal with IV infusion of a calcium salt (ex; calcium gluconate)

170
Q

How to monitor serum drug levels?

A

How monitoring is done depends on the dosing schedule employed (once daily dosing or the use of dividing doses)

171
Q

When once daily dosing is employed for drugs, what do we measure?

A

When once-daily dosing is employed, we need to measure only trough levels.

172
Q

When drawing blood samples for aminoglycoside levels, how to measure PEAK level?

A

Samples of peak levels should be taken 30 minutes after giving an IM injection or after completing a 30 minute IV infusion

173
Q

When drawing for aminoglycoside levels, what is sampling for trough levels dependent on?

A

Sampling for trough levels depends on the dosing schedule.

174
Q

For patients receiving divided doses of aminoglycosides, when should trough samples be taken?

A

For patients receiving divided doses, trough samples should be taken just before the next dose.

175
Q

For patients receiving once daily doses of aminoglycosides, when should trough samples be taken?

A

For patients receiving once-daily doses, a single sample can be drawn 1hour before the next dose. The value should be very low, preferably close to zero.

176
Q

What were the first drugs available for the systemic treatment of bacterial infections?

A

Sulfonamides

177
Q

Primary use of Sulfonamides

A

UTI

178
Q

How do sulfonamides suppress bacterial growth?

A

Sulfonamides suppress bacterial growth by inhibiting synthesis of tetrahydrofolate, a derivative of folate.

179
Q

Purpose of folate in all cells?

A

Folate is required by all cells to make DNA, RNA, and proteins;

180
Q

What step in folate synthesis does sulfonamide block?

A

Sulfonamides block the step in which PABA is combined with pteridine to form dihydropteroic acid. Because of their structural similarity to PABA, sulfonamides act as competitive inhibitors of this reaction.

181
Q

Adverse effects of Sulfonamides

A
  1. Hypersensitivity reactions
  2. Blood dyscrasias
  3. Kernicterus
  4. Renal damage from crystalluria
181
Q

Hypersensitivity Reactions from Sulfonamides- most severe?

A

The most severe hypersensitivity response to sulfonamides is Stevens-Johnson syndrome, a rare reaction with a mortality rate of about 25%.

182
Q

Hematologic Effects of Sulfonamides:

A

Sulfonamides can cause hemolytic anemia in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency.

183
Q

Adverse Effect of Kernicterus from using Sulfonamides

A

Kernicterus is a disorder in newborns caused by the deposition of bilirubin in the brain.

184
Q

Renal damage from Sulfonamides

A

Because of their low solubility, older sulfonamides tended to come out of solution in the urine, forming crystalline aggregates in the kidneys, ureters, and bladder. These aggregates cause irritation and obstruction, sometimes resulting in anuria and even death.

185
Q

Silver Sulfadiazine and Mafenide

A

These sulfonamides are employed to suppress bacterial colonization in patients with second- and third-degree burns.

186
Q

Difference between application of Silver sulfadiazine and mafenide?

A

Local application of mafenide is painful,

Application of silver sulfadiazine is pain free.

187
Q

What drug is similar to sulfonamides in that it suppresses synthesis of tetrahydrofolate- needed for bacteria to make folate?

A

Trimethoprim

188
Q

What is Trimethoprim’s mechanism of action?

A

Trimethoprim inhibits dihydrofolate reductase, the enzyme that converts dihydrofolate to its active form: tetrahydrofolate

189
Q

Trimethoprim/Sulfamethoxazole (TMP/SMZ):

A

The antimicrobial effects of TMP/SMZ result from inhibiting consecutive steps in the synthesis of tetrahydrofolate.

190
Q

Therapeutic uses for TMP/SMZ:

A

The combination is especially valuable for:

UTIs,

otitis media,

bronchitis,

shigellosis, and

pneumonia caused by P. jiroveci and Pneumocystis pneumonia and

GI infection

191
Q

Two urinary antiseptics are available: They are only used for UTIs

A
  1. Nitrofurantoin
  2. Methenamine
192
Q

Drugs in Nitrofurantoin family?IGNORE THIS SLIDE I THINK ITS WRONG!

A

[Furadantin, Macrodantin, Macrobid]

193
Q

What do Nitrofurantoin do at low concentrations?

A

Nitrofurantoin [Furadantin, Macrodantin, Macrobid] is a broad-spectrum antibacterial drug, producing bacteriostatic effects at low concentrations and bactericidal effects at high concentrations.

194
Q

What do Nitrofurantoin do at high concentrations?

A

Nitrofurantoin [Furadantin, Macrodantin, Macrobid] is a broad-spectrum antibacterial drug, producing bacterioSTATIC effects at low concentrations and bacteriCIDAL effects at high concentrations.

195
Q

Methenamine [Hiprex, Urex]- mechanism of action

A

Methenamine [Hiprex, Urex] is a prodrug that, under acidic conditions, breaks down into ammonia and formaldehyde.

The formaldehyde denatures bacterial proteins, causing cell death.

196
Q

Tuberculosis is caused by what:

A

Tuberculosis is caused by Mycobacterium tuberculosis

197
Q

How is M. tuberculosis transmitted?

A

Is transmitted from person to person by inhaling infected sputum that has been aerosolized, usually by coughing or sneezing.

198
Q

Where is initial infection of M. tuberculosis?

A

Initial infection is in the lungs

199
Q

What happens in most cases of M. tuberculosis?

A

In most cases, immunity to M. tuberculosis develops within a few weeks, and the infection is brought under complete control.

As a result, approximately 90% of individuals with primary infection never develop clinical or radiologic evidence of disease.

200
Q

What happens if immune system fails to control primary infection of M. tuberculosis?

A

If the immune system fails to control the primary infection, clinical disease (tuberculosis) develops.

201
Q

What happens to lungs when you have the clinical disease of Tb?

A

The result is necrosis and cavitation of lung tissue.

Lung tissue may also become caseous (cheese-like in appearance).

In the absence of treatment, tissue destruction progresses, and death may result.

202
Q

First line drugs for Tb:

A
  1. Isoniazid (MH)
  2. Rifampin
  3. Rifapentine, rifabutin, pyrazinamide, ethambutol
203
Q

Adverse Effects of Isoniazid

A

Hepatotoxicity

Peripheral neuropathy

Optic neuritis- bc drug crosses blood brain barrier

Anemia

204
Q

How does using isoniazid result in peripheral neuropathy?

A

Peripheral neuropathy results from isoniazid-induced deficiency in pyridoxine (vitamin B6).

If peripheral neuropathy occurs, it can be reversed by administering pyridoxine (but much higher doses needed)

205
Q

Adverse Effects of Rifampin

A

Hepatotoxicity- toxic to liver and can lead to hepatitis

Discoloration of Body Fluids- red orange color to urine, sweat, tears

GI disturbances

206
Q

Second line Antituberculosis Drugs

A

levofloxacin and moxifloxacin

three injectable drugs (capreomycin, amikacin, streptomycin),

and three other drugs (PAS, ethionamide, and cycloserine).

kanamycin

207
Q

Fluroquinolones- what spectrum and what use?

A

the fluoroquinolones are broad-spectrum agents that have multiple applications.

208
Q

Benefits of Fluoroquinolones

A

Benefits derive from disrupting DNA replication and cell division.

209
Q

How are Fluoroquinolones administered?

A

All of the systemic fluoroquinolones can be administered orally.

210
Q

Prototype Fluoroquinolone

A

Ciprofloxacin

211
Q

Side Effects of Fluoroquinolones

A

GI

CNS

Tendon Rupture* rare but a big deal I guess???

Phototoxicity

Candida infections

Increased risk of C.diff infection

Older pt issues

212
Q

GI side effects taking Fluoroquinolones

A

Nausea/Vomiting, diarrhea, abdominal pain

213
Q

CNS side effects of Fluoroquinolones

A

Dizziness, headache, restlessness, confusion, rarely seizures

214
Q

Candida infections side effects of taking Fluoroquinolones

A

Pharynx and vagina

215
Q

Effects of taking Fluoroquinolones in old people

A

Confusion

Somnolence

Psychosis

Visual disturbances

216
Q
A

PATHO/PHARM I (28 decks)

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