class 3 Flashcards

1
Q

Nonpathogenic

A

◦ Usually do not cause disease unless conditions change
◦ Part of normal flora
◦ Often beneficia

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2
Q

Pathogens

A

Disease causing

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3
Q

Pathogens/germs that are disease causing microbes

A

◦ Bacteria and viruses
◦ Chlamydiae, Rickettsiae, & Mycoplasmas
◦ Fungi, Protozoa
◦ Helminths (worms), Prions, Algae

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4
Q

where are rickettsiae found

A

Rickettsiae (gram negative bacteria found in ticks, lice, fleas,
mites)

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5
Q

Pathogenicity

A

the capacity of microbes to cause
disease

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6
Q

Nosocomial infections

A

occur in health care facilities (often spread by direct contact or via contaminated objects). Also referred to as Hospital acquired infections (HAI)

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7
Q

Example of hospital acquired infections

A

C-diff. MRSA, VRE, …(more serious infections), usually resistant to antibiotics

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8
Q

Infection control requires two approaches

A

◦ Standard Precautions used in all
settings with all clients when body fluids
may be exchanged.
◦ Specific Precautions in clients
diagnosed with a particular infection—
these are used in addition to standard
precautions.

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9
Q

Characteristics of bacteria

A

 Unicellular -Single-celled microorganisms
 Rigid cell wall; unlike human cells (no
cell wall) ◦ Gram (+) or Gram (-) cell wall
 Some secrete toxins ◦ Exotoxins (gram +) ◦ Endotoxins (gram -) ◦ Enzymes
 Capable of cell division ◦ Reproduce by binary fission; if rapid a large infection can develop quickly
 Independent survival ◦ Do not require living tissue to survive
 Some can form spores ◦ Encapsulated; survive long time
 Aerobic and anaerobic; indiscrete
nucleus

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10
Q

On a gram negative bacteria, what can the outer membrane stop from entering

A

penicillin

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11
Q

characteristics of binary fission

A
  • very virulent
  • rapid onset of infection
  • fever stops binary fission
  • stops proliferation
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12
Q

what is a bacterial mutation

A

Errors made when duplicating their genetic codes
Occur spontaneously and randomly
This may result in a bacteria that is able to survive in harsher conditions, change the shape of its organelles, or perhaps grow faster
May result in drug resistance for a microorganism

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13
Q

Prevention of Resistant Strains

A

Prevent Infections when possible

Diagnose and treat infections properly

Use antimicrobials wisely

Prevent transmission

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14
Q

viral infections require what to replicate

A

a host cell

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15
Q

host resistance

A

The ability of a host to resist a pathogen
Healthy people can resist infection

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16
Q

what factors can decrease ones host resistance

A

for example infants, homeless people, use of steroids

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17
Q

What is an Opportunistic Infection?

A

an infection caused by pathogens that take advantage of an opportunity not normally available. These opportunities can stem from a variety of sources, such as a weakened immune system

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18
Q

what is virulence and what is it characterized by

A

the degree of pathogenicity of a
specific microbe (A highly virulent microbe
produces disease when present in small numbers)
characterized by
◦ Invasiveness, Adherence, Ability to avoid host defences
◦ Toxicity (Exotoxins and Endotoxins)

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19
Q

exotoxins

A

Exotoxins are proteins released by bacteria into surrounding tissue and has the ability
to inactivate or kill host cells

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20
Q

endotoxins

A

Endotoxins are harmful non-protein chemicals that are part of the outer wall of gram negative bacteria; They cause macrophages to release large amounts of cytokines, causing generalized inflammation, fever, and chills.

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21
Q

Phases of Acute Infection

A

 Exposure- microorganism enters body
 Incubation – time b/t entry into body and clinical signs
 Prodromal- infected person feels unwell
 Acute Period – clinical manifestations peak
 Convalescence – signs subside, return to normal

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22
Q

if sputum is purulent that indicates what type of infection

A

bacterial

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23
Q

id sputum is clear that indicates what type of infection

A

viral

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24
Q

lymphadenopathy

A

swollen lympth nodes

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25
Q

Arthralgia

A

joint pain

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26
Q

Leukocytosis indicates what type of infection

A

bacterial

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27
Q

Leukopenia indicates what type of infection

A

viral

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28
Q

increased neutrophils indicate what

A

bacterial infection

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29
Q

Parasitic & allergic responses are determined by elevated what in the blood

A

eosinophils

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30
Q

neutropenia indicates what type of infection

A

viral

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31
Q

lymphocytosis indicates what type of infection

A

viral

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32
Q

Serous exudate

A

watery, consists primarily of fluid with
small amout of WBC and protein

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33
Q

Fibrinous Exudate

A

thick and sticky with high cell &
fibrin content (increase risk of scar tissue)

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34
Q

Purulent exudate

A

think, yellow-green in color,
contains more leukocytes & cell debris &
microorganisms – indicates infection (pus)

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35
Q

Absess

A

localized pocket of purulent exudate or pus in a solid tissue

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36
Q

Hemorrhagic exudate

A

Damaged blood vessels

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37
Q

2 complications of infection

A

sepsis (infection of blood)
chronic infection

38
Q

what is sepsis

A

 Severe bacterial infection; life-threatening emergency
 Uncontrolled & overwhelming inflammatory response:
(+++ inflammatory cytokines)
circulatory shock
 Development of SIRS (Systemic inflammatory response syndrome)
 Leads to tissue damage, organ failure, death

39
Q

super bug

A

Bacteria that are resistant to the majority of antibiotics commonly used today.
◦ Resistant bacteria that cause pneumonia, urinary tract infections and skin infections are just a few of the dangers we now face
MRSA, VRSA, VRE, C. diff

40
Q

what can cause super bugs

A

overuse or missuse of antibiotics

41
Q

Treatment of Infection

A

Antimicrobial drugs
Vaccination
Antiviral drugs
Antifungal drugs
Symptom reduction
◦ Antipyretics
◦ NSAIDs

42
Q

what is Pneumonia

A

Inflammation of the alveoli and bronchioles
Normally our airway distal to the larynx is sterile (no bugs)
Caused by:
◦ Bacterial Infections
◦ Viral Infections – inflammation can make pt susceptible to bacterial invasion
◦ Fungal infections – usually only opportunistic

43
Q

what is a secondary infection

A

a bacterial or viral illness that develops following a first illness. The second infection may develop because a person’s immune system is stressed or weakened.

44
Q

both classifications of pneumonia

A

Typical (bacterial)
◦ Causes inflammation and exudation of fluid in the air-filled spaces of the alveoli

Atypical (viral or mycoplasmal) (less symptoms)
◦ Infection of the alveolar septum and interstitium of the lung = interstitial pneumonia
◦ Flu-like symptoms, little exudate within the alveoli

45
Q

Bacterial (Typical) Pneumonia
Classification (2)

A

Lobar
◦ An acute bacterial infection involving a large portion or an entire lobe of a lung
Bronchopneumonia
◦ Patchy consolidation with the involvement of more than one lobe
◦ Both have exudate in the alveoli

46
Q

community acquired pneumonia

A

◦ Infections from organisms in the community, acquired outside of hospital or diagnosed within 48 hrs of admission
◦ Can be bacterial or viral

47
Q

hospital acquired pneumonia

A

(90% bacterial) [Nosocomial]
◦ Not present on admission to hospital
◦ Develops ≥48 hrs post admission, most are bacterial

48
Q

Ventilator-Associated pneumonia [Nosocomial]

A

[Nosocomial]
Acquired ≥48 hrs post endotracheal intubation

49
Q

Bactericidal

A

kills bacteria

50
Q

Bacteriostatic

A

prevents growth and reproduction of bacteria

51
Q

Mechanisms of Antibacterial Agents (4)

A

 Drugs that damage bacterial cell wall

 Drugs that damage cell membrane

 Drugs that inhibit protein synthesis

 Drugs that inhibit DNA replication or bacterial cell division

52
Q

Mechanisms of Resistance

A

 Pathogen destroys drug
 Pathogen prevents drug entry or pumps drug out of itself
 Pathogen alters target site of drug or undergoes mutation or adapts to drug

53
Q

Bacteria change physiology to become resistant by

A

 Replicating rapidly
 Mutating spontaneously and randomly
 Acquiring resistance and promoting resistance to other bacteria via conjugation

54
Q

Antibiotics should not be used for

A

viral infections or coughs

55
Q

Combining antibiotics can decrease what

A

their effectiveness and promotes resistant strains

56
Q

Empirical therapy

A

use of broad spectrum antibiotics used before labs or reports come back to report the specific infection

57
Q

Prophylactic therapy

A

treatment of antibiotics to prevent infection, ex before surgery

58
Q

Therapeutic response

A

signs and symptoms are improving

59
Q

Sub-therapeutic response

A

signs and symptoms are not improving

60
Q

Patient factors affect choice of anti-infective

A

 Host defenses and immune system status
 Local tissue conditions – for some infections, it is difficult to get a therapeutic
concentration to site of infection
 Allergy history and drug hypersensitivity
 Pregnancy, age, genetics

61
Q

superinfections

A

Superinfections (secondary infections) develop when host flora is damaged by
antibiotic as nutrients and space become available for pathogens to grow

 Host flora being in competition with each other for space and nutrients is called
microbial antagonism
 Host flora limit space and nutrients for pathogenic bacteria
 Broad spectrum antibiotics are more likely to cause superinfections

62
Q

Peptidoglycan molecules form a set of chains called penicillin-binding
proteins (PBPs) because

A

penicillins and related antibiotics bind to them

63
Q

penicillin mechanism of action

A

Inhibits bacterial cell wall synthesis by binding to penicillin binding proteins (PBPs) – causing lysis the breakdown of the bacteria membrane (destruction)

64
Q

characteristics of penicillin

A

 Mainly active against grampositive bacteria
 Most have narrow spectrum of
antimicrobial activity
 Widely distributed to tissues
 Nearly all are rapidly excreted
by kidneys.
 Short half-lives
 Penicillin’s do not kill other
cells in the body

65
Q

penicillin allergies

A

Allergic reactions occur in 0.7 to
4% of cases

 Urticaria, pruritus, angioedema

 Those allergic to penicillin’s have
a fourfold to sixfold increased
risk of allergy to other β-lactam
antibiotics

 Cross-reactivity between
penicillin’s and cephalosporins is
between 1 and 18%

 Common adverse effects include:

 Nausea, vomiting, diarrhea,
abdominal pain

66
Q

Cephalosporins mechanism of action, and what they are used for

A

interferes with bacterial cell wall
synthesis (bactericidal action)

 Most common adverse effects are allergy, rash, GI complaints
 Eliminated by kidneys
 Use with caution in nursing mothers and patients with renal impairment

67
Q

Prototype Drug Cefotaxime (Claforan) (class cephalosoporins)

A

 Therapeutic effects and uses
 Third generation cephalosporin with borad spectrum activity against both Grampositive and Gram-negative infections
 Infections of the respiratory tract, urinary tract, genital infections, meningitis,
septicemia, endocarditis, bone and joint infections
 Infection prophylaxis in surgical patients

68
Q

Cefotaxime (Claforan) adverse effects

A

 Mild diarrhea, abdominal cramps, rash, pruritis, redness, edema
 Potential cross-sensitivity with penicillin’s if allergies exist – potential anaphylaxis
 Seizures

69
Q

Tetracyclines mechanism of action

A

Are bacteriostatic (inhibit bacterial growth)
Inhibit protein synthesis
Stop many essential functions of the bacteria

70
Q

what are tetracyclines used for

A

 Active against both Gram-positive and Gram-negative bacteria
 Drugs of choice for Lyme disease, H. pylori ulcers, and chlamydia
 bacteriostatic

71
Q

Tetracyclines Adverse Effects

A

Strong affinity for calcium
 Discoloration of permanent teeth and tooth enamel in fetuses and children (under 8), or nursing infants if taken by
the mother
 May slow fetal skeletal development if taken during pregnancy
 Alteration in intestinal flora may result in:
 Superinfection (overgrowth of nonsusceptible organisms such as
Candida)
 Diarrhea
 Pseudomembranous colitis

72
Q

Macrolids mechanism of action

A

inhibits protein synthesis

73
Q

what are Marcrolids used for

A

 Most effective against Gram-positive bacteria

 Alternative drugs for patients allergic to penicillin

 Generally, well tolerated and safe

 Decrease hepatic metabolism of other drugs thus drug interactions are possible

 Bacteriostatic in low doses, can be bactericidal in high doses

74
Q

what macrolids are not well tolerated

A

erythromycin

75
Q

Prototype Drug Erythromycin (Eryc) therapeutic effects and uses ( marcolide)

A

 Strep infections (streptococcus pyrogens)
 Mild to moderate upper and lower respiratory tract infections
 Syphilis & Lyme disease
 Gonorrhea & Chlamydia

76
Q

Prototype Drug Erythromycin (Eryc) adverse effects

A

 Adverse effects
 Nausea, vomiting, abdominal cramping
 Phlebitis, intense pain at IV injection site

 Serious adverse effects
 Cholestatic hepatitis
 Anaphylaxis
 Ototoxicity (hearing loss, vertigo, dizziness)
 Cardiotoxicity including palpitations, chest pain, arrhythmias

77
Q

what are Aminoglycosides used for

A

 Used to kill Gram-negative bacteria such as Pseudomonas spp., Escherichia
coli, Proteus spp., Klebsiella spp., Serratia spp.

 Often used in combination with other antibiotics for synergistic effects (never
used alone to treat gram + infections

 Reserved for serious gram neg (-) infections

  • only given through IV

-bacteriostatic

78
Q

Aminoglycosides cause serious toxicities such as

A

 Nephrotoxicity (renal damage)
 Ototoxicity (auditory impairment and vestibular damage [eighth
cranial nerve])

79
Q

Prototype Drug Gentamicin (Garamycin) mechanism of action

A

inhibits protein synthesis

80
Q

Prototype Drug Gentamicin (Garamycin) therapeutic effects and uses ct (aminoglycoside)

A

 Serious infections caused by aerobic, Gram-negative bacilli
 A few Gram-positive bacteria, including some strains of MSRA

81
Q

Aminoglycosides (Gentamycin): Adverse
Effects & Interactions

A

 Ototoxicity and nephrotoxicity are
the most significant

 Others include:
 Headache
Paresthesia
Fever
Superinfections
Vertigo
Skin rash
Dizziness

82
Q

Fluoroquinolones mechanism of action

A

Block Bacterial DNA Replication

83
Q

what is Fluoroquinolones used for

A

activity on all Gram
-negative bacteria, with some activity on
Gram-positive bacteria

 Commonly used for urinary tract
infections, GI, respiratory and skin
infections

  • good bioavailability and oral absorption
84
Q

Fluoroquinolones adverse effects

A

 Cartilage toxicity leading to tendon abnormalities
 GI toxicity
 Hypersensitivity reactions
 Nerve damage
 Phototoxicity / photosensitivity
 Hepatotoxicity
 Resistance

85
Q

Prototype Drug Ciprofloxacin (Cipro) therapeutic effects and uses (fluoroquinolone)

A

 Urinary tract infections
 Sinusitis
 Pneumonia
 Skin, bone, and joint infections
 Infectious diarrhea
 Certain eye infections

86
Q

what are Sulfonamides used for and mechanism of action

A

 Active against broad spectrum of microorganisms; classified based on
absorption and excretion qualities

 Suppress DNA replication by inhibiting synthesis of folic acid (folate) – folic
acid is necessary for thymine metabolism

 Adverse effects include hypersensitivity reactions, blood abnormalities,
nausea, vomiting, anorexia

 Some strains are resistant to sulfonamides

87
Q

Prototype Drug TrimethoprimSulfamethoxazole therapeutic uses and effects

A

 UTI prophylaxis and UTI
 Prophylaxis and treatment of p. carinii and shigella
 Acute episodes during chronic bronchitis
 Off-label for other indications depending on sensitivity of microbe

88
Q

Prototype Drug Vancomycin (Vancocin) therapeutic effects and uses, mechanism of action

A

 Severe Gram-positive infections resistant to safer antibiotics
 Off-label uses for meningitis and antibiotic-induced pseudomembranous colitis
 Mechanism of action
 Inhibits synthesis of bacterial cell wall

89
Q

Prototype Drug Vancomycin (Vancocin) adverse effects

A

“red man” syndrome
 Flushing, hypotension, tachycardia, rash on upper body
 Nausea, rash, fever, chills

 Serious adverse effects
 Confusion, seizures, and hallucinations
 Extravasation leading to tissue necrosis (if IV leaks)
 Ototoxicity, Nephrotoxicity
 Anaphylaxis

90
Q

Common therapies for UTI (2)

A

 Sulfonamides
 Fluoroquinolones

91
Q

Prototype Drug Nitrofurantoin therapeutic effect and use, mechanism of action

A

 Therapeutic effects and uses
 Uncomplicated acute cystitis, usually for prophylaxis of recurrent UTI

 Mechanism of action
 Intermediates attack bacterial ribosomal proteins, prevent DNA and RNA synthesis,
and prevent protein synthesis, also inhibits cell wall synthesis