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Therapy: year 3 > Introduction to infectious disease > Flashcards

Introduction to infectious disease Flashcards

1
Q

What are ID caused by?

A

bacteria, viruses, pathogens, fungi

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2
Q

what are the ways they are spread?

A

pateint to patient, vector to patient,(animal to patient), environment to patient (hospital), patients own flora

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3
Q

Organisms that live on body concern?

A

no they can be harmless or even helpful, under certain conditions that may cause disease

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4
Q

What are pathogens?

A

Organism that can cause host tissue damage and intitae a immune reponse that usualy reuslts in infection

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5
Q

what is the basic approach to identifying ID?

A
  1. establish infection
  2. fever does not always mean infection
  3. determine sites of infection
  4. deternine pathogens
  5. select apporpriate antimicrobial therpay
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6
Q

how can we establish an infection?

A
  1. careful history and phsycial
  2. s and s
  3. predisposing factors
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7
Q

what are the signs and symptoms we can use to identify an infection?

A

-fever
-increased WBC
- Acute Phase reactants (ESR, CRP, Procalcitonin)

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8
Q

what should we know about fever? other causes? specifically drugs?

A

fact: lowest in the morning and highest in the evening

other causes:
- maligancy (epecailly CNS), autoimmune diseae, stress, drugs

Drugs:
- anticonvulsants, sulfa-containing compounds, antiarrhythmics, antipsychotic, beta-lactams

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9
Q

What should we know about WBC? other causes, and drugs

A

Fact: infection can cause mobilization of granulocytes and lymphocytes

Other causes:
malignancy, inflammatory disorders, stress, drugs

Drugs:
- corticosteroids
- epinephrine
- lithium

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10
Q

if an increase in lymphocytes indicates what?

A

viral infection

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11
Q

if an increase in neutrophils indicates what?

A

bacterial or fungal infection

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12
Q

what are acute phase reactions?

A

ESR - erythrocyte sedimentation rate

CRP - C- reactive protein

procalcitonin -

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13
Q

Expand on ESR

A

-can show inflammatory activity in the body

  • measure the distance RBC falls in a test tube within an hour
  • Further RBC have fallen the greater the inflammatory response of the immune system
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14
Q

Expand on CRP

A
  • made in the liver
  • levels increase when there is an inflammatory response
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15
Q

Procalcitonin

A
  • biomarker release in reponse to bacterial infections
  • used to distinguish etiology of infectious process
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16
Q

S and S mild vs severe

A

mild - sore throat, small sore on skin

Severe - painful cough, gross production of sputum

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17
Q

S and S localized vs deep-seated

A

localized: Skin - swelling , erythema, tenderness and purulent drainage

Deep-seated: meningitis, pneumonia - must be determined from tissue or fluid sample

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18
Q

What do clinicans usualy look for? then what is the next step?

A

determine a focus:
- cough - prob lungs
- leg sore - prob and ulcer, cut
- child pulling ear - probably inner ear canal

the next step is to determine what organisms are common for that area?

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19
Q

Gram-positive Cocci

A

Staph : S.aureus, S.epidermis
Strep : Pneumococcus, viridians
Enterococcus: E.Faecalis, E.Faecium

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20
Q

Gram positive bacilli

A

Corynebacteria

Listeria

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21
Q

Antimicrobial coverage for MSSA

A

Cloxacillin, cefazolin, Caphaleixin

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22
Q

hospital-acquired MRSA

A

Vancomycin, daptomycin, clindymin( linezolid),

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23
Q

Community-acquired pneumonia (penicillin-susceptible)

A

penicillin, ampicillin

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24
Q

Community-acquired pneumonia (penicillin-resisitant)

A

3 gen cephalosporin (not ceftazidime), a quinolone (not cipro), vancomycin

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25
Q

community acquired MRSA

A

Clindamycin, SNX-TMP, doxycycline

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26
Q

Enterococcus

A

Ampicillin or vancomycin (depending on resistance)

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27
Q

Gram-negative cocci

A

Moraxella,

Neisseria: meningitis, gonorrhea

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28
Q

gram-negative bacilli

A

a bunch

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29
Q

Easy to kill gram-negative

A

HPEK M SS

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30
Q

antimicrobial to kill easy to kill gram-negative

A

amoxicillin, amox/clavulate, 2nd gen cephalosporines for milder infections

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31
Q

antimicrobial to kill hard-to-kill gram-negative

A

SPACE

  • MAFIA PCC:
    meropenem, aminoglycosides, FQ (not moxi), imipenem, pip/tazo, cefepime, ceftazidime
32
Q

what HTK are hard to get?

A

Pseudomonas and acinobacter

33
Q

What are the anaerobes?

A

Peptococcous, Peptostreptoccoucs, bacteroides, fuscobacterium, prevotella

34
Q

When treated do we need o know the pathogen right away to pick an agent?

A

no we can use a broad spectrum and then use a more specific one when we need more trageted therapy

35
Q

Colonization def

A

presence of an organism without inflammatory response

36
Q

Contamination def

A

the presence of an orgaism acquired during specimen sampling without evidence of host inflammtoyr repsonse

37
Q

Infections

A

presence of an organism that initiates a host inflammatory response

38
Q

when patients is acutley ill febrile what should we do?

A

do blood cultutres before antibbiotics are initiated

T>= 38.5 degress celsius

39
Q

what types of results should be evaluated? useful results

A

blood, sputum, urine, wound, or sinus drainage

  • not always useful reuslts
40
Q

what can we evalute to detrmine the lilkeyl pathogen?

A

Blood cultutre, blood, sputum, urine, sinus darainge, wound, spinal fluid in menigitis, joint aspirations in septic joints, abcess/cullulitis drainag

41
Q

what areas are heavily colonized with a variety of bacteria?

A

skin, oropharynx, ears, throat, and perineum

  • concern if revocered from blood, venous cathether or prosthetic devices
42
Q

what are some considerations for interpreting results if the sample is from the CSF?

A

glucose, WBC, proteins

43
Q

what are some considerations for interpreting results if the sample is from the Sputum?

A

diffiucly to interpret, most reliable if from bronchoscopy or deep suctioning or an intubated patient

44
Q

what are some considerations for interpreting results if the sample is from the urine?

A

cats, nitrites, polymicrobila. pyruia

45
Q

MIC and types

A

minmum inhibtory concentration - lowest Ab dose that prevents growth after 24 hours

S - susuctible,
I - intermediate or indtermine
R - resistant

46
Q

Pharmacokinetics

A

what body does to drug

47
Q

Pharmacodynamics

A

what drug does to body

48
Q

What info do we need from he patient’s history?

A
  1. acquitsion of infection
  2. previous infections or colonization
  3. Previous antibiotic use
  4. site of infection and most liley pathogen
49
Q

Time-dependent killing

A
  • above MIC by 2-4 times
  • higher cocnetraion doesn’t work better
  • minimla to no PA
50
Q

Concentration-dependent killing

A
  • more durg more death
  • have P- need 10more then MIC AE
51
Q

drug class most knonw for PAE?

A

Aminoglycosides

52
Q

when do we prefer bacteriocidial?

A
  • when immuncomprmises
  • in sever life threatening infection ) endocarditis or meningitis)
53
Q

Baterostatiic drugs?

A

M
T
L

54
Q

Drug factors: tissue pentration

A

if it cannot reach the site of infection, usueless

55
Q

Abscess

A

they can inactiavte drugs so muct be drained

56
Q

meningitis

A

cafazolin can work against bacterila but not penetrate CNS

57
Q

Moxifloxicin

A

low renal clearance, don’t use for UTI

58
Q

Nitrofuratoin

A

is metabolized before reached urinary tract in poor renal failure

59
Q

Daptomycin

A

inactivated by lung surfactant - bad for lung infection

60
Q

If we are severly ill what should we be aware of?

A

oral absorption may be hindered

61
Q

drug that can cause increase in seizures

A

imepenem

62
Q

Aminoglycosdies SE

A

nephrotocityc, ototcity

63
Q

Glycopetides SE

A

red man syndorme

64
Q

Datomycin (lipopetide)

A

hepatoxicity

65
Q

Sulfonamides and trimethoprim

A

HIV patients caution

66
Q

When is combination therapy indicated?

A
  1. boraden spectrum of acticivty
  2. Synergisc effects
  3. when risk of failure is catastrphic (rex: resp infection in ICU with SPACE)
67
Q

How can we monitor effectiveness?

A
  1. fever resolves in 24-48 hours
  2. patient compliants dimish
  3. pneumia scans will still show evdience fo damage for a while
68
Q

when is IV - PO stepdown therapy indicated?

A
  1. overall improvemnt
  2. lack of fever for 24 hours
  3. decrease in WBC
  4. Functioning GI tract
  5. taking other meds by mouth
  6. tolerating oral diet (no nauseou or vomiting)
69
Q

draugs that have better oral bioavailibilty then IV

A

FQ, Metronidazle, SMX-TMP, clindamycin,

70
Q

Duaration of therpay for UTI Drugs

A

nitor- 5 d
TMP -SMX - 3 days
Fosfomycin - 1 d

febrile UTI 7-14 d

rest 7 d

71
Q

Pneumoina

A

5-7 d

72
Q

COPD

A

5-7 days

73
Q

Streptococoal pharyangitis

A

10 days

74
Q

acute otis media

A

10 days

75
Q

Intraabodimal

appendicitis

Absecss infection

A

no more then 24 post opertaion

only before

less then 7 days

76
Q

Bacteremia

A

7 days

77
Q

osteoarticular

A

weeks

Therapy: year 3 (14 decks)

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