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Pharmaco For Pod > wk 5- antimicrobial therapy > Flashcards

wk 5- antimicrobial therapy Flashcards

1
Q

primary pathogens

A

cause disease in individuals despite immune status

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2
Q

opportunistic pathogens

A

cause disease in individuals whose natural defences are compromised

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3
Q

infectivity

A

ability for pathogen to establish in a host

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4
Q

virulence

A

how harmful pathogens are once established in a host

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5
Q

incubation period

A

time between the invasion by the pathogen and appearance of clinical features of infection (signs and symptoms)

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6
Q

period of infectivity

A

time the patient is infectious to others

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7
Q

bodys normal flora and defence system

A

normal flora: bodys microorganisms living in particular areas of the body

defence: different processes and barriers in the body that prevent infection eg (cilia, skin, mucus, tears, macropahges)

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8
Q

different types of pathogens and how they cause disease

A

virus
bacteria
fungi
protozoa
helminths

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9
Q

signs and symptoms of local and systemic infections

A

local: (involves skin or single organ)
-red
-hot
-pain
-loss of function
-exudate
-delayed wound healing

systemic: (involves whole body)
-fever >37.5C normal tempt is 36-37C
-chills/sweats
-diaarhoea, vomiting, nauesea
-headache
-fatigue
-etc

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10
Q

stages of infection

A
  1. incubation stage: pathogen is replicating. no symptoms
  2. prodromal stage: host begins to feel unwell with nonspecific signs/symptoms, fever, muscle aches, headache, fatigue
  3. acute stage: microbes are destroying specific host cells and systems. more specific symptoms occur
  4. convalescent stage: bodys defence mechanism has confined microbes and healing of damaged tissue has begun. health returns to normal.
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11
Q

ways to diagnose an infection

A
  • no single definitive test
    combination of clinical signs and laboratory tests (WBC count, ESR, CRP, blood, urine, wound culture)
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12
Q

blood tests- WBC what 2 major classes does it include and what are the types of infection you can conclude from the test

A

2 major classes
1. granulocytes: engluf and digest.
-neutorphils, monocytes, basphils, eosinophils

  1. lymphocytes: recognition of microbes

types of infections from WBC count
1. leukocytosis: increase of WBC- most common acute bacterial infection
2. leukopenia: decrease of WBC- long infection
3. increase in eosinophil count- allergic reaction

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13
Q

ESR what does it do when theres an infection, with other populations and when is it used

A

Large increases during infection, inflammation and plasma cell dyscrasias

also increases with age, pregnancy and anaemia

useful for monitoring resposne over time to antibiotics, example lower ESR means theres a response to antibiotics

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13
Q

CRP

A

increase when theres inflammation/ infection

good for determining severity as it reflects disease activity and response to treatment as it rises and falls quickly as response

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14
Q
A
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14
Q

clinical questioning SITDOWNSIR

A

s- site
i- intensity
t- type
d- duration
o- onset
w- with other symptoms?
n- aggrevated by?
s- spread?
i- incidence
r- relieved by

15
Q
A
16
Q

what tests to use if you want to monitor treatment (antibiotics)

A

CPR
ESR

17
Q

what tests to use if you want to assess if theres an infection and if its longstanding or acute

A

WBC count

18
Q

what tests to use for systemically ill patients

A

culture blood, urine, mucus etc before administration of antibiotic

19
Q

gram positive and negative

A

positive: retains only purple stain
neg: retains only red stain

tells us the difference in structure of cell wall

response to antibiotics varies with the type of bacteria

20
Q

how long do wound cultures take

A

24-48hours

21
Q

bacteria components

A

single celled organisms
unique cell wall
some have flagella (move)
some have fimbria (attachement to host tissue)
DNA

dont have membrane bound organelles
dont have nucleus

22
Q

principles of antimicrobial treatment

A
  • accurate diagnosis
  • empirical treatment initially
  • switch to narrow spectrum after culture/sensitivity testing
  • cost effective
  • shortest duration possible
  • host characteristics
  • adverse effects
  • when to refer
23
Q

goals of AMT

A

destroy/suppress growth of pathogen with selective toxicity so the normal host defences can control the ifnection

24
Q

pharmocokinetic properties of antimicrobials

A

PK- concerned with the time course of antimicrobial concentration

T>MIC: time that the plasma concentration remains above the Minimum inhibitory concentration

25
Q

pharmacodynamic properties of antimicrobials

A

PD- concerned with antimicrobial concentration and the antimicrobial effect

MIC: minimum inhibitory concentration of the antimicrobial

26
Q

types of killing patterns of antimicrobial drugs

A
  1. concentration dependent (higher the peak blood level, the better the effect, suboptimal dosing can lead to resistance)
    -ciprofloxacin
  2. time dependent (T>MIC for atleast 60% of time to produce a good effect)
    -penicillin, erythromycin
27
Q

bactericidal and example

A

cause cell death and lysis
-penicllin

28
Q

bacteriostatic

A

inhibit growth allowing hist defence system time to remove

29
Q

targets of antimicrobial action

A
  1. cell wall synthesis inhibitors (bactericidal)
  2. disruption of membrane permeability (bactericidal/static)
  3. protein synthesis inhibitors (bctericidal)
  4. essential metabolite
    synthesis inhibitiors (bacteriostatic)
30
Q

unwanted effects of antimicrobial drugs

A
  • superinfection: imbalance of pathogen/non pathogen gut flora which can cause a secondary infection by allowing oathogenic organisms to proliferate area

-antibiotic related colitis: inflammtion of wall of colon, dont use anti diarrhoeal medicines

-hypersensitivity reactions: preformed antibodies or immune cells with antigens

-drug resistance: not enough dosing to kill pathogen but for it to adapt

31
Q

antimicrobial resistance

A

when pathogens no longer respond to medicine making the infection harder to treat

32
Q

intrinsic v acquired resistance

A

intrinsic: organisms make up that specifies the resistance (eg cell wall)

acquired: organism mutates or acquires new DNA creating a resistance organism

33
Q

mechanisms of antimicrobial resistance

A
  1. barrier to entry- change in cell wall/outer membrane composition
  2. efflux pump- antibiotic from inside bacteria to external environment
  3. formation of biofilm- protective membrane that prevents penetration
  4. enzyme inactiviation
  5. alteration of target sites
  6. increased synthesis of target
  7. target adapation
34
Q

microbes commonly involved in antimicrobial resistance

A
35
Q

preventing antimicrobial resistance

A
  • correct selection, dose and time for use (misuse, mis prescribing) - AMR stewardship
  • monitoring
  • hand hygiene/PPE
  • disinfecting/cleaning
  • vaccination

Pharmaco For Pod (10 decks)

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