Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology 3001 > Pathophysiology and Treatment of Sepsis > Flashcards

Pathophysiology and Treatment of Sepsis Flashcards

1
Q

What is the definition of sepsis?

A

Life-threatening organ dysfunction caused by a dysregulated response to infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the definition of septic shock?

A

A subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality than sepsis alone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Who are most at risk of developing sepsis?

A
  • Very young (>1 year)
  • Older adults (>75 years)
  • Those with impaired immune systems due to illness or medications
  • Those who have had surgery/invasive procedure in last 6 weeks
  • Anyone with breach of skin integrity (cuts, burns, blisters, skin infection)
  • IV drug users
  • People with indwelling lines or catheters
  • Woman who are preganant, have given birth or had a termination of pregancy or miscarriage in last 6 weeks
  • Neonates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How often is the pathogen causing sepsis in a patient actually identified?

A

Only around half of cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the key causitive Pathogens for sepsis?

A
  • Neisseria meningitidis
  • Streptococcus pneumoniae
  • Streptococcus pyogenes
  • Staphylococcus aureus (including MRSA)
  • Salmonella typhimurium
  • Klebsiella pneumoniae
  • Gram negative bacilli
  • Candida species
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What kind of organisms are asplenics highly suseptibal to?

A

Encapsulated organisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What can cause breaching of the host?

A
  • Catheters
  • Wounds
  • Burns
  • Thorn pricks
  • Insect bites
  • Epithelial cell damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the main factors affecting infection?

A
  • Virulence of pathogen (presence or absence of endotoxin)
  • Bioburden (CFU)
  • Portal of entry
  • Host susceptibility
  • Temporal evolution
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Name some immune molecules / cells / receptors inolved in the first line of defence against pathogenic insult

A
  • Complement
  • Mannose-binding lectin (MBL)
  • Phagocytes
  • Toll-like receptors (TLRs)
  • Nucleoside-binding oligomerisation domain receptors (NLRs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Name some inflammatory markers produced by the host?

A
  • Interleukins (ILs)
  • Tumour Necrosis Factor alpha (TNFa)
  • Reactive oxygen species (ROS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does TLR4 recognise?

A

LPS (which is present on many gram-negative bacteria)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the three stages of the immune and inflammatory pathways?

A
  • Access
  • Recognition
  • Response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Where is lipoteichoic acid present?

A

The cell wall of gram-positive bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the host molecule that identifies peptidoglycans?

A

CD14

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What host cell molecule identifies lipoteichoic acid?

A

Macrophage scavenger receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What type of host molecule recognises bacterial DNA?

A

The nucleotide binding oligomerisation domain (NOD-1, NOD-2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What does a vast increase in cytokines and effector molecules cause in response to infection in the body?

A 
Increased
- Intravascular coagulation 
- Stress hyperglycaemia 
- Cytopathic dysoxia 
Decreased 
- fibrinolysis
- Circulatory control 
- Endothelial integrity
Organ failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the effects of TNFa and IL-2 on the body:

A

Acute phase response

  • Fever
  • Hypotension
  • Increased HR
  • Corticosteroid and ACTH release
  • Release of neutrophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the effects of IL-1 and TNFa on the CVS?

A
  • Generalised vasodilation (NO)
  • Increased vascular permeability (activated leukocytes)
  • Intravascular fluid loss
  • Myocardial depression (tissue hypoxia)
  • Circulatory shock
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What happens to albumin levels in the blood during septic shock?

A

Decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

When is a patient screened for sepsis?

A
  • Patient presents with unexplained illness
  • Clearly looks unwell and has a likely infctive cause
  • OR presents with (or deteriorates to) an individual parameter score of 3 or aggregate score of 4 or higher on FEWS chart
22
Q

Expain the sepsis screening tool (for non-haematology patients)

A 
- FEWS alert 3 or greater
Assess for SIRS 
- Temperature < 36 C or > 38
- HR > 90 bpm
- WCC > 12 or <4 x10^9/l
- RR > 20 bpm
SEPSIS if any evidence of infection or new infection developing
23
Q

What does SIRS stand for?

A

Systemic Inflammatory Response Syndrome

24
Q

When can a patient be classified as having SIRS?

A

Having at least 2 of the following

  • Fever >38 C or hypothermia <36 C
  • Tachycardia >90
  • Tachypnea >20 breaths/min
  • Leucocytosis >12 x10^9 or leucopoenia <4x10^9/l
25
Q

How quickly should the sepsis 6 be completed in?

A

1 hour

26
Q

When is serum lactate produced?

A

When cells become hypoxic

27
Q

SEPSIS SIX

A
  • Give supplementary oxygen (aim for SPO2 of >94%)
  • Blood cultures
  • IV antibiotics
  • Fluid resuscitation
  • Serum lactate and Hb
  • Strict fluid balance
28
Q

What should the target Hb be?

A

> 7 g/dL

29
Q

What should the general prescribing considerations be in sepsis?

A
  • Patient history (underlying disease, immune status, prior antibiotic use, prior infection, or colonization with multidrug-resistant organisms)
  • Potential source of infection
  • Microbial resistance patterns within the community hospital, or intensive care unit
  • Patient organ dysfunction
  • Associated drug toxicities (such as nephrotoxicity with aminoglycosides)
30
Q

If source is respiratory what should be done?

A
  • Cover with broad spectrum, consider pseudomonas and MRSA
31
Q

If the source is urine what should be done?

A

Cover for G-ve and pseudomonas

32
Q

If the source is abdo what should be done?

A

Cover for G-ve/+ve and anaerobes

33
Q

If the source is soft tissue/joint what should be done?

A

Cover for G-ve/+ve/anaerobes

34
Q

If the source is CNS what should be done?

A

Cover for meningitis

35
Q

If BP is low what should be added in?

A

IV fluids, oxygen and possible vasopressors

36
Q

What should the recommended initial broad-spectrum therapy to treat sepsis consist of?

A

1 or more drugs with activity against all likely pathogens (bacterial, fungal, and/or viral)

37
Q

If fungal infection is likely what therapy should be undertaken?

A

Empiric antifungal therapy

38
Q

What should the first-line of antibiotics be in sepsis?

A

Amoxicillin + Gentamicin

39
Q

What antibiotics should be administered if MRSA is suspected or for sever sepsis?

A

Piperacillin + Vancomycin

40
Q

If the patient has a true penicillin allergy what antibiotics should be administered?

A

Vancomycin + Ciprofloxacin + Metronidazole

41
Q

What antibiotics are considered ‘broad spectrum’?

A
  • Amoxicillin
  • Piperacillin-tazobactam
  • Ciprofloxacin
42
Q

Amoxicillin properties

A
  • Broad spectrum

- Not so good for Staph aureus/G -ve

43
Q

Gentamicin properties

A
  • Good against some G+ve
  • Good against many G-ve
  • By extension good against pseudomonas
  • Not useful versus anaerobes
44
Q

Peperacillin-tazobactam properties

A
  • Broader spectrum
  • Anti-pseudomonal
  • G+ve (but not versus MRSA)
  • G-ve
  • Anaerobes
45
Q

Vancomycin properties

A
  • Good against G+ve including MRSA, some G-ve
46
Q

Ciprofloxacin properties

A

Broad spectrum including pseudomonas

47
Q

Metronidazole properties

A

Good against anaerobes

48
Q

How do you test if the antimicrobial is working?

A
  • Frequent observations
  • Repeat cultures
  • Test levels of different molecules (procalcitonin test)
49
Q

What antibiotics should be administered if a patient is suspected to have meningococcal infection (meningitis)?

A
  • Community setting - IV?IM Benzylpenicillin or Cefotaxime

- Hospital setting - IV Ceftriaxone

50
Q

What can be the short-term effects of sepsis?

A
  • Organ dysfunction

- Coagulation disorders

51
Q

What can be the longterm effects of sepsis?

A
  • Neurological dysfunction

- Increased mortality rate for at least a year

Pathology 3001 (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions