302 Bacterial pathogenesis and sepsis Flashcards

1
Q

What in the membrane makes gram negative bacteria negative?

A

Lipopolysaccharide and proteins and pores on the outside

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2
Q

What are the different classifications of streptococci?

A

alpha: haemolytic (partial)
Beta: haemolytic (complete)
Gamma: non-haemolytic

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3
Q

Samples of what, from the body, are usually sterile?

A

urine and blood

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4
Q

Where is staph aureus a normal commensal of?

A

The nose (60%)

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5
Q

Which bacteria mainly causes cellulitis

A

Streptococcus pyogenes

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6
Q

What is necrotising fasciiatis?

A

A deeper strep pyogenes infection with signs of sepsis

It gets deeper and behaves differently and releases extensive tissue damage

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7
Q

How do you recognise necrotising fasciatis?

A

-Out of proportion pain
-Bruising and blistering
-Generalised toxaemia
-Renal impairment
-Very high CRP
-Raised creatine kinase sometimes

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8
Q

What are the superficial infections causes by strep pyogenes?

A

Pharyngitis
Cellulitis

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9
Q

What are the deeper infections caused by strep pyogenes?

A

Severe soft tissue infection
myositis
Necrotising fasciitis

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10
Q

What are some autoimmune sequalae of s.pyogenes infection?

A

Rheumatic fever
Glomerulonephritis

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11
Q

Why is lipopolysaccharide considered an endotoxin?

A

It stimulates a powerful immune response

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12
Q

Which bacteria is a common contaminant of urine and blood?

A

Staph epidermidis

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13
Q

What host responses in sepsis causes further disease

A

Dissemination
Cellular damage
Organ damage

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14
Q

What is SIRS?

A

Systemic inflammatory response syndrome

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15
Q

What are some cardiovascular changes in sepsis?

A

Early distributive shock (warm peripheries)
-Peripheral vasodilatation

Then hypovolaemic shock (cold peripheries)
-Capillary leak, peripheral and pulmonary oedema
-Low filling pressure (fluid responsive)

Late cardiogenic shock (cold peripheries)
-Cardiac myocyte suppression
-High filling pressure (not fluid responsive)

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16
Q

What are some effects of pro-inflammatory cytokines in sepsis?

A

↑Vascular permeability
↓Vascular resistance
↓Cardiac contractility
Fever and Diarrhoea
Metabolic changes: Insulin resistance and Protein catabolism
↑Neutrophil migration, adhesion
↑Coagulation

17
Q

What is the coagulation response in sepsis?

A

-Coagulation homeostasis disrupted early and profoundly in sepsis

Coagulation and inflammation closely linked:
-Coagulation factors – pro-inflammatory activity
-Anticoagulation factors – anti-inflammatory activity

During sepsis this causes:
-Platelet activation
-Activation of coagulation cascades
-Down-regulation of anticoagulant mediators
-Consumption of coagulation factors
-The term “consumption coagulopathy” is used. The extreme form of which is “Disseminated Intravascular Coagulation”

18
Q

What does TLR4 detect?

A

Lipopolysaccharide (LPS)

19
Q

What is PAMP?

A

Pathogen Associated Molecular Pattern
Eg. Lipopeptides
Peptidoglycans
Flagellin
Microbial DNA / RNA

20
Q

What is PRR?

A

Pattern Recognition Receptor
Eg. LRs1-11
CD14
NOD1 and 2
Beta integrins

21
Q

What is toxic shock syndrome?

A

Caused by Staphylococcus aureus or Streptococcus pyogenes

Because they release Superantigen exotoxins

22
Q

What is the difference between antigens and superantigens?

A

Antigens: trigger T cell responses in tiny proportions of resting T cells

Superantigens: trigger T cell responses in up to 20% of all resting T cells

23
Q

What is the SOFA score?

A

Sequential Organ Failure Assessment

It assesses if the patient actually has sepsis:
Patients need to have infection and organ damage

24
Q

What is CRP?

A

Synthesised by hepatocytes
Regulated by IL6
Following stimulus
Peak 48hrs
t½ 19 hours
Clearance constant in renal disease
Minimal genetic variation
Production impaired in severe liver disease