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ECC > 4: Sepsis > Flashcards

4: Sepsis Flashcards

1
Q

What is the difference between sepsis and endotoxaemia?

A

Sepsis is a systemic bacterial infection whereas endotoxaemia is LPS from bacterial cell wall in the blood

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2
Q

Does endotoxaemia or sepsis cause shock?

A

Both can

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3
Q

What conditions cause endotoxaemia in the horse?

A

FPT, neonatal septicaemia, intestinal ischaemia (so treat for this at the time of colic surgery)

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4
Q

In what species is endotoxaemia not seen?

A

Cats

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5
Q

When can cows get endotoxaemia?

A

Toxic mastitis

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6
Q

When can dogs get endotoxaemia?

A

Pyometra

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7
Q

What receptor recognises gram +ve?

A

TLR2

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8
Q

What receptor recognises gram -ve?

A

TLR4

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9
Q

How does endotoxaemia cause cell death?

A

Caspases activate cell death pathway

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10
Q

What normally restricts endotoxin to the intestinal lumen?

A

The mucosa

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11
Q

What usually removed endotoxin in the blood?

A

Hepatic macrophages

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12
Q

Which kind of bacteria produce LPS?

A

Gram -ves

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13
Q

What does the hydrophobic core do?

A

Protects lipid A of endotoxin in the centre

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14
Q

What increases host reaction to the endotoxin by 1000x?

A

A small glycoprotein

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15
Q

What also enhances response to the endotoxin?

A

CD14

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16
Q

What does MD2 do?

A

A TLR4 co-receptor which induces LPS to contact TLR4

17
Q

What pathway is induced by TLR4?

A

NFkB

18
Q

How many signalling pathways does TLR2 activate compared to TLR4?

A

Less

19
Q

What are two examples of inflammatory mediators?

A

Cytokines and prostaglandins

20
Q

What are signs of endotoxaemia?

A

Pain, increased heart rate, decreased intestinal motility, pale MMs, depression, fever, haemoconcentration, leukopaenia

21
Q

Which drug can bind lipid A?

A

Polymixin B

22
Q

What is a problem with using polymixin B?

A

Can be nephrotoxic, so care if decreased perfusion

23
Q

Why can NSAIDs be good for shock?

A

Prevent prostglandin production, prevent early haemodynamic effects

24
Q

Where is COX1 produced?

A

Constitutively expressed, produces PGs responsible for intestinal mucosa repair

25
Q

Where is COX2 expressed?

A

Upregulated in inflammation and produces excessive PGs

26
Q

What is a problem with COX-2 selective inhibitors?

A

Can worsen coagulopathy

27
Q

Why is IVFT good in endotoxaemia?

A

Improves tissue perfusion, dilutes toxins

28
Q

Why is amikacin good for endotoxaemia?

A

An aminoglycoside - rapidly kills without lysis

ECC (7 decks)

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