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JG Year 1 > 140 Sepsis > Flashcards

140 Sepsis Flashcards

1
Q

How much IV fluids should be given to a pt with sepsis?

A

20ml/kg

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2
Q

What are the characteristics of SIRS?

A
  • Temp 38
  • RR >20
  • HR >90
  • WBC >12,000 or <4,000
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3
Q

What addition to SIRS would indicate sepsis?

A

Clinical picture of infection

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4
Q

What is severe sepsis?

A

Sepsis with signs of hypoperfusion, hypotension or organ dysfunction

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5
Q

What is classes as hypotension?

A

Systolic <90 or 40mmHg below baseline

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6
Q

What is septic shock?

A

Sepsis with refractory hypotension

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7
Q

Which protein on a macrophage’s surface does bacterial LPS bind to?

A

CD14

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8
Q

What is the outcome of LPS encountering a macrophage?

A

Release of TNF –> IL-1

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9
Q

What is the outcome of LPS coming into contact with endothelial cells?

A

Increased vascular permeability

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10
Q

What effect does LPS have on the liver?

A
  • Release of acute phase proteins
  • Hypoglycaemia
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11
Q

What effect does increased vascular permeability have on the body?

A

Hypotension

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12
Q

What is the physiological effect of IL-1? (3 listed)

A
  • Fever
  • Increased adhesiveness of endothelial cells and leukocytes
  • Endothelial procoagulant activity
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13
Q

What are the cardiac/ circulatory complications of sepsis? (3 listed)

A

Decreased myocardial functions (contractility) Decreased peripheral vascular resistance –> decreased BP

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14
Q

What are the pulmonary complications of sepsis?

A
  • Increased pulmonary water content due to increased capillary permeability
  • –> decreased compliance and gas exchange
  • –> ARDS
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15
Q

What are the renal complications of sepsis? (3 listed)

A
  • fatty change
  • acute tubular necrosis
  • → renal failure (due to low BP),
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16
Q

What are the coagulation complications of sepsis? (2 listed)

A
  • Thrombocytopaenia
  • DIC
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17
Q

What are the neurologic complications of sepsis? (3 listes)

A
  • confusion
  • delerium
  • coma
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18
Q

What are the hepatic complications of sepsis? (3 listed)

A
  • bile stasis
  • focal necrosis
  • jaundice
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19
Q

Which type of sepsis can cause adrenal insufficiency?

A

meningococcal sepsis

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20
Q

What is the average mortality of a pt with sepsis?

A

30days

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21
Q

Which 2 age groups have an increased susceptibility to sepsis?

A
  • neonates
  • elderly
22
Q

What is the reduction in mortality from sepsis with early treatment?

A

35% –> 25%

23
Q

Which antibiotic is best used to treat Staph aureus in sepsis?

A

Flucloxacillin (+/- fusidic acid or gentamycin)

24
Q

Which antibiotic is best used to treat Staph pneumoniae in sepsis?

A

Benzyl penicillin IV

25
Which antibiotic is best used to treat Enterococcus in sepsis?
Amoxicillin
26
Which antibiotic is best used to treat *E. coli* in sepsis?
Cefuroxime
27
Which antibiotic is best used to treat Pseudomonas spp. in sepsis?
Ciprofloxacin / Gentamycin / Ceftazidine
28
Which antibiotic is best used to treat *N*. *meningtidis* in sepsis?
Cefotaxime / Benzyl penicillin / chloramphenicol
29
Name 3 new treatments of sepsis
* antiendotoxin agents * antimediator drugs * antithrombotic agents
30
Which circulating cells are activated and recruited to the site of inflammation to differentiate into macrophages and dentritic cells?
Monocytes
31
What are the complications affecting the GIT in sepsis?
patchy mucosal haemorrhage and necrosis
32
Immunosuppression happens in late sepsis, what phenotype do T-cells change into from Th1?
Th2
33
What antibody is produces when an antigen is presented to CD4+ Th2 cells in Type 1 hypersensitivity reaction?
IgE
34
Which cells produce the IgE in a Type 1 hypersensitivity reaction?
B lymphocytes
35
Which cells do IgE bind to and cause degranulation?
Mast cells and basophils
36
What is the result of degranulation of pharmalogically active mediators in Type 1 hypersensitivity reactions? (initial response - 3 listed)
* Vasodilation, * vascular leakage * SM spasm
37
What is the result of degranulation of pharmalogically active mediators in Type 1 hypersensitivity reactions? (late-phase response - 5 listed)
* Mucosal oedema * mucous secretion * leukocyte infiltration * epithelial damage * bronchospasm
38
What is the result of mitochondrial death in sepsis?
Cell death even if adequate O2 is being administered
39
What is hypovoloaemic shock?
\>20% loss in body fluids from the circulation
40
What is cardiogenic shock?
Failure of the heart eg in IHD causing pulmonary oedema etc
41
Name 3 causes of obstructive shock
* PE * cardiac tamponade * tension pneumothorax
42
What is the cause of maldistributive shock?
Abnormal dilation of the small arteries commonly due to infections or allergy
43
What tests should be done to diagnose shock? (8 listed)
* Bloods * FBC * U&E * glucose * ABG * lactate * blood cultures * ECG * x-ray
44
Why are blood lactate levels raised in sepsis?
Due to anaerobic metabolism - critically low O2 delivery to the mitochondria
45
What is the dose of IM adrenaline given in anaphylaxis?
1:1000 = 1mg/ml
46
What is the MOA of noradrenaline?
* Acts on α1 and α2 adrenergic receptors to cause vasoconstriction * Also acts to cause dilation of the coronary arteries acting on β adrenergic receptors there
47
What is the indication for using noradrenaline?
* Low BP in eg septic shock. (NB it is a specialised ITU drug)
48
What is the MOA of adrenaline?
* Acts on α and β receptor sites of sympathetic effector cells * Prominent effects are on the β receptors of the heart, vascular and other SM
49
What is the indication for using atropine?
Low HR - antimuscarinic (parasympatholytic) drug
50
What is the MOA of atropine?
* Antimuscarinic - antagonises muscarine-like actions of ACh * It can abolish bradycardia or asystole * Counteracts the peripheral dilatation and abrupt decrease in BP caused by choline esters

JG Year 1 (27 decks)

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