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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
Q

Which antibiotic is best used to treat Enterococcus in sepsis?

A

Amoxicillin

26
Q

Which antibiotic is best used to treat E. coli in sepsis?

A

Cefuroxime

27
Q

Which antibiotic is best used to treat Pseudomonas spp. in sepsis?

A

Ciprofloxacin / Gentamycin / Ceftazidine

28
Q

Which antibiotic is best used to treat N. meningtidis in sepsis?

A

Cefotaxime / Benzyl penicillin / chloramphenicol

29
Q

Name 3 new treatments of sepsis

A
  • antiendotoxin agents
  • antimediator drugs
  • antithrombotic agents
30
Q

Which circulating cells are activated and recruited to the site of inflammation to differentiate into macrophages and dentritic cells?

A

Monocytes

31
Q

What are the complications affecting the GIT in sepsis?

A

patchy mucosal haemorrhage and necrosis

32
Q

Immunosuppression happens in late sepsis, what phenotype do T-cells change into from Th1?

A

Th2

33
Q

What antibody is produces when an antigen is presented to CD4+ Th2 cells in Type 1 hypersensitivity reaction?

A

IgE

34
Q

Which cells produce the IgE in a Type 1 hypersensitivity reaction?

A

B lymphocytes

35
Q

Which cells do IgE bind to and cause degranulation?

A

Mast cells and basophils

36
Q

What is the result of degranulation of pharmalogically active mediators in Type 1 hypersensitivity reactions? (initial response - 3 listed)

A
  • Vasodilation,
  • vascular leakage
  • SM spasm
37
Q

What is the result of degranulation of pharmalogically active mediators in Type 1 hypersensitivity reactions? (late-phase response - 5 listed)

A
  • Mucosal oedema
  • mucous secretion
  • leukocyte infiltration
  • epithelial damage
  • bronchospasm
38
Q

What is the result of mitochondrial death in sepsis?

A

Cell death even if adequate O2 is being administered

39
Q

What is hypovoloaemic shock?

A

>20% loss in body fluids from the circulation

40
Q

What is cardiogenic shock?

A

Failure of the heart eg in IHD causing pulmonary oedema etc

41
Q

Name 3 causes of obstructive shock

A
  • PE
  • cardiac tamponade
  • tension pneumothorax
42
Q

What is the cause of maldistributive shock?

A

Abnormal dilation of the small arteries commonly due to infections or allergy

43
Q

What tests should be done to diagnose shock? (8 listed)

A
  • Bloods
    • FBC
    • U&E
    • glucose
    • ABG
    • lactate
    • blood cultures
  • ECG
  • x-ray
44
Q

Why are blood lactate levels raised in sepsis?

A

Due to anaerobic metabolism - critically low O2 delivery to the mitochondria

45
Q

What is the dose of IM adrenaline given in anaphylaxis?

A

1:1000 = 1mg/ml

46
Q

What is the MOA of noradrenaline?

A
  • 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
Q

What is the indication for using noradrenaline?

A
  • Low BP in eg septic shock.

(NB it is a specialised ITU drug)

48
Q

What is the MOA of adrenaline?

A
  • 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
Q

What is the indication for using atropine?

A

Low HR - antimuscarinic (parasympatholytic) drug

50
Q

What is the MOA of atropine?

A
  • 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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