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Week 140 - Collapse > Sepsis > Flashcards

Sepsis Flashcards

0
Q

E.coli, Klebsiella, Enterobacteria, Pseudomonas aeruginosa and Neisseria gonorrhoea eater all what type of bacteria:
Gram -ve
Gram +ve?

A

Gram -ve

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1
Q

Streptococcus pneumoniae, Staphylococcus aureus and Listeria monocytogenes are all what type of bacteria:
Gram -ve
Gram +ve?

A

Gram +ve

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2
Q

List 3 changes that occur in the capillaries during sepsis.

A

Vasodilation
Intravascular coagulation
Increased permeability

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3
Q

What does TNF do in sepsis?

A

Mimics sepsis syndrome

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4
Q

What does interleukin 1 (IL-1) in sepsis?

A

Induce fever; increase endothelial and leukocyte adhesion; triggers procoagulant activity

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5
Q

What effects do IL-2, -4, -6 and -8 have in systemic inflammation?

A 
Hypotension
Leaky capillaries
Reduced myocardial contractility
Synthesis of acute phase proteins e.g. Fibrinogen
Leukocyte chemo taxis
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6
Q

What does Nitric oxide cause in sepsis?

A

Hypotension

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7
Q

What are the key clinical features of septic shock?

A

Hypotension
Low urine output
Pyrexia
Tachycardia / pnoea

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8
Q

Define “shock”

A

Inadequate cellular perfusion and O2 uptake with consequent tissue hypoxia and organ failure

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9
Q

What 4 things can lead to organ failure in the late stages of shock?

A

Failure to autoregulate peripheral circulation
Abnormal distribution of blood flow with organs
Direct cellular toxicity
Prevention of O2 uptake and utilisation

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10
Q

Define sepsis

A

Suspected or proven infection with SIRS (systemic inflammatory response syndrome)

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11
Q

Define severe sepsis

A

Suspected or proven infection with SIRS plus organ dysfunction (perhaps hypotension that improves with fluid administration)

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12
Q

Define septic shock

A

Severe sepsis plus hypotension despite adequate volume resuscitation

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13
Q

Which anatomical systems are most commonly the source of infection in septic patients?

A

Respiratory
Intra-abdominal
Urinary

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14
Q

What are common clinical signs of severe sepsis?

A

Visible signs of acute inflammation (redness, swelling, heat, pain - if skin, mottling if vascular etc)
Systemic signs of inflammation - fever, tachycardia, tachypnoea, hypoxaemia, raised CRP, leukocytosis.
Organ failure - altered mental status, cardiac, respiratory, renal or gut failure

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15
Q

What does low urine output tell you?

A

That a patient is dehydrated or that the kidneys are not being well perfused and therefore other organs probably aren’t either

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16
Q

What are the main characteristics of innate immunity?

A

Rapid onset
Non-specific (Can damage healthy / normal tissues)
Consists of mechanical barriers, certain inflammatory cells, chemical mediators

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17
Q

What are the main cells that are involved in innate immunity?

A

Mast cells
Macrophages
Neutrophils

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18
Q

What is the initial role of a Toll-like receptor?

A

To stimulate an innate immune reaction once they have detected exotoxins, endotoxins or other microbial components (PAMPS)

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19
Q

What do cytokines do in acute inflammation?

A

Facilitate vascular changes and recruit other inflammatory cells (along with other mediators)

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20
Q

Which Toll-like receptors detect lipopolysaccharide?

A

TLR2 and TLR4

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21
Q

Which Toll-like receptor recognises gram +ve bacteria?

A

TLR2

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22
Q

Which Toll-like receptor recognises gram -ve bacteria?

A

TLR4

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23
Q

Name the chemical mediators of inflammation

A 
Complement system
Kinin system
Vasoactive amines (histamine and serotonin)
Prostaglandins, leukotrienes
Cytokines and chemokines
Nitric Oxide
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24
Q

What systemic effect do the inflammatory mediators prostaglandin, Nitric Oxide and histamine have?

A

Cause vasodilation

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25
Q

What systemic effect do vasoactive amines, the complement cascade, bradykinin and leukotrienes have in inflammation?

A

They increase vascular permeability

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26
Q

What role do chemokines, IL1, TNF and bacterial products have during inflammation?

A

Chemotaxis, recruit and activate leukocytes

27
Q

What 3 elements in acute inflammation will cause fever?

A

IL-1, TNF and prostaglandins

28
Q

What do prostaglandins and bradykinin commonly contribute to during inflammation?

A

Pain

29
Q

What results from the activity of neutrophil and macrophage lysosomal enzymes, oxygen metabolises and nitric oxide in inflammation?

A

Tissue damage

30
Q

List the key stages of inflammation (there are 7)

A
  1. Injury (organism invasion /toxin)
  2. Mast cell degranulation
  3. Macrophage activation
  4. Activation of complement cascade and other mediators
  5. Vascular dilatation and increased permeability
  6. Recruitment of neutrophils, migration into tissue and activation
  7. Phagocytosis and destruction of microbe
31
Q

What do mast cells release during granulation?

A

Histamine

32
Q

Which cells dominate mediation in adaptive immunity?

A

B- And T-lymphocytes

33
Q

Chronic inflammation, allergy and hypersensitivity are all expressions of what type of immunity?

A

Adaptive immunity

34
Q

What role does adaptive immunity have in sepsis?

A

Amplification of the inflammatory response

35
Q

Antigen-specific immunoglobulin facilitates what in adaptive immunity?

A

Opsonisation and phagocytosis of microbes

36
Q

What type of cytokines do T-helper-1 cells secrete?

A

Pro-inflammatory cytokines

37
Q

What type of cytokines do T-helper-2 cells secrete?

A

Anti-inflammatory cytokines

38
Q

What does leukocytosis mean?

A

An increase in WBC count

39
Q

In Systemic Inflammatory Response Syndrome what proteins are characteristically secreted?

A

Procalcitonin and C-reactive protein

40
Q

What effect does the increase in nitric oxide do in sepsis?

A

Causes vasodilation

41
Q

Which cells produce intravascular cytokines in sepsis? (E.g. TNF, IL-1, IL-8)

A

Leukocytes, monocytes and endothelial cells

42
Q

Severe sepsis is defined by what characteristics resulting from intravascular cytokines activity?

A

Widespread endothelial injury
Vascular dilatation and increased permeability
Hypotension

43
Q

What happens to pro-coagulant and anti-coagulant factors in severe sepsis?

A

Pro-coagulant factors increase and anti-coagulant factors decrease

44
Q

What is the net effect of the disturbance in coagulation factors in sepsis?

A

Intravascular thrombosis (DIC) in small blood vessels. also, as platelets and clotting factors are used up in the thrombosis process the levels circulating in the blood are reduced putting the individual at risk of bleeding also.

45
Q

Fibrin and thrombin are examples of what?

A

An pro-coagulation factors

46
Q

What is the role of plasmin in sepsis?

A

It is an anti-coagulant protein which breaks down clotting factors such as fibrin

47
Q

What substances lead to DIC?

A

Intravascular organisms, LPS (lipopolysaccharide), and many cytokines esp. TNF

48
Q

What is DIC?

A

Stands for: Disseminated Intravascular Coagulation; is widespread intravascular coagulation

49
Q

What is a major result of DIC?

A

Tissue ischaemia

Together with hypotension can lead to organ ischaemia and therefore failure

50
Q

What does tissue ischaemia lead to?

A

Anaerobic glycolysis and metabolic acidosis

51
Q

High levels of what in blood tests evidence metabolic acidosis?

A

Lactate

52
Q

What does the production of IL-10, the conversion of T-helper-1 to T-helper-2 cells and apoptosis of lymphocytes contribute to?

A

Immunosuppression that often features late in sepsis

53
Q

List the management priorities in sepsis

A

Early recognition of signs of organ dysfunction (e.g. Urine output)
Antibiotics to treat the initial infection
Oxygen; Fluids
Nutrition
Organ support

54
Q

What type of hypersensitivity reaction is anaphylactic shock described as?

A

A severe systemic Type 1 - immediate hypersensitivity

55
Q

List examples of type 1 hypersensitivity reactions

A

Bronchial asthma; allergic rhinitis; allergic conjunctivitis; hay fever; allergic gastroenteritis; systemic anaphylaxis

56
Q

What is a type 1 hypersensitivity reaction?

A

A rapidly developing immunologic reaction

57
Q

How does anaphylaxis differ from rhinitis, for example?

A

It is a severe systemic rather than moderate local reaction

58
Q

What cells are principally involved in immediate type 1 hypersensitivity reactions?

A

T-cells, B-cells, mast cells and eosinophils

59
Q

Name the primary mast cell mediators

A

Histamine, proteases and chemotactic factors

60
Q

Name the secondary mast cell mediators in type 1 HRs

A

Prostaglandins, leukotrienes, PAF and cytokines

61
Q

What clinical signs and symptoms result from release of primary and secondary mast cells mediators?

A

Smooth muscle spasm, oedema, leukocyte infiltration and mucous secretion

62
Q

List some common symptoms of systemic anaphylaxis

A 
Itching, hives, skin erythema
Bronchspasm (contraction)
Laryngeal oedema or obstruction - hoarseness
Vomiting, cramps, diarrhoea
Hypotension and shock
63
Q

How should you manage anaphylaxis?

A 
ABC
Adrenalin (500 micrograms IM - ideally)
Antihistamines
Bronchodilators
Steroids
64
Q

How does adrenalin help treat anaphylaxis?

A

1) It inhibits further mast cell degranulation
2) Acts on alpha receptors in blood vessels - constricts them to increase BP and redirect blood to vital organs
3) Acts on beta receptors in heart and lungs to open airways and make heart beat faster and stronger

65
Q

What does T- and B-cell involvement imply about anaphylaxis?

A

The individual has to have been exposed to the allergen prior to the anaphylactic episode

Week 140 - Collapse (3 decks)

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