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Medicine Year 1 - Semester 2 - Part 2 > Sepsis > Flashcards

Sepsis Flashcards

1
Q

Statistics regarding sepsis

A

Accounts for 1/5 of all deaths globally

3 million deaths in children <5

85% of cases are in Low+Middle income countries

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2
Q

Sepsis in the UK

A

1 dies in the UK every 12 minutes

2 in 5 have major complications of sepsis (major disability/ limitation)

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3
Q

qSOFA score

A

Used to rapidly identify sepsis.

Features include:

Respiratory rate : 22/min or greater
Systolic blood pressure : 100 mmg Hg or less

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4
Q

What does qSOFA look at ?

A

Organ dysfunction

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5
Q

Sepsis

A

Life-threatening organ dysfunction caused by a dysregulated host response to infection.

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6
Q

Septic shock

A

A subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone.

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7
Q

Septic Shock features

A

Subset of sepsis
Organ Dysfunction

  • Persistent hypotension requiring vasopressors to maintain MAP>= 65 mmHg
  • Serum lactate >= 2mmol/L
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8
Q

SIRS

A

Systemic Inflammatory Response Syndrome

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9
Q

What does SIRS do ?

A

Reflects the usual, expected and useful host immune responses.

Typically, represent responses to infection.

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10
Q

Key features of SIRS - systematic inflammatory response syndrome

A

2 or more of:

Temperature >38 or <36

Heart rate >90/min

Resp rate >20/min

White cell count > 12,000/mm3

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11
Q

Data on SIRS

A

Now thought to lack both specificity and sensitivity

Sepsis is not an inevitable consequence of escalating inflammation.

Sepsis involves anti- and pro- inflammatory pathways.

SIRS is still useful but has limitations

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12
Q

Non-infection causes

A

Severe burns
Pancreatitis
Severe trauma
Ischaemia- reperfusion injury

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13
Q

Inflammation

A

Automated, early, rapid and protective responses

Directed at the site of infection, injury or trauma

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14
Q

Features of inflammation

A

Heat
Pain
Redness
Swelling

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15
Q

Celsus Tetrad

A

Calor
Dolor
Rubor
Tumor

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16
Q

Heat

A

Inhibiting or Mitigating pathogen expansion

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17
Q

Pain

A

Protective alert mechanism, encouraging withdrawal/action

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18
Q

Redness

A

Increased blood flow, facilitating access to site of injury

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19
Q

Swelling

A

Local fluid accumulation, cellular influx, pro-thrombotic, creating a seal

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20
Q

Localised regulated inflammation

A

Resident cells able to immediately recognise and response

Use of surface receptors, signal transduction and downstream responses to effect immediate changes

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21
Q

What are Toll-like receptors ?

A

Critical (host) cell receptors

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22
Q

Function of TLRs

A

TLRs and CLRs identify and signal downstream responses to attempt to address pathogen.

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23
Q

PRRs

A

Pattern Recognition receptors

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24
Q

Function of PRRs

A

Pattern recognition receptors are evolved to recognise abnormal patterns

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25
PAMP
Pathogen Associated Molecular Patterns
26
Function of PAMPs
Pathogen Associated Molecular Patterns trigger such responses
27
NLRs
Nod-like receptors
28
CLRs
C-lectin type receptors
29
Most severe type of sepsis
Gram negative sepsis through TLR4
30
What is TLR4 associated with ?
LPS Lipopolysaccharide
31
Function of TLR4
TLR4 is the major receptor for lipopolysaccharide (LPS), the major trigger for gram-negative sepsis.
32
Action of TLR4
TLR4 uses 2 accessory molecules in a complex
33
Function of TLR3
TLR3 is expressed on the endoscope inner surface - well placed to recognise PAMPs - specifically Virus associated (RNA) PAMPs
34
What is TLR5 associated with ?
Flagellin
35
Downstream effects of TLRs
Inflammatory cytokines response
36
Function of activated TLRs
Regulate genes responsible for: - Cardiovascular regulation - Immune regulation - Hormonal control - Coagulation - Metabolism - Bio-energetic systems
37
What is implicated in downstream drivers of inflammation by TLR activation ?
Mitochondrial function
38
What is found in activated TLRs ?
Pro-inflammatory cytokines, chemokine and cytokine receptor genes found in cells with activated TLR are up-regulated e.g. TNFalpha, IL-1, IL6
39
Results of activated TLRs
Increased blood flow MHC expression Cortisol, oestrogen, adrenaline Platelet activation Metabolism - increased Mitochondrial - varied responses
40
Results of dysregulated inflammation
SIRS / Sepsis
41
Describe dysregulated inflammation
Systemic vasodilation and reduced blood volume. Impaired O2 delivery, intravascular coagulation - reduced blood flow Lactic acidosis, cellular dysfunction and multi-organ dysfunction. ATP levels fall, mitochondria function and cell performance falls Mitochondria dysfunction can lead to cell death (tissue necrosis) but NOT in sepsis. In sepsis, Mitochondria may adopt a low energy state. This may explain recovery of organ function once systemic inflammation resolves.
42
Systemic vasodilation and reduced blood volume
Poor organ perfusion with TNF-alpha, IL-1, IL-6 and endothelial cell activation
43
Describe mitochondria in sepsis
IN sepsis, the mitochondria may adopt a low energy state.
44
Key feature of dysregulated inflammation
Lactic acidosis Cellular dysfunction ATP levels fall Mt (mitochondria) function falls
45
State the major role of mitochondria
Generation of ATP Production of reactive oxygen species (ROS) Note: Mitochondria consume >95% of the body's oxygen supply
46
Functions of mitochondria
Generation of heat, thermoregulation Cell signalling Intracellular calcium regulation Inflammasome assembly Initiation of cell death
47
What is the mitochondria the site of ?
Site of production (e.g. cortisol) OR action (e.g. oestrogen) of several hormones Synthesis of heme and iron-sulfur clusters (cofactors in the electron transport chain)
48
How is the electrochemical gradient generated ?
An electrochemical gradient is generated across the inner mitochondrial membrane. The result proton gradient in complex V (ATP synthase) drives ADP to ATP.
49
ROS
Reactive oxygen species
50
Describe mitochondrial dysfunction in sepsis
Impaired ATP generation Micro- and Macrovascular (endothelial) complications Increased ROS, in response to PAMPs, DAMPs Pro-inflammatory cytokine release Hyper-inflammatory release
51
Mitochondrial dysfunction
Electron transport chain complex dysfunction (I, III, IV)
52
What does mitochondrial dysfunction lead to ?
Compromised immune function Compromised metabolic function of end-organisms : multi-organ dysfunction Hyper-inflammatory state, loss of haemostasis
53
Impact of dysregualted inflammation on Mt
Impaired perfusion, reduced O2 to tissues to fuel electron transport and ATP generation. Hormonal alterations affect Mt function.
54
What damages Mitochondria (Mt) ?
NO, CO, HS and the ROS inhibit Mt respiration and damage Mt proteins
55
What is down-regulated in early septic processes ?
Genes transcribing Mt proteins are down-regulated early in septic processes.
56
Metabolic consequences of dysregulated inflammation ?
ATP levels fall, but in sepsis cell death does not occur (as would be expected in other low ATP situations) This may lead to dysfunction and 'damaging' mitochondrial biogenesis, aggravating pro-inflammatory responses.
57
Mitochondria as 'quality control' in sepsis
Critical roles in: Supplying energy and metabolic intermediated for immune cell activation Influencing inflammatory and cell death pathways
58
Mitophagy
Destruction of dysfunctional mitochondria to limit associated damage cascades
59
DAMPS
Damage associated molecular patterns
60
Describe proposed mitochondrial / cell hibernation
Mt adopt decreased metabolic rate to compensate for reduced ATP concentration. Decrease in cell functionality within tissue/ system - organ dysfunction So, when inflammation resolves, the organ can recover
61
Function of mitochondrial research
Better understand fundamental processes relevant to many diseases.
62
What does sepsis lead to ?
Sepsis is the result of infection that leads to tissue damage - distal to the site of infection Dys-regulated inflammation following infection
63
Key risk factors for sepsis
Elderly >75 Very young <1 Impaired immune systems - due to illness/treatments Post-operative (6 weeks)
64
Impaired immune system
Cancer, Chemotherapy, DM, Splenectomy, Sickle cell, Steroids
65
State some other risk factors for sepsis
Loss of skin integrity: cuts, burns, IV drug users Women - pregnancy/ postnatal Neonatal - GBS (group B strep), PROM (prem rupture of membranes)
66
Pathogens causing sepsis
Neisseria meningitidis Strep pneumoniae Strep pyogenes Staph aureus Salmonella typhimurium Aspergillus fumigatus
67
Types of sepsis
Bacterial Viral Fungal
68
Presentation of sepsis
Wide range of symptoms and signs May include source of infection / trigger Usually reflects broad systemic response of sepsis
69
Things to consider in the presentation of sepsis
Localising symptoms/signs that point to the underlying cause General symptoms or signs that reflect the severity of sepsis
70
Localising symptoms/signs that point to the underlying cause
Dysuria Red hot knee Inflamed site around cannula Diarrhoea
71
General symptoms or signs that reflect the severity of sepsis
Reduced consciousness Tachypneoa Light-headedness Low BP
72
Clinical findings - CNS
Headache Photophobia Confusion Seizure
73
Clinical findings - Respiratory
Productive cough Haemoptysis Breathlessness
74
Clinical findings - Cardiovascular
Murmur Chest pain
75
Clinical findings - GI
Diarrhoea Abdominal pain
76
Clinical Findings - renal
Loin pain Dysuria Anuria
77
Clinical Findings - Joints/Skin
Erythema Swelling Tenderness Cyanotic / Mottled
78
Clinical findings - other
Fever Migrane Severe myalgia
79
SOFA
Sequential organ failure assessment score
80
qSOFA - memory aid
15 22 00 <15 altered mental state GCS >22 respiratory rate <100 blood pressure - low
81
ROC curve values - diagnostic
0.7-0.8 OK 0.8-0.9 Very good >0.9 excellent
82
qSOFA diagnostic score
0.81 Very good diagnostic tool
83
Early immune response
TLRs Release of IL-1, IL-6, IL-8 etc Activation of complement, coagulation and phagocytes
84
Cellular immune response
Activation of B cells, neutrophils, myeloid derived suppressor cells
85
Humoral immune response
Production of immunoglobulins (IgM, IgG)
86
Anti-inflammatory events
Decrease of HLA-DR expression T-cell exhaustion Apoptosis of immune cells (lymphocytes, monocytes and antigen presenting cells )
87
Describe sepsis
System-wide release of cytokines, mediators and pathogen related molecules Activation of coagulation ad complement pathways Widespread inflammation, tissue damage, multi-organ dysfunction.

Medicine Year 1 - Semester 2 - Part 2 (53 decks)

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