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Session 3 Flashcards

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1
Q

What is the definition of sepsis?

A

A life-threatening organ dysfunction due to a dysregulated host response to infection.

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2
Q

What is the definition of septic shock?

A

Subset where profound circulatory, cellular and metabolic abnormalities increase mortality.

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3
Q

Why are definitions important in medicine?

A
  • Common language to improve communication between professionals, and with their patients
  • Educating public about condition
  • Criteria/threshold for intervention
  • Eligibility for clinical trials
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4
Q

What is a main characteristic of sepsis?

A

Inflammation

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5
Q

What are the 3 steps that happen in sepsis?

A

1) VASODILATATION
Allows platelets, fibrin and white cells to enter - responsible for redness and warm peripheries

2) CAPILLARY LEAKAGE
Allows white blood cells to enter the tissues - causes oedema

3) AMPLIFICATION
Cytokine upregulation

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6
Q

What are the effects of sepsis on airways?

A

No effect unless infection from throat or neck, but can be affected by reduced consciousness

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7
Q

What are the effects of sepsis on breathing?

A

Tachypnoea - Lung oedema due to capillary leakage prevents optimal oxygen exchange, and patients will breathe faster to compensate. May also be caused by trying to remove acidic carbon dioxide from lungs.

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8
Q

What are the effects of sepsis on circulation?

A
  • Hypovolaemia (reduced volume) due to vasodilation + capillary leakage
  • Hypotension
  • Lower TPR = tachycardia (heart pumping faster to compensate)
  • Will eventually result in end organ damage
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9
Q

What are the effects of sepsis in terms of ‘disability’?

A
  • Reduced blood flow to brain

- Confusion, drowsiness, reduced consciousness

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10
Q

What are the effects of sepsis in terms of ‘exposure’?

A
  • Hypothalamic response to infection - high temperature

- Elderly mount different response, so a temp. under 36 degrees may mean they are very ill

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11
Q

What is the SEPSIS symptom list?

A 
Slurred speech/confusion
Extreme shivering/muscle pain
Passing no urine in a day
Severe breathlessness
It feels like you're going to die
Skin mottled or discoloured
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12
Q

What is the overall mortality rate for sepsis?

A

28.9% (67,000 deaths)

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13
Q

Who is especially at risk of sepsis?

A
  • Children under 1 y/o - cannot give history!
  • Elderly/frail
  • Pregnant and 6 wk post partum ladies (immunocompromised)
  • Patients with impaired immunity due to illness/meds
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14
Q

How is sepsis diagnosed?

A
  • Patient triggering early warning score (NEWS2)
  • Patient looks ill
  • Signs of infection
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15
Q

What is the NEWS2?

A
  • System used to identify and respond to patients at risk of clinical deterioration
  • For use in non-pregnant adults (16+)
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16
Q

What are the 6 different physiological measurements in NEWS2?

A
  • Respiration rate
  • Oxygen saturation
  • Systolic BP
  • Pulse rate
  • Levels of consciousness/new confusion
  • Temperature
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17
Q

Does a NEWS2 score provide a diagnosis?

A

No, it helps to identify patients at risk of clinical deterioration who need an urgent review. (5+ = think sepsis)

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18
Q

Is a high score on NEWS2 always indicative of a need for clinical review?

A

No - some patients who will score high will be at their end of life care and at that point it is most important to provide them comfort.

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19
Q

What is red flag sepsis?* (look at example)

A

Criteria to recognise patients with a high likelihood of organ dysfunction.

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20
Q

How is sepsis managed?

A
  • SEPSIS 6: six tasks delivered within the first hour of sepsis recognition
    Give oxygen
    Take cultures
    Give antibiotics (PRIORITY)
    Consider fluids - may not be appropriate for people in heart failure
    Take haemoglobin and lactate
    Monitor urine output
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21
Q

How to do a gram stain?*

A
  • Collect 5ml of blood into designated bottle
  • Put in automated blood culture incubator
  • Colour of bottle will change at the bottom (will go red if positive blue if negative)
  • Can then gram stain and do an antibiotic sensitivity test
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22
Q

What is a purpuric rash?

A

A rash which does not fade after being pressed and viewed through a glass.

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23
Q

What are 2 example symptoms of meningitis?

A
  • Photophobia

- Neck stiffness

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24
Q

What are supportive investigations for meningitis?

A
  • CRP
  • Blood gases
  • FBC, electrolyte, urea count
  • Liver function tests
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25
What are specific investigations for meningitis?
- Cerebrospinal fluid | - Throat swab
26
How is an investigation of cerebrospinal fluid performed?
- Obtained by lumbar puncture - Transported to lab - Glucose and protein estimation (low glucose, high protein) - Appearance - should appear clear but will be cloudy in meningitis - Gram stain
27
What is the meningococcus bacteria?
(eg. Neisseria meningitides) - Spread by aerosols and nasopharyngeal secretion - Polysaccharide capsular antigen prevents phagocytosis - Outer membrane acts as endotoxin
28
How to treat sepsis/meningitis?
- Antibiotics that cross blood brain barrier (CEFTRIAXONE) - Vaccination (Men ACWY) - Prophylaxis for close contacts which are traced by public health England
29
What are the 'key players' in adaptive immunity?*
- Naive T-cells = cells that are not activated and have not yet encountered an antigen - Pathogens - ANTIGEN PRESENTING CELLS - allow the antigens from pathogens to be recognised by the T-cells and therefore allow action
30
What kind of information do the antigen-presenting cells provide for the lymphocyte?
Sense, capture, process and present the pathogen.
31
What are two types of naive T-cells?
- Dendritic cells (tissue) | - Langerhans cells (skin)
32
What are effector T-cells?
Cells that have previously encountered the antigen and are capable of performing effector functions during an immune response (active response to stimulus).
33
What are two types of effector T-cells?
- Macrophages (phagocytic) | - B cells (antibody response)
34
What order are the immunoglobulins produced by the B cells?
- IgM produced first - Help received from t-cells to then produce IgG second - No IgG production in some.
35
Where are antigen-presenting cells located?
- Mucosal membranes (MALT), associated lymphoid tissues) - Skin ( SALT) - Blood - plasmacytoid cells, viral - Lymph nodes - trigger B cells - Spleen
36
What is the diversity in PRRs?
Extracellular and intracellular have different PRRs.
37
How are whole microbes captured compared to soluble particles?
- Macropinocytosis (soluble) | - Phagocytosis (whole)
38
What PRRs can sense Staph. aureus and Strep. pneumoniae? * (LOOK AT NOTES)
TLR1 and TLR2.
39
What PRRs can sense N. meningitides and E. coli?*
TLR4 and TLR5.
40
What TLRs are expressed on the nucleus to sense viruses and why?*
Viruses replicate in the nucleus. - TLR3 (dsRNA) - TLR7 + TLR8 (ssRNA, norovirus) - TLR9 (dsDNA, adenovirus)
41
Please refer to L6 slide 9 note on the whole process of antigen processing, expression and presentation to correct t-cells.
Ok :)
42
What are pathogens presented by?
Major Histocompatibility Complex (MHC)
43
What is the Human Leukocyte Antigen (HLA)?
Gene complex encoding MHC.
44
What is the haplotype?
A set of MHC alleles inherited together from one parent and present on chromosome.
45
What cells express MHC class 1?
ALL nucleated cells as can be attacked by viruses. (intracellular microbes)
46
What cells express MHC class 2?
APCs, dendritic cells, B cells and macrophages (extracellular microbes)
47
What are key features of MHC I AND MHC II?
- Codominant expression = 6 of each class in each individuals, more presentation allowed - Polymorphic genes = different individuals respond to different microbes (so that one disease cannot eradicate a population) - Presentation of microbial peptides
48
Why is HIV untreatable?
The virus mutates MHC I so that it cannot present antigens.
49
How do intracellular microbes get processed?*
- Viral protein is present in cytosol and is marked for destruction by proteasome (not host protein) - Viral peptide from proteasome destruction transported to ER by TAP1/TAP2 proteins - Formation of MHC 1 complex if right match - MHC-1 will migrate to cell surface to be recognised by natural killer t-cells
50
What kind of cells are intracellular pathogens presented to?
CD8+ T cells = will destroy the infected cell
51
Define the endogenous pathway again.*
- Virus antigen can be expressed on APC or any infected target cell - Naive CD8+ T cells will be activated in lymphoid tissue - All infected cells killed
52
How are extracellular microbes processed?*
EXOGENUS PATHWAYS - Microbes are captured by phagocytosis/micropinocytosis (always in vesicle) - Microbe degraded in endosome - Vesicles fuse with vesicles containing MHC-II - Peptide-MHC complex formed if right match - Presented on surface to CD4+ T cells
53
Where does the exogenous pathway occur?
Only in antigen presenting cells
54
Why would it be bad if everyone had the same MHC molecules/genes?
- Would mean that everyone would react the same to diseases | - e.g. one disease could wipe out the world
55
How are peptides presented by the MHC molecules?
- Peptide binding cleft - Broad specificity - Responsive T cells
56
What is a MHC-I complex made of?*
- 3 alpha cells (binding cleft between alpha-1 and alpha-2) - Small beta chain for stability - Can present around 9 amino acids
57
What is a MHC-II complex made of?*
- 2 alpha chains - 2 beta chains - Binding cleft above alpha-1 and beta-1 subunits - Can present around 30 amino acids
58
What is meant by broad specificity?
Many peptides can be presented by the same MHC molecule and so many microbes are recognised.
59
What is meant by responsive T cells?
- Different types of T cells recognise different microbes - CD4+ = extracellular - CD8+ = intracellular
60
What is the clinical importance of MHC molecules?
- Different hosts can deal with microbes at different levels - No 2 individuals have the same set: will not be wiped out by single disease - Different susceptibility to infections (strong vs weak responses)
61
What are elite controllers/long-term nonprogressors?
- Specific to HIV mainly - Individuals who can maintain undetectable virus levels and remain asymptomatic without antiretroviral therapy. - High CD4 cell counts maintained
62
What are some clinical issues with MHC molecules?
- Causes of organ transplant rejection: mismatch of HLA between donor and recipient, so seen as foreign - HLA association with autoimmune diseases
63
What are the HLA associations with autoimmune diseases?
- Ankylosing spondylitis: HLA-B27 allele present in almost all patients - Type 1 diabetes: HLADQ2 allele in 50-75% of patients

Infection (10 decks)

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