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ESA3 > Infection S3 - Innate Immunity & Acute Sepsis > Flashcards

Infection S3 - Innate Immunity & Acute Sepsis Flashcards

0
Q

What are the clinical features of SIRS?

A

Two or more of:

  • Temperature >36 or >38
  • Heart rate >90 bpm
  • Respiratory rate >20/min
  • WBC count >4x10^9/L or >12x10^9/L
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1
Q

What is a purpuric rash?

A

A dark purple rash that does not fade upon application of pressure (glass tumbler test)

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2
Q

What is sepsis?

A

A generalised response to a documented or presumed infection with the presence of SIRS

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3
Q

What is SIRS?

A

Systemic Inflammatory Response Syndrome

It’s a response to a non specific insult eg ischaemia, trauma, infection

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4
Q

Define bacteraemia

A

The presence of bacteria in the blood (+/-) clinical features

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5
Q

Define septicaemia

A

Clinical term meaning generalised sepsis

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6
Q

Define severe sepsis

A

SIRS + organ dysfunction/hypoperfusion (due to infection)

Characterised by reduced urine output and hypotension

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7
Q

Define septic shock

A

Severe sepsis + persistent hypotension despite administration of IV fluids

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8
Q

How does sepsis interfere with coagulation?

A

Cytokines initiate production of thrombin and thus promote coagulation
Cytokines also inhibit fibrinolysis
Coagulation cascade leads to micro vascular thrombosis
This causes organ ischaemia, dysfunction and failure
Micro vascular thrombosis is the leading cause of shock and multi organ failure

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9
Q

What urgent investigations should be undertaken if sepsis is suspected?

A 
Full blood count (FBC)
Urea
Electrolytes
EDTA bottle for PCR
Blood sugar
Liver function tests
C-reactive protein (CRP)
Clotting studies
Blood gases
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10
Q

What are the ‘Sepsis Six’?

A

Six actions to be completed within an hour of seeing a suspected septic patient:
1- Deliver high flow O2
2- Take blood and other cultures, consider source control
3- Administer empirical IV antibiotics
4- Measure serum lactate
5- Start IV fluid resuscitation
6- Commence accurate urine output measurement

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11
Q

What is an “empirical antibiotic”?

A

A broad spectrum antibiotic treatment that’s decided upon based on the doctor’s best guess at the pathogen responsible for the infection

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12
Q

Define the immune system

A

Cells and organs which contribute to immune defences agains infectious and non-infectious conditions

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13
Q

Define infectious disease

A

When a pathogen succeeds in evading and/or overwhelming the hosts’ immune defences

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14
Q

What factors determine the outcome of the host-pathogen relationship?

A

Number of organisms present
Virulence of the pathogen
The host’s immune response

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15
Q

What are the roles of the immune system?

A

Pathogen recognition
Containing/eliminating the infection
Regulating itself
Remembering pathogens

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16
Q

How does the immune system identify pathogens?

A

By cell surface and soluble receptors

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17
Q

How does the immune system contain/eliminate the infection?

A

By clearance and killing mechanisms

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18
Q

Why does the immune system regulate itself?

A

To ensure minimum damage to the host (in other words, to allow complete resolution)

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19
Q

Why does the immune system recognise pathogens?

A

To prevent a recurrence of the disease

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20
Q

What protection does innate immunity confer?

A

Immediate:

  • Fast (within seconds)
  • Recognises groups of pathogens
  • Lacks memory
  • No change in intensity
21
Q

What protection does adaptive immunity confer?

A

Long-lasting:

  • Slow (3-4 days)
  • Specific to one pathogen
  • Immunologic memory
  • Increases in intensity
22
Q

How does innate immunity work?

A
  • First line of defence is factors that limit entry and growth of pathogens
  • Second line of defence is factors that will contain and clear the infection
23
Q

What are the types of first line defence?

A

Physical barriers
Physiological barriers
Chemical barriers
Chemical barriers

24
Q

Give examples of physical barriers in the innate immune system

A 
> Skin
> Mucous membranes:
- Mouth
- Respiratory tract
- GI tract
- Urinary tract
> Bronchial cilia
25
Q

Give examples of physiological barriers in the innate immune system

A

Diarrhoea (food poisoning, allergies)
Vomiting (food poisoning, hepatitis, meningitis)
Coughing (pneumonia)
Sneezing (sinusitis)

26
Q

Give examples of chemical barriers in the innate immune system

A
  • Low pH (eg in the skin pH=5.5, stomach pH=1-3, vagina pH=4.4)
  • Anti microbial molecules (eg IgA in tears & saliva, lysozyme in sebum, perspiration & urine, mucous on mucous membranes, beta defensins in epithelium)
27
Q

Give examples of biological barriers in the innate immune system

A

Normal flora: non-pathogenic microbes in strategic locations eg vagina, nasopharynx, GI tract, mouth, throat

28
Q

What are the immunological benefits of normal flora?

A
  • They compete with pathogens for attachment sites and resources
  • They produce anti microbial chemicals
  • They synthesise vitamins eg K, B12, other B vitamins)
29
Q

Give examples of normal flora which inhabit the skin

A 
Staphylococcus aureus
Staphylococcus epidermidis
Streptococcus pyogenes
Candida albicans
Clostridium perfringens
30
Q

Give examples of normal flora which inhabit the nasopharynx

A

Streptococcus pneumoniae
Neisseria meningitidis
Haemophilus species

31
Q

How do problems with normal flora occur?

A

When normal flora is displaced from its normal location to a sterile location
When normal flora overgrown and becomes pathogenic when host becomes immuno-compromised
When normal flora is depleted by antibiotics

32
Q

How may normal flora be displaced to a sterile location?

A

Breaching skin integrity (surgery, injection drug users, IV lines, burns)
Fecal-oral route (food borne infection)
Fecal-perineal-urethral route (UTI in women)
Poor dental hygiene/work (dental extraction, gingivitis, flossing)

33
Q

Is bacteraemia always serious?

A

No. Dental work is the most common route for harmless bacteraemia
However serious infection ensues in high risk patients:
-Asplenic/hypo splenic
-Patients with damaged or prosthetic valves
-Patients with a history of infective endocarditis

34
Q

When could normal flora overgrow and become pathogenic in immunosupressed patients?

A

Diabetes
AIDS
Malignant diseases
Chemotherapy (neutrophils)

35
Q

Give examples of clinical problems when normal flora is depleted by antibiotics

A

Intestine- severe colitis (clostridium difficile)

Vagina- thrush (candida albicans)

36
Q

What are the types of second line defence?

A

Phagocytes
Chemicals
Inflammation

37
Q

How do phagocytes contribute to innate immunity?

A

By recognising, engulfing and destroying microbes

38
Q

How are microbes/pathogens identified/recognised?

A

PAMPs
PRRs
Opsonisation

39
Q

Describe PAMPs

A

Pathogen-associated molecular patterns
Carbohydrates, lipids, proteins, nucleic acids which have been released by pathogens
Eg lipopolysaccharide, flagellin, mannose-rich glycans, peptidoglycan

40
Q

Describe PRRs

A

Pathogen recognition receptors
Bind to the PAMPs
Eg TLR2, 4, 5

41
Q

Describe opsonisation

A

When coating proteins (opsonins) bind to microbial surfaces to enhance recognition and attachment of phagocytes, leading to engulfment and destruction
Essential in clearing encapsulated bacteria

42
Q

Give examples of opsonins

A

Complement proteins: C3b, C4b
Antibodies: IgG, IgM
Acute phase proteins: CRP (C reactive protein), MBL (mannose-binding lectin)

43
Q

Briefly describe phagocytosis

A

1-Chemotaxis and binding of phagocyte to microbe
2-Ingestion of microbe
3-Formation of phagosome
4-Fusion to lysosome to form phagolysosome
5-Digestion of microbe by enzymes
6-Formation of residual body containing indigestible material
7-Discharge/exocytosis of waste materials

44
Q

Describe a respiratory burst

A

Quick release of many toxic oxygen products in close proximity to microbes, eg O NO HO, hydroxyl radical and hypohalite

45
Q

Describe the oxygen independent pathways of destroying microbes

A 
Lysozyme
Lactoferrin
Transferrin
Cationic proteins (cathepsin)
Proteolytic and hydrolytic enzymes
46
Q

What chemicals are used in the innate im hun System?

A

Cytokines

The complement system

47
Q

Briefly describe the complement system

A

20 serum proteins

C1-C9 most important

48
Q

What are the anti microbial actions of the complement proteins?

A

C3a & C5a: recruitment of phagocytes
C3b-C4b: opsonisation of pathogens
C5-C9: killing of pathogens, membrane attack complex

49
Q

How may the complement system be activated?

A

The MBL pathway: initiated when MBL (a PRR) binds to mannose-containing protein residues eg those found on salmonella and Candida albicans
The alternative pathway: initiated by microbial cell surface constituents eg lipopolysaccharide on Escherichia coli

50
Q

What are the actions of TNF alpha, IL-1 and IL-6?

A

Liver: produce opsonins CRP & MBL
Bone marrow: neutrophil mobilisation
Hypothalamus: increases body temperature
Inflammatory actions: vasodilation, increased vascular permeability, attract neutrophils

51
Q

How can the innate immune system cause SIRS/sepsis?

A

LPS & other microbial toxins cause overreaction of the TLR4 receptor (controlling neutrophils, endothelium, monocytes) and complement
This causes an excessive inflammatory response due to coagulopathy, vasodilation, leaky capillaries and floods of cytokines causing reduced tissue/organ perfusion, leading to sepsis and multi organ failure

ESA3 (17 decks)

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