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ESA 3 > Infection Session 3- Sepsis And Innate Immunity > Flashcards

Infection Session 3- Sepsis And Innate Immunity Flashcards

1
Q

What is sepsis?

A

Life threatening organ dysfunction due to dysregulated host response to infection- septic shock is persisting hypotension requiring treatment to maintain blood pressure despite fluid rescue situation

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2
Q

What is bacteraemia?

A

Presence of bacteria in the blood

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3
Q

What is the sepsis six bundle?

A 
Oxygen
Blood cultures
IV antibiotics
Fluid challenge
Lactate
Measure urine output
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4
Q

What urgent investigations can be done for sepsis?

A 
FBC
Urea and electrolytes
ECTA bottle for PCR
Blood sugar
Liver function tests
CRP
Coagulation studies
Blood gases
Other microbiology samples
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5
Q

Which pathogen causes meningococcal meningitis?

A

Neisseria meningitidis

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6
Q

How is meningococcal meningitis spread?

A

Direct contact with respiratory secretions

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7
Q

How can the inflammatory cascade cause sepsis?

A

Endotoxins binds to macrophages so cytokines locally stimulate inflammatory response to promote wound repair and recruit RE system.
Cytokines released into circulation stimulating GF, macrophages and platelets.
Infection not controlled cytokines lead to activation of humoral cascades and RE system
CIRCULATORY INSULT

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8
Q

How can cytokines cause shock and multi organ failure?

A

Cytokines initiate production of thrombin and promote coagulation and inhibit fibrinolysis. Coagulation cascade leads to macrovascular thrombosis and organ ischaemia, dysfunction and failure

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9
Q

What supportive care can be offered for sepsis?

A

Early referral to ITU
Sepsis six
Regular monitoring and reassessment

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10
Q

What antibiotic is used to treat meningitis and why?

A

Ceftriaxone- penetrates into CSF

Not used for neonates/elderly

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11
Q

What are some of the life threatening complications of sepsis?

A 
Irreversible hypotension
Respiratory failure
Acute kidney injury
Raised intracranial pressure
Ischaemic necrosis of digits/hands/feet
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12
Q

What type of bacteria is neisseria meningitidis?

A

Gram -ve diplococcus

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13
Q

What are the serogroups of neisseria meningitidis based on?

A

Polysaccharide capsular antigen- evades immune response by preventing phagocytosis
Outer membrane acts as endotoxin

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14
Q

What percentage of young adults carry meningococcal disease?

A

25%

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15
Q

How is meningococcal disease spread?

A

Aerosols and nasopharyngeal secretions

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16
Q

How many cases of meningococcal disease per year and which type?

A

1000 cases per year, mainly group B

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17
Q

What is the fatality rate of meningococcal disease?

A

About 10%

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18
Q

What are the 2 ways to prevent meningococcal disease?

A

Vaccination-ACYW or men C

Antibiotic prophylaxis

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19
Q

Define immune system

A

Cells and organs that contribute to immune defences against infectious and non-infectious conditions

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20
Q

Define infectious disease

A

When the pathogen succeeds in evading and/or overwhelming the host’s immune defences

21
Q

What are the 4 main parts of the immune response?

A

Pathogen recognition- cell surface and soluble receptors
Containing/eliminating the infection- killing and clearance mechanisms
Regulating itself- minimum damage to host
Remembering pathogens- preventing disease from recurring

22
Q

What are the main differences between innate and adaptive immunity?

A 
Innate = immediate protection, adaptive = long lasting protection
Innate = fast, adaptive = slow
Innate = lack of specificity, adaptive = specificity
Innate = lack of memory, adaptive = immunologic memory
Innate = no change in intensity, adaptive = changes in intensity
23
Q

What are the 4 barriers of innate immunity?

A

Physical barriers
Physiological barriers
Chemical barriers
Biological barriers

24
Q

What physical barriers exist within the body?

A

Skin
Mucous membranes (mouth, resp tract, GI tract, urinary tract)
Bronchial cilia

25
Q

What are the physiological barriers in innate immunity?

A

Diarrhoea - food poisoning
Vomiting- food poisoning, hepatitis, meningitis
Coughing- pneumonia
Sneezing- sinusitis

26
Q

What chemical barriers exist in the innate immune system?

A

Low pH- skin 5.5, stomach 1-3, vagina 4.4

Antimicrobial molecules- IgA, lysozyme, mucus, beta defensins, gastric acid and pepsin

27
Q

What are the biological barriers of innate immunity?

A

Normal flora- non pathogenic microbes, strategic locations, absent in internal organs/tissues
Benefits- compete with pathogens for attachment sites and resources, produce antimicrobial chemicals, synthesise vitamins

28
Q

How can normal flora be displaced from its normal location to sterile location?

A

Breaching skin integrity = skin loss, surgery, injection drug users, IV lines
Fecal-oral route = foodborne infection
Fecal-perineal-urethral = UTI

29
Q

What is the main way normal flora is displaced from its normal location (not to a sterile location)?

A

Poor dental hygiene/dental work - common cause of harmless bacteraemia

30
Q

When can normal flora overgrow and become pathogenic?

A

When host is immunocompromised- diabetes, AIDS, malignant diseases and chemotherapy

31
Q

Give 2 examples of diseases that can be caused by normal flora being depleted by antibiotics

A

Severe colitis in intestine caused by clostridium difficile

Thrush in vagina caused by candida albicans

32
Q

What are the second line of defence in innate immunity?

A

Phagocytes and chemicals

33
Q

What are the main types of phagocytes?

A

Macrophages
Monocytes
Neutrophils

34
Q

Where are macrophages found and what is their function?

A

Present in all organs
Function is phagocytosis (and presenting microbial antigens to T cells in AI)
Produce cytokines and chemokines

35
Q

Where are monocytes found and what is their function?

A

Present in blood (5-7%)

Recruited at infection site and differentiate into macrophages

36
Q

Where are neutrophils found and what is their function?

A

Present in blood (60% of blood leukocytes)
Increased during infection
Recruited by chemokines to the site of infection
Ingest and destroy pyogenic bacteria: staph aureus and strep pyogenes

37
Q

What other cells are important in innate immunity and what is their function?

A

Basophils/mast cells- early actors of inflammation, important in allergic response
Eosinophils- defence against multicellular parasites
Natural killer cells- kill all abnormal host cells
Dendritic cells- present microbial antigens to T cells (acquired immunity)

38
Q

What does PAMPs stand for?

A

Pathogen associated molecular patterns

39
Q

Give some examples of PAMPs and what they relate to

A

Lipopolysaccharides- gram -ve bacteria
Peptidoglycan- gram +ve bacteria
Mannose rich glycine- all mycobacteria
Flagellum- bacterial flagella

40
Q

What is opsonisation of microbes?

A

Opsonins bind to the microbial surfaces leading to enhanced attachment of phagocytes and clearance of microbes

41
Q

Give some examples of opsonins

A

Complement proteins- C3b
Antibodies- IgG
Acute phase proteins- CRP

42
Q

What are the two phagocyte intracellular killing mechanisms?

A

Oxygen dependant pathway

Oxygen independant pathways

43
Q

Describe the oxygen dependant pathway (respiratory burst)

A

Toxic O2 products for the pathogens- hydrogen peroxide, hydroxyl radical, nitric oxide, singlet oxygen , hypohalite

44
Q

What molecules are used in oxygen independant pathways?

A

Lysozyme
Lactoferrin/transferrin
Cationic proteins
Proteolytic and hydrolysis enzymes

45
Q

Describe the 2 activating pathways in the complement system

A

Alternative pathway- initiated by cell surface microbial constituents
MBL pathway- initiated when MBL binds to mannose containing residues of proteins found on many microbes

46
Q

What are the microbial actions of complement and which serum proteins are responsible?

A

Recruitment of phagocytes- C3a and C5a
Opsonisation of pathogens- C3b to C4b
Killing of pathogens, membrane attack complex- C5 to C9

47
Q

What are the anti-microbial actions of macrophage-derived TNF/IL-1/IL-6 and where do they occur?

A

Liver (opsonins)- CRP and MBL (complement activation)
Bone marrow- neutrophil mobilisation
Inflammatory actions- vasodilation, vascular permeability, adhesion molecules = attraction of neutrophils
Hypothalamus- increased body temp

48
Q

What can result in reduced phagocytosis and what causes this?

A

Decreased spleen function- asplenic and hyposplenic patients
Decreased neutrophil number- cancer chemotherapy, certain drugs, lymphoma and leukaemia
Decreased neutrophil function- chronic granulomatous disease, chedial-hiyashi syndrome (no phagolysosomes formation)

ESA 3 (18 decks)

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