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Immunology > Acute inflammation > Flashcards

Acute inflammation Flashcards

1
Q

What do we mean by inflammation?

A

The reaction of living, vascularised tissue to injury

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2
Q

How do we recognise infection?

A

Cutaneous inflammation- skin

Red, warm, swollen, tender, loss of function

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3
Q

Name examples of inflammation

A

Obstructions- gallstone cholecystitis, appendicitis
Reaction to infection- pneumonia, shingles
Burns, ulcer, Gout,
After necrosis- stroke, myocardial infarction

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4
Q

What does inflammation do?

A

Deliver concentrated, activated defensive materials to the innate immune system in fluid- phagocytes, plasma proteins

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5
Q

What is exudate?

A

Delivered cells, protein, fluid

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6
Q

What is inflammation?

A

Delivery and battle

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7
Q

Name tissue sentinel cells

A

Pericytes, mast cells, tissue macrophages, DC

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8
Q

Name blood sentinel cells

A

Monocytes, NK cells, resident liver macrophages

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9
Q

What danger signals trigger inflammation by activating the innate immune response?

A

Mild physical trauma
Specific molecular patterns
Perturbed cellular homeostasis
Missing self molecules

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10
Q

What does mild physical trauma cause?

A

Degranulates mast cells (secretion of cytoplasmic granules)

short-lived Histamine released

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11
Q

What are specific molecular patterns?

A

PAMPS

DAMPS

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12
Q

What is perturbed cellular homeostasis?

A

Surveillance of vital systems/ effector triggered immunity

Phosphorylation status, ion balance, mitochondrial status- signals converge to activate a cytoplasmic PRR

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13
Q

What are missing self molecules?

A

Cell surface molecules that prevent immune attack

MHC Class 1, Complement inhibitors

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14
Q

What are the vascular changes in inflammation?

A

Accelerated by active changes in small blood vessels- dilation of arteriole, leakiness of capillary bed

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15
Q

What does arteriole dilation do?

A

Vasoactive mediators initiate and sustain response (nitric oxide from endothelium/ cytokines)
Capillary bed opens fully, fluid leak= fluid slows/ more viscous and concentrated= stasis/ more oxygen delivery

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16
Q

What causes local tissue swelling?

A

Fluid leaving leaky vessels, caused by active structural changes to endothelium in venules in response to vasoactive mediators

17
Q

What are the vasoactive mediators that cause the leaky vessels?

A 
Endothelial contraction opens gap
Initial- histamine
Rapid- bradykinin
Delayed- cytokines
Transcytosis channels- VEGF
18
Q

What is the clot protein that escapes with the fluid?

A

Fibrinogen- made in liver, forms insoluble polymer that clots, scaffolding for cells

19
Q

How do passive leaks occur?

A

At sites of epithelial injury until endothelium regenerates
(sunburn/ leucocyte transmission)
Angiogenesis- new leaky capillaries

20
Q

What limits tissue swelling?

A

The space around the swelling- more= more swelling
Exudate in soft brain tissue- necrosis, no space (pressure)
Extra fluid reduces joint stability
Skin- lots of compartments

21
Q

What are the types of exudate in clinical practice?

A

Pus
Fibrinous
Serous
Haemorrhagic

22
Q

What is pus?

A

Neutrophil and enzyme rich

Opaque, greenish, chemotactic microorganisms

23
Q

What is fibrinous exudate?

A

Few cells
Greyish sticky fibrin coating- polymer
Restricts escape of infecting agents

24
Q

What is serous exudate?

A

Few cells, watery exudate
Serum-like, little fibrinogen/ platelets
Burn blister

25
Q

What is haemorrhagic exudate?

A

Vascular destruction

26
Q

How do circulating neutrophils get to an injury site?

A

Leucocytes passively marginate (roll along) on passing into venules, pushed by haemodynamic of blood flow
Slow= more neutrophils contact endothelium
Change in cell adhesion molecules expressed
Transmigration

27
Q

How are circulating neutrophils and vascular endothelium activated?

A

DAMP, cytokines and chemokines from DAMP activated cells like pericytes

28
Q

How do neutrophils exit into the tissue?

A

Contact, capture and rolling- histamine, DAMP and cytokines TNF/ IL1 cause endothelium to expose sticky selectins on surface
Firm adhesion, spreading, crawling- cytokines increase endothelial surface adhesion molecules firmly bind to neutrophils
Transmigration- crawling neutrophils encounter platelets, mover to endothelial junction to exit using proteases

29
Q

What is the process of transmigration?

A

Crossing basement membrane
Pericyte guides molecules
Extravasated neutrophils have transcriptional burst (ATP mitochondria) releasing cytokines, chemokines and growth factors- screen perivascular tissue
Move by chemotaxis along fibrin matrix scaffold to injury site

30
Q

Name self agents that cause neutrophil chemotaxis

A

Coagulation products
Complement C5a and C3a
Cytokine IL-8

31
Q

Name foreign agents that cause neutrophil chemotaxis

A 
Bacterial endotoxin (LPS)
f-met-leu-phe peptides- tag on peptides
32
Q

How do resident macrophages shield trivial injury?

A

Sporadic- cloak tissue microlesions, single muscle fibre

Above density of tentacles= neutrophils activated and swarm initiated

33
Q

How does the nature of the exudate change with time?

A

Fluid then Neutrophil peak then macrophage peak
Extravasating neutrophils leave trail of granule proteins along endothelium and extravasating tissue, recognised by monocytes coming next
Neutrophils secrete tenderising proteins, engage process of repair

34
Q

What is the nociceptive system?

A

Noxious stimuli are processed by specialised neural pathways (pain)

35
Q

What are the types of pain processed?

A

Direct physical stimulation
Chemical mediators- bradykinin, ATP, serotonin, histamine
Itching- histamine and proteases
Reduced pain threshold (hyperalgesia)- prostaglandin, amines, cytokines
Deep visceral pain- autonomic/ more complex than somatic pain

36
Q

How does pain and stress stimulate the autonomic nervous system?

A

Adrenaline/ noradrenaline
Indirect pain- capsular stretch, secondary inflammation
No pain nerve fibres= no pain innervation/ psychological

37
Q

How are the lymphatics involved in inflammation?

A

Terminal lymphatics proliferate and drain some of the exudate- carry guide molecules that lead into dendritic cells/ post-phagocytic macrophages/ neutrophils
Draining lymph rich in immune cells, cytokines and proteins

38
Q

What are the systematic effects of inflammation?

A

Hormonal cytokine effects distant to the injury

  • Fever (prostaglandin synthesis in hypothalamus)
  • Acute phase proteins (fibrinogen, C-reactive proteins, serum amyloid A)
  • Leucocytosis (accelerated neutrophilia release from marrow)
  • Sickness behaviours
39
Q

What are the sickness behaviours?

A

Listlessness, fatigue, decreased appetite, irritability and social withdrawal, heightened pain sensitivity, anhedonia (inability to feel pleasure)
Cytokine-induced depression- inflammatory cytokines alter CNS neurotransmitter (serotonin and dopamine) availability

Immunology (12 decks)

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