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med year 1 > Inflammatory Arthritis: Acute inflammation pathology > Flashcards

Inflammatory Arthritis: Acute inflammation pathology Flashcards

1
Q

How long does acute inflammation response last for?

A

3 days no more

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2
Q

List 5 cardinal signs of acute inflammation:

A

calor(hot), dolor (pain), tumor(swelling), rubor (redness - vessel dilate to allow for blood to rush to site), functio laesa (loss of function)

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3
Q

What is inflammation caused by?

A
  • Caused by necrosis (unintentional cell death and rupture of membranes - can cause raised neutrophils count) (DAMPs) or infection (PAMPs/MAMPs) - pathogen/microbe associated infection
    • Allowing inflammatory cells + plasma proteins to escape from blood vessels
    • Characterised by neutrophils
    • cytokine transmitted to bone marrow and undergo hyperplasia
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4
Q

5Rs of inflammation

A
  • Recognition (of agent causing injury) - toll like receptor recogonise
  • Recruitment (of leucocytes ie cytokine)
  • Removal of agent
  • Regulation of response (depend on how long should be active)
  • Resolution
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5
Q

Process of Inflammation

A
  1. PAMPs and DAMPs produced
  2. Recognised by dendritic cells (in the skin) + macrophages + mast cells - all have Toll-like receptors (specific to patterns that are PAMPs or DAMPs
  3. Cytokines produced, IL1
  4. Recruits neutrophils and monocytes (become macrophages) - chemotaxis
  5. Phagocytosis of microbes/dead cells
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6
Q

what is Hageman Factor?

A
  • Due to infection, clotting factor VII (Hageman factor) comes in contact with collagen (blood vessels)
  • Activates coagulation cascade (and wound blood flow will stop), complement system (trigger accute inflammation)
  • Activates Kinin system - hageman factor cleaves kallikrein which cleaves high molecular weight (HMW) kininogen, producing bradykininHageman factor → kallikrein → HMW kininogen → bradykinin
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7
Q

What is Bradykinin Functions?

A
  • Vasodilation (rubor,calor, dalor ie painful)
  • Increased vascular permeability (cells lining blood vessels (endothelial layer) activated and actin contact - cause junctions to break)
  • Pain - sensitises nerve endings
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8
Q

Describe the Complement System

A
  • Complement proteins produced in liver
  • Circulates in blood inactively, activated in three way ( trigger needed)…
    • Classical Pathway - binding to IgG or IgM
    • Alternative Pathway - binding to microbes
    • Lectin Pathway - lectin binding to mannose on bacteria
  • Results in C3 Convertase which splits in C3a and C3b
    • C3a - anaphylatoxin that recruits leukocytes → mast cells release histamine and recruite other cells
    • C3b - opsonin (eat me signal for bacteria) signal protein for macrophages
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9
Q

Functions of Complement: Formation of anaphylatoxins

A
  • Mast cells secrete histamine
  • C5a-and-C3a-chemotaxis attracts neutrophils, monocytes, eosinophils, basophils
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10
Q

Functions of Complement: Opsonisation

A
  • C3b coats microbes
  • Neutrophils and macrophages have C3b receptors, enables phagocytosis
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11
Q

Functions of Complement:Cell lysis

A

Formation of membrane attack complex (C5b, C6, C7, C8, C9), cell filled with water causing lysis → T shaped tunnel through wall of bacteria allowing water to flood in - T cell complex

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12
Q

Functions of Complement:Immunoglobulin clearance

A

Removal of immune complex from circulation

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13
Q

Describe the function of Mast Cells

A
  • Activated by tissue trauma, complement proteins (C3a, C5a), cross linking of IgE
  • Immediate response = vasodilation of arterioles, increased vascular permeability
  • Delayed response = production of arachidonic acid derivatives e.g leukotrienes
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14
Q

What is the Arachidonic Acid Cycle?

A

Phospholipids converted to arachidonic acid using enzyme, phospholipase A2

all components are derived from plasma membrane

Two mechanisms

  1. Reacts with COX1 and COX2, forming prostaglandins (PG)
  2. PGI2 and PGD2 = vasodilation, vascular permeability
  3. PGE2 = pain, fever - needed to stop denaturing of proteins
  4. Acts on 5-lipogenase, forming leukotrienes (LT)
  5. LTC4, LTD4, LTE4 = vasoconstriction, bronchospasm and vascular permeability
  6. LTB4 = neutrophil attraction + activation
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15
Q

what do Steroids do?

A

anti-inflammatory drug - prevents transcription of phospholipase A2, stops production of PGs and LT

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16
Q

what do NSAIDs do?

A

(aspirin, ibuprofen) - inhibits COX1 + COX2, stops production of PGs

17
Q

what is Leukocyte Extravasation?

A

neutrophils in bone marrow and stimulus in skin so neutrophils have to come into contact with it:

  1. Margination - vasodilation slows blood
  2. Rolling - cytokines activate selectins act as speed bumps, binds to neutrophils, causing them to ‘roll’
  3. Adhesion - integrins activated, increases affinity for adhesion between neutrophils and endothelial cells
  4. Transmigration and chemotaxis - neutrophils attracted to bacterial products, IL8, C5a, LTB4 (strong chemoattractants) - present in tissue around vessel and draw neutrophils toward them
  5. Phagocytosis
  6. Destruction of phagocytosed material
  7. Resolution
18
Q

Describe Phagocytosis and O₂-Dependent Killing:

A

how neutrophils kills:

  1. Microbe digested, ingested in phagosome
  2. Phagosome merges with lysosomes forming phagolysosomes
  3. Degraded via lysosomal enzymes, reactive oxygen species, nitrogen species
  4. Active enzyme converts oxygen → superoxide + hydrogen peroxide
  5. Myeloperoxidase converts hydrogen peroxide → hypochlorite (or bleach)
  6. Killing of pathogen
19
Q

What is O₂-Independent Killing?

A
  • Occurs via enzymes in leukocytes secondary granules in cytoplasm
    • Lysozymes in macrophages, major basic proteins in eosinophils
  • Less effective
20
Q

What is and happens in Resolution?

A
  • Neutrophils die from apoptosis, disappearing after 24 hours
  • Era of macrophages begin, main controllers of next inflammatory process
21
Q

What happens with the Arrival of Macrophages?

A
  • Peaks 2-3 days after inflammation
  • Follows the same margination, rolling, adhesion etc…
  • Phagocytosis aided with opsonins
22
Q

what are Systemic Effects of acute inflammation?

A
  • Lipopolysaccharides (a pyrogen) from bacteria cause macrophages to produce IL1, TNF
    • Increases COX activity, output of acute phase proteins e.g CRP, white cell production
    • Increase insulin resistance, promoting type 2 diabetes
    • TNF can accelerate atherosclerosis and promote thrombosis
23
Q

what are the Outcomes of Inflammation?

A
  • Macrophages produce IL10, TGF-β - ends inflammation, reparation begins
  • Prolonged acute inflammation causes macrophages to produce IL8 - recruits more neutrophils
  • Macrophages produce fibrogenic growth factors - forming an abscess (neurophill in small space)
  • Possible chronic inflammation - activation of CD4+ helper T cells

med year 1 (12 decks)

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