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Pathology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Acute inflammation, brief summary of processes

A

Infective organism/foreign material/dead cell molecules are released Mast cells, platelets release preformed mediators PRRs are stimulated on macrophages, DC, epithelium - these activate transcription factors - production of cytokines => inflammatory response

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2
Q

What is the vascular response to acute inflammation

A

want to deliver cells/chemical mediators/proteins to tissue - vasodilation -> increase blood flow - increased vascular permeability - allow plasma proteins to leave circulation - endothelial cell activation - increased adhesion of leukocytes + migration through wall

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3
Q

Endothelium - what is its normal function? (4)

A
  • semi-permeable barrier (junctional complexes) - prevents blood clottin (NO + prostacyclin) - role in vascular tone: - release NO, prostacyclin -> vasodilation - release endothelin -> vasoconstriciton resist leukocyte adhesion produce growth factors + cytokines (IL-1, TNFa) specialised morphology in certain areas
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4
Q

What mediators are released from endothelium to induce vasodilation

A

NO, prostacyclin

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5
Q

What mediators are released from endothelium to induce vasoconstriction

A

endothelin

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6
Q

What are the two major components of acute inflammation?

A

Vascular changes - vasodilation -> increase blood flow - increased vascular permeability - allow plasma proteins to leave circulation - endothelial cell activation - increased adhesion of leukocytes + migration through wall Cellular events - cellular recruitment: emigration of leukocytes from circulation, accumulation at site of injury - activation of leukocytes

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7
Q

What are 4 mechanisms by which there may be an increase in vascular permeability?

A
  1. retraction of endothelial cells 2. endothelial injury (burns, toxins) 3. leukocyte-mediated vascular injury 4. increased transcytosis
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8
Q

retraction of endothelial cells (to increase vascular permeability) - which blood vessels are affected - what stimulates it - mechanism - how long does it last

A

venules stimulated by histamine, NO junctions loosen, gaps form rapid, short-lived

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9
Q

endothelial injury (to increase vascular permeability) - which blood vessels are affected - what causes it - how long does it last

A

arterioles, capillaries, venules burns, microbial toxins stimulate rapid, and may be long-lived (hrs->days)

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10
Q

leukocyte-mediated vascular injury (to increase vascular permeability) - which blood vessels are affected - what stimulates it - how long does it last

A

venules, pulmonary capillaries occurs in the late stages of inflammation, the leukocytes release enzymes to stimulate it long-lived

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11
Q

increased transcytosis (to increase vascular permeability) - which blood vessels are affected - what stimulates it - mechanism

A

venules induced by VEGF - proteins move through in larger amount, due to increased transporters

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12
Q

What is diapedesis

A

the process of WBC moving through endothelial wall

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13
Q

Cardinal features of acute inflammation

A

redness heat swelling pain loss of function

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14
Q

what are the cellular components of acute inflammation

A

Early on - neutrophils (6-72hrs) Later (2-3 days) - macrophages

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15
Q

Neutrophils - what is their action in acute inflammation

A

↑production in bone marrow (due to IL1, IL6, TNFa), released from bone marrow and are recruited to the site of inflammation role: phagocytose + kill - also role in debridement of dead dissue then apoptose

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16
Q

Macrophages - role in acute inflammation

A

come in 2-3 days one roles - APC - phagocytosis - secretion of mediators mediators: - chemokines - proteases (tissue destruction) - cytokines + growth factors

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17
Q

Macrophages in acute inflammation - which cytokines do they release, and what is their role

A

TGFb, PDGF, FGF - stimulate repair - proliferation, angiogenesis IL-1, TNF - endothelial activation IL-1, IL-6, TNF - acute phase response

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18
Q

what is the main cell type that produces IL1 and TNF?

A

macrophage

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19
Q

phagocytosis in macrophages - describe process

A

microbes bind phagocytic receptors - though opsonins phagocyte membrane zips up around -> form phagosome phagosome meets with lysosome -> phagolysosome -> degradation (lysosomal enzymes, ROS, NO)

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20
Q

Oedema - definition - types of oedema, and when they occur

A

abnormal increase in interstitial fluid (1) transudate - normal vascular permeabiliy - mostly fluid - few proteins - occurs due to ↑hydrostatic pressure or ↓plasma protein pressure (2) exudate - due to ↑vascular permeability - fluid + cells + protein + fibrin - different types of fibrin (diff % fluid/nt/fibrin) (3) impaired lymphatic drainage

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21
Q

what is fibrin? role in inflammation histology

A

coagulative protein (coag. cascade initiation) liver = fibrinogen; changes to fibrin when exposed to collagen in tissues in inflammation - often have vessel damage - want it to clot. - also probably helps to provide scaffolding for cells to migrate histo: fine, pink rods

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22
Q

What are the 3 types of exudate? what are their components, examples when they occur, histology

A

(1) purulent/suppurative - neutrophil rich - usually due to bacterial infection examples: =abscess (focal area of tissue necrosis + nts) (the necrosis is due to mediators released by bact/nt that damage tissue) = perforation - can occur in GIT, nts release granule contents histology - nts ————————————————————– (2) fibrinous - fibrin-rich - generally occurs on serous surface (pleura, pericardium) examples: fibrinous pleuritis, fibrinous pericarditis, acute appendicitis. can lead to adhesions histo: - serosal surface, predominantly fibrin macro: fibrin is pale, white/brown ——————————————————————- serous - fluid example: blister

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23
Q

What is hyperemia? What is vasocongestion?

A

hyperemia = Increase in blood due to active process of vasodilation - inflammation, exercise vasocongestion = passive - less outflow of blood from tissue - eg venous obstruction

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24
Q

which inflammatory mediators act to cause vasodilation what are they released from (3)

A

(1) histamine (mast cells, in response to IL-1) (2) prostaglandins (mast cells, macrophages, endothelial cells) (3) NO (endothelial cells)

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25
Q

which inflammatory mediators act to cause ↑vascular permeability what are they released from (4)

A

histamine (mast cells) serotonin (platelets) bradykinin (plasma proteins - kininogens - are activated) leukotrienes (plasma cell membranes - mast cells, leukocytes)

26
Q

which inflammatory mediators act to cause endothelial activation what are they released from (2)

A

TNF, IL-1 = macrophages (also endothelial + mast cells)

27
Q

which inflammatory mediators act to cause chemotaxis what are they released from (4)

A

complement components bacterial components (plasma) chemokines leukotriene B4 (leukocytes, some macrophages)

28
Q

which inflammatory mediators act to cause tissue damage what are they released from (3)

A

neutrophil granule contents ROS NO (endothelium, macrophages)

29
Q

which inflammatory mediators act to cause pain what are they released from (2)

A

prostaglandins (mast, macrophages, endothelial cells) bradykinin (plasma protein) these act on nerve endings in tissue

30
Q

fever

A

IL-1, IL-6, TNF -> act on hypothalamus to produce PGE2

31
Q

What are 4 outcomes of acute inflammation? What does the outcome depend on?

A
  1. abscess formation 2. resolution 3. healing by repair 4. chronic inflammation Outcome depends on - tissue type - extent of damage - type/duration of injury
32
Q

When may acute inflammation result in abscess formation

A

neutrophil response + tissue destruction

33
Q

When might acute inflammation result in resolution?

A

Tissue damage is minimal, and neutralised Healing: - regrowth of dead cells - regeneration

34
Q

When might acute inflammation result in healing by repair?

A

There is tissue damage, but it is neutralised Healing is through organisation (scar formation) - granulation tissue formation - phagocytosis

35
Q

When might acute inflammation result in chronic inflammation?

A

Tissue is destroyed, and there is a persistent damaging agent there is organisation (scar tissue formation) + continued inflammation

36
Q

Healing occurs through…

A

granulation tissue

37
Q

Granulation tissue - what are its main components (4)

A

(1) Inflammatory cells - macrophages - lymphocytes - eosinophils (2) New blood vessels - mainly capillaries (3) fibroblast migration + proliferation (4) deposition of ECM (by fibroblasts)

38
Q

What is the purpose of granulation tissue?

A

Generates scar tissue through organisation

39
Q

Granulation tissue - what is the function of macrophages, and lymphocytes

A

phagocytose debris, release growth factors lymphocytes - CD8 - kill

40
Q

Granulation tissue - formation of new blood vessels - how does this occur? -

A

(1) degradation of BM by matrix metalloproteinases (MMP) loss of cell-cell contact b/w endothelial cells (2) migration + proliferation of endothelial cells (angiogenic stimulus) (3) maturation of cells, recruitment of pericytes + smooth muscle cells (4) new vessels = leaky - VEGF secreted by various mesenchymal cells is important

41
Q

Which cytokines are involved in stimulating fibroblast migration + proliferation

A

PDGF, TGFb, FGF

42
Q

Healing, describe the progressive changes in healing tissue at 1wk, few weeks, and 6-8weeks

A

~1week - very cellular + vascular histology - tiny spots of haemorrhage - fibro/myofibroblasts, macrophages, lymphocytes, neutrophils, oedema ~few weeks - more fibrous histology - more collagen deposition - more dense ~6-8 weeks - mature scar tissue - poorly cellular (pale)- a few fibroblasts - macrophages/lymphocytes have migrated away - dense connective tissue

43
Q

Which growth factors are involved in organisation/repair? what are they released by what is their function what do they lead to

A

EGF, VEGF, FGF, PDGF, TGFb released by macrophages, mesenchymal cells, endothelial cells, platelets function - are ligands - receptors mostly have tyrosine kinase activity -> activate signal transduction pathways -> activate transcription of transcription factors - these control entry/progression into cell cycle - eg cMYC, cJUN, p53 lead to - proliferation of epithelium, endothelium, fibroblasts

44
Q

what is healing by primary intention?

A

narrow wound, closely apposed edges (suture to acheive this) => small area to heal

45
Q

what is healing by primary intention?

A

larger wound to fill -> longer healing w/ more problems

46
Q

How does wound healing occur?

A

(1) inflammatory phase - acute inflammation Blood vessels contract, clot is formed, then blood vessels dilate to let in cells, antibodies, growth factors etc reach the wounded area. (2) proliferation phase Wound is rebuilt with granulation tissue, with new blood vessels (angiogenesis) Epithelial cells resurface the wound, a process known as ‘epithelialisation’. (3) Maturation - after wound has closed remodelling of collagen from type III to type I. Cellular activity reduces and the number of blood vessels in the wounded area regress and decrease.

47
Q

What cells are involved in chronic inflammation?

A

Macrophages (may be multinucleate - fuse together to fight, form giant cells) Lymphocytes Plasma cells (lots of RER -> purple) Eosinophils also germinal centres

48
Q

Granulomatous inflammation - histology - how does it form

A

can only see this histologically - epithelioid macrophages - giant cells +/- necrosis immune granulomas (cf foreign body granulomas) immune granulomas - cell mediated response (delayed type sensitivity) - macrophages are presenting antigen to CD4s - CD4s release INFg + IL-2 INFg - activate macrophages to become epithelioid IL-2 activate t lymphocytes -> Th1 response

49
Q

What is a foreign body granuloma?

A

Granuloma - well circumscribed collection of altered macrophages (epithelioid macrophages) [epithelioid macrophages = elongated nucleus, assocaited with multinucleate cells] => cells are fusing together to get rid of a foreign object/persistent inflammation (cf immune granuloma - where the macrophages are presenting antigens - and you get a delayed type hypersensitivity; here Mo -> IL-1 -> stimulate epithelioid macrophages formation)

50
Q

In what conditions do you see granulomatous inflammation?

A

Diseases - TB, leprosy, syphilis, fungal, parasitic Unknown cause - sarcoidosis, Crohn’s Deposition of exogeneous/endogeneous irritant materials (suture, urate crystals, keratin) Lymphomas

51
Q

How do viral infection inflammatory reactions deviate from typical patterns?

A

don’t see neutrophils do see lymphocytes (CD8) usually no erythema/swelling

52
Q

how does the inflammatory reaction in ‘acute’ rheumatic fever differ from typical pattern of inflammation

A

don’t see neutrophils do see lymphocytes, macrophages usually no erythema/swelling

53
Q

how does the inflammatory reaction in hypersinsitivity type 1 + parasitic infection differ from a typical pattern of inflammation

A

many eosinophils + mast cells

54
Q

Describe the role of TNF/IL-1 in inflammation

A

(1) Microbial products/cytokines/toxins activate macrophages (2) Macrophages release IL-1, TNF (3) These have local effects: a. changes in vascular endothelium: - ↑leukocyte adhesion molecule expression - produce IL-1, chemokines - ↑procoagulant activity, ↓anticoagulant activity b. leukocyte changes - activation - production of cytokines c. fibroblast chagnes - proliferation - ↑collagen synthesis (4) and systemic effects - fever -leukocytosis - ↑acute phase proteins - ↓apetite - ↑sleep => end up with - inflammation - repair - systemic manifestations of inflammation

55
Q

What are the systemic effects of IL-1, TNF, IL-6 in acute and chronic inflammation

A
  • fever, rigors, chills - malaise, anorexia - leukocytosis - ↑acute phase proteins - weight loss
56
Q

how do IL-1, TNF, IL-6 cause leukocytosis in inflammation?

A

stimulate bone marrow to ↑production in acute - get neutrophilia

57
Q

what are acute phase proteins?

A

CRP, fibrinogen, serum amyloid A (SAA) protein, complement factors, hepcidin => produced by hepatocytes main actions - opsonins, antimicropbial

58
Q

What is the ESR test? What about CRP?

A

Erythrocyte sedimentation rate - how quickly RBC sediment process: - fibrinogen + Ig’s bind to RBC -> form roleaux -> sediment more rapidly if ↑Ig -> ↑ESR => marker of inflammation ========= CRP - also test for inflammation IL-1, IL-6, TNF - increase release of CRP from liver

59
Q

what are some effects of chronically increased stimulation of acute phase proteins?

A

IL-1, TNF, IL-6 increase acute phase protein production => elevated serum amyloid A (SAA) protein -> secondary amyloidosis in RA, TB etc. => choronically elevated hepcidin -> limits Fe availability => anaemia

60
Q

leukocyte migration from blood vessels

  • which blood vessels
  • mechanism
A

occurs in post-capillary venules

vasocongestion -> more cells come into contact with endothelium, also leukocytes are attracted by chemokines

endothelium has upregulated receptors (due to ↑TNFa, IL-1)

  • cells are rolling along, stick to this epithelium
  • E-selectin first
  • then ICAM for tight binding
  • gaps are forming, PECAM-1 is found near the gaps - cells bind this and move through

the movement is driven further by chemotaxis

61
Q

Acute vs chronic inflammation

  • timing + onset
  • duration
  • features
  • what arm of immune system
  • aims
A

Acute

Chronic

Timing and onset

Earliest response, rapid onset

Later response

Duration

Mins- days

Weeks, months, years

Features

  • neutrophils
  • fluid + protein exudate
  • vasodilation
  • macrophages
  • macrophages
  • lymphocytes
  • plasma cells
  • associated fibrosis/scarring

What arm of immune system

Is non-specific => innate

Development of actual immune response

Aims

  • Mediate local defenses
  • destroy infective agents
  • remove debris

Pathology (3 decks)

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