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MCD Cell Pathology > inflammation > Flashcards

inflammation Flashcards

inflammation: explain and compare the pathology and histological features of acute, chronic and granulomatous inflammation; list the sequelae of inflammation

1
Q

purpose of inflammation

A

protective response removing cause and consequences of injury, setting stage for potential healing

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2
Q

how is inflammation triggered

A

various cell types and soluble mediators

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3
Q

how is inflammation regulated

A

leukocyte and vascular responses

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4
Q

what must the tissue be in order for inflammation to occur

A

vascularised

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5
Q

define acute inflammation

A

rapid non-specific leukocyte and vascular response to cellular injury, orchestrated by mediators from injured cells

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6
Q

cardinal signs of acute inflammation

A

rubor (redness), calor (heat), tumour (swelling), dolor (pain), loss of function

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7
Q

process of acute inflammation

A

alteration in calibre of blood vessels increase flow → structural changes to microvasculature, allowing proteins and leukocytes through → emigration, accumulation and activation of leukocytes at focus of injury

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8
Q

vasodilation in acute inflammation: what introduces it and what follows it

A

vasodilation (early manifestation causing heat and redness) introduced by mediators including histamine (richest source in mast cells) and nitric oxide, followed by increased permeability (diameter increases and flow decreases, causing stasis)

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9
Q

acute inflammation: mechanism of increasing vascular permeability

A

histamine causes endothelial cells to contract, increasing interendothelial spacing

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10
Q

define exudate

A

mass of cells and fluid that has seeped out of blood vessels

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11
Q

contents of exudate

A

high protein content, purulent (pus formed by suppuration), serous (serum), fibrinous (fibrin), high specific gravity, cells and cell debris (including leukocytes)

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12
Q

functions of exudate

A

dilutes and “walls off” pathogens, permits spread of soluble inflammatory mediators, provides substrate for inflammatory cell migration

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13
Q

consequence of very high intravascular fluid losses

A

haemorrhages

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14
Q

2 reasons for leukocyte response in inflammation

A

recognise and kill bacteria and eliminate foreign and necrotic material by phagocytosis, produce and activate multiple factors and mediators to interact with other cells to amplify inflammatory response

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15
Q

what is the first leukocyte into a damaged area

A

neutrophil

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16
Q

how do neutrophils enter damaged area

A

extravasation

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17
Q

function of neutrophils in inflammation

A

phagocytosis and degranulation

18
Q

examples of receptors activated by leukocytes during inflammation

A

cytokines, chemokines, complement proteins

19
Q

why must the acute inflammatory response terminate

A

prevent overactivation of leukocytes causing long-term harm

20
Q

4 ways or contributors for terminating acute inflammatory response

A

mediators and neutrophils have short half-lives, macrophages release anti-inflammatory products, mast cells and lymphocytes produce anti-inflammatory products (lipoxins), cause of inflammation (e.g. bacteria) removed

21
Q

what non-specific leukocytes are present in acute inflammation

A

neutrophils, eosinophils, mast cells

22
Q

role of macrophages in acute inflammation

A

phagocytosis (destroy pathogen directly or stimulate another pathway, and once cleared, dies), cytokine release, wound repair and fibrosis, anti-inflammatory effects

23
Q

define chronic inflammation

A

prolonged duration of inflammation, where inflammation, tissue injury and attempts at tissue repair coexist

24
Q

when does chronic inflammation occur

A

may follow acute inflammation, or arise as insidious, low-grade smouldering inflammation

25
Q

what causes insidious, low-grade smouldering inflammation

A

persistent infection, prolonged exposure to toxins, autoimmunity or persistent foreign body

26
Q

what cells are present in the mononuclear cell filtrate of chronic inflammation

A

eosinophils, macrophages, T-lymphocytes and plasma B-lymphocytes (antibodies); neutrophils may be present if co-existing with acute inflammation)

27
Q

following tissue destruction, what is damaged tissue replaced with in chronic inflammation

A

connective tissue

28
Q

difference in macrophage presence in chronic inflammation

A

macrophages persist, causing tissue destruction and can trigger inflammatory cascade

29
Q

define angiogenesis and prominence in chronic inflammation

A

formation of new blood vessels; prominent in chronic inflammation

30
Q

define granulomatous inflammation

A

distinctive pattern of chronic inflammation showing granuloma formation

31
Q

what is granuloma formation

A

aggregate of activated macrophages

32
Q

why is there an aggregate of activated macrophages

A

attempts to eliminate resistant pathogen, triggered by strong, specific T-lymphocyte reaction

33
Q

causes of granulomatous inflammation

A

infection, foreign material, tumour reaction, diseases (e.g. Crohn’s, TB)

34
Q

acute vs chronic inflammation: leukocytes

A

neutrophils vs macrophages

35
Q

acute vs chronic inflammation: soluble factors

A

histamine vs cytokines

36
Q

acute vs chronic inflammation: outcome on cells

A

prominent necrosis vs prominent scar tissue

37
Q

acute vs chronic inflammation: onset

A

immediate vs delayed

38
Q

acute vs chronic inflammation: duration

A

a few days vs weeks/months/years

39
Q

acute vs chronic inflammation: outcomes

A

complete restoration and progression to chronic inflammation vs scar tissue formation and disability

40
Q

positive long term consequences of inflammation

A

removal of pathogen, cessation of inflammatory response, healing of tissue damage

41
Q

negative long term consequences of inflammation

A

excessive tissue damage and scarring, systemic involvement with multiorgan failure leading to septic shock

MCD Cell Pathology (12 decks)

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