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Transition block 1 > Pathology - inflammation > Flashcards

Pathology - inflammation Flashcards

1
Q

What are some vascular changes that occur in response to injury?

A
  • Changes in flow and vessel caliber and vasodilation
  • These first involve arterioles and then capillary beds
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2
Q

What chemicals mediate vasodilation and what is the result of vasodilation?

A

Mediated by histamine and nitric oxide and results in increased heat (calor) and redness/erythema (rubor)

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3
Q

What are some cellular changes that occur in response to injury?

A

Stasis, white cell margination, rolling, adhesions, migration

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4
Q

How is white cell margination able to occur after injury?

A

Vasodilatation occurs which slows the rate of blood flow making cells able to move peripherally - especially larger white cells

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5
Q

Name some chemical mediators that are expressed after injury

A
  • Selectins - expressed on endothelial cell surface
  • Integrins - bind to vessel walls, cell matrix and other cells
  • Vascular cell adhesion molecule (VCAM)
  • Intercellular adhesion molecule (ICAM)
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6
Q

What chemicals cause release of inflammatory mediators in cells?

A
  • Histamine and thrombin increase selectin expression
  • TNF and IL-1 increase endothelial expression of VCAM and ICAM
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7
Q

What substance increaes the affinity of VCAMs and ICAMs for integrins?

A
  • Chemokines from the site of injury bind to proteoglycans on endothelial cell surface.
  • These proteoglycans then increase the affinity of VCAMs and ICAMs for integrins
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8
Q

What happens as a result of vascular permeability in response to injury?

A
  • Leaky blood vessels - loss of proteins
  • Change in osmotic pressure - water follows protein - swelling
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9
Q

What happens in chemotaxis?

A

Cells follow a chemical gradient and move along it

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10
Q

What are the 3 phases of phagocytosis?

A
  1. Recognition and attachment
  2. Engulfment
  3. Killing and degradation
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11
Q

What is involved in the recognition and attachment stage of phagocytosis?

A
  • Mannose receptors
    • Bacterial surface glycoproteins and glycolipids contain terminal mannose residues.
    • Mammalian glycoproteins and glycolipids do not
  • Scavenger receptors - similar to mechanism that phagocytes recognise low density lipoprotein
  • Opsonins - bacteria etc are coated with proteins making them stand out, include components of the complement cascade as well as Ig
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12
Q

What is involved in the engulfment stage of phagocytosis?

A
  • Pseudopods
  • Vesicle formation - phagosome
  • Joins with lysosome - phagolysosome
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13
Q

What is involved in the killing and degradation stage of phagocytosis?

A
  • Reactive oxygen species
    • NADPH oxidase - oxygen gains an electron from NADPH and becomes superoxide
  • Reactive nitrogen species
    • Nitric oxide synthase - combines NO with superoxide and produces ONOO
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14
Q

What are the clinical features of inflammation according to Celsus?

A

Rubor (erythema), calor (heat), tumor (swelling), dolor (pain) and loss of function

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15
Q

What mediates the pain/dolor part of the inflammatory response?

A

Prostaglandins and bradykinin

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16
Q

What is the main cell of acute inflammation?

A

Neutrophil

17
Q

What is the resolution stage of inflammation?

A

Complete restoration of the tissue to normal after removal of inflammatory components

18
Q

What is needed for effective resolution?

A
  • Minimal cell death
  • Tissue has capacity to repair (e.g. GI tract frequently replaces epithelium)
  • Good vascular supply
  • Injurious agent easily removed
19
Q

What is suppuration?

A
  • Pus - contains living, dying and dead cells, neutrophils, bacteria and inflammatory debris (fibrin)
  • May be termed an abscess
20
Q

When a space is filled by pus and walled off what is it called?

A

An empyema

21
Q

When does organisation occur as part of the inflammatory process?

A

Mucosa where damage goes beyond the basement membrane favours healing by organisation and repair, not resolution

22
Q

When can resolution occur as part of the inflammatory healing process?

A
  • Erosions and abrasions describe injury with basement membrane intact.
  • These heal rapidly with complete resolution
23
Q

How is granulation tissue formed?

A
  • Defect is slowly infiltrated by capillaries and then by myofibroblasts
  • Deposit collagen and smooth muscle cells
  • Given constituents it looks very red
24
Q

What happens when there is too much scarring and fibrosis of the liver?

A
  • Cirrhosis occurs - results in liver failure
  • The liver has some regenerative capacity but can be overwhelmed
25
Q

What happens as a result of liver cirrhosis?

A
  • Liver failure - loss of liver function, can’t remove toxins and can’t make any proteins
  • Plus, large volume of blood flows throughout the liver so can result in vascular disturbances
26
Q

What factors favour chronic inflammation?

A
  • Suppuration
  • Persistence of injury
  • Infectious agent e.g. virus
  • Type of injury - autoimmune, transplant rejection
27
Q

What is a granuloma?

A

Aggregate of epitheloid histiocytes

28
Q

What can cause granuloma formation?

A
  • Foreign bodies:
    • Endogenous - keratin, bone, crystals
    • Exogenous - talc, asbestos, suture material, oil
  • Specific infection, parasites, syphilis
  • Mycobacterium - TB
29
Q

What is the characteristic feature of a granuloma caused by TB?

A

Caseous necrosis - cheesy necrosis

30
Q

How does hypoxia cause cell injury and then acute inflammation?

A
  • No oxygen = No ATP
  • No ATP:
    • Na/K ATPase fails -> increased K + swelling
    • Ca pump fails -> increased intracellular Ca
    • increased Ca stimulates; ATPase, phospholipase (membrane damage), proteases (membrane and cytoskeleton damage), endonuclease (DNA damage and breakdown) and mitochondrial permeability (release pro death factors)
31
Q

What are the first signs in cells after an MI?

A
  • Cells shrink, become red, nucleus shrinks and becomes dark
  • Marginal contraction bands appear
32
Q

What happens in the first 24 hours following an MI?

A

Cell contents leaked, complement cascade initiated and acute inflammation

33
Q

At what point is the heart most susceptible to cardiac rupture post-MI?

A
  • 3-7 days post-MI
  • Necrosis and neutrophils may be all that is holding it together if the full thickness is affected
34
Q

What happens after the acute inflammation response to an MI (48 hours)?

A
  • Resolution, restitution and chronic inflammation
  • As time progresses, neutrophils fade and are replaced by macrophages
  • At this point definite changes can be seen at autopsy - presence of macrophages causes a yellow appearance
35
Q

Would resolution ever occur after an MI?

A
  • Only if it was short lived and if the injury was mild and blood supply was good
  • MI - blood supply is by definition poor, generally once cell death has occurred resolution is unlikely
36
Q

Describe the process of restitution after an MI

A

Progressive scarring - macrophages fade and are replaces by fibroblasts

37
Q

How long after an MI do fibroblasts start to work?

A

Occurs progressively after 2 weeks and is complete at 6 weeks, so if an MI occurred more than 6 weeks ago it is impossible to date it i.e. could be 7 weeks or 7 years

38
Q

What is the issue with scarring of the heart post-MI?

A
  • Scar tissue has replaced an area of muscle so the muscle can’t function as well which results in a weaker heart -> heart failure
  • Scar tissue can also damage the nerves innervating the heart causing ineffective pace making

Transition block 1 (11 decks)

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