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MCD Cell Pathology > 4 Inflammation > Flashcards

4 Inflammation Flashcards

1
Q

*Q: What is inflammation a reaction to? Development?

A

A: Reactions of living vascularised tissue to sub-lethal cellular injury

Evolutionary development to protect against infection and trauma

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2
Q

*Q: Describe acute inflammation. Length? Involves release of? Typical of which 2 responses?

A

A: = Transient and early response to injury

Hours/few days

Involves release of chemical mediators

Typical vascular and leucocyte response

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3
Q

*Q: Describe chronic inflammation. Length? Usually due to? What does it not contain? Compared to acute, what is not as prominent?

A

A: Inflammation of prolonged duration in which active inflammation, tissue destruction and attempts at repair occur simultaneously

Weeks/months/years

=Usually due to persistent injury causing agent

no exudate

Necrosis is not as prominent as in acute inflammation

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4
Q

*Q: What is a Granuloma. What does granulation tissue contain?

A

A: = collection of immune cells known as histiocytes (macrophages) that form when the immune system attempts to wall off substances it perceives as foreign but is unable to eliminate

lots of fibroblasts producing granulomatous tissue

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5
Q

Q: What are the 4 components of inflammatory responses and healing?

A

A: -cells

  • extra cellular matrix
  • soluble factors
  • vessels
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6
Q

Q: Which cells are involved in inflammatory responses and healing? (5)

A

A: -neutrophils

  • macrophages
  • lymphocytes
  • eosinophils
  • mast cells
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7
Q

Q: What forms of extra cellular matrix are involved in inflammatory responses and healing? (3)

A

A: -collagen

  • proteoglycans
  • fibroblasts
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8
Q

Q: Which soluble factors are involved in inflammatory responses and healing? (4)

A

A: -antibodies

  • cytokines
  • complement system
  • coagulation system
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9
Q

Q: What are the 5 cardinal signs of a inflammation/vascular event? Include what causes them.

A

A: CALOR: Caused by histamine mediated vasodilation

TUMOR (Oedema - increased fluid in interstitial fluid): Caused by histamine mediated increase in permeability of vessels

dolor=pain

RUBOR: Blood flow isn’t as fast so you get redness

Loss of Function: Due to swelling and pain

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10
Q

Q: What is histamine? Produced by? Packaged into?

A

A: Vasoactive amine

Produced by mast cells

Packaged into granules inside mast cells - when antigen binds to IgE on the surface of mast cells - causes cross-linking and degranulation

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11
Q

Q: What can histamines lead to? Dysregulation leads to?

A

A: Vasodilation and Increased Vascular Permeability

allergy (Type 1 Hypersensitivity)

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12
Q

Q: What is a ‘complement’? released when? Stimulate? (3)

A

A: circulating proteins that are synthesises in the liver and released during acute inflammation

  • mast cell degranulation
  • neutrophil chemotaxis
  • opsonisation
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13
Q

Q: What are cytokines

A

A: broad range of chemicals that modulate function of other cells

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14
Q

Q: Name drugs/chemicals that target these Inflammatory Mediators:

  • Histamine
  • Prostaglandins
  • IL-1 and TNF
A

A: = Anti-histamines
= Aspirin
= Anti-TNF antibodies

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15
Q

Q: What is hydrostatic pressure?

A

A: the pressure exerted by a fluid at equilibrium at a given point within the fluid, due to the force of gravity

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16
Q

Q: What is colloid osmotic pressure?

A

A: form of osmotic pressure exerted by proteins in a blood vessel’s plasma that usually tends to pull water into the circulatory system

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17
Q

Q: What’s the relationship between hydrostatic and colloid osmotic pressure?

A

A: oppose eachother

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18
Q

Q: What is exudate? Specific gravity? Cause?

A

A: fluid with a high content of protein and cellular debris which has escaped from blood vessels and has been deposited in tissues or on tissue surfaces WITH high specific gravity

usually as a result of inflammation

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19
Q

Q: What is transudate? Specific gravity? Cause?

A

A: fluid that remains in the vessels which has low protein and few cells with low specific gravity

usually result of disturbances in hydrostatic and colloid osmotic pressure, NOT CAUSED BY INFLAMMATION

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20
Q

Q: What is specific gravity?

A

A: ratio of the density of a substance to the density of a reference substance

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21
Q

Q: What does exudate consist of? (4) Describe 2 in terms of pathogen.

A

A: fluid, cells, proteins including fibrin, antibodies

Fluid - dilutes pathogen and allows soluble mediators to spread

Fibrin - walls off pathogen to stop it spreading. Gives inflammatory cells substrate to hold on to/migrate through

22
Q

Q: What are the 3 types of exudate? Give an example for each.
Which has lowest protein content?
Which is more due to traumatic injury?
Describe the content of one. (4)

A

A: Serous = fluid filled

  • EXAMPLE: Blister
  • Lower protein content of all the exudates

Fibrinous = High fibrin content

  • More due to traumatic injury
  • EXAMPLE: Viral Pericarditis

Purulent = pus filled

  • Combination of fibrin, inflammatory cells, debris and fluid
  • EXAMPLE: peritonitis following bowel perforation
23
Q

Q: Describe the pathway of neutrophil action in acute inflammation. (5)

A

A: 1. Enter tissue

  1. Migrate to site of cell injury - chemotaxis
  2. Become activated
  3. Carry out their designated role - e.g. phagocytosis
  4. Interact with other cell types - release of soluble mediators
24
Q

Q: Why are neutrophils described as key players in inflammation? Main role? (3)

A

A: FIRST CELLS to the damaged area

  • Kill bacteria and recruit more cells
  • Phagocytosis
  • Degranulation
25
Q

Q: What is involved in cellular egress? (4)

A

A: -margination

  • rolling and adhesion
  • transmigration (diapedesis)
  • chemotaxis
26
Q

Q: What is margination in cellular egress?

A

A: cells being pushed to the edges of vessels

27
Q

Q: Describe rolling and adhesion in cellular egress. (3)

A

A: Once at the margin they can bind to endothelial cells through selectins on the neutrophil and endothelial cells

The selectin bonds are loose - the neutrophil rolls along the side of the blood vessel and is slowed down

As it slows down more permanent bonds are formed which fixes the neutrophil to the vessel wall

28
Q

Q: Describe transmigration in cellular egress. (2)

A

A: Neutrophil dissolves basement

Enters interstitium

29
Q

Q: What is ‘killing’ in phagocytosis? By? (4)

A

A: Destruction of phagocytosed material in vacuole

By free radicals, lysozyme, lactoferrin (binds iron and stops bacteria reproducing), major basic protein (produced by eosinophils - cytotoxic to helminth parasites)

30
Q

Q: What’s the importance of eosinophils? (2)

A

A: Important in allergic and parasitic causes of inflammation

31
Q

Q: What’s the importance of mast cells?

A

A: Important in allergic diseases

32
Q

Q: What are the 4 ways inflammatory responses are controlled?

A

A: -Mediators and neutrophils have short half life

  • Stimulus (e.g. bacteria) removed
  • Mast cells and lymphocytes release anti-inflammatory products (lipoxins)
  • Macrophages release anti-inflammatory products
33
Q

Q: How does an acute inflammatory response evolve into a chronic one? (3)

A

A: -Breakdown of myofibres

  • Fewer neutrophils in chronic inflammation
  • Other cell types involved
34
Q

Q: What is the cause of chronic inflammation? 4 examples. Which 3 cells are involved? Abundance?

A

A: Persistent Damage

  • Persistent infection
  • Prolonged exposure to toxic agent
  • Autoimmunity
  • Foreign body (e.g. splinter)

-Macrophages
-Lymphocytes
-Plasma Cells
(high)

35
Q

Q: Do monocytes/ macrophages live for less or more time than neutrophils? What’s the role of M? (2) When are they more abundant? (2)

A

A: -M live longer

  • phagocytosis
  • Control many other inflammatory cells - by releasing cytokines

Increased in viral and atypical bacterial infections

36
Q

Q: What is granulomatous inflammation? What does it involve? 4 causes?

A

A: FORM OF CHRONIC INFLAMMATION - shows granuloma formation

-Involves specific immune reaction T cells

  • Infection
  • Foreign Material
  • Reaction to Tumours
  • Immune Diseases (e.g. Crohn’s, sarcoid)
37
Q

Q: Describe the histological features of granulomatous inflammation. (2)

A

A: -Macrophages in the middle and lymphocytes around the outside

-Horseshoe shaped nuclei - fused macrophages - seen at latter stages of granulomatous inflammation

38
Q

Q: How do acute and chronic inflammation differ in terms of:

main cell involved?
main soluble factor involved?
prominent feature?
onset?

A

A: neutrophils, M

histamines, cytokines

necrosis, scar tissue

immediate, delayed

39
Q

Q: 2 outcomes of acute inflammation? 2 for chronic?

A

A: -complete resolution
-progression to chronic inflammation

  • scar tissue formation
  • disability
40
Q

Q: What are positive outcomes of inflammation? (3)

A

A: Remove causative agent

Cessation of inflammatory reaction

Healing of tissue damage to preserve integrity and function (resolution)

41
Q

Q: What are the negative effects of inflammation? (2- 2,2) Examples? (2)

A

A: LOCAL:

  • Excess local tissue damage/scarring
  • Secondary effects on nearby tissue - e.g. bronchoconstriction in asthma

SYSTEMIC:

  • Systemic inflammatory reaction
  • Secondary multi-organ failure

EXAMPLE: Septic Shock, Amyloid (in response to inflammatory reaction, the liver produces amyloid proteins which can deposit in various organs)

42
Q

Q: What are the 2 parts to wound healing?

A

A: RESOLUTION = regeneration of normal functional parenchymal cells

REPAIR = connective tissue and SCAR TISSUE formation

43
Q

Q: What occurs during ‘resolution’? What are the 2 conditions for it to occur? Give an example.

A

A: Tissue architecture returns to normal

  • Tissue contains cells that are capable of regeneration to replace lost cells
  • Little structural damage done as cells need a framework to build on (basement membrane)

Pneumococcal pneumonia

44
Q

Q: When does the ‘repair’ part of wound healing occur? What occurs? Process? (3)

A

A: Tissue loss is too great and cells are unable to regenerate

Replace normal tissue with fibrous scar tissue

Process:

  • Fibroblasts - produce collagen
  • Collagen - strong scar type collagen
  • Remodelling - reorganisation of collagen fibres for maximal tensile strength
45
Q

Q: Describe what hinders repair? (7) Include 2 subheadings.

A

A: General

  • Poor nutrition (protein needed for collagen production)
  • Vitamin Deficiency (C needed by fibroblasts to make collagen, A needed for epithelial regeneration)
  • Mineral Deficiency
  • Suppressed Inflammation

Local

  • Poor blood supply
  • Persistent foreign body (e.g. splinter)
  • Movement (e.g. broken bones need casts to hold the bones in place)
46
Q

*Q: What are the 3 complications of repair?

A

A: -keloid formation

  • contractures
  • impaired organ function
47
Q

Q: How do you get keloid formation? Where?

A

A: Excess collagen deposition

You can get scar tissue formation other than at the site of original injury

48
Q

Q: Describe contractures as a complication of repair. What happens if it occurs across a joint?

A

A: Fibrous scar tissue contracts as part of its maturing process

If this happens across a joint, you can get reduced joint mobility

49
Q

Q: How can complications of repair cause impaired organ function?

A

A: Fibrous scars forming in organs will cause loss of functional tissue which affects organ function

50
Q

Q: Where are neutrophils produced? Where do they abide?

A

Q: bone marrow

circulate in blood and migrate into damaged tissue

51
Q

Q: What is neutrophil degranulation?

A

A: release contents of cytoplasmic granules including enzymes, free radicals and soluble mediators

52
Q

Q: Where do monocytes/macrophages originate? Difference?

A

Q: bone marrow

circulate in small numbers as monocytes in blood

once in tissue they’re called macrophages

MCD Cell Pathology (6 decks)

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