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MCD - Cell pathology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Define inflammation

A

Reactions of living vascularised tissue to sub-lethal injury

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2
Q

What are the three types of inflammation and what are the main cell involved?

A

Acute; transient and early responses to injury, involves release of chemical mediators
-Neutrophil

Chronic: inflammation of prolonged duration, usually due to persistent injury causing agent.

  • Macrophages
  • lymphocytes
  • neutrophil exudate

Granulomatous (type of chronic inflammation):FORM of chronic inflammation: shows granuloma formation. Clusters of macrophages. Involves specific immune reaction T cells.
-Lymphocytes and Macrophages

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3
Q

What are the clinical features of acute inflammation?

A

LOCAL

  • Rubor *redness
  • calor * heat
  • tumor *swelling
  • dolor *pain
  • Functio Leasa- loss of function

SYSTEMIC:
Fever
Shock

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4
Q

What causes:

  • Calor
  • Tumor
  • Rubor
  • Loss of function
A

Calor: caused by histamine mediated vasodilation
Tumor: oedema, increased fluid in interstitial fluid
caused by histamine mediated increase in permeability of vessels
Rubor: blood flow isn’t as fast so you get redness
Loss of Function: due to swelling and pain

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5
Q

What triggers histamine release and what is it and what effect do histamines have?

A
  • Vasoactive amine
    -produced by mast cells
    -packaged into granules inside mast cells- when antigen binds to IgE on the surface of mast cells to the Fc receptor on mast cells - causes cross-linking and degranulation
    Histamines cause: vasodilation + increased vascular permeability
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6
Q

What is an exudate?

A

Fluid with high protein content and cellular debris, which leaves blood vessels and deposits in tissues or on tissue surfaces, usually as a result of inflammation

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7
Q

What is a transudate?

A

Fluid escape from vessels due to disturbances in hydrostatic and colloid osmotic pressure – NOT CAUSED BY INFLAMMATION:

  • Low protein
  • Cell poor
  • Low specific Gravity
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8
Q

What are the functions of exudate?

A
  • 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
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9
Q

What are the 4 types of exudates and how do they differ?

A

Serous – fluid filled – lowest protein content of the three exudates
Fibrinous – high fibrin content – more due to traumatic injury
Purulent – pus filled –combination of fibrin, inflammatory cells, debris and fluid.
Haemorrhagic

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10
Q

What is the main histological feature of acute inflammation?

A
  • Lots of neutrophils, these kill bacteria and recruit more cells, and degranulation.
  • there will also be eosinophils and mast cells
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11
Q

What are the steps in the leukocyte exiting the vessel lumen ( extravasation)

A
  • Margination ( cells being pushed to the edges of the vessels)
  • Rolling
  • Adhesion : bind to endothelial cells through selectins on neutrophils, selectin bonds loose, causing neutrophil to roll and slow down which fixes it to the vessel wall as more permanent bonds are formed.
  • Transmigration (diapedesis) across endothelium through vessel wall: neutrophil dissolves basement and enters interstitium
  • migration through tissues: chemotaxis, flow to site of inflammation.
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12
Q

What are eosinophils and mast cells important for

A

Important in allergic diseases ( both mast and eosinophils)

-and parasitic causes of inflammation (eosinophil ONLY)

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13
Q

Define chronic inflammation and what is it caused by?

A

inflammation of prolonged duration in which active inflammation, tissue destruction and attempts at repair occur simultaneously
caused by:
-persistent damage e.g. persistent infection, prolonged exposure to toxic agent..

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14
Q

What are the three main cell types involved in chronic inflammation and these will also be abundant for histological features?

A

Macrophages
Lymphocytes
Plasma Cells

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15
Q

What is an important difference between acute and chronic inflammation?

A

Acute inflammation produces an exudate whereas chronic inflammation doesn’t, necrosis is also not very prominent as it is in acute, and granulation tissue is formed while trying to repair in chronic.

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16
Q

What are the histological features of granulomatous inflammation and what is caused by ?

A
  • macrophages in the middle and lymphocytes around the circle
  • horseshoe nuclei-fused macrophages-seen at latter stages of this inflammation

Caused by:
infection, foreign material, reaction to tumours, immune disease e.g. crohns

17
Q

State differences in acute and chronic inflammation

cells involved
what it releases
what happens mainly
when it happens
outcome
A

Acute:

  • neutrohils
  • histamine
  • prominent necrosis
  • immediate onset
  • Outcomes: complete resolution, progress to chronic
CHronic:
-monocytes/macrophage
-cytokines
-prominent scar tissue
-delayed onset
-scar tissue formation
disability
18
Q

What is the good outcome of inflammation and in what circumstance can this occur?

A

Resolution – healing of tissue damage to preserve integrity and function.
Can occur if:
-tissue contains cells that are capable of regeneration to replace lost cells.
-little structural damage done: basement membrane there

19
Q

What is ‘Repair’ in terms of wound healing?

A

connective tissue and scar tissue formation
-replace normal tissue with fibrous scar tissue made by collagen: fibroblasts- produce collagen, collagen- strong scar type collagen, remodelling- reorgansiation of collagen fibres for maximum tensile strength

20
Q

Give an example of resolution and how it takes place.

A

Pneumococcul lobar pneumonia
Inititally you get exudation Then you get red hepatisation (erythrocytes move into the alveolar cells) Erythrocytes break down to give Grey hepatisation – Provided the basement membrane is still there – the body can remove the problem

21
Q

What are three main complications of repair? Describe each of them

A

Keloids formation – excess collagen deposition . You can get scar tissue formation other at the site of original injury.
Contractures – fibrous scar tissue contracts after a while, if the scar tissue is over a joint it can affect joint mobility
Impaired organ function- fibrous scars forming in organs will cause loss of functional tissue. This affects organ function.

22
Q

How are these inflammatory mediators treated?
Histamine
Prostaglandins
IL-1 and TNF

A

Histamine = Anti-histamines
Prostaglandins= Aspirin
IL-1 and TNF= Anti-TNF antibodies

23
Q

Define Hydrostatic pressure

A

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

24
Q

Define 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.

25
Q

What are the cellular events in acute inflammation?

A

NEUTROPHIL action:
1. Enter tissue
2. Migrate to site of cell injury - chemotaxis
3. Become activated
4. carry out their designated roles e.g. phagocytosis
5. Interact with other cell types- release of soluble mediators that aid inflammatory process
Neutrophils contain cytoplasmic granules

26
Q

What are the ways in which phagocytosis works?

A

Opsonisation:

  • Opsonins attach to bacteria
  • enhances neutrophil recognition and attachment
  • makes the bacteria more recognisable and more readily phagocytosed

Ingestion:
-Pathogen is phagocytosed

Killing:

  • Destruction of phagocytosed material in vacuole
  • By free radicals, lysozyme, lactoferrin (binds iron and stops bacteria reproducing).
27
Q

How are inflammatory reactions controlled?

A
  • mediators and neutrophils have shorter half life
  • stimulus removed
  • mast cells and lymphocytes release anti-inflammatory products
  • macrophages release anti-inflammatory products
28
Q

How does it turn from acute to chronic inflammation

A
  • breakdown of myofibres
  • fewer neutrophils in chronic inflammation
  • other cell types involved
29
Q

define resolution

A

regeneration of normal functional parenchymal cells

30
Q

what are Harmful effects of Chronic inflammation

A

Amyloidosis
In response to chronic inflammation anywhere in body, liver produces and releases increased amounts of serum amyloid A protein into the blood.

In some cases this is deposited in tissue as dense protein (amyloid).

31
Q

what hinders repair>

A

Protein needed for collagen production.

Vitamin deficiency
Vitamin C – needed by fibroblasts to make collagen
Vitamin A- required for epithelial regeneration
Mineral deficiency
e.g. Zinc

MCD - Cell pathology (7 decks)

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