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MCD- IC > Cell pathology 4- Inflammation > Flashcards

Cell pathology 4- Inflammation Flashcards

1
Q

What is inflammation

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

Describe acute inflammation (5)

A 
Transient and early response to injury 
Hours/few days 
Involves release of chemical mediators 
Typical vascular and leucocyte response 
NOT the same as infection
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3
Q

Describe chronic inflammation (3)

A

Inflammation of prolonged duration
Weeks/months/years
Usually due to persistent injury causing agent

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4
Q

What five cells are involved in inflammatory response

A

Neutrophils-
Produced in bone marrow, circulate in blood, contain cytoplasmic granules
Involved in phagocytosis
Degranulation

Macrophages
Phagocytosis
Control other inflammatory cells
Release cytokines

Lymphocytes

Eosinophils-
Seen with allergic and parasitic causes of inflammation

Mast cells
Also seen in allergic diseases

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5
Q

What three parts of ECM are involved in inflammatory response

A

Collagen
Proteoglycan
Fibroblasts

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6
Q

What soluable factors are involved in inflammatory response

A

Antibodies
Cytokines
Complement system
Coagulation system

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7
Q

5 cardial signs of inflammation

A

Rubor- Redness
Blood flow isn’t as fast so you get redness

Calor- Heat
Caused by histamine mediated vasodilation

Tumor- Swelling
Oedema - increased fluid in interstitial fluid
Caused by histamine mediated increase in permeability
of vessels

Dolor- Pain

Functio laesa- loss of function
Due to swelling and pain

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8
Q

What is histamine
Where is it produced
What is it packaged into
What does its secretion lead too

A

Vasoactive amine
Produced by mass cells
Packaged into granules inside mast cells - when antigen binds to IgE on the surface of mast cells - causes cross-linking and degranulation
Leads to: Vasodilation and Increased Vascular Permeability
Dysregulation - allergy (Type 1 Hypersensitivity)

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9
Q

3 targeting inflammatory medications

A

Histamine = Anti-histamines

Prostaglandins = Aspirin

IL-1 and TNF = Anti-TNF antibodies

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10
Q

Types of exudates

A

Purlent= pus filled

Serous= Fluid filled

Fibrinous= High fibrin content

Hemorrhagic

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11
Q

Describe the action of Neutrophils in inflammatory response

A

Enter tissue

Migrate to site of cell injury - chemotaxis

Become activated

Carry out their designated role - e.g. phagocytosis

Interact with other cell types - release of soluble mediators

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12
Q

How do cells get to site of injury

A

Margination, Rolling, Adhesion, Transmigration, Chemotaxis, Phagocytosis

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13
Q

Describe the process of margination

A

Cells pushed to edges of vessel

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14
Q

Process of rolling and adhesion

A

Selectins on endothelial cells and leucocytes bind white blood cells to endothelial cells

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15
Q

Process of Transmigration

A

Neutrophil dissolves basement, enter interstitium

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16
Q

Process of chemotaxis

A

Follow chemical gradient followed to site of inflammation

17
Q

What are the soluble factors in exudates (5)

A 
Factors made by local cells
Vasoactive amines
Cytokines
Antibodies
proteins
18
Q

Process of phagocytosis

A

Opsonisation
Opsonins (various protein/chemical mediators) attach to bacteria
Enhances neutrophil recognition and attachment

Ingestion
Phagocytosis (engulfment) and entrapment in vacuoles
Killing

Destruction in vacuole by free radicals, lysozyme, lactoferrin, major basic protein

19
Q

Describe the control of Inflammatory Reaction

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

20
Q

How can the acute inflammation return to normal

A

If resolution or repair occur

21
Q

Histological Features of Acute Inflammation

A

There are lots of Neutrophils

There will also be mast cells and eosinophils

22
Q

Histological Features of Chronic Inflammation

A

Macrophages, lymphocytes and plasma cells will be abundant

23
Q

What hinders repair

A

Not having enough:
Protein
Vit C- fibroblasts
Vit A- required for epithelial regeneration

Poor blood supply
Persistent foreign body
Movement

24
Q

What are the Complications of repair

A

Keloid Formation
Excess collagen deposition
You can get scar tissue formation other than at the site of original injury

Contractures
Fibrous scar tissue contracts as part of its maturing process
If this happens across a joint, you can get reduced joint mobility

Impaired Organ Function
Fibrous scars forming in organs will cause loss of functional tissue
This affects organ function

25
Q

What are the causes of chronic inflammation

A 
Persistent damage
Persistent infection
Prolonged exposure to toxic agent
Autoimmunity 
Foreign body
26
Q

What is Granulomatous inflammation and name 4 causes

A

Particular form of chronic inflammation showing granuloma formation
Cluster of macrophages
Involves specific immune reaction T cells

Causes 
Infection – TB, fungi
Foreign material 
Reaction to tumours
Immune diseases (sarcoid, Crohn’s)
27
Q

What is the ‘good’ outcome of inflammation

A

Removal of causative agent

Cessation of the inflammatory reaction

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

28
Q

What is the ‘bad’ outcome

A

LOCAL
Can cause excess local tissue damage and scarring
Secondary effects on nearby tissue
E.g. Bronchoconstriction in asthma

SYSTEMIC
Can evolve into systemic inflammatory reaction and secondary multi-organ failure
E.g. Septic shock
Amyloid

29
Q

Difference between repair and resolution

A

RESOLUTION = regeneration of normal functional parenchymal cells

REPAIR = connective tissue and SCAR TISSUE formation

30
Q

When can resolution occur?

A

Tissue contains cells able to regenerate to replace lost cells E.g. Liver
Little structural damage done

31
Q

When does repair occur

A

Tissue loss too great, and cells unable to regenerate
Replace normal tissue with fibrous scar tissue

Fibroblasts – produce collagen
Collagen – strong “scar” type collagen
Remodelling – reorientation of collagen fibres for maximal tensile strength

MCD- IC (58 decks)

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