Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology Year 2 > 3. Acute and chronic inflammation > Flashcards

3. Acute and chronic inflammation Flashcards

1
Q

Inflammation

A 
The host response to  tissue damage
Protective response
 – to remove/ contain cause, initiate repair and reinstate useful function
Stops when injurious agent is eliminated
Essential for healing.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Triggers of Inflammation

A 
Foreign Body
Infection
Ischaemia/infarction
Physical/chemical injury 
Immune reactions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Acute inflammation

A

Rapid host response - vascular and cellular reaction
Vascular changes to maximise movement of plasma proteins to site of injury:
Vasodilation - increased blood flow to the area of injury, redness and heat (ERYTHEMA). induced by histamine and nitric acid.
Increased permeability follows, - to fluid leaking into the extravascular tissue. This leads to swelling (OEDEMA)
Together this creates blood stasis, pooling the blood at site of inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

VASCULAR PERMEABILITY

A

Endothelial cells of vessel wall contract
Endothelial injury
Transcytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Endothelial cells of vessel wall contract

A

increasing inter-endothelial spaces, triggered by histamine, bradykinin, leukotriens, substance P etc. It is the Immediate transient response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Endothelial injury

A

leading to endothelial cell death, vessel wall is damaged and there is immediate extravascular leakage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Transcytosis

A

leading to increased transport of fluids/proteins through cell channels. Promoted by specific factors triggered by inflammation eg VEGF

Together these mechanisms cause leakage of intravascular fluid into the extravascular spaces.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Cellular reaction

A

Main aim of inflammation is to recruit leucocytes to area of damage. by adhering them to vessel wall
Neutrophils and macrophages ingest and kill bacteria and necrotic cells, as well as promoting repair.
These white blood cells need to be recruited from the vessel lumens.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Margination:

A

Red blood cells flow in centre of vessel lumen and WBCs flow peripherally. In stasis, more wcc fall into peripheral flow.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Rolling:

A

This leads to an increased amount of leucocytes to roll along then edge of the damaged endotehlium. Mediated by selectins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Adhesion:

A

The leucocytes finally stop and adhere to the endothelium. Cytokines secreted by by injured cells encourage the adhesion of the leucocytes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Transmigration:

A

Leucocyte is then encouraged to pass through endothelium to extravascular space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Chemokines

A

stimulate migration and leucocyte move towards the chemical concentration gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

(towards site of injury where the chemokines are being produced)

A

PECAM-1 – platelet endothelial cell adhesion molecule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Chemotaxis:

A

Exogenous (bacteria ) and endogenous (cytokines/complement) substances attract the leucocytes towards the area of injury.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Neutrophils

A

appear at 6-24 hours, monocytes appear at 24-48hours. Neutrophils are more common in circating blood and respond to chemokines.

17
Q

Function of leucocytes

A 
Receptors on the leucocytes recognise foreign microbes
These include:
-Toll 
-G protein 
-Opsonin receptors 
-Cytokine receptors
18
Q

Toll

A

like receptors present on cell surface of leucocytes and attach to bacteria products

19
Q

G protein

A

coupled receptors recognise N-formymethionyl of bacteria as well as chemokine breakdown

20
Q

Opsonin receptors

A

recognoze microbes that have been coated with proteins ( antibodies/complement) or opsonins, thus called opsonization. This targets them for phagocytosis

21
Q

Cytokine receptors

A

are present on leucocytes respond to the cytokines produced in response to microbes.

22
Q

Phagocytosis

A

Through these receptors the leucocyte recognises and attaches itself to bacteria or damaged cell
leucocytes - engulfs the cell/particle
leucocyte - kills and degrades the offending agent, removing its harmful effects.
This continues until all foreign and damaged products are removed, so healthy cells remain and healing and repair can begin.

23
Q

Outcomes

A

Complete resolution
Healing with connective tissue replacement (fibrosis)
Following substantial tissue destruction, some cells cannot regenerate.
Connective tissue replaces area or damage.
Progression to chronic inflammation
- Acute problem is not resolved due to persistent injury or interference with healing.

24
Q

Chronic inflammation

A

Caused by:
Persistent infection: microorganisms difficult to remove e.g. parasite, mycobacteria.
Immune mediated inflammation: reaction against host tissue leading to auto-immune diseases.
Prolonged exposure to toxic agent : silica, asbestos, lipids (atherosclerosis)
Predominantly show infiltration of mononuclear cells: macrophages, lymphocytes and plasma cells.
( Macrophages destroy damaged cells and promote repair)
Tissue destruction following prolonged inflammatroy reaction
Signs of attempts at healing: connective tissue repair, increased growth of small blood vessels and fibrosis

25
Q

Granulomas

A

Cellular attempt to contain offending agent it cannot eradicate

Strong activation of macrophages and T lymphocytes, leading to injury of normal tissues.

e.g Tuberculosis which leads to caseating lesions in the lungs.

26
Q

Clinical signs

A 
Redness (rubor)
Heat	(calor)	
Swelling	(tumor)
Pain (dolor)
Loss of function
27
Q

Signs and Symptoms (1)

A 
Fever
Tachycardia
Hypotension
Raised WCC
Raised CRP
28
Q

Signs and Symptoms (2)

A

Anorexia
General malaise
Weight loss (chronic inflammation)
Sepsis- large amount of toxins stimulate cytokines, can lead to cardiovascular failure (septic shock)

29
Q

Acute Inflammation

A

Rapid response
Short lived
NEUTROPHILS predominate
Aim is complete resolution

30
Q

Outcomes of acute inflammation

A

Complete resolution
Healing by fibrosis (scar formation)
Abscess formation
Chronic inflammation

31
Q

Chronic inflammation

A 
Prolonged (weeks/months)
Can develop from acute inflammation but frequently doesn’t:
persistent infection 
prolonged exposure to toxins
autoimmune reactions
32
Q

Can it be harmful? How?

A

Exaggerated or inappropriate inflammatory response = allergies, hypersensitivity reactions and autoimmune diseases

Poor inflammatory response is the basis for immunodeficiency conditions/diseases; some are acquired and some are hereditary

33
Q

What can we do about it?

A

Medications
Non-steroidal anti-inflammatories (NSAIDs)
Anti-histamines
Steroids
Targeted biologics against immune response proteins e.g anti TNF

34
Q

What happens if there is no inflammatory response?

A

Defective inflammation →
Increased susceptibility to infection
Delayed healing of wounds
Tissue damage

Eg. hereditary immunodeficiency conditions, post-chemotherapy, medications

35
Q

Acute appendicitis

A

Peak age 10-30 years
Central abdominal pain which localises to right iliac fossa; worse on movement; may have nausea/vomiting
Pyrexia, raised HR, raised WCC and CRP
Management – appendicectomy
Complications – perforation leading to peritonitis, abscess formation

36
Q

Septic Arthritis

A

Red hot swollen joint
Unable to move joint as limited by pain
Pyrexia, tachycardia, raised WCC and CRP
Risk factors: prosthetic joint, recent surgery/trauma to knee, age, RA, Immunodeficiency
Treatment – Joint aspirate, IV antibiotics, sepsis 6

37
Q

Minor Injury

A 
Sprained ankle
Muscle cells are damaged 
Leads to swelling pain heat etc
Inflammatory response is of no benefit
REST – prevent further injury
ICE – reverse vasodilation
COMPRESS – reduce oedema
ELEVATE – prevent blood stasis
ANTI- INFLAMMATORY
38
Q

Rheumatoid Arthritis

A

Chronic autoimmune inflammatory condition
Leading to warm swollen, stiff and painful joints.
Vessels also can become involved – Vasculitis, leading to circulatory problems.
Immune systems views host cell as foreign, leading to a chronic inflammatory response.
macrophages, lymphocytes (T cell) and plasma attempt to remove foreign agent. Instead healthy joints are destroyed.
Treatment: Steroids, DMARDs, biologics

39
Q

Peptic Ulcers

A

Acute inflammatory response e.g. h pylori/excess acid
Necrotic inflammed mucosa falls away and is exposes to stomach acid/ h pylori and does not repair, leading to chronic inflammation
At risk of developing bleed/perforation
Treatment – PPIs / histamine receptor agonist/ antibiotics

Pathology Year 2 (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions