Brainscape's Knowledge GenomeTM

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


See full index

Year One: Pesky Things > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

Define inflammation(3)

A

a defensive reaction (innate immune response) of a macro-organism against injury caused by trauma, toxic chemicals, or an invading pathogen.

  • Protective response, but also a potentially harmful process: Components of inflammation that can destroy microbes can also injury bystander normal tissue
  • Rapid response to tissue injury; minutes/hours to develop and of relative short duration (hours or days).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Triggers of acute inflammation…

A
    1. Infections Bacteria, viruses, parasites, fungi, toxins
    1. Tissue damage
    1. Foreign bodies: Splinters, sutures, dirt
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What can damage to tissue be due to

A

o Physical agents: Frost bites, burns, radiation (ionising, UV)
o Chemical agents: Chemical burns, irritants, bites
o Mechanical injury & ischemia: Trauma, tissue crush, reduced blood flow

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

What is the purpose of acute inflammation?(5)

A
  • Alert the body and initiate appropriate immune response
  • Limit spread (of infection and/or injury)
  • Protect injured site from becoming infected
  • Eliminate dead cells/tissue
  • Create the conditions required for healing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Summarise the steps in acute inflammation(5)

A
  • Recognition of injury
  • Recruitment of leucocytes
  • Removal of injurious agent
  • Regulation (closure of inflammatory response)
  • Resolution/Repair of affected tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Signs of acute inflammation…(5)

A
  • Heat (Latin: Calor) Increased blood flow (hyperaemia) to injured area Swelling
  • Increased blood flow and metabolic activity Redness (Rubor)
  • (Tumor) Fluid accumulation due to permeability of vessels
  • Pain (Dolor) Release of pain mediators; pressure on nerve ends
  • Loss of function (Functio laesa) Damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Systematic changes of acute inflammation

A
  1. Fever
  2. Neutrophilia- GM-CSF (cytokine) stimulation of bone marrow to replenish dead neutrophils
  3. • Acute phase reactants.
  4. • Complications. In rare cases causing a sever systemic inflammatory reaction called sepsis or a form of inflammatory response syndrome (SIRS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the molecules that cause fever?

A
  1. Endogenous pyrogens (IL-1, TNF-α)- acts on preoptic areas of hypothalamus to raise the temperature
    - Exogenous pyrogens (microbial components)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Name some acute phase reactants as part of the systemic changes

A
  • C-reactive protein (CRP), fibrinogen, complement, serum amyloid A protein (SAP)
  • Produced in the liver
  • Induced by the cytokines IL-6, IL-1, TNF-alpha
  • Increased Fibrinogen => stacking of RBCs => faster sedimentation rate (Increased ESR (Erythrocyte Sedimentation Rate)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

The components of an acute inflammatory response…

A
  • Vascular: acute changes in local vasculature. Vasodilatation, plasma exudation and oedema
  • Cellular: infiltration of inflammatory cells. Cell recruitment, phagocytosis, NETosis
  • Humoral: release of inflammatory mediators. Complement, plasma factors, clotting cascade, cytokines and chemokines
  • Resolution: Inflammation is controlled and self-limiting. Healing, regeneration and repair of tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Summarise what happens in vascular events

A
  1. Vasodilation

2. Increased vascular permeability

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

What happens during vasodilation in vascular events?(3)

A

– Vasodilation: an increase in vascular diameter
Induce by histamine and serotonin released by injured cells, mast cells and macrophages
• This results in hyperaemia (increase in blood volume to the area) (Redness)
• The increased blood volume heats up the tissues (Heat)

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

What happens during increased vascular permeability?(3)

A
  • Leading to leakage of fluids into the tissues (Swelling)
  • As exudate accumulates, pressure increases. Nerve endings are stimulated by the excess fluid and inflammatory mediators (Pain).
  • Endothelial cell activation increasing their expression of adhesion molecules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why does gaps appear between endothelial?

A

Gaps occur due to contraction of e.g myosin and shortening of individual endothelial cells

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

What does loss of proteins like albumin and fibrinogen from the plasma?

A

the tissue increase the osmotic pressure/gradient, leading to fluid leakage to the area, causing oedema.
• Cell transmigration

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

What is inflammatory exudate due to?

A

due to increased vessel permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What other substances enter tissues or serous tissues?

A

Water, salts, small plasma proteins (fibrinogen) inflammatory cells, red blood cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Why does transudate occur?

A

fluid leaks due to altered osmotic/hydrostatic pressure; vessel permeability normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the mediators of inflammation?

A
  • Macrophages
  • Neutrophils
  • Mast cells
  • Platelets
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

• Humoral factors of inflammation…

A
  • Complement
  • Plasma factors
  • Clotting cascade
  • Cytokines
  • Chemokines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are proinflammatory cytokines?

A

• Activated tissue resident macrophages secrete the inflammatory cytokines

  1. • Mast cells in the tissue secrete Histamine
    • These chemical signals released by activated macrophages and mast cells at the injury site cause endothelial activation, vasodilation and increased vascular permeability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Which factors regulate and repair tissue?

A

the release of immunoregulatory factors (TGF-)

23
Q

Summarise the steps in neutrophil recruitments

A
    1. Margination & rolling mediated by selectins
    1. Integrin activation by chemokines
    1. Firm adhesion to endothelium mediated by integrins and cell adhesion
    1. Transmigration through endothelium into tissue
24
Q

Describe transmigration through endothelium into tissue

A

Neutrophils migrate through interendothelial spaces
Neutrophils pass through vessel wall and enter tissue
Migrate (chemotaxis) through tissue towards inflamed site
Gradient of chemoattractants guides migration in tissues

25
Q

Describe the Chemotaxis (attraction and movement) to inflamed site

A
  1. Movement of cells through tissue towards inflamed sites
  2. Guided by chemoattractants:
  3. Produced at site of infection/damage
  4. Diffuse into adjacent tissue and form a gradient
26
Q

What are the components of chemotaxis?

A

Bacterial components (peptides containing N-formyl-methionine-leucine-phenylalanine; lipids)
- Chemokines (IL-8)
Complement(C5a)
- Leukotriene B4 (LTB4

27
Q

What are selectins?

A
  • Mediate rolling of neutrophils
  • Expressed by activated endothelium
  • Endotelial selectins bind to ligands on neutrophils
28
Q

What is the difference between P-selectin and E-selectin?

A

o P-selectin – pre-formed granules

o E-selectin – induced by IL-1 and TNF- (cytokines produced by macrophages, mast cells, endothelial cells at site of inflammation)

29
Q

Which type of cells express L-selectin

A

L- selectin= ligands on endothelium

30
Q

What do endothelial selectins bind to?

A

ligands on neutrophils

31
Q

What are ligands? Give two examples

A

carbohydrates (PSGL-1, sialyl-Lewisx)

32
Q

Why is interaction between selectins and ligands slow?

A

requiring repetitive contacts- As cells are flowing low affinity interaction IS disrupted by flowing blood => repetitive binding and detaching => rolling; slow down

33
Q

What are integrins?

A

• Integrins bind to ligands on endothelium
2.• Integrin ligands are induced by IL-1 and TNF-a (cytokines produced by macrophages, mast cells, endothelial cells at site of inflammation)
• Results in firm adhesion of neutrophils to endothelium
• Integrins are activated to change to high affinity configuration

34
Q

Name some integrin ligands

A

intercellular adhesion molecule-1; VCAM-1 = vascular cell adhesion molecule-1

35
Q

Summarise the adhesion molecules involved in neutrophil recruitment

A
  1. selectins
  2. integrins
  3. Immunoglubulin superfamily cell adhesion molecules CAMS
36
Q

Mechanisms involved in pathogen destruction…

A
  • Release of granule content
  • Phagocytosis
  • Generation of reactive oxygen/nitrogen species
37
Q

Formation of Neutrophil Extracellular Traps (NETs) (netosis)… (3)

A
  • Mesh of nuclear content (chromatin)
  • Mesh traps microbes
  • Contains anti-microbial molecules
38
Q

Neutrophil granules…

A
  • Specific granules (small)
  • Lysozyme, collagenase, gelatinase, lactoferrin, alkaline phosphatase
  • Azurophil granules (large)
  • Myeloperoxidase, lysozyme, defensins, acid hydrolases, proteases (elastase, cathepsin G, collagenases, proteinase 3)
  • Granule content can cause tissue damage
39
Q

Describe the variation in times of leucocyte infiltration

A
  • Neutrophils (6-24h); short lived; die in tissues (24/48h)

* Monocytes (24-48h); survive longer, proliferate

40
Q

What are the other types of inflammatory responses apart from neutrophils?

A

Eosinophils (allergies, parasite infections)

• Lymphocytes (viral infections)

41
Q

Summarise the outcomes of acute inflammation

A

If the inflammatory trigger is eliminated then inflammation resolves
- Recruited cells die (neutrophils have a short life span in tissue)
- Inflammatory mediators are degraded (most are short-lived)
- Activation of regulatory mechanisms (anti-inflammatory)
- Activation of tissue repair mechanisms
If the inflammatory response does not reach a critical threshold of activation the mechanisms of regulation are not promoted effectively

42
Q

Complete resolution…

A

Damaging agent removed

b. Injured tissue is replaced by cells of the same type
c. There is no change in tissue structure/function

43
Q

How can normal tissue be restored?

A

only restored if the residual tissue is structurally intact

44
Q

What is fibrosis- repair by replacement?

A

a. Injured tissue is replaced with connective tissue
b. Scarring can alter tissue function
c. TGF-β which is released by macrophages promotes fibrosis

45
Q

Describe abscess

A
  • A mass of necrotic (dead) tissue
  • Is caused by pyogenic (pus-forming) bacteria
  • Can become chronic if it’s not reabsorbed/drained
46
Q

Describe the types of regenerative ability

A
  • High regeneration ability (labile tissues; divide continuously)
    o Epithelial cells (e.g. skin, airways, gut, blood cells)
    o Sometimes you can get perfect regeneration with no scarring.
  • Immediate regeneration ability (stable tissues)
    o Normal state: quiescent cells (G0/G1) – when injury leads to cell division
    o May regenerate when injured
    ▪ E.g. liver, kidney, pancreas, endothelial cells, fibroblasts
    o If there is extensive injury then you may get scarring
  • No/little regeneration ability (permanent tissues)
    o Neurons, myocardium, skeletal muscle
    o Heal with fibrosis, scarring, loss of function
47
Q

Factors that favour tissue resolution…

A

Minimal destruction

  • Minimal cell death
  • Good regeneration ability of injured tissue
  • Fast clearance of infection
  • Quick removal of dead tissue (debris)
  • Removal of foreign material (sutures, bone fragments)
  • Immobilisation of wound edges (sutures)
48
Q

Factors that prevent tissue healing…

A
  • Infection
  • Diabetes
  • Poor general health/nutrition (protein/vitamin C deficiency)
  • Old age
  • Drugs; corticosteroids
  • Extensive injury
  • Poor vascular supply
  • Extensive haemorrhage
  • Foreign bodies
  • Pressure/torsion/movement on wound edges - dehiscence
49
Q

Summarise the types of inflammatory exudate

A

serous
purulent
fibrinous
haemorrhagic

50
Q

Serous

A
  • A few cells, no/few microbes
  • Fluid derived from plasma / secreted by mesothelial cells
  • Serous cavities (pleura, peritoneum, pericardium)
  • Skin blisters (burns, viral infections)
51
Q

Purulent

A
  • Pus: many leucocytes (neutrophils), dead cells, microbes
  • Pus-producing bacteria (pyogenic) e.g. Staphylococcie.g. acute appendicitise.g. abscess (localised collection of purulent inflammation)
52
Q

Fibrinous

A
  • fibrin deposition (derived from fibrinogen in plasma)
  • large vascular leaks (fibrinogen exits blood & enters tissue)
  • serous cavities (meninges, pleura, pericardium) can lead to scarring if not cleared (fibroblasts => collagen
53
Q

Haemorrhagic

A
  • red blood cells predominates

* blood vessel rupture, trauma

54
Q

What is PAF?

A

platelet activating factor

Year One: Pesky Things (20 decks)

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