Brainscape's Knowledge GenomeTM

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


See full index

Molecular Bio: Pathology > Inflammation > Flashcards

Inflammation Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

What is the difference between acute inflammation and chronic inlfmammtion?

A

Acute inflammation has a rapid onset, short duration and results in fluid, plasma protein and cellular exudate to site of injury. Results in neutrophilic leukocyte accumulation.

Chronic inflammation has an insidious onset, long duration, attracts lymphocytes and macrophages to site of injury and results in scarring.

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

Define inflammation:

A

A protective response intended to eliminate the cause and consequence (necrotic cells and tissue) of cell injury.

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

List the 5 stages of acute inflammation:

A
  1. Recognition
  2. Recruitment
  3. Removal
  4. Resolution
  5. Regulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How are PRR used to recognise the cause and consequence of injury?

A

They detect the cause or consequence of injury and release chemical mediators that initiate vascular and cellular changes that lead to the recruitment of leukocytes to the site of injury.

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

How do PAMPS recognise the cause and consequence of injury?

A
  • They are toll like receptors: Recognise patterns that are unique to bacteria, viruses and other pathogens.
  • detect eg. Lipopolysaccharides (LPS), Lipoteichoic acid, unique surface glycans, viral RNA.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How do DAMPS recognise the cause and consequence of injury?

A
  • They are Inflammasomes: recognise products of dead cells and some microbial products.
  • detect eg. Uric acid, ATP, decreased K+ concentration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Define vascular change:

A

Rapid response designed to deliver leukocytes and plasma protein to the site of injury.

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

Provide examples of vascular change:

A
  • vasodilation
  • increased vascular permeability
  • stasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the mediators of vascular change?

A

Immediate and short term mediators:

  • histamine, bradykinin, leukotrienes (chemical mediators)
  • endothelial cell contraction

Slow, prolonged mediators:

  • IL-1 and TNF
  • Changes in cytoskeleton
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the features of vascular change?

A
  • increased hydrostatic pressure
  • accumulation of interstitial fluid
  • ultrafiltrate
  • low protein concentration, few cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

List the 5 steps leading to leukocyte recruitment at site of injury:

A
  1. Margination
  2. Rolling
  3. Adhesion
  4. Transmigration
  5. Migration/chemotaxis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is leukocyte adhesion in inflammation mediated by?

A

Integrins, which have a low affinity until activated by chemokines.

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

What is chemotaxis?

A

A chemical gradient produced by exogenous (infection) and endogenous (host factor) sources.

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

What are the cardinal signs of inflammation?

A
  • heat : vasodilation causes increased blood flow to region
  • redness: vasodilation, congestion
  • swelling: vasodilation and vascular permeability leading to extravasation of fluid.
  • pain: compression of tissues and direct effect of inflammatory mediators
  • loss of function: direct effect of injury, or due to pain and swelling.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Define opsonization:

A

a process by which a pathogen is marked for ingestion and destruction by phagocytes.

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

Which cellular functions do leukocyte activation enhance?

A
  • phagocytosis
  • intracellular destruction of phagocytosed microbes and debris
  • release of substances that destroy extracellular microbes and degrade tissue
  • produce cellular mediators to amplify the inflammatory response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What does the phagolysosome do?

A

facilitates killing and degradation of the phagocytosed material (by the production of free radicals and the action of powerful enzymes)

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

What occurs when phagocytosis is initiated?

A

the signalling cascade that leads to cytoskeletal rearrangements and assembly of actin by the phagosome is activated.

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

What is the respiratory burst?

A

A reaction that leads to the production of reactive oxygen species (ROS) through the action of an enzyme called NADPH oxidase/phagocytic oxidase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How do lysozyme kill?

A

Oligosaccharide coat degradation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How do Major basic protein kill?

A

Cytotoxic to parasites

22
Q

How do defensins kill?

A

Create holes in microbe membranes

23
Q

Why is activity of neutral proteases (eg. elastase, collagenase, cathepsins) checked by anti-proteases?

A

in order to limit damage to host tissue

24
Q

What happens in resolution of inflammation?

A

Damage can effectively be replaced or regenerated with same cells or repaired by scar formation, so that the function of the tissue is restored.

25
Q

What are lipoxins?

A

A chemical mediator produced as a product of AA metabolism. It acts as an inflammation inhibitor.

26
Q

How do lipoxins inhibit inflammation?

A

Lipoxins inhibit pro-inflammatory effect of Leukotrienes (which are another product of AA metabolism) by chemotaxis and inhibiting neutrophil adhesion.

27
Q

What are plasma derived mediators?

A

They are inactive precursors circulating in the plasma and activated at the site of inflammation. Once active, they amplify their response through a system of enzymatic cascades that produce molecules with different activities.

28
Q

What stimuli conduct histamine release?

A
  • activation of complement
  • physical injury
  • binding of IgE
  • other chemical mediators such as cytokines
29
Q

What are similarities and differences between Prostaglandins & Leukotrienes?

A

Prostaglandins- produced by action of cyclooxygenase facilitate vasodilation and increased vascular permeability.

Leukotrienes- produced by action of 5-lipoxygenase facilitate chemotaxis and increased vascular permeability.

Both are AA metabolites (eicosanoids) and have short range so must act locally.

30
Q

What does release of histamine do?

A

Each release facilitates the vasodilation and increased vascular permeability that enables the formation of the inflammatory exudate (mass of cells and fluid that has seeped out of blood vessels or an organ) and recruitment of leukocytes to the site of injury.

31
Q

What is released by tissue resident cells in response to inflectional injury?

A

IL-1 and TNF

32
Q

What is released by leukocytes recruited as part of the inflammatory response

A

IL-6

33
Q

What result do release of cytokines (IL-1, IL-6 and TNF) have on the brain, liver and bone marrow?

A

give rise to the clinical and pathological systemic effects of inflammation.

34
Q

What do pyrogens do in the brain?

A

Pyrogens act on the brain and lead to synthesis of prostaglandins that act on the hypothalamus to reset the temperature set point.

35
Q

Elevated levels or action of what acute phase proteins identify non-specific markers of inflammation?

A
  • C-reactive protein (CRP)
  • Serum amyloid A (SAA)
  • Fibrinogen
36
Q

What pathogen does increased neutrophilia count indicate?

A

Bacteria

37
Q

What pathogen does increased lymphocytosis count indicate?

A

Viral infection

38
Q

What pathogen does increased eosinophilia count indicate?

A

hypersensitivities and parasitic infections.

39
Q

When does sepsis occur?

A

In response to severe microbial infection, the presence of bacteria and their products in the blood leads to enormous production of cytokines (TNF and IL-1)

40
Q

In sepsis, what life threatening clinical effects occur?

A
  • Disseminated intravascular coagulation (formation of blood clots in blood vessels)
  • Metabolic disturbances affecting regulation of glucose (insulin resistance and hyperglycaemia)
  • Systemic vasodilation - leading to hypotensive shock
41
Q

When is inflammation considered serous?

A

When it is composed of a watery acellular exudate

42
Q

How does an inflammation become serous?

A
  • vasodilation
  • can also be secreted by mesothelial cells that form the linings of these cavities. This can occur in response to injury caused by irritation (eg. blister by burn or viral infection).
43
Q

How is fibrinous inflammation resolved?

A

Through fibrinolysis (enzymatic breakdown of fibrin and phagocytosis by macrophages). If this does not occur, then repair can lead to the formation of a scar through the deposition of collagen. This process of scarring, described as organization, can restrict/compromise the function of the heart.

44
Q

What is ‘pus’?

A

An exudate that has a significant cellular component -particularly neutrophils.

45
Q

Why is pus yellow?

A

Exudate is yellow because of the heme of MPO (which is produced by neutrophils to kill pathogen).

46
Q

Define ‘abscesses’:

A

Suppurative inflammation that occurs in a confined space.

47
Q

Define Primary chronic inflammation:

A

Injury that involves chronic inflammation without an initial acute inflammatory response, or as a consequence of an unresolved acute inflammation.

48
Q

List 4 associated reasons for chronic inflammation:

*hint: Persian Hypochondriacs Proliferate Rapidly

A
  1. Persistant infections
  2. Hypersensitivity (immune mediated disease)
  3. Prolonged exposure to toxic agents
  4. Result of primary granulomas
49
Q

What do M1 (Classically activated) macrophages do?

A

Involved in microbicidal actions and inflammation

50
Q

What do M2 (Alternatively activated) macrophages do?

A

Have principle role in tissue repair and have anti-inflammatory effects.

51
Q

What is IFN-gamma?

A

A cytokine that is type II class of interferons.

52
Q

Describe the morphology of a granuloma and explain

how it occurs

A
  • Macrophages will develop an epithelial-like appearance (large, pink, flat) = epithelioid cells
  • Macrophages may also fuse to form multi-nucleated giant cells
  • T cells present and there may be recruitment of fibroblasts as part of repair process and deposition of connective tissue forming the scar

Molecular Bio: Pathology (6 decks)

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