Brainscape's Knowledge GenomeTM

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


See full index

Pathology > Inflammation and Wound Healing > Flashcards

Inflammation and Wound Healing Flashcards

1
Q

Describe and recognise different leukocytes

A

Neutrophils- segmented nucleus
Eosinosphils- reddy coloured, granular
Monocytes- bean shaped or oval nucleus, fluffy looking
Lymphocytes- round nucleus, can hardly see any cytoplasm

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

Describe and differentiate cellular and non-cellular components of acute and chronic inflammation

A

Cellular components- leucocytes, blood vessels, plasma, extracellular matrix
Non cellular components- chemical mediators

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

Explain the differences between and exudate and a transudate

A

Exudate- extravascular fluid that has escaped into interstitial tissue due to increased permeability of blood vessels.
Turbid to opaque appearance.
Trnasudate- clear of lightly coloured fluid. Low protein content, due to haemodynamic imbalances

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

Describe the vascular changes seen in acute inflammation and explain the consequences of these changes

A

Increased vascular flow- vasodilation (opening of capillary bed) increases blood flow to area. Circulation slows, stasis,
onset of cellular evens.
Increased vascular permeability- vasodilation→ vascular leakage
Increased hydrostatic pressure in capillary bed due to increased blood flow- fluid outflow into interstitial tissue

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

Classify the mechanisms of endothelial mediated vascular leakage

A

Chemical mediators eg histamine. Endothelial contraction, gap formation between endothelial cells
Cytokines an dhypoxia. Endothelial retraction, gap formation
Direct injury eg severe burns. Necrosis of endothelial cells, detachment of endothelial cells.

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

Explain the mechanism of leukocyte extravasation

5 steps

A

1) Rolling of leukocytes on endothelium
cytokine induced activation of endothelium → tethering of leukocytes to activated
endothelium and rolling on selectins

2) Activation of leukocytes
Activation of leukocytes by chemokines displayed on endothelium → spreading and firm adhesion of
activated leukocytes to endothelium via integrins.

3) Stable adherence of leukocytes to endothelium

4) Transmigration of leukocytes through the vessel wall [= diapedesis, extravasation]
Transmigration through endothelial lined vessel wall; neutrophil can complete this process in 2 – 9 minutes!

5) Leukocyte migration in interstitial tissues toward a chemotactic stimulus

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

Describe how and why the type of leukocyte in an inflammatory response changes over time

A

Main type of leuocyte varies with time of inflammation and type of injurious stimulus
First 24 hrs. neutrophils dominate
After 24 hrs replaced by macrophages due to short life of neutrophils

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

Describe the movement of leukocytes in extravascular tissues in an acute inflammatory response

A

Leukocytes move by extending pseudopods which pulls remainder of the cell into direction of extension
Step by step migration in response to chemo attractants (chemokines)
a) exogenous
- bacterial products (peptides, lipids)
b) endogenous
- components of complement system (C5a)
- leukotrienes (lipoxygenase pathway products)
- cytokines (chemokines)
bind to specific receptors on leukocytes, mobilisation of Ca, assembly of contractile elements, cell movement.

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

Describe the process and purpose of phagocytosis

Three steps

A
  1. recognition and attachment- phagocytic cell receptors to PAMPS on bacterial cells. Opsonisation of microbes increase
    efficiency of phagocytosis
  2. engulfment- pseudopods flow around particle, enclose microbe within phagosome, fusion with lysosome
  3. = phagolysosome. Degranulation of lysosomal granules
  4. killing or degradation- oxygen dependent mechanisms. Free radical. Activation of NADPH oxidase in phagosomal
    membrane. Oxidation of proteins and lipids lead to destruction on microbe
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Give examples of the source and function of different chemical mediators of inflammation
-> plasma and cell derived

A

a) plasma-derived
- in plasma as precursors, need to be activated
b) cell-derived
- within intracellular granules → secretion
- newly synthesised in response to stimulus

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

Give examples of the source and function of different chemical mediators of inflammation
–>vaso active amines

A

Histamine. Within mastc ells, preformed in granules. Released with degranulation (C3a C5a)
Serotonin. In platelets and mast cells. Released with platelet aggregation
→Dilation of arterioles, constriction of large arteries. Induction of endothelial gaps

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

Give examples of the source and function of different chemical mediators of inflammation
–>plasma proteases

A

→ complement system. Culminates in the lysis of microbes by membrane attack complex
→ kinin system. Triggered by intrinsic clotting pathway. Activation of bradykinin, endothelial gaps form
→ clotting system. Thrombin- leukocyte adhesion. Factor X- endothelial gap formation.

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

Formulate a morphological diagnosis, using descriptors for duration, severity and distribution

A
  • exact nomenclature includes:
    a) degree: mild, moderate, severe
    b) duration: acute, subacute, chronic
    c) distribution: focal, multifocal, disseminated, diffuse
    d) type of inflammation
    e) organ-itis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe and explain different types of exudate seen in acute inflammatory responses

A

Serous- thin fluid from blood serum. Mainly serosal surfaces (catarrhal inflammation)
Fibrinous- serum with larger molecules (fibrin). Clotted exudate. Mucosa and serosal surfaces, lungs, joints. Can easily be
peeled off
suppurative- dominated with neutrophils- pus. Normally induced by bacteria. Necrotic tissue, neutrophils and fibrin
transformed into yellowish mass by neutrophilic enzymes
haemorrhagic- exudate with red blood cells. Severe damage to blood vessels
necrotising- exudation and severe tissue necrosis. Often leads to ulcer, replaces whole depth of epithelial lining.

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

Correctly use nomenclature for describing purulent inflammation in different spaces/tissues

A

serous - thin fluid eg blisters
fibronous- scrambled egg
suppurative- pus
translucent/ opaque on radiographs on spaces which should be transparent. Greyish appearance where it should black

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

Describe the four possible outcomes of acute inflammation and the factors which influence the outcome

A
  1. Complete resolution
  2. Abscess formation
  3. Progression to chronic inflammation ( when acute inflammation cannot be resolved)
  4. Healing by fibrosis ( after substantial tissue injury/tissue does not regenerate)
17
Q

Provide examples of injury that is more likely to result in chronic inflammation

A

Persistent infections
Prolonged irritation
Cellular immune response- autoimmunity

18
Q

Describe the histological features of chronic inflammation

A

A) Active inflammation (mononuclear cells)
Macrophages- THE cells of chronic inflammation.
Persistent accumulation due to continued recruitment, local proliferation. Immobilisation of macrophages.
Lymphocytes- continuous interaction with macrophages
Plasma cells- Ig producing B cells
B) Tissue destruction- mainly induced by inflammatory cells. Leukocyte induced tissue injury.
C) Attempts at healing/repair.
Connective tissue replaces damaged tissue
Proliferation of small blood vessels (angiogenesis)

19
Q

Explain the components and the mechanisms involved in fibrosis

A

Fibrosis- deposition of collagen fibres as an attempt to replace lost tissue.

  1. Angiogenesis
  2. Migration and proliferation of fibroblasts
  3. Extracellular matrix deposition (synthesised by fibroblasts)
  4. Tissue remodelling (replacement of granulation tissue with scar. Alterations in composition of ECM)
20
Q

Describe the different morphological patterns of chronic inflammation
-Chronic proliferative inflammation

A

→ formation of granulation tissue
(new small blood vessels and proliferating fibroblasts)
→chronic recurring inflammation:
chronic proliferative inflammation with acute bouts (recruitment of additional neutrophils)

21
Q

Describe the different morphological patterns of chronic inflammation
-abscess

A

cause: suppurative inflammation buried in tissues, organs or confined spaces
- necrosis of tissue due to:
1) bacterial toxins
2) reduced perfusion
- emigration of neutrophils → phagocytosis of bacteria → necrosis (liquefaction; early phase of abscessation)

22
Q

Describe the different morphological patterns of chronic inflammation
-Ulcers

A

= local defect / excavation on the surface of an organ / tissue due to sloughing of inflammatory necrotic tissue
mainly seen in: oral cavity, stomach, intestines, urogenital tract, skin
chronic stage: wall formation, scarring

23
Q

Describe the different morphological patterns of chronic inflammation
-granulomatous inflammation

A
  • predominant cell type: activated macrophage
  • granuloma: focal area of granulomatous inflammation
    • centre: macrophages, epithelioid cells [necrosis]
    • periphery: lymphocytes, plasma cells
      [+ rim of fibroblasts and connective tissue]
      1) foreign body granuloma
      2) immune granuloma
24
Q

Define a granuloma

A

Focal area of granulomatous inflammation. Macrophages in centre. Multinucleated giant cells .
lymphocytes at periphery. Rim of fibroblasts and connective tissue

25
Q

Define granulation tissue

A

ingrowth of new blood vessels into deposited fibrin during repair.

26
Q

Define granulomatous inflammation

A

macrophage dominated chronic inflammation . occurs when injurious agent cannot
by phagocytosed and degraded easily eg mycobacteria

27
Q

Describe the principles of healing by primary intention

A

Wounds with opposed edges (eg surgery)
Within 24hrs blood clot formed (fibrin). Neutrophils appear. Epidermis thickens at edge
2-7 days epithelial cells grow along basement membrane, replaces full thickness. Neutrophils replaced by macrophages
granulation tissue invades and fills space. Fibroblasts deposit collagen which bridges wound
2-4 weeks. Accumulation of collagen- scar. Inflammation has disappeared
scar remodels, strengthens repair

28
Q

Describe the principles of healing by secondary intention

A

within 2-3 days:. blood clot with necrotic tissue. neutrophils appear. Larger defect in epidermis and dermis
within 1-2 weeks:- granulation tissue fills deficit
epithelialisation begins at margins
within 3-6 weeks: Maturation of granulation tissue, with contraction of wound. epithelialisation progresses
across granulation tissue
months- epithelialisation complete. contraction of wound produces irregular scar. loss of adnexae eg hair follicles and
glands

29
Q

When does healing by secondary intention occur?

A 
o	infarction
o	inflammatory ulceration
o	abscess formation
o	surface wounds with large defects
o	differences to healing by first intention:
	a) more intense inflammatory reaction
	b) formation of larger amount of granulation tissue
	c) wound contraction
30
Q

Explain the consequences of wound healing by secondary intention

A 
larger defect (scar).
Loss of function of that tissue.
Loss of associated glands etc

Pathology (1 decks)

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