Brainscape's Knowledge GenomeTM

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


See full index

Tissue Pathology > Connective Tissue > Flashcards

Connective Tissue Flashcards

1
Q

5 types of CT

A

Areolar tissue
Adipose
White fibrous
Yellow elastic
Reticular

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

Homeostasis in wound healing

A

Establishes the fibrin provisional wound matrix and platelets, provide initial release of cytokines and growth factors in the wound

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

Inflammation in wound healing

A

Mediated by neutrophils and macrophages
Removes bacteria and denatured matrix components
Source of growth factors and cytokines
Prolonged elevated inflammation => retards healing due to high levels of proteases and reactive oxygen that destroys essential factors

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

Proliferation in wound healing

A

Fibroblasts supported by new capillaries, proliferate and synthesise disorganised ECM
Basal epithelial cells proliferate and migrate over the granulation tissue to close the wound surface

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

Remodelling in wound healing

A

Fibroblasts and capillary density decreases and initial scar tissue is removed and replaced by ECM that is more similar to normal skin
Result of balanced regulated activity of proteinases

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

Tissue regeneration

A

Remaining cells of an injured organ regrow to offset the missed cells
Cornerstone of tissue engineering leading to NEW growth

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

Embryonic wound healing

A

Early gestation foetus can heal wounds without scar
Foetal dermis -> regenerate non-disrupted collagen matrix -> identical to original tissue

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

Foetal collagen Vs post-natal collagen Vs adult collagen

A

Foetal:
Type III collagen rapidly deposited => fine reticular network => indistinguishable

Post-natal:
Ratio of type I to type III increases => more strength and rigidity => may impeded cellular migration and regeneration

Adult:
Collagen synthesis delayed while fibroblasts proliferate

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

Hyaluronic acid

A

Net negative charge traps and impede water molecules which allows resistance to deformation and facilitates cellular movement

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

Hyaluronic acid in foetal wound healing

A

More Hyaluronic acid => more HA receptors
In scarless foetalwounds => HA increased more rapidly than adult
Less pro inflammatory cytokines such as IL-1 and TNFalpha that downregulate HA expression

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

Adhesion proteins in foetal wounds

A

Enhanced ability to upregulate tenascin and fibronectin which mediate ECM attachment and attract fribroblasts, keratinocytes and endothelial cells to site of injury
=> rapid deposition of an organised matrix => less scarring

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

Inflammatory cells in foetal wound healing

A

Immune system not fully developed
Embryo is undergoing rapid growth and differentiation

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

Role of TGFbeta in wound healing

A

Inflammation
Stimulatory angiogenesis
Fibroblast proliferation
Collagen synthesis and deposition
Remodelling of the new ECM
Foetal platelets produce less PDGF, TGF-B1 and TGF-B2

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

TGF beta in foetal wound healing

A

High levels of TGFbeta3 from keratinocytes and fibroblasts
Low levels of TGFbeta1 and TGFbeta2
High levels of fibroblast growth factor
PDGF not detected

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

IL6 in wound healing

A

Stimulates monocyte chemotaxis and macrophage activation

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

IL8 in wound healing

A

Attracts neutrophils and stimulates neovascularisation

17
Q

Interleukin expression in wound healing Adult Vs Foetal

A

Adult:
Elevation in IL6 and IL8 up to 72 hours

Foetal:
IL6 and IL8 elevation not present after 12 hours
Significantly lower expression
Addition of IL6 to foetal wounds produces a scar in normally scarless wounds

18
Q

How do we detect EMT?

A

Loss of surfactant production
Gain of ECM or metalloproteinase secretion
Differences in N and E Cadherin
Differences in cytoskeletal proteins e.g. loss of cytokeratins,gain of vimentin

19
Q

Type 1 EMT

A

Tissue and organ formation during embryogenesis

20
Q

Type 2 EMT

A

Normal wound healing, tissue regeneration and fibrosis, and plays a role in excessive tissue repair
Associated with inflammation; normally terminated once repair is completed
In organ fibrosis type 2 EMT can continue to respond to ongoing inflammation => organ destruction

21
Q

Type 3 EMT

A

Indicates acquisition of migratory phenotype by malignant epithelial cells associated with tumour invasiveness and metastasis

22
Q

Fibrosis

A

Thickening and scarring of CT usually as result of injury
Excess accumulation of ECM components
Drives end-stage organ failure

23
Q

Idiopathic pulmonary fibrosis

A

Disease of the lung; parenchymal scarring; death
Inability of alveolar epithelium to regenerate after injury

24
Q

Type 1 alveolar cells

A

Provide thin walled gas exchange surface

25
Q

Type 2 alveolar cells

A

Functions as stem cells, contributing to alveolar renewal and repair
-facultative progenitor cells (not always functional)
-favouring of excessive ECM deposition and fibrosis

26
Q

Myofibroblasts in IPF

A

Origin is controversial
ATII cells that have undergone EMT may be source
Critical in pathogenesis of IPF

27
Q

IPF modulated by:

A

Repetitive injury
Inefficiency of ATII cells => abnormal repair and failure of alveolar regeneration
Aberrant pathway activation

28
Q

IPF 7 keys factors at play

A

Aberrant activation of:
[1] Wnt/B-catenin
[2] Sonic hedgehog
[3] TGF-Beta and other developmental pathways

[4] ZEB transcription factors initiated by extracellular ligand binding
=> downregulation of [5] E Cadherin expression in epithelial cells

Profibrotic environment created in which collagen-producing [6]fibroblasts and myofibroblasts accumulate through different mechanisms such as proliferation and differentiation of resident lung fibroblast

[7] cell environment e.g. ROS

29
Q

______ master switch in induction of fibrosis.

A

TGFbeta

30
Q

Inability to respond to ________ affords protection from bleomycin-induced fibrosis

A

TGFbeta1

31
Q

TGFbeta-SMAD dependent canonical pathway

A

TGFbeta binds receptor and promotes SMAD 2/3 phosphorylation
Active SMAD 2/3 forms complex with SMAD4
Complex binds to promoter region of target genes ass. With EMT

HSP90 is suggested to contribute in both canonical and non-canonical TGFbeta signalling pathways in IPF

32
Q

TGFbeta independent non-canonical pathway

A

Transduce through Ras-MAPK and P13K-Akt
Role for ubiquitin-proteasome pathway
- Skp2 and Fbw7 are E3 ubiquitin ligases
- Skp2 promotes p27 degradation
- Fbw7 promotes telomere protection protein 1 degradation
P27 is a kinase inhibitor and acts as a cell cycle inhibitor
TPP1 acts to protect chromosomes

33
Q

Wnt signalling in EMT

A

TGFbeta stim canonical Wnt in a p38 dependent manner by decreasing expression of endogenous Wnt aganosit Dickkopf-1 -> Wnt binds Fed, inducing its phosphorylation -> cytosolic beta-catenin accumulation -> translocated to nucleus -> interacts with transcription factors => EMT

34
Q

SMAD co-activator

A

Beta catenin

35
Q

Other pathways involved in EMT(4)

A

Wnt
Delta-notch
NFkB
Shh

Tissue Pathology (6 decks)

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