Satia Cellula Injury Flashcards

1
Q

What are the two major forms of cell death?

A

Necorsis and apoptosis

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2
Q

What is coagulative necrosis?

A

Desaturation of intracytoplasmic proteins

dead tissue is firm then soft

typically in ischaemic injury EXCEPT THE BRAIN

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3
Q

WHAT IS COLLQUATIVE NECROSIS?

A

Seen in brain e.g. stroke

glial reaction at periphery with cyst formation

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4
Q

What is caseous necrosis?

A

Characteristic of TB
macro - cheese like
micro - no structure

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5
Q

What is gangrenous necrosis?

A

Necrosis with putrefaction of tissues due to certain bacteria e.g. Clostridia or Streptococci

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6
Q

What makes tissue black in gangrenous necrosis?

A

Iron sulfide from degraded haemoglobin

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7
Q

What causes gas gangrene?

A

C perfringens

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8
Q

What type of necrosis is seen in malignant hypertension?

A

Fibrinoid necrosis

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9
Q

What are some mediators of apoptosis?

A

p53
bcl-2
fas (CD 95)
Caspases

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10
Q

How is bcl-2 related to tumours

A

inhibits apoptosis, therefore expression leads to failure of initiation of apoptosis

overexpressed in neoplasia

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11
Q

What is pyknosis

A

nuclear shrinking

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12
Q

what is karyorrhexis

A

nuclear fragmentation

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13
Q

What disease increase apoptosis?

A

HIV
Neurodegenerative diseases

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14
Q

What are labile cells?

A

Good capacity for regeneration
e.g. surface epithelial cells constantly being replaced by cells from deeper

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15
Q

What are stable cells?

A

divide at a slower rate under physiological conditions
replaced by mitotic division of mature cells and lost cells are rapidly replaced e.g. liver and renal tubular epithelium

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16
Q

What are permanent cells?

A

Never divide in post natal life cannot be replaced if lost

e.g. nerve cells

17
Q

Outline the process of organisation

A

Fibrinous exudate
Removal of fibrin and dead tissue by phagocytes
Migration of fibroblasts and capillaries forming granulation tissue
Replacement of exudate by vascularised fibrous tissue
eventually a collagen rich scar develops

18
Q

Describe the formation of granulation tissue

A

Capilary endothelial cells grow into the area to be repaired
Fibroblasts are stimulated to divide
Fibroblasts secrete collagen and matrix components
Fibroblasts acquire muscle filaments and become myofibroblasts

19
Q

What is proud flesh?

A

excessive granulation tissue protruding above the wound surface

20
Q

Issues with organisation

A

Fibrous adhesions in the peritoneum ma cause intestinal obstruction

obliteration of the pericardial space - constrictive pericarditis

21
Q

Issues with wound contraction

A

Stenosis
Stricture
Scarring in muscle = contracture
Contractures following burns

22
Q

Describe healing by primary intention

A

Edges opposed
Fibrin helps to stick the edges together
Capillaries bridge the gap
Fibroblasts invade fibrin network
After 10 days wound is strong and sutures can be removed
remodelling

23
Q

Describe healing by secondary intention

A

Tissue loss
Phagocytes remove debris
Formulation of granulation tissue at base of wound
Myofibroblasts cause contraction
Re-epithelialisation
Tissue deficit replaced by scar tissue

24
Q

What is keloid?

A

Excessive fibroblast proliferation and collaagen production
Collagen deposits beyond and above wound
covered by normal epithelium

25
Describe Hyperophic scar
Does not extend beyond wound borders
26
Describe bone repair
Haematoma Macrophages invade haematoma with polymorphs and fibroblasts new vessels grow Fibrosis by the end of the week Osteoblasts grow into haematoma and form trabeculae of woven bone The new bone is called callus Internal callus is within the medullary cavity External callus is related to the periosteum Woven bone replaced by lamellar bone Remodelling takes place in the direction of mechanical stress
27
What factors affect bone remodelling?
Movement misalignment interposition of soft tissues infection pre-existing bone disease
28
What is wallerian degeneration
Is the process that occurs when a nerve is cut or crushed. - It occurs when the part of the axon separated from the neuron's cell nucleus degenerates. - It usually begins 24 hours following neuronal injury and the distal axon remains excitable up until this time. - The degeneration of the axon is followed by breakdown of the myelin sheath, a process that occurs by infiltration of the site with macrophages. - Eventually regeneration of the nerve may occur although recovery will depend on the extent and manner of injury
29
What is Neuropraxia?
Nerve intact but electrical conduction is affected Full recovery Autonomic function preserved Wallerian degeneration does not occur
30
What is neurotmesis?
Disruption of the axon, myelin sheath and surrounding connective tissue. Wallerian degeneration occurs
31
What is axontmesis
Axon is damaged and the myelin sheath is preserved. The connective tissue framework is not affected. Wallerian degeneration occurs
32
Erosion vs Ulcer of GIT
Erosion is loss of part of thickness of mucosa Ulcer is loss of full thickness
33
Where in the GI tract do anastomoses heal the best?
Upper
34
What tumours are produced by UV light?
BCC SCC and malignant melanoma