Cellular Injury Flashcards

1
Q

What are the two major forms of cell death

A
  • Necrosis

- Apoptosis

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2
Q

List the 6 types of necrosis

A
  • Coagulative
  • Colliquative
  • Caseous
  • Gangrenous
  • Fibrinoid
  • Fat
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3
Q

When does coagulative necrosis occur

A

Ischaemic injury (except in the brain)

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4
Q

When does colliquative necrosis occur

A

Seen in the brain due to a lack of supporting stroma

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5
Q

What is caseous necrosis characteristic of

A

TB

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6
Q

Why is gangrenous tissue black

A

Due to iron sulphide from degraded Hb

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7
Q

What bacteria causes Gas Gangrene

A

Clostridium perfringens

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8
Q

What type of necrosis is associated with Malignant hypertension

A

Fibrinoid

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9
Q

Describe Fibrinoid necrosis

A

Necrosis of arteriole smooth muscle wall with seepage of plasma into the tunica media and deposition of fibrin

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10
Q

Define Apoptosis

A

Energy-dependent process for the deletion of unwanted individual cells. It is characterised by the activation of endogenous endonuclease.

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11
Q

What is the role of p53

A
  • Checks the integrity of the genome prior to mitosis

- Switches cells with damaged DNA into apoptosis

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12
Q

What is the role of bcl-2

A

Inhibits apoptosis

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13
Q

List the morphological features of apoptosis

A
  • Cell shrinkage with intact plasma membrane
  • Nuclear shrinking (pyknosis)
  • Nuclear fragmentation
  • Margination of chromatin
  • Surface blebbing of a cell
  • Formation of apoptotic bodies
  • Fragments are either shed or phagocytosed
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14
Q

Outline the differences between the fates of dead cells that underwent apoptosis vs necrosis

A
  • Apoptosis = phagocytosed by neighbouring cells

- Necrosis = phagocytosed by neutrophils and macrophages

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15
Q

In terms of the process of healing, what is meant by regeneration

A

Total healing of a wound with restitution of the original tissues in their usual amounts, arrangement and function

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16
Q

In terms of the process of healing, what is meant by repair

A

The process where the original tissue is not totally regenerated and the defect is made good to a variable extent by scar tissue

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17
Q

How are cells classified according to their capacity to renew

A
  1. Labile cell
  2. Stable cell
  3. Permanent cell
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18
Q

Which cell type has the greatest capacity to renew

A

Labile cell

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19
Q

Give examples of labile cell tissues

A
  • Skin
  • Oesophagus
  • Vagina
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20
Q

Give examples of stable cell tissues

A
  • Liver

- Renal tubular epithelium

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21
Q

Give examples of permanent cell tissues

A
  • Nerve
  • Striated muscle
  • Myocardium
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22
Q

Outline the process of organisation in tissue repair

A
  1. Fibrinous exudate produced
  2. Removal of fibrin, dead tissue, and phagocytes
  3. Migration of fibroblasts and capillaries forming granulation tissue
  4. Replacement of exudate by vascularised fibrous tissue
  5. Eventually a collagen-rich scar develops
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23
Q

What does granulation tissue consist of

A
  • Capillary loops

- Myofibroblasts

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24
Q

What complications are associated with organisation in wound healing

A
  • Abdominal adhesions

- Constrictive pericarditis

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25
Q

Outline the process of wound healing by primary intention

A
  • Edges of wound opposed
  • Fibrin ‘sticks’ edges together
  • Capillaries bridge tiny gap
  • Fibroblasts invade fibrin network
  • Suitable strength regained within 10 days
  • Remodelling occurs from then on
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26
Q

Outline the process of wound healing by secondary intention

A
  • Tissue loss
  • Phagocytes remove any debris
  • Formation of granulation tissue in base of wound
  • Myofibroblasts cause wound contraction
  • Re-epithelialisation covers defect
  • Scar tissue formation
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27
Q

What causes Keloid scarring

A

Excessive fibroblast proliferation and collagen production

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28
Q

What differentiates Keloid scars from Hypertrophied scars

A

Collagen deposition beyond the confines of the wound

29
Q

What is the outcome of Hypertrophied scars

A

Usually settle spontaneously within 18 months

30
Q

What type of insult is most likely to cause a Keloid scar

A

Burns

31
Q

List the stages of skin graft ‘take’

A
  1. Adherence
  2. Plasmic imbibition
  3. Inosculation
32
Q

What occurs during the adherence stage of skin graft ‘take’ and how long does this take

A
  • Fibrin bonds the graft to the recipient site

- <12 hours

33
Q

What occurs during plasmic imbibition stage of skin graft ‘take’ and how long does this take

A
  • Graft absorbs essential nutrients from recipient bed

- 24-48 hours

34
Q

What occurs during inosculation stage of skin graft ‘take’ and how long does this take

A
  • Revascularisation of the graft

- 48-72 hours

35
Q

Which type of skin graft ‘takes’ better and why

A

Split thickness - thinner and therefore more likely to survive the imbibition phase

36
Q

When will primary bone healing occur

A

When strain is <2%

37
Q

When will secondary bone healing occur

A

When strain is 2-10%

38
Q

What are the 3 phases of secondary bone healing

A
  1. Inflammatory phase
  2. Reparative phase
  3. Remodelling phase
39
Q

By what method does primary bone healing occur

A

Haversian remodelling

40
Q

What occurs during the inflammatory phase of secondary bone healing

A
  • Haematoma forms and provides a source of haematopoetic cells capable of secreting growth factors
  • Macrophages, neutrophils and platelets release several cytokines
  • Fibroblasts and mesenchymal cells migrate to the fracture site and granulation tissue forms around fracture ends
41
Q

When does the inflammatory stage become fully established

A

Within 7 days

42
Q

What occurs during the reparative phase of secondary bone healing

A
  • Primary callus forms within 2 weeks
  • Bridging of soft callus forms if bone ends not touching
  • Fibroblasts lay down disordered matrix of Type 2 collagen
  • Endochondral ossification mineralises the soft callus to form hard callus and woven bone
43
Q

When does hard callus begin to form

A

14 days post-fracture

44
Q

What occurs during the remodelling phase of fracture healing

A
  • Begins midway through repair phase

- Woven bone is converted to lamellar bone with ordered architecture

45
Q

What is Wolff’s law

A

Change in the internal structure of bone in response to load

46
Q

Where are the osteoblasts that produce new bone derived from

A

Periosteum

47
Q

When may complete restitution occur in liver damage

A

If the damage is confined to the hepatocytes only

48
Q

What occurs to cardiac cells when damaged

A

Replaced with scar tissue

49
Q

How do GI mucosal ulcers heal

A
  • Granulation tissue in the base

- Centripetal growth of surface epithelium

50
Q

What nutritional deficiencies can negatively impact wound healing

A
  • Vitamin C deficiency

- Zinc deficiency

51
Q

What are the three types of radiation-induced DNA damage

A
  1. Strand breaks
  2. Base alterations
  3. Cross-linking
52
Q

What is the effect of radiotherapy on the bone marrow

A
  • Suspends renewal of all cell lines
  • Granulocytes are reduced before erythrocytes
  • Increased incidence of leukaemia in long-term survivors
53
Q

What is the effect of radiotherapy on the intestines

A
  • Loss of surface epithelium causes diarrhoea

- Full thickness damage causes fibrosis and stricture formation

54
Q

What tissue have the most marked acute response to radiotherapy

A
  • Gut epithelium
  • Bone marrow
  • Skin
  • Gonads
55
Q

What is the effect of radiotherapy on the kidneys

A
  • Gradual loss of parenchyma results in loss of renal function
  • Endarteritis obliterans of small vessels will cause intrarenal artery stenosis and HTN
56
Q

What constitutes a low-voltage electrical injury

A

<1000 volts

57
Q

What constitutes a high-voltage electrical injury

A

> 1000 volts

58
Q

How may high-voltage electrical injuries affect the kidneys

A

Rhabdomyolysis

59
Q

What is used to treat hydrofluoric acid burns

A

Calcium gluconate (as can cause lethal hypocalcaemia)

60
Q

Outline the 3 components of Jackson’s burn wound model

A
  1. Zone of necrosis
  2. Zone of stasis
  3. Zone of hyperaemia
61
Q

What occurs in the zone of necrosis

A
  • Area of maximum damage

- Rapid and irreversible cell death due to coagulation of cellular proteins

62
Q

What occurs in the zone of stasis

A
  • Adjacent to the zone of necrosis
  • Compromised tissue perfusion due to damaged microcirculation
  • Can progress to necrotic tissue if left untreated
63
Q

What occurs in the zone of hyperaemia

A
  • Outermost burn zone
  • Tissue perfusion is increased due to local inflammatory mediator release
  • Usually completely recovers
64
Q

What factors can cause progression of the zone of stasis to necrosis

A
  • Hypoperfusion
  • Infection
  • Oedema
65
Q

At what extent of burn coverage is a systemic response seen

A

20%

66
Q

What are the features of superficial epidermal burns

A
  • Erythema
  • No blistering
  • Good capillary refill
  • Painful
  • NOT included in TBSA calculations
67
Q

What are the features of superficial dermal burns

A
  • Pink
  • Blistered and oedematous
  • Good capillary refill
  • Extremely painful
68
Q

What are the features of deep dermal burns

A
  • Red
  • Fixed staining or petechial points
  • Reduced or absent capillary refill
  • Reduced or absent sensation
  • Less painful
69
Q

What are the features of full-thickness burns

A
  • Appear thick
  • Can be white or black
  • Absent capillary refill
  • Absent sensation
  • Painless