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Clinical Diagnosis > Lecture 2- Cell Damage, Change, Necrosis & Wound Healing > Flashcards

Lecture 2- Cell Damage, Change, Necrosis & Wound Healing Flashcards

1
Q

What are genetic causes of cell death and damage?

A

Chromosomal / gene defect

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2
Q

What are physical causes of cell death and damage?

A

Thermal Damage, radiation, trauma

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3
Q

What are nutritional causes of cell death and damage?

A

Deficiency, or excess dietary substances e.g. iron / vitamins

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4
Q

What are immune causes of cell death and damage?

A

Autoimmune Conditions

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5
Q

What are endocrine causes of cell death and damage?

A

Deficient or excessive hormone activity

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6
Q

What are chemical causes of cell death and damage?

A

Drugs, solvents

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7
Q

What are Anoxia causes of cell death and damage?

A

Abnormal respiratory / circulatory function

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8
Q

What are Infective causes of cell death and damage?

A

Virus, bacteria, fungi, parasites

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9
Q

What is Atrophy in cells?

A

Reduction in the size of cells

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10
Q

What is Hypertrophy in cells?

A

Increase in the size of cells

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11
Q

What is involution in cells?

A

Decrease in the number of cells

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12
Q

What is hyperplasia in cells?

A

Increase in the number of cells

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13
Q

What is metaplasia in cells?

A

Stable change to another cell type

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14
Q

What is hydropic swelling in cells?

A

water inclusion

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15
Q

What is fatty change in cells?

A

Fat inclusion

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16
Q

What needs to happen following an acute inflammatory response for cell resolution to occur?

A

Damaging Stimulus Needs to be Removed

Cell debris is cleared from the site

The specialised cells have the capacity to regrow / regenerate.

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17
Q

What are the 2 ways in which cell death occurs?

A

Necrosis (cells simply die)
or
Apoptosis (an active process)

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18
Q

What is Apoptosis?

A

Unlike necrosis, abnormal or unwanted cells are eliminated.

DNA or proteins are damaged beyond repair,
so the cells kill themselves by fragmentation of the cell without complete loss of membrane integrity.

Does not trigger an inflammatory response

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19
Q

What are examples of Apoptosis?

A

In Health – embryogenesis & development
Tadpole to a frog
Menstrual cycle
– the breakdown of the endometrium

In Disease:
Chemotherapy – apoptosis is a major mechanism in chemotherapy induced cell death.

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20
Q

What is necrosis?

A

Death of a cell or group of cells,
usually due to severe hypoxia, physical or chemical injury.

Damage to cell membranes is severe
lysosomal enzymes enter the cytoplasm and digest the cell
& cellular contents leak out.

21
Q

What is Coagulative Necrosis?

A

Appears firm and pale (as if cooked)
Outline of the dead cells are maintained
Eg. Myocardial Infarction

22
Q

What is liquefactive (colliquative) Necrosis?

A

Appears semi liquid due to dissolution of tissue by the
action of hydrolytic enzymes.
E.g. Cerebral infarction (arterial occlusion)

23
Q

What is caseous necrosis?

A

Appears soft & white, resembling cream cheese.
The original architecture can be seen
E.g. Tuberculosis

24
Q

What is fat necrosis?

A

Foci of hard, yellow material seen in dead adipose tissue.
e.g. liberation of pancreatic enzymes into the peritoneal cavity (Acute pancreatitis)

25
Q

What is Gangrene?

A

Complication of necrosis.
Tissues are invaded by bacteria which release proteolytic enzymes.
The enzymes degrade the necrotic tissue releasing foul smelling gas.
The tissue becomes green or black due to breakdown of heamoglobin.

Examples:
- Obstruction of blood supply in the bowel, is almost inevitably followed by gangrene.
- Diabetic foot

26
Q

What are the most sensitive cells to damage?

A

Cardiac Arrest Example- cessation of oxygen (hypoxia) to the whole body follows.

Most sensitive cells are the large neurons of the hippocampus & cerebellum which die after 2-5mins without oxygen.
Prolonged hypoxia causes damage to the majority of the pyramidal cells
The most robust cells are fibroblasts. These can remain even after all the parenchymal cells have been destroyed.

(It all comes down to the varying metabolic capacities of the different cells types to survive ATP depletion and calcium influx!)

27
Q

How are damaged proteins removed?

A

Damaged proteins are removed by a cell stress response & autophagy.
(this is called sublethal cell damage and is associated with recognisable structural changes).

28
Q

The critical factor in determining whether a cell follows an necrotic or apoptotic pathway to death seems to be on how much cellular ATP is available. True or false

A

True

29
Q

If damaging stimulus to a cell is massive, what happens?

A

The cell is killed immediately without passing through the stages of apoptosis or necrosis.

Examples of this include:
Severe heat – burns
Strong acids

30
Q

What is the final response to tissue injury?

A

Healing

31
Q

What does the capacity for tissue regeneration depend on?

A

Proliferative ability
Type and Severity of the damage
Most Importantly, regeneration is NOT possible if the STEM CELLS are destroyed.

32
Q

What 2 processes are involved in regeneration?

A
  1. Proliferation of surviving cells to replace lost tissue
  2. Migration of surviving cells Into the vacant space.

The factors which control healing & repair are complex; they include the production of a large variety of growth factors.

33
Q

What does wound healing show?

A

Epithelial regeneration (healing of the epidermis)

Repair by scarring
(healing of the dermis)

34
Q

What is stage 1 of organisation and repair?

A

(coagulation / Inflammation)
Pre-existing capillaries in the undamaged tissue form new capillaries by budding into the damaged area.

The damaged area is also infiltrated by macrophages, fibroblasts, and myofibroblasts.
Macrophages phagocytose inflammatory exudate and dead tissue

Vascular granulation
a fragile complex of interconnecting capillaries, macrophages and support cells replace the area of tissue damage.

35
Q

What is stage 2 of organisation and repair?

A

(tissue formation)
There is progressive growth of fibroblasts and myofibroblast.
the tissue is filled with:
complex capillary network
proliferating fibroblasts
& a few residual macrophages (fibrovascular granulation tissue).

With continued proliferation of the fibroblasts and active collagen synthesis, many of the newly formed capillaries regress until a comparatively small number of vascular channels remain, connecting the damaged area of tissue to the normal undamaged area around it – providing nutrients for the fibroblasts.

36
Q

What is stage 3 of organisation and repair?

A

(remodelling)
The intervening spaces between the vessels become progressively filled with fibroblasts synthesizing collagen (FIBROUS GRANULATION TISSUE).

The fibroblasts align themselves so that they deposit collagen in a mainly uniform pattern- running in a direction that provides maximum strength (for the physical stresses encountered).

Contraction of the area of granulation tissue frequently occurs, partly through the contractile effects of the myofibroblasts; the size of the damaged area is therefore reduced.

37
Q

What is stage 4 of organisation and repair?

A

(remodelling)
Production of dense collagen by the fibroblasts forms a collagenous scar

Once the fibroblasts have synthesized sufficient collagen to fill the defect, they assume a resting status – known as fibrocytes.

38
Q

What is the difference between organisation and repair?

A

The process whereby the inflammatory exudate is replaced by granulation tissue is called organisation of the exudate

The process where the granulation tissue is subsequently replaced by fibrous scar is called fibrous repair.

39
Q

What is organisation and repair?

A

When there has been substantial structural damage to the tissue stroma,
healing does not occur through resolution of the exudate,
but by a process known as organisation and repair.

						This eventually leads to 
						the formation of a scar.
40
Q

What are the 2 patterns of healing?

A

HEALING BY FIRST INTENTION (Primary Union)
HEALING BY SECOND INTENTION (Secondary union)

41
Q

Where do HEALING BY FIRST INTENTION (Primary Union) occur?

A

Occurs in clean, incises wounds. An example is a planned surgical incision

42
Q

Where do HEALING BY SECOND INTENTION (Secondary union) occur?

A

Occurs in open wounds, particularly where there has been significant loss of tissue, necrosis or infection

43
Q

What is the difference between first and second intention healing?

A

In secondary intention healing, there is a higher amount of tissue loss and separation of edges or infected wounds.

These wounds are filled by an abundance of granulation tissue which forms the margins of the wound.

The same process occurs as in healing by primary intention, but there is a more intense inflammatory process & considerable more wound contraction
- This means the scar takes on the shape of the original wound

44
Q

What is a keloid scar?

A

Keloid scar – overproduction of collagen.

45
Q

What are the factors that influence healing?

A

Inadequate Nutrition – Protein is required for collagen synthesis, as are Vit. C & Zinc
Ischemia
Infection
Foreign Material (continued infection / inflammation)
Steroids – hinder the formation of granulation tissue and their immunosuppressive effects may predispose to local infection.
Diabetes – Poor wound healing for several reasons.

46
Q

When does chronic inflammation occur?

A

Following acute inflammation if the causal agent is not removed

Or

“Primary” - there is no acute inflammation.
Examples – Tuberculosis, leprosy, auto-immune diseases, Crohn’s

47
Q

What are the key effector cells in chronic inflammation?

A

Lymphoid cells and macrophages are the key effector cells in chronic inflammation.

Macrophages not only act as phagocytic cells but they become activated to fulfil immunological and secretory functions.
Once activated they secrete:
Platelet activating factor & arachidonic acid metabolites (mediators of acute inflammation)
Cytokines, IL-1 TNFalpha (stimulate fibroblast proliferation and collagen synthesis)
Growth Factors (growth of blood vessels, division & migration of fibroblasts)
Proteases & hydrolytic enzymes (dissolution of extracellular material)
Plus a lot of other chemical processes which are involved in specific chronic diseases..!

48
Q

What is Granulomatous Inflammation?

A

A special type of chronic inflammation

In certain diseases, the acute inflammatory response, dominated by neutrophils is quickly replaced by an immune based cellular response
It is characterized by aggregation of macrophages & lymphocytes

The macrophages form clusters called granulomas.
Examples include - Tuberculosis
Sarcoidosis
Crohn’s Disease

49
Q

What is the transmission process of Tuberculosis?

A

1 - initial infection and replication of Mtb in macrophages
2 - Infected Macrophages
3 - Recruitment of innate and adaptive immune cells
4 - Solid granuloma, containment of Mtb
5 - Infected cells undergo necrosis resulting in the formation of the caseum
6 - Caseating granuloma
7 - Granuloma cavitation and dissemination of Mtb in the lung

Clinical Diagnosis (22 decks)

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