Cell Injury Flashcards

1
Q

Define cell injury

A

If the limits of adaptive responses to a stimulus are exceeded or if the cells are exposed to injurious agent or stress , deprived of essential nutrients or become compromised by mutations that effect the essential cellular constituents a sequence of reactions follows called as cell injury

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2
Q

Different tissue responses to cell injury

A

1.Altered physiological stimuli: cellular adaptation. Hyperplasia
Hypertrophy atrophy metaplasia
2.acute reversible injury : cellular swelling
Fatty change
Acute Irreversible injury: necrosis and apoptosis
3. Chronic injury: intracellular accumulations, calcification
4. Sublethal injury over a long span: cellular aging

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3
Q

Mechanism of cell injury

A
  1. Atp depletion
  2. Membrane damage/ defects in memb permeability
  3. Mitochondrial damage
  4. Accumulation of reactive o2 species……
  5. Influx of intracellular Ca++ causing damage to dna nd proteins
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4
Q

Role of ca++

A

Failure of ca++ pump leads to influx of ca++ causing activation of various enzymes that have damaging effects
Phospholipase
Protease
Endonuclease
Atpase….

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5
Q

Why does inflammation occur in necrosis

A

Necrotic cells lose their membrane integrity leading to the release of intracellular contents into the extracellular space

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6
Q

What are free radicals

A

Free radicals are chemical species that have a single unpaired electron in their outermost orbit

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7
Q

Generation of free radicals

A

1radiant energy absorption: uv rays and x rays
2. Reduction oxidation reactions
3. During inflammation
4. Transition metals like iron copper
5. Enzymatic metabolism
6. Nitric oxide

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8
Q

Pathological effects of free radicals

A
  1. Lipid peroxidation in membranes
  2. Oxidative modification of proteins
  3. Lesions in dna
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9
Q

Neutralization of free radicals

A
  1. Spontaneous deacy: these are inherently unstable.
    O2^- decays into O2 in presence of water
  2. Non enzymatic: antioxidants in the cytosol- lipid soluble vitamins like A and E
    Ascorbic acid
    Glutathione
    Iron copper
    Transferin lactoferin ferritin ceruloplasmin
  3. Enzymatic:
    .Catalase: h2o2 into o2 and h20
    .Superoxide dismutase:
    mn sod and cu zn sod
    . Glutathione peroxidase
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10
Q

What are fatty changes

A

The term steatosis or fatty change refers to the abnormal accumulation of TG within parenchymal cells

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11
Q

Causes of fatty change

A

Alcohol abuse
Toxins
Protein malnutrition
DM
Obesity
Anoxia

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12
Q

Sites of fatty change

A

Liver
Heart
Muscle
Kidney

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13
Q

What causes fatty change in heart

A

Hypoxia eg. anaemia
Myocarditis eg. Diptheria

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14
Q

Pathological calcification

A

It is the abnormal tissue deposition of ca salts with smaller amts of other mineral salts
2 forms: dystrophic cal
Metastatic calc.

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15
Q

Dystrophic calcification causes

A

When deposition occurs locally in dying tissue despite normal serum levela of ca and in absence of derrangement in ca metabolism
1. In areas of necrosis
2. Atheromas of advanced atherosclerosis
3. Aging or damaged heart valves
4. Tuberculous lymphnode

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16
Q

Metastatic calc causes

A

The deposition of ca salts in otherwise normal tissues.
1. Inc secretion of pth
2. Resorption of bone tissue
3. Vit D related disorders
4. Renal failure
5. Milk alkali syndrome
6. Al intoxication

17
Q

Sites of metastatic calc

A

Intestinal tissues if gastric mucosa
Kidneys
Lungs
Systemic arteries
Pulmonary veins

18
Q

Chemical agents causing cell injury

A

Glucose or salt in hypertonic solution
O2 in high concentration
Env and air pollutants
Insecticides
Herbicides
Industrial or occupational hazard
Recreational drugs

19
Q

Imp free radicals

A

Reactive o2 species
Superoxides
Hydrogen peroxide
Hydrxyl ion
Reactive nitrogen species
No
Onoo-
No2-
Ccl3 derived from ccl4

20
Q

Define necrosis

A

Spectrum of morphological changes that follows cell death in living tissue largely resulting from progressive degradative action of enzymes on lethally injured cell

21
Q

Apoptosis define

A

It is a pathway of cell death that is induced by a tightly regulated intracellular program in which cells that are destined to die activate enzymes that degrade the cells own nuclear dna and cytoplasmic proteins

22
Q

Nuclear changes in necrosed cell

A

1.Karyolysis: basophilia of chromatin may fade reflecting dnase activity
2. Pyknosis: nuclear shrinkage and increased basophilia
3. Karyorrhexis: pyknotic or partially pyknotic nucleus undergoes fragmentation and disappears totally

23
Q

Define gangrene

A

It is necrosis of tissue with superimposed putrefaction

24
Q

Types of gangrene

A

Dry gangrene : because of lack of arterial blood supply.
Moist gangrene: due to obstruction of both arterial and venous drainage. Particularly in moist areas
Gas gangrene: caused mainly by clostridium perfringes
Rarely by c. Histolyticum
C. Novyi and c. Septicum

25
Which type of gangrene is most dangerous
Gas gangrene because it is caused by anaerobic bacteria c. Perfringes And can cause toxaemia and septicemia which can lead to death
26
Bed sores
It is seen in moist gangrene. These are pressure sores that develop over bony prominences in indivisuals with limited mobility such as those who are bed ridden Sustained mechanical pressure causes lack of blood supply and ischemia in the area and subsequent necrosis.
27
Morphology of dry gangrene
Macroscopic: area is cold dry shrivelled and mummified. It is black due to fes. Foul smelling Hemolysed rbc produces iron. Putrefaction produces h2s. These combine to form black feS Microscopic: Zone of inflammation Zone of separation Zone of gangrenous tissue
28