Cell injury and death Flashcards

1
Q

Name 5 causes of Cell injury

A

Hypoxia (Lack of oxygen)

Physical agent

Chemical agent

biological agent

Immunological response

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2
Q

What is the major cause of Hypoxia

A

Ischaemia

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3
Q

What are the forms of immunological reactions causing problem

A

Hypersensitive state and autoimmunity

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4
Q

What is the pathogenesis of cell injury

A

All stresses and noxious influences exert their effects at the molecular or biochemical level
- Structural changes after biochemical derangement
- Histochemical or ultrastructural changes (minutes to hours after injury)
- Changes by light microscopy or on gross examination (hours to days)

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5
Q

Name 4 biochemical mechanism and how does they cause damage

A
  1. Mitochondrial damage
    ==> Calcium efflux ==>Loss Mitochondrial membrane potential ==> Impair Oxidative phosphorylation

–> Reduce ATP production
–> Release ROS that damages lipid, protein and DNA

  1. Entry of Calcium ion
    –> Increase mitochondrial permeability to cause Calcium efflux
    —> Activates phospholypase (dmg cell membrane), endonuclease (Dmg DNA) and Protease (Break down membrane and cytoskeletal proteins)
    –>Promote apoptosis
  2. Membrane damage
    –> Cell membrane: Loss of cellular components
    –> Lysosomal membranee: Enzyme digestion of cellular component
  3. Protein misfolding, DNA damage
    –> activation of pro-apoptotic protein
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6
Q

What are the 5 reversible injury and the 2 main type of irreversible injury

A
  1. Intracellular oedema
  2. Fatty change
  3. Hyaline degeneration
  4. Intracellular accumulation
  5. Sublethal nuclear damage

Necrosis, Apoptosis

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7
Q

What is intracellular oedema

A

Derangement of cell membrane causes influx of Na+ ion along with water to cause cell swelling

Or in other words, influx of isotonic solution

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8
Q

What is Fatty change

What is the cells most prone to it

What is the causes of it

A

It means the non-adipocytes appears like a adipocyte, with abnormal accumulation of fat in the cell

Liver, heart muscle, Renal Tubule

Chemical injury, Hypoxia, Starvation &wasting disease, DM

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9
Q

What is Hyaline degeneration

What is the appearance of hyaline degeneration under H&E staining

A

The situation when Smooth muscle is replaced by fibrous connective tissue

Homogeneous glassy, pink alteration (intracellular & extracellular)

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10
Q

What are usually accumulated in intracellular accumulations

And their causes

A

Lipofuscin (Pigment of aging)

Lysosomal storage disease (ie The lack of functional lysosome causing big moelcules to accumulate)

Haemosiderin (due to uptake of excess iron by cell)

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11
Q

For sublethal Nuclear damage

At what cells will the damage cause heritable disease

Else what will be the problem

A

Germ cell

Neoplasia

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12
Q

What is the difference between cell apopotosis and necrosis in terms of the effect caused

A

Apoptosis affects single cells within living tissues, usually wont lead to disruption in tissue function

While necrosis means a sheet of cells dying together, disrupting tissue structure

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13
Q

Will apopotosis and necrosis cause

Acute inflammation

Scaring

Are they phyiological or pathological

Cell size change

Cell membrane damaged

A

Apoptosis no. Necrosis Yes

Apoptosis no. Necrosis May

Apoptosis: Both
Necrosis: Pathological

Necrosis: Enlarged
Apoptosis: Shrinked

Necrosis: Yes
Apoptosis: Intact but structure altered

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14
Q

What are the physiologucal causes for apoptosis

A

-programmed cell destruction during
embryonic development

– normal cell turnover in adult organs

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15
Q

What are the pathological causes for apoptosis

A

– UV or ionizing radiation
– cytotoxic T cells
– Cell mediated immunity
– drugs
– tumour cell death

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16
Q

What is the intrinsitc pathway for apopotosis

A

Mitochondrial pathway

Which involves
-> Removal of growth factor
–> DNA damage (by radiation, toxin, free radical)
–> Protein misfolding (ER stress, ie stress brought by Failure in second folding of protein)

17
Q

What is the extrinsic factor causing apoptosis

A

Receptor-ligand interactions
–> Fas (a kind of Tumour Necrosis Factor receptor)

18
Q

What are the steps of apoptosis

A

–> DNA fragmentation
–> Chromatin and Cytoplasm condensation
–> The remenant forms apoptotic body
–> Phagocytosed by adjacent cell

19
Q

How are the apoptotic body appear under H&E staining. Why

A

It is darkyl stained as the chromatin fragment is very eosinophilic

20
Q

What are the 2 ways of the cell clearing up the remenant in necrosis

A

Autolysis (lysosomal hydrolase of the necrotic cell)

Heterolysis (by immigrant leucocytes

21
Q

What are the 3 steps of the Nuclear change in necrosis

A

Pyknosis (irrevesible condensation of chromatin)

Karoyorrhexis (Fragmentation of nucleus)

Karyolysis (dissoluton of nuclear component)

22
Q

Name 5 types of necrosis

A

Coagulative necrosis
Liquefaction necrosis
Caseous necrosis
Fat necrosis
fibrinoid necrosis

23
Q

What is coagulative necrosis

What are the 2 causes for that. Arrange in descending order of the probability

What type of organ does it usually happen

A

It means death due to lack of blood supply

Infartion (blockage of vessel, ie prolonged ischemia), ischemia

Solid organ (not the brain

Preserved tissue architecture with loss of nucleus

It becomes an acidophilic (pink) and opague tombstone

24
Q

What is liquefaction necrosis

What are the causes

What does it involve to remove the cell debris

Does the tissue structure affected

What is left behind

A

The death tissue softens and appears liquid like and a pus develops

Bacterial infection
Ischaemic necrosis of brain

Power hydrolytic enzymes

Yes

Cystic space

25
Q

What is caseous Necrosis

A

A type of necrosis that the dead cells look like cheese

26
Q

What is the difference between caseous Necrosis and the coagulative necrosis

A

Caseous necrosis cause tissue structure to be destroyed while coagulative necrosis dont

27
Q

In caseous necrosis, what is surrounding the amorphous mass

It is the characteristic of an particular pathogen infection. WHat is that

A

Glanulomatous wall

Mycobacteria

28
Q

What is fat necrosis

What is the white chalky white patches formed. How is it formed in Acute pancreatitis

Why complications is caused in acute pancreatitis

A

Death of fat tissue due to injury and loss of blood supply

Soap. The pancreatic lipase breaks down Triglyceride into fatty acid and glycerol

The fatty acid combines with Calcium to form soap

The enzyme leaked will attack other pancreatic cells to release more enzymes

29
Q

Name an example of fat necrosis due to traumatic

What does it provoke

What is observable

A

Breast

Chronic inflammation hence giant cell reaction

Formation of a hard indurated mass

30
Q

What is fibrinoid necrosis

Name 3 examples of Fibrinoid Necrosis

A

Tissue death is accompanied by fibrin deposit

Rheumatoid nodule, Arthus reaction, arteriolar lesions of malignant hypertension

31
Q

What are the problems brought by necrosis

A

➢ Loss of function
➢ Release of cell contents
➢ Acute inflammation
➢ Effects of repair and regeneration
➢ Dystrophic calcification
➢ Infection

32
Q

What molecule level can we use to track acute pancreatitis

A

Lipase and proteas

33
Q

What will the destruction of lung tissue cause

A

Emphysema hence respiratory failure

34
Q

For the gangrene of bowel, what is the problem

A

The bowel can burst and leak the content to the cavity

35
Q

What is autophagy

What is the function of it

A

Lysosomal digestion of the cel’s own cell component

involves sequestration of cellular organelles
into cytoplasmic autophagic vacuoles
(autophagosomes) that fuse with lysosomes
and digest the enclosed material.

Help Host defense against certain microbes

Help adapt nutrient deprivation