Cell injury and death Flashcards
Name 5 causes of Cell injury
Hypoxia (Lack of oxygen)
Physical agent
Chemical agent
biological agent
Immunological response
What is the major cause of Hypoxia
Ischaemia
What are the forms of immunological reactions causing problem
Hypersensitive state and autoimmunity
What is the pathogenesis of cell injury
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)
Name 4 biochemical mechanism and how does they cause damage
- Mitochondrial damage
==> Calcium efflux ==>Loss Mitochondrial membrane potential ==> Impair Oxidative phosphorylation
–> Reduce ATP production
–> Release ROS that damages lipid, protein and DNA
- 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 - Membrane damage
–> Cell membrane: Loss of cellular components
–> Lysosomal membranee: Enzyme digestion of cellular component - Protein misfolding, DNA damage
–> activation of pro-apoptotic protein
What are the 5 reversible injury and the 2 main type of irreversible injury
- Intracellular oedema
- Fatty change
- Hyaline degeneration
- Intracellular accumulation
- Sublethal nuclear damage
Necrosis, Apoptosis
What is intracellular oedema
Derangement of cell membrane causes influx of Na+ ion along with water to cause cell swelling
Or in other words, influx of isotonic solution
What is Fatty change
What is the cells most prone to it
What is the causes of it
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
What is Hyaline degeneration
What is the appearance of hyaline degeneration under H&E staining
The situation when Smooth muscle is replaced by fibrous connective tissue
Homogeneous glassy, pink alteration (intracellular & extracellular)
What are usually accumulated in intracellular accumulations
And their causes
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)
For sublethal Nuclear damage
At what cells will the damage cause heritable disease
Else what will be the problem
Germ cell
Neoplasia
What is the difference between cell apoptosis and necrosis in terms of the effect caused
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
Will apopotosis and necrosis cause
Acute inflammation
Scaring
Are they phyiological or pathological
Cell size change
Cell membrane damaged
Apoptosis no. Necrosis Yes
Apoptosis no. Necrosis May
Apoptosis: Both
Necrosis: Pathological
Necrosis: Enlarged
Apoptosis: Shrinked
Necrosis: Yes
Apoptosis: Intact but structure altered
What are the physiologucal causes for apoptosis
-programmed cell destruction during
embryonic development
– normal cell turnover in adult organs
What are the pathological causes for apoptosis
– UV or ionizing radiation
– cytotoxic T cells
– Cell mediated immunity
– drugs
– tumour cell death
What is the intrinsitc pathway for apopotosis
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)
What is the extrinsic factor causing apoptosis
Receptor-ligand interactions
–> Fas (a kind of Tumour Necrosis Factor receptor)
What are the steps of apoptosis
–> DNA fragmentation
–> Chromatin and Cytoplasm condensation
–> The remenant forms apoptotic body
–> Phagocytosed by adjacent cell
How are the apoptotic body appear under H&E staining. Why
It is darkyl stained as the chromatin fragment is very eosinophilic
What are the 2 ways of the cell clearing up the remenant in necrosis
Autolysis (lysosomal hydrolase of the necrotic cell)
Heterolysis (by immigrant leucocytes
What are the 3 steps of the Nuclear change in necrosis
Pyknosis (irrevesible condensation of chromatin)
Karoyorrhexis (Fragmentation of nucleus)
Karyolysis (dissoluton of nuclear component)
Name 5 types of necrosis
Coagulative necrosis
Liquefaction necrosis
Caseous necrosis
Fat necrosis
fibrinoid necrosis
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
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
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
The death tissue softens and appears liquid like and a pus develops
Bacterial infection
Ischaemic necrosis of brain
Power hydrolytic enzymes
Yes
Cystic space
What is caseous Necrosis
A type of necrosis that the dead cells look like cheese
What is the difference between caseous Necrosis and the coagulative necrosis
Caseous necrosis cause tissue structure to be destroyed while coagulative necrosis dont
In caseous necrosis, what is surrounding the amorphous mass
It is the characteristic of an particular pathogen infection. WHat is that
Glanulomatous wall
Mycobacteria
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
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
Name an example of fat necrosis due to traumatic
What does it provoke
What is observable
Breast
Chronic inflammation hence giant cell reaction
Formation of a hard indurated mass
What is fibrinoid necrosis
Name 3 examples of Fibrinoid Necrosis
Tissue death is accompanied by fibrin deposit
Rheumatoid nodule, Arthus reaction, arteriolar lesions of malignant hypertension
What are the problems brought by necrosis
➢ Loss of function
➢ Release of cell contents
➢ Acute inflammation
➢ Effects of repair and regeneration
➢ Dystrophic calcification
➢ Infection
What molecule level can we use to track acute pancreatitis
Lipase and proteas
What will the destruction of lung tissue cause
Emphysema hence respiratory failure
For the gangrene of bowel, what is the problem
The bowel can burst and leak the content to the cavity
What is autophagy
What is the function of it
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
