cell death and injury part 2

Question 1

What is apoptosis

Answer 1

Programmed cell death
Cell death with shrinkage
Regulated intracellular program where a cell activates enzymes that degrade its own nuclear DNA and proteins
- DNA breakdown is non random and there us internucleosomal cleavge of DNA.

Question 2

stages of apoptosis

Answer 2

initiation- involves caspase 9
execution- involves caspase 3 & 6
degradation and phagocytosis

*extrinsic and intrinsic pathway activate caspase enzymes

Question 3

explain the intrinsic pathway in apoptosis

Answer 3

• initiating signal comes from within the cell.
• triggered by irreparable DNA damage, withdrawal of GF/hormones
• p53 protein is activated and causes the outer mitochondrial membrane to become leaky. Cytochrome C is released from the mitochondria and this causes activation of caspases.

Question 4

explain the extrinsic pathway of apoptosis

Answer 4

initiated by extracellular signals
triggered by cells that are a danger e.g tumour cells, virus infected cells
TNFα is one of these signals secreted by T killer cells. It binds to cell membrane receptors and causes activation of caspases

Question 5

define gangrene

Answer 5

necrosis visible to the naked eye

Question 6

define infarction

Answer 6

necrosis caused by a reduction in arterial blood flow

Question 7

define infarct

Answer 7

an area of necrotic tissue which is the result of loss of arterial blood supply.

Question 8

types of infarct

Answer 8

coagulative -dry
liquefactive -wet
white infarct-solid organs. occlusion of end artery. wedge shaped
red infarct -haemorrhagic. loose tissue

Question 9

what do the complications of infarction depend on

Answer 9

if there is an alternative blood supply
speed of ischaemia
tissue involved
oxygen content of the blood

Question 10

what is ischaemia-reperfusion injury and causes?

Answer 10

if blood flow is returned to a damaged but not yet necrotic tissue damage sustained can be worse than if blood flow hadn’t returned.
causes - increased production of oxygen free radicals from reoxygenation. increased number of neutrophils resulting in more inflammation and increase tissue injury . delivery of complement proteins and activation of the complement pathway.

Question 11

mechanisms of abnormal intracellular accumulations

Answer 11

abnormal metabolism
alterations in protein folding and transport
deficiency of critical enzymes
inability to degrade phagocytksed partciles

Question 12

affects of build up of fluid/water in cells

Answer 12

severe cellular distress e.g hypoxia
sodium and water enter the cell and form discrete droplets
hydropic swellings(entire cell swollen) leads to entire organ swollen

Question 13

what is steatosis

Answer 13

accumulation of triacylglycerides

caused by chronic alcohol misuse, obesity , diabetes mellitus

Question 14

complications of steatosis

Answer 14

liver and metabolic dysfunction
liver failure
liver cirrhosis
sudden death

Question 15

accumulation of proteins

Answer 15

intracellular accumulation leads to eosinophilic pink droplets or aggregations in the cytoplasm of cells

Question 16

what is α1-antitrypsin deficiency

Answer 16

liver produces incorrectly folded α1-antitrypsin protein (a protease inhibitor)
cannot be packaged by ER, accumulates within ER and is not secreted
systemic deficiency- proteases in lungs act unchecked resulting in emphysema

Question 17

effects of hypercalaemia

Answer 17

bone diesel
renal stones
confusion , drowsiness, coma, pyschosis
thirst , polyuria