cell injury

Question 1

causes of cell death/injury

Answer 1

hypoxia, physical agents e.g cold, radiation or trauma, chemical agents e.g alcohol, microorganisms, immune mechanisms, dietry insufficiency or excess (obese) or genetic abnormalities (e.g errors of metabolism)

Question 2

what is hypoxia and what are the different types

Answer 2

area/ whole body not getting enough oxygen. hyperaemic hypoxia - low o2 levels due to something like altitude, anaemic hypoxia due to haemoglobin not being able to carry enough oxygen, ischaemic hypoxia- interruption to blood supply or histolytic hypoxia - inability to utilise oxygen e.g from cyanide poisoning

Question 3

how does the immune system damage body cells

Answer 3

hypersensitivity- e.g hives from an overly vigorous immune reaction or autoimmune - e.g graves disease where immune system unable to distinguish self cells and attacks them

Question 4

which components of the cell are susceptible to injury

Answer 4

cell membrane, nucleus, proteins and mitochondria

Question 5

describe reversible hypoxic injury

Answer 5

due to lack of oxygen there is low oxidative phosphorylation and low oxygen. results in low ATP production meaning the Na pump stop working allowing Na to diffuse in, with water following causing the cell to swell. as well as this there is more anaerobic glycolysis meaning more lactate in the blood decreasing the pH. This causes ribosome to detach from the ER meaning less protein synthesis and lipid deposition

Question 6

describe irreversible hypoxic injury

Answer 6

ca2+ pump fails meaning Ca2+ conc increases inside cell activating enzymes including; ATPase- reduces ATP, phospholipase- degrades membrane, protease- degrades membrane and cytoskeleton and endonuclease- causes nuclear chromatin damage.

Question 7

how the cold/ heat causes cell damage

Answer 7

crystallises or dissolves cell membrane.

Question 8

how cyanide toxicity damages cell membrane

Answer 8

inactivates enzymes involved in oxidative phosphorylation meaning no ATP produced

Question 9

how free radicals damage cells

Answer 9

when there is an imbalance between mechanisms to control radicals and the number of radicals then it results in lipid peroxidation and damage to proteins, carbs and DNA which cause potentially carcinogenic mutations

Question 10

what are heat shock proteins

Answer 10

look up

Question 11

how injured cells look under microscope

Answer 11

lighter pink cytoplasm because of it being diluted by water moving in from failure of sodium pump. organelles are also swollen, chromatin clumps due to low pH and later on nucleus fragments. lysosomes rupture from swelling and enzymes are released digesting cell contents.

Question 12

what is oncosis

Answer 12

cell death with swelling, prior to death

Question 13

what is necrosis

Answer 13

morphological changes after cell death

Question 14

what are the different types of necrosis and their definitions

Answer 14

coagulative- protein denaturation dominates and proteins clump together forming solid dead cells where architecture is preserved. liqeffective- mainly enzymes release leading to liquifying of contents, looks very viscous under microscope. caseous- looks like clotted cheese, associated with infections. fat necrosis- release of free fatty acids which react with calcium to form chalky deposits, this is due to deposition of adipose tissue

Question 15

define gangrene

Answer 15

visible necrosis, the clinical word for necrosis

Question 16

define infarction

Answer 16

a cause of necrosis which can result in gangrene caused by reduction of arterial flow (verb)

Question 17

define an infarct

Answer 17

area of narcotic tissue which results in loss of arterial blood supply (noun)

Question 18

define the differences between dry, wet and gaseous gangrene

Answer 18

dry = modified by exposure to air (coagulative necrosis) 
wet= modified by infection (liquefactive necrosis)
gas= wet gangrene where anaerobic bacteria produce gas (liquefactive)

Question 19

what are the most common causes of infarction

Answer 19

thrombosis - blood clot which obstructs the blood flow and embolism- detached solid, liquid or gaseous material which is carried to a site elsewhere in the body. however tissues can also become infarcted by twisting and compression of blood vessels which restrict the flow

Question 20

types of ischaemic necrosis (infarct) due to thrombosis for example

Answer 20

coagulative (e.g myocardial infarct), liquefactive (e.g cerebral infarct) and can also be a red or white infarct

Question 21

what is a white infract

Answer 21

blockage of end artery suppling (only artery supplying that organ) haemorrhage. shows white wedge shape where there is no blood supply. commonly occurs in the heart, kidney and spleen

Question 22

what is a red infarct

Answer 22

due to bleeding. blood inside dead tissue. organ has dual blood supply meaning that if one end artery becomes blocked the other still supplies the tissue with blood but not enough to fully supply it. happens in lung because has dual blood supply and loose tissue

Question 23

what does the consequence of infarction depend on

Answer 23

whether there is an alternate blood supply, the speed of the ischaemia, what tissue is involved (much more dangerous in brain than in muscle because adapted for anaerobic respiration) and the oxygen content of the blood

Question 24

what is apoptosis

Answer 24

cell death, a non random, active process where enzymes break down DNA and cell proteins

Question 25

when does apoptosis occur (physiological reasons)

Answer 25

during embryogenesis (sporting fingers), or during involution (the shrinkage of an organ in old age or when inactive, e.g. of the uterus after childbirth)

Question 26

when apoptosis occur (pathological reasons)

Answer 26

when cells are damage e.g with DNA damage or during cytotoxic T cell killing of virus infected or neoplastic (skin graft) cells

Question 27

explain the basic process of apoptosis

Answer 27

during initiation the cell and the nucleus shrink, during execution the nuclei fragments and the during degeneration cell breaks up into apoptic bodies which are later cleared by macrophages. no inflammation because no enzymes released externally

Question 28

intrinsic triggers of apoptosis

Answer 28

something goes wrong inside cell e.g DNA damage. P53 protein is activated and mitochondria membrane becomes leaky. caspases are activated and clear target proteins/DNA

Question 29

extrinsic triggers of apoptosis

Answer 29

dangerous cells e.g tumours or contain virus. TNTa binds to receptor resulting in the activation of caspases

Question 30

difference between apoptosis and oncosis

Answer 30

apoptosis is controlled and there is no inflammation whereas oncosis is more pathological and results in the release of many enzymes meaning many surrounding cells are affected and lots of inflammation occurs

Question 31

name some examples of molecules which are related from injured cells

Answer 31

potassium, enzymes and myoglobin

Question 32

effect of potassium release

Answer 32

usually have small amounts in extracellular fluid. if this rises may cause heart to stop. any celll injury means the K+ is related and will result in cardiac arrhythmia (irregular heart beat)

Question 33

effect of enzyme release

Answer 33

troponin is related by myocytes after injury. shows if someone has had a myocardial infarction.

Question 34

effect of myoglobin release

Answer 34

related by any dead/damaged muscle. rhabdmyololysis shows large amounts of myoglobin related due to trauma

Question 35

discuss water and electrolyte accumulation in cells

Answer 35

when cell is damaged cells become enlarged because water enters the cell. this is very dangerous in brain because the pressure can damage the brain or spinal cord by pressing on important structures and by restricting blood flow into the brain.

Question 36

discuss lipid accumulation in cells

Answer 36

steatosis (accumulation of TAG) is often seen in the liver of diabetics, obese and alcoholics. cholesterol can’t be broken down it can only be removed (via the liver) therefore when there is an excess of things needing to be broken down fat is stored in vesicles which can lead to the formation of foam cells and atherosclerotic plaque

Question 37

discuss protein accumulation in cells

Answer 37

Mallory’s hyaline- damaged keratinocytes build up in hepatocytes. This happens in alcoholic liver disease
alpha 1 antitrypsin deficiency- when unable to correctly fold alpha 1 trypsin meaning it can’t be packaged and accumulates in the ER. if unchecked can cause emphysema

Question 38

exogenous pigment accumulation

Answer 38

air pollution e.g carbon is phagocytosed by macrophages causing blackened lymph nodes.harmless unless in large amounts- can cause fibrosis and emphysema = coal worker pneumoconiosis or anthracosis(milder).Y
This is due to build up of carbon in lungs. also accumulate during tattoo. sometimes pigment also reaches lymph node.

Question 38

exogenous pigment accumulation

Answer 38

air pollution e.g carbon is phagocytosed by macrophages causing blackened lymph nodes.harmless unless in large amounts- can cause fibrosis and emphysema = coal worker pneumoconiosis or anthracosis(milder).Y
This is due to build up of carbon in lungs. also accumulate during tattoo. sometimes pigment also reaches lymph node.

Question 39

endogenous pigment accumulation

Answer 39

haemosiderosis- forms when overload of iron is deposited in haemosiderms (iron storage molecule) from bruise.
hameochromatosis- overload of haemosidersms in many organs. happens because too much is absorbed from diet and its damaging because can’t get rid of it. when builds up in pancreas causes diabetes and in liver causes chirrosis. treatment is to remove blood and give blood with reduced iron.
jaundice- accumulation of bilirubin when can’t leave via bile duct due to obstructed flow. bilirubin becomes deposited in tissues= yellow skin

Question 39

endogenous pigment accumulation

Answer 39

haemosiderosis- forms when overload of iron is deposited in haemosiderms (iron storage molecule) in many organs. happens because too much is absorbed from diet and its damaging because can’t get rid of it. when builds up in pancreas causes diabetes and in liver causes chirrosis. treatment is to remove blood and give blood with reduced iron.
jaundice- accumulation of bilirubin when can’t leave via bile duct due to obstructed flow. bilirubin becomes deposited in tissues= yellow skin

Question 40

why can germ cells keep replicating forever and other cells can’t

Answer 40

have mechanism to maintain telomere length due to enzyme telomerase. other cells can’t do this which is why they enter replicative senesce which is a point where telomere length to short to replicate. unfortunately cancer cells also have ability to replicate forever

Question 41

what is metastatic calcification

Answer 41

further away from site of dying tissue due to hypercalcaemia from calcium homeostasis disruption. hydroxyapatite crystals deposited throughout tissues in body. increased PTH means more bone resorption, can happen during renal failure or tumour. destruction of bone tissue is down to disease, imoblisition and tumours especially myeloma.

Question 42

what are the effects o chronic excessive alcohol intake on the liver

Answer 42

fatty change (retention of lipids in liver), acute alcoholic hepatitis(inflammation of liver) and finally cirrhosis ( liver does not function properly due to long-term damage. This damage is characterized by the replacement of normal liver tissue by scar tissue). progressive order of disease.