cell injury Flashcards

1
Q

what is reversible cell injury?

A

cells adapt to changes in environment, return to normal once stimulus is removed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is irreversible cell injury?

A

permanent, cell death is a consequence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what determines if an injury is reversible or not?

A

type,duration, severity of injury

susceptibility/adaptability of cell, nutritional status, metabolic needs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

give causes of cell injury

A
hypoxia
physical agents
chemicals/drugs
infections
immunological reactions
nutritional imbalance
genetic defects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is hypoxia?

A

deficiency of oxygen
causes:anemia/resp failure
disrupts oxidative resp processes- decreased ATP
cells can still release energy via anaerobic mechanisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is ischaemia?

A

reduction in blood supply to tissue, caused by blockage of arterial supply or venous drainage, depletion of nutrients, more severe than hypoxia- anaerobic energy release stops

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

describe physical agents

A

mechanical trauma- affects structure, cell membranes
extremets of temp affect proteins + chemical reactions
ionising radiation=DNA damage
electric shock=burn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

describe chemicals/drugs

A

simple chemicals in excess cause osmotic damage
poisons, environmental
occupational hazards cause inflammation
alcohol, smoking and recreational drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

describe immunological reactions

A

anaphylaxis
auto-immune reactions
cause damage as a result of inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

describe too little nutritional imbalance

A

scurvy, rickets, anorexia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

describe too much nutritional imbalance

A

hypervitaminosisA/D, obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

describe genetic defects

A

sickle cell anaemia
inborn error of metabolism
more subtle variations in genetic make up determine susceptibility to cell injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

describe mechanisms of reversible injury

A

aerobic resp/ATP synthesis
plasma membrane integrity
enzyme and structural protein synthesis
DNA maintenance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

describe cloudy swelling

A

cells incapable of maintaining ionic and fluid homeostasis
failure of pumps in membrane
build up of intracellular metabolites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

describe fatty change

A

accumulation of lipid vacuoles in cytoplasm caused by disruption of fatty acid metabolism so that triglycerides cannot be released from cell esp. liver
occurs with toxic and hypoxic injury
macroscopically liver enlarged and pale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is necrosis?

A
cell death usually due to pathology
irreversible
protein denaturation and lysosomal digestion of cell
inflammatory response
phagocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is pyknosis?

A

nucleus shrinks, darker staining

18
Q

what is karyorrhexis?

A

nucleus fragments

19
Q

what is karyolysis?

A

blue staining DNA in nucleus is digested by endonucleases- loss of blue = necrosis

20
Q

what are the cytoplasmic changes of necrosis?

A

appears paler, swollen, mose eosinophilic because of denaturation of cytoplasmic structural and enzyme proteins

21
Q

describe 1-coagulative necrosis

A

no proteolysis of dead cells due to denaturation of enymes
architecture of tissue preserved for days
no nucleus
cells digested by lysosomes of leukocytes
localised=infarct

22
Q

describe liquefactive necrosis

A

digestion of dead tissues so tissue in liquid viscous state
focal bacterial or fungal infections
necrotic material thick pale yellow in colour

23
Q

describe caseous necrosis

A

friable white appearance
mostly seen in TB infection
granuloma-fragmented cells and granular debris surrounded by inflammatory cells

24
Q

describe gangrenous necrosis

A

coagulative necrosis with superimposed bacterial infection- liquefactive

25
Q

describe fat necrosis

A

focal areas of fat destruction

fat cells may be liquefied by activated pancreatic enzymes

26
Q

describe fibrinoid necrosis

A

immune reactions in b.v

immune complexes are deposited in artery walls together with fibrin that leaks out of the vessels

27
Q

what are the effects of necrosis?

A

functional-depends on organ/tissue
inflammation
release of cell contents activates inflammation
cell remains phagocytosed
necrotic area replaced by scar
if remains not removed calcium salts may be deposited

28
Q

what is apoptosis?

A
genetically programmed cell death
orderly elimination of unwanted cells
required E
distinct pathways involved
no inflammation
29
Q

what are 5 pathological triggers of apoptosis?

A

hypoxia/ischaemia
viral infection
DNA damage
caspases activated by enzymes that trigger apop
cell contents degraded by enzymes activated by cell

30
Q

what are the physiological roles of apoptosis?

A

deletion of cell populations during embryogenesis
hormone change dependent involution
cell deletion in proliferating cell populations to maintain constant no. cells
deletion of inflammatory cells after an inflammatory response
deletion of self reactive lymphocytes in thymus

31
Q

describe the morphology of apoptosis

A
cell shrinkage
chromatin condensation
membrane intact
cytoplasmic blebs
break off to form apoptotic bodies
phagocytosed
32
Q

what can accumulate intracellularly?

A

excessive normal cellular constituent- water, lipid, glycogen
abnormal endogenous/exogenous material- carbon, silica, metabolites, cholesterol

33
Q

describe cholesterol accumulation

A

atherosclerosis- in macrophages and smooth muscle cells in b.v walls
found at sites of haemorrhage and necrosis

34
Q

what is amyloid?

A

fibrillar protein material deposited as a result of pathogic processes leading to increased prod. of these proteins, deposited in extracellular location in various tissues and organs

35
Q

what is pathological pigmentation?

A

build up of pigmented substances in cytoplasm

endogenous and exogenous

36
Q

what is endogenous pigmentation?

A

lipofuscin-cellular lipid breakdown products
melanin
haemosiderin-localised bruising
bilirubin

37
Q

what is exogenous pathological pigmentation?

A
carbon deposition
in macrophages in alveoli of lungs 
black pigment=anthracosis
inhaled soot/smoke
tattoos
heavy metal salts
38
Q

describe dystophic pathologic calcification

A

deposits of calcium phosphate in necrotic tissue

serum ca normal

39
Q

describe metastatic pathologic calcification

A

deposits of calcium salts in normal vital tissue with raised serum ca levels
often seen it ct of b.v
can compromise function of tissue

40
Q

what are 4 causes of raised serum calcium?

A

increased PTH eg tumous
destruction of bone tissue
excess vit. D
renal failure - causes secondary hyperparathyroidism