Cell Injury Flashcards
1
Q
what does the degree of cell injury depend on
A
type of injury, severity of injury and type of tissue
2
Q
what is hypoxia
A
decreased oxygen supply
3
Q
what is ischaemia
A
decreased blood supply
4
Q
Give 4 causes of hypoxia
A
- Hypoxaemic
- Anaemic
- Ischaemic
- Histiocytic
5
Q
what is hypoxaemic hypoxia
A
when the arterial content of oxygen is low e.g from reduced oxygen in higher altitudes
6
Q
what is anaemic hypoxia
A
decreased ability of haemoglobin to carry oxygen
7
Q
what is ischaemic hypoxia
A
interruption to blood supply
8
Q
what is histiocytic hypoxia
A
inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes
9
Q
what type of hypoxia is cyanide poising an example of
A
histiocytic hypoxia
10
Q
what 2 ways does the immune system damage the bodys cells
A
- Hypersensitivity reactions
2. Autoimmune reactions
11
Q
what are hypersensitivity reactions
A
where the host tissue id injured due to an overly vigorous immune reaction
12
Q
what is an autoimmune reaction
A
where the immune system fails to distinguish self from non self
13
Q
which parts of the cell are most susceptible to injury
A
cell membranes, DNA, proteins and mitochondria
14
Q
what happens during reversible injury caused by hypoxia
A
during a lack of oxygen there will be a lack of oxidative phosphorylation in the mitochondria decreasing atp production. This means the Na,K,ATPase stops. Na, Ca and water move into the cell. Ribosomes also detach from RER reducing protein synthesis. Glycolysis will increase, decreasing the pH of the cell.
15
Q
why do you get a fatty liver in hypoxia
A
the ribosomes fall off RER, so hepatocytes cant make the proteins which metabolise fats so they accumulate in the liver cells
16
Q
what happens if hypoxia is prolonged
A
there is a massive influx of calcium which activates enzymes such as:
- ATPase - so less ATP is produced
- Proteases - breaks down cytoskeleton
- Endonucleases - DNA is degraded
17
Q
what are free radicals
A
reactive oxygen species with a single unpaired electron in their outer orbit
18
Q
what is the most dangerous type of free radical
A
hydroxyl (OH)
19
Q
what 3 free radicals are particularly significant in cells
A
hydroxyl, superoxide (O2-) and hydrogen peroxide
20
Q
how are free radicals produced (5)
A
- oxidative phosphorylation
- Inflammation (neutrophils produce free radicals in oxygen dependant phagocytosis)
- radiation
- contact with iron or copper
- drugs
21
Q
what is hemachromatosis
A
excess of iron
22
Q
what is Wilson’s disease
A
excess of copper
23
Q
how does the body control free radicals (3)
A
- vitamins A, C and E donate electrons to free radical
- metal carrier and storage proteins which bind to iron and copper
- enzymes neutralise free radicals
24
Q
which metal carrier and storage proteins bind to iron and copper
A
transferrin and ceruloplasmin
25
what enzymes neutralise free radicals
superoxide dismutase, catalase
26
how do free radicals injure cells
causes lipid peroxidation, oxidises proteins, carbohydrates and DNA causing their shape to change and breakage of cross links
27
what is lipid peroxidation
when a free radical take an electron from a lipid, causing a chain reaction generating further free radicals
28
how do cells protect against injury
heat shock proteins try to help misfolded proteins reform (chaperone proteins)
29
give an example of a heat shock protein
ubiquitin
30
what is pyknosis
when the cytoplasm of injured cells looks very pink under a microscope as the proteins denature and clump together. the nucleus shrinks and become dull
31
what is karyorrhexis
when the nucleus begins to dissolves
32
what is karyolysis
when the nucleus is fully dissolved
33
what changes can be seen in reversible injury under an electron microscope
the cell swells and forms blebs as the cytoskeleton is broken down by proteases (due to calcium). The chromatin clumps. Lysosomes start to leak content. Ribosomes detach
34
what changes can be seen in irreversible cell injury under an electron microscope
lysosomes erupt releasing digestive enzymes, holes for in the membrane, nucleus dissolves and myelin figures form
35
how do you diagnose cell death
test their function. dead cells will have holes in their membrane so by putting cells in a dye and seeing which cells take up the die will show which cells are dead
36
what is oncosis
cell death with swelling
37
what is necrosis
the morphologic changes that occur after a cell has died (12-24 hours after)
38
what are the 2 main types of necrosis
coagulative and liquefactive
39
what are the 2 specialised types of necrosis
caseous and fat necrosis
40
what causes coagulative necrosis
ischaemia of solid organs (organs with lots of CT support)
41
what causes liquefactive necrosis
ischaemia of loose organs (e.g. the brain)
42
what happens in coagulative necrosis
protein denature and clump, so cytoplasm looks more pink. Architecture of cells is preserved
43
what happens in liquefactive necrosis
enzymes are released from lysosomes causing digestion of tissues
44
what is caseous necrosis
necrosis associated with infections (TB). Cells break down and lose their architecture
45
what is fat necrosis
when enzymes (especially digestive enzymes in the pancreas) break down lipids to give fatty acids which then react with calcium to from calcium soap depositions
46
what does gangrene mean
necrosis visible to the naked eye
47
what is an infarction
necrosis caused by the reduction of arterial blood flow
48
what is an infarct
an area of necrotic tissue which is the result of loss of arterial blood supply
49
what is dry gangrene
necrosis modified by exposure to air (form of coagulative necrosis)
50
what is wet gangrene
necrosis modified by infection (form of liquefactive necrosis)
51
what is gas gangrene
where there is a bacterial infection that produces gas inside tissues anaerobically
52
what is a thrombosis
formation of a blood clot inside a blood vessel
53
what is an embolism
where part of a thrombus breaks off and blocks a blood vessel
54
why are some infarcts white
occlusion of end arteries to solid organs (coagulative necrosis) means theres no blood so the area looks white
55
why are some infarcts red
there is occlusion of a vessel in loose tissue but because of the anastomoses other vessels supply blood to this area which leaks out
56
what is ischaemia reperfusion injury
when blood flow is returned to damage tissue and results in increased production of free radicals, increased number of neutrophils (causes inflammation) and delivery of complement proteins
57
what happens if potassium leaks out of cells
can stop the heart from beating
58
when does myoglobin leak out of cells
when there''s damage to skeletal muscle. the myoglobin then blocks the glomerulus in the kidney and leaks out the in the urine
59
what is Rhabdomyolysis
break down of skeletal muscle
60
what is apoptosis
cell death with shrinkage induced by regulated intracellular signals to activate enzymes to degrade its own DNA and proteins
61
what is the characteristical DNA break down in apoptosis
DNA is cleaved inbetween nucleosomes giving similar lengths of DNA
62
true or false: apoptosis is a passive process
false - its an active process
63
what happens in apoptosis
enzymes degrade DNA and proteins. Membrane integrity is maintained, lysosomal enzymes are not involved. Budding occurs and the apoptic bodies break off
64
when does apoptosis occur physiologically
1. embryogenesis to form digits
| 2. in response to hormone levels
65
when do apoptosis occur pathologically
1. cytotoxic T cells killed infected cells
2. when cells are damaged
3. Graft versus host disease (bone marrow transplant is seen as foreign)
66
which 2 mechanism initiate apoptosis
intrinsic and extrinsic
67
what do the 2 mechanisms of initiating apoptosis result in
activation of caspases which are enzymes which cause DNA and protein cleavage
68
how is intrinsic apoptosis carried out
triggered by signals inside the cells (DNA damage or withdrawal of hormones). this activates the p53 protein making the outer mitochondrial membrane leaky. Cytochrome C is released from the mitochondria causes activation of capases
69
how is the extrinsic apoptosis carried out
trigger by extracellular signals including the TNF alpha signal which is secreted by T killer cells and binds to death receptors on the cell membrane which activates caspases
70
why are apoptotic bodies phagocytosed
they have proteins on their surface which are recognised by phagocytes
71
true of false: apoptosis is the death of groups of cells
false - this is necrosis. apoptosis is the breakdown of single cells
72
what happens to the nucleus in necrosis
it undergoes pkinosis, karyorrhexis and karyolysis
73
what happens to the nucleus in apoptosis
fragments
74
what is hydropic swelling
accumulation of fluid in cells
75
what causes hydropic swelling
energy supply is stopped so sodium and water flood into the cell causing swelling
76
what is steatosis
accumulation of triglycerides
77
where is steatosis normally seen
in the liver
78
what causes steatosis
alcohol, diabetes, obesity and toxins
79
what does steatosis look like under a microscope
white gap as the prep for the slide dissolves the fat
80
what cells does cholesterol accumulate in
smooth muscle cells and macrophages
81
what is xanthomas
accumulation of cholesterol in people with hyperlipidaemia
82
when do proteins accumulate in cells
1. alcoholic liver disease (Mallory hyaline)
2. alpha1 antitrypsin deficiency - protein is folded properly so accumulates in ER. Means that proteases aren't broken down
83
what pigments can accumulate in cells
1. soot - taken up by alveoli macrophages
| 2. tattoos - phagocytosed by macrophages in dermis and some pigment will reach lymph nodes
84
what is haemosiderin
iron storage molecule which forms when there an excess of iron.
85
what is haemosiderosis
deposition of haemosiderin in organs due to an overload of iron
86
what are the symptoms of haemochromatosis
liver damage, heart dysfunction, endocrine failure (especially pancreas)
87
what accumulates in jaundice
bilirubin (breakdown product of heme)
88
how is bilirubin excreted
taken from tissues by albumin to the liver where its conjugated and excreted in bile
89
how does bilirubin levels rise
when bile flow is obstructed
90
what is dystrophic calcification of tissues
localised depositions of calcium salts
91
what is metastatic calcification of tissues
deposition of calcium salts around the body
92
why does dystrophic calcification occur
local changes causes production of hydroxyapatite crystals
93
what causes metastatic calcification
hypercalcaemia caused by disturbances in calcium metabolism depositing hydroxyapatite crystals throughout the body
94
what causes hypercalcaemia
1, increased secretion of the Parathyroid hormone resulting in bone resorption
2. destruction of bone tissue
95
what enzyme do germ cells and stem cells contain that allow them to divide indefinitely
telomerase
