Cell injury/death Flashcards

(110 cards)

1
Q

how can cell injury be visualised?

A

gross appearance

microscopic features

ultrastructural features

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2
Q

intercellular Ca2+ levels ….. during cell injury. Why?

A

Increase

b/c of low ATP levels, low Ca pump activity, and plasma membrane damage

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3
Q

How does cellular pH change during cell injury?

A

pH decreases

due to failure of aerobic glycolysis, ditch to anaerobic glycolysis and build up of lactic acid.

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4
Q

how does fat necrosis occur?

A

adipocytes destroyed due to trauma or release of lipases from damaged pancreatic tissues

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5
Q

intracellular Na+ ….. during cell injury. Why?

A

increase

b/c low ATP disrupts na/K pump, water build up in cell

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6
Q

How is apoptosis regulated?

A

Genes

inhibitors - growth factors, sex steroids, ECM

inducers - viruses, loss of matrix attachment

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7
Q

what condition would you see Mallory hyaline?

A

Alchohol lover diesease

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8
Q

in apoptosis cell size is ……..

A

reduced

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9
Q

in apoptosis plasma membrane is ………

A

intact

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10
Q

in necrosis cell size is ……….

A

enlarged

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11
Q

in necrosis plasma membrane is ……….

A

disrupted

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12
Q

necrosis is a …….. cause of cell death

A

pathological

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13
Q

what 2 mechanisms can lead to cell death?

A

necrosis

apoptosis

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14
Q

what are capsizes?

A

family of protease enzymes

essential role in programmed cell death

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15
Q

examples of physiological apoptosis

A

embryogenesis/fetal development

death of cells that have served purpose

hormone dependent involution - shedding of lining during menstruation

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16
Q

what are heat shock proteins?

A

family of chaperone proteins

induced during environmental, physical or chemical stress

limit damage and facilitate cellular recovery

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17
Q

example of heat shock protein?

A

ubiquitin

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18
Q

examples of apoptosis inducers?

A

growth factor withdrawal

glucocorticoids

free radicals

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19
Q

examples of apoptosis inhibitors

A

growth factors

sex steroids

viral proteins

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20
Q

examples of chemical agents and drugs that can cause cellular injury

A

Cyanide

alcohol or therapeutic drugs

O2 in high concentrations

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21
Q

examples of dietary imbalance that could cause cellular injury

A

insufficiency - anorexia, malnourished

excess - obesity or diabetes

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22
Q

What are some examples of enzymes that Ca2+ activates in irreversible injury?

A

Proteases
phospholipases
endonucleases
ATPases

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23
Q

What are some examples of immunological reactions that can cause cellular injury?

A

self antigen reaction

hypersensivity reactions

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24
Q

examples of infections that can cause cell injury

A

Worms

viruses

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25
examples of pathological apoptosis
Neoplasia Autoimmune AIDS
26
examples of physical agents that can cause cell injury
direct trauma extremes of temperature radiation electric shock
27
What are the 2 pathways for apoptosis?
Extrinsic - external death receptors activated by ligand Intrinsic - withdrawal of growth factors/hormones, molecules released form mitochondria
28
What are the 2 types of calcification?
Dystrophic Metastatic
29
What are the 3 main effects at a cellular level of reduced ATP?
Reduced activity of Na+ pumps Increased anaerobic glycolysis detachment of ribosomes
30
What are the 3 phases of apoptosis?
initiation execution degradation/phagocytosis
31
What are the 3 stages of nuclear change in irreversible injury?
Pyknosis - nuclei condensed and dense karyorrhexis- nuclei break into fragments karyolysis - nuclei dissolved
32
What are the external receptors in extrinisic apoptosis?
Fas Receptor TNF receptor
33
What are the type of necrosis?
Coagulative - protein denaturation Liquefactive - degradation of tissue by enzymes Caseous necrosis - chess like Fat necrosis Fibrinoid necrosis
34
What are the types of gangrene
wet gangrene - bacteria Dry gangrene - air Gas gangrene - gas forming bacteria
35
What are white deposits made of in fat necrosis
Fatty acids and calcium
36
What are white infarcts
Arterial insufficiency due to robust stromal support preventing haemorrahage entering necrotic area
37
what can cause a Hypoxaemic hypoxia
low arterial O2 content high altitude cardiorespiratory failure
38
What can cause an infarction
Thrombosis Embolism External compression of vessel
39
what can cause anaemic hypoxia
low O2 carrying capacity anaemia CO poisoning
40
causes of cell injury (7)
Hypoxia chemical agents and drugs Infections immunological reactions dietary imbalance genetics physical agents
41
what can cause histiocytic hypoxia
disabled oxidative phosphorylation cyanide paracetamol poisoning
42
what can cause hypoxia(4)
Hypoxaemic hypoxia anaemic hypoxia ischaemic hypoxia histiocytic hypoxia
43
What can cause ischaemic hypoxia
interruption to blood supply blocked vessel heart failure
44
What can cause metastatic calcification
Parathyroid overactivity Vitamin D overdose Maligant tumour (PTHrp) Prolonged immobilisation
45
What can occur to a cell that cannot adapt to a stress
Cell injury occurs
46
What can occur to a cell that cannot adapt to a stress
Cell injury occurs
47
What caspase do both extrinsic and intrinsic pathway for apoptosis activate
Caspase 3
48
What colour urine seen in myoglobinuria
Brown breakdown of muscle cause damage to kidneys
49
What do the consequences of infarct depend on
if tissue has alternative blood supply How quickly ischaemia occured How vulnerable tissue is to hypoxia Oxygen content of blood
50
What factors released from mitochondria in intrinsic apoptosis
Bcl2 Bax p53
51
What is apoptosis
Energy dependant programmed cell death
52
What is calcification
Abnormal deposition of calcium salts in tissues
53
What is gangrene
clinical term to describe visible necrosis
54
What is haemosiderin
iron storage complex iron released from heme stored as haemosiderin
55
What is infarction
obstruction of blood vessel to organ or region of tissue
56
What is ischaemia-Reperfusion injury
Return of blood to ischemic tissue results in production of O2 -derived free radicals, which further damage tissue.
57
What is mallory's hyaline
Damaged protein seen in hepatocytes
58
what is oncosis
Cell death with swelling which eventually leads to necrosis
59
What is Steatosis
abnormal retention of fat (lipids) within a cell or organ
60
What is the appearance in fibrinoid necrosis
Bright pink and amorphous appearance
61
What is the apperance of caseous necrosis
Cheese like appearance
62
What is the effect of detachment of ribosomes in cell injury
Decreased protein synthesis lipid deposition
63
What is the function of caspase 3
Cleave proteins leading to chromatin condensation nuclear fragmentation and blebbing occurs
64
What is the gross apperance in coagulative necrosis
Firm Pale wedge of tissue
65
What is the morphological hallmark of cell death?
Loss of the nucleus
66
What is the morphological hallmark of irreversible cellular injury?
Membrane damage
67
What is the morphological hallmark of reversible cell injury?
Cellular swelling
68
most dangerous/reactive free radical?
Hydroxyl
69
What is the only organ that does not yield coagulative necrosis following an ischaemic infarct?
Brain
70
What is the role of Bcl2?
Prevent cytochrome C release from mitochondria hence inhibits apoptosis
71
What molecules are released by cells due to cell injury and death
Potassium Enzymes myoglobin
72
What molecules can accumulate intracellularly(5)
Water lipids proteins carbohydrates pigments
73
What occurs if cell injury is severe and progressive
Irreversible injury occurs
74
What occurs to a cell when the stress applied is mild
Injury can be reversible and homeostasis can be returned
75
What pattern of necrosis is characteristic of pancreatitis-mediated damage of peripancreatic fat?
Fat necrosis
76
What pattern of necrosis is characteristically seen in Tuberculosis?
Caseous necrosis; with granulomas
77
What physiological process does hypoxia affect
Oxidative phosphorylation
78
What structural changes occur in irreversible cell injury
membrane blebbing lysosomes rupture swelling of ER and loss of ribosomes swollen mitochondria nuclear condensation myelin figures appear
79
What structural changes occur in reversible cell injury
clumping of chromatin swelling of ER and mitochondria
80
What two main processes are seen in necrosis
Denaturation of intracellular proteins Enzymatic digestion by lysosomes
81
What type of free radical is made through inflammation?
Superoxide Ions via NADPH Oxidase action Made during oxygen-dependent killing by neutrophils.
82
What type of free radicals are formed via ionising radiation?
Hydroxyl (OH) free radicals via hydrolysis of water
83
What type of free radicals are made via the Fenton Reaction?
Hydroxyl radicals via Fe2+
84
What type of tissue calcification is associated with normal serum Ca?
Dystrophic calcification Metastatic calcification occurs in normal tissue. Dystrophic calcification occurs in necrotic tissue.
85
What ultrastructural components of the cell are involved in morphological changes in cell injury?
Cell membranes nucleus proteins mitochondria
86
Where are lipofuscin granules usually seen
liver and heart
87
Where can free radicals be produced from(5)
Chemical and radiation injury ischaemia-reperfusion Cellular ageing high O2 concentration Phagocytosis
88
Where do red infarcts occur
Organs with dual blood supply Organs with loose stromal support
89
Where do red infarcts occur
Organs with dual blood supply Organs with loose stromal support
90
Where is caseous necrosis seen in
Granulomatous inflammation
91
Where is dystrophic calcification seen
necrotic tissue
92
Where is fat necrosis seen
Breast tissue where it can mimic a breast tumour Pancreas in pancreatitis where lipase released from pancreas
93
Where is fibrinoid necrosis usually seen
immune reactions with blood vessels
94
Where is liquefactive necrosis usually seen
Brain and abscess formation
95
Which enzyme functions to eliminate H2O2?
catalase
96
Which enzyme functions to eliminate Superoxide Radicals?
superoxide dismutase
97
Which enzyme functions to primarily eliminate Hydroxyl radicals (OH)?
Glutathione peroxidase
98
Which enzyme secreted by CD8+ T cells functions to create pores in the membrane of target cells
perforin
99
Which enzyme secreted by CD8+ T cells functions to enter the pores made by Perforin and activate Caspases?
granzyme
100
Which mechanism of cell death is always followed by acute inflammation?
necrosis
101
Which mechanism of cell death is associated with shrunken cells with more eosinophilic cytoplasm?
apoptosis
102
Which mechanism of cell death is not followed by acute inflammation?
apoptosis
103
Which metabolic process is the source of physiological generation of free radicals?
oxidative phosphorylation
104
Which organs are white infarcts commonly seen
heart Spleen kidney
105
Why does a cell swell in reversible injury
Reduced activity of Na pump Na accumulates in cell H2O follows Na H2O retained by cell
106
Why is necrotic material in liquefactive necrosis creamy yellow
Presence of dead leukocytes and is called pus
107
Why is rhabdomyolysis serious
Myoglobin produced as a breakdown product of muscle and causes damage to kidneys and eventually renal failure
108
........ is a protein that leaks out of the inner mitochondrial matrix when Bcl2 is inactivated.
cytochrome c then activates capsize and starts apoptosis
109
........is a cause of decreased O2 carrying capacity that classically presents with cyanosis and chocolate-coloured blood.
Methaemoglobinaemia involves oxidation of haem Fe2+ to Fe3+, which cannot bind to O2.
110
........is a phenomenon seen in fat necrosis that involves the release of fatty acids via trauma or pancreatic lipase and subsequent joining of Ca with those fatty acids.
Saponification