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Y1 - PP > Lecture 2 - Cell Injury And Cell Death > Flashcards

Lecture 2 - Cell Injury And Cell Death Flashcards

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1
Q

What are the general cell responses to injury?

A

Cell adapts to the injury
Injured cell repairs if damage is reversible
Cell dies

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2
Q

What happens when the heart becomes damaged?

A

Myocytes have to work harder
Adaptation - Cardiac myocytes hypertrophy
Ventricular hypertrophy
More O2 for bigger cells needed
Hypoxia
Myocardial infarction/arrhythmia

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3
Q

What are the 2 types of causes to cell injury?

A

Environmental
Non-environmental

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4
Q

What are some environmental causes of cell injury?

A

HYPOXIA
TOXINS
Immune mediated
Physical agents
Infection
Nutritional

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5
Q

What are some non-environmental causes of cell injury?

A

Genetics
Ageing

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6
Q

What is hypoxia?

A

Oxygen deprivation

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7
Q

What are the 4 different causes of hypoxia

A

Hypoxaemic hypoxia
Anaemic hypoxia
Ischaemic hypoxia
Histiotoxic hypoxia

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8
Q

What is Hypoxaemic hypoxia?

A

Arterial content of oxygen is low

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9
Q

What is Anaemic hypoxia??

A

Haemoglobin has a reduced ability to carry oxygen (Anaemic or CO poisoning etc…)

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10
Q

What is Ischaemic hypoxia?

A

Interruption to blood supply

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11
Q

What is Histiotoxic hypoxia?

A

Inability to utilise oxygen due to disabled oxidative phosphorylation enzymes

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12
Q

What may be a cause of Histiotoxic hypoxia?

A

Cyanide poisoning

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13
Q

How quickly are neurones affected by hypoxia?

A

Affected after a few minutes

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14
Q

What are some immune mediated cases of hypoxia and what type of reactions are they?

A

Hypersensitivity reactions (anaphylaxis in allergy)

Autoimmune reactions (Graves disease of the thyroid)

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15
Q

What are hypersensitivity reactions?

A

Excessive immune response to non self antigens causing injury

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16
Q

What is an autoimmune reaction?

A

Immune system over reacts to a self antigens causing tissue damage

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17
Q

What do most mechanisms of cell injury lead to which causes damage?

A

Lack of ATP

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18
Q

What are the 2 main mechanisms of cell injury?

A

Depletion of ATP
Oxidative stress (free radicals)

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19
Q

What are the 6 mechanisms of cell injury?

A

Depletion of ATP
Oxidative stress (free radicals)
Direct mitochondrial damage
Direct membrane damage
Disruption to calcium homeostasis
Direct damage to DNA and proteins

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20
Q

How does Hypoxia result in ATP depletion?

A

Less O2
Less oxidative phosphorylation
Less ATP synthesised by mitochondria

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21
Q

What are the 3 ways reduced ATP affects the cell?

A

Affects pH
Calcium homeostasis of cells lost (calcium influx)
Protein synthesis

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22
Q

How does reduced ATP lead to pH being affected?

A

Increased anaerobic respiration
Increased lactic acid build up

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23
Q

How does reduced ATP cause calcium influx into cells?

A

ATP sensitive Na+/K+ pumps affected
Na+ and water enter cell
Calcium also enters the cells

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24
Q

How does reduced cell ATP lead to protein synthesis being affected?

A

Ribosomes detach from ER
Reduced protein synthesis
Causes abnormal protein build up

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25
How does calcium influx cause irreversible cell damage?
Calcium activates enzymes like ATPases Phospholipases Proteases Endonucleases
26
Why is activation of phopholipases by excess calcium bad?
Breaks down membranes which can lead to cell contents leaking out
27
What is the affect of activating proteases by excess calcium?
Cleaves proteins
28
What is the affect of activating endonucleases by excess calcium?
Breaks down DNA
29
Where are Free radicals generated?
The ETC Ischaemic-repercussion injury Cellular ageing Antimicrobial killing by phagocytosis (respiratory burst)
30
What are some examples of free radicals/ROS?
Hydroxyl Superoxide O2- Hydrogen peroxide H2O2
31
What are the 3 ways which free radicals cause damage?
Lipids Proteins DNA
32
How do free radicals damage lipids?
LIPID PEROXIDATION Unsaturated fatty acids get attacked producing more free radicals causing a chain reaction Damages membranes causing calcium influx
33
How do free radicals damage proteins?
Causes cross linking (disulphide bonds) Oxidation of protein is Cleaving proteins
34
How do free radicals damage DNA?
Single or double stranded breaks
34
How do free radicals damage DNA?
Single or double stranded breaks
35
How does the body control number of free radicals?
Antioxidants Transport proteins Enzymes
36
What are some examples of antioxidants?
Vitamins C and E (Vit C regenerates reduced Vit E) GSH Abscorbic acid
37
What a re one transport proteins which help control free radicals?
Iron binds to transferrin Copper binds to ceruloplasmin
38
What is Wilsons disease?
Improper copper metabolism
39
What are some enzymes which control free radicals in the body?
Superoxide dismutase (SODs) GSH peroxidase
40
What is the function of heat shock proteins?
Help deal with free radical damage Help repair and refold damaged proteins or label them for degradation
41
What are some indications that injured cells are reversibly injured?
Swelling Clumped chromatin Ribosome dispersion Cytoplasmic blebs
42
What are some indications that cells have been damaged irreversibly?
Membrane defects Nuclear changes Lysis of ER Lysosome rupture
43
Why do cells swell?
Failure of Na/K+ pump
44
Why does chromatin clump?
Reduced pH
45
What is apoptosis?
Individual programmed cell death
46
Is apoptosis pathological or physiological?
Can be both
47
What does physiological mean?
Normal
48
What happens to the size of cells in apoptosis?
Cells shrink NO INFLAMMATION
49
What are the enzymes which induce apoptosis?
Caspases
50
What are the 2 pathways for apoptosis?
Intrinsic (mitochondrial) Extrinsic (death receptor)
51
How does intrinsic/mitochondrial apoptosis work?
Mitochondria release cytochrome C Activates caspase enzymes Caspase induces apoptosis
52
How does extrinsic/death receptor apoptosis work?
Death receptor released by T killer cells Death receptors bind to cell membrane activating caspase
53
What is the Definiton of necrosis?
The morphological changes that occur after a cell has been dead some time (12-24hrs)
54
What happens tot cell size in necrosis?
Cells swell
55
What happens to the nuclei of cells in necrosis?
Pyknosis (shrinkage) Karyorrhexis (fragmentation) Karyolysis (dissolution)
56
Is Necrosis Physiological or Pathological?
ALWAYS PATHOLOGICAL
57
What are the different types of necrosis?
Coagulative (Main type) Liquefactive (Main type) Caseous Fat necrosis Fibrinoid
58
What type of organs does coagulative necrosis affect?
Solid organs
59
What is the definition of coagulative necrosis? How does this appear histologically?
Proteins denature and coagulate Retains ghost outline of cells and tissue architecture
60
What tissue does liquefactive necrosis affect? How is architecture affected? Why does Liquefactive necrosis happen?
Loose tissue COMPLETE LOSS OF ARCHITECTURE Proteins broken down by enzymes
61
What is Caseous necrosis and what does it indicate?
Seen in LUNG Indicates TB Cheese like What type of giant cell is seen with this infection? Langhans giant cell
62
What is fat necrosis?
Direct trauma to fatty areas
63
Compare how the DNA is cleaved in apoptosis Vs Necrosis:
Apoptosis = DNA cleaved neatly between nucleosomes Necrosis = DNA randomly cleaved
64
Is there inflammation in Necrosis?
Yes None in Apoptosis
65
What are the 3 important molecules released by injured cells which can be measured in the blood?
Potassium Enzymes Myoglobin
66
Why excess potassium bad?
Cardiotoxic Too much K+ stops the heart
67
What cells relase K+? When do cells release K+?
All cells when undergoing necrosis
68
What enzymes are tested for in the liver function test? What proteins are tested for in the liver function test?
AST/ALT Aspartate Transaminase and Alanine Transaminase Bilirubin and Albumin
69
What enzymes are released into the blood following a myocardial infarction?
Troponin Troponin I and Troponin T
70
What enzymes are released into the blood in pancreatitis?
Amylase
71
When is myoglobin released into the blood?
When skeletal muscle is damaged Prolonged intense exercise
72
Why is myoglobin in the blood a problem?
Myoglobin = TOXIC TO KIDNEYS
73
What is characteristic of Rhabdomyolysis?
Dark brown tea coloured urine
74
How do falls in the elderly lead to Rhabdomyolysis getting myoglobin into the blood?
Blood flow restricted on area that’s been fallen on Ischaemic Hypoxia of skeletal muscle
75
Why do Intracellular accumulations occur in cell injury?
Struggle to remove due to deranged metabolism
76
What are the 3 types of accumulation?
Normal cel accumulations Abnormal accumulations Pigment
77
Features of abnormal cellular accumulations:
Reversible or permanent Harmful Toxic
78
Cerebral oedema is what type of accumulation?
Normal accumulation Water
79
What is cerbral oedema?
Hypoxia cell injury of neurones Less ATP ATP sensitive Na+ pump affected Na+ enters cell with water Brain swells
80
Why is cerebral oedema so dangerous?
Brain is in skull so as it swells it has no where to go
81
How does the brain get further damaged in cerebral oedema?
Brain compressed on skull Blood supply cut out (Ischaemic hypoxia) Liquefactive necrosis
82
What is an example of an abnormal cell component accumulation?
Fatty liver disease Liver cell injured Fat accumulates
83
What is Gangrene?
When necrosis is visible to the naked eye BUT its NOT a type of necrosis
84
What is an infarction?
Infarction is NOT a type of necrosis!! But it is a cause of necrosis It causes necrosis by reduction in arterial blood flow/loss of blood suppply (ischaemic hypoxia normally the cause of necrosis) Might be due to an embolism for example
85
What is Ischaemia?
Inadequate blood supply to tissue
86
What can Ischaemia cause?
Infarction Which could in turn cause gangrene
87
What are the 2 types of gangrene?
Dry and Wet
88
What is Dry gangrene?
Necrotic area exposed to air
89
What type of necrosis is dry gangrene?
Coagulative necrosis
90
What is wet gangrene?
Necrosis caused by infection
91
What type of necrosis causes wet gangrene?
Liquefactive necrosis
92
Give some examples of dry gangrene and their appearance:
Gangrenous toes Umbilical cord of new born (physiological) Leaf like appearance
93
What is gas gangrene and when does it usually happen?
Road traffic accidents (skin scrapped across dirty surface) Infected with anaerobic bacteria
94
What is a white infarct?
White in colour due to no haemorrhage
95
What is a red infarct?
Red in colour due to haemorrhage
96
Where do white infarcts usually happen?
Solid organs (spleen/kidney/heart) Tissues loose blood flow
97
Where do red infarcts usually happen?
In organs with a dual blood supply
98
How does a red infarct happen?
Haemorrhaging into dead tissues usually from capillaries
99
What is pathological calcification?
Abnormal deposition of calcium within tissues
100
What is localised (dystrophic) pathological calcification?
Calcium migrates to dead tissues Calcium metabolism s normal
101
What is generalised (metastatic calcification?
Deposition in other wise normal tissue Metabolic error causing high levels of circulating calcium
102
How does excess alcohol cause liver disease?
Ethanol = toxin Decreased NAD:NADH ratio Increased fatty acid synthesis Fat accumulates
103
What is alcoholic hepatitis?
Florid inflammation of the liver
104
What is released by hepatocytes in liver disease?
ALT and AST
105
Once liver has undergone cirrhosis, is the damage reversible?
NO IRREVERSIBLY INJURED
106
What are the complications of liver disease?
Bleeding Encephalopathy Ascites
107
What is Encephalopathy?
Confusion due to toxins accumulating which would normally be removed by the liver
108
Why does Ascites occur with liver disease?
Less protein synthesis in liver (less albumin) means plasma oncotic pressure is lower so less tissue fluid drawn back into blood

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