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Pathological Processes > PP 1 Cell Injury And Death > Flashcards

PP 1 Cell Injury And Death Flashcards

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1
Q

2 causes of cell injury

A

Environmental
Non environmental

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2
Q

Environment cause of cell injury

A

Hypoxia
Toxins/poisons
Immune mediated
Physical agents
Infection
Nutritional/dietary

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3
Q

Non environmental causes of cell injury

A

Genetics
Ageing

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4
Q

Hypoxia meaning

A

Oxygen deprivation

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5
Q

Causes of hypoxia

A

Hypoxaemic hypoxia
Anaemic hypoxia
Ischaemic hypoxia
Histotoxic hypoxia

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6
Q

What is hypoxaemic hypoxia?

A

Arterial content of O2 is low

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7
Q

What is anaemia hypoxia?
Example

A

Decreased ability of haemoglobin to carry oxygen
e.g. carbon monoxide poisoning

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8
Q

What is ischaemic hypoxia?

A

Interruption of blood supply

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9
Q

What is histotoxic hypoxia?

A

Inability to utilise O2 due to disabled oxidative phosphorylation enzyme

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10
Q

How long does it take for neurones to be affected by hypoxia?

A

A few minutes

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11
Q

why is CPR needed ASAP in cardiac arrest?

A

Neurones are affected by hypoxia after a few minutes
To prevent brain damage

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12
Q

How long does it take for skeletal muscle to be affected by hypoxia?

A

A few hours

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13
Q

Examples of toxins

A

Poison
Pollutant
Insecticides
Herbicides
Asbestos
Alcohol
Drugs

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14
Q

What is a hypersensitivity reaction?
Example

A

Injury secondary to excessive immune reaction to a non self antigen
E.g. anaphylaxis

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15
Q

Physical agents examples

A

Trauma
Extreme temp. - frost bite, burns
Electric currents
Radiotherapy

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16
Q

Types of microbes

A

Bacterial
Viral
Parasitic
Fungal

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17
Q

Nutritional/dietary issues which can cause cell injury

A

Obesity
Anorexia
Dietary deficiency or excesses - B12/folate/vit D/fat

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18
Q

Issues due to genetics/ageing

A

Inborn errors of metabolism
Enzyme deficiencies
Dysfunctional proteins

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19
Q

What happens in reversible cell damage?

A
  • swelling: due to Na+/K pump failure
  • cytoplasmic blebs
  • clumped chromatin: due to reduced pH
  • ribosome dispersion: lack of ATP to hold together
  • membrane remains intact
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20
Q

What happens in irreversible cell damage?

A
  • nuclear changes
  • membrane defects > causes lysis of ER
  • lysosome rupture
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21
Q

What is cell death due to?

A

Irreversible cell injury

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22
Q

Types of cell death

A

Apoptosis
Necrosis

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23
Q

Apoptosis meaning

A

Individual programmed cell death

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24
Q

Describe apoptosis

A

Single cell death
Cell shrinks
Plasma membrane preserved
Organelles contract
DNA cleaved between nucleosides
Dead cells taken up by phagocytosis

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25
Pathways of apoptosis
Intrinsic (mitochondrial) Extrinsic (death receptor)
26
Intrinsic pathway of apoptosis
Mitochondria released cytochrome C Activates caspases which induce apoptosis
27
What are caspases?
Enzymes involved in cell death
28
Extrinsic pathway of apoptosis
Death receptors attach to cell membrane which activates caspases > apoptosis
29
What are death receptors secreted by?
T killer cells
30
Describe necrosis
Grouped cell death Cell swells Plasma membrane destroyed Organelles swell and break down DNA is degraded randomly Dead cells start inflammatory process
31
Characteristic nuclear changes in necrosis
Pyknosis Karyorrhexis Karyolysis
32
What is pyknosis?
Nuclear shrinkage
33
What is karyorrhexis?
Nuclear fragmentation
34
What is karyolysis?
Nuclear dissolution
35
Main types of necrosis
Coagulative Liquefactive
36
Other types of necrosis
Caseous Fat necrosis Fibrinoid necrosis
37
What type of necrosis is often a sign of TB?
Caseous necrosis
38
Describe coagulative necrosis
Solid organs Retains ghost outline of cells Protein denaturation > release of proteases
39
Describe liquefactive necrosis
Damage of loose tissue Complete loss of architecture Tissue breakdown due to release of proteases Often in soft organs within collagenous framework *e.g.brain* or areas of many neutrophils
40
Describe fat necrosis
Direct trauma onto fatty areas Many adipocytes *e.g. Acute pancreatitis*
41
Molecules released by dead cells
Potassium Myoglobin Enzymes
42
Who have high levels of myoglobin?
Extreme sports athletes Older people after a fall Due to over worked muscles
43
What is myoglobin highly toxic to?
Kidneys
44
What does high levels of myoglobin cause?
Rhabdomyolysis
45
Sign of rhabdomyolysis
Tea coloured urine
46
What could tea coloured urine indicate?
Rhabdomyolysis
47
Gangrene meaning
Necrosis visible to naked eye
48
Infarction meaning
Necrosis cause by reduction in arterial blood flow
49
What can ischaemia cause?
Infarction
50
What can an infarction cause?
Gangrene
51
Type of gangrene
Dry Wet Gas
52
What is dry gangrene due to? What type of necrosis is seen?
Due to necrosis being exposed to air Coagulative necrosis
53
What is wet gangrene due to? What type of necrosis is seen?
Due to necrosis being exposed to infection Liquefactive necrosis
54
What is gas gangrene due to? What does it look like? Where is it commonly seen?
- Due to wet gangrene being infected by anaerobic bacteria - visible palpable bubbles of gas within tissue - Often in traffic accidents
55
Where is gas gangrene often see?
Traffic accidents
56
Complications of infarctions depend on…
- alternative blood supply? - speed of ischaemia - tissues involved - O2 content of blood
57
What is pathological calcification?
Abnormal deposition of calcium within tissues
58
Types of pathological calcification
Dystrophic/localised Metastatic/generalised
59
Where does dystrophic calcification occur?
Areas of dying tissues Atherosclerotic plaques Within neoplastic growths Ageing or damaged heart valves TB lymph nodes
60
Where does metastatic calcification occur?
Body wide Hydroxyapatite crystals deposited in normal tissues in cases of hypercalcaemia
61
Mechanisms of cell injury
- **depletion of ATP** - direct mitochondrial damage - direct membrane damage - disruption of calcium homeostasis - **oxidative stress (free radicals)** - direct damage to DNA and proteins
62
How does hypoxia cause ATP deletion?
1- cells deprived of oxygen 2- reduction in oxidative phosphorylation 3- mitochondrial ATP production stops
63
Effect of reduction in ATP
- **Anaerobic glycolysis** > decrease in cell pH > affects enzymes - **ATP needed for NA+/K+ pump** > cell swelling + Ca2+ enters cells > irreversible cell damage - **Ribosomes detach from ER** > reduce protein synthesis
64
What does a Ca2+ influx cause?
Irreversible cell damage
65
What does excess calcium activate?
ATPases Phosphilpases Proteases Endonucleases
66
What do ATPases do?
Catalyses the hydrolysis of the phosphate bond in ATP to ADP
67
What do endonucleases do?
Breakdown DNA
68
What is a free radical?
Atom with unaired electron
69
Is necrosis always only pathological, only physiological or both?
Pathological only
70
What are free radicals generated in?
Chemical/radiation injury Cellular ageing Anti-microbial killing by phagocytosis Ischaemia-reperfusion injury
71
What is the most dangerous free radical?
OH° hydroxyl
72
What do free radicals damage?
Lipid Protein DNA
73
What antioxidants help the body control free radicals?
- free radical scavengers - ascrobic acid - glutathione GSH
74
Enzymes used to control free radicals
- superoxidase dismutase SOD + catalase - glutathione peroxidase
75
How does superoxide dismutase control free radicals?
- **SOD**: 2 superoxides > 2H2O2 - **catalase**: 2H2O2 > 2H2O + O2
76
Heat shock protein function
Help repair + refold damaged proteins Label proteins for degeneration
77
Infarction meaning
Necrosis due to ischaemia
78
Describe caseous necrosis
Structureless Reduced individuality > looks like a clump Often in TB
79
What does the body have to control free radical damage?
Heat shock proteins *e.g. ubiquitin*
80
What transport proteins are used to control free radicals?
Iron binds by transferrin Calcium binds by ceruloplasmin
81
What are the most common free radicals?
Hydroxyl Superoxides Hydrogen peroxide
82
Where is Liquefactive necrosis often seen?
Often in soft organs within collagenous framework *e.g.brain* Areas of many neutrophils
83
Where does coagulative necrosis occur?
Solid organs *e.g heart, liver, kidneys, spleen*
84
Is there haemorrhage associated with white or red infarcts?
Red
85
Where do white infarcts occur? What are they due to? What shape are they often in? Is there associated haemorrhage?
- solid organs *e.g.spleen, kidney, heart* - occlusion of end artery - wedge shaped - no associated haemorrhage
86
Where do red infarcts occur? Is there associated haemorrhage?
- organs with dual blood supply *e.g. intestines, lungs* - associated with haemorrhage into dead tissue

Pathological Processes (14 decks)

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