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S1 L2 Flashcards

1
Q

What is cell injury?

A

any disruption, physical or chemical, that results in the loss of a cell’s or tissue’s ability to maintain homeostasis

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2
Q

What do the degrees of cell injury depend on?

A

Duration of injury
Type of injury
Severity of injury
Type of tissue

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3
Q

What can cause cell injury?

A

Hypoxia
Toxins
Physical agents: direct trauma, extreme of temp, pressure changes, electrical currents
Radiation
Microorganisms
Immune mechanisms =acute and chronic inflammation, hypersensitivity, autoimmune reactions.
Dietary insufficiency and deficiencies, dietary excess
Genetic abnormalities – inborn errors of cell function, autoimmunity.

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4
Q

What is hypoxia?

A

Oxygen deprivation

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5
Q

What is ischaemia?

A

Loss of oxygen and other substrates= more rapid and severe cell injury

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6
Q

What are the causes of hypoxia?

A

Hypoaxemic
Anaemic
Ischaemic
Histiocytic

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7
Q

What is hypoxaemic hypoxia?

A

Arterial content of oxygen is low =the oxygen pressure in the blood being too low to saturate haemoglobin
Reduced inspired pO2 altitude
Reduced absorption secondary to lung disease

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8
Q

What is anaemic hypoxia?

A

Decreased ability of haemoglobin to carry oxygen

=anaemia or CO poisoning

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9
Q

What is ischaemic hypoxia?

A

Interruption of blood supply

Blockage of a vessel or heart failure

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10
Q

What is histiocytic hypoxia?

A

Inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes
E.g. cyanide poisoning

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11
Q

What things are toxic?

A 
Glucose and salt in hypertonic solutions
High conc of O2
Poisons
Pollutants
Insecticides
Herbicides
Absbetos
Alcohol
Narcotic drugs
Medicines
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12
Q

How does the immune system damage the body’s cells?

A

Hypersensitivity reactions host tissue is injured secondary to overly vigorous immune reaction
Autoimmune reactions- immune system fails to distinguish self from non-self

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13
Q

Which cell component are most susceptible to injury?

A

Cell membranes inc organellar membranes
Nucleus- DNA
Proteins- Enzymes
Mitochondria- oxidative phosphorylation

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14
Q

What happens at the molecular level in hypoxia?

A

Blood vessel is occulded
Deprives tissue of oxygen
Mitochondrial ATP production stops
Decreased ATP
NA-K pump decreases in activity= influx of Ca2+, H2O, Na, effluent of K+= cellular swelling, loss of Microvilli, bless, ER swelling
In the absence of oxygen, the cell will carry put anaerobic respiration to provide ATP.
Increase of glycolysis = increase in lactic acid = decrease in pH and glycogen = clumping of nuclear chromatin
Detachment of ribosomes- decrease protein synthesis = lipid deposition
The cell will initiate a stress (heat-shock) response to repair damage.

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15
Q

What happens in prolonged hypoxia?

A

Increased cytotoxic calcium enters the cell due to the failure of the Na+/Ca2+ exchanger and activates multiple enzymes= irreversible cell injury resulting in cell death. These enzymes and their effects:
Phospholipase- Destruction of the cell membrane
Proteases- Damage membrane proteins and the cell cytoskeleton
ATPase- Further loss of ATP
Endonucleases-Cleavage of the DNA backbone and clumping of nuclear chromatin

The cellular organelles will then begin to swell, enzymes will be released and damage other cellular components, and the damaged cell membrane begins to bleb

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16
Q

What happens after cell death?

A

release many of its intracellular molecules (such as potassium, cell specific enzymes, myoglobin) into the surrounding tissue= general toxic effects on the neighbouring cells and cause local irritation and inflammation.
Different cell types have different molecules, and so levels of these molecules in blood tests can be useful for diagnosis

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17
Q

What are free radicals?

A

Single unpaired electron in outer orbit

Unstable configuration= reaction with other molecules

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18
Q

Name three free radicals that are of biological significance in cells.

A

Hydroxyl (OH)
Superoxide (O2)
Hydrogen peroxide (H2O2)

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19
Q

How are free radicals produced?

A

Normal metabolic reactions
Inflammation: respiratory burst
Radiation
Contact with unbound metals in body: Fe in Fenton reaction and Cu
Drugs and chemicals: liver metabolism of paracetamol or carbon tetrachloride by P450 system

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20
Q

How do free radicals injure cells?

A

Causes oxidative imbalance
Target lipids in cell membrane= lipid peroxidation causing further formation of free radicals
Oxidised proteins, carbs, DNA= form cross links, bend out of shape, break, mutagentic

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21
Q

How does the body control free radicals?

A

Anti-oxidant scavengers: donate electrons to the free radical- vitamins A, C, E
Metal carrier and storage proteins (transferring, ceruloplasmin): sequester iron and copper
Enzymes neutralise free radicals: superoxide dismutase, catalase, glutathione peroxidase

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22
Q

How can cell protect itself against injury?

A

Heat shock proteins= mend misfiled proteins and maintain cell viability
Unfoldases or chaperonins

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23
Q

What does a hypoxic cell look like under a microscope?

A

Cytoplasmic changes
Nuclear changes
Abnormal cellular accumulations

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24
Q

What changes can we see in a cell undergoing reversible injury?

A 
Blebs
Generalised swelling
Clumping of nuclear chromatin
Autophagy by lysosomes
ER swelling
Dispersion of ribosomes
Mitochondrial swelling
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25
What can we see under a microscope of irreversible injury?
``` Rupture of lysosomes and autolysis Nucleus: pyknosis, karyolysis, karyorrhexis Defects in cell membrane Myelin figures ER lysis ```
26
Describe the nuclear changes seen in irreversible cell injury
Pyknosis-Irreversible condensation of chromatin and nuclear shrinkage. Karyolysis-Dissolution of the nucleus. Karryorrhexis-Destructive fragmentation of the nucleus.
27
What are abnormal cellular accumulations?
When metabolic processes become deranged Occurs with sublethal or chronic injury Can be reversible, harmless or toxic Can derive from: cell’s own metabolism, extracellular space, outer environment
28
What are the main five groups of intracellular accumulations?
``` Water and electrolytes Lipids Carbohydrates Proteins Pigments ```
29
When does fluid accumulate in the cells?
``` Hydropic swelling When energy supplies cut off Severe cellular distress Na and water flood into cell Problem in brain ```
30
When do lipids accumulate in the cell?
Steatosis- acculturation of triglycerides in liver | Asymptomatic if mild
31
What are the causes of steatosis?
Alcohol Diabetes mellitus Obesity Toxins
32
How does cholesterol accumulate in the body?
Excess sorted in cells in vesicles Accumulates in smooth muscle cells and macrophages in atherosclerotic plaques = foam cells Present in macrophages in skin and tendons of people with hereditary hyperlipidaemias=xanthomas
33
How do proteins accumulate in the cells?
Eosinophilic droplets or aggregates in the cytoplasm | Seen in alcoholic liver disease: Mallory’s hyaline (damaged keratin filaments)
34
How is protein accumulation seen in a1-antitrypsin deficiency?
Liver produces incorrectly folded a1-antitrypsin protein (a protease inhibitor) Cannot be packaged by ER, accumulates within ER and is not secreted Systemic deficiency- proteases in lung act unchecked resulting in emphysema
35
When do pigments accumulate in cells?
Carbon/coal dust/soot-urban air pollutant is inhaled and phagocytosis by alveolar macrophages Anthracosis and blackened peribronchial lymph nodes Usually harmless unless in large amounts = fibrosis and emphysema
36
How do tattoos get into skin?
Pigment pricked into skin and phagocytosed by macrophages in dermis – remains there Some pigment reaches draining lymph nodes
37
What is haemosiderin?
Iron storage molecule Derived from haemoglobin, yellow/brown Forms when there is a systemic of local excess of iron e.g. bruise With systemic overload of iron, haemosiderin is deposited in many organs = haemosiderosis Seen in haemolytic anaemias, blood transfusions and hereditary haemochromatosis
38
What is hereditary haemochromatosis?
Increased intestinal absorption of dietary iron | Iron deposited in skin, liver, pancreas, heart and endocrine organs
39
What are the symptoms of hereditary haemochromatosis?
Liver damage Heart dysfunction Multiple endocrine failures esp of pancreas
40
What is the treatment of haemochromatosis?
Repeated bleeding
41
What is accumulating in jaundice?
Accumulation of bilirubin Bile flow obstructed or overwhelmed, bilirubin in blood rises and jaundice results Deposited in tissues extra cellular lay or in macrophages
42
What happens when membranes are leaky?
Cause local inflammation General toxic effects on body May appear in high concentrations in blood and can aid in diagnosis
43
What important things leak out of a cell?
Myoglobin Enzymes Potassium
44
What happens when tissues are calcified?
Abnormal deposition of calcium salts within tissues Can be localised (dystrophic) or generalised (metastatic) Dystrophic is more common- occurs in an area of dying tissue, atherosclerotic plaques, aging or damaged heart valves, in tuberculous lymph nodes, some malignancies
45
Describe metastatic calcification
Systemic and occurs throughout the body hypercalcaemia due to abnormal calcium metabolism, resulting in hydroxyapatite crystals being deposited in tissues. Usually symptomless but, in some cases, can pose a serious risk to health
46
What are the causes of dystrophic calcification?
Local change/disturbance favours nucleation of hydroxyapatite crystals Can cause organ dysfunction e.g. atherosclerosis, calcified heart valve
47
What causes hypercalecaemia?
Increased secretion of PTH resulting in bone resorption | Destruction of bone tissue e.g. tumours, accelerated bone turnover, immobilisation
48
What is oncosis?
Cell death with swelling, characterised by ATP depletion.
49
What is necrosis?
Described the morphological changes that occur after a cell has died (this is not a process, but an appearance).
50
What are the two main types of necrosis?
Coagulative- protein denaturation e.g. ischaemia of solid organs Liquefactive (colliquitive) enzyme release e.g. ischaemia in loose tissues; presence of many neutrophils
51
What does coagulative necrosis look like?
Occurs in solid organs such as the liver Denaturation of protein dominates over release of active proteases Cellular architecture is preserved e.g ghost outline of cells
52
What does liquefactive necrosis look like?
Happens in loose and soft tissues such as the lungs and the brain Enzyme degradation is substantially greater than denaturation Leads to enzymatic digestion of tissues
53
What is caseous necrosis?
Associated with infections esp TB A form of cell death in which the tissue has a cheese-like appearance, seen under the microscope as a mix of coagulative and liquifactive states. Contains amorphous (structureless) debris
54
What is fat necrosis and what does it look like?
characterized by the action of digestive enzymes on fat released from adipocytes. In fat necrosis the enzyme lipase releases fatty acids from triglycerides. The fatty acids then complex with calcium to form soaps. These soaps appear as white chalky deposits.
55
What is gangrene?
Necrosis visible to the naked eye
56
What is infarction?
Necrosis caused by reduction in arterial blood flow | Can result in gangrene
57
What is infarct?
An area of necrotic tissue which is the result of loss of arterial blood supply- an area ischaemia necrosis
58
What is dry gangrene?
Necrosis modified by exposure to air- coagulative necrosis
59
What is wet gangrene?
Necrosis modified by infection- liquefactive necrosis
60
What is gas gangrene?
Wet gangrene where the infection is with anaerobic bacteria that produce gas
61
What are the commonest causes of infarction?
Thrombosis | Embolism
62
Why are some infarcts white?
=anaemic infarcts Occlusion of an end artery Often wedge-shaped Coagulative necrosis
63
Why are some infarcts red?
``` =haemorrhagic infarct Loose tissue Dual blood supply Numerous anastomoses Prior congestion Raised venous pressure Re-perfusion ```
64
What is the consequence of infarction?
Can range from none to death
65
What does the consequence of infarction depend on?
Alternative blood supply Speed of ischaemia Tissue involved Oxygen content of the blood
66
What is ischaemia-reperfusion injury?
If blood blow is returned to the damaged but not yet necrotic tissue, damage sustained can be worse than if blood flow hadn’t been returned
67
What are the causes of ischaemia- reperfusion?
Increased production of oxygen free radicals with reoxygenation Increased number of neutrophils resulting in more inflammation and increased tissue injury Delivery of complement proteins and activation of the complement pathway
68
What is apoptosis?
Cell death with shrinking which occurs as a normal and controlled part of the growth and development of an organism.
69
When does apoptosis occur physiologically?
In order to maintain a steady state Hormone-controlled involution Embryogenesis- stain for apoptotic cells in the developing paw of a foetal mouse
70
When does apoptosis occur pathologically?
Cytotoxic T cell killing of virus-infected or neoplasticism cells Cell DNA is damaged- non-random, internucelosomal cleavage of DNA Graft rests host disease
71
What are the three phases of apoptosis?
Initiation- triggered by intrinsic or extrinsic factors Execution- Activation of caspases which cause cleavage of DNA and proteins in the cytoskeleton. Degradation and phagocytosis- The cell shrinks and splits into small apoptotic bodies containing organelles. These are engulfed by neighbouring cells
72
How is apoptosis triggered?
Intrinsic and extrinsic mechanisms that activate caspases
73
What are caspases?
Enzymes that control and mediate apoptosis | Cause cleavage of DNA and proteins of the cytoskeleton
74
How is the intrinsic pathway initiated and carried out?
Initiating signal comes from within the cell Triggers: most commonly irreparable DNA damage, withdrawal of growth factors or hormones# P53 proteins is activated= outer mitochondrial membrane becoming leaky Cytochrome C is released from mitochondria = activation of capases
75
How is the extrinsic pathway initiated and carried out?
Initiated by extracellular signals Triggers: cells that are in danger e.g. tumour cells, virus-infected cells TNFa secreted by T killer cells= binds to cell receptor =death receptor Causes activation of capases
76
How are apoptotic bodies phagocytosed?
Both intrinsic and extrinsic pathways cause the cells to shrink and break up into apoptotic bodies Apoptotic bodies express proteins on their surface= recognised by phagocytes or neighbouring cells Degradation takes place within the phagocyte/neighbour
77
Compare apoptosis and necrosis
Apoptosis Shrinkage and chromatin condensation Budding Apoptotic bodies phagocytosed with no inflammation Necrosis Swelling Blebbing with disruption of cell membrane Release of proteolytic enzymes with important inflammatory reaction
78
Can cells live forever?
``` As cells age, they accumulate damage over time Hayflick limit (around 50 times a cell can divide). a cell can no longer replicate= replicative senescence telomeres become shorted with each cell division= once at a critical length- cell with undergo apoptosis ```

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