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ESA 2 SK > MoD 1&2 Cell Injury > Flashcards

MoD 1&2 Cell Injury Flashcards

0
Q

What is hypoxia?

A

Reduced O2 levels to cells/tissue

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1
Q

Name some methods of cell injury

A

Hypoxia, toxins, heat, cold, trauma, radiation, micro-organisms, immune mechanisms

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2
Q

What is is ischaemia?

A

Interruption of blood supply to cells/tissue

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3
Q

Why is injury seen quicker in ischaemia than hypoxia?

A

Because in ischaemia there is a lack of metabolic substrates as well as oxygen. E.g glucose for glycolysis

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4
Q

Distinguish between hypoxaemic, anaemic, ischaemic and histiocytic

A

Hypoxaemic- arterial content of oxygen low e.g reduced inspired pO2 at altitude
Anaemic- decreased ability of haemoglobin to carry oxygen e.g anaemia, CO poisoning
Ischaemic- interruption to blood supply e.g blocked vessel, heart failure
Histiocytic- inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes e.g cyanide poisoning

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5
Q

Name the 4 cell components that are the principal targets of cell injury

A

Cell membranes
Nucleus
Proteins- cytoskeleton and enzymes
Mitochondria

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6
Q

What % of normal concentration must ATP fall under for vital cell functions to become compromised?

A

5-10%

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7
Q

What occurs in reversible hypoxic injury?

A

Loss of activity of Na+/K+ pump so Na+ rises in cell, water enters and so cell and organelles swell. Ca2+ enters damaging cell components
Glycolytic ATP production occurs creating lactic acid, lowering cell pH which reduces enzyme activity and causes chromatin to clump.
Ribosomes detach from ER and protein synthesis disrupted causing accumulations of fat and denatured proteins

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8
Q

What does irreversible hypoxic injury usually occur as?

A

Necrosis

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9
Q

What is a key event in irreversible injury?

A

Development of profound disturbances in membrane integrity and massive cytosolic accumulation of Ca2+

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10
Q

Where does the Ca2+ come from in cell injury?

A

Enters from outside cell across damaged plasma membrane and is released from stores in organelles like the ER and mitochondria

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11
Q

What does the high intracellular calcium activate?

A

ATPases (further decreasing ATP conc), phospholipases (further damaging membrane), proteases ( membrane damage and cytoskeletal proteins) and endonucleases (damage DNA)

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12
Q

How does lysosomal membrane damage cause harm to the cell?

A

Lysosomal enzymes leak into cytoplasm and damage cell

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13
Q

How can we detect cell injury in blood samples?

A

Ca2+ entering irreversibly damaged cells allows intracellular contents to leak out across cell membrane and be detected in blood. E.g if liver cells damaged transaminases will be detected in blood

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14
Q

What is ischaemia-reperfusion injury?

A

When blood flow is returned to a tissue which has been subject to ischaemia and the tissue injury is worse than if blood flow wasn’t restored

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15
Q

What is ischaemia-reperfusion injury due to?

A

May be:
Increased production of oxygen free radicals with reoxygenation
Increased neutrophils following reinstatement of blood supply causing more inflammation and injury
Delivery of complement proteins and activation of complement pathway

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16
Q

What types of injury are free radicals particularly produced in?

A

Chemical and radiation injury, ischaemia-reperfusion injury, cellular aging, high oxygen concentrations

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17
Q

How do free radicals injure cell membranes?

A

Cause lipid peroxidation of lipids in cell membrane

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18
Q

How do free radicals cause damage within the cell?

A

Damage proteins and nucleic acids, known to be mutagenic.

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19
Q

What physiological roles do free radicals have in the body?

A

Made by leucocytes for killing bacteria and used in cell signalling

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20
Q

Which 3 free radicals are of biological significance?

A

OH. Hydroxyl- most dangerous
O2- superoxide
H2O2 hydrogen peroxide

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21
Q

How can OH. be formed?

A

Radiation directly lyses water
Fenton and Haber-Weiss reactions (note H2O2 and O2- are substrates)
Fe2+ + H2O2 -> Fe3+ + OH- + .OH
O2- + H+ + H2O2 -> O2 + H2O +.OH

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22
Q

What is oxidative stress?

A

Build up of free radicals within a cell or tissue

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23
Q

What makes up the antioxidant system?

A

Enzymes: SOD O2- ->H2O2
Catalases and peroxidases complete removal H2O2 -> O2 + H2O
Free radical scavengers that neutralise free radicals: Vit A,C,E and glutathione
In extracellular matrix storage proteins e.g transferrin and ceruplasmin sequester transition metals which catalyse free radical formation

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24
Q

What are heat shock proteins?

A

Proteins that refold misfolded proteins and make sure protein destroyed if unable to refold. Important in maintaining protein viability and so maximising cell survival

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25
Q

What three main alterations can be seen under light microscope in injured cells?

A

Cytoplasmic changes- reduced pink staining due to inc water then inc pink staining due to detaching ribosomes and accumulation of denatured proteins
Nuclear changes-subtly clumped chromatin(reversible) followed by pyknosis(shrinkage), karryohexis(fragmentation) and karryolysis(dissolution)
Abnormal intracellular accumulations

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26
Q

What reversible changes can be seen with an electron microscope?

A

Swelling of cell and organelles(Na+/K+ pump failure)
Cytoplasmic blebs
Clumped chromatin due to low pH
Ribosome detachment (failure of energy dependent attachment system)

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27
Q

What irreversible changes can be seen with electron microscope?

A

Further swelling
Nuclear changes- pyknosis, karryolysis, karryohexis
Swelling and rupture of lysosomes
Membrane defects
Myelin figures(damaged membranes)
ER lysis due to membrane defects
Amorphous densities in swollen mitochondria

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28
Q

Define oncosis

A

Spectrum of changes occurring prior to cell death

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29
Q

Define necrosis

A

Morphological changes following cell death in living tissue due to progressive degradative action of enzymes on lethally injured cell

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30
Q

Define apoptosis

A

Cell death induced by regulated intracellular program where cell activates enzymes to degrade its own nuclear DNA and proteins

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31
Q

How is necrotic tissue removed?

A

Enzymatic degradation and phagocytosis by white cells

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32
Q

What is dystrophic calcification?

A

When necrotic tissue remains and calcifies

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33
Q

What are the two main types of necrosis

A

Coagulation and liquifactive

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34
Q

What is coagulative necrosis?

A

Necrosis where protein denaturation dominates over active protease release giving dead tissue a solid consistency.
Cellular architecture preserved giving ‘ghost outline’.
This only seen in first few days as tissue incites acute inflammatory reaction

35
Q

What is liquifactive necrosis?

A

Where enzyme degradation greater than denaturation giving liquid consistency?

36
Q

Where is coagulative necrosis found?

A

Most solid organs where ischaemia is cause of death

37
Q

Where is liquifactive necrosis found?

A

Seen in massive neutrophil infiltration like abscesses as neutrophils release proteases so often in bacterial infections
Seen in brain as it’s a fragile tissue without robust collagen matrix for support.

38
Q

What is caseous necrosis?

A

Cheesy appearance macroscopically.
Amorphous (structureless) debris seen, associated with infections especially TB.
Associated with granulomatous inflammation

39
Q

What is fat necrosis?

A

Destruction of adipose tissue. Often from lipase release in acute pancreatitis, also from direct trauma to fat tissue like breast giving irregular scar which mimics nodule of breast cancer.

40
Q

What happens to the free fatty acids released in fat necrosis?

A

They react with calcium to form chalky deposits (calcium soaps) in fatty tissue that can be seen on x rays and with the naked eye in surgery and autopsy

41
Q

What is gangrene?

A

clinical term used to describe necrosis that is visible to the naked eye

42
Q

What is ‘wet’ gangrane?

A

where underlying process is liquifactive necrosis

43
Q

What is ‘dry’ gangrene?

A

Where underlying process is coagulative necrosis

44
Q

Which type of gangrene is more serious and often due to infection? What can it lead to?

A

Wet

Scepticaemia

45
Q

Where is gangrene most often seen in clinical practise?

A

Ischaemic limbs

46
Q

What is infarction?

A

An area of of tissue death caused by obstruction of tissue’s blood supply (ischaemia).

47
Q

What are most infarctions due to?

A

Thrombosis or embolism. Occasionally due to compression or twisting of vessels e.g testicular torsion or volvolus of bowel

48
Q

What type of necrosis does MI show?

A

Coagulative

49
Q

What is a white infarct and where does it occur?

A

Infarct with little haemorrhage due to occlusion of an end artery. Occurs in solid organs as solid nature of tissue prevents haemorrhage from neighbouring capillaries. e.g spleen, kidney, heart.

50
Q

What shape are white infarcts and what type of necrosis is shown?

A

Wedge shaped with occluded artery at apex. Coagulative.

51
Q

What is a red infarct?

A

red(haemorrhagic infarct) is where there is extensive haemorrhage into the dead tissue

52
Q

Where do red infarcts occur?

A

Organs with dual blood supply e.g lung (Secondary arterial supply not enough to rescue tissue)
Where numerous anastomoses present (where capillary beds of two arterial supplies combines) e.g intestines
Loose tissue with poor stromal support
Sites of previous congestion
Raised venous pressure causing reduced arterial filling pressure and engorging tissue with blood.

53
Q

The consequences of infarcts depend on:

A

Whether tissue has alternative blood supply e.g lung and forearm
How quickly ischaemia occurred (if slowly other perfusion pathways may develop)
How vulnerable tissue is to hypoxia
Oxygen content of blood (if patient anaemic more serious)

54
Q

When is apoptosis a physiological process?

A

Killing cells no longer needed to remain in a steady state, during hormone controlled involution, cytotoxic T cell killing of virus infected cell and in sculpting od digits in embryogenesis

55
Q

How do apoptotic cells appear under a light microscope?

A

Shrunken, intensely eosinophilic cells with chromatin condensation, pyknosis and nuclear fragmentation. affects single cells or small clusters

56
Q

How do apoptotic cells appear under an electron microscope?

A

Cytoplasmic blebbing seen that progresses to fragmentation into membrane bound apoptotic bodies which are removed by macrophage phagocytosis

57
Q

Why doesnt apoptosis cause inflammation?

A

There is no leakage of cell contents

58
Q

What are the three phases of apoptosis?

A

Initiation, execution and degradation/phagocytosis

59
Q

What happens in initation of apoptosis?

A

Inrinsic- damage leads to increased mitochondrial permeability releasing cytochrome c which interacts with APAF1 and caspase 9 to form an apoptosome that activates caspases.
Extrinsic- binding of external ligands like TRAIL to ‘death receptors’ activates caspases.

60
Q

What happens in degradation of apoptosis?

A

Cells break into apoptotic bodies which express molecules on surface inducing phagocytosis by neighbouring cells or phagocytes

61
Q

What are the important apoptotic molecules?

A

p53- guardian of genome, mediates in response to DNA damage
cytochrome c, APAF1, caspase 9- make up apoptosome
Bcl-2 inhibits cytochrome c release and so apoptosis
death ligands and receptors TRAIL and TRAIL-R
Caspases- effector molecules e.g caspase 3

62
Q

What can abnormal cellular accumulations consist of?

A

normal cellular constituents (water, lipids, proteins carbs)
abnormal substances e.g exogenous like minerals or endogenous like abnormal metabolism products
pigments

63
Q

What is steatosis, where is it seen and what is the cause?

A

triglyceride accumulation often seen in liver.
Liver steatosis caused by alcohol abuse, diabetes mellitus, obesity and toxins e.g carbon tetrachloride. When mild doesnt affect function

64
Q

What are foam cells and where are they found?

A

smooth muscle cells and macrophages that accumulate cholesterol and appear to have a foamy cytoplasm.
Found in atherosclerotic plaques and in skin and tendons of those with hyperlipidaemias (xanthomas)

65
Q

What is Mallory’s hyaline?

A

accumulation of damaged protein seen in hepatocytes in alcoholic liver disease due to altered keratin filaments

66
Q

What occurs in alpha1-antitrypsin deficiency?

A

misfolded alpha1-antitrypsin accumulates within the ER in liver as it cannot be packaged, or secreted. This means proteases in lung act unchecked and emphysema develops as lung tissue is broken down

67
Q

What exogenous pigments can accumulate in cells?

A

carbon/coal dust. phagocytosed by macrophages in lung and seen as blackened lung tissue or blackened peribronchial lymph nodes. Can cause pneumoconiosis.
Tattooing

68
Q

What endogenous pigments can accumulate within cells?

A

Lipofusin-brown pigment in aging cells from free radicsal damage. causes no harm
Haemosiderin- yellow/brown from excess iron. Seen in bruises, and as haemosoderosis in organs occurring in haemolytic anaemias
Bilirubin-bile pigment-yellow

69
Q

What is pathological calcification?

A

abnormal deposition of calcium salts within tissues. Either dystrophic or metastatic

70
Q

Where does dystrophic calcification occur?

A

dying tissue, atherosclerotic plaques, aging or damaged heart valves, tuberculus lymph nodes. NO abnormality in calcium metabolism or serum concentration

71
Q

Where does metastatic calcification occur?

A

Normal tissue when there is hypercalcaemia secondary to disturbances in calcium metabolism. Asymptomatic.

72
Q

What are the 4 main causes of metastatic hypercalcaemia?

A

Inc PTH secretion causing bone resorption
Destruction of bone sue to primary bone tumours e.g leukaemia, Paget’s disease, immobilisation
Vit D related disorders
Renal failure

73
Q

What is replicative senescence?

A

the decline in a cells ability to replicate as it ages due to the shortening of telomeres every time a cell divides

74
Q

What maintains telomere size in germ and stem cells?

A

Enzyme telomerase

75
Q

What pathological cells produce telomerase?

A

cancer cells

76
Q

How does metabolic tolerance to alcohol occur?

A

induction of CYP2E1 increasing ethanol metabolism (and other drugs metabolised by this system)

77
Q

How does excessive alcohol intake damage the liver?

A

Steatosis which when marked leads to hepatomegaly. (reversible and asymptomatic)
Acute alcoholic hepatitis- hepatocyte necrosis, mallory body formation, neitrophil infiltrate. Symptoms of fever, liver tenderness and jaundice (usually reversible)
Cirrhosis- occurs in 10-15% of alcoholics. Hard shrunken liver histologically appearing as micronodules of regenerating hepatocytes surrounded by bands of collageb. (irreversible, serious and sometimes fatal)

78
Q

What is depleted and what accumulates in paracetamol overdose?

A

glutathione depleted

NAPQI accumulates

79
Q

How does NAPQI damage the liver?

A

binds with sulphydryl groups on liver cell membranes causing hepatocyte necrosis and liver failure 3-5 days after large overdose

80
Q

Who has low glutathione reserves making paracetamol overdose more dangerous?

A

those who took alcohol with the paracetamol
those alcohol dependent
malnourished people
people on enzyme inducing drugs like carbamazepine
HIV positive people and those with AIDS

81
Q

What is the antidote to paracetamol overdose and how does it work?

A

N-acetylcysteine (NAC) increases the availability of hepatic glutathione

82
Q

How is it decided whether to administer NAC?

A

Take serum paracetamol conc 4 hours after overdose

83
Q

What does aspirin do?

A

stops platelet aggregation by dtopping platelet thromboxane production

84
Q

What are the consequences of aspirin overdose?

A

Stimulates respiratory centre giving respiratory alkalosis. Compensatory mechanisms then give metabolic acidosis (fall in serum pH shows srs poisoning) by intefering with carb fat and protein metabolism to give ketone bodies, lactate and pyruvate. can cause acute GI bleed.

85
Q

What are petechaie?

A

small red or purple spots caused my small capillary haemorrhage

ESA 2 SK (35 decks)

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