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Pathological Processes > S1L2 - Cell Injury > Flashcards

S1L2 - Cell Injury Flashcards

1
Q

How do free radicals cause cell injury

A
  • Target lipids in cell membranes, cause lipid peroxidation. Generates further lipid free radicals (autcatalytic chain reaction)
  • Oxidise proteins, carbohydrates and DNA. Molecules change shape, broken or cross linked (disulphide bonds). Mutagenic and therefore may be carcinogenic if not fixed.
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2
Q

How does irreversible cell injury occur?

A

When the changes in the environment overwhelms the adaptive response of the cell.

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3
Q

What does the degree of injury depend on?

A
  • Type of injury
  • Severity of injury
  • Duration of injury
  • Type of tissue
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4
Q

What kind of things cause cell injury?

A 
Hypoxia 
Toxins (chemical agents)
Physical agents (Trauma, extreme temperature, Changes in pressure, electrical currents)
Radiation
Microorganisms
Immune mechanisms
Dietary insufficiency or excess
Genetic abnormalities
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5
Q

How do cells react to cell injury?

A

May respond with an increased or decreased level of activity to attempt to maintain homeostasis.
This is the adaptive response. When cells reach the limit of their adaptive response, they become injured.

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6
Q

What cellular components are targets of cellular injury?

A

Cell membranes
Nucleus
Proteins
Mitochondria

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7
Q

What is the difference between hypoxia and ischaemia?

A

Hypoxia = oxygen deprivation

Ischaemia = loss of blood supply (includes lack of oxygen, substrates and nutrients)

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8
Q

Name 4 causes of hypoxia

A

1) Hypoxaemic hypoxia - oxygen concentration in arterial blood is low. Occurs at high altitudes, or due to reduced absorption of oxygen due to lung disease.
2) Anaemic hypoxia - decreased ability of haemoglobin to carry oxygen. Caused by anaemia and carbon monoxide poisoning
3) Ischaemic hypoxia - decreased blood supply. Cause by blockage of vessel, and heart failure
4) Histiotoxic hypoxia - inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes. Caused by cyanide poisoning

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9
Q

Summarise hypoxic cell injury

A
  1. Deprived of oxygen
  2. Mitochondrial ATP production through oxidative phosphorylation stops
  3. The ATP-driven membrane ionic pumps can no longer operate. (na/K ATPase)
  4. Sodium and water leak into the cell causing cell swelling and stretching the plasma membrane. K+ efflux
  5. Cell activates anaerobic glycolysis pathways.
  6. PH decreases as lactic acid is produced from glycolysis. Clumping of nuclear chromatin
  7. Calcium enters the cell as the Na+/Ca2+ pump reverses, causing cellular damage.
  8. Enzymes leak from lysosomes causing attack on cellular components
  9. Cell starts blebbing
  10. Cell death
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10
Q

Name some toxic substances

A 
Glucose and salt in hypertonic solutions
High concentration of oxygen
Poisons
Pollutants
Insecticides
Herbicides
Asbestos
Alcohol
Narcotic drugs
Medicines
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11
Q

What is ischaemia-reperfusion injury?

A

When blood flow is returned to a damaged but not yet necrosis tissue, damage sustained can be worse than if blood flow was not returned.

May occur due to increased production of oxygen free radicals with reoxygenation. Increased no. of neutrophils results in more inflammation and tissue injury. Delivery of complement proteins and activation of complement pathway.

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12
Q

How does the immune system damage body cells?

A

Hypersensitivity reactions - injury is secondary to an overly vigorous immune reaction

Autoimmune reaction - immune system fails to distinguish self from non-self.

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13
Q

What are free radicals?

A

Reactive oxygen species/reactive nitrogen species. Have a single unpaired electron in outer orbit. Unstable configuration allows free radical to react with and oxidise other molecules, producing more free radicals.

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14
Q

How are free radicals produced?

A 
Chemical injury
Radiation injury
Ischaemia-reperfusion injury
Cellular ageing  
Inflammation (immune response)
Metabolism
Air pollution
Smoking
High oxygen concentrations
Drugs and chemicals
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15
Q

Name 3 Reactive oxygen species molecules

A

OH. Hydroxyl (most dangerous)
H2O2 hydrogen peroxide
O2-. Superoxide

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16
Q

What are the body’s defence mechanisms against free radicals?

A
  1. Enzymes.
    Superperoxide dismutase/catalase
    Glutathione peroxidases
  2. Free radical scavengers.
    Neutralise free radicals by donating electrons. Vitamins A, C and E and glutathione
  3. Storage proteins that sequester transition metals. As transitional metals catalyse the formation of free radicals, proteins that sequester them (Fe2+ and Cu2+) reduce free radical formation.
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17
Q

What are heat shock proteins?

A

Protect the body against injury when submitted to stress. Are produced in the heat shock/cellular stress response. Aim to mend mis-folded proteins and maintain cell viability. Example is ubiquitin.

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18
Q

Describe the appearance of injured/dying cells under a light microscope.

A
  1. Oncosis (swelling) - due to intake of sodium and water. Watery cytoplasm.
  2. Nuclear changes
    - Pyknosis - shrinking of the nucleus due to condensation of the chromatin
    - Karyorrhexis - fragmented nucleus
    - Karyolysis - nucleus dissolves
  3. Cytoplasmic changes
  4. Abnormal intracellular accumulations.
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19
Q

What cell injury can be observed under an electron microscope? (reversible/irreversible)

A

Reversible:
Swelling (due to failure of primary active transporters), clumping of chromatin due to reduced pH (lactate), Ribosomes separating from RER as limited ATP, cytoplasmic blebbing.

Irreversible:
Increased cell swelling, nuclear changes(pyknosis, karyolysis, keryorrhexis), Rupture of lysosomes, Membrane defects, Lysis of ER, myelin figures.

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20
Q

What are the mechanisms of intracellular accumulations

A
  1. Abnormal metabolism
  2. Alterations in protein folding and transport
  3. Deficiency of critical enzymes
  4. Inability to degrade phagocytosed particles
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21
Q

What are the 5 main groups of intracellular accumulations?

A 
Water and electrolytes 
Lipids
Carbohydrates
Proteins
Pigments
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22
Q

What is Steatosis?

A

Accumulation of triglycerides. Often seen in the liver. Can be seen due to excessive alcohol intake, diabetes, obesity or toxins.

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23
Q

What occurs when cholesterol accumulates in cells?

A

Cholesterol is insoluble and cannot be broken down. Eliminated through liver. Excess cholesterol is stored in vesicles and accumulates in smooth muscle cells and in macrophages. Cholesterol forms atherosclerotic plaques and foam cells. May present as xanthomas.

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24
Q

What occurs when proteins aggregate in the cells?

A

Seen as eosinophilia droplets in cytoplasm.

  • Alcoholic liver disease - Mallory hyaline (damaged keratin filaments in the cytoplasm of hepatocytes)
  • alpha 1 antitrypsin deficiency - liver produces incorrectly folded alpha 1 antitrypsin protein, which cannot be packaged and accumulates in the ER.
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25
Q

What causes accumulation of pigment within cells?

A

Endogenous - Bruises. Deposition of haemosiderin, an iron storage molecule. Derived from haemoglobin.

Exogenous - Inhaled carbon, coal dust, soot. Urban air polluters. Inhaled and phagocytosed by alveolar macrophages. Presented as blackness on the outside of lungs on lymphatic system and on peribronchial lymph nodes. Usually harmless. Also tattoos.

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26
Q

What is hereditary haemochromatosis

A

Genetically inherited disorder.
Increased intestinal absorption of dietary iron.
Iron deposited in organs, causing liver cirrhosis and scarring of pancreas. Results in liver damage, heart dysfunction and multiple endocrine failures (esp. of pancreas).
Treat with repeated bleeding.

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27
Q

What is oncosis?

A

Cell death with swelling. Occurs in cells injured by hypoxia.

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28
Q

What is jaundice?

A

Accumulation of bilirubin (bright yellow). Breakdown product of haemoglobin. Bilirubin consists of stacks of broken porphyria rings that have lost their iron. Usually eliminated in the bile but if bile flow is obstructed bilirubin in blood rises, resulting in jaundice.

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29
Q

What is apoptosis?

A

Cell death with shrinkage. Occurs when cells enzymes degrade its own nuclear DNA and proteins.

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30
Q

What are the 2 main types, and the 2 special types of necrosis?

A

Main Types
- Coagulative and liquifactive.

Special types
-Caseous and fat necrosis

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31
Q

When can myoglobin be found in the urine?

A

Myoglobin is relaeased from striated muscle (skeletal and myocardium) when damaged.

32
Q

What is pathological calcification?

A

Abnormal deposition of calcium salts within tissues.
May be localised (dystrophic) or generalised (metastatic).
Dystrophic is more common, occurring in dying tissue, in atherosclerotic plaques, aging or damaged heart valves.

Metastatic calcification occurs secondary to disturbances in calcium metabolism. Hydroxyapatite crystals deposited in normal tissues.

33
Q

What is hypercalcaemia?

A

High blood calcium levels. Primary hypercalcaemia is due to parathyroid hyperplasia or tumour resulting in increased parathyroid hormone and therefore increased bone reabsorption. Secondary is due to renal failure and retention of phosphate. Ectopic is secretion of PTH-related protein by malignant tumours.
Destruction of bone tissue also releases calcium into blood.

34
Q

What a coagulative necrosis?

A

Protein denaturation. Denatured proteins tend to coagulate. Example is ischaemia of solid organs.
Cellular architecture is somewhat preserved with visible ghost outline of the cell.

35
Q

What is liquifactive necrosis?

A

Autolysis due to proteins undergoing dissolution by the cells own enzymes. Example is ischaemia in loose tissues; presence of many neutrophils. Occurs in the brain. Leads to enzymatic digestion of tissues

36
Q

What is necrosis?

A

The morphological changes that occur after a living organism has been dead for some time (4-24hrs). It is an appearance, not a process. Inflammation often seen.

37
Q

What is caseous necrosis?

A

Contains amorphous structureless debris. Associated with tuberculosis. No ghost outline.

38
Q

What is fat necrosis?

A

Necrosis in adipose tissue. Seen in alcoholics, often seen in pancreas.

39
Q

What is gangrene?

A

Not necrosis. Term to describe necrosis that is visible to the naked eye.

40
Q

What is infarction?

A

Refers to the cause of necrosis, namely ischaemia. Can result in gangrene.

41
Q

What is an infarct?

A

An area of ischaemic necrosis.

42
Q

What molecules are released during cell death?

A

Myoglobin
Potassium
Enzymes

Levels of these substances in the blood can be measured and help in diagnosis.

43
Q

What are the commonest causes of infarction?

A

Thrombosis - thrombus in left anterior coronary artery.

Embolism -piece of clot, foreign object, other bodily substance becomes stuck in blood vessel and obstructs blood flow.

44
Q

What occurs in apoptosis?

A

Cell death with shrinkage. Due to activation of internally controlled suicide programme where cell activate enzymes that degrade its own nuclear DNA and proteins. Normal process.
Under light microscope, appear intensely eosinophilic. DNA breakdown is non random unlike oncosis. Requires energy.
Does not induce inflammation as there is not leak of cell contents, as removed by macrophage phagocytosis.

45
Q

What is the difference between physiological and pathological apoptosis?

A

Physiological = Hormone controlled. In order to maintain a steady state.

Pathological = cytotoxic T cells kill neoplasticism or virus infected cells. Occurs when cells are damaged (esp. when its DNA)

46
Q

What are the 3 main phases of apoptosis?

A

Initiation
Execution
Degradation and phagocytosis

47
Q

What are the mechanisms that trigger apoptosis?

A

Intrinsic and extrinsic mechanisms. Both activated by caspase enzymes.

48
Q

What are caspases?

A

Enzymes that control and mediate apoptosis. Do so by causing cleavage of DNA and proteins of the cytoskeleton

49
Q

What is oncosis?

A

Cell death by swelling. Characterised by the formation of neoplasms or tumors.

50
Q

What is the difference between apoptosis and oncosis?

A

Apoptosis = programmed cell death. shrinkage and chromatin condensation. Budding. Apoptotic bodies phagocytosed by macrophages with no inflammation. Usually physiological role.

Oncosis = necrosis, swelling. Blebbing, disruption of cell membrane. Release of proteoglycan enzymes causing inflammatory reactions. Pyknosis, karyolysis and karyorrhexis. Pathological role

51
Q

What damage occurs during cellular aging?

A

Accumulate damage to cellular constituents and DNA.
Reach replication senescence after certain number of divisions. Length of telomeres shorten after each division, and eventually reach a critical length, after which the cell can no longer divide.

52
Q

What is telomerase?

A

Telomerase is produced in germ cells and stem cells. It maintains the length of the telomeres on chromosomes, effectively stopping replicative senescence. Also produced by cancer cells.

53
Q

What happens to a cell after it reaches the limits of its adaptive response?

A

Undergoes reversible injury or become irreversibly injured and die.

54
Q

How are free radicals harmful?

A

They:

  • Attack lipids in cell membranes and cause lipid peroxidation.
  • Damage proteins, carbohydrates and nucleic acids.
  • Are mutagenic
55
Q

What are foam cells?

A

type of macrophage that localize to fatty deposits on blood vessel walls, where they ingest low-density lipoproteins and become laden with lipids, giving them a foamy appearance

56
Q

What is hydropic swelling?

A

When Na+ and water flood into cells. An indicator of cellular distress.

57
Q

What is anthracosis?

A

Anthracosis the asymptomatic, milder type of pneumoconiosis as caused by the accumulation of carbon in the lungs due to repeated exposure to air pollution or inhalation of smoke or coal dust particles”

58
Q

What is rhabdomyolysis?

A

Rhabdomyolysis is when large amounts of myoglobin is released, caused by excessive exercise, burns, excessive drug abuse. Tea coloured urine. May cause renal failure as it blocks kidney tubules.

59
Q

When does necrosis occur?

A

When cell membranes are damaged and lysosomal enzymes are released into the cytoplasm and digest the cell.

60
Q

What is dystrophic calcification?

A

Calcification of necrotic tissue. Dystrophic calcification occurs in dying tissue, in atherosclerotic plaques, aging or damaged heart valves.

61
Q

What is gas gangrene?

A

Gas gangrene a type of wet gangrene where the tissue has become infected with anaerobic bacteria that produce visible and palpable bubbles of gas within the tissues.

62
Q

What is the difference between wet and dry gangrene?

A 
Wet = infection with a mixed bacterial culture. Liquifactive necrosis 
Dry = exposure to air results in drying. Coagulative necrosis
63
Q

What’s the difference between a red infarct and a white infarct?

A

Red infarct = haemorrhagic. Haemorrhage into dead tissue, dual blood supply.
White infarct = anaemic. Occurs in solid organs after the occlusion of an end artery. Coagulative necrosis.

64
Q

What are the consequences of an infarct?

A

Consequences of an infarct - none to death, depending on alternative blood supply, speed of ischaemia, tissue involved and oxygen content of the blood.

65
Q

What are apoptotic bodies?

A

Cells that have undergone apoptosis. Contain cytoplasm, organelles and often nuclear fragments. Removed by macrophage phagocytosis.

66
Q

Describe the intrinsic activation pathway of apoptosis

A

Intrinsic pathway = Initiating signals come from within the cell, usually triggered by irreparable DNA damage or withdrawal of growth factors or hormones. P53 protein is activated and the outer mitochondrial membrane becomes leaky. Cytochrome C released form the mitochondria, resulting in activation of cascades.

67
Q

Describe the extrinsic initiating pathway of apoptosis

A

Extrinsic pathway = Initiated by extracellular signals. Triggered by tumour cells or virus-infected cells. Signal secreted by T killer cells. That binds to cell membranes receptor. This activates the cascades.

68
Q

What is dystrophic calcification?

A

Calcification of dying tissue, in atherosclerotic plaques, within some neoplastic growths, in aging or damaged heart valves and in tuberculous lymph nodes.

69
Q

What is metastatic calcification?

A

Hydroxyapatite crystals are deposited in normal tissues throughout the body when there is hypercalcaemia secondary to disturbances in calcium metabolism. It is usually asymptomatic however, it can be lethal.
Symptoms can regress if hypercalcaemia is corrected

70
Q

What are the 4 mechanisms of intracellular accumulations?

A
  1. Abnormal metabolism
  2. Alterations in protein folding and transport
  3. Deficiency in critical enzymes
  4. Inability to degrade phagocytosed particles.
71
Q

What is hypercalcaemia caused by?

A

Hypercalcaemia is caused by:

  1. Increased secretion of PTH resulting in bone resorption. Primary due to parathyroid hyperplasia or tumour, secondary due to renal failure and the retention of phosphate, ectopic by secretion of PTH-related protein by malignant tumors.
  2. Destruction of bone tissue - leukaemia, immobilisation, Paget’s disease of bone
72
Q

What is replicative senescence?

A

The decline in a cells ability to replicate over time.

73
Q

What are telomeres?

A

The ends of chromosomes. They shorten after each replication and their length determines whether or not a cell can divide.

74
Q

How are apoptotic bodies targeted for phagocytosis?

A

Apoptotic bodies express proteins on their surface that allows them to by recognised by phoagocytes or neighbouring cells. These neighbouring cells or phagocytes engulf the apoptotic cell where they are then degraded.

75
Q

what is oxidative stress?

A

cellular damage by oxidation from free radicals overwhelms the antioxidant system.

76
Q

why might an infarct appear red?

A 
haemorrhage
loose tissue
dual blood supply
numerous anastomoses
prior congestion
raised venous pressure
re-perfusion
77
Q

what is haemosiderin?

A

an iron storage molecule derived from haemoglobin
gives pigment to bruises
can be deposited in many organs in systemic iron overload.

Pathological Processes (7 decks)

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