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Pathological Processes > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

What kind of things can cause cell injury?

A
  • Hypoxia (most important in medicine)
  • Toxins
  • Physical agents
    • extreme temperatures
    • direct trauma
    • changes in pressure
    • electric currents
  • Radiation
  • Micro-organisms
  • Immune mechanisms
  • Dietry insufficiency and deficiency e.g. obesity damages hepatocytes
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2
Q

What is hypoxia?

A

A deficiency in the amount of oxygen reaaching the tissues.

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3
Q

What is ischaemia?

A

An inadequate blood supply to an organ or part of the body.

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4
Q

What are the causes of hypoxia?

A
  • Hypoxaemic hypoxia
  • Anaemic hypoxia
  • Ischaemic hypoxia
  • Histiocytic hypoxia
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5
Q

What are the causes of ischaemia?

A

Main cause is atherosclerosis but can also be caused by a blood clot.

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6
Q

What is hypoxaemic hypoxia?

A

When the arterial content of oxygen is low. Can be caused by:

  • Reduced inspired pO2 at high altitudes
  • Reduced absorption secondary to lung disease
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7
Q

What is anaemic hypoxia?

A

The decreased ability of haemoglobin to carry oxygen. Can be caused by:

  • anaemia
  • carbon monoxide poisoning
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8
Q

What is ischaemic hypoxia?

A

Interruption of the blood supply from blockage of a vessel or heart failure.

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9
Q

What is histiocytic hypoxia?

A

Inability to utilise oxygen in cells due to lack of function in oxidative phosphorylation enzymes. This can be caused by cyanide poisoning.

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10
Q

How does hypoxia affect different cells?

A

The survival rates of cells under hypoxia are dependant upon the cell type. For example, fibroblast can survive hypoxic condition for a few hours and then return to their normal state whereas neurones can only survive for a few minutes and the damage is irreversible.

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11
Q

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

A
  1. Hypersensitivity reactions - host tissue is injured secondary to an overly vigorous immune reaction e.g. urticaria
  2. Autoimmune reaction - immune system fails to distinguish self from non-self (e.g. Graves disease)
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12
Q

What is urticaria?

A

Hives

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13
Q

Which cell components are most susceptible to injury?

A
  1. Cell membranes (both plasma and intracellular membranes)
  2. Nucleus: DNA
  3. Proteins: Structural enzymes
  4. Mitochondria: Oxidative phosphorylation

Different forms of injury attack different key structures e.g. frostbite and free radicals damage membranes primarily.

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14
Q

What happens at the molecular level in initial and prolonged hypoxia?

A
  1. Cell is deprived of oxygen.
  2. Mitochondrial ATP production stops. ATP levels have to drop to 5-10% before they affect the cell.
  3. The ATP-driven membrane ionic pumps run down.
  4. Sodium and water seep into the cell.
  5. The cell swells, and the plasma membrane is stretched.
  6. Glycolysis enables the cell to limp on for a while.
  7. The cell initiates a heat-shock (stress) response, which will probably not be able to cope if the hypoxia persists.
  8. The pH drops as cells produce energy by glycolysis and lactic acid accumulates.
  9. Calcium enters the cell.

Roughly up to this point damage is reversible.

  1. Calcium activates:
  • phospholipases, causing cell membranes to lose phospholipid
  • proteases, damaging cytoskeletal structures and attacking membrane proteins
  • ATPase, causing more loss of ATP
  • endonucleases, causing the nuclear chromatin to clump.
  1. The ER and other organelles swell.
  2. Enzymes leak out of lysosomes and these enzymes attack cytoplasmic components.
  3. All cell membranes are damaged and start to show blebbing.
  4. At some point, the cell dies, possibly killed by the burst of a bleb.
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15
Q

When does cell injury become irreversible?

A

Difficult to say but thought to be related to the influx of Ca2+

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16
Q

What are free radicals?

A

Reactive oxygen species. A single unpaired electron in the outer orbit that is unstable and highly reactive. This normally produces other free radicals and damages cells.

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17
Q

Give three examples of biological free radicals

A
  1. OH♦ (hydroxyl) - most dangerous
  2. O2- (superoxide)
  3. H2O2 (hydrogen peroxide)
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18
Q

When are free radicals produced?

A
  • In normal metabolic reactions e.g. oxidative phosphorylation
  • Inflammation: oxidative burst of neutrophils
  • Radiation (water is converted to hydroxyl)
  • Contact with unbound metals (iron and copper)
    • free radical damage occurs in haemochromatosis and Wilson’s disease
  • Drugs and chemicals
    • P450 metabolism of paracetamol and carbon tetrachloride in the liver
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19
Q

How does the body control free radicals?

A
  • Enzymes:
    • Superoxide dismutase (SOD)
    • Catalases
    • Peroxidases
  • Storage proteins that sequester transition metals in the extracellular matrix. Transferrin and ceruloplasmin sequester iron and copper, which catalyse the formation of free radicals.
  • Free radical scavengers that neutralise free radicals. Vitamins A, C and E and glutathione are free radical scavengers.
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20
Q

How do free radicals injure cells?

A

Through oxidative imbalance (free radicals overwhelming the antioxidant system). Mainly target lipids in cell membranes causing lipid peroxidation; autocatalytic reaction occurs. Proteins, carbohydrates and DNA are also oxidised and are broken, cross-linked or mutated.

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21
Q

What are heat shock proteins?

A

Proteins that try and protect the cell against injury. Examples are unfoldases or chaperonins that attempt to mend misfolded proteins and maintain cell viability. Ubiquitin is an example that is found in all cells. Present in low concentrations in unstressed cells.

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22
Q

What morphological changes occur in the cell during lethal hypoxia?

A
  • Cytoplasmic changes
    • paler due to swelling with water then darker due to clumping and coagulation of proteins
  • Nuclear changes - chromatin clumps due to lower pH
    • pyknosis
    • karyorrhexis
    • karyolysis
  • Abnormal cellular accumulations
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23
Q

What is pyknosis?

A

a thickening, especially the degeneration of a cell in which the nucleus shrinks in size and the chromatin condenses to a solid, structureless mass or masses

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24
Q

What is karyorrhexis?

A

Rupture of the cell nucleus in which the chromatin disintegrates into formless granules that are extruded from the cell.

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25
Q

What is karyolysis?

A

The dissolution of the nucleus of a cell.

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26
Q

What is the morphology of a dying (reversible injury) cell under a microscope?

A
  • Blebs in cell membrane
  • Generalised swelling
    • ER
    • Mitochondrial
  • Clumping of nuclear chromatin
  • Autophagy by lysosomes
  • Aggregation of intramembranous particles on the cell membrane
  • Dispersion of ribosomes
  • Small densities in mitochondria
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27
Q

What is the morphology of cell death (irreversible) under a microscope?

A
  • Rupture of lysosomes and then autolysis
  • Nucleus
    • pyknosis
    • karyolyisis
    • karyorrhexis
  • Defects in cell membrane
  • Myelin figures (folding on phospholipid bilayers to resemble myelin sheath - creates holes in the cell membranes)
  • Lysis of ER
  • Mitochondrial swelling and large densities
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28
Q

How can cell death be diagnosed?

A

Difficult to pinpoint when the cell actually dies yet once in the irreversible state damaged cells will take up and dye and cells that can still be saved will not which can be visualised microscopically.

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29
Q

What is oncosis?

A

Cell death with swelling, the spectrum of changes that occur in injured cells prior to death.

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30
Q

What is necrosis?

A

The morphological change within a living organism that occurs after a cell has been dead for some time (12-24 hours). Often confused with oncosis.

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31
Q

What are the two main types of necrosis?

A
  • Coagulative
  • Liquefactive (colliquitive)
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32
Q

What are two other special types of necrosis?

A
  • Caseous
  • Fat Necrosis
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33
Q

Why are there two types of necrosis?

A
  • Coagulative necrosis
    • caused by protein denaturation
    • ischaemia of solid organs (kidney, liver and heart)
  • Liquefactive necrosis
    • caused by enzyme release
    • ischaemia of loose tissues e.g. brain
    • presence of many neutrophils
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34
Q

What does coagulative necrosis look like?

A
  • Denaturation of proteins dominates over release of active proteases
  • Cellular architecture is somewhat preserved producing a ‘ghost outline’ of cells
  • Eosinophilic cells undergo karyolysis.
    • immune cells are attracted to the dead tissue to mop it up.
  • The appearance of necrosed cells depends on how long they have been dead for.
35
Q

What does liquefactive necrosis look like?

A
  • Enzyme degradation is substantially greater than denaturation
    • leads to greater enzymatic digestion (liquefaction) of tissues
  • Cellular debris remains and the presence of neutrophils

Image: Coronal section of the brain. Due to ischemia, tissue has undergone oncosis and necrosis. Swelling around the site of necrosis as neutrophils are attached to the dead tissue (inflammation of the tissue increases swelling and surrounding damage.

36
Q

What is caseous necrosis and what does it look like?

A
  • Cell death occurs centrally around an area of inflammation
  • Contains structureless debris (like coagulative necrosis)
  • Associated with infections especially tuberculosis
    • A uniformly eosinophilic center (necrosis) surrounded by a collar of lymphocytes and activated macrophages (giant cells, epithelioid cells). The entire structure formed in response to tuberculosis is known as a granuloma.
  • Macroscopically lungs appear white soft and cheesy (see image)
37
Q

What is fat necrosis and what does it look like?

A
  • pancreatic lipase activation causing hydrolysis of triglyceride in fat cells under necrotic conditions.
    • fatty acids bind with calcium to form sop crystals (saponification)
  • Occurs in breast tissue (not enzyme-mediated) due to trauma or pancreas in acute pancreatitis
  • Gross appearance is chalky yellow/white deposits in peripancreatic tissue
  • Microscopically there are pale outlines of fat cells filled with basophilic-staining calcified areas
38
Q

What does gangrene mean?

A

Necrosis visible to the naked eye/ an appearance of necrosis.

39
Q

What does infarction mean?

A

Necrosis caused by a reduction in arterial blood flow.

  • a cause of necrosis
  • can result in gangrene
40
Q

What is an infarct?

A

An area of necrotic tissue caused by a loss of arterial blood supply/ an area of ischaemic necrosis

41
Q

What is the difference between wet and dry gangrene?

A

Dry gangrene = necrosis modified by exposure to air, without any infection occurring (coagulative necrosis)

  • irreversible and tissue is lost
  • less likely to get an infection
  • occurs in the umbilical cord

Wet gangrene = necrosis modified by infection (liquefactive necrosis)

42
Q

What is gas gangrene?

A

Wet gangrene that is infected by anaerobic bacteria that produce a gas. Serious condition as wet gangrene allows bacteria to get into the blood supply. Normally found in patients who have had a motocross accident.

43
Q

What are the commonest causes of infarction?

A

Thrombosis:

  • Blood clot forming within a blood vessel

Embolism

  • Blood clot that has formed and travels in the blood supply to a separate location blocking off a blood vessel e.g the brain causing a stroke.
44
Q

What are other ways a tissue can become infarcted?

A
  1. Testicular taution
    • spermatic cord twists, blood vessels become occluded
  2. Pressure from herniation
    • tissue becomes gangrenous
  3. Twisting of the sigmoid colon
    • normally in the elderly
    • bacteria continue to produce gas; can rupture then lead to peritonitis
45
Q

What does infarcted tissue look like?

A

White or red depending on the amount of haemorrhaging there is into the infarct.

46
Q

When does infarcted tissue appear white?

A

White

  • ‘anaemic’ infarct
  • occurs in solid organs (those with good stromal support)
  • after occlusion at the end of the artery (an artery that is the sole source of arterial blood to a segment of an organ)
  • often wedge-shaped
  • coagulative necrosis
47
Q

When does infarcted tissue appear red?

A

When the infarct is haemorrhagic (extensive blood into dead tissue).

  • in loose tissue e.g. lungs
  • organs with a dual blood supply
  • numerous anastomoses
  • prior congestion
  • raised venous pressure
  • re-purfusion
48
Q

What is a congestion?

A

An abnormal or excessive accumulation of fluid.

49
Q

What are anastomoses?

A

The connection of two divergent (different directions) structures.. e.g. blood vessels or loops of intestine

50
Q

What are the consequences of infarction?

A

Depends on factors (see below) but can range from nothing to death.

Factors:

  • alternative blood supply
  • speed of ischaemia
  • tissue involved
  • oxygen content of the blood (anaemic pts are more prone to ischaemia)
51
Q

What is ischaemia-reperfusion injury?

A

If blood flow is returned to damaged but not yet necrotic tissue, damage sustained can be worse than if blood flow had not been returned.

Causes:

  • increased production of free oxygen radicals with reoxygenation
  • increased number of neutrophils, therefore, more inflammation and increased tissue injury
  • delivery of complement proteins and activation of the complement pathway
52
Q

When membranes are leaky can molecules leak out as well?

A

Yes, has local and systemic effects.

  • local inflammation
  • general toxic effects
  • high concentrations in blood and can aid diagnosis
53
Q

What can leak out of cells after membrane damage?

A
  • Potassium
    • stops heart and causes cardiac arrest
    • occurs in severe burns and tumour lysis syndrome.
    • used in surgery: heart is bathed in potassium solution to stop the heart and operate.
  • Enzymes
    • Can be used a biomarker e.g. troponin for myocardial infarction
  • Myoglobin in Rhabdomyolysis
    • leaks out of skeletal muscle when there has been severe muscle damage (trauma or strenuous exercise)
    • urine goes brown as myoglobin products damage renal tubes
54
Q

What is apoptosis?

A

cell death with shrinkage, induced by a regulated intracellular program where a cell activates enzymes that degrade it’s own nuclear DNA and proteins. Can be characterised microscopically by non-random internucleosomal cleavage of DNA.

55
Q

What are the features of apoptosis?

A
  • Requires ATP (active process)
  • Enzymes are activated that degrade nuclear DNA and proteins
  • Membrane integrity is maintained, there is no localised inflammatory response
  • Lysosomal enzymes are not involved
  • Quick process, cells are removed within hours
  • Can be pathological or physiological
56
Q

When does apoptosis occur physiologically?

A
  • Maintaining a steady state/ cell populations
  • Hormone controlled involution
    • Uterus shrinks to original size after pregnancy
    • Ovaries shrink after the menopause
  • Embryogenesis
    • removing of webbed fingers
57
Q

When does apoptosis occur pathologically?

A
  • Cytotoxic T cell killing of virus-infected or neoplastic cells
  • When cells are damaged, particularly with damaged DNA
  • Graft versus host disease (GvHD)
    • occurs after an allogeneic transplant to treat leukaemia
    • donated cells/ bone marrow attacks the hosts cells
58
Q

What does apoptosis look like?

A
  • Clumping of chromatin underneath the nuclear membrane (condensation)
  • Cell fragments and blobs into apoptotic bodies.
59
Q

How does apoptosis occur?

A

Three phases:

  1. Initiations
  2. Execution
  3. Degradation and Phagocytosis
60
Q

What is the initiation of execution of apoptosis?

A

Trigged by two mechanisms

  • intrinsic pathway (mitochondrial-mediated)
  • extrinsic pathway (death receptor-mediated)

Both lead to the activation of caspases through intial activation of caspase 8

  • capases are enzymes that control and mediate apoptosis by cleaving DNA and proteins in the cytoskeleton
61
Q

How is the intrinsic pathway carried out?

A
  • initiating signal comes from within the cell
  • triggered by:
    • irreparable DNA damage
    • withdrawal of growth factors or hormones
  • p53 protein is activated resulting in the outer mitochondrial membrane to become leaky.
  • cytochrome C is released from the mitochondria which causes the activation of caspases
62
Q

How is the extrinsic pathway initiated and carried out?

A
  • initiated by extracellular signals
  • triggers:
    • tumour cells
    • virus infected cells
  • TNF alpha is an example of a signal
    • secreted by T killer cells
    • binds to Fas receptor (death receptor)
    • results in activation of caspases
63
Q

How and why are apoptotic bodies phagocytosed?

A
  • Apoptotic bodies express proteins on their surface
    • recognised by phagocytes or neighbouring cells and are engulfed
  • Degradation takes place in another cell to prevent inflammation
64
Q

Compare the structural changes in oncosis/necrosis and apoptosis.

A
65
Q

Where do abnormal cellular accumulations come from?

A
  • Derangement of metabolic processes
  • Sublethal or chronic injury
  • Can be reversible, harmless or toxic
  • Derive from:
    • cell’s own metabolism
    • extracellular space e.g. spilled blood
    • outer environment e.g. dust
66
Q

What kind of things can accumulate in cells?

A

Five main groups:

  • water and electrolytes
  • lipids
  • carbohydrates
  • proteins
  • ‘pigments’
67
Q

When does fluid accumulate in cells?

A
  • Hydropic swelling: reversible cell swelling characterised by an influx of water and sodium chloride.
  • Occurs when energy supplies are cut off e.g. hypoxia
  • Confers severe cellular distress
  • Problematic in the brain
    • encased in the skull - limited swelling can occur before herniation of cerebellar vermis exerting pressure on the medulla which can lead to respiratory arrest.
    • gross examination: swelling causes gyri to widen and flatten and sulci to narrow
68
Q

When do lipids accumulate in cells?

A

Process is called steatosis (accumulation of triglycerides)

  • Normally seen in the liver as fat metabolism occurs here.
  • Asymptomatic if mild
  • Causes:
    • Alcohol (reversible in 10 days)
    • Diabetes mellitus
    • Obesity
    • Toxins e.g. carbon tetrachloride

Cholesterol

  • Cannot be broken down and is insoluble, only eliminated through the liver
  • Excess cholesterol is stored in vesicles
  • Accumulates in smooth muscle cells and macrophages in atherosclerotic plaques.
  • Also present in macrophages of skin and tendons of people with hereditary hyperlipidaemias
    • Lesions are called xanthomas
69
Q

What does steatosis look like?

A

Liver is enlarged and has fatty deposits. Histologically, large spaces between cells of where triglycerides were (fat is dissolved when during processing of tissues).

70
Q

What are hereditary hyperlipidaemias?

A

Inherited disorder causing elevated levels of cholesterol and triglycerides in the blood. Affects 1-2% of the population. Xanthomas (fatty lesions of cholesterol and triglycerides) can develop on the skin. mainly affecting the knees, elbows, hands and buttocks.

71
Q

In what clinical conditions do proteins accumulate in cells?

A
  • Histologically seen as eosinophilic (pink) droplets or aggregations in the cytoplasm.
  • Alcoholic liver disease
    • Mallory’s hyaline (damaged keratin filaments)
  • Alpha1-antitrypsin deficiency (A1ATD)
    • Liver produces incorrectly folded alpha1-antitrypsin protein (a protease inhibitor that calms inflammation and stops localised tissue damage)
    • A1AT cannot be packaged by ER; accumulates and is not secreted (seen histologically).
    • Systemic deficiency; proteases in lungs are uninhibitedly resulting in emphysema.
    • Emphysema and liver cirrhosis are clinical conditions of A1ATD.
72
Q

When do pigments accumulate in cells?

A

Carbon/coal dust /soot - urban air pollutant

  • Inhaled and phagocytosed by alveolar macrophages
  • Anthracosis and blackened peribronchial lymph nodes
    • “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”
  • Normally presents in the elderly
    • harmless unless in large amounts which can lead to fibrosis and emphysema (coal workers pneumoconiosis).

Tattooing

  • Pigments are phagocytosed by macrophages in the dermis and remain there. Pigment may reach draining lymph nodes.
73
Q

When do endogenous pigments accumulate?

A

Haemosiderin

  • Iron storage molecule
  • Derived from haemoglobin
  • Forms when there is a systemic or local excess of iron e.g. bruise
  • In systemic overload of iron, haemosiderin is deposited in many organs (haemosiderosis)
  • Clinical conditions haemosiderosis is seen in:
    • haemolytic anaemia
    • blood transfusion
    • hereditary haemochromatosis
74
Q

What is hereditary haemochromatosis?

A
  • Genetically inherited disorder - causes increased intestinal absorption of dietary iron.
  • Iron is deposited in skin, liver, pancreas, heart and endocrine organs.
    • associated with cirrhosis of liver and pancreas
  • Symptoms:
    • Liver damage
    • Heart dysfunction
    • Endocrine failures (especially the pancreas)
    • Diabetes (‘bronze diabetes’)
    • Bronze skin
  • Treatment is repeated bleeding.
75
Q

What accumulates in jaundice?

A
  • Accumulation of bilirubin - bright yellow
    • breakdown product of haemoglobin, stacks of broken porphyrin rings
  • Formed in all cells of the body but must be eliminated in bile
  • Albumin conjugated with bilirubin to be processed in the liver and excreted in bile
    • if bile flow is obstructed or overwhelmed bilirubin in blood rises and jaundice results.
  • Deposited in tissues extracellularly (yellow staining of sclerae) or macrophages (histologically seen as yellow deposits in cells)
76
Q

What are the mechanisms of intracellular accumulations?

A
  1. Abnormal metabolism e.g. steatosis
  2. Alterations in protein folding and transport e.g. A1AT
  3. Deficiency in critical enzymes
  4. Inability to degrade phagocytosed particles e.g. tattoo pigments
77
Q

When does calcification of tissues occur?

A
  • Abnormal deposition of calcium salts within tissues
  • Can be:
    • Dystrophic (localised)
    • Metastatic (generalised)
78
Q

What is dystrophic calcification?

A
  • Localised
  • More common than metastatic
  • Occurs in:
    • an area of dying tissue
    • atherosclerotic plaques
    • ageing or damaged heart valves
      • only valves of the left side of the heart are affected possibly due to the lower pH of blood in the right side of the heart
    • tuberculous lymph nodes
    • malignancies
  • Reduces that elasticity of blood vessels making them stiff
  • Normal serum calcium and phosphate
79
Q

Why does dystrophic calcification occur?

A

From necrosis of tissue; when the phospholipid bilayer gets damaged calcium binds to it forming calcium phosphate deposits. Can cause organ dysfunction.

80
Q

Why does metastatic calcification occur?

A
  • Hypercalcaemia secondary to disturbances in calcium metabolism
  • Hydroxyapatite crystals are deposited in normal tissues throughout the body
  • Normally asymptomatic but may be lethal
  • Able to regress if the cause of hypercalcaemia is corrected
81
Q

What causes hypercalcaemia?

A
  • Increased secretion of parathyroid hormone (PTH) resulting in bone resorption.
    • Primary = parathyroid hyperplasia or tumour
    • Secondary = due to renal failure and the retention of phosphate
    • Ectopic = secretion of PTH-related protein by malignant tumours e.g. carcinoma of the lung
  • Destruction of bone tissue
    • Primary tumours of bone marrow e.g. leukaemia, multiple myeloma
    • Diffuse skeletal metastases
    • Paget’s disease of bone - accelerated bone turnover.
    • Immobilisation
82
Q

Can cells live forever?

A
  • Cells gather damage to cellular constituents and DNA as they age
    • reach replicative senescence after a certain no. of divisions
  • Telomeres (repetitive sequence caps)
    • shorten after each replication
    • at critical length, the cell can no longer divide (ageing)
    • germ, stem and cancer cells contain telomerase which maintains telomeres at their origin length
83
Q

Describe the movement of ions and water into a cell after an infarction

A

Ca2+ and Na+ and water influx

K+ efflux

84
Q

What change seen microscopically indicates irreversible cell injury?

A

Pyknosis - shrinkage of the nucleus with clumping of chromosomes and hyperchromasia

Pathological Processes (9 decks)

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