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Mechanisms of Disease > Lecture 1.1: Cell Injury and Death > Flashcards

Lecture 1.1: Cell Injury and Death Flashcards

1
Q

What are Potential Causes of Cell Injury? (7)

A
  1. Hypoxia
  2. Chemical Agents and Drugs
  3. Infections
  4. Immune-Mediated Processes
  5. Nutritional Imbalance
  6. Genetic Derangement
  7. Physical Agents
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2
Q

Causes of Cell Injury (7)

A
  1. Hypoxia
  2. Chemical agents and drugs
  3. Infections
  4. Immune-mediated processes
  5. Nutritional imbalance
  6. Genetic derangement
  7. Physical agents
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3
Q

Types of Hypoxia: Hypoxaemic Hypoxia and why it occurs

A

Low arterial O2

Cardiorespiratory failure or in reduced inspired O2 at high altitudes

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4
Q

Types of Hypoxia: Anaemic Hypoxia and why it occurs

A

Decreased O2 carrying capacity in blood

Anaemia or CO poisoning

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5
Q

Types of Hypoxia: Ischaemic Hypoxia and why it occurs

A

Interruption to blood supply

Blocked vessel or heart failure

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6
Q

Types of Hypoxia: Histiocytic Hypoxia and why it occurs

A

Unable to use O2 due to disabled oxidative phosphorylation enzymes

Cyanide or paracetamol poisoning

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7
Q

Causes of Cell Injury: Chemical Agents and Drugs (5)

A

• Oxygen in high concentration
• Glucose and salt in hypertonic concentrations
• Trace amounts of poisons: cyanide and arsenic
• Daily exposures: Air and environmental pollutants, insecticides and asbestos
• Drugs: Recreational (alcohol) and therapeutic drugs

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8
Q

Causes of Cell Injury: Infection

A

Worms can lead viruses

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9
Q

Causes of Cell Injury: Immune-Mediated Processes

A

By reacting to endogenous self antigens (autoimmune disease)

Hypersensitivity reaction as a result of vigorous immune reaction results in host tissue damage (utricaria and hives)

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10
Q

Causes of Cell Injury: Nutritional Imbalance

A

• Dietary Insufficiency (Deprived Populations,
Anorexia Nervosa)
• Dietary Excess (Obesity, Diabetes,
Atherosclerosis, Cancer)

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11
Q

Causes of Cell Injury: Genetic Derangements

A

• Genetic Abnormalities
• Inborn Errors of Metabolism

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12
Q

Causes of Cell Injury: Physical Agents

A

• Mechanical trauma
• Extremes of temperature (Burns and Deep Cold)
• Sudden change in atmospheric pressure
• Radiation
• Electric shock

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13
Q

What can Irreversible Cell Injury lead to?

A

• Necrosis
• Apoptosis

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14
Q

Nuclear Changes that occur when Irreversible Cell Injury occur

A

Live Cells: Nuclei are normal morphology
Pyknosis: Nuclei are condensing & dense
Karyorrhexis: Nuclei break up into fragments
Karyolysis: Nuclei are dissolved

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15
Q

Which Free Radicals have Particular Biological Significance?

A

• OH• (hydroxyl ions) -the most dangerous
• O2- (superoxide anion radical)
• H2O2 (hydrogen peroxide)
• Reactive oxygen species (ROS)
• Nitric oxide (NO) made by microphages,
endothelia, and neurones

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16
Q

How does Free Radical Production occur?

A

• Chemical and Radiation Injury
• Ischaemia: Reperfusion Injury
• Cellular Ageing
• High Oxygen Concentrations
• Killing of Pathogens by Phagocytes (ROS)

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17
Q

What do Free Radicals cause increased production of?

A

• Activated leucocytes in response to toxins or
infectious agents
• UV Light
• Ionizing radiation
• Pollutants

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18
Q

What is the role of Heat Shock Proteins (HSP)?

A

• In cell injury, the heat shock response aims to
‘mend’ mis-folded proteins and maintain cell
viability
• Many HSP’s are Chaperonins
• Provide optimal conditions for denatured protein
folding, preventing protein aggregation and also
label misfolded proteins for degradation
• Increase HSP expression and can protect cells
against subsequent, otherwise lethal, insults

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19
Q

What is an example of a Heat Shock Proteins (HSP)?

A

Ubiquitin

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20
Q

What are the two main processes seen in Necrosis?

A
  1. Denaturation of intracellular proteins
  2. Enzymatic digestion by lysosomes inherent to
    the dying cell and lysosomes of leukocytes that
    are part of inflammatory reaction
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21
Q

How long does it take for the earliest (microscopic) effects of necrosis to become apparent?

A

4 to 12 hours

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22
Q

Types of Necrosis (5)

A
  1. Coagulative Necrosis
  2. Liquefactive Necrosis
  3. Caseous Necrosis
  4. Fat Necrosis
  5. Fibrinoid Necrosis
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23
Q

Types of Necrosis: Coagulative Necrosis

A

• Commonest form
• Occurs in most organs
• A result of protein denaturation
• Gross: Firm, pale wedge of tissue, can be soft
later on
• Microscopy: “ Ghost Cells”

24
Q

Types of Necrosis: Liquefactive Necrosis

A

• Usually seen in brain
• Seen in infections resulting in abscess formation
• Degradation of tissue by enzymes
• The necrotic material is frequently creamy
yellow because of the presence of dead
leukocytes and is called pus (neutrophils)

25
Types of Necrosis: Caseous Necrosis
• “Cheese like” gross appearance • Amorphous debris surrounded by histiocytes resulting in a granulomatous inflammation
26
Types of Necrosis: Fat Necrosis
• Destruction to adipocytes as a consequence of trauma or secondary to release of lipases from damaged pancreatic tissue • Fat necrosis causes fatty acids which react with calcium to form white deposits in fatty tissue • Seen in breast tissue and can mimic breast tumour on radiology and is biopsied to exclude cancer
27
Types of Necrosis: Fibrinoid Necrosis
• Usually seen in immune reactions involving blood vessels • Deposits of “immune complexes,” with fibrin that has leaked out of vessels • Bright pink and amorphous appearance in H&E stains • These are called “fibrinoid” (fibrin-like) by pathologists
28
What is Infarction?
• Necrosis caused by inadequate blood supply to the affected area • Necrosis developing can be coagulative or liquefactive
29
Possible Aetiologies of Infarctions
• Thrombosis • Embolism • Twisting of Blood Supply • External compression of vessel
30
What is White Infarct?
• Solid organ- Robust stromal support limits haemorrhage into necrotic area from adjacent capillaries • Arterial insufficiency • End artery • Common site: heart, spleen, kidney
31
What is Red Infarct/Haemorrhagic Infarct?
• Organs with dual blood supply and those with numerous anastamoses between capillary beds • Organs that have loose stromal support • Raised venous pressure leading to increased capillary pressure and tissue pressure resulting in arterial insufficiency
32
What is Gangrene?
It is the clinical term to describe Visible Necrosis
33
What is Wet Gangrene?
It is necrosis modified by bacteria
34
What is Dry Gangrene?
It is necrosis modified by air
35
What is Gas Gangrene?
It is necrosis modified by gas forming bacteria
36
Ways to Visualise Cell Injury (3)
Naked Eye: Gross Appearance Light Microscope: Microscopic Features Electron Microscope: Ultrastructural Features
37
What is Apoptosis?
• Energy dependent programmed cell death • Characteristic non random internucleosomal cleavage of DNA
38
How is Apoptosis different to Necrosis? (4)
• Apoptosis does not result in an inflammatory response • Apoptosis is singluar cells whilst necrosis is contiguous groups of cells • Cells enlarged (swelling) in necrosis but reduced (shrinkage) in apoptosis • Necrosis always pathological, apoptosis often physiological
39
Examples of Physiological Apoptosis
• Embryogenesis and foetal development (loss of webbing as hand develops) • Hormone dependent involution (shedding of endometrium at menstruation) • Cell deletion in proliferating cell populations (regulation of immune system or intestinal crypts) • Death of cells that have served their function (neutrophils and lymphocytes)
40
Apoptosis in Pathologic Conditions
• Neoplasia • Autoimmune conditions • AIDS - HIV proteins may activate CD4 on uninfected T helper lymphocytes with apoptosis leading to immunodepletion
41
Regulation of Apoptosis
• Apoptosis is regulated by many genes • Inhibitors (growth factors, extracellular cell matrix , sex steroids, viral proteins) • Inducers (growth factor withdrawal, loss of extracellular matrix attachment, glucocorticoids, viruses, free radicals, ionising radiation)
42
How is the Mechanism of Apoptosis initiated?
Activation of a cascade of caspases (cysteine-dependent aspartate-directed proteases) Two pathways both resulting in activated caspase 3 which cleave proteins causing chromatin condensation, nuclear fragmentation and blebbing
43
Mechanism is Apoptosis: Extrinsic Pathway
External “death receptors” (TNF receptors or Fas receptors) are activated by a ligand
44
Mechanism is Apoptosis: Intrinsic Pathway
Withdrawal of growth factors or hormones causes molecules to be released from mitochondria (e.g. Bcl2, Bax, p53)
45
What happens to the Apoptotic cell after initiation, extrinsic and intrinsic pathway occur?
Apoptotic cell eventually phagocytised by macrophages or histiocytes or by neighbouring cells but there is no acute inflammation
46
Molecules released as a result of Cell Injury and Death: Calcium
As calcium enters damaged membranes, other molecules leak out: • Can cause local inflammation • May have general toxic effects on body • May appear in high concentrations in blood and can aid in diagnosis
47
Molecules released as a result of Cell Injury and Death: Myoglobin
Rhabdomyolysis can be serious with myoglobin as a breakdown product of muscle causing damage to the kidneys and even renal failure requiring dialysis Typical brown urine in myoglobinuria
48
Are Abnormal Cellular Accumulations reversible?
• May be reversible • Can be harmless or fatal
48
Why and When do Abnormal Cellular Accumulations occur?
• They occur as a result of sub-lethal or chronic injury • Occurs when metabolic processes are deranged
49
Mechanisms (Effects) of Intracellular Accumulations (4)
• Abnormal metabolism • Alterations in protein folding and transport • Deficiency of critical enzymes • Inability to degrade phagocytosed particles
50
What are examples of Intracellular Accumulations?
• Water and Electrolytes/ Fluid (Vacuoles or Hydropic Swelling ) • Lipids • Carbohydrates • Proteins • Pigments (Exogenous and Endogenous)
51
Examples of Endogenous Pigments (3)
• Haemosiderin • Haemosiderosis • Hereditary Haemochromatosis • Bilirubin
52
What is Dystrophic Calcification?
• It is a type of deposition • Calcification occurring in degenerated or necrotic tissue
53
Metastatic Pathological Calcification
• Parathyroid overactivity – tumour or hyperplasia • Vitamin D overdosage • Malignant tumours e.g. breast and lung, bone • Paget’s disease • Prolonged immobilisation
54
What is Cellular Ageing?
It is the progressive decline in the resistance to stress and other cellular damages, causing a gradual loss of cellular functions and resulting eventually in cell death
55
Excessive Alcohol Intake

Mechanisms of Disease (11 decks)

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