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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
Q

Types of Necrosis: Caseous Necrosis

A

• “Cheese like” gross appearance
• Amorphous debris surrounded by histiocytes
resulting in a granulomatous inflammation

26
Q

Types of Necrosis: Fat Necrosis

A

• 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
Q

Types of Necrosis: Fibrinoid Necrosis

A

• 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
Q

What is Infarction?

A

• Necrosis caused by inadequate blood supply to
the affected area
• Necrosis developing can be coagulative or
liquefactive

29
Q

Possible Aetiologies of Infarctions

A

• Thrombosis
• Embolism
• Twisting of Blood Supply
• External compression of vessel

30
Q

What is White Infarct?

A

• Solid organ- Robust stromal support limits
haemorrhage into necrotic area from adjacent
capillaries
• Arterial insufficiency
• End artery
• Common site: heart, spleen, kidney

31
Q

What is Red Infarct/Haemorrhagic Infarct?

A

• 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
Q

What is Gangrene?

A

It is the clinical term to describe Visible Necrosis

33
Q

What is Wet Gangrene?

A

It is necrosis modified by bacteria

34
Q

What is Dry Gangrene?

A

It is necrosis modified by air

35
Q

What is Gas Gangrene?

A

It is necrosis modified by gas forming bacteria

36
Q

Ways to Visualise Cell Injury (3)

A

Naked Eye: Gross Appearance
Light Microscope: Microscopic Features
Electron Microscope: Ultrastructural Features

37
Q

What is Apoptosis?

A

• Energy dependent programmed cell death
• Characteristic non random internucleosomal
cleavage of DNA

38
Q

How is Apoptosis different to Necrosis? (4)

A

• 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
Q

Examples of Physiological Apoptosis

A

• 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
Q

Apoptosis in Pathologic Conditions

A

• Neoplasia
• Autoimmune conditions
• AIDS - HIV proteins may activate CD4 on
uninfected T helper lymphocytes with apoptosis
leading to immunodepletion

41
Q

Regulation of Apoptosis

A

• 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
Q

How is the Mechanism of Apoptosis initiated?

A

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
Q

Mechanism is Apoptosis: Extrinsic Pathway

A

External “death receptors” (TNF receptors or Fas receptors) are activated by a ligand

44
Q

Mechanism is Apoptosis: Intrinsic Pathway

A

Withdrawal of growth factors or hormones causes molecules to be released from mitochondria (e.g. Bcl2, Bax, p53)

45
Q

What happens to the Apoptotic cell after initiation, extrinsic and intrinsic pathway occur?

A

Apoptotic cell eventually phagocytised by macrophages or histiocytes or by neighbouring cells but there is no acute inflammation

46
Q

Molecules released as a result of Cell Injury and Death: Calcium

A

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
Q

Molecules released as a result of Cell Injury and Death: Myoglobin

A

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
Q

Are Abnormal Cellular Accumulations reversible?

A

• May be reversible
• Can be harmless or fatal

48
Q

Why and When do Abnormal Cellular Accumulations occur?

A

• They occur as a result of sub-lethal or chronic
injury
• Occurs when metabolic processes are deranged

49
Q

Mechanisms (Effects) of Intracellular Accumulations (4)

A

• Abnormal metabolism
• Alterations in protein folding and transport
• Deficiency of critical enzymes
• Inability to degrade phagocytosed particles

50
Q

What are examples of Intracellular Accumulations?

A

• Water and Electrolytes/ Fluid (Vacuoles or
Hydropic Swelling )
• Lipids
• Carbohydrates
• Proteins
• Pigments (Exogenous and Endogenous)

51
Q

Examples of Endogenous Pigments (3)

A

• Haemosiderin
• Haemosiderosis
• Hereditary Haemochromatosis
• Bilirubin

52
Q

What is Dystrophic Calcification?

A

• It is a type of deposition
• Calcification occurring in degenerated or
necrotic tissue

53
Q

Metastatic Pathological Calcification

A

• Parathyroid overactivity – tumour or hyperplasia
• Vitamin D overdosage
• Malignant tumours e.g. breast and lung, bone
• Paget’s disease
• Prolonged immobilisation

54
Q

What is Cellular Ageing?

A

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
Q

Excessive Alcohol Intake

A

Mechanisms of Disease (11 decks)

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