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BDS2 PMI > PMI03-2009 > Flashcards

PMI03-2009 Flashcards

1
Q

What affects a cell’s response to injury?

A

Type, duration and severity of stimulus

Cell type, status, capability, genetic makeup

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2
Q

What are the two ways in which a cell can respond to injury?

A

Adaptation

Death

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3
Q

What is a labile cell? Give an example.

A

Continually cycling/replicating

Keratinocytes

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4
Q

What is a stable cell? Give an example.

A

Cell that has temporarily exited the cell cycle (G0), “quiescent”

Liver cells

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5
Q

What is a permanent cell? Give an example.

A

Terminally differentiated cell

Neurons/heart cells/RBCs/skeletal muscle cells

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6
Q

What type of cell is likely to be more inclined to adapt to injury/stimuli?

A

Labile cell

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7
Q

What type of cell is likely to be more inclined to die in response to injury/stimuli?

A

Permanent cell

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8
Q

What is hyperplasia?

A

Increase in the number of cells within a tissue or organ without an associated increase in size of cells

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9
Q

When does hyperplasia occur in response to a stimulus?

A

When cells are able to divide (labile and stable cells)

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10
Q

Give a physiological example of hyperplasia in response to a stimulus.

A

Hyperplasia of glandular tissue in female breast during puberty (hormonal)

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11
Q

Give a pathological example of hyperplasia in response to a stimulus.

A

Hyperplasia of prostate during hormonal imbalance

Chronic hyperplastic candidiasis (fungal infection)

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12
Q

What is hypertrophy?

A

Increase in size of cells without increasing in number

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13
Q

When does hypertrophy occur in response to a stimulus?

A

When cells are not able to divide (permanent cells)

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14
Q

Give a physiological example of hypertrophy in response to a stimulus.

A

Increase in muscle bulk following exercise

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15
Q

Give a pathological example of hypertrophy in response to a stimulus.

A

Left cardiac ventricle hypertrophy in heart failure (hypertension increases load)

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16
Q

Why are hyperplasia and hypertrophy often seen together?

A

They are responses to similar stimuli

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17
Q

What is atrophy?

A

Reduction in the size of an organ as a result of a reduction in the size and number of cells

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18
Q

Give a physiological example of atrophy in response to a stimulus.

A

Changes in vaginal epithelium due to menopause (hormonal)

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19
Q

Give a pathological example of atrophy in response to a stimulus.

A

Atrophic buccal epithelium in Lichen Planus (lymphoid infiltration)

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20
Q

What may cause atrophy?

A

Mutations

Poor nourishment

Loss of hormonal support

Loss of nerve supply to organ

Lack of organ/muscle use

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21
Q

What is metaplasia?

A

Change from one differentiated cell type to another

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22
Q

Why does metaplasia occur?

A

To better equip the affected area against the insult

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23
Q

Give an example of metaplasia relating to the oral cavity.

A

Squamous metaplasia of glandular epithelium

Trauma causes metaplasia of duct cells of minor salivary glands (cuboidal to squamous)

24
Q

What is dysplasia?

A

Disordered stratification and disordered maturation

25
Q

What causes dysplasia?

A

Persistent noxious agents (eg carcinogens)

26
Q

What can metaplasia progress to after sufficient length and exposure of a stimulus?

A

Dysplasia

27
Q

What is reversible injury?

A

Cell changes that can be restored to normalcy with removal of stimulus

28
Q

What is irreversible injury?

A

Stressors exceed the capacity of the cell to adapt

Permanent changes lead to cell death

29
Q

What are the possible causative agents of cell adaptation or death?

A

Physical = trauma, thermal, radiation

Chemical = carbon monoxide, cigarette smoke, ethanol

Infectious = toxins, metabolic products, lysis, DNA damage, viruses

Oxygen deprivation = hypoxia, ischaemia, anaemia

Immunologic = complement activation, cell-mediated cytotoxicity, autoimmunity, hypersensitivity

Genetic abnormality

Nutritional deficiency

30
Q

What are the possible mechanisms of cell injury?

A

Disruption of metabolism

  • ATP depletion
  • mitochondrial damage

Nutrient/growth factor deprivation

Free radical/ROS formation

DNA damage by ROS

Membrane disruption

Inflammatory cell action

31
Q

What stimuli may cause ROS formation?

A

Ionising radiation

Inflammation

Some drugs and metals

32
Q

What can ROS damage in a cell?

A

Membranes

DNA

Other molecules in metabolic pathways

33
Q

What are the two types of cell death?

A

Apoptosis

Necrosis

34
Q

What are the five types of cell adaptation?

A

Hyperplasia

Hypertrophy

Atrophy

Metaplasia

Dysplasia

35
Q

Describe necrosis.

A

Membrane damage is irreparable and leads to swelling

Pathological and not energy-dependent

Initial increased eosinophilia due to degradation of cytoplasmic RNA

Later loss of nuclear definition (karyolysis) as it loses its basophilia

Bursting of cell elicits an inflammatory response

36
Q

What are the steps leading up to karyolysis?

A

Pyknosis = condensation of nucleus so it appears darker

Karyorrhexis = fragmentation

Karyolysis

37
Q

What are the different types of necrosis?

A

Coagulative

Liquefactive

Caseous

Fat

Gangrene

Fibrinoid

38
Q

What is coagulative necrosis?

A

Most common form of necrosis

Structural pattern of necrotic tissue is maintained

Commonly caused by ischaemia and infarction

39
Q

What is a common cause of coagulative necrosis?

A

Ischaemia and infarction

40
Q

Give an example of where you might see coagulative necrosis?

A

Renal cortex - tubular structure remains

41
Q

What is liquefactive necrosis?

A

Changes in organ results in a collection of liquid, viscous material and no cell outlines visible

Common with CNS tissue necrosis

Formation of pus on infection

42
Q

What is caseous necrosis?

A

Necrotic tissue resembles soft cheese microscopically - soft, white, proteinaceous dead cell mass

Typical for certain types of granulomatous inflammation, esp TB

43
Q

What disease typically displays caseous necrosis?

A

Tuberculosis

44
Q

What is fat necrosis?

A

Action of lipases on fatty tissues produces grossly visible, chalky white areas

Seen in breast, omentum and pancreatitis

45
Q

What is gangrenous necrosis?

A

Necrosis of an appendage usually due to ischaemia

Green-black = due to breakdown of Hb

Coagulative or liquefactive necrosis can occur depending on secondary infection

46
Q

What is fibrinoid necrosis?

A

Connective tissues and arterial walls are infiltrated by strongly eosinophilic hyaline material that shows characteristics of fibrin

47
Q

Describe apoptosis.

A

Regulated and targeted programmed cell death

Energy-dependent

Can be physiological or pathological

Cell shrinkage and does not elicit inflammatory response

48
Q

What may trigger apoptosis?

A

DNA damage

Protein misfolding

Viral infection

49
Q

What are the two pathways of apoptosis?

A

Extrinsic/death receptor-mediated pathway

Intrinsic/mitochondrial-dependent pathway

50
Q

Describe the extrinsic/death receptor-mediated pathway.

A

Death/Fas ligand binds death/Fas receptor

Activates cascade of initiator caspases which will activated executioner caspases

Eventual activation of caspase 8 which causes activation of caspase 3

Leads to dismantling of DNA and cytoskeletal proteins

51
Q

Describe the intrinsic/mitochondrial-dependent pathway.

A

Cytochrome C release after DNA damage causes downstream activation of caspase 9 which activates caspase 3

52
Q

What are the morphological state of apoptosis?

A

Early stages characterised by shrinkage of nucleus and cytoplasm (reversible)

Progresses to formation of membrane-bound bodies containing organelles (apoptotic bodies)

Apoptotic bodies phagocytosed by inflammatory cells

53
Q

Give an example of physiological apoptosis.

A

Lymph node germinal centres - B cell negative selection

54
Q

Give an example of pathological apoptosis.

A

Atrophy in oral Lichen Planus is caused by apoptosis

Induced by lymphocytes within the lamina propria

55
Q

Contrast necrosis and apoptosis.

A

Necrosis

  • pathological
  • involves groups of cells
  • swelling of cell
  • not energy-dependent
  • elicits an inflammatory response

Apoptosis

  • physiological or pathological
  • involves individual cells
  • shrinking of cell
  • energy-dependent
  • no inflammation elicited
56
Q

What is autophagy?

A

A response to cell stress

Ability of cell to recycle its own contents

57
Q

Describe the process of autophagy.

A

Starts with formation of isolation membrane

Isolation membrane elongates to isolate off subcellular organelles = autophagosome

Autophagosome merges with lysosomes

Degradation and deconstruction of organelles, ready to be reused

BDS2 PMI (21 decks)

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