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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
What causes dysplasia?
Persistent noxious agents (eg carcinogens)
26
What can metaplasia progress to after sufficient length and exposure of a stimulus?
Dysplasia
27
What is reversible injury?
Cell changes that can be restored to normalcy with removal of stimulus
28
What is irreversible injury?
Stressors exceed the capacity of the cell to adapt Permanent changes lead to cell death
29
What are the possible causative agents of cell adaptation or death?
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
What are the possible mechanisms of cell injury?
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
What stimuli may cause ROS formation?
Ionising radiation Inflammation Some drugs and metals
32
What can ROS damage in a cell?
Membranes DNA Other molecules in metabolic pathways
33
What are the two types of cell death?
Apoptosis Necrosis
34
What are the five types of cell adaptation?
Hyperplasia Hypertrophy Atrophy Metaplasia Dysplasia
35
Describe necrosis.
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
What are the steps leading up to karyolysis?
Pyknosis = condensation of nucleus so it appears darker Karyorrhexis = fragmentation Karyolysis
37
What are the different types of necrosis?
Coagulative Liquefactive Caseous Fat Gangrene Fibrinoid
38
What is coagulative necrosis?
Most common form of necrosis Structural pattern of necrotic tissue is maintained Commonly caused by ischaemia and infarction
39
What is a common cause of coagulative necrosis?
Ischaemia and infarction
40
Give an example of where you might see coagulative necrosis?
Renal cortex - tubular structure remains
41
What is liquefactive necrosis?
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
What is caseous necrosis?
Necrotic tissue resembles soft cheese microscopically - soft, white, proteinaceous dead cell mass Typical for certain types of granulomatous inflammation, esp TB
43
What disease typically displays caseous necrosis?
Tuberculosis
44
What is fat necrosis?
Action of lipases on fatty tissues produces grossly visible, chalky white areas Seen in breast, omentum and pancreatitis
45
What is gangrenous necrosis?
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
What is fibrinoid necrosis?
Connective tissues and arterial walls are infiltrated by strongly eosinophilic hyaline material that shows characteristics of fibrin
47
Describe apoptosis.
Regulated and targeted programmed cell death Energy-dependent Can be physiological or pathological Cell shrinkage and does not elicit inflammatory response
48
What may trigger apoptosis?
DNA damage Protein misfolding Viral infection
49
What are the two pathways of apoptosis?
Extrinsic/death receptor-mediated pathway Intrinsic/mitochondrial-dependent pathway
50
Describe the extrinsic/death receptor-mediated pathway.
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
Describe the intrinsic/mitochondrial-dependent pathway.
Cytochrome C release after DNA damage causes downstream activation of caspase 9 which activates caspase 3
52
What are the morphological state of apoptosis?
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
Give an example of physiological apoptosis.
Lymph node germinal centres - B cell negative selection
54
Give an example of pathological apoptosis.
Atrophy in oral Lichen Planus is caused by apoptosis Induced by lymphocytes within the lamina propria
55
Contrast necrosis and apoptosis.
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
What is autophagy?
A response to cell stress Ability of cell to recycle its own contents
57
Describe the process of autophagy.
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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