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pharmacology > Cellular pathology - stress and death - non synchronous > Flashcards

Cellular pathology - stress and death - non synchronous Flashcards

1
Q

State the mechanisms of cell injury.

A

Biochemical mechanisms:
- Loss of energy
- Mitochondrial damage
- Loss of calcium homeostasis
- Defects in plasma membrane permeability
- Generation of reactive oxygen species and other free radicals

Reperfusion injury

Chemical injury

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2
Q

What are the three mechanisms that free radicals can damage cells?

A
  1. Lipid peroxidation of membranes: double bonds in polyunsaturated membrane lipids are vulnerable to attack by oxygen free radicals
  2. DNA fragmentation: free radical react with thymine in nuclear and mitochondrial DNA to produce single strands
  3. Protein cross-linking: Free radicals promote protein cross-linking, resulting in increased degradation or loss of activity
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3
Q

Describe the mechanism of reperfusion injury.

A
  • Restoration of flow may expose compromised cells to high Ca2+
  • Reperfusion increases free radical production from comprised mitochondria and circulating inflammatory cells
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4
Q

What is hypertrophy?

A
  • Increase in size of organs and cells due to protein accretion; a response to increased work load
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5
Q

What is hyperplasia?

A

Increase in cell number and organ size; response to hormonal stimulation or compensatory to damage

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6
Q

What is dysplasia?

A

Change in cellular organisation, size and organ architecture; response to irritation and damage

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7
Q

What is metaplasia?

A

Substitution of one cell type for another within an organ; in response to diff. conc. or assortment of growth factors which is a response to irritation or injury

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8
Q

What is atrophy and/or hypoplasia?

A

Decrease in cell size and number; response to decreased work load, hormonal or neuronal stimulation etc.

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9
Q

What is sub-lethal cellular injury?

A
  • Cell recovers after removal of damaging stimulus
  • Characteristics: cell and/or organelle swelling, alteration in protein synthesis
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10
Q

What is hydropic degeneration?

A

Disruption of ionic and fluid homeostasis; failure of energy dependant membrane pumps
- Swelling of organelles and consequent cellular enlargement
- Cytoplasm becomes pale, formation of intracellular vacuoles

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11
Q

What is fatty change?

A
  • Affects cells with key role in lipid metabolism
  • Metabolic or hypoxic injury
  • Appearance of lipid vacuoles inside cell
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12
Q

What is lethal cellular injury?

A
  • Severe damage stimulus
  • Prolonged sub-lethal damage
  • Leading to cell death: necrosis or programmed cell death
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13
Q

What is necrosis?

A
  • Cell death by injury; mechanical damage, exposure to toxic chemicals
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14
Q

What is programmed cell death?

A
  • Cell death by suicide
  • internal or external cellular/biological signals
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15
Q

Describe he process of necrosis

A
  • Cells receive structural or chemical insult
  • Cells and organelles swell up
  • Activation of lysosomal enzymes
  • Enzymatic digestion of cells
  • Membrane digestion and leakage
  • Nucleus disintegrates
  • ‘Cell ghosts’
  • Invasion of phagocytes and inflammation
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16
Q

What is coagulative necrosis?

A
  • Dead tissue appears firm and pale
  • Architecture and tissue outline preserved
  • Occurs in cells with fewer lysosomes
  • Injury damage enzymes so blocks proteolysis
17
Q

What are the causes of coagulative necrosis?

A
  • Occlusion of arterial bloody supply: kidney, heart
  • Proteins released from dead cells aid diagnosis
18
Q

What is liquefactive necrosis?

A
  • Dead tissue appears semi-solid
  • Dissolution of tissue: hydrolytic enzymes
19
Q

What are the causes of liquefactive necrosis?

A
  • Bacterial/fungal infections
  • Ischaemia in central nervous system
  • Liquefactive pattern: cerebral infarction
  • Neurons have high lysosomal content
  • Lack extracellular structural proteins,
    reticulin, collagen etc
20
Q

What is enzymatic fat necrosis?

A
  • Escape of lipase
  • Damage fats, producing fatty acids with Ca2+ ions appears grossly as soft chalky, white areas
21
Q

What is caseous necrosis?

A
  • Bacterial liquefaction
  • Coagulative and liquefactive necrosis most characteristic of granulomatous inflammation
22
Q

What is gangrenous necrosis?

A

Term for necrosis that is advanced and grossly visible

23
Q

What is dry gangrene?

A

Mostly coagulation necrosis, site dried up before bacteria could overgrow

24
Q

What is wet gangrene?

A

Mostly liquefactive necrosis

25
Q

What is autophagic cell death?

A
  • Cytoplasm is actively destroyed long before nuclear changes appear
26
Q

What is apoptosis?

A
  • Chromatin marginates and cell and nucleus fragment before morphological changes are seen
27
Q

In which situations does apoptosis occur?

A
  • Embryonic development
  • Cell turnover in adult tissues
  • T-cell clonal deletion
  • Normal involutional processes
  • Atrophic processes
  • Deletion of damaged cells
28
Q

Describe the process of apoptosis.

A
  • Active cell death
  • Requires energy and RNA and protein synthesis
  • Characteristic morphological features
  • DNA cleaved, chromatin condenses
  • Cells shrink
  • Formation of apoptotic body
  • Cleared by phagocytosis
  • No inflammation = NO TISSUE DAMAGE
29
Q

What makes a cell decide to commit suicide?

A
  • Withdrawal of positive growth signals
  • Receipt of negative death signals
  • Interference in cell death pathway mechanism
  • Failure to replicate
  • Incorrect mechanistic signalling activation
30
Q

What are the two pathways that initiate apoptosis and where do they converge?

A
  • Intrinsic / mitochondrial apoptosis: regulated by mitochondria
  • Extrinsic apoptosis: activated by ligation of death receptors
  • These pathways converge at the execution phase
31
Q

What morphological changed occur during apoptosis?

A

a. Normal cell
b. Shrinks and then condensed chromatin collapses into crescents around nuclear envelope
c. Membrane bulges and blebs
d. Chromatin condenses and cell blebs into discrete packages
e. Cell finally breaks into a number of apoptotic bodies
f. Apoptotic bodies are phagocytosed

32
Q

Compare apoptosis and necrosis.

A

DNA: internucleosomal cleavage v random degradation
Nucleus: chromosome margination v pyknosis
Membrane integrity: persists until late v compromised early
Mitochondria: Appear normal v swollen
Inflammation: No v Yes
Pattern: Individual cells v multiple cells
Cell volume: decreases v increases early
Cell fragmentation: yes (apoptotic bodies) v no (cell lysis)

pharmacology (40 decks)

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