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Pharmacology > Cellular Pathology > Flashcards

Cellular Pathology Flashcards

1
Q

What are the causes of cell damage?

A 
Hypoxia
Ischaemia 
Chemical exposures
Physical damage
Microbiological infections
Immune reactions
Genetic + inborn genetic errors
Nutritional deficiencies
Ageing
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2
Q

Why do cells have to adapt to stress exposure?

A

Maintain steady physiological + functional state

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3
Q

How do cells adapt?

A

Increase cell activity
Decrease activity
Alter morphology

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4
Q

What are the biochemical cell injuries?

A 
Loss of energy (ATP/O2 depletion)
Mitochondrial damage
Loss of Ca2+ homeostasis
Defects in membrane permeability
Generation of reactive O2 species + free radicals
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5
Q

What are the two types of cell injury?

A

Reperfusion

Chemical

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6
Q

What happens if free radicals not neutralised?

A

Can damage cells

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7
Q

How many mechanisms do free radicals damage cells by?

A

3

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8
Q

What is the 1st free radical damage mechanism?

A

Lipid peroxidation of membranes

Double bonds in poly unsaturated membrane lipids vulnerable to O2 FR

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9
Q

What is the 2nd free radical damage mechanism?

A

DNA fragmentation

FR react with thymine in nuclear + mitochondrial DNA = single strand breaks

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10
Q

What is the 3rd free radical damage mechanism?

A

Protein cross-linking

FR promote protein cross-linking = increased degradation + loss of activity

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11
Q

What is the mechanism for reperfusion injury?

A

Restoration of flow may expose compromised cells to high [Ca2+]
Reperfusion increase FR production
From compromised mitochondria + inflammatory cells

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12
Q

What is hypertrophy?

A

Increase in size of organs + cells due to protein accretion

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13
Q

What is hypertrophy in response to?

A

Increased work load/hormone stimulation

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14
Q

In hypertrophy what happens to permanently differentiated cells?

A

They cannot resume the cell cycle to increase number = get bigger

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15
Q

What is hyperplasia?

A

Increase cell number + organ size

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16
Q

What is hyperplasia in response to?

A

Hormone stimulation/damage

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17
Q

In hyperplasia what happens to cells?

A

Stem cells resume cell cycle to increase number

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18
Q

What is dysplasia?

A

Change in cellular organisation, size + organ architecture

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19
Q

What is dysplasia in response to?

A

Irritation + damage

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20
Q

What is metaplasia?

A

Substitution of one cell type for another within an organ

Indigenous cells are replaced by cells better suited to abnormal environment

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21
Q

What is metaplasia in response to?

A

Different conc or assortment of growth factors

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22
Q

What is atrophy (hypoplasia)?

A

Decrease in cell size + number

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23
Q

What is atrophy in response to?

A

Decreased work loads, hormonal/neuronal stimulation, blood supply, nutrition or aging in adults or during development

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24
Q

What are the type of cellular damage?

A

Sub-lethal cellular injury
Lethal cellular injury
Necrosis
Programmed cell death

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25
Q

What is sub-lethal cellular injury?

A

Blebbing of membrane

Alteration in protein synthesis/organelle genesis

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26
Q

What are examples of sub-lethal cellular injury?

A

Hydropic degeneration

Fatty change

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27
Q

What is lethal cellular injury?

A

Several damage to stimuli
Prolonged sub-lethal damage
Leads to cell death

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28
Q

What is necrosis?

A

Cell death by injury
Mechanical damage
Exposure to toxic chemicals

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29
Q

What is programmed cell death?

A

Cell death by suicide

Internal/external cellular signals

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30
Q

Describe the process of necrosis

A 
Cells receive chemical or structural insult
Swell up
Activation of lysosomal enzymes
Enzymatic digestion of cells
invasion of phagocytes + inflammation
Tissue damage
Passive cell death
31
Q

Describe coagulative necrosis

A

Dead tissue = pale + firm

Architecture + tissue outline preserved

32
Q

Where does coagulative necrosis occur?

A

Cells with few lysosomes

33
Q

What does coagulative necrosis do?

A

Damages enzymes = blocks proteolysis

34
Q

What are the causes of coagulative necrosis?

A

Occlusion of arterial blood supply (kidney + heart)

Proteins released from dead cells aid diagnosis

35
Q

Describe liquefactive necrosis

A

Dead tissue = semi-solid

Dissolution of tissue: hydrolytic enzymes

36
Q

What are the causes of liquefactive necrosis?

A

Bacterial/fungal infections

Ischaemia in CNS

37
Q

What is the liquefactive necrosis pattern?

A

Cerebral infarction
Neurons have high lysosomal content
Lack extracellular structural proteins - eg. collagen

38
Q

Describe enzymatic fat necrosis

A

Escape of lipases

Damages fat = soft, chalky white areas

39
Q

What is an example of enzymatic fat necrosis?

A

Acute pancreatitis
Vague cellular outline
Lost peripheral nuclei
Cytoplasm pink amorphous mass

40
Q

Describe caseous necrosis

A

Bacterial liquefaction
Coagulative + liquefactive necrosis
Caused by tuberculosis

41
Q

What are the signs of caseous necrosis?

A

Confluent cheesy tan granulomas

Extensive tissue destruction = cavitation

42
Q

Describe gangrenous necrosis

A

Necrosis grossly advanced + visible

43
Q

What are examples of gangrenous necrosis?

A

Dry gangrene

Wet gangrene

44
Q

What is dry gangrene?

A

Mostly coagulated

Site dried up before bacteria could over grow

45
Q

What is wet gangrene?

A

Mostly liquefactive

Foul-smelling oozing foot infection

46
Q

What are the two types of programmed cell death?

A

Autophagic cell death

Apoptosis

47
Q

What is autophagic cell death?

A

Cytoplasm actively destroyed long before nuclear changes appear

48
Q

What is apoptosis?

A

Chromatin marginates + cell and nucleus fragment before morphological changes are seen

49
Q

What are examples of apoptosis?

A

Embryonic development
Cell turnover in adult tissues
T-cell clonal deletion

50
Q

Since apoptosis is active cell death what does it require?

A

Energy
RNA
Protein synthesis

51
Q

Describe the process of apoptosis

A

Cell shrinks + chromatin condenses
Cell blebs + chromatin condenses
Cell fragments into apoptotic bodies
Apoptotic bodies phagocytosed by neighbouring cells

52
Q

Why does apoptosis happen?

A

Withdrawal of positive (growth) signals
Receipt of negative (death signals)
Interference in cell death pathway mechanism
Failure to replicate

53
Q

What are the negative (death) signals?

A

Increased oxidants
DNA damage
Death activators = TNF alpha

54
Q

What are the 2 pathways that initiate apoptosis?

A

Intrinsic/mitochondrial apoptosis = regulated by mitochondria
Extrinsic apoptosis = activated by ligation of death receptors

55
Q

What happens to DNA involved in apoptosis?

A

Internucleosomal cleavage

56
Q

What happens to DNA involved in necrosis?

A

Random degradation

57
Q

What happens in the nucleus in apoptosis?

A

Chromosome margination

58
Q

What happens in the nucleus in necrosis?

A

Pyknosis

59
Q

What happens to membrane integrity in apoptosis?

A

Persists till late

60
Q

What happens to membrane integrity in necrosis?

A

Compromised early

61
Q

What happens to mitochondria in apoptosis?

A

Appears normal

62
Q

What happens to mitochondria in necrosis?

A

Appears swollen

63
Q

Is there inflammation in apoptosis?

A

NO

64
Q

Is there inflammation in necrosis?

A

YES

65
Q

What is the pattern of apoptosis?

A

Individual cells

66
Q

What is the pattern of necrosis?

A

Multiple cells

67
Q

What happens to cell volume in apoptosis?

A

Decreases

68
Q

What happens to cell volume in necrosis?

A

Increases

69
Q

Is there cell fragmentation in apoptosis?

A

YES (apoptotic bodies)

70
Q

Is there cell fragmentation in necrosis?

A

NO (cell lysis)

71
Q

Where does nephrotoxicity of antibiotic Gentamicin occur?

A

Proximal tubule cells in kidney

Drug accumulates in cells

72
Q

What does accumulation of Gentamicin cause?

A

Phospholipid dialysis

= releases degrative enzymes

73
Q

What does Gentamicin act on?

A

Mitochondria = activates apoptosis

74
Q

Is Gentamicin OK in low doses?

A

YES

Pharmacology (40 decks)

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