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POM Y1 Imperial > Cell Injury & Fate > Flashcards

Cell Injury & Fate Flashcards

1
Q

What are the two types of cell injury?

A

Lethal and sublethal

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2
Q

What is lethal cell injury?

A

Produces cell death

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3
Q

What is sublethal cell injury

A

Reversible cell damage can progress to cell death

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4
Q

What is an example of direct cell injury?

A

Myocardial infarction

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5
Q

How does a myocardial infarction occur?

A

Direct cell injury due to ischaemia, causes cell death through infarction, hypertrophy insufficiently compensates increased demand
Sub-lethally damaged cells can be recovered

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6
Q

What are the 8 causes of cell injury?

A 
Oxygen deprivation, chemical agents
Infectious agents
Immunological agents
Genetic agents
Nutritional imbalance
physical agents
aging
HICGINPA
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7
Q

What three factors contribute to the cellular response to injurious injury?

A

Severity
Duration
Type

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8
Q

What consequences of injurious stimuli depend upon?

A

Type of cell

Status

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9
Q

Which intracellular mechanisms are vulnerable to injury?

A

Cell membrane integrity
ATP generation
Protein synthesis
Integrity of the genetic apparatus

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10
Q

What is atrophy?

A

Shrinkage in the cellular size, by the loss of cell substance

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11
Q

What is an example of atrophy?

A

Dementia
Amyloid Beta, phosphorylation of tau, dissociates from the MF and accumulates into filamentous neurofibrillary tangles, reduction in neural function, apoptosis

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12
Q

What is hypertrophy?

A

Enlargement of cells, consequently resulting in an increase in size of the organ
Hypertrophy response to physiological or pathological stresses

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13
Q

What is hyperplasia?

A

An increase in the number of cells in an organ

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14
Q

Whatis metaplasia?

A

Reversible change whereby an adult type cell is replaced by another

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15
Q

What lines the cervix?

A

Squamous epithelium

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16
Q

What lines the internal endocervical canal?

A

Columnar epithelium

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17
Q

During cervical expansion what happens to the exposed columnar epithelial cells?

A

The columnar epithelium cells react to external factors (Vaginal pH) and change into squamous epithelial
These changes are reversible

18
Q

What is barrets Oesophagus?

A

Acid reflux induces metaplasia

Squamous lined epithelium exchanged into columnar epithelium

19
Q

What is dysplasia?

A

Precancerous cells which show genetic and cytological feature, not invading underlying tissue

Cells do not express malignancy, have not invaded the basal lamina

20
Q

What is the clinical significance of cervical cancer screening?

A

Aims to identify cells in the dysplastic stage marks patients with an increased risk of cancer

21
Q

What stage does alcohol-induced fatty liver begin at?

A

Steatosis

22
Q

What does ethanol consumption do to the liver?

A

Ethanol metabolism to shift the redox state of liver and inhibit beta oxidation due to sterol regulatory element binding protein I being activated
Lipogenic enzymes

23
Q

What does ethanol metabolites do?

A

Activates element binding protein 1 (lipogenic enzymes)

Fatty deposits cause fatty liver disease

24
Q

What is ballooning degeneration?

A

Hepatocytes increase in size

25
Q

What is necrosis?

A

Confluent cell death associated with inflammation

26
Q

What is coagulative necrosis?

A

Substance changes, molecular structure does not
Tissue retains the same structure
Nuclei are absent, neutrophil polymorphs present
The architecture of dead tissue is preserved

27
Q

What is coagulative necrosis associated with?

A

Ischemia infarction

28
Q

What are the four types of necrosis?

A

Liquefactive, caseous, fat and coagulative

29
Q

What is liquefactive necrosis?

A

Results in a transformation of the tissue into a liquid viscous mass
Cellular death proceeds into lysosomal digestion, formation of pus filled cysts

30
Q

What is caseous necrosis?

A

Activated cytolytic T lymphocytes kill M TB infected macrophages, resulting in collateral damage.
Host degenerates self tissue to control uninhibited multiplication of bacilli.

31
Q

What composition is the necrotic area?

A

Granular

32
Q

What is fat necrosis?

A

Release of lipases digests and hydrolyzes triglycerides to free fatty acids and glycerol
FFAs combine with calcium in the extracellular fluid and deposits.
Blue area is calcium

33
Q

What ion do FFAs combine with in the extracellular fluid?

A

Calcium

34
Q

What is apoptosis?

A

Controlled and programmed cell death

35
Q

What is the distinctive comparison between apoptosis and necrosis?

A

Necrosis is associated with inflammation
Apoptosis concerns the death of individual cells
Active cell death requires ATP
Both physiological and pathological

36
Q

How is the intrinsic pathway of apoptosis triggered?

A

Response to internal stimuli (biochemical stress, DNA damage)

37
Q

Which gene is activated that halts the cell cycle?

A

P53 gene, initiates gene repair

38
Q

What do dead cells phagocytose in?

A

Phagocytosis into membrane vesicles –> apoptotic bodies

39
Q

Why is there no inflammation?

A

Vesicles result in no cytoplasmic leakage

40
Q

What are the causes of apoptosis?

A
  1. Embyrogenesis
  2. Deletion of auto-reactive T cells in the thymus
  3. Hormone dependent physiological involution
  4. Cell deletion in proliferating populations
  5. Irreparable DNA damage that triggers cell suicide pathways
41
Q

What are light microscopic changes associated with reversible injury?

A

Fatty change and cellular swelling

42
Q

What is necroptosis?

A

Programmed cell death associated with inflammation.Many causes e.g viral infections

POM Y1 Imperial (34 decks)

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