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

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18
Q

What is barrets Oesophagus?

A

Acid reflux induces metaplasia

Squamous lined epithelium exchanged into columnar epithelium

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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

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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?

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
What is necrosis?
Confluent (Region of cells) associated with inflammation
26
What is coagulative necrosis?
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
What is coagulative necrosis associated with?
Ischemia infarction
28
What are the four types of necrosis?
Liquefactive, caseous, fat and coagulative
29
What is liquefactive necrosis?
Results in a transformation of the tissue into a liquid viscous mass Cellular death proceeds into lysosomal digestion, formation of pus filled cysts
30
What is caseous necrosis?
Activated cytolytic T lymphocytes kill M TB infected macrophages, resulting in collateral damage. Host degenerates self tissue to control uninhibited multiplication of bacilli.
31
What composition is the necrotic area?
Granular
32
What is fat necrosis?
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
What ion do FFAs combine with in the extracellular fluid?
Calcium
34
What is apoptosis?
Controlled and programmed cell death
35
What is the distinctive comparison between apoptosis and necrosis?
Necrosis is associated with inflammation Apoptosis concerns the death of individual cells Active cell death requires ATP Both physiological and pathological
36
How is the intrinsic pathway of apoptosis triggered?
Response to internal stimuli (biochemical stress, DNA damage)
37
Which gene is activated that halts the cell cycle?
P53 gene, initiates gene repair
38
What is BCL-2?
Consists of pro and anti apoptotic members balance determines the direction of apoptosis Establishes molecular switch
39
What is the extrinsic apoptotic pathway?
Triggers apoptosis in response to external stimuli, by ligand binding at death receptors on the cell surface
40
What family of receptors do death receptors concern with?
Tumour necrosis factor receptor
41
what is the execution phase in regards to apoptosis?
Cascade activiation of caspases
42
What is the initiator caspase?
Caspase 8
43
What does caspase 8 do?
The initiator caspase cleaves pro-caspases into active executioner caspases PRO --> EXECUTIONER
44
What are the functions of executioner caspases?
Cause the degradation of cellular structures (cytoskeleton and nucleus)
45
What is pyknosis?
Nuclear shrinkage
46
What is karyorrhexis?
Fragmentation
47
What do dead cells phagocytose in?
Phagocytosis into membrane vesicles --> apoptotic bodies
48
Why is there no inflammation?
Vesicles result in no cytoplasmic leakage
49
What are the causes of apoptosis?
Embryogenesis: Death of intermediate cells between fingers Deletion of autoreactive T cells in the thymus Shedding of the endometrium Response to DNA damage that irreparable