Adaptation, Injury & Cell Death Flashcards
(53 cards)
How do cells adapt to a stressor (5)?
Atrophy Hyperplasia Hypertrophy Metaplasia Dysplasia
What are the causes of atrophy (5)?
Decrease workload
« » neuronal stimulation
« » hormonal « »
Insufficient blood flow
« » nutrition
How atrophy occur (mechanism)?
Decrease in prot synthesis
Increase PROT DEGRADATION
Or AUTOPHAGY
Ingest its own organelles (attempt to conserve energy and survive)
Eg.: lack of nutrients activates UBIQUITIN ligase (E3) to attach multiple ubiquitin mol onto unnecessary prots.
Prots w/ attached ubiquitin mols are transported towards PROTEASOMES.
Proteasome job: degrade prots & recycles aa
In atrophy, which pathway is use for the degradation of prots?
Ubiquitin-proteasome pathway
What are the causes of hypertrophy (2)?
Increase workload
« » hormonal stimulation (growth factor, anabolic steroids)
What are the 2 types of hypertrophy and explain it
Physiological = n d/t increase demand
Pathological = compensatory following a disease (eg.: myocardial infarct)
How hypertrophy occurs (mechanism) (3)?
Increase prot and cell synthesis
Optimization of cell fct
Enzymatic induction (liver)
Optimization: muscle hypertrophy, some myosin chains are replaced by more energetically efficient chains.
Increase metabolism via MECHANICAL: stress TROPHIC: growth factor Trigger induce gene transcription Induce prot/c synthesis Increase functionnality
Give an example of hypertrophy of functional enzymes (enzymatic induction in the liver).
Chronic alcoholics
Become + tolerant to higher dose of alcohol
Because they have a GREATER NMB of liver ENZYMES & they work FASTER
Liver enzymes: responsible for breakdown and metabolism of alcohol.
What is the difference b/w pathological hyperplasia and cancer?
Hyperplasia occurs in response to ABNORMAL STIMULUS
It STOPS if the stimulus is REMOVED
Cancer: proliferation despite absence of stimulus
What is metaplasia?
A substitution of cell from one type to another.
Give an example of metaplasia
Substitution of normal COLUMNAR epithelium into SQUAMOUS metaplasia in airways of SMOKERS
(From ciliated to squamous)
Squamous cells: survival advantage in presence of smoke
BUT
Decrease in ciliary mvt increase ACCUMULATION of TOXIC particles in the lung
Cause LUNG CANCER in long term
How metaplasia occur (mechanism)
Reprogramming of STEM CELLS to differentiate into a different phenotype.
What is dysplasia?
Metaplasia cells w/ ABNORMAL structure and fct
New fct can be unrelated to any of the know cell types
If exposed for a long time to a stressor CAN become PERMANENT
What part of the cell are more vulnerable to cell injury (5)?
Mitochondria
Plasma membrane
ER
Protein synthesis
Nucleus/DNA
What type of cells are more vulnerable to ischemia?
Neurons
What are the major causes of cell injury(9)? Pense aux cours de la session jusqu’à présent
Hypoxia
Free radical
Physical
Chemical
Biological
Immune reactions
Genetic abnormalities
Nutritional imbalance
Aging
What is hypoxia?
Oxygen deficiency
Define ischemia
Inadequate blood supply to cells
Major cause of hypoxia
Name 4 causes of ischemia
Atherosclerosis
Thrombus
Embolism
Vessel spasm
Compression
Name 2 types of cell death d/t ischemia
Myocardial infarct
Stroke
Name 3 types of hypoxia caused by poor oxygenation of the blood
Severe anemia
Carbon monoxide poisoning
Pneumonia
Explain the mechanism of hypoxic injury
Decrease of 02
Decrease ATP prod (via oxidative phosphorylation)
Voir p.10
Severe ischemia lead to which ion influx?
Calcium
In severe ischemia calcium influx activates which enzymes?
ATPase
Protease
Phospholipase
Nuclease
Damage plasma membrane/nuclear membrane (d/t an increase in phospholipid & membrane prot breakdown)
If cell dies = necrosis
