Cell Adpatation and Death Flashcards
Three Types of Cells:
- Labile (continuously dividing)
- Stable (quiescent)
- Permanent (non-dividing)
Labile Cells
(continuously dividng)
- epithelial e.g. GIT, urinary tracts, lining of exocrine ducts
- hemopoietic stem cells
Stable Cells
(Quiescent)
- Epithelial e.g. liver, kidneys, pancreas
- Smooth Muscle cells, fibroblasts, endothelial cells
Permanent
(non-dividing)
- cardiac & skeletal myocytes, CNS neurons
Apoptosis
Cell suicide/ programmed cell death
- no inflammation or scarring
- does not affect surrounding cells
- active dismantling of the cell
- can be physiological or pathological
- needed for healthy functioning of body
Necrosis
uncontrolled cell death - creates infarct stimulation of acute inflammation - loss/reduction of tissue function (scarring, calcification, death) - always pathological - passive - damages surrounding cells
Tissue Patterns of Necorsis
- Coagulative: hypoxic death (not brain)
- Liquefactive: localised bacterial infection, brain
- Casecous: TB lesions
- Fat: Adipose Tissue
Apoptosis vs Necrosis
- apoptosis occurs in physciolohy and pathology, necrosis is pathological
- apoptosis is active, necrosis passive
- a single cell can die by apoptosis, a necrotic cell kills neighbouring cells
- apoptosis does not stimulate inflammation, necrosis does
what do tissues need?
- nerve innovation
- blood & lymphatic supply
- defence against invasions
what do cells need?
- function plasma membrane
- ability to make RNA & proteins
- the ability to copy & taset DNA
- functional cytoskeletal proteins
- energy (ATP)
- antioxidant defences
- ability to remove waste
- ability to repair or destroy redundant & damaged organelles
- chemistry - temperture, pH etc.
cellular change/adaptations
- Autophagy
- Atrophy
- Hyperplasia
- Hypertrophy
- Metaplasia
Tissue atrophy vs Infarction
Atrophy involves: apoptosis & autophagy
Infarct involves: ischaemic or haemorrhagic
Two types of cell death
Necrosis and Apoptosis
Apoptosis - Physiological Conditions
- embryo-genesis
- loss of cell in proliferation
- removal of self-reactive lymphocytes
- death of inflammatory cells after their function are over
Apoptosis - Pathological
- injured cells which can’t be repaired (DNA damage, miss folded proteins, viral infection)
Necrosis - Pathological conditions
Ischemia or Hypoxia, trauma, radiation, infection, cancer, extreme temps, toxins, immunological conditions.
What determines whether a stimulus causes atrophy or infarction?
How suddenly and severely the stress if applied. Slow, partial introduction of stress may allow the cell to slowly adapt (autophagy and apoptosis). Sudden application of severe stress causes necrosis and infarction.
what effect does aging have on cells
As we age, the ability for our cells to undergo autophagy declines meaning that cells are more likely to just undergo apoptosis. All our functional tissue, except for the prostate gland in men, atrophies with age
after abortion or birth what cellular process would occur in the uterus over the ensuing weeks?
The epithelial cells that had undergone hyperplasia will undergo apoptosis.
The smooth muscle cells that had undergone hypertrophy will undergo autophagy.
The body tries to conserve energy so if cells are unused/unneeded, they will shrink &/or die by apoptosis
where is the prostate gland located and what are its functions?
The prostate is a multi-lobed epithelial gland that surrounds the male urethra just below (inferior to) the bladder. The secretions from the prostate gland form part of the ejaculate, which provide nutrients to the sperm and show antibacterial properties.
Age related enlargement of prostate
failure of apoptosis rather than hyperplasia. old cells that should be dying are being kept alive thus leading to increase in size
Age-related enlargement of bladder
The enlarged prostate, causes constriction of the urethra leading to urinary retention within the bladder. The bladder undergoes hypertrophy in response to increased pressure caused by urethral obstruction by the enlarged prostate
what could cause the testicle to atrophy?
Anything that slowly puts pressure on the tissue thus slowly reducing blood supply, nerve innervation etc. Some possible examples include a cyst (fluid-filled sack) or a tumour growing & placing pressure on the normal tissue causing the cells to shrink through autophagy and die by apoptosis; reduced blood supply caused by the arterial disease atherosclerosis; hormonal abnormalities
Brain and Kidney Atrophy
In young people tissue atrophy often includes both autophagy and apoptosis but as we get older, we just see apoptosis. These stressors have been applied slowly which has given the cells time to actively die through apoptosis
Heart atrophy: changes & possible causes
When a heart is obviously atrophied, it may be due to chronic nutrient deprivation (starvation) or, cachexia the wasting syndrome that is associated with some cancers and chronic conditions like renal failure.
If the person had been cured of heart atrophy, would the heart have returned to its original size and composition?
The myocardium of the heart is comprised of permanent cells (cardiac myocytes) so the cells are unable to proliferate. Therefore, the cells lost by apoptosis would never be replaced but the cells that had shrunk through autophagy could undergo hypertrophy restoring the overall size of the organ. However, it would not have the same functional reserve that it once had
How does atrophy differ between young and elderly tissues?
In young healthy tissues that are subjected to stress, some cells will often choose to shrink through autophagy while others die by apoptosis. As we age, the ability for our cells to undergo autophagy declines meaning that cells are more likely to just undergo apoptosis. All of our functional tissue, with the exception of the prostate gland in men
Senile Atrophy
Senile atrophy is typically caused by reduced hormones/growth factors and is exacerbated by vascular disease.
What has caused the heart to undergo hypertrophy, would this be an example of hyperplasia as well, explain your answer?
Increased workload causes the cardiac myocytes to adapt and increase in size (hypertrophy). The heart cells are permanent and so will not divide (undergo hyperplasia).
what might lead to hypertrophy of the right ventricle?
Increased workload of the right ventricle typically caused by pulmonary hypertension as the right ventricle pumps blood into the pulmonary circuit
when can hypertrophy of the heart be beneficial?
The hypertrophy allows the heart to continue to supply blood to target tissues, if it didn’t get larger and keep up with the demand necrosis/infarction would occur in tissues due to lack of blood supply.
Is there any problem with having hypertrophy of the heart?
The hypertrophy uses up some of the reserve capacity of the heart and so if it is faced with greater demands, it is more likely to fail. As hypertrophy increases, muscle contraction becomes less efficient, and the valves of the heart may malfunction all of which increases the risk of myocardial infarction &/or failure.
Are there differences between cardiac hypertrophy in response to exercise versus pathology?
The hearts of athletes are often hypertrophied but usually more uniformly across the chambers. Unlike in pathology where hypertension is chronic, an athlete may have huge increases in cardiac output during their workout, but their resting heart rate is usually lower than average. While the athlete’s heart hypertrophies, we often see an increase in elastic fibres, capillary density, mitochondrial number and energy efficiency
what form of cell death has occurred in myocardial infarction and what are some causes?
Necrosis. Sudden, complete blockage of a blood vessel; ruptured blood vessel & haemorrhaging; burns (chemical, electrical, thermal); some infections, severe trauma like a crush injury; direct cell injury through surgery or foreign object including a blade, bullet etc
