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A in depth but concise summary of Cell Adaptation and Cell Death $16.29   Add to cart

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A in depth but concise summary of Cell Adaptation and Cell Death

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This is a summary of vital aspects of Cell Adaptation, For example, what is meant by ‘cell adaptation’? Define 3 types of cell adaptation, and give a physiological and pathological example of each. Needed to answer exam question. Cell Death-The different stages are described in depth.

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Cell Adaptation
What is meant by ‘cell adaptation’? [20%]

- adaptations are reversible changes, which occur to allow the cell to
survive and continue to function in face of the environmental stresses
placed upon them.
- cellular adaptations -occur in response to perturbation of environmental conditions and can be
changes in:
- size
- number
- metabolic activity
- functions
-adaptations can be classified as:
1. Physiological adaptations - occur in response to hormones/endogenous mediators
2. Pathological adaptations - occur in response to stress - allowing cells to modify their structure
and function & therefore escape injury

Define 3 types of cell adaptation, and give a physiological and
pathological example of each. [80%]

• HYPERTROPHY:
-An increase in the size of cells which results in an increase in
the size of the organ.
-No increase in cell no. - cells become larger owed to an increase in
the synthesis of structural components within these cells.
-Hypertrophy occurs when cells are incapable of dividing i.e.
non-dividing cells (e.g. myocardial fibres)
-Hypertrophy may occur along with 'hyperplasia'*-resulting in
Hypertrophy of organ (increased organ size)
-Hypertrophy is caused by either an increased functional demand
eg: inc. demand on striated muscle: myocardial/skeletal muscle-
cardiac / skeletal muscle hypertrophy.
OR
-Hypertrophy is also caused by hormonal/growth factor secretion eg:
oestrogen - causing hypertrophy in uterus

• PHYSIOLOGICAL HYPERTROPHY: (SKELETAL MUSCLES)

-When muscle workload is increased, striated muscle cells in
skeletal muscles respond by undergoing hypertrophy (eg:
weightlifters-inc. functional demand / preganacy- mediated by
oestrogen).
this maybe because these cells they only have a limited ability
to divide.
-These stressed, striated muscle cells synthesize more proteins,
resulting in more Myofilaments, which increases the force
myocytes can generate, giving rise to increased strength in the
organ (an adaptation to the change in environmental demand
/stresses)
-2 main biochemical pathways involved in muscle hypertrophy

, are the P13K/AKT pathway and signalling downstream of GPCR.
-Another mech. associated with muscle hypertrophy is the switch
of contractile proteins from adult to fetal/neonatal forms
eg: the alpha isoform of the myosin heavy chain is
replaced by the beta isoform.
-This beta form has a slower more energetically economical
mechanism of contraction.
-Hypertrophy is LIMITED (a limit is reached where the
enlargement of muscle mass can no longer compensate for the
increased burden).
-This limit can be illustrated via : cardiac hypertrophy (once limit is
reached several degenerative changes occur in myocardial fibres:
-fragmentation
-loss of myofibrillar contractile elements
-These show how adaptation to stress can progress to functionally
significant cell injury if the stress is not relieved

• PATHOLOGICAL HYPERTROPHY: (CARDIAC MUSCLES)

- when muscle workload is increased, striated muscle cells in
the heart respond by undergoing hypertrophy (as they only
have a limited ability to divide)
- This happens when increased workload is placed upon the
heart e.g. through systemic hypertension i.e. increased
resistance in the systemic circulatory system which forces
the heart to pump harder and faster to keep blood
circulating.
- Mechanisms of cardiac hypertrophy involve @ least 2 types of
signals
Mechanical triggers such as stretch:
Trophic triggers such as activation of alpha adrenergic receptors
- These triggers activate signal transduction pathways - lead to
induction of genes - stimulate synthesis of numerous cellular
proteins (inc. growth factors and other structural proteins).
-This results in the synthesis of more proteins and myofibrils per
cell resulting in more Myofilaments, which increases the force
myocytes can generate.
- This achieves improved performance & thus a balance between
the increased demand on cells and the cells functional capacity.
-Some examples of pathological hypertrophy :
-Cardiac muscle of the left ventricle undergoes hypertrophy
because of increased outflow pressure eg systemic
hypertension, aortic valve disease
-Cardiac muscle of the right ventricle undergoes hypertrophy
because of increased outflow pressure eg pulmonary
hypertension, pulmonary valve disease.
-Arterial smooth muscle undergoes hypertrophy in hypertension.

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