GENERAL PATHOLOGY

2. Adaptations of Cellular
Growth& Differentiation
BY
DR ABDUL AZIZ SHAIKH
MBBS,M.PHIL(HISTOPATHOLOGY)
ASSISTANT PROFESSOR

3. Adaptations
Adaptations are reversible changes in
the size, number,
phenotype, metabolic activity, or
functions of cells in
response to changes in their
environment

4. Hypertrophy
Hypertrophy refers to an increase in
the size of cells, that
results in an increase in the size of
the affected organ.
The hypertrophied organ has no new
cells, just larger cells.

5. Hypertrophy
The increased size of the cells is due to
the synthesis and assembly of additional
intracellular structural components
Cells capable of division may respond to
stress by undergoing both hyperplasia
and hypertrophy,

6. Hypertrophy
whereas in non dividing (e.g., myocardial
fibers) increased tissue mass is due to
hypertrophy
Hypertrophy can be physiologic or pathologic;
the former is caused by increased functional
demand or by stimulation by hormones and
growth factors

7. Hypertrophy
The striated muscle cells respond to
increased metabolic demands mainly by
undergoing hypertrophy.
The most common stimulus for hypertrophy
of muscle is increased work load. For
example, the bulging muscles of bodybuilders

10. Hypertrophy
In the heart, the stimulus for hypertrophy is usually
chronic hemodynamic overload, resulting from
either hypertension or faulty valves
 In both tissue types the muscle cells synthesize
more proteins and the number of myofilaments
increases.
 This increases the amount of force each myocyte
can generate, and thus increases the strength and
work capacity of the muscle as a whole.

11. Hypertrophy
The massive physiologic growth of the uterus during
pregnancy is a good example of hormone-induced
enlargement
Uterine hypertrophy is stimulated by estrogenic
hormones acting on smooth muscle through
estrogen receptors, eventually resulting in
increased synthesis of smooth muscle proteins and
an increase in cell size.

12. Mechanisms of Hypertrophy
Hypertrophy of the heart becomes
maladaptive
and can lead to heart failure, arrhythmias
and sudden death .
There are three basic steps in the
molecular pathogenesis of cardiac
hypertrophy

14. Mechanisms of Hypertrophy
The integrated actions of mechanical sensors
(that are triggered by increased workload),
growth factors
(including TGF-β, insulin-like growth factor 1
[IGF1],fibroblast growth factor), and vasoactive
agents (e.g.,
α-adrenergic agonists, endothelin-1, and
angiotensin II).

15. Mechanisms of Hypertrophy
These signals originating in the cell
membrane activate
a complex web of signal transduction
pathways.
Two such biochemical pathways involved
in muscle
hypertrophy are the phosphoinositide 3-

16. Mechanisms of Hypertrophy
AKT pathway (postulated to be most
important in physiologic, e.g.,
exercise-induced, hypertrophy) and
signaling downstream of G-protein–
coupled receptors (induced by many
growth factors and vasoactive
agents,and thought to be more
important in pathologic hypertrophy).

17. Mechanisms of Hypertrophy
These signaling pathways activate a set of transcription
factors such as GATA4, nuclear factor of activated T
cells (NFAT), and myocyte enhancer factor 2 (MEF2).
These transcription factors work coordinately to increase
the synthesis of muscle proteins that are responsible for
hypertrophy.

19. Alberuni iprs
Thursday 11TH
JUNE 2020

20. Hyperplasia
Hyperplasia is defined as an increase in the
number of
cells in an organ or tissue in response to a
stimulus.
Hyperplasia can only take place if the tissue contains
cells capable of dividing;
thus increasing the number of cells. It can be
physiologic
or pathologic

21. Physiologic Hyperplasia
Physiologic hyperplasia due to the action of
hormones or growth factors occurs in several
circumstances:
when there is a need to increase functional capacity
of hormone sensitive organs; when there is need for
compensatory increase after damage or resection.

22. Physiologic Hyperplasia
Hormonal hyperplasia: the proliferation
of the glandular epithelium of the
female breast at puberty and during
pregnancy,usually accompanied by
enlargement (hypertrophy) of the
glandular epithelial cells.

23. Physiologic Hyperplasia
The compensatory hyperplasia
comes from the study of liver
regeneration. In individuals who
donate one lobe of the liver for
transplantation, the remaining
cells proliferate so that the organ
soon grows back to its original size.

24. Physiologic Hyperplasia
Marrow is remarkable in its
capacity to undergo rapid
hyperplasia in response to a
deficiency of terminally
differentiated blood cells.

25. Physiologic Hyperplasia
For example, in the setting of an
acute bleed or premature
breakdown of red cells(hemolysis),
feedback loops involving the growth
factor erythropoietin are activated
that stimulate the growth of red cell
progenitors, allowing red cell
production to increase as much as
8-fold

26. Pathologic Hyperplasia
Most forms of pathologic hyperplasia are
caused by
excessive or inappropriate actions of
hormones or growth
factors acting on target cells. Endometrial
hyperplasia is
an example of abnormal hormone-induced
hyperplasia

29. An example of hypertrophy would be
(a) liver regeneration after partial hepatectomy
(b) breast development at puberty
(c) the uterus during pregnancy
(d) the uterus during menstruation
(e) a papillomavirus induced skin wart

30. ANS
(c) enlargement of the uterus during
pregnancy (an example of hormonal
hyperplasia and hypertrophy)

31.  (a) liver regeneration after partial
hepatectomy (compensatory hyperplasia)
(b) breast development at puberty
(hormonal hyperplasia) (c) enlargement of
the uterus during pregnancy (an example of
hormonal hyperplasia and hypertrophy) (d)
the uterus during menstruation (atrophy)
(e) a papillomavirus induced skin wart
(pathologic hyperplasia)

32. The pattern of cell death that is characterized by
conversion of a single cell to an acidophilic body,
usually with loss of the nucleus but with preservation
of its shape to permit recognition of cell boundaries is
termed
A. Apoptosis
B. Caseous necrosis
C. Fibrinoid necrosis
D. Liquefactive necrosis

33. ANS
Apoptosis

34. A pathologist notes cloudy swelling, hydropic change
and fatty change in the liver of a patient with a history of
alcohol abuse. These morphological changes are all
examples of
A. Early neoplastic change
B. Hyaline change
C. Patterns of cell death
D. Postmortem artefact
E. Reversible cell injury

35. ANS
E. Reversible cell injury

36. Metapalsia
(a) can be caused by vitamin B12 deficiency
(b) preserves the mucus secretion in the
respiratory tract
(c) is typically irreversible
(d) describes the underlying pathology of Barrett’s
oesophagus
(e) is an increase in the number and size of cells
in a tissue

37. ANS
(d) describes the
underlying pathology of
Barrett’s oesophagus