ADAPTATIONS Flashcards

1
Q

Define Adaptation

A

Adaptations are reversible changes in the size, number, phenotype, metabolic activity, or functions of cells in response to:

1) changes in physiologic states
2) some pathologic stimuli

TO REACH
new but altered steady states

TO ALLOW
the cell to survive and continue to function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the types of adaptations

A

1- HYPERTROPHY: increase in the size of the cells and functional activity
2- HYPERPLASIA: increase in cell number
3- ATROPHY: Decrease in the size of cells and metabolic activity
4- METAPLASIA: change in the phenotype of cells
5- DYSPLASIA: Abnormal growth or development, but NOT CONSIDERED ADAPTATION, first step of neoplastic transformation, still reversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe hypertrophy

A

1- It is the increase in the size of cells, that results in an increase in the size of the affected organ
2- THey are bigger for synthesis and assembly of additional intracellular structural components
3- May coexist with hyperplasia adn contribute to increased size
4- Not capable of division

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Explain hypertrophy in striated muscle cells

A

1- Caused by increased functional demand or by
stimulation by hormones and growth factors
2- Hypertrophy of striated muscle cells
1) skeletal muscles in response to increased workload
2) heart for chronic hemodynamic overload
(hypertension or faulty valves)
The muscle cells syntetize more proteins and the
number of myofilaments increases.
Increase in the force of the muscle
In the heart can lead to heart failure, arrhythmias and
sudden death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Example of normal physiological hypertrophy

A

Pregnancy: hypertrophy of
muscle fibers of the uterus due to
estrogenic hormones.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Explain the mechanism of myocardial hypertrophy

A
1• Increased protein synthesis
-->increased cell size --> increased
organ size
2• Nondividing cells produce more
protein and membrane without
division
3• Mechanosensors, PI3K /Akt signaling
pathway important in exercise-­
induced growth
4• Growth factors, vasoactive agents,
hormones mediate stress-­induced
response
5• Unrelieved stress eventually results
in irreversible injury
6• Expression of fetal or embrionic proteins
-­contractile proteins (more energetically economical contraction)
-­atrial natriuretic factor (ANF) (causes salt secretion by the kidney,
decreases blood volume and pressure, reduce hemodynamic load).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Explain the epidemiology Cardiac hypertrophy

A

1• Prolonged hypertrophy is a highly important risk factor for the development of
heart failure
2• Cardiac hypertrophy includes a group of inherited conditions that produce
hypertrophy of the myocardium in the absence of an alternate cause (e.g.
aortic stenosis or hypertension).
3• It is the most common cause of sudden cardiac death in young people and
affects 1 in 500 of the population.
4• The majority of cases are familial autosomal dominant, due to mutations in the
genes encoding sarcomeric proteins .
5• The most common causes of cardiac hypertrophy are mutations of the β-­
myosin heavy chain and myosin-­binding protein C.
6• Often asymptomatic
7• Symptoms: CHEST PAIN and atrial fibrillation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe Hyperplasia

A
  1. Definition: Increase in the number of cells in
    an organ or tissue in response to a stimulus.

2• frequently occur together with hypertrophy
(same stimulus)

3• Only in tissues composed by cells
capable of dividing

4• physiologic or pathologic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Examples of physiological hyperplasia

A

1) Hormonal:

  1. proliferation of the glandular epithelium of the
    female breast at puberty and during pregnancy, usually
    accompanied by enlargement (hypertrophy) of the glandular
    epithelial cells.
  2. Endometrial profileration during normal menstrual cycle

2) Compensatory:

  1. after damage or resection. Best example is
    liver and bone marrow regeneration.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Explain Pathologic Hyperplasia

A
  1. Caused by excessive or inappropriate actions of hormones or
    growth factors acting on target cells.
  2. Pathologic hyperplasias are abnormal, but can regresses if the
    hormonal stimulation is eliminated.
3. Hyperplasia is distinct from cancer but pathologic hyperplasia
constitutes a fertile soil in which cancerous proliferations may
eventually arise (endometrium hyperplasia increases risk for
developing endometrial cancer).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Example of pathologic hyperplasia

A

1- Endometrial hyperplasia: pathologic when the balance
between estrogens and progesterone is disturbed;;
abnormal menstrual bleeding/Abnormal vaginal bleeding

2- Benign prostatic hyperplasia: induced by androgens.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Explain the mechanism of Hyperplasia

A
  1. Growth factor-­driven proliferation of mature cells

2. Proliferation of tissue stem cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe Atrophy

A

1- Defintion: Reduction in the size of an organ or tissue due to
a decrease in cell size and number.

2- Could physiologic or pathologic

3- Physiologic atrophy
during fetal development.
decrease in the size of the uterus that occurs shortly after parturition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the casues of pathological atrophy?

A

1• Decreased workload (atrophy of disuse).
Es: skeletal muscle atrophy after immobilization

2• Loss of innervation (denervation atrophy).
Metabolism of skeletal muscle are dependent on its nerve supply.

3• Diminished blood supply.
Es: brain and heart atrophy for atherosclerosis (senile atropy)

4• Inadequate nutrition.
Use of skeletal muscle proteins as a source of energy
marked muscle wasting (cachexia)

5• Loss of endocrine stimulation.
Physiologic atrophy of the endometrium, vaginal
epithelium, and breast due to loss of estrogen stimulation after menopause

6• Pressure.
Tissue compression by benign tumor can cause atrophy as a result of ischemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Explain the mechanism of atrophy

A

1- Decreased protein synthesis for
reduced metabolic activity.

2- Increased protein degradation by the
ubiquitin-­proteasome pathway.

3- Increased autophagy (“self-­eating”)
starved cell eats its own components
in an attempt to reduce nutrient
demand to match the supply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe Metaplasia

A

1- Definiton: reversible change in which one differentiated cell type
(epithelial or mesenchymal) is replaced by another cell type.

2- Example:
1- Metaplasia of the respiratory epithelium
2- Metaplasia of esophageal epithelium

3- Metaplasia is not a normal physiologic process and may be
the first step toward neoplasia

17
Q

Explain respiratory epithelium metaplasia

A
1) Due to:
• chronic irritation of trachea of
cigarette smoke
Why: stratified squamous epithelium is
more able to survive
2) Complicances:
• loss of important mechanisms of
protection against infection (mucus
secretion and the ciliary action of the
columnar epithelium)
• the influences that predispose
to metaplasia, if persistent,
can initiate malignant
transformation in metaplastic
epithelium.
18
Q

Explain Esophageal epithelium metaplasia

A

1 - Glandular, or Barrett’s metaplasia of the normal esophageal squamous mucosa
has occurred here, with the appearance of intestinal-­like columnar cells,
secondary to gastric reflux. Cancers may arise in these areas.

19
Q

Explain the mechanism of metaplasia

A

1- Reprogramming of epithelial stem cells or of undifferentiated
mesenchymal cells present in connective tissue.

2- Due to signals generated by cytokines, growth factors, and
extracellular matrix components in the cells’ environment.

3- These external stimuli promote the expression of genes that drive
cells toward a specific differentiation pathway.

20
Q

Example of dysplasia

A

This is cellular dysplasia in the uterine cervix. The normal cervical
squamous epithelium has become transformed to a more disorderly
growth pattern, or dysplastic epithelium. This is farther down the road
toward neoplasia, but dysplasia is still a potentially reversible process.