Describe the causes and clinical importance of hyperplasia.

Hyperplasia is of two types:

A. Physiologic hyperplasia

B. Pathologic hyperplasia.

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.

So physiologic hyperplasia may be

• Hormonal: proliferation of the glandular epithelium of the female breast at puberty and during pregnancy.
• Compensatory: Liver regeneration after donation of a lobe of liver.

Pathologic hyperplasia:

Most forms of pathologic hyperplasia are caused by excessive or inappropriate actions of hormones or growth factors acting on target cells.

1. Endometrial hyperplasia
2. Benign prostatic hyperplasia
3. Hyperplasia is a characteristic response to certain viral infections, such as papillomaviruses, which cause skin warts and several mucosal lesions composed of masses of hyperplastic epithelium.

What do you mean by Apoptosis? What are the causes of Apoptosis?

Apoptosis:

Apoptosis is a pathway of cell death that is induced by a tightly regulated suicide program in which cells
destined to die activate intrinsic enzymes that degrade the cells’ own nuclear DNA and nuclear and cytoplasmic proteins.

Causes of Apoptosis:

Apoptosis occurs normally both during development and throughout adulthood, and serves to remove unwanted, aged, or potentially harmful cells. It is also a pathologic event when diseased cells become damaged beyond repair and are eliminated.

Apoptosis in Physiologic Situations:

• The destruction of cells during embryogenesis, including implantation, organogenesis, developmental involution, and metamorphosis.
• Involution of hormone-dependent tissues upon hormone withdrawal, such as endometrial cell breakdown during the menstrual cycle, ovarian follicular atresia in menopause, the regression of the lactating breast after weaning, and prostatic atrophy after castration.
• Cell loss in proliferating cell populations, such as immature lymphocytes in the bone marrow and thymus and B lymphocytes in germinal centers that fail to express useful antigen receptors.
• Elimination of potentially harmful self-reactive lymphocytes, either before or after they have completed their maturation, so as to prevent reactions against one’s own tissues.
• Death of host cells that have served their useful purpose, such as neutrophils in an acute inflammatory response, and lymphocytes at the end of an immune response.

Apoptosis in Pathologic Conditions:

• DNA damage. Radiation, cytotoxic anticancer drugs, and hypoxia can damage DNA, either directly or via production of free radicals.
• Accumulation of misfolded proteins.
• Cell death in certain infections, particularly viral infections, in which loss of infected cells is largely due to apoptosis that may be induced by the virus (as in adenovirus and HIV infections) or by the host immune response (as in viral hepatitis).
• Pathologic atrophy in parenchymal organs after duct obstruction, such as occurs in the pancreas, parotid gland, and kidney.

What are the causes of cell injury?

Causes of Cell Injury: 

The causes of cell injury range from the external gross physical violence of an automobile accident to subtle internal abnormalities, such as a genetic mutation causing lack of a vital enzyme that impairs normal metabolic function. Most injurious stimuli can be grouped into the following broad categories.

1. Oxygen Deprivation. Causes of hypoxia include reduced blood flow (celled ischemia), inadequate oxygenation of the blood due to cardiorespiratory failure, and decreased oxygen-carrying capacity of the blood, as in anemia or carbon monoxide poisoning (producing a stable carbon monoxyhemoglobin that blocks oxygen carriage) or after severe blood loss.

2. Physical Agents. Physical agents capable of causing cell injury include mechanical trauma, extremes of temperature (burns and deep cold), sudden changes in atmospheric pressure, radiation, and electric shock.

3. Chemical Agents and Drugs. Oxygen at high concentrations is toxic, Arsenic, Cyanide, Mercuric salts.

4. Infectious Agents. Rickettsiae, Bacteria, Fungi, and higher forms of parasites.

5. Immunologic Reactions. Injurious reactions to endogenous self-antigens are responsible for several autoimmune diseases.

6. Genetic Derangements.

7. Nutritional imbalance. Protein-calorie deficienciency, Deficiencies of specific vitamins, Atherosclerosis, Obesity.

Causes or risk factors of childhood malignancy.

Causes (risk factors) of childhood malignancy:

• Race
• Chemotherapeutic agent (Alkylating agents)
• Ionizing radiation in utero
• Down syndrome
• Family history
• EBV
• Immunodeficiency
• Genetic factor