cell adaptation

• Adaptations are reversible changes in cells' number, size, phenotype, metabolic activity, or function in response to environmental changes.
• An adaptation to stress can lead to significant cell injury if the stress is not relieved.

Physiologic Adaptations

• Represent cellular responses to normal hormonal or endogenous chemical stimuli.
• Can result from hormone-induced breast and uterus enlargement during pregnancy or mechanical stress.

Pathologic Adaptations

• Enable cells to modulate their structure and function under stress, such as squamous metaplasia in smokers' bronchial epithelium.

1. Hypertrophy

• An increase in cell size that results in an organ's enlargement.
• There are no new cells, just bigger cells, enlarged by an increased number of structural proteins and organelles.
• Occurs in tissues incapable of cellular division.

Physiologic Cellular Hypertrophy

• Enlargement of the uterus during pregnancy.
• Increased workloads on striated muscle cells in skeletal and heart muscle.

Pathologic Cellular Hypertrophy

• Cardiac enlargement occurs with hypertension or aortic valve disease.

Notes

• Ischemia causes reversible injury, while ischemic coagulative necrosis causes irreversible injury.
• In myocardial hypertrophy, the left ventricular wall is thicker than 2 cm (normal, 1-1.5 cm).
• Triphenyltetrazolium chloride colors viable myocardium magenta; failure to stain indicates enzyme loss after cell death.

2. Hyperplasia

• Occurs when tissues contain cells capable of replication, often with hypertrophy, in response to the same stimuli.

Physiologic Hyperplasia

• Hormonal hyperplasia exemplifies glandular epithelium proliferation in the female breast during puberty and pregnancy.
• Hormones cause this increase in number e.g. puberty
• Compensatory hyperplasia occurs when residual tissue grows after removing part of an organ.
  • E.g. hepatocytes regenerate with injury because of polypeptide growth factor.

Pathologic Hyperplasia

• Caused by abnormal stressors, such as excessive hormonal or growth factor stimulation.

• Endometrial hyperplasia exemplifies hormone imbalance, causing continuous bleeding; doctors may take tissue samples for analysis.

• Benign prostatic hyperplasia causes frequent urination due to an enlarged prostate.

• Papillomaviruses, or HPV, can cause warts.

• Myocytes and neurons don't regenerate; hepatocytes regenerate only if there is injury; epithelial cells regenerate continuously.

3. Atrophy

• Cell shrinkage results from lost cell substances due to decreased nutrient supply or disuse.
• It involves decreased synthesis and breakdown of cellular organelles.

Causes

• Decreased workload- Can be due to immobilization of the lymph node during healing process
• Loss of Innervation
• Diminished Blood Supply
• Inadequate Nutrition- Body mass reduced, like in conditions of marasmus
• Loss of Endocrine Stimulation- Menopausal women
• Aging (Senile Atrophy

Mechanism of Atrophy

• Combination of decreased protein synthesis and increased protein degradation in cells.
• Reduced metabolic activity = decrease protein synthesis
• Degradation of cellular proteins mainly involves the ubiquitin-proteasome pathway.
  • Due to cachexia malignancy or chronic underlying causes
• Increased autophagy where cells are scarred and eat their own

Physiologic Atrophy

• Occurs as a natural consequence of maturation.
  • atrophy of the thymus and lymphoid tissues during puberty
• Sexual organs and brain begin to undergo physiologic atrophy at about 50 years of age.

Senile Atrophy

• Characterized by ✓ dry, lusterless, wrinkled skin because of atrophy of sweat and sebaceous glands ✓ loss of fat, gray hair, atrophy of the ligaments, brittle bones that easily break

Pathologic Atrophy

• A decrease in size of tissues or organs
• Usually as a consequence of disease

4. Metaplasia

• Metaplasia is a reversible change in which one adult cell type (epithelial or mesenchymal) is replaced by another adult cell type.
• Response to chronic irritation that makes cells better able to withstand the stress
• Usually induced by altered differentiation pathway of tissue stem cells
• May result in reduced functions or increased propensity for malignant transformation
• change in phenotype of differentiated cells, often in response to chronic that makes cells suited
• usually induced by altered differentiation pathway of tissue stem cells
• may result in reduced functions or increased propensity for malignant transformation

Epithelial Metaplasia

• Epithelium exposed to mechanical trauma or chronic prolonged inflammation.
• Prolonged vitamin A deficiency
• Most commonly leads to replace columnar cells by stratified squamous epithelium.
• Respiratory passages.
• . linings of gland ducts
• . mucosal lining of endocervix

Mesenchymal Metaplasia

• Connective tissue- fibroblasts transform toward differentiated forms like fat, osteoblasts, or tissue macrophages.
• Under some circumstances cells may accumulate abnormal amounts of various substances may be harmless or associated with varying degrees of injury

Intracellular Accumulations

• The substance may be located: -Cytoplasm -Within organelles (typically lysosomes) -In the nucleus
• May be synthesized by the affected cells or may be produced elsewhere.

Mechanism/ Pathways of Abnnormal Intracellular Accumulations

• I. Inadequate removal a normal stubstance defects in mechanisms packaging and transporting:

  • fatty change in the liver
  • The packaging and transporting are governed by golgi
  • apparatus which produces proteins have defects on processes
  • Example of these normal substances cholesterol in ell synthesis

• II. Accumulation a normal endogenous sustance:

  • Genetic defects in folding, packaging, transport, as with a1- antitrypsin

• III. Failure to degrade a metabolite:

• inherited enzyme deficiencies -Accumulation endogenous material cell can't utilize

Abnormal Intracellular Accumulations

1. Fatty Change (Steatosis)

• Fatty change to any abnormal accumulation of triglycerides with Parenchymal cell

• Causes of Steatosis: -protein malnutrition -diabetes mellitus -obesity -anoxia- inhibits fatty acid oxidation

• Common causes faty change in the liver (fatty liver)

  • Alcohol abuse and diabetes -Hepatotoxins inhibits fatty acid oxidation

• Anoxia. inhibits fatty acid oxidation

• starvation- increase fatty mobilization

• Accumulation Fat in Hepatocytes -Increased up take triglycerides -overproduction of fat cells -Decrease secretion of cells

Accumulation Intacellular Proteins

• Mallori Body of Hyalin eosinophilic cytoplasmic inclusion in liver cells alcoholic. Damaged within the hepatocytes

Deposition of an Abnormal Exogenous Substance:

Accumulation of carbon, Silica particles Coal worker's diseases, Anthracosis

• Aggregates of hyperphosphorylated tau protein that typically stabilize nerve microtubules.

• Accumulation results in primary marker of Alzheimer's disease

• Glycogen accumulates in cells, and disorders collectively disrupt glycogen storage or glycogenosis.

Pigments:

Pigments can be either normal (physiologic) or the pathological conditions

• Endogenus pigment the produce within tissue serves function

• Exogenus pigments- foreign, food, medication and injections

• Nonhematogenus Melanin Lipofuscin Chromaffin

   Melanin endogenous screens
    The basal in accumulate( freckles)
  

• Lipofuscin(Wear tear pigment)is

• Complexes that lipid,brain, etc.

• Nonlurious the cell

Pathologic Calcification

Abnormal composition calcium smaller

1. Dysthophic Calcification when the the normal levels Coagulative) Liquefactive) Fat Caeseous lungs) Gangrenous extremeties) Fibrinoid of arteries(

Pathogenesis dysthophic calcification Intrancellulaor cells regulate calcium

2. Metabolic Calcification whenever there.

Four causes hypercalcemia

hormone Destruction:

Decreased reabsorption lead cause of parahyroidism.

Four major causes of Hypercalcemia

• Increased Secretion of parathyroid hormone
  • Due to either primary parathroid tumors or production of parathyroid hormone-related Malignant Tumor
• Destruction of bone
  • Tumors-increased catabolism multiple nyeloma or leukemia metastases
• Renal failure
  • Phosphate retention
  • Secondary hyperparathy

Definition

• calcium soils dead irreversible Hystrophile
• Derange
• Hipercalcemia reverable
• Hipercalcemia Regardless of the examination granules