Cellular Adaptation 2024 PDF

Ministry of Higher Education and Stage: 2nd Scientific Research Module: mechanism of Wasit University disease College of medicine...

Ministry of Higher Education and Stage: 2nd Scientific Research Module: mechanism of Wasit University disease College of medicine Lecturer Title : cellular adaptation Dr. Zainab abbas alquraishy M.B.Ch.B C.A.B.H.S, DipRCPath Department of pathology and forensic medicine HOMEOSTASIS Normal cell is in a state of functional and structural balance with❖.neighboring cells ADAPTATION Adaptations are reversible functional and structural responses to❖ more severe physiologic stresses and some pathologic stimuli, during which new but altered steady states are achieved, allowing the cell to. survive and continue to function When the stress is eliminated the cell can recover to its original state❖ without any harmful consequences :ADAPTATION RESPONSE Adaptations are reversible changes in the size, number, phenotype, metabolic❖ activity, or functions of cells in response to changes in their environment Hypertrophy Hyperplasia Atrophy Metaplasia.Its aim is to escape from cell injury :The adaptive responses include.Atrophy.1.Hypertrophy.2.Hyperplasia.3.Metaplasia.4 :Atrophy This refers to a decrease in the size of the cell by loss of cell substance. When sufficient numbers of cells are involved, the entire organ or tissue decreases in size i.e. become.atrophic :Causes of atrophy include.Decrease workload e.g. muscular atrophy due to immobilization as in fractured limb.1 Denervation (loss of nerve supply) e.g. paralysis of a limb due to nerve injury or.2.poliomyelitis.Ischemia e.g. brain atrophy as an ageing phenomenon due to atherosclerosis.3.Under nutrition, as in starvation and Kwashiorkor.4 Loss of endocrine stimulation e.g. atrophy of the gonads in hypopituitarism and senile.5.endometrial atrophy (decrease estrogen secretion from the ovary) The aim of this adaptation (atrophy) is to bring into balance cell survival in the face of reduced blood supply, nutrition etc.- the cells become smaller with diminished function and thus reduced metabolic needs.and by doing so they escape injury The reduction in size is due to reduction in the number of its structural components e.g.-.mitochondria, myofilaments, endoplasmic reticulum etc Because of the above cell debris accumulate; some resist digestion by intracellular-.enzymes and become enclosed by a membrane (residual bodies) e.g. lipofuscin granules When the latter is present in sufficient amount it imparts a brown discoloration to the.affected tissue (brown atrophy of the heart) If the cause is severe or persistent, the atrophic cell gets injured and eventually dies to.be replaced by fibrosis mechanisms of atrophy- Atrophied cells had decrease in cell size and organelles, which may reduce❖.the metabolic needs of the cell sufficiently to permit its survival Atrophy results from decreased protein synthesis and increased protein -.degradation in cells (ubiquitin-proteasome pathway).Protein synthesis decreases because of reduced metabolic activity ❖ atrophy is also accompanied by increased autophagy, with resulting❖.increases in the number of autophagic vacuoles Autophagy (“self eating”) is the process in which the starved cell eats its ❖.own components in an attempt to find nutrients and survive A. Normal brain of a young adult. B. Atrophy of the brain in an old male with atherosclerotic disease. Atrophy of the brain is due to aging and reduced blood supply. Note that loss of brain substance narrows the gyri and widens the sulci. The meninges have been stripped from the right half of each specimen to reveal the surface of the brain.  B A A. Is a normal testis. B. Atrophic testis Bilateral atrophy may complicate chronic alcoholism, hypopituitarism, atherosclerosis, chemotherapy or radiation, and severe prolonged illness. Atrophy in skeletal muscle :Hypertrophy This Refers to increase in the size of cells and as a consequence the size of the.organ or tissue containing them (opposite to atrophy) It is due to synthesis of more structural components within the cell (more-.enzymes, more mitochondria and more myofilaments etc.).It can be physiological or pathological- Examples include.Uterus in pregnancy (physiological: hormonal).1.Skeletal muscles in athletes (physiological: increased workload).2 Left ventricle in systemic hypertension (pathological) increased workload; the.3.(ventricle has to contract against increased pressure in the aorta The excessive workload induces increase in cellular constituents i.e. more-.enzymes, more mitochondria (ATP production) and more myofilaments The aim is to achieve equilibrium between the demand and the cell's.functional capacity if the burden persists the hypertrophy reaches a limit beyond which the enlarged muscle is no longer able to compensate for the increased work and.cardiac failure ensues.At this point there is lysis and loss of myofibril's contractile elements : mechanism of hypertrophy❖ activation of cell receptors, gens, growth factors leading to synthesis of.proteins and cell organelles In the heart, the stimulus for hypertrophy is usually chronic❖ hemodynamic overload, resulting from either hypertension or faulty.valves  Uterine hypertrophy in pregnancy On the left is a normal uterus showing the normal mass of smooth muscle in its wall. On the right is a uterus from a pregnant women, in which the striking increase in mass of smooth muscle is evident. At cellular level this is due to both hyperplasia and hypertrophy of uterine smooth muscle.  Normal Vs hypertrophied uterine smooth muscle cells A B A. Small spindle-shaped uterine smooth muscle cells from a normal uterus. Compare this with (B) large, plump hypertrophied smooth muscle cells from a gravid uterus (same magnification). Comparison between normal heart (left) & hypertrophied heart (right) :Hyperplasia This refers to an increase in the number of cells in an organ or tissue leading.to an increase in its size Hyperplasia and hypertrophy are closely related and often occur together- (e.g. in estrogen induced enlargement of the uterus during pregnancy; there.is both hyperplasia and hypertrophy of the myometrium).Not all adult cell types have the same capacity for hyperplasia- Those capable of cell division (labile cells) can undergo profound hyperplastic growth e.g. those of the epidermis, mucosal surfaces, hepatocytes,.fibroblasts and bone marrow cells On the contrary, nerve cells and those of the heart (myocardial cells) and-.skeletal muscle fibers have no capacity for hyperplasia (permanent cells) Intermediate among the above two are those of bone, cartilage and smooth.muscle cells.Hyperplasia is divided into physiological and pathological :A. Physiological hyperplasia is either Hormonal (e.g. proliferation of the breast glandular epithelium in females at.puberty or during pregnancy).Compensatory (e.g. after partial hepatectomy).2 B. Pathological hyperplasia is mostly either due to Excessive hormonal stimulation (e.g. endometrial hyperplasia) or.The effect of growth factors on target cells (as in wound healing).2 : Mechanism of hyperplasia❖ Hyperplasia is the result of growth factor–driven proliferation of mature cells and, in some cases, by increased output of new cells from.tissue stem cells  Endometrial hyperplasia The prominent folds of endometrium in this uterus (opened to reveal the endometrial cavity) are an example of hyperplasia. The hyperplasia involves both endometrial glands and stroma. Multiple papules with rough, pebble-like surfaces at infection sites : Metaplasia.This refers to replacement of one mature cell type by another mature cell type- It may represent an adaptation of cells more sensitive to stress by other cells that.are more resistant to the adverse environment -:Examples include - Squamous metaplasia of the laryngeal and bronchial respiratory epithelium.1.due to habitual smoking Squamous metaplasia of the urothelium in the urinary bladder due to Bilharzia.2.or vesical stone Columnar metaplasia of esophageal squamous epithelium as a result of.3.prolonged reflux of acidic gastric juice into the esophagus In the mesenchymal cells e.g. Formation of bone in long standing fibrosis of.4.soft tissue as a result of injury Metaplasia of normal columnar (left) to squamous epithelium (right) in a bronchus Barrett esophagus: Metaplastic transformation (arrow) of the normal esophageal stratified squamous epithelium (Lt) to mature columnar epithelium Dysplasia This refers to disturbed proliferation of cells associated with atypical.cytological changes that involve cell size, shape, and organization It is not an adaptive process but considered here because of its close-3.relation to hyperplasia It is most commonly encountered in lining epithelia, mostly squamous e.g. that of the uterine cervix and metaplastic squamous epithelium of the.respiratory passages (in habitual smokers) The increased proliferative activity produces greater amounts of DNA and.thus the nuclei appear more hyperchromatic - Although there is an increase in mitotic activity, there are usually no-.abnormal mitoses. The latter is usually met with in cancerous states Dysplastic changes are often found adjacent to foci of cancer indicating that.it is a stage that precedes development of frank malignancy.However, dysplasia does not necessarily progress to cancer Hypoplasia Incomplete development of an organ with reduced cell numbers Degenerative changes: calcification & hyaline change Hyaline change This refers to intra- or extra-cellular homogeneous, pinkish.alteration in sections stained with H& E -:Examples of intracellular hyaline change include Hyaline droplets within renal tubular epithelium in cases of proteinuria. 2. Russel.bodies in plasma cells.Viral inclusions (nuclear or cytoplasmic).3.Alcoholic hyaline in liver cells (Mallory bodies).4 -:Extracellular hyalinization may be encountered in.Collagen in old scar.Hyalinization of arteriolar walls associated with hypertension and diabetes.2.Amyloid deposition.3