Pathology Lecture 2: Cell Injury - PDF

Pathology lecture (2) CELL INJURY Pathology  The normal ability of cells to maintain stable physiologic parameters. Cellular dysfunction→ Organ dysfunction →Clinical expression.  Variety of changes (molecular and st...

Pathology lecture (2) CELL INJURY Pathology  The normal ability of cells to maintain stable physiologic parameters. Cellular dysfunction→ Organ dysfunction →Clinical expression.  Variety of changes (molecular and structural) of the stressed cell due to external & internal environmental changes (altered homeostasis) a) Ischemia : as arterial occlusion b) Inadequate oxygenation: heart or lung disease c) Decreased oxygen carrying capacity of the RBCs: anemia  Viruses, bacteria, fungi  Trauma, heat, cold, radiation  Concentrated acids, alkalies, poisons, drugs  Autoimmune diseases.  Excess as in obesity or deficient as in protein and vitamins deficiency. Effects of cell injury depend on: 1. The nature, duration and severity of injurious agents. 2. The type and state of injured cell : Very sensitive to hypoxia (2-5 min) Can adapt hypoxia for (2-6 hours) Cell affection could be in the form of one of the following: 1- Adaptation 2- Reversible cell injury 3- Irreversible cell injury 4- Intracellular and extracellular deposits. Pathology Modification of cell structure and functions in response to excess physiologic or pathologic stress to preserve the vitality of cells.(growth disturbance due to stress) It is reversible. Too much stress exceeds the cell’s adaptive capacity leads to injury. 1. Atrophy. 2. Hyperatropgy. 3. Hyperplasia. 4. Metaplasia. 5. Dysplasia. Pathology  Decrease in size of organ by decrease in size and/or number of its cells.  Cells become smaller due to: 1. Decreased protein synthesis. 2. Increased protein degradation. 3. Cell deaths.  Due to: decreased workload, decreased blood supply, decreased nutrition, decreased hormones or denervation.  Aging  Disuse atrophy: after bone  Uterus atrophy: after labor. fracture.  Thymus atrophy: after  Neurogenic atrophy: denervation. puberty.  Thermal atrophy: undescended testis.  Ischemic, nutritional & Endocrinal.  Increase in size of organ due increase in size of its constituent cells.  Increased synthesis of structural proteins & organelles due to: 1. Increased functional demand [e.g. Mechanical]. 2. Growth factor 3. Hormons.  Uterine hypertrophy  Left ventricular hypertrophy in  Muscle hypertrophy in athletes. systemic hypertension Pathology  Enlargement of organ due to increase in number of its component cells.  Cell proliferation due to: 1. Increased functional demand [e.g. compensatory]. 2. Growth factor stimulation. 3. Hormonal stimulation  Hyperplasia of female breast  Bone marrow after hemorrhage. in puberty, pregnancy and  Skin or mucous membrane lactation. around ulcer.  Liver cells after partial destruction.  Prostate and endometrium (hormones)  Change of one type of tissue to another type of same category, epithelium to epithelium or connective tissue to connective tissue.  Always pathological  Reprogramming of stem cells, differentiate along a new pathway to tolerate physical or chemical stress.  Reprogramming Reversible Respect histogenic boundaries with Risk of malignancy  Squamous metaplasia of respiratory epithelium in smokers.  Intestinal metaplasia of esophagus in reflux esophagitis (Barrette’s esophagus).  Squamous metaplasia of urinary bladder in bilharziasis. Pathology  Degeneration (Sublethal) caused by mild injurious agent of short duration.  Affects active functioning cells with higher rate of metabolism more than supporting stromal cells.  The functional and morphologic changes are reversible if the damaging stimulus is removed. Cloudy swelling & Hydropic degeneration. Fatty change.  Caused by severe injurious agent of long duration 1. Necrosis. 2. Apoptosis (single cell death). Mild (in cloudy) and excess (in hydropic) intracellular water accumulation. Caused by mild injury or injury of short duration. Occurs in organs rich in mitochondria e.g. renal tubules mostly proximal convoluted tubules, cardiac muscles and hepatocytes. Mitochondrial function is disrupted first → Decreased ATP leading to; increase in intracellular Na & Lactic acid.The increase in the cytoplasmic osmotic pressure helps intra-cellular water accumulation → cell swelling Pathology The affected organ appears: swollen, soft, bloodless and pale due to compression of the capillaries by the swollen cells. Outer surface: smooth with tense capsule and rounded borders. Cut surface: appears cloudy (less glistening), opaque and bulges outwards. Cloudy swelling  The cells are swollen with compressed capillaries in between.  The nucleus is normal  The cytoplasm is granular. Hydropic degeneration  The cells are swollen with compressed capillaries in between.  The nucleus is normal.  The cytoplasm is pale and shows multiple vacuoles. Pathology Reversible cell injury characterized by accumulation of neutral fat in functioning cells Hypoxia. Bacterial toxins of acute and chronic infections. Chemical agents as alcohol, phosphorous and carbon tetrachloride. The affected organ appears: swollen, soft, pale yellow. Outer surface: smooth with tense capsule and rounded borders. Cut surface: appears yellow, bulges outwards and greasy to touch. The cells appear swollen and show multiple tiny cytoplasmic vacuoles The fat globules fuse together forming a big globule that pushes and flattens the nucleus against the cell membrane giving the cell a signet ring appearance. The swollen cells compress the intercellular capillaries. Fat special stains done on frozen sections During routine staining of sections by Hx and E fat is dissolved during preparation by the organic solvents. For demonstration of fat, frozen sections are used and stained by a. Sudan III and oil red O…….Orange red - Osmic acid…….Black