pathology

1. Chapter Two adaptation and injury

3. Irreversible Injury (cell death) Reversible Injury adaptation normal When cells encounter physiological stresses or pathological stimuli, they undergo adaptation, achieving a new a steady state and preserving viability. If the adaptive capacity is exceeded, cell injury develops. Within certain limits, injury is reversible. with severe and persistent stress, irreversible injury results.

6. Incomplete occlusion of coronary artery Complete or prolonged occlusion hypertesion Prolonged starvation

18. Types of adaptation

23. Fig 2-5

24. Cerebral atrophy - Alzheimers:

30. Hydropic change in ischemic - kidney Microvilli

31. Muscle ischemic atrophy:

36. Hydronephrosis

41. Fig 2-6

44. Heart hypertrophy in hypertension: Left Ventricle

47. HYPERPLASIA

50. PARTIAL HEPATECTOMY Priming Proliferation Growth lnhibition GROWTH FACTORS AND CYTOKINES HGF TGF-  EGF TNF-  IL-6 Others ADJUVANTS Norepinephrine Insulin Glucagon Thyroid hormone GROWTH INHIBITORS TGF-  Others Growth factors Adjuvanis Matrix degradation

81. Irreversible Injury Reversible Injury adaptation normal

84. Cellular swelling

98. mucoid degeneration

101. Chemical nature of amyloid fibrils Two major forms: AL (amyloid light chain protein) AA (amyloid-associated protein): Derived from serum AA (12kd) synthesized in liver and elevated in inflammatory states.

102. Minor forms of amyloid fibrils: Transthyretin (TTR): A mutant form of a serum protein in familial amyloid polyneuropathy. A variant of TTR in aging. Beta-2-microglobulin (the component of class I MHC molecules) in long-term hemidialysis.

103. Minor forms of amyloid fibrils: Beta-2-amyloid protein forms the core of cerebral plaques and deposits within cerebral vessel walls in Alzheimer disease, deriving from a transmembrane glycoprotein precursor.

104. Minor forms of amyloid fibrils: Transthyretin (TTR): A mutant form of a serum protein in familial amyloid polyneuropathy. A variant of TTR in aging. Beta-2-microglobulin (the component of class I MHC molecules) in long-term hemidialysis.

105. Minor forms of amyloid fibrils: Beta-2-amyloid protein forms the core of cerebral plaques and deposits within cerebral vessel walls in Alzheimer disease, deriving from a transmembrane glycoprotein precursor.

121. Metastatic calcification Affecting Interstitial tissue of gastric mucosa Kidneys Lungs Pulmonary veins Systemic arteries

122. Section C CELL DEATH

128. 1)Three pattern of nuclear changes Karyolysis (DNase activity) Pyknosis (DNA condensation) Karyorrhexis (fragmentation of pyknotic nucleus)

134. Coagulation necrosis Denatures of both structural and enzymatic proteins by injury or the subsequent increasing intracellular acidosis.

135. Renal Infarction - Coagulative

136. Splenic Infarction - Coagulative necrosis

137. Infarction - Adrenal gland:

139. Caseous necrosis A subtype of coagulation necrosis White and cheesy Tuberculosis Completely obliterated tissue architecture

142. Extensive Caseous necrosis Tuberculosis

145. Liver abscess: Liquifactive necrosis

146. Stroke- Liquifactive necrosis

154. Caseous necrosis - Tuberculosis

155. Gangrene - Amputated Diabetic foot

158. Gangrene Intestine - Thrombosis.

167. Section D APOPTOSIS

171. Necrosis Apoptosis Stimuli Hypoxia Physical Toxins Pathological Histology Cell swelling Single cell Coagulation N Chromatin Disruption of condensation organelles Apoptotic bodies DNA Random Internucleosomal breakdown Diffuse

172. Necrosis Apoptosis Mechanism ATP depletion Gene activation Membrane Endonuclease injury Free radicals Tissue Inflammation No inflammation reaction Phagocytosis of apoptotic bodies

175. Biochemical features of apoptosis 1.PROTEIN CLEAVAGE: Caspases (cysteine protease) Nuclear scaffold Cytoskeletal protein 2.PROTEIN CROSS-LINKING: Transglutaminase Cytoplasmic protein  shrunken shalls  apoptotic bodies Biochemical features of apoptosis

176. 3. DNA breakdown: 50-300 kb pieces Ca2+, Mg2+ dependent endonucleases DNA oligonucleosomes DNA ladders (also seen in necrosis) 4. PHAGOCYTIC RECOGNITION Receptors on macrophages for the surface components (phosphatidylserine, thrombospondin) on apoptotic bodies.

183. normalcell Cellular swelling, chromatin cluping Membrane damage Nuclear chromatin condensation and fragmentation Cytoplasmic budding and apoptosisi body Phagocytosisi of apoptosis body The sequential ultrastructual changes in necrosis and apoptosis

184. Apotosis of hepatocytes

185. Comparison of cell death by apoptosis and necrosis

191. Telomerase in ageing: Germ Cells Somatic Cells

193. Pathology of elderly