Musculoskeletal group case 1
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Both pigs had a vitamin E and selenium deficiency which led to increased free radicals and oxidative cell injury. This caused massive liver necrosis in Pig 1. Pig 2 had a gastric ulcer and epicardial hemorrhage due to microangiopathy from the deficiency. Both pigs also had skeletal muscle necrosis and calcification because the deficiency damaged cell membranes and mitochondria.
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Cell injury is defined as the functional and morphologic effects of a variety of stresses on the cell from various etiologic agents which result in change in its internal and external environment.
The term cell injury is used to indicate a state in which the capacity for physiological adaptation is exceeded.
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Host Factors: Type of cell, Nutritional status of cell etc.
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Cell injury can be reversible or irreversible, leading to cell death. Reversible injury causes pathological changes that can be reversed when the stressor is removed, while irreversible injury causes permanent changes and cell death. Cell injury is caused by various stressors like hypoxia, physical/chemical agents, microbiological agents, genetic defects, and nutritional imbalances. The key targets of injury are the mitochondria, cell membrane, proteins, cytoskeleton, and DNA. Injury disrupts cellular energy production and increases reactive oxygen species, calcium influx, and damage to membranes and DNA/proteins. This can lead to either reversible injury or the irreversible processes of necrosis or apoptosis.
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Cell Injury and its causes ppt pdf
Cell Injury in hindi
Cell injury is defined as the functional and morphologic effects of a variety of stresses on the cell from various etiologic agents which result in change in its internal and external environment.
The term cell injury is used to indicate a state in which the capacity for physiological adaptation is exceeded.
This may occur when the stimulus is excessive or when the cell is no longer capable to adapt without suffering some form of damage.
Cellular response to stress may vary depending upon following two factors:
Host Factors: Type of cell, Nutritional status of cell etc.
Factors pertaining to injurious agent: Its type, dose etc.
Etiology/Causes
Hypoxia and Ischaemia
Physical Agents
Chemicals and Drugs
Microbial Agents
Immunologic Causes
Nutritional Derangements
Ageing
Psychogenic Cause
Iatrogenic Cause
Idiopathic Disease
#rohitkumartrivedi
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Adjustments which the cells make in response to stresses.
Adjustments may be for physiologic need or response to non-lethal pathogenic injury (Pathologic adaptation).
Adaptive responses are reversible on withdrawal of stimulus.
If the irritant stimulus persists for longer duration or is more lethal, the cell may not be able to survive.
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This document discusses various types of cell injury and cell death. It describes how cells transition from a normal state to a reversibly injured state to irreversibly injured and eventually dead through apoptosis or necrosis. The main causes of cell injury are oxygen deprivation, physical or chemical agents, infections, immune reactions, genetics, and nutritional imbalances. The key mechanisms of injury are ATP depletion, mitochondrial damage, calcium dysregulation, oxidative stress, membrane damage, and DNA/protein damage. Different patterns of necrosis like coagulative, liquefactive, and caseous are described. Apoptosis and other forms of programmed cell death like necroptosis are also outlined. Intracellular accumulations in various diseases are briefly discussed.
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3. Specific causes of injury like ischemia and hypoxia can lead to ATP loss, pH changes, impaired sodium pumping, and decreased protein synthesis, ultimately causing reversible or irreversible cell injury.
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athero-(meaning porridge) referring to the soft lipid-rich material in the centre of atheroma, and
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2. Vasculitis refers to inflammation of blood vessels which has various immune-mediated forms that can affect large, medium, or small vessels.
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2122metabolism.ppt
A proper diet requires balancing carbohydrates, fats, proteins, vitamins, minerals and water. Carbohydrates provide energy and are obtained from plants. Lipids provide insulation and energy storage while proteins are needed for building tissues. Vitamins and minerals assist enzymes and are obtained from foods. The body metabolizes nutrients through cellular respiration to produce energy in the form of ATP. Free radicals can damage cells but antioxidants neutralize them.
Iron overload
1. Iron overload, also known as hemochromatosis, occurs when the body absorbs more iron than it loses, causing excess iron to accumulate and damage organs. It is commonly caused by a genetic disorder or frequent blood transfusions.
2. Hepcidin regulates iron levels in the body. Iron overload results from low hepcidin leading to increased iron absorption in the gut and spleen.
3. Treatment involves regular phlebotomy to remove excess iron from the body. Phlebotomy can prevent organ damage if started early and allows patients to live normally once iron levels are normalized.
cell injury.pptx
Cell injury can be reversible or irreversible, leading to cell death. Reversible injury causes pathological changes that can be reversed when the stressor is removed, while irreversible injury causes permanent changes and cell death. Cell injury is caused by various stressors like hypoxia, physical/chemical agents, microbiological agents, genetic defects, and nutritional imbalances. The key targets of injury are the mitochondria, cell membrane, proteins, cytoskeleton, and DNA. Injury disrupts cellular energy production and increases reactive oxygen species, calcium influx, and damage to membranes and DNA/proteins. This can lead to either reversible injury or the irreversible processes of necrosis or apoptosis.
Free Radicals
This document discusses free radicals and their role in various diseases and conditions. It covers how free radicals are involved in cancer development, aging, and other diseases like diabetes, hypertension, neurological disorders, and cataracts. It also discusses how antioxidants from foods and supplements can help reduce free radical damage and risk or progression of these conditions. The document provides details on specific antioxidants like vitamins C and E and their effects. It also summarizes recent research on uses of antioxidants in treatments.
Antioxidant medical
This document discusses reactive oxygen species (ROS), antioxidants, and their roles in various disorders. It begins by defining ROS as unstable molecules that can damage cells, and listing their sources. ROS are necessary in small amounts but can cause issues in excess. Antioxidants help neutralize ROS and prevent oxidative damage. The document then examines the roles of ROS and antioxidants in specific disorders like diabetes, cardiovascular disease, chronic fatigue, cancers, pregnancy complications, and male infertility. It provides treatment options like antioxidant supplementation to help control ROS levels and reduce related disease complications.
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Atherosclerosis is caused by plaques made of lipid and fibrous tissue building up in the vessel walls. It is the most common type of arteriosclerosis. The plaques can rupture, leading to thrombosis and blockages that cause issues like heart attacks or strokes. Risk factors include hyperlipidemia, hypertension, smoking, and diabetes. Macrophages play a key role by taking up lipid in the plaques. Atherosclerosis can affect arteries throughout the body and cause peripheral vascular disease, mesenteric ischemia, or cerebrovascular disease in addition to coronary artery disease.
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The document summarizes common diseases affecting neonatal and growing pigs. For neonatal pigs, it lists Escherichia coli, transmissible gastroenteritis coronavirus, Clostridium perfringens type C, coccidiosis, and rotavirus. For growing pigs, it lists Brachyspira hyodysenteriae causing swine dysentery, Lawsonia intracellularis causing proliferative enteropathy, and Salmonella Typhimurium which can infect humans. It also provides images showing the pathogenesis of proliferative enteropathy caused by L. intracellularis.
Bone rounds 3 1-11
This document discusses several nutritional disorders that can occur in chickens including rickets, manganese deficiency, riboflavin deficiency, and others. Rickets is caused by calcium or phosphorus deficiencies and results in bending of bones. Manganese deficiency causes chondrodystrophy, displacing the gastrocnemius tendon. Riboflavin deficiency causes curled toe paralysis. Nutritional deficiencies can be caused by inadequate levels of vitamins and minerals like calcium, phosphorus, vitamin D3, thiamine, riboflavin, pyridoxine, and manganese.
Musculoskeletal tumors
Musculoskeletal tumors can originate from a multistep accumulation of mutations leading to unregulated cell proliferation. Osteosarcoma is the most common type of bone tumor, arising from osteoblasts. It is diagnosed through radiography, cytology, and histopathology. Grading is based on features like pleomorphism and mitoses. Treatment involves surgery with chemotherapy. Variants include osteoblastic, chondroblastic, telangiectatic and fibroblastic subtypes. Multilobular tumor of bone is a slow growing but potentially malignant tumor appearing as islands of bone or cartilage surrounded by spindle cells. Chondrosarcoma arises from cartilage and osteochondroma involves cartilage capped bone protrusions.
Lecture 12 disturbances in growth and differentiation
This document discusses several topics related to embryology, teratology, oncology, and cell biology. It covers coordinated events in embryology, cell differentiation and regeneration, renal dysplasia vs chronic renal failure. It also discusses teratology including causes of birth defects, developmental syndromes, errors of morphogenesis, and relationships between genotype and phenotype. Further, it covers mutations including types of chromosome mutations, molecular diagnostics, single gene mutations, and diagnosis of single gene mutations. Finally, it discusses disturbances of cell proliferation, the cell cycle, cell cycle regulation, and cancer genetics.
Parvoviral myocarditis in puppies
All 4 puppies submitted for evaluation showed signs of heart failure and respiratory distress. On post-mortem examination, 3 of the 4 puppies showed gross lesions consistent with heart failure, including pulmonary edema and congestion. Microscopic examination found histologic lesions typical of parvoviral myocarditis in the hearts of all 3 puppies examined, including lymphocytic inflammation and intranuclear inclusions. Immunohistochemistry confirmed the presence of canine parvovirus-2 in the hearts of 2 puppies. No other significant infectious agents were identified in the heart or lungs of the puppies.
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Lecture 12 disturbances in growth and differentiation
Lecture 12 disturbances in growth and differentiation
Musculoskeletal group case 1
- 1. Musculoskeletal Group Case #1 4/21/08 Brian Caserto
- 2. Lesion Cause Relationship Pig 1 Massive/ Centrilobular Hepatic Necrosis Vit E/ Selenium Deficiency increased free rad oxidative necrosis Vit E- Cell membranes Free radical scavenger Selenium Cytosol free radical scavenger Pig 2 Gastric Ulcer Microangiopathy Induced by Vit E Selenium def Local ischemia infarciton necrosis and ulceration Epicardial Hemorrhage Microangiopathy Vessel damage hemorrhage Both Pigs Skeletal muscle necrosis and calcification Vit E Sel Def cell membrane damage decreased Mitochondrial ATP ER cant sequester Ca++ Hypercontraction myofiber coagulation
- 3. Oxidative cell injury and necrosis Antioxidant deficiency Increased Cellular free radicals Cell membrane damage Mitochondrial membrane damage Vitamin E Vitamin E Selenium- Glutathione peroxidase Mitochondria
- 4. Liver Affected Tissues Blood Vessels Skeletal Muscle Necrosis Ischemia and infarction Hemorrhage Myocyte degeneration and calcification Thrombosis Necrosis
- 5. Vitamin E Selenium Membrane protectors Cytosol protectors Cellular Defense against oxidant injury Free Radicals: Superoxide anion Hydrogen peroxide Hydroxyl radical Glutathione peroxidase: 2GSH + H 2 O 2 -> GS–SG + 2H 2 O Glutathione reductase: GS–SG + NADPH + H + -> 2 GSH + NADP + .
- 6. Vitamin E- Alpha Tocopherol Vitamin C- Ascorbic Acid
- 8. Liver: Massive to centrilobular necrosis
- 9. Liver: Massive to centrilobular necrosis
- 10. Liver: Massive to centrilobular necrosis Necrosis
- 15. Skeletal muscle: Necrosis and calcification Necrosis
- 16. Skeletal muscle: Necrosis and calcification White areas are necrotic and gritty (calcification)
- 17. Skeletal muscle: Necrosis and calcification Muscle fibers are disrupted and hypercellular
- 18. Skeletal muscle: Necrosis and calcification Calcification