HomeCoursesMEDSCI 203: Mechanisms of DiseaseLecture 24 Lecture 24 1. What are symptoms of diabetes? "thirst (polydispsia), frequent urination (polyuria)"What are symptoms of diabetes?== "thirst (polydispsia), frequent urination (polyuria)" 2. What is diabetes insipidus?=Â = Deficiency in vasopressin What is diabetes insipidus?=Â = Deficiency in vasopressin 3. How can ADH deficiency occur? Problem with secretion in hypothalamus (eg. tumour compressing neuron) or with V2 receptor in kidneyHow can ADH deficiency occur?== Problem with secretion in hypothalamus (eg. tumour compressing neuron) or with V2 receptor in kidney 4. What causes diabetes mellitus? HyperglycaemiaWhat causes diabetes mellitus?== Hyperglycaemia 5. What is the effect of hyperglycaemia on the tissues?= =Dehydration What is the effect of hyperglycaemia on the tissues?= =Dehydration 6. What does the body do with all the fluid absorbed from the tissues? Excretes in urine (polyuria)What does the body do with all the fluid absorbed from the tissues?== Excretes in urine (polyuria) 7. What happens with excess glucose in blood? "Excreted, as once glucose transporters are saturated additional glucose cannot be reabsorbed"What happens with excess glucose in blood?== "Excreted, as once glucose transporters are saturated additional glucose cannot be reabsorbed" 8. What test can signify diabetes mellitus? "Glucosuria, blurred vision"What test can signify diabetes mellitus?== "Glucosuria, blurred vision" 9. What can hyperglycaemia increase the risk of? "CV disease, renal failure, neuropathy, blindness, infections"What can hyperglycaemia increase the risk of?== "CV disease, renal failure, neuropathy, blindness, infections" 10. Where is insulin produced? Beta cells in islets of langehans in pancreaseWhere is insulin produced?== Beta cells in islets of langehans in pancrease 11. What does insulin do? Stores glucose in liver as glycogenWhat does insulin do? ==Stores glucose in liver as glycogen 12. What is glucose used for? Energy productionWhat is glucose used for?== Energy production 13. What does glucagon do?== Converts glycogen to glucose 14. What happens to insulin vs glucagon in hypoglycaemia? "Decreased insulin, increased glucagon"What happens to insulin vs glucagon in hypoglycaemia? =="Decreased insulin, increased glucagon" 15. What is Type I diabetes mellitus? Dysfunction in insulin productionWhat is Type I diabetes mellitus?== Dysfunction in insulin production 16. What is Type II diabetes mellitus? Dysfunction in insulin receptor pathwayWhat is Type II diabetes mellitus?== Dysfunction in insulin receptor pathway 17. What happens to glycogen in diabetes mellitus type I? "Decreased insulin, increased glucagon, decreased glycogen, hyperglycaemiea"What happens to glycogen in diabetes mellitus type I?== "Decreased insulin, increased glucagon, decreased glycogen, hyperglycaemiea" 18. What causes dysfunction of insulin receptor pathways in DMT2? "Genetic predisposition, FFAs"What causes dysfunction of insulin receptor pathways in DMT2?== "Genetic predisposition, FFAs" 19. What transporters facilitate glucose uptake? "GLUT1, GLUT4"What transporters facilitate glucose uptake?== "GLUT1, GLUT4" 20. What activates GLUT4 receptors? Insulin in peripheral cells such as skeletal muscleWhat activates GLUT4 receptors? ==Insulin in peripheral cells such as skeletal muscle 21. What does the body do to obtain energy if glucose is not available? Anaerobic respirationWhat does the body do to obtain energy if glucose is not available? ==Anaerobic respiration 22. What is the negative effect of chronic anaerobic respiration? "Increase in ketone bodies => ketoacidosis of the blood, weight loss"What is the negative effect of chronic anaerobic respiration?== "Increase in ketone bodies => ketoacidosis of the blood, weight loss" 23. What are likely causes of T1 DM? Autoimmune diseaseWhat are likely causes of T1 DM?== Autoimmune disease 24. What are the factors of T1 DM autoimmune diseases? "Environmental triggers, genetic predisposition"What are the factors of T1 DM autoimmune diseases?== "Environmental triggers, genetic predisposition" 25. What destroys beta cells in the islets of Langerhan? Inflammatory lymphocytesWhat destroys beta cells in the islets of Langerhan?== Inflammatory lymphocytes 26. What could cause insulitis (lymphocytic infliltration of islets of Langerhan? "Viral infection, environmental triggers"What could cause insulitis (lymphocytic infliltration of islets of Langerhan? =="Viral infection, environmental triggers" 27. What may be genetic factors of T1 DM? "Abnormal expression of MHC antigens (HLADR3, HLADR4)"What may be genetic factors of T1 DM?== "Abnormal expression of MHC antigens (HLADR3, HLADR4)" 28. How do we know T2 DM is genetically predisposed? Monozygotic twins both susceptibleHow do we know T2 DM is genetically predisposed?== Monozygotic twins both susceptible 29. What are major causes of T2 DM? "Lack of exercise, excess food consumption"What are major causes of T2 DM?== "Lack of exercise, excess food consumption" 30. How do lifestyle factors cause T2 DM? Increased glucose > increased FFAs > hypertrophy of adipocytes > increased release of adipokines > FFA acumulation in skeletal muscle and liverHow do lifestyle factors cause T2 DM?== Increased glucose > increased FFAs > hypertrophy of adipocytes > increased release of adipokines > FFA acumulation in skeletal muscle and liver 31. What else do adipokines do? "Inflammatory ""go"" signals"What else do adipokines do?== "Inflammatory ""go"" signals" 32. What do FFAs and inflammation cause? Dysfunction of intracellular signalling (eg. GLUT4 insertion)What do FFAs and inflammation cause?== Dysfunction of intracellular signalling (eg. GLUT4 insertion) 33. How can T2 DM progress to chronic dysfunction? Hyperinsulinaemia => beta cell dysfunciton or insulin resistanceHow can T2 DM progress to chronic dysfunction?== Hyperinsulinaemia => beta cell dysfunciton or insulin resistance 34. What is the difference between T1 DM and chronic T2 DM insulin production/resistance? T2 DM not autoimmune mediated but inflammatory signals from adipocytesWhat is the difference between T1 DM and chronic T2 DM insulin production/resistance?== T2 DM not autoimmune mediated but inflammatory signals from adipocytes 35. What is the effect of chronic hyperglycaemia on proteins? Glucose binds to amino acids => Advanced glycosylation end products (AGEs)What is the effect of chronic hyperglycaemia on proteins?==Glucose binds to amino acids => Advanced glycosylation end products (AGEs) 36. What does glycation of proteins result in? "Damage to protein structure => blood vessel, nerve, connective tissue damage/change"What does glycation of proteins result in?== "Damage to protein structure => blood vessel, nerve, connective tissue damage/change" 37. What proteins have impaired function as a result of glycation? "Basement membrane, myelin, collagen"What proteins have impaired function as a result of glycation?== "Basement membrane, myelin, collagen" 38. How does hyperdlycaemia cause osmotic swelling and cell damage? High glucose > aldose reductase conversion of glucose into sorbitol > sorbitol accumlulation creates dysfunction to Na/K ATPaseHow does hyperdlycaemia cause osmotic swelling and cell damage?== High glucose > aldose reductase conversion of glucose into sorbitol > sorbitol accumlulation creates dysfunction to Na/K ATPase 39. How does excess food intake activate protein kinase c? Increased glucose and FFAs > increased DAG > activation of PKCHow does excess food intake activate protein kinase c?== Increased glucose and FFAs > increased DAG > activation of PKC 40. What does activation of PKC do? "Increases permeability of blood vessels, proliferation of endothelial and smooth muscle cells, ECM production, cytokine production, glycation"What does activation of PKC do? =="Increases permeability of blood vessels, proliferation of endothelial and smooth muscle cells, ECM production, cytokine production, glycation" 41. What is the result of the toxic effect of glucose? "Angiopathy, nephropathy, retinopathy, neuropathy"What is the result of the toxic effect of glucose?== "Angiopathy, nephropathy, retinopathy, neuropathy" 42. How does hyperglycaemia cause macro angiopathy?= =Increase in atherosclerosis How does hyperglycaemia cause macro angiopathy?= =Increase in atherosclerosis 43. How does hyperglycaemia cause atherosclerosis? "Activation of PKC, glycation, inflammation, plasminogen inhibitor => inhibition of fibrinolysis"How does hyperglycaemia cause atherosclerosis?== "Activation of PKC, glycation, inflammation, plasminogen inhibitor => inhibition of fibrinolysis" 44. How does hyperglycaemia cause nephropathy and retinopathy? Damage to small blood bessels in kidney and retinaHow does hyperglycaemia cause nephropathy and retinopathy?== Damage to small blood bessels in kidney and retina 45. What is scarring in glomeric blood vessels called? GlomerusclerosisWhat is scarring in glomeric blood vessels called? ==Glomerusclerosis 46. What is a complication of retinal angiopathy? "Angiogenesis produces leaky blood vessels causing increaed exudate, lipid deposition and scarring"What is a complication of retinal angiopathy?== "Angiogenesis produces leaky blood vessels causing increaed exudate, lipid deposition and scarring" 47. What damages schwann cells? "Sorbitol, glycation, PKC activation"What damages schwann cells?== "Sorbitol, glycation, PKC activation" 48. How does DM increase infection? "Decreased leukocyte function, decreased cytokine secretion of macrophages, increased ketoacidosis => fungal infection susceptibility"How does DM increase infection?== "Decreased leukocyte function, decreased cytokine secretion of macrophages, increased ketoacidosis => fungal infection susceptibility" Loading...
