Презентация Water Salt Balance 2008

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  Metabolic disorders Part 3 07. 12. 08  Metabolic disorders Part 3 07. 12.

  Typical mechanisms of carbohydrate metabolism disorders 1. Disorders of digestion and absorption 2. Disorders Typical mechanisms of carbohydrate metabolism disorders 1. Disorders of digestion and absorption 2. Disorders of the gluconeogenesis and glycolysis 3. Altered synthesis and breakdown of glycogen (glycogenoses) 4. Disorders of glucose uptake by the cells 5. Hypoglycemia, hyperglycemia

  Normal blood glucose concentration – 3, 3 -5, 5 mmol/l Normoglycemia Peripheral cells. Intestine Normal blood glucose concentration – 3, 3 -5, 5 mmol/l Normoglycemia Peripheral cells. Intestine Liver ( glycogenolysis , glycogenesis, gluconeogenesis )Insulin Counter hormones — +Glucostat – maintenance of the constant blood glucose level

  Regulation of blood glucose level Glucose counter regulatory hormones:  elevation of blood glucose. Regulation of blood glucose level Glucose counter regulatory hormones: elevation of blood glucose. Lowering of blood glucose: Insulin Catecholamines Glucagon Cortisol Growth hormone Thyroid hormons

  The effects of insulin on metabolism Type of metabolism Liver cells Fat cells Muscle The effects of insulin on metabolism Type of metabolism Liver cells Fat cells Muscle Glucose ↓ gluconeogenesis; ↓ glycogenolysis; ↑ glycolysis; ↑ glycogenesis ↑ glucose uptake; ↑ glycerol synthesis ↑ glucose uptake; ↑ glycolysis; ↑ glycogenesis Fat ↑ lipogenesis; ↓ lipolysis ↑ synthesis of triglycerides; ↑ fatty acid synthesis; ↓ lipolysis — Protein ↓ protein breakdown — ↑ amino acid uptake; ↑ protein synthesis

 Features of type 1 and 2 diabetes Features of type 1 and 2 diabetes

  Insulitis – a mechanism of the type I diabetes mellitus Insulitis – a mechanism of the type I diabetes mellitus

  Role of viruses in the pathogenesis of T 1 DM Role of viruses in the pathogenesis of T 1 DM

  Proposed mechanisms of ββ -cell death Proposed mechanisms of ββ -cell death

  Pathogenesis of diabetic ketoacidosis Deficiency of insulin; excess of counter regulatory hormons Decreased glucose Pathogenesis of diabetic ketoacidosis Deficiency of insulin; excess of counter regulatory hormons Decreased glucose utilization Increased glucose production. Increased mobilization of fatty acids Ketonemia Ketonuria Hyperglycemia Glucosuria Osmotic diuresis Blood hyperosmolarity and dehydration. Metabolic acidosis CNS impairment Circulatory disorders (hypotension, tachycardia)Coma

  Normal state Diabetic ketoacidosis Normal state Diabetic ketoacidosis

  Pathogenesis of T 2 DM Pathogenesis of T 2 DM

  1. Prereceptor level ( anomalous insulin ) 2. Receptor level ( decreased number of 1. Prereceptor level ( anomalous insulin ) 2. Receptor level ( decreased number of insulin receptors, decreased affinity of the receptors ) 3. At the level of glucose transport ( decreased number of GLUT) 4. Postreceptor level ( disorders of signal transduction and kinase phosphorylation )Mechanisms of insulin resistance

  Components of the insulin resistance syndrome Components of the insulin resistance syndrome

  Consequences of hyperglycemia ● Glucosuria ,  polyuria ,  secondary polydipsia … ● Consequences of hyperglycemia ● Glucosuria , polyuria , secondary polydipsia … ● Blood hyperosmolarity, tissue dehydration, hyperosmolar coma ● Non-enzymatic glycation of proteins (albumins, hemoglobin etc. ) – formation of advanced glycation end-products ● Endothelial dysfunction ( micro- and macroangiopathy ) ● Formation of autoantigens (autoimmune reactions)

  Role of lipid glycation in the pathogenesis of atherosclerosis (macroangiopathy) in diabetes Role of lipid glycation in the pathogenesis of atherosclerosis (macroangiopathy) in diabetes

  Cellular effects of advanced glycation end-products Cellular effects of advanced glycation end-products

  Advanced glycation end-products mediated vessel injury: pathogenesis of diabetic microangiopathy Advanced glycation end-products mediated vessel injury: pathogenesis of diabetic microangiopathy

  Major clinical manifestations of diabetes: - Retinopathy - Cerebrovascular disease - Premature coronary artery Major clinical manifestations of diabetes: — Retinopathy — Cerebrovascular disease — Premature coronary artery disease — Autonomic dysfunction (gastroparesis, diarrhea) — Peripheral vascular disease — Peripheral neuropathy (pain, loss of sensation) — Nephropathy (( renal failure ))

  Diabetic foot ulcers: peripheral arterial disease + diabetic neuropathy Diabetic foot ulcers: peripheral arterial disease + diabetic neuropathy

  Diabetes is currently one of the leading causes of renal failure Normal gromerulus Diabetic Diabetes is currently one of the leading causes of renal failure Normal gromerulus Diabetic nephropathy

  Diabetes is a leading cause of blindness in the USA Diabetic retinopathy Diabetes is a leading cause of blindness in the USA Diabetic retinopathy

  • Increased utilization of glucose by the cells  –  increased insulin production, • Increased utilization of glucose by the cells – increased insulin production, treatment with insulin – formation of insulin-like growth factors • Disorders of glycogenolysis ( glycogenoses, liver cirrhosis ) • Disorders of glucose reabsorption ( renal diabtes ) • Prolonged intensive physical exercise Mechanisms of hypoglycemia

  Mechanisms of compensation in hypoglycemia ● Activation of sympathetic nervous system  ( glycogenolysis Mechanisms of compensation in hypoglycemia ● Activation of sympathetic nervous system ( glycogenolysis ) ● Increased production of glucose counter regulatory hormones , gluconeogenesis , activation of lipolysis and decreased utilization of glucose

  Hypoglycemic coma Blood glucose of less than 2, 0 -1, 5 mmol/l Amount of Hypoglycemic coma Blood glucose of less than 2, 0 -1, 5 mmol/l Amount of glucose in the neurons Brain hypoxia. Energy deficiency in the neurons Water and electrolyte imbalance. Injury of the neuronal membranes Cellular hyperhydratation Disturbed electrogenesis cortex function Excitation of the neurons of the spinal cord. Excitation, seizures Coma

  Basics of Body Fluids • Water is primary body fluid. 40-60 of weight in Basics of Body Fluids • Water is primary body fluid. 40%-60% of weight in adult. Affected by age, sex, & body fat. • Distribution: 2 major compartments-ICF & ECF. • ICF: in cells. 2/3 of body fluid in adults. • ECF: outside cells. 1/3 of body fluid. 4 compartments-intravascular, interstitial, lymph, & transcellular

  Schematic representation of body fluid compartments in man (70 kg) Schematic representation of body fluid compartments in man (70 kg)

  Basics of Body Fluids • Intravascular: plasma • Interstitial: surrounds the cells; 3/4 ECF Basics of Body Fluids • Intravascular: plasma • Interstitial: surrounds the cells; 3/4 ECF • Transcellular: CSF, pericardial, pleural, etc • Lymph: lymphatic system

  Water Balance Water Balance

  Edema – pathological accumulation of the fluid within the extravascular space, i. e. , Edema – pathological accumulation of the fluid within the extravascular space, i. e. , interstitium and/or cells Main mechanisms of edema: 1. Increased microvascular permeability (hypersensitivity type I); 2. Decreased lymph drainage (elephant leg); 3. Increased hydrostatic pressure in the capillaries (venous congestion); 4. Decreased oncotic pressure of the blood (hypoproteinemia); 5. Severe retention of water and salts (renal failure)