DM 6 Disorders of carbohydrate & Lipid metabolism PDF

Approach to the patient with disorders of carbohydrate & Lipid metabolism GENERAL PATHOLOGY 3º Prof. Luis D’Marco, MD, MSc, PhD.  ROADMAP Diabetes Hypercholesterolaemia Diabetes management...

Approach to the patient with disorders of carbohydrate & Lipid metabolism GENERAL PATHOLOGY 3º Prof. Luis D’Marco, MD, MSc, PhD.  ROADMAP Diabetes Hypercholesterolaemia Diabetes management hypertriglyceridemia 1 3 5 2 4 6 Diabetes emergencies Lipid metabolism Mixed hyperlipidaemia 2  Diabetes mellitus Clinical syndrome characterised by an increase in plasma blood glucose (hyperglycaemia). T1DM is generally considered to result from autoimmune destruction of insulin-producing cells (β cells) in the pancreas, leading to marked insulin deficiency, whereas T2DM is characterised by reduced sensitivity to the action of insulin and an inability to produce sufficient insulin to overcome this ‘insulin resistance’. NOT ENTERING  Diabetes mellitus Hyperglycaemia causes both acute and long-term problems: Acutely, high glucose and lack of insulin can result in marked symptoms, metabolic decompensation and hospitalization. Chronic hyperglycaemia is responsible for diabetes-specific ‘microvascular’ complications affecting the eyes (retinopathy), kidneys (nephropathy) and feet (neuropathy).  Diabetes mellitus There is a continuous distribution of blood glucose in the population, with no clear division between people with normal values or abnormal ones. The diagnostic criteria for DM (a fasting plasma glucose of ≥126 mg/dL or glucose 2 hours after an oral glucose challenge of ≥200mg/dL) have been selected to identify a degree of hyperglycaemia that, if untreated, carries a significant risk of microvascular disease. Less severe hyperglycaemia is called ‘impaired glucose tolerance’. Kids with obesity not diabetes junk food less sport less access to health  - Type 1 Diabetes Mellitus Immune-mediated (type 1A) Idiopathic (type 1B) Etiologic - Type 2 Diabetes Mellitus Classification - Other Specific Types of Diabetes Genetic defects of beta-cell function: Maturity-onset diabetes of the young (MODY) Mellitus Genetic defects in insulin action: Insulin receptor mutations and other disorders Diseases of the exocrine pancreas Endocrinopathies: Cushing’s syndrome, acromegaly, and other disorders Drug- or chemical-induced: Glucocorticoids most common Infections Uncommon forms of immune-mediated diabetes - Gestational Diabetes Mellitus Metabolic actions of insulin increating = food in the stomach release it help beta cell to secrete insulin if no food in stomach = no release (secretion of beta cell but less) if medication stimulate incretin = ralease increase insulin of the ca enter secretion vesicle with insulin from ER depol of cells K and GLUT cotransporter Insulin secretion in response to intravenous or oral glucose eat = high insulin secretion but if IV lower insulin when drink glucose : 1 st phase insulin secretion = acute 2 nd phase = with time Processing of pro-insulin into insulin and C-peptide insulin release from pancrease at the same time as C peptide but in blood seperate C peptide half life is higher than insulin used to test the long term insulin production type 1 diabetes = no production of insulin = C peptide = almost 0 type 2 = higher level of C peptide = more insulin secreted due to insulin resistance higher level of C peptide = more fat around the heart and coronary calcification = more CV risk Major metabolic pathways of fuel metabolism and the actions of insulin 1 muscle energy 2 storage of glucose fat storage need energy if a lot of energy needed Ketone (not good too much) release into blood  Investigations insulin = lipogenic hormone = forma grassa Blood and glucose higher 160 / 170 glucose pass Urine glucose in urine 100% filter by glomerulus normally reabsorbed except diabetes Interstitial glucose divises Urine and blood ketones Liver release ketone Glycated haemoglobin glycated haemoglobin = long term study of glucose level (3 mth) C-peptide Urine protein diabetic = kidney problems = CV didease Islet autoantibodies Type 1 type 1 = lean no fat = no insulin type 2 = bigger patient or type 1 patient with a lot of insulin treatment = bigger  Pathogenesis of type 1 diabetes type 1  Natural history of type 2 diabetes keep eating a lot = pancreas release insulin a lot B cell destruction progression become like type 1 Patient = normal level or hypoglycemia -> hyperinsulineamia = patient hungry treatment = diet and medication to improve insulin resistance = stimulation of GLUT 3 and 4 (muscle adipose tissue and liver ) Acute metabolic complications of insulin deficiency type 1 no sugar for energy = break down other component spill over of FFA very dangerous CV metabolic acidosis