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Diabetes
BMS263
| Term | Definition |
|---|---|
| Pancreas | Both an exocrine and endocrine gland. Different cell types produce specific hormones which are secreted directly into the blood stream. a cells- Glucagon; b cells- Insulin |
| Regulation of Insulin Secretion | Stimulated by increased BGL, blood amino acid levels, responses to a meal & some anti-diabetic drugs. Inhibited by Adrenaline, somatostatin and some drugs (Thiazide diuretics) |
| Release of Insulin | 2 phase release of insulin in response to increased BGL. Initial rapid release phase (release of stored hormone). Slower delayed phase (release of newly synthesised & stored hormone). Response is abnormal in Diabetes Mellitus |
| Actions of Insulin | Fuel storage hormone (anabolic).Facilitates uptake & storage of glucose, amino acids & fats after meal. Reduces BGL. Inhibits glycogenolysis & gluconeogenesis. Stim glycogen synthesis. Increase facilitated transport of gluc via Glut-4 transport |
| Mechanism of Insulin Action | Bind to insulin receptors on target cells. Activates tyrosine kinase enzyme. Initiate cascade of phosphorylation reaction. Act or deactivate metabolic pathways. Glut-4 trans move to plasma membrane of muscle & fat cells. Rapid increase in glucose uptake |
| Glucagon | Secreted by the pancreatic a cells in response to low BGL. Fuel mobilising hormone. Increases BGL. Stimulates glycogenolysis Stimulates gluconeogenesis. Inhibits glycogenesis. Increases lipolysis. More fatty acids available. Less dependence upon BG |
| Actions of Glucagon | Stimulates release of catecholamines. Increases release of GH and ACTH. Although glucagon generally opposes the action of insulin, glucagon can also stimulate insulin secretion (negative feedback loop) |
| Factors That Inhibit Glucagon | Stimulate glucagon secretion: Low BGL, High protein meals, Exercise, Stress; Inhibit glucagon secretion: High BGL, Insulin, Amylin (co-secreted with insulin) |
| Incretins | Peptide hormones secreted from the digestive tract in response to food. ‘Alert’ pancreatic β cells to impending rise in BGL. Cause increased insulin secretion. E.g. GLP-1 OR GIP. Response to incretins is reduced in diabetics |
| CNS Input | Regulates energy balance (TH secretion) & glucose homeostasis (Stim insulin sensitivity & Inhibit glucose production). Availability of peripheral nutrients detected & alters physiology. Vagal output inhibit gluconeogenesis in liver. Controls leptin |
| Leptin | Stimulates insulin sensitivity & the release of an appetite suppressant |
| Diabetes Mellitus | Chronic disorder -->high BGL. 7th leading cause of death in Aus. 5.9% of population. Risk of developing closely associated with central obesity. Rapid rise mirrors other nutrition-related ‘lifestyle’ diseases (obesity, CV & chronic renal disease) |
| Glycosuria | When BGL exceeds the renal threshold, excess glucose is secreted by the kidney into urine |
| Polyuria | Osmotic diuresis (excess urination) |
| Polydipsia | Excessive thirst (often caused by dehydration) |
| Hyperglycaemia | High BGL. Occur when glucose not readily taken up into cells & glycogen fails to store glucose in liver. BGL exceeds renal threshold excess secreted by kidney. Resulting in Glycosuria, Polyuria & Polydipsia, dry skin & mouth, drowsy, ab pain |
| Pathophysiology of T1D | 15% of diabetes. Juvenile onset (often <20 yr). Usually non-obese. Usually no family history. Low/absent insulin levels. No insulin resistance. Insulin receptors normal. Treatment involves insulin |
| Pathophysiology of T2D | 85% of Diabetes. Maturity onset (often >35 yr). Usually obese. Often family history. Variable insulin levels. Insulin resistance present. Low or defective insulin receptors. Treatment: diet, oral hypoglycaemic agents, insulin |
| T1DM | Damage to pancreatic b cells. Usually due to autoimmune disease. Lack of insulin (Require exogenous insulin). Possible genetic predisposition. Due to abnormal carbohydrate metabolism, much greater breakdown of fats & protein - Ketoacidosis |
| Diabetic Ketoacidosis | Waste products from fatty acid breakdown accumulate (Ketone bodies). Acidosis occurs. Triggered by stress, such as infection, increases hormones that antagonise insulin action, e.g. adrenaline & cortisol. Excessive lipolysis & fatty acid metabolism |
| Diabetic Coma | Due to accumulation of ketone bodies (acidity), ventilation increases (rapid & deep breaths). Dehydration (due to hyperglycaemia). Stupor & coma. Treatment involves exogenous insulin, hydration, & bicarbonate can be used to correct acidosis |
| Dehydration from hyperglycaemia | Excessive hyperglycaemia causes diuresis (more urine production) leading to dehydration. Water moves out of cells, to dilute the more concentrated extracellular body fluids |
| T2DM | Usually have functioning b cells, so produce at least some insulin. Insulin secretion may be impaired &/or insulin resistance due to decrease receptor # &/or function & abnormal cell-signalling post-receptor. Associated with hypertension & hyperlipidaemia |
| Hyperosmolar Coma | Hyperglycaemia=hyperosmolar state (Diuresis). Insulin activity inhibit excessive lipolysis & ketoacidosis. Severe dehydration (not acidosis) results in hypovolaemia, hypotension, high osmolarity & coma. Treatment:hydration & correcting electrolyte balance |
| Long Term Complications of Diabetes | Microvascular (thickening basement membrane & endothelial hyperplasia, ischaemia, neuropathy, renal disease & diabetic retinopathy; Macrovascular (Atherosclerosis, thrombosis, coronary artery disease, stroke, & cardiomyopathy. Increased infection risk |
| Metabolic Syndrome | High triglycerides, Low HDL, Hypertension, Elevated fasting BGL Increased waist circumference, Inflammatory markers, endothelial dysfunction & coagulation may be abnormal. Predisposes individuals to CVD |
| Hypoglycaemia | Low BGL. Increased anxiety, blurry vision, chilly sensation, cold sweating, increased pulse rate and weakness, shakiness, pallor, confusion, drowsiness, faintness, headache, nausea or increased appetite. Mild to moderate or Severe (Already unconscious) |
| Glucagon | Used in severe hypoglycaemia & to terminate insulin coma. Only useful if liver glycogen is available. Not useful in starvation or where glycogen stores already depleted. Protein (must be administered IM, IV, or SC injection. Short HL & duration of action |
| Management of Diabetes | Blood glucose monitoring, Insulin replacement, Oral hypoglycaemic agents (dependent upon at least some pancreatic insulin production & secretion), Lifestyle factors (Diet, alcohol, exercise, cigarette smoking), antihypertensives & lipid-lowering drugs |
| Diet for Diabetes | Reduce high sugar & fat food intake, increase fibre. Better glycaemic control with high fibre diets. Reduces BGL fluctuations. Saturated fats decrease insulin activity. Avoid hyperglycaemic substances, e.g. large amounts of caffeine can raise BGL |
| Alcohol | Promotes hypoglycaemia. Blocks formation, storage & breakdown of glycogen. Reduced food intake & Impairs judgement |
| Exercise | Sedentary life-style increases risk of T2DM & CVD. Exercise increases glycaemic control & enhances utilisation of glucose. Long term, exercise training decreases BGL fluctuations & hyperglycaemia. Each exercise bout runs the risk of hypoglycaemia |
| Cigarette Smoking | Nicotine can reduce absorption of subcutaneous insulin which raises BGL, decreases responsiveness to insulin, increases risk of CV disease. Nicotine is a potent vasoconstrictor |
| Glycosylated Haemoglobin | Provides an indication of the average BGL over the past 3 months. Used as an indicator of the efficiency of long-term management of diabetes. Commonly recommended that this test is done every 3-6 months |
| Insulin Replacement | Essential for treatment of T1DM. Formulations: Recombinant human insulin, Bovine or Porcine insulin (rarely used) & may elicit immune response. Human insulin identical to insulin produced by human pancreas. Absorbed faster & shorter duration of action |
| Insulin Formulations | Ultra short acting, short acting, intermediate acting, long acting. Pre-mixed formulations. Preparations differ in their amino acid sequence |
| Ultra Short Acting Insulin Pharmacokinetics | Ultra short acting preparations have the following advantages: More rapid onset of action, earlier peak effect, shorter duration of action. T1D may also require a intermediate or long acting insulin to maintain basal insulin activity |
| Long Acting Insulin Pharmackinetics | Insulin glargine - forms microcrystals in the tissues after injection, slowly releases insulin but may cause pain; & Insulin detemir – binds to albumin in plasma and tissues, slowly releases insulin but may cause local reaction |
| Insulin Administration | Given subcutaneously. Alternated injection sites to reduce local effects. Supplied in vials, pens, cartridges or pumps for delivery |
| Insulin Dosage | Dosage depends on: weight, diet, lifestyle, type of insulin used, other meds & BGL. Will alter depending on injection site (minimise local reaction including lipodystrophy), body temp, physical activity & blood flow |
| Lipodystrophy | Abnormal distribution of fat in the body. Can alter insulin absorption. Caused by injections into the same site |
| Rebound Effect | Hypoglycaemia followed by rebound hyperglycaemia. “Dawn phenomenon”, increase of BGL in early hours due to nocturnal GH levels (as well as adrenaline and cortisol due to activation of sympathetic nervous system as a reaction to LOW BGL) |
| Biguanides | Increase glucose uptake & utilises skeletal muscle. Reduce gluconeogenesis, LDL & VLDL. Increase insulin sensitivity (Increased # insulin receptors & affinity). Hypo low risk. Contraindicated: patients risk lactic acidosis. May combo hypoglycaemic agents |
| Sulfonylureas | Stim insulin secretion (depolarise B cells). Increase insulin sensitivity. Decrease glycogenolysis, gluconeogenesis & BGL. Take w food avoid Hypo (common side effect). Bind strongly to plasma albumin. Weight gain, GIT disturbances. DDI: alcohol & NSAIDS |
| Repaglinide | Stimulates B cells to produce insulin. Improves insulin secretion in response to glucose load. Similar action to sulfonylurea (instead acts on ATP-K Channels). Adverse effects: Hypo & GIT disturbances |
| Glitazones | Enhance sensitivity of peripheral tissues & liver to insulin (occurs after few weeks). Reduce insulin resistance. Alters gene expression to alter glucose & lipid metabolism. Increase glucose uptake. Anaemia, weight gain, risk heart failure, periph oedema |
| Oral Hypoglycaemic Agents | Dependent upon at least some pancreatic insulin production & secretion, so usually can’t be used to treat type 1 diabetes. Biguanides, Sulfonylureas, Repaglinide, Glitazones) & α-glucosidase inhibitors |
| Incretin Enhancers | Mimic effects of incretins, or increase endogenous incretin levels &/or activity. Increase glucose-dependent insulin secretion. Enhance b cell proliferation. Slows gastric emptying. Reduce appetite. Some reduce glucagon secretion |
| α-Glucosidase Inhibitor | Delays digestion and absorption of carbs. Leads to smaller increase in BGL after meals. Common adverse effects including flatulence, loose stools and ab pain |
Created by:
Mandyrox300
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