logging in or signing up Diabetes Mellitus Silvestre Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINTLite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 3071 Category: Education License: All Rights Reserved Like it (1) Dislike it (0) Added: February 29, 2008 This Presentation is Public Favorites: 4 Presentation Description No description available. Comments Posting comment... By: WISDOMTOOTH (16 month(s) ago) Nice Presentation. Please let me know how to download Saving..... Post Reply Close Saving..... Edit Comment Close By: nickpueju (31 month(s) ago) great... Saving..... Post Reply Close Saving..... Edit Comment Close By: ta2008 (43 month(s) ago) need ppt Saving..... Post Reply Close Saving..... Edit Comment Close Premium member Presentation Transcript Diabetes Mellitus: Diabetes Mellitus Barbara S. Hays Winter, 2006Blood Glucose (normal serum level 65 – 105 mg): Blood Glucose (normal serum level 65 – 105 mg) Inside CNS Brain uses glucose as primary fuel Brain cannot store/produce glucose Outside CNS Fatty acids: stored as Glycogen (liver/muscles) Triglycerides (fat cells)Blood glucose, cont.: Blood glucose, cont. Outside CNS, continued Endocrine portion of pancreas: Islets of Langerhans Alpha cells make glucagon “counterregulatory”, acts opposite of insulin Beta cells make insulin Allows body cells to store and use carbohydrate, fats, and proteinHyperglycemia: Hyperglycemia When blood glucose becomes high INSULIN allows glucose to enter cells Liver Production /storage of glycogen Inhibits glycogen breakdown Increased protein & fat synthesis (VLDL formation) Muscles Promotes protein and glycogen synthesis Fat cells Promotes storage of triglyceridesHyperglycemia: Hyperglycemia Drowsy Flushed ThirstyHypoglycemia: Hypoglycemia Glucagon: causes release of glucose from liver “glycogenolysis (breakdown of glycogen to glucose) “glyconeogenesis of glucose not available Lipolysis (breakdown of fat) Proteolysis (breakdown of amino acids)Hypoglycemia: Hypoglycemia Weak, sweaty Confused/irritable/ disorientedDiabetes Mellitus (problem with glucose metabolism): Diabetes Mellitus (problem with glucose metabolism) Major health problem US/worldwide Complications [lousy blood vessels] Blindness Renal failure Amputations [heart attacks and strokes] [OB/neonatal complications]Diabetes Mellitus: Diabetes Mellitus The good news: Blood glucose control reduces complications of Diabetes!Diabetes Mellitus: Diabetes Mellitus Absence (or ineffectiveness of ) insulin Cellular resistance Cells can’t use glucose for energy Starvation mode Compensatory breakdown of body fat/protein Ketone bodies from faulty fat breakdown Metabolic acidosis, compensatory breathing (Kussmal’s breathing)Diabetes Mellitus: Diabetes Mellitus HYPERGLYCEMIA: fluid/electrolyte imbalance. Polyuria Sodium, chloride, potassium excreted Polydipsia from dehydration Polyphagia: cells are starving, so person feels hungry despite eating huge amounts of food. Starvation state remains until insulin is available.Diabetes Mellitus: Diabetes Mellitus Complications of chronic hyperglycemia Macrovascular complications Cardiovascular disease (heart attack) Cerebrovascular disease (strokes) Microvascular Blindness (retinal proliferation, macular degeneration) Amputations Diabetic neuropathy (diffuse, generalized, or focal) Erectile dysfunctionClassifying Diabetes Mellitus: Classifying Diabetes Mellitus Type I Diabetes: autoimmune Beta cell destruction in genetically susceptible person Some viral infectionsClassifying Diabetes Mellitus: Classifying Diabetes Mellitus Type II Diabetes Reduction in ability of most cells to respond to insulin Poor control of liver glucose output Decreased beta-cell function (eventual failure)Diabetes Mellitus: Diabetes Mellitus Major risk factors Family history Obesity Origin (Afro-American, Hispanic, Native American, Asian-American) Age (older than 45) History of gestational diabetes High cholesterol HypertensionDiabetes Mellitus: Diabetes Mellitus Prevention of effects: combination approach Increased exercise Decreases need for insulin Reduce calorie intake Improves insulin sensitivity Weight reduction Improves insulin action Triad of Treatment: Triad of Treatment Diet Medication Oral hypoglycemics Insulins Exercise Diabetes treatment: Diabetes treatment Exercise Under physician supervision Check glucose priorDiabetes treatment: Diabetes treatment Diet Lower calorie Fewer foods of “high glycemic index” Spread meals evenlyDiabetes treatment: Diabetes treatment Anti-Diabetic medications Oral hypoglycemic agents (“Easy” p 297) Sulfonylureas Thiazolidinediones Biguanides Alpha-glucosidase inhibitors D-phenylalinine derivatives Combinations Insulins (“Easy” Prototype Pro p 393)Sulfonylureas: Sulfonylureas Stimulate pancreas to secrete insulin Glyburide (Diabeta) [Prototype Pro p 393] Glucotrol (Glipizide) Diabenese (chlorpropamide) Adverse reactions Hypoglycemia Water retention/edema Photosensitivity May need to add insulin in times of stressBiguanides: Biguanides Decreases liver production of glucose Decreases intestinal absorption of glucose Improves cell sensitivity to insulin Example: Metformin GI upset, flatulence Cardiac (CHF, MI)Thiazolidinediones: Thiazolidinediones Increase cellular sensitivity to insulin Pioglitazone (Actos) Rosiglitazone (Avandia) Client should have liver enzymes checked periodicallyD-Phenylalanine derivatives: D-Phenylalanine derivatives Nateglinide (Starlix) Rapid onset, short half-life Good for those with rapid post prandial rise in blood glucoseCombinations: Combinations Glucovance Glyburide and Metformin Avandamet Avandia and Metformin [come tell me when you run into this question…]Insulin: Insulin Made in beta cells of the pancreas Moves glucose into cells (thus acts like growth hormone in a way) Moves potassium into cells (can buy time in emergencies)Insulin preparations (“Easy” p 390) given ONLY with syringes marked in “units”: Insulin preparations (“Easy” p 390) given ONLY with syringes marked in “units” Rapid acting (lispro, asparte) Short acting (regular) Intermediate acting (NPH) Long acting Ultralente [Glargine/Lantus] Your learning: Your learning Onset of action Peak (blood glucose will be lowest then) DurationRapid acting insulin: Rapid acting insulin Lispro (Humolog, Novolog Aspart) Onset of action “15-30” minutes [may come on in 5 minutes…] Peak of action 1 - 2 hours Duration 3 – 4 hoursShort acting insulins: Short acting insulins Regular (clear so can be given IV) Onset of action 0.5 to 1 hour Peak of action 2 – 4 hours Duration of action 6 – 8 hoursIntermediate acting insulins: Intermediate acting insulins NPH, Lente (chemicals added. Cloudy) Onset of action 1 – 4 hours Peak of action 4 – 12 hours Duration of action 18 – 24 hoursLong acting insulins: Long acting insulins Ultralente Onset of action 4 – 8 hours Peak of action 18 hours Duration of action 24 – 36 hoursOnce a day insulin: Once a day insulin Glargine/Lantus Cannot be diluted or mixed in syringe with any other insulin Slow, steady release Daily dosing [usually at bedtime] Refrigerated or tosses every 14 daysCombination insulins: Combination insulins 70/30 (70% NPH and 30% regular) Humolog 70/30 (Humolog and regular) Fewer injections Rotate sites to decrease lipodystrophyMiscellaneous: Miscellaneous Byetta for type II Diabetics taking sulfonylureas or combination Mimics physiologic glucose control Inhances insulin secretion only in presence of hyperglycemia Insulin secretion decreases as blood glucose approaches normal Neutontin for Diabetic nerve painSome things to know: Some things to know Insulin moves potassium into cells Good for emergency situations Dangerous if potassium level already lowSome things to know…: Some things to know… HHNK (Hyperglycemic Hyperosmolar Non-Ketotic Coma). Also called HHNK HNKS [syndrome] Like dibetic ketoacidosis, without the ketones Type II diabetic, makes enough insulin to avoid ketones, but sugar guilds up to dangerous levels -> cellular dehydration Some things to know…: Some things to know… Dawn Phenomenon vs Somogi’s effect Dawn phenomenon Blood sugar rises in early morning Somogi’s (rebound) effect Blood sugar rise in morning as reaction to hypoglycemic time during the nightSome things to know…: Some things to know… Diabetic foot care Dry, cracked skin + poor circulation could = loss of a limb For the most part nurses don’t trim nails of diabetic clients. Refer to Podiatrist.Typical diabetic foot ulcer: Typical diabetic foot ulcer You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.
Diabetes Mellitus Silvestre Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINTLite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 3071 Category: Education License: All Rights Reserved Like it (1) Dislike it (0) Added: February 29, 2008 This Presentation is Public Favorites: 4 Presentation Description No description available. Comments Posting comment... By: WISDOMTOOTH (16 month(s) ago) Nice Presentation. Please let me know how to download Saving..... Post Reply Close Saving..... Edit Comment Close By: nickpueju (31 month(s) ago) great... Saving..... Post Reply Close Saving..... Edit Comment Close By: ta2008 (43 month(s) ago) need ppt Saving..... Post Reply Close Saving..... Edit Comment Close Premium member Presentation Transcript Diabetes Mellitus: Diabetes Mellitus Barbara S. Hays Winter, 2006Blood Glucose (normal serum level 65 – 105 mg): Blood Glucose (normal serum level 65 – 105 mg) Inside CNS Brain uses glucose as primary fuel Brain cannot store/produce glucose Outside CNS Fatty acids: stored as Glycogen (liver/muscles) Triglycerides (fat cells)Blood glucose, cont.: Blood glucose, cont. Outside CNS, continued Endocrine portion of pancreas: Islets of Langerhans Alpha cells make glucagon “counterregulatory”, acts opposite of insulin Beta cells make insulin Allows body cells to store and use carbohydrate, fats, and proteinHyperglycemia: Hyperglycemia When blood glucose becomes high INSULIN allows glucose to enter cells Liver Production /storage of glycogen Inhibits glycogen breakdown Increased protein & fat synthesis (VLDL formation) Muscles Promotes protein and glycogen synthesis Fat cells Promotes storage of triglyceridesHyperglycemia: Hyperglycemia Drowsy Flushed ThirstyHypoglycemia: Hypoglycemia Glucagon: causes release of glucose from liver “glycogenolysis (breakdown of glycogen to glucose) “glyconeogenesis of glucose not available Lipolysis (breakdown of fat) Proteolysis (breakdown of amino acids)Hypoglycemia: Hypoglycemia Weak, sweaty Confused/irritable/ disorientedDiabetes Mellitus (problem with glucose metabolism): Diabetes Mellitus (problem with glucose metabolism) Major health problem US/worldwide Complications [lousy blood vessels] Blindness Renal failure Amputations [heart attacks and strokes] [OB/neonatal complications]Diabetes Mellitus: Diabetes Mellitus The good news: Blood glucose control reduces complications of Diabetes!Diabetes Mellitus: Diabetes Mellitus Absence (or ineffectiveness of ) insulin Cellular resistance Cells can’t use glucose for energy Starvation mode Compensatory breakdown of body fat/protein Ketone bodies from faulty fat breakdown Metabolic acidosis, compensatory breathing (Kussmal’s breathing)Diabetes Mellitus: Diabetes Mellitus HYPERGLYCEMIA: fluid/electrolyte imbalance. Polyuria Sodium, chloride, potassium excreted Polydipsia from dehydration Polyphagia: cells are starving, so person feels hungry despite eating huge amounts of food. Starvation state remains until insulin is available.Diabetes Mellitus: Diabetes Mellitus Complications of chronic hyperglycemia Macrovascular complications Cardiovascular disease (heart attack) Cerebrovascular disease (strokes) Microvascular Blindness (retinal proliferation, macular degeneration) Amputations Diabetic neuropathy (diffuse, generalized, or focal) Erectile dysfunctionClassifying Diabetes Mellitus: Classifying Diabetes Mellitus Type I Diabetes: autoimmune Beta cell destruction in genetically susceptible person Some viral infectionsClassifying Diabetes Mellitus: Classifying Diabetes Mellitus Type II Diabetes Reduction in ability of most cells to respond to insulin Poor control of liver glucose output Decreased beta-cell function (eventual failure)Diabetes Mellitus: Diabetes Mellitus Major risk factors Family history Obesity Origin (Afro-American, Hispanic, Native American, Asian-American) Age (older than 45) History of gestational diabetes High cholesterol HypertensionDiabetes Mellitus: Diabetes Mellitus Prevention of effects: combination approach Increased exercise Decreases need for insulin Reduce calorie intake Improves insulin sensitivity Weight reduction Improves insulin action Triad of Treatment: Triad of Treatment Diet Medication Oral hypoglycemics Insulins Exercise Diabetes treatment: Diabetes treatment Exercise Under physician supervision Check glucose priorDiabetes treatment: Diabetes treatment Diet Lower calorie Fewer foods of “high glycemic index” Spread meals evenlyDiabetes treatment: Diabetes treatment Anti-Diabetic medications Oral hypoglycemic agents (“Easy” p 297) Sulfonylureas Thiazolidinediones Biguanides Alpha-glucosidase inhibitors D-phenylalinine derivatives Combinations Insulins (“Easy” Prototype Pro p 393)Sulfonylureas: Sulfonylureas Stimulate pancreas to secrete insulin Glyburide (Diabeta) [Prototype Pro p 393] Glucotrol (Glipizide) Diabenese (chlorpropamide) Adverse reactions Hypoglycemia Water retention/edema Photosensitivity May need to add insulin in times of stressBiguanides: Biguanides Decreases liver production of glucose Decreases intestinal absorption of glucose Improves cell sensitivity to insulin Example: Metformin GI upset, flatulence Cardiac (CHF, MI)Thiazolidinediones: Thiazolidinediones Increase cellular sensitivity to insulin Pioglitazone (Actos) Rosiglitazone (Avandia) Client should have liver enzymes checked periodicallyD-Phenylalanine derivatives: D-Phenylalanine derivatives Nateglinide (Starlix) Rapid onset, short half-life Good for those with rapid post prandial rise in blood glucoseCombinations: Combinations Glucovance Glyburide and Metformin Avandamet Avandia and Metformin [come tell me when you run into this question…]Insulin: Insulin Made in beta cells of the pancreas Moves glucose into cells (thus acts like growth hormone in a way) Moves potassium into cells (can buy time in emergencies)Insulin preparations (“Easy” p 390) given ONLY with syringes marked in “units”: Insulin preparations (“Easy” p 390) given ONLY with syringes marked in “units” Rapid acting (lispro, asparte) Short acting (regular) Intermediate acting (NPH) Long acting Ultralente [Glargine/Lantus] Your learning: Your learning Onset of action Peak (blood glucose will be lowest then) DurationRapid acting insulin: Rapid acting insulin Lispro (Humolog, Novolog Aspart) Onset of action “15-30” minutes [may come on in 5 minutes…] Peak of action 1 - 2 hours Duration 3 – 4 hoursShort acting insulins: Short acting insulins Regular (clear so can be given IV) Onset of action 0.5 to 1 hour Peak of action 2 – 4 hours Duration of action 6 – 8 hoursIntermediate acting insulins: Intermediate acting insulins NPH, Lente (chemicals added. Cloudy) Onset of action 1 – 4 hours Peak of action 4 – 12 hours Duration of action 18 – 24 hoursLong acting insulins: Long acting insulins Ultralente Onset of action 4 – 8 hours Peak of action 18 hours Duration of action 24 – 36 hoursOnce a day insulin: Once a day insulin Glargine/Lantus Cannot be diluted or mixed in syringe with any other insulin Slow, steady release Daily dosing [usually at bedtime] Refrigerated or tosses every 14 daysCombination insulins: Combination insulins 70/30 (70% NPH and 30% regular) Humolog 70/30 (Humolog and regular) Fewer injections Rotate sites to decrease lipodystrophyMiscellaneous: Miscellaneous Byetta for type II Diabetics taking sulfonylureas or combination Mimics physiologic glucose control Inhances insulin secretion only in presence of hyperglycemia Insulin secretion decreases as blood glucose approaches normal Neutontin for Diabetic nerve painSome things to know: Some things to know Insulin moves potassium into cells Good for emergency situations Dangerous if potassium level already lowSome things to know…: Some things to know… HHNK (Hyperglycemic Hyperosmolar Non-Ketotic Coma). Also called HHNK HNKS [syndrome] Like dibetic ketoacidosis, without the ketones Type II diabetic, makes enough insulin to avoid ketones, but sugar guilds up to dangerous levels -> cellular dehydration Some things to know…: Some things to know… Dawn Phenomenon vs Somogi’s effect Dawn phenomenon Blood sugar rises in early morning Somogi’s (rebound) effect Blood sugar rise in morning as reaction to hypoglycemic time during the nightSome things to know…: Some things to know… Diabetic foot care Dry, cracked skin + poor circulation could = loss of a limb For the most part nurses don’t trim nails of diabetic clients. Refer to Podiatrist.Typical diabetic foot ulcer: Typical diabetic foot ulcer