Download Free Medical Diabetes Mellitus PowerPoint Presentation

Diabetes Mellitus PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "Diabetes Mellitus" by Dr Mohamed El Houseny Shams.

This medical PowerPoint presentation talks about diabetes mellitus, commonly referred to as diabetes. Diabetes mellitus is a chronic condition characterized by high levels of sugar (glucose) in the blood. Glucose is the main source of energy for the bodys cells, but it needs insulin, a hormone produced by the pancreas, to enter cells and be used as fuel.

In people with diabetes, the pancreas either does not produce enough insulin (type 1 diabetes), or the body cannot effectively use the insulin it produces (type 2 diabetes). As a result, glucose builds up in the blood, leading to high blood sugar levels.

Tags : Diabetes Mellitus, diabetes, high levels of sugar, type 1 diabetes, type 2 diabetes, endocrinology, endocrinology PowerPoint presentation

Published on : Apr 18, 2023 | Views : 4247 | Downloads : 17

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

1 Diabetes Mellitus Dr Mohamed El Houseny Shams
Slide 2-

2 What is diabetes? Diabetes mellitus (DM) is a chronic condition that is characterised by raised blood glucose levels (Hyperglycemia).
Slide 3-

3 Regulation of Plasma Glucose Level
Slide 4-

4 How Insuline Decrease Plasma Glucose Level?
Slide 5-

5 Classification of DM 1. Type 1 DM It is due to insulin deficiency and is formerly known as. Type I Insulin Dependent DM (IDDM) Juvenile onset DM 2. Type 2 DM It is a combined insulin resistance and relative deficiency in insulin secretion and is frequently known as. Type II Noninsulin Dependent DM (NIDDM) Adult onset DM
Slide 6-

6 3. Gestational Diabetes Mellitus (GDM): Gestational Diabetes Mellitus (GDM) developing during some cases of pregnancy but usually disappears after pregnancy. 4. Other types: Secondary DM
Slide 7-

7 Etiology 1. Etiology of Type 1 Diabetes
Slide 8-

8
Slide 9-

9 2. Etiology of Type 2 Diabetes
Slide 10-

10 a
Slide 11-

11
Slide 12-

12
Slide 13-

13
Slide 14-

14
Slide 15-

15 Epidemiology Type 1 DM It is due to pancreatic islet β-cell destruction predominantly by an autoimmune process. Usually develops in childhood or early adulthood It accounts for upto 10% of all DM cases Develops as a result of the exposure of a genetically susceptible individual to an environmental agent
Slide 16-

16 Type 2 DM It results from insulin resistance with a defect in compensatory insulin secretion. Insulin may be low, normal or high! About 30% of the Type 2 DM patients are undiagnosed (they do not know that they have the disease) because symptoms are mild. It accounts for up to 90% of all DM cases
Slide 17-

17 Risk Factors Type 1 DM Genetic predisposition In an individual with a genetic predisposition, an event such as virus or toxin triggers autoimmune destruction of b-cells probably over a period of several years.
Slide 18-

18 Risk Factors Type 2 DM Family History Obesity Habitual physical inactivity Previously identified impaired glucose tolerance (IGT) or impaired fasting glucose (IFG) Hypertension Hyperlipidemia
Slide 19-

19
Slide 20-

20 Carbohydrate Metabolism Carbohydrates are metabolized in the body to glucose. CNS uses glucose as its primary energy source. This is independent of insulin. Glucose is taken by the muscle to produce energy (insulin required). Glucose is stored in the liver as glycogen and in adipose tissues as fat. Insulin is produced and stored by the β-cells of the pancreas
Slide 21-

21 Carbohydrate Metabolism (Cont’d) Postprandial glucose metabolism in normal individuals: After food is ingested, blood glucose concs rise and stimulate insulin release. Insulin action: glucose uptake by the tissues liver glycogen formation and glycogen breakdown lipid synthesis and inhibits fatty acid breakdown to ketone bodies Promotes protein synthesis
Slide 22-

22 Carbohydrate Metabolism (Cont’d) Fasting glucose metabolism in normal individuals: In the fasting state, insulin release is inhibited. Hormones that promote an increase in blood glucose are released: Glucagon, epinephrine, growth hormone, glucocorticoids, and thyroid hormones. Glycogenolysis Gluconeogenesis: AA are transported from muscle to liver and converted to glucose. TG are broken down into free FAs as an alternative fuel source.
Slide 23-

23 Pathophysiology Type 1 DM Type 1 DM is characterized by an absolute deficiency of insulin due to immune- mediated destruction of the pancreatic b-cells In rare cases the b-cell destruction is not due to immune mediated reaction (idiopathic type 1 DM)
Slide 24-

24
Slide 25-

25 Pathophysiology Type 1 DM There are four stages in the development of Type 1 DM: Preclinical period with positive b-cell antibodies Hyperglycemia when 80-90% of the β- cells are destroyed. Transient remission (honeymoon phase). Establishment of the disease
Slide 26-

26 Pathophysiology Time (years) Birth
Slide 27-

27 Pathophysiology Type 2 DM Type 2 DM is characterized by the presence of both insulin resistance (tissue insensitivity) and some degree of insulin deficiency or b- cell dysfunction Type 2 DM occurs when a diabetogenic lifestyle (excessive calories, inadequate caloric expenditure and obesity) is superimposed upon a susceptible genotype
Slide 28-

28 Pathophysiology Type 2 DM Glucose mg/dL Relative b- cell Function % 250 200 150 100 50 0 b-cell failure 300 250 200 150 100 50 0 Fasting blood glucose Post-meal glucose Years of diabetes
Slide 29-

29 Laboratory Tests 1. Glucosuria To detect glucose in urine by a paper strip Semi-quantitative Normal kidney threshold for glucose is essential 2. Ketonuria To detect ketonbodies in urine by a paper strip Semi-quantitative
Slide 30-

30 Laboratory Tests (Cont’d) 3. Fasting blood glucose Glucose blood concentration in samples obtained after at least 8 hours of the last meal 4. Random Blood glucose Glucose blood concentration in samples obtained at any time regardless the time of the last meal
Slide 31-

31 Laboratory Tests (Cont’d) 5. Glucose tolerance test 75 gm of glucose are given to the patient with 300 ml of water after an overnight fast Blood samples are drawn 1, 2, and 3 hours after taking the glucose This is a more accurate test for glucose utilization if the fasting glucose is borderline
Slide 32-

32 Laboratory Tests (Cont’d) 6. Glycosylated hemoglobin (HbA1C) HbA1C is formed by condensation of glucose with free amino groups of the globin component of hemoglobin Normally it comprises 4-6% of the total hemoglobin. Increase in the glucose blood concentration increases the glycated hemoglobin fraction. HbA1C reflects the glycemic state during the preceding 8-12 weeks.
Slide 33-

33 Laboratory Findings (Cont’d) 7. Serum Fructosamine Formed by glycosylation of serum protein (mainly albumin) Since serum albumin has shorter half life than hemoglobin, serum fructosamine reflects the glycemic state in the preceding 2 weeks Normal is 1.5 - 2.4 mmole/L when serum albumin is 5 gm/dL.
Slide 34-

34 Self Monitoring Test Self-monitoring of blood glucose Extremely useful for outpatient monitoring specially for patients who need tight control for their glycemic state. A portable battery operated device that measures the color intensity produced from adding a drop of blood to a glucose oxidase paper strip. e.g. One Touch, Accu-Chek, DEX, Prestige and Precision.
Slide 35-

35
Slide 36-

36 Diagnostic Criteria Any one test should be confirmed with a second test, most often fasting plasma glucose (FPG). This criteria for diagnosis should be confirmed by repeating the test on a different day.
Slide 37-

37
Slide 38-

38 Clinical Presentation Type 1 DM Polyuria Polydipsia Polyphagia Weight loss Weakness Dry skin Ketoacidosis Type 2 DM Patients can be asymptomatic Polyuria Polydipsia Polyphagia Fatigue Weight loss Most patients are discovered while performing urine glucose screening
Slide 39-

39 Treatment Relieve symptoms Reduce mortality Improve quality of life Reduce the risk of microvascular and macrovascular disease complications Macrovascular complications: Coronary heart disease, stroke and peripheral vascular disease Microvascular Complications: Retinopathy, nephropathy and neuropathy Desired outcome
Slide 40-

40 How to achieve the goals ? Near normal glycemic control reduce the risk of developing microvascular disease complications Control of the traditional CV risk factors such as smoking, management of dyslipidemia, intensive BP control and antiplatelet therapy. Treatment
Slide 41-

41 Treatment General approaches Medications Dietary and exercise modification Regular complication monitoring Self monitoring of blood glucose Control of BP and lipid level
Slide 42-

42 Treatment Glycemic goals
Slide 43-

43 Treatment Complication monitoring Annual eye examination Annual microalbuminuria Feet examination BP monitoring Lipid profile
Slide 44-

44 Treatment Self-monitoring of blood glucose Frequent self monitoring of blood glucose to achieve near normal level More intense insulin regimen require more frequent monitoring
Slide 45-

45 Treatment Nonpharmacological therapy For type 1 the goal is to regulate insulin administration with a balanced diet In most cases, high carbohydrate, low fat, and low cholesterol diet is appropriate Type 2 DM patients need caloric restriction Diet
Slide 46-

46 Treatment Nonpharmacological therapy Artificial sweeteners: e.g. Aspartame, saccharin, sucralose, and acesulfame Safe for use by all people with diabetes Nutritive sweeteners: e.g. fructose and sorbitol Their use is increasing except for acute diarrhea in some patients Diet (Cont’d)
Slide 47-

47 Treatment Nonpharmacological therapy Exercise improves insulin resistance and achieving glycemic control. Exercise should start slowly for patients with limited activity. Patients with CV diseases should be evaluated before starting any exercise Activity
Slide 48-

48
Slide 49-

49 TreatmentPharmacological therapy Insulin (Type 1 and Type 2 DM) Sulfonylurea (Type 2 DM) Biguanides (Type 2 DM) Meglitinides (Type 2 DM) Thiazolidinediones Glitazones (Type 2 DM) a-Glucosidase inhibitors (Type 2 DM)
Slide 50-

50 Strategy for Controlling Hyperglycemia Serum Sugar Cellular Uptake Absorption from Diet Biosynthesis in Liver Insulin a-Glucosidase Inhibitors Pancreas Sulfonylureas Meglitinide Biguanides; thiazolidinediones Biguanides Pharmacological Treatment of Type 2 DM
Slide 51-

51 1. Sulfonylureas Pharmacological effect Stimulate the pancreatic secretion of insulin
Slide 52-

52 Sulfonylureas (Cont’d) Classification First generation e.g. tolbutamide, chlorpropamide, and acetohexamide Lower potency, more potential for drug interactions and side effects Second generation e.g. glimepiride, glipizide, and glyburide higher potency, less potential for drug interactions and side effects All sulfonylurea drugs are equally effective in reducing the blood glucose when given in equipotent doses.
Slide 53-

53 Major Pharmacokinetic Properties of Sulfonyl Ureas
Slide 54-

54 Sulfonylureas (Cont’d) Adverse effects Hypoglycemia Hyponatremia (with tolbutamide and chlorpropamide) Weight gain HbA1c: 1.5 – 1.7% reduction. FPG: 50 – 70 mg/dL reduction. PPG: 92 mg/dL reduction. Efficacy
Slide 55-

55 Sulfonylureas (Cont’d) Drug interactions
Slide 56-

56 2. Short-acting Secretogogues Pharmacological effect Stimulation of the pancreatic secretion of insulin The insulin release is glucose dependent and is decreased at low blood glucose With lower potential for hypoglycemia (incidence 0.3%) Should be given before meal or with the first bite of each meal. If you skip a meal don’t take the dose! Repaglinide Nateglinide
Slide 57-

57 Secretogogues (Cont’d) Adverse effect Incidence of hypoglycemia is very low about 0.3 % Drug Interactions Inducers or inhibitors of CYP3A4 affect the action of repaglinide Nateglinide is an inhibitor of CYP2C9
Slide 58-

58 3. Biguanides Pharmacological effect Reduces hepatic glucose production Increases peripheral glucose utilization Metformin (Glucophage) Adverse effects Nausea, vomiting, diarrhea, and anorexia Phenformin: another biguanide, was taken off the market because it causes lactic acidosis in almost 50% of patients As a precaution metformin should not be used in patients with renal insufficiency, CHF, conditions that lead to hypoxia
Slide 59-

59 4. Glitazones (PPARg Agonists) PPARg Agonists: Peroxisome proliferator-activated receptor g gonists Rosiglitazone - Pioglitazone Reduces insulin resistance in the periphery (Sensitize muscle and fat to the action of insulin) and possibly in the liver The onset of action is slow taking 2-3 months to see the full effect Edema and weight gain are the most common side effects. (no hepatotoxicity) Pharmacological effect
Slide 60-

60 5. a-Glucosidase Inhibitors Pharmacological effect Prevent the breakdown of sucrose and complex carbohydrates The net effect is to reduce postprandial blood glucose rise The effect is limited to the luminal side of the intestine with limited systemic absorption. Majority eliminated in the feces. Postprandial glucose conc is reduced. FPG relatively unchanged. Average reduction in HbA1c: 0.3-1.0% - Acarbose - Miglitol
Slide 61-

61 Pharmacotherapy :Type 2 DM General considerations: Consider therapeutic life style changes (TLC) for all patients with Type 2 DM Initiation of therapy may depend on the level of HbA1C HbA1C < 7% may benefit from TLC HbA1C 8-9% may require one oral agent HbA1C > 9-10% my require more than one oral agent
Slide 62-

62 Pharmacotherapy :Type 2 DM Obese Patients >120% LBW: Metformin or glitazone Add SU or short-acting insulin secretagogue Add Insulin or glitazone
Slide 63-

63 Pharmacotherapy :Type 2 DM Non-obese Patients <120% LBW: SU or short-acting insulin secretagogue Add Metformin or glitazone Add Insulin
Slide 64-

64 Pharmacotherapy :Type 2 DM Elderly Patients with newly diagnosed DM : SU or short-acting insulin secretagogue or a-glucosidase inhibitor or insulin Add or substitute insulin
Slide 65-

65 Pharmacotherapy :Type 2 DM Early insulin resistance : Metformin or glitazone Add glitazone or metformin Add SU or short-acting insulin secretagogue or insulin
Slide 66-

66 Clinical Trials: Diabetes Mellitus 1- Diabetes Prevention Program Population: Over-weight patients with impaired glucose tolerance. Intervention: Low-fat diet and 150 min of exercise per week. Results: Decrease the risk of progression to Type 2 DM by 58%
Slide 67-

67 Pharmacotherapy :Type 1 DM The choice of therapy is simple All patients need Insulin
Slide 68-

68 Insulin Anabolic Glucose uptake Glycogen synthesis Lipogenesis Protein synthesis Triglyceride uptake Pharmacological effect: Anticatabolic Inhibits gluconeogenesis Inhibits glycogenolysis Inhibits lipolysis Inhibits proteolysis Inhibits fatty acid oxidation
Slide 69-

69 Insulin (Cont’d) The number of units/ml e.g. U-100 , U-20, U-10 Strength Source Pork: Differs by one a.a. Beef-Pork Human (recombinant DNA technology)
Slide 70-

70 Insulin (Cont’d) Changing the properties of insulin preparation can alter the onset and duration of action Lispro: (Monomeric) absorbed to the circulation very rapidly Aspart: (Mono- and dimeric) absorbed to the circulation very rapidly Regular: (Hexameric) absorbed rapidly but slower than lispro and aspart Onset and duration of effect
Slide 71-

71 Insulin (Cont’d) Lent insulin: Amorphous precipitate of insulin and zinc and insoluble crystals of insulin and zinc. Releases insulin slowly to the circulation NPH: R-insulin + Protamine zinc insulin. Releases insulin slowly to the systemic circulation Insulin glargine: Prepared by modification of the insulin structure. Precipitate after S.C. injection to form microcrystals that slowly release insulin to the systemic circulation (N.B. cannot be mixed with other insulins) Onset and duration of effect
Slide 72-

72 Insulin (Cont’d) Rapid-acting insulin e.g. Insulin lispro and insulin aspart Short-acting insulin e.g. Regular insulin Intermediate-acting insulin e.g. NPH and Lente insulin Long-acting insulin e.g. Insulin Glargine Mixture of insulin can provide glycemic control over extended period of time e.g. Humalin 70/30 (NPH + regular) Onset and duration of effect
Slide 73-

73 Insulin (Cont’d) Hypoglycemia Treatment: Patients should be aware of symptoms of hypoglycemia Oral administration of 10-15 gm glucose IV dextrose in patients with lost consciousness 1 gm glucagon IM if IV access is not available Skin rash at injection site Treatment: Use more purified insulin preparation Lipodystrophies (increase in fat mass) at injection site Treatment: rotate the site of injection Adverse effects
Slide 74-

74 Insulin (Cont’d) Drugs interfering with glucose tolerance The most significant interactions are with drugs that alter the blood glucose level: Diazoxide Thiazide diuretics Corticosteroids Oral contraceptives Streptazocine Phenytoin All these drugs increase the blood glucoseconcentration. Monitoring of BG is required
Slide 75-

75 Insulin (Cont’d) Methods of Insulin Administration Insulin syringes and needles Pen-sized injectors Insulin Pumps
Slide 76-

76 Pharmacotherapy :Type 1 DM The goal is: To balance the caloric intake with the glucose lowering processes (insulin and exercise), and allowing the patient to live as normal a life as possible
Slide 77-

77 Pharmacotherapy :Type 1 DM Breakfast Lunch Supper Insulin Concentration Time of day Normal insulin secretion during he day - Constant background level (basal) - Spikes of insulin secretion after eating
Slide 78-

78 Pharmacotherapy :Type 1 DM -The insulin regimen has to mimic the physiological secretion of insulin With the availability of the SMBG and HbA1C tests adequacy of the insulin regimen can be assessed More intense insulin regimen require more intense monitoring
Slide 79-

79 Pharmacotherapy :Type 1 DM Example: 1- Morning dose (before breakfast): Regular + NPH or Lente 2- Before evening meal: Regular + NPH or Lente Require strict adherence to the timing of meal and injections
Slide 80-

80 Pharmacotherapy :Type 1 DM Modification NPH evening dose can be moved to bedtime Three injections of regular or rapid acting insulin before each meal + long acting insulin at bedtime (4 injections) The choice of the regimen will depend on the patient
Slide 81-

81 Pharmacotherapy :Type 1 DM How much insulin ? A good starting dose is 0.6 U/kg/day The total dose should be divided to: 45% for basal insulin 55% for prandial insulin The prandial dose is divided to - 25% pre-breakfast - 15% pre-lunch - 15% pre-supper
Slide 82-

82 Pharmacotherapy :Type 1 DM Example: For a 50 kg patient The total dose = 0.6X50 = 30 U/day 13.5 U for basal insulin (45% of dose) Administered in one or two doses 16.5 U for prandial insulin (55% of dose) The 16.5 U are divided to: - 7.5 U pre-breakfast (25%) - 4.5 U pre-lunch (15%) - 4.5 U pre-supper (15%)
Slide 83-

83 Pharmacotherapy :Type 1 DM Monitoring Most Type 1 patients require 0.5-1.0 U/kg/d The initial regimen should be modified based on: Symptoms SMBG HbA1C
Slide 84-

84 Pharmacotherapy :Type 1 DM Monitoring
Slide 85-

85 Pharmacotherapy :Type 1 DM Insulin Pump Therapy This involves continuous SC administration of short-acting insulin using a small pump The pump can be programmed to deliver basal insulin and spikes of insulin at the time of the meals Requires intense SMBG Requires highly motivated patients because failure to deliver insulin will have serious consequences
Slide 86-

86 Pharmacotherapy :Type 1 DM Insulin Pump
Slide 87-

87 II. Surgery Islet transplantation has been investigated as a treatment for type 1 diabetes mellitus in selected patients with inadequate glucose control despite insulin therapy. Observations in patients with type 1 diabetes indicate that islet transplantation can result in insulin independence with excellent metabolic control Ref. Shapiro A.M. J., et al. N Engl J Med 2000; 343:230-238, Jul 27, 2000
Slide 88-

88 Diabetes Mellitus Complications 1. Hypoglycemia Cause: Missing meals or excessive exercise or too much insulin Symptoms: Tachycardia, palpitation, sweating, nausea, and vomiting. Progress to mental confusion, bizarre behavior and coma Treatment: Candy or sugar IV glucose Glucagon 1 gm IM Identification: MedicAler bracelet
Slide 89-

89 Diabetes Mellitus Complications 2. Diabetes retinopathy Microaneurysm Hemorrhage Exudates Retinal edema other
Slide 90-

90 Diabetes Mellitus Complications 3. Diabetes nephropathy 30-40 % of all type 1 DM patients develop nephropathy in 20 years 15-20 % of type 2 DM patients develop nephropathy Manifested as: Microalbuminuria Progressive diabetic nephropathy leading to end-stage renal disease
Slide 91-

91 Diabetes Mellitus Complications Diabetes nephropathy (Cont’d) All diabetic patients should be screened annually for microalbuminurea to detect patients at high risk of developing progressive diabetic nephropathy Tight glycemic control and management of the blood pressure can significantly decrease the risk of developing diabetic nephropathy. ACE-inhibitors are recommended to decrease the progression of nephropathy
Slide 92-

92 Diabetes Mellitus Complications 4. Diabetes neuropathy Autonomic neuropathy: Manifested by orthostatic hypotension, diabetic diarrhea, erectile dysfunction, and difficulty in urination.
Slide 93-

93 Diabetes Mellitus Complications 5. Peripheral vascular disease and foot ulcer Incidence of gangrene of the feet in DM is 20 fold higher than control group due to: - Ischemia - Peripheral neuropathy - Secondary infection
Slide 94-

94 Special Patient Population 1. Adolescent Type 2 DM Type 2 DM is increasing in adolescent Lifestyle modification is essential in these patients If lifestyle modification alone is not effective, metformin the only labeled oral agent for use in children (10-16 years)
Slide 95-

95 Special Patient Population 2. Gestational DM Dietary control If blood glucose is not controlled by dietary control, insulin therapy is initiated One dose of NPH or NPH + regular insulin (2:1) given before breakfast. Adjust regimen according to SMBG. Sulfonylureas: Effective, but require further studies to demonstrate safety.
Slide 96-

96 Special Situations 3. Diabetic ketoacidosis It is a true emergency Usually results from omitting insulin in type 1 DM or increase insulin requirements in other illness (e.g. infection, trauma) in type 1 DM and type 2 DM Signs and symptoms: Fatigue, nausea, vomiting, evidence of dehydration, rapid deep breathing, fruity breath odor, hypotension and tachycardia
Slide 97-

97 Special Situations Diabetic ketoacidosis (Cont’d) Diagnosis Hyperglycemia, acidosis, low serum bicarbonate, and positive serum ketones Abnormalities: - Dehydration, acidosis, sodium and potassium deficit Patient education is important
Slide 98-

98 Special Situations Diabetic ketoacidosis (Cont’d) Management: Fluid administration: Rapid fluid administration to restore the vascular volume, IV infusion of insulin to restore the metabolic abnormalities. Titrate the dose according to the blood glucose level. Potassium and phosphate can be added to the fluid if needed. Follow up: Metabolic improvement is manifested by an increase in serum bicarbonate or pH.