DIABETES  MELLITUS by dr aftab ahmed
Upcoming SlideShare
Loading in...5
×
 

DIABETES MELLITUS by dr aftab ahmed

on

  • 3,248 vues

DEDICATED TO MY TEACHERS

DEDICATED TO MY TEACHERS

Statistics

Vues

Total Views
3,248
Views on SlideShare
3,248
Embed Views
0

Actions

Likes
7
Downloads
250
Comments
3

0 Ajouts 0

No embeds

Accessibilité

Détails de l'import

Uploaded via as Microsoft PowerPoint

Droits d'utilisation

© Tous droits réservés

Report content

Signalé comme inapproprié Signaler comme inapproprié
Signaler comme inapproprié

Indiquez la raison pour laquelle vous avez signalé cette présentation comme n'étant pas appropriée.

Annuler
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Votre message apparaîtra ici
    Processing...
Poster un commentaire
Modifier votre commentaire

DIABETES  MELLITUS by dr aftab ahmed DIABETES MELLITUS by dr aftab ahmed Presentation Transcript

  •  
  • DIABETES MELLITUS DR AFTAB AHMED RAJPUT FCPS PART 2 TRAINEE MEDICAL UNIT 2 PMCH,NAWAB SHAH
  • PRESENTATION OUTLINES
    • DM AND ITS CLASSIFICATION
    • PATHOPHYSIOLOGY OF DM
    • CLINICAL FEATURES OF DM
    • INVESTIGATIONS
    • DIAGNOSTIC CRITERIA FOR DM
    • MANAGEMENT OF DM
  • DIABETES MELITUS
    • … a metabolic disorder of multiple aetiology characterised by chronic hyperglycaemia with disturbances of carbohydrate, fat and protein metabolism resulting from defects in insulin secretion, insulin action or both
  • CURRENT IMPACT OF DM
    • 6 th leading cause of death by disease
    • Decreases life expectancy of middle-aged people by 5-10 years
    • 2-4 x greater risk of death d/t heart disease
      • Compounding factors include: duration of disease, glycemic control, HTN, smoking, dyslipidemia, decreased activity, and obesity
    • Leading cause of blindness in 25-74 year olds
    • Leading cause of non-traumatic amputations
    • Responsible for 25-30% of all new dialysis patients
  • CLASSIFICATION OF DM
    • TRADITIONALY DM HAS BEEN DIVIDED INTO
    • PRIMARY DM
    • IN WHICH THERE IS DEFECT IN INSULIN PRODUCTION AND/OR ITS ACTION
    • 2NDRY IN WHICH ANY DISEASE CAUSES EXTENSIVE DEMAGE OF PANCREATIC ISLET e.g,pancratitis,tumors,drugs,iron overload ,surgical removal of pancreatic substance and certain endocrinopathies that antagonize the action of insulin.
  • CLASSIFICATION
    • In 1997 AMERICAN DIABETES ASSOCIATION RECOMMENDED A NEW CLASSIFICATION BASED ON ETIOLOGY.
    • THERE IS NO DISTINCTION BETWEEN PRIMARY AND 2NDRY DM AND DESCRIPTION BASED ON AGE OF ONSET OR TYPE OF TREATMENT HAVE BEEN ELIMINATED.
  • CONTI……..
    • 1. Type 1 diabetes (b-cell destruction, leads to absolute insulin deficiency) •Immune-mediated (TYPE 1A)
    • • Idiopathic (TYPE 1B)
    • 2. Type 2 diabetes ( insulin resistance with relative insulin deficiency )
    • 3. Genetic defects of b -cell function
    • • Maturity-onset diabetes of the young (MODY), caused by mutations in :
    • • Hepatocyte nuclear factor 4a [HNF-4a] (MODY1)
    • • Glucokinase (MODY2)
    • • Hepatocyte nuclear factor 1a [HNF-1a] (MODY3)
    • • Insulin promoter factor [IPF-1] (MODY4)
    • • Hepatocyte nuclear factor 1b [HNF-1b] (MODY5)
    • • Neurogenic differentiation factor 1 [Neuro D1] (MODY6)
    • • Mitochondrial DNA mutations
  • CONTI……
    • 4. Genetic defects in insulin processing or insulin action
    • • Defects in proinsulin conversion
    • • Insulin gene mutations
    • • Insulin receptor mutations
    • 5. Exocrine pancreatic defects
    • • Chronic pancreatitis
    • • Pancreatectomy
    • • Neoplasia
    • • Cystic fibrosis
    • • Hemachromatosis
    • • Fibrocalculous pancreatopathy
    • 6. Endocrinopathies
    • Cushing syndrome
    • Hyperthyroidism
    • Pheochromocytoma
    • Glucagonoma
    • Acromegaly
  • CONTI……
    • 7. Infections
    • Rubella
    • Cytomegalovirus
    • Coxsackie virus B
    • Epstein barr virus
    • 8. Drugs
    • Glucocorticoids
    • interferon
    • Protease inhibitors
    • b-adrenergic agonists
    • Thiazides
    • Nicotinic acid
    • 9. Genetic syndromes associated with diabetes
    • Down syndrome
    • Kleinfelter syndrome
    • Turner syndrome
    • 10. Gestational diabetes mellitus
  • PATHOPHYSIOLOGGY OF DM
    • The pancreas functions as both an exocrine and an endocrine gland
    • Exocrine function is associated with the digestive system because it produces and secretes digestive enzymes
    • Endocrine Function: produces two important hormones in Islets of Langerhans, insulin and glucagon
      • They work together to maintain a steady level of glucose, or sugar, in the blood and to keep the body supplied with fuel to produce and maintain stores of energy.
  • Pancreatic Hormones
    • Insulin (beta cells)
      • stimulates the uptake of glucose by body cells thereby decreasing blood levels of glucose  
    • Glucagon (alpha cells)
      • stimulates the breakdown of glycogen and the release of glucose, thereby increasing blood levels of glucose
    • Glucagon and insulin work together to regulate & maintain blood sugar levels
    • Glycogen
      • Polysaccharide consisting of numerous monosaccharide glucoses linked together. Stored as an energy source in liver & muscles
  • EFFECTS OF INSULIN
  •  
  • CONTIN…….
      • Type One Diabetes (10-15%)
        • results when the body’s immune system destroys its own beta cells in the pancreas. No insulin production is then possible.
      • Type Two Diabetes (85-90%) results from either
        • Insulin resistance (overweight people)
        • Inadequate insulin production (lean people)
        • A combination of both
    • Gestational Diabetes
    • Diabetes diagnosed during pregnancy
    • Increased health risk to mother and baby
    • May require insulin injections
    • Goes away after birth, but increased risk of developing Type 2 DM for mother and child
  • Pathophysiology of type 1 diabetes
  •  
  • Type One Diabetes
    • Usually under 30 yrs of age
    • Autoimmune disorder
    • Sudden onset of severe symptoms
    • Rapid weight loss
    • Total lack of insulin in the body
    • Insulin injections essential for life
    • Ketones produced
    • Genetic predisposition, though 80% have no relatives with the disease
  • Pathophysiology of type 2 diabetes
  •  
  • Type Two Diabetes
    • Usually over 40 yrs of age though the age of diagnosis is getting younger
    • Gradual onset with mild symptoms
    • Most produce a normal amount of insulin but it is unable to work properly due to insulin resistance
    • Many have complications at diagnosis
  • What is Insulin Resistance?
    • condition in which the body does not utilise insulin efficiently
    • Insulin resistance is the decreased response of the liver and peripheral tissues (muscle, fat) to insulin
      • Insulin resistance is a primary defect in the majority of patients with Type 2 diabetes
  • Insulin resistance syndrome (syndrome x,metabolic syndrome,REAVEN’S SYNDROME)
    • Metabolic syndrome is a name for a group of risk factors that occur together and increase the risk for CAD, STROKE, and type 2 diabetes
    • The two most important risk factors for metabolic syndrome are:
    • Extra weight around the middle and upper parts of the body (central obesity). The body may be described as "apple-shaped."
    • Insulin resistance, in which the body cannot use insulin effectively. Insulin is needed to help control the amount of sugar in the body. As a result, blood sugar and fat levels rise.
    • Other risk factors include:
    • Aging
    • Genes that make more likely to develop this condition
    • Hormone changes
    • Lack of exercise
    • metabolic syndrome is present if ONE have three or more of the following signs:
    • Blood pressure equal to or higher than 130/85 mmHg
    • Fasting blood sugar (glucose) equal to or higher than 100 mg/dL
    • Large waist circumference (length around the waist):
      • Men - 40 inches or more
      • Women - 35 inches or more
    • Low HDL cholesterol:
      • Men - under 40 mg/dL
      • Women - under 50 mg/dL
    • Triglycerides equal to or higher than 150 mg/dL
    • Tests that may be done to diagnose metabolic syndrome include:
    • Blood pressure measurement
    • Glucose test
    • HDL cholesterol level
    • LDL cholesterol level
    • Total cholesterol level
    • Triglyceride level
  • Type 2 Diabetes Risk Factors
    • Increasing age
    • Obesity – especially abdominal
      • Women with BMI > 35 compared to 22 have a 93 fold increased risk
      • Men with BMI > 35 have 40 fold increased risk
    • Physical inactivity
    • Family history
    • Ethnic background
    • High blood pressure
    • High Cholesterol
    • Previous gestational diabetes
  • Characteristics of Diabetes Type 1 Type 2
    • Usually under 30
    • Rapid onset
    • Normal or underweight
    • Little or no insulin
    • Ketosis common
    • Make up 15% of cases
    • Autoimmune plus environmental factors
    • Low familial factor
    • Treated with insulin, diet and exercise
    • Usually over 40
    • Gradual onset
    • 80% are overweight
    • Most have insulin resistance
    • Ketosis rare
    • 85% of diagnosed cases
    • Part of metabolic insulin resistance syndrome
    • Strongly hereditary
    • Diet & exercise, progressing to tablets, then insulin
  • CLINICAL FEATURES OF DM
    • Diabetes Mellitus Type 1
    • Clinical Manifestations:
      • Polyuria – increased urine
      • Polydipsia – increased thirst
      • Polyphagia – increased hunger
        • 3 ‘Ps”
      • Weight loss
      • Fatigue
      • Nausea, vomiting
    • Ketoacidosis may be a presenting sign
  • Diabetes Mellitus Type 1
    • Usually develop symptoms over a short period of time, and the condition is often diagnosed in an emergency setting
    • In addition to high glucose levels, acutely ill type 1 diabetics have high levels of ketones.
      • As cells cannot get glucose, they burn fats as an alternate energy source
      • Ketones are produced by the breakdown of fat and muscle, and are toxic at high levels
      • Ketones in the blood cause a condition called "acidosis” or “ketoacidosis" (low blood pH)
      • Urine testing detects ketones in the urine
      • Blood glucose levels are also high.
  • Diabetes Mellitus Type 2
    • Type 2 Clinical Manifestations:
      • Polydipsia – increased thirst
      • Polyuria – increased urine
      • Polyphagia – increased hunger
      • Fatigue
      • Blurred vision
      • Slow healing infections
      • Impotence in men
  • INVESTIGATION AND LABORATORY FINDINGS
    • URINALYSIS
    • BLOOD TESTING PROCEDURES
    • LIPOPROTEIN ABNORMALITIES IN DIABETES
  • URINALYSIS
    • Urine glucose
    • Ketones
    • Protein(microalbuminia)
  • Blood tests
    • BLOOD GLUCOSE
    • GLYCELATED HAEMOGLOBIN (HBA1C)
    • BLOOD LIPIDS(TOTAL CHOLESTROL,LDL,HDL,TRIGLYCERIDE)
  • Other test
    • Routine blood count and coagulation screen
    • Arterial blood gases an any emergency like diabetic ketoacidosis
    • Serum electrolyte and urea-creatinine
    • Lipid profile
    • Liver function test
    • Chest x ray
    • ECG
  • DIAGNOSTIC CRITERIA FOR DM
    • Blood glucose levels - venous samples
    • 1 sample is diagnostic if symptoms are present; 2 samples if asymtomatic :
      • Fasting plasma glucose of > 7.0mmols(126MG/DL)
      • Random plasma glucose of > 11.1mmols ( 200MG/DL)
      • Plasma glucose of > 11.1(mmols (200MG/DL)2 hours after an oral glucose tolerance test (OGTT
  • GTT
    • Venous Plasma
    • Fasting >126MG/DL DIABETES
    • Fasting 110MG/DL TO< 126MG/DL Impaired Fasting Glycaemia
    • 2 hour level > 200MG/DL DIABETES
    • 2 hour 140MG/DL –200MG/DL Impaired Glucose Tolerance
  • Impaired Fasting Glucose (IFG)
    • Fasting plasma glucose > (100MG/DL)and (120) mmol/l
    • Intermediate state between normal glucose tolerance and diabetes
    • Present in 5% of the population and increasing with age
    • Has greater risk CVD
  • Impaired Glucose Tolerance (IGT)
    • Fasting plasma glucose < 126MG/DLand OGTT 2 hour value >140MG/DL but <200MG/DL
    • Intermediate state between normal glucose tolerance and diabetes
    • Individuals often manifest hyperglycaemia only when challenged with oral glucose in an OGTT
    • 2-5% of people with IGT progress to diabetes per year
    • IGT associated with increase risk of developing cardiovascular disease
  • MANAGEMENT OF DM
  • Cornerstones of Diabetes Management
    • Healthy eating
    • Exercise
    • Monitoring
    • Medication/Insulin
    • Health Care Team
  • Management of Diabetes
    • Type One: Insulin + Healthy Eating + Exercise
    • Type Two :
    • Healthy eating + exercise
    • then Healthy eating + exercise + tablets
    • then Healthy eating + exercise + tablets + insulin
  • Diabetes Mellitus
    • Role of Diet in Diabetic Management
    • A. Goals for diabetic therapy include
    • 1. Maintain as near-normal blood glucose levels as possible with balance of food with medications
    • 2. Obtain optimal serum lipid levels
    • 3. Provide adequate calories to attain or maintain reasonable weight
  • Diabetes Mellitus
    • B. Diet Composition
    • 1. Carbohydrates: 60 – 70% of daily diet
      • Carbohydrates convert quickly to sugars
        • Advice patient to consume a similar amount of carbs at each meal
        • Medications can work on a consistent glucose response from foods
    • 2. Protein: 15 – 20% of daily diet
    • 3. Fats: No more than 10% of total calories from saturated fats
  • Diabetes Mellitus
    • 4. Fiber: 20 to 35 grams/day; promotes intestinal motility and gives feeling of fullness
    • 5. Sodium: recommended intake 1000 mg per 1000 kcal
    • 6. Sweeteners approved by FDA instead of refined sugars
    • 7. Limited use of alcohol: potential hypoglycemic effect of insulin and oral hypoglycemics
  • Exercise & Weight Loss
    • Benefits of a 10kg weight loss
      • Fall of 50% in fasting glucose
      • Fall of 10% total cholesterol
      • Fall of 15% LDL
      • Fall of 30% triglycerides
      • Rise of 8% HDL
      • Fall of 10 mmHg systolic, 20 mmHg diastolic
      • SIGN guidelines
  • Oral Hypoglycemics
  • Oral Hypoglycemics
    • All taken orally in the form of tablets.
    • Pts with type 2 diabetes have two physiological defects:
    • Abnormal insulin secretion
    • Resistance to insulin action in target tissues associated with decreased number of insulin receptors
  • Oral Anti-Diabetic Agents Sulfonylureas Drugs other than Sulfonylurea
  • Sulfonylureas (Oral Hypoglycemic drugs) Tolbutamide Acetohexamide Tolazamide Chlorpropamide Glipizide Glyburide (Glibenclamide) Glimepiride Short acting First generation Intermediate acting Long acting Long acting Short acting Second generation
  • FIRST GENERATION SULPHONYLUREA COMPOUNDS * Good for pts with renal impairment ** Pts with renal impairment can expect long t1/2 Tolbutamid short-acting Acetohexamide intermediate-acting Tolazamide intermediate-acting Chlorpropamide long- acting Absorption Well Well Slow Well Metabolism Yes Yes Yes Yes Metabolites Inactive * Active +++ ** Active ++ ** Inactive ** Half-life 4 - 5 hrs 6 – 8 hrs 7 hrs 24 – 40 hrs Duration of action Short (6 – 8 hrs) Intermediate (12 – 20 hrs) Intermediate (12 – 18 hrs) Long ( 20 – 60 hrs) Excretion Urine Urine Urine Urine
  • SECOND GENERATION SULPHONYLUREA COMPOUNDS Glipizide Short- acting Glibenclamide (Glyburide) Long-acting Glimepiride Long-acting Absorption Well Well Well Metabolism Yes Yes Yes Metabolites Inactive Inactive Inactive Half-life 3 – 4 hrs Less than 3 hrs 5 - 9 hrs Duration of action 10 – 16 hrs 12 – 24 hrs 12 – 24 hrs Excretion Urine Urine Urine
  • MECHANISM OF ACTION OF SULPHONYLUREAS 1) Release of insulin from β-cells 2) Reduction of serum glucagon concentration 3) Potentiation of insulin action on target tissues
  • SIDE EFFECTS OF SULPHONYLUREAS 1) Nausea, vomiting, abdominal pain, diarrhea 2) Hypoglycaemia 3) Dilutional hyponatraemia & water intoxication (Chlorpropamide) 4) Weight gain
  • CONTRAINDICATIONS OF SULPHONYLUREAS 1) Type 1 DM ( insulin dependent) 2) Parenchymal disease of the liver or kidney 3) Pregnancy, lactation 4) Major stress
  • Drugs other than Sulfonylurea Metformin Biguanides α-Glucosidase Inhibitors Thiazolidinediones Acarbose Rosiglitazone Pioglitazone Repaglinide Nateglinide Meglitinides
  • MEGLITINIDES e.g. Repaglinide, Nateglinide PHARMACOKINETICS Taken orally Rapidly absorbed ( Peak approx. 1hr ) Metabolized by liver t 1/2 = 1 hr Duration of action 4-5 hr
  • MEGLITINIDES (Contd.) MECHANISM OF ACTION Bind to the same K ATP Channel as do Sulfonylureas, to cause insulin release from β-cells.
  • MEGLITINIDES (Contd.) CLINICAL USE Approved as monotherapy and in combination with metformin in type 2 diabetes Taken before each meal, 3 times / day Does not offer any advantage over sulfonylureas; Advantage: Pts. allergic to sulfur or sulfonylurea SIDE EFFECTS: Hypoglycemia Wt gain ( less than SUs ) Caution in pts with renal & hepatic impairement.
  • BIGUANIDES e.g. Metformin PHARMACOKINETICS Given orally Not bind to plasma proteins Not metabolized Excreted unchanged in urine t 1/2 2 hr
  • BIGUANIDES (Contd.) MECHANISM OF ACTION 1. Increase peripheral glucose utilization 2. Inhibits gluconeogenesis 3. Impaired absorption of glucose from the gut
    • Advantages of Metformin over SUs
    • Does not cause hypoglycemia
    • Does not result in wt gain
    • ( Ideal for obese pts )
  • BIGUANIDES (Contd.) SIDE EFFECTS 1. Metallic taste in the mouth 2. Gastrointestinal (anorexia, nausea, vomiting, diarrhea, abdominal discomfort) 3. Vitamin B 12 deficiency (prolonged use) 4. Lactic acidosis ( rare – 01/ 30,000-exclusive in renal & hepatic failure)
  • 1. Hepatic impairment 2. Renal impairment 3. Alcoholism 4. Heart failure BIGUANIDES (Contd.) CONTRAINDICATIONS
    • Obese patients with type 11 diabetes
    • 2. Alone or in combination with sulfonylureas
    BIGUANIDES (Contd.) INDICATIONS
  • α-GLUCOSIDASE INHIBITORS e.g. Acarbose PHARMACOKINETICS Given orally Not absorbed from intestine except small amount t 1/2 3 - 7 hr Excreted with stool
  • MECHANISM OF ACTION Inhibits intestinal alpha-glucosidases and delays carbohydrate absorption, reducing postprandial increase in blood glucose α-GLUCOSIDASE INHIBITORS (Contd.)
  • SIDE EFFECTS Flatulence Loose stool or diarrhea Abdominal pain Alone does not cause hypoglycemia α-GLUCOSIDASE INHIBITORS (Contd.)
  • INDICATIONS Patients with Type 11 inadequately controlled by diet with or without other agents( SU, Metformin) Can be combined with insulin may be helpful in obese Type 11 patients (similar to metformin) α-GLUCOSIDASE INHIBITORS (Contd.)
  • THIAZOLIDINEDIONE DERIVATIVES New class of oral antidiabetics e.g.: Rosiglitazone Pioglitazone
  • PHARMACOKINETICS
    • 99% absorbed
    • Metabolized by liver
    • 99% of drug binds to plasma proteins
    • Half-life 3 – 4 h
    • Eliminated via the urine 64% and feces 23%
    THIAZOLIDINEDIONE DERIVATIVES (Contd.)
  • MECHANISM OF ACTION
    • Increase target tissue sensitivity to insulin by:
    • reducing hepatic glucose output & increase glucose uptake & oxidation in muscles & adipose tissues.
    • They do not cause hypoglycemia (similar to metformin and acarbose ) .
    THIAZOLIDINEDIONE DERIVATIVES (Contd.)
  • ADVERSE EFFECTS
    • Mild to moderate edema
    • Wt gain
    • Headache
    • Myalgia
    • Hepatotoxicity
    THIAZOLIDINEDIONE DERIVATIVES (Contd.)
  • INDICATIONS Type 11 diabetes alone or in combination with metformin or sulfonylurea or insulin in patients resistant to insulin treatment. THIAZOLIDINEDIONE DERIVATIVES (Contd.)
  • DPP-4 Inhibitor
    • Inhibits the dipeptidyl-peptidase 4 enzyme
    • Enhances the incretin hormones
    • GLP-1 (Glucagon-like peptide 1)
    • GIP (glucose-dependent insulinotropic polypeptide)
  • Incretin Hormones
    • Stimulate insulin response from beta cells in a glucose-dependent manner
    • Inhibit gastric emptying
    • Reduces food intake and body weight
    • Inhibit glucagon secretion from alpha cells in a glucose-dependent manner
  • DPP-4 Inhibitor
    • Available product: Januvia (Sitagliptin)
    • Once daily dosing
    • Indicated for use with metformin or thiazolidinedione
    • Dosing adjustment for renal impairment
    • Adverse effects: Diarrhea, upper respiratory infection
    • Expensive
      • INSULIN THERAPHY
  • Diabetes Mellitus
    • Medications
    • A. Insulin
    • 1. Sources: standard practice is use of human insulin prepared by alteration of pork insulin or recombinant DNA therapy
    • 2. Clients who need insulin as therapy:
    • a. All type 1 diabetics since their bodies essentially no longer produce insulin
    • b. Some Type 2 diabetics, if oral medications are not adequate for control (both oral medications and insulin may be needed)
    • c. Diabetics enduring stressor situations such as surgery, corticosteroid therapy, infections, treatment for DKA
    • d. Women with gestational diabetes who are not adequately controlled with diet
    • e. Some clients receiving high caloric feedings including tube feedings or parenteral nutrition
    • Insulin Degradation
    • Hydrolysis of the disulfide linkage between A&B chains.
    • 60% liver, 40% kidney(endogenous insulin)
    • 60% kidney,40% liver (exogenous insulin)
    • Half-Life 5-7min (endogenous insulin)
    • Delayed-release form( injected one)
    • Category B ( not teratogenic)
    • Usual places for injection: upper arm, front& side parts of the thighs& the abdomen.
    • Not to inject in the same place ( rotate)
    • Should be stored in refrigerator& warm up to room temp before use.
    • Must be used within 30 days.
  •  
  • TYPES OF INSULIN PREPARATIONS 1. Ultra-short-acting 2. Short-acting (Regular) 3. Intermediate-acting 4. Long-acting
  •  
  • 3. Intermediate - acting insulins e.g. isophane (NPH) Turbid suspension Injected S.C.(Only) Onset of action 1 - 2 hr Peak serum level 5 - 7 hr Duration of action 13 - 18 hr Insulin mixtures 75/25 70/30 50/50 ( NPH / Regular )
  • 3. Intermediate - acting insulins (contd.) Lente insulin Turbid suspension Mixture of 30% semilente insulin 70% ultralente insulin Injected S.C. (only) Onset of action 1 - 3 hr Peak serum level 4 - 8 hr Duration of action 13 - 20 hr
  • 3. Intermediate - acting insulins (contd.) Lente and NPH insulins Are roughly equivalent in biological effects. They are usually given once or twice a day. N.B: They are not used during emergencies (e.g. diabetic ketoacidosis).
  • 4. Long – acting insulins e.g.Insulin glargine Onset of action 2 hr Absorbed less rapidly than NPH&Lente insulins. Duration of action upto 24 hr Designed to overcome the deficiencies of intermediate acting insulins Advantages over intermediate-acting insulins: Constant circulating insulin over 24hr with no pronounced peak. More safe than NPH&Lente insulins due to reduced risk of hypoglycemia(esp.nocturnal hypoglycemia). Clear solution that does not require resuspention before administration.
  • Methods of Adminisration
    • Insulin Syringes
    • Pre-filled insulin pens
    • External insulin pump
    • Under Clinical Trials
    • Oral tablets
    • Inhaled aerosol
    • Intranasal, Transdermal
    • Insulin Jet injectors
    • Ultrasound pulses
  • COMPLICATIONS OF INSULIN THERAPY 1. Severe Hypoglycemia (< 50 mg/dl )– Life threatening Overdose of insulin Excessive (unusual) physical exercise A meal is missed 2. Weight gain 3. Local or systemic allergic reactions (rare) 4. Lipodystrophy at injection sites 5. Insulin resistance 6. Hypokalemia
  •