All what you have to know about Diabetes Mellitus
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All what you have to know about Diabetes Mellitus

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All what you have to know about Diabetes Mellitus is here.Introduction of Diabetes,Regulation of blood glucose,Predisposing factors of DM,Clinical presentation,DM and pregnancy ,Diabetes ketoacidosis ...

All what you have to know about Diabetes Mellitus is here.Introduction of Diabetes,Regulation of blood glucose,Predisposing factors of DM,Clinical presentation,DM and pregnancy ,Diabetes ketoacidosis ,Complications of DM ,Diagnosis ,Dietary management of DM & Prevention of DM.
Student seminar on Diabetes Mellitus presented by 2007/2008 Batch students of Faculty of Medicine,University of Peradeniya,Sri Lanka.

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All what you have to know about Diabetes Mellitus All what you have to know about Diabetes Mellitus Presentation Transcript

  • Why DIABETES?  One of the commonest health problem  Affects almost all systems of the body  5%– 10% of total health care expenditure is spent on DM
  • Trend of The disease  Each year 7 million people develop diabetes (each 10 seconds 2 people develop DM)  2.3.8 million people die out of DM each year (one person per each 10 seconds)
  • Future  By 2007,246 million people were affected worldwide  By 2025 380 million people are expected to have the disease
  • Content ● Introduction - Group 1& 2 ● Regulation of blood glucose - Group 3 & 4 ● Predisposing factors of DM - Group 5 & 6 ● Clinical presentation - Group 7 & 8 ● DM and pregnancy - Group 9 & 10 ● Diabetes ketoacidosis - Group 11 & 12 ● Complications of DM - Group 13 & 14 ● Diagnosis - Group 15 & 16 ● Dietary management of DM - Group 17 & 18 ● Prevention of DM - Group 19 & 20
  • Groups 1 & 2
  • What is Diabetes mellitus ?  DM is the most common metabolic disorder encountered in clinical practice.  Diabetes - Greek word means ‘a passer through a siphon’.  Mellitus – Greek word for ‘sweet’
  • Classification of DM  Type 1 - Insulin dependent DM Insulin deficiency due to autoimmune mediate pancreatic islet cell destruction.  Type 2 - Non insulin dependent DM Due to tissue insulin resistance. Associated with ; - increasing age - obesity - ethnicity - family history.
  • Clinical differences between Type 1 and Type 11 Diabetes Type 1 Type 11 Ketosis prone Yes Uncommon Insulin requirement Yes- absolute insulin Often later in disease- deficiency insulin deficiency+_ deficiency Onset of symptoms Acute Often insidious Obese Uncommon Common Age at onset - years Usually < 30 >30 Family history of 10% 30% diabetes Concordance in 30- 50% 90-100% monozygotic twins
  • Epidemiology  More than 120 million people worldwide are suffering from DM.  It is estimated that it will affect 220 million by year 2020.
  • Prevalence of diabetes in Sri Lanka
  • Symptoms  Weight loss.  Polyuria – increased urine excretion.  Polydipsia – excessive thirst and water ingestion.
  • Causes  Increased prevalence of DM is related to;  excessive caloric intake  reduced physical activity.
  • Nature of the Disease  Usually irreversible.  Strongly linked to obesity.  Patients can have a reasonably normal life style.
  • Insulin  Coded by chromosome 11 and synthesized in the beta cells of the pancreatic islets.  About 50% of secreted insulin is extracted and degraded in the liver and kidney
  • Action of Insulin  Prime target organ is the liver.  Is the key hormone involved in the storage and controlled release of the chemical energy available from food within body.
  • Metabolic Changes  Abnormal carbohydrate metabolism. (Normal blood glucose level 3.6- 6.1 mmol /l)  Abnormal lipid homoeostasis. Hyperglycemia
  • Complications of Diabetes  Macrovascular diseases  Coronary heart disease  Peripheral vascular disease  Amputations  Microvascular diseases  Retinopathy  Nephropathy  Neuropathy
  • Prevention & Treatment  Combination approach.  Increased exercise  Decreases need for insulin  Reduce calorie intake  Improves insulin sensitivity  Weight reduction  Improves insulin action
  • Group 3/4
  • •Normal plasma glucose: 3.9-8.3 mM •Plasma glucose is tightly regulated by hormones: Insulin: ↓Plasma glucose Glucagon Epinephrine Cortisol ↑Plasma glucose Growth hormone
  • Correlation Between Plasma Glucose & Insulin Levels
  • Metabolism of Insulin •Insulin has no plasma carrier proteins •Short plasma half-life (3-5 min) • ~50% of insulin is removed during the first pass through the liver
  • Biological Effects of Insulin • Major target tissues for insulin:  liver, skeletal muscle, & adipose tissue. • Insulin ↑glucose uptake in muscle and adipose tissue by regulating glucose transporter (GLUT4). • Glucose transporter in the liver (GLUT 2) is not regulated by insulin.
  • GLUCAGON The most important hormone in increasing plasma glucose. Glucagon is a single chain polypeptide (29 amino acids).
  • REGULATION OF GLUCAGON SECRETION
  • ROLE OF GLUCAGON IN GLUCOSE REGULATION Glucagon opposes the metabolic actions of insulin. The major site of action: liver. The important metabolic effects of glucagon in the liver include: Carbohydrates: ↑gluconeogenesis(glucose production) ↑glycogenolysis(glycogen breakdown) ↓glycogen synthesis
  • Fat: ↑Ketogenesis(ketoneproduction) Protein: ↓Hepatic protein synthesis ↑protein catabolism in the liver Glucagon DOES NOT affect muscle proteins.
  • REGULATION OF BLOOD GLUCOSE BY INSULIN & GLUCAGON
  • Overall: •Insulin ↓plasma glucose by promoting glucose uptake & its storage. •Glucagon ↑plasma glucose by increasing liver glucose output.
  • GLUCOSE REGULATION DURING EXERCISE- ROLE OF EPINEPHRINE
  • Group 5 & 6
  • Diet Starch  White bread, sugared breakfast cereals & potatoes, which all have especially high glycemic index values & low fiber contents predispose diabetes.  Potatoes ,in particular, can become dietery handgrenades for diabetics when served as French fries.
  • Diet continue...  Refined sugars  Nothing increases blood sugar more readily than ingesting sugar. So high fructose corn syrup, candy & sweets such as cakes are not good for diabetics at all .  Saturated fats  Fats do compound many risk factors for & complications from diabetes such as obesity, hardening of arteries & heart attack or stroke.  Eg: butter, margarine, whole milk
  • Emotional Stress  Highly stressed life deeply influences the metabolism of the body. Even grief, anxiety, worry, death of any close person, etc. may alter the blood sugar level and lead to the disease.  Energy mobilization is a primary result of the fight & flight response. So stress stimulates the release of various hormones like glucocorticoids which elevate blood glucose level.
  • Obesity  When a person is overweight, the cells in the body become less sensitive to the insulin due to the high circulating levels of leptin.  There is some evidence that fat cells are more resistant to insulin than myocytes.  If a person has more fat cells than muscle cells, then the insulin become less effective overall,& glucose remain circulating in the blood instead of being taken in to the cells to be used as energy.
  • Sedentary Life  A sedentary life style is damaging to health & bears responsibility for the growing obesity problems.  Inactivity & being overweight go hand in hand towards a diagnosis of type 2 diabetes.  Muscle cells have more insulin receptors than fat cells, so a person can decrease insulin resistance by exercising.
  • Smoking  smoking 16 to 25 cigarettes a day increases your risk for Type 2 diabetes to three times that of a non-smoker..  Increases complications esp. Retinopathy, Cardiovascular conditions •There is also evidences that links cigarette smoking with microvascular diseases in diabetes. •Smoking can cause chronic pancreatitis which leads to diabetes.
  • Ethnicity  Incidence high in  African, Americans, Asians, American Indians, Hispanic, Caucasians, Latinos, Mexican-American, Europeans Age •It has been observed that as one grows older, particularly above 45 years of age, in them the chances to develop diabetes are increased. •It is chiefly because due to old age, the person becomes less active, tends to gain weight, leading to pancreatic dysfunction.
  • Genetic Predisposition  People who belong to family background having history of diabetes are 25% more prone to develop diabetes. • The concordance of type 1 DM in identical twins ranges between 30% and 70% The major susceptibility gene for type 1 DM is located in the HLA region on chromosome 6 • The concordance of type 2 DM in identical twins is between 70% and 90% •if both parents have type 2 DM, the risk approaches 40%
  • Gestational Diabetes Human placental Peripheral tissues Lactogen Insulin resistance Estrogen Pancreas Progesterone •Increased Fat stores •Prolactin •Changes in insulin receptor most women revert to normal glucose tolerance post-partum, but have a substantial risk (30– 60%) of developing diabetes mellitus later in life.
  • Infections  Mumps, Coxsackie B, Cytomegalovirus, Kilham rat virus and rubella infections can damage the pancreas.  Coxsackie virus is the commonest viral cause  Some viruses can trigger or maintain autoimmune beta cell damage.
  • Barker and Hales hypothesis  Evidence, mainly from animals, suggests that maternal and therefore fetal malnutrition during a critical early phase of fetal development can reduce Beta-cell mass and permanently impair insulin secretory reserve.
  • Other factors  Endocrine  Acromegaly 25%  Cushing’s Disease 30%  Glucagonoma 90%  Drugs that decrease insulin sensitivity  Glucocorticoids  Beta-2 receptor antagonists  OCP
  • Groups 7 & 8
  • “ The history of diabetic symptoms is of the greatest importance and an accurate appreciation of their severity far exceeds an estimation of the blood sugar as a means of assessing the need for treatment.” (John Malins, Clinical Diabetes Mellitus, Eyre & Spottiswoode, 1968)
  • Clinical presentation Acute Sub acute Symptoms Symptoms •Acute & Sub acute presentations often overlap. But,  Asymptomatic diabetes can occur.
  • Acute presentation Young people often present with a 2-3 weeks history and report the classical triad of symptoms. Thirst Polyuria 1.Thirst 2.Polyuria 3.Weight loss If not  Ketonuria treated Ketoacidosis
  • Sub acute presentation  Clinical onset over several months, years  In older patients  Classical triad of symptoms are typically present. But complain of,  visual – blurring  pruritus vulvae (female)  balanitis (male) lack of energy  dry mouth  dysphagia
  • balanitis Visual blurring Pruritus vulvae
  • Other symptoms  Somnolence (the tendency to fall asleep)  Myopia  Nausea, headache  Tiredness, fatigue  Malaise  Hyperphagia - predilection for sweet foods
  • Complications  Macrovascular  Microvascul ar diseases diseases Cardiovascular diseases Nehpropathy Eg: Coronary artery diseases Neuropathy Stroke Retinopathy • Foot infections • Erectile dysfunctions gangrene
  • Asymptomatic diabetes  No symptoms or ill health.  Accidently detected ; as glycosuria or hyperglycemia on routine investigations (for other purposes).  Both are not diagnostic of diabetes but indicates a high risk of developing diabetes.
  • Diabetes and pregnancy Group 9 and 10
  • 1. Already diagnosed diabetes mellitus woman getting pregnant – Preexisting diabetes. 2. A woman who hasn’t been diagnosed diabetes, exhibit high blood glucose levels during pregnancy – Gestational diabetes
  • Gestational diabetes  Gestational diabetes is defined as “Any degree of glucose intolerance with onset or first recognition during pregnancy"  Gestational diabetes generally has few symptoms and it is most commonly diagnosed by screening during pregnancy..
  • Gestational diabetes During Human placental lactogen pregnancy level & Cortisol level increase • Both are insulin antagonists. • Cortisol gluconeogenesis glucose utilization Blood glucose • HPL insulin sensitivity glucose utilization
  • Risk factors • Obesity BMI > 30 • Family history of diabetes • Previous babies having high birth weight ( >4.5kg ) • Previous still birth • Previous babies with congenital abnormalities
  • Maternal complications  Pre-eclampsia (pregnancy induce hypertension )  Antepartum hemorrhage due to placental abbruption  Microvascular  Nephropathy  Retinopathy  Neuropathy  Macrovascular  Coronary artery disease  Hyperglycaemia / hypoglycaemia / ketoacidosis  Infection  Thrombo – embolic disease
  • Fetal & neonatal complications  Increase risk of miscarriage & congenital fetal abnormalities  Neural tube defects, congenital heart diseases & spinal anomalies  Sacral agenesis (caudal regression syndrome)  Fetal macrosomia  Late still birth  Respiratory distress syndrome  Hypoglycaemia  Polycythaemia  Hyperbilirubinaemia  Hypomagnesemia Macrosomia
  • Diagnosis of maternal diabetes  Glucose challenge test (>140mg/dl)  Oral glucose tolerance test.  Random blood sugar. Normal fasting glucose -<7mmol/l Impaired glucose intolerance -7.8- 11.1mmol/l Random blood glucose -<11.1mmol/l If Diabetes RBG>11.1mmol/l mellitus If FBG>7mmol/l
  • Management Diabetic women are advised to maintain the blood sugar level close to normal range for 2 to 3 months in advance, before planning for pregnancy. Antenatal care  Frequent review  Increase insulin dose  Vigorous treatment for infection  Regular urine analysis to detect nephropathy At term,  Should not be allowed to continue beyond 38 weeks.  Caesarean section if needed.  Delivery before 36 weeks – Dexamethasone.  Monitor the blood glucose & urine ketone body regularly
  • Newborn,  Anticipate & treat asphyxia  Cross monitoring blood glucose level for the first 72h  Early breast feeding  Look for congenital malformation.  Random blood sugar and give dextrose if necessary. On descharge  Check the fasting blood sugar  Complete family early & follow family planning method.
  • References  Obstetrics by Ten Teachers
  • DIABETIC KETOACIDOSIS GROUP 11 & 12 07/08 BATCH
  • Introduction  Major medical emergency  Principally with type 1 diabetes  High blood sugar with ketones in urine and blood  Body can’t use glucose due to insulin shortage
  • Main cause – Type 1 diabetes Usually occurs in following circumstances • Undiagnosed diabetes • Interruption to insulin therapy • Stress due to any illness (Also occurs in type 2 diabetes)
  • Mechanism of Diabetes Ketoacidosis In adipose cells insulin inhibit the action of intracellular enzyme “Hormone-sensitive lipase”
  • Development of Signs and Symptoms  Diabetic ketoacidosis appears to require Insulin deficiency coupled with a relative or absolute increase in glucagon concentration  Increased glucagon induces maximal gluconeogenesis and also impairs peripheral utilization of glucose resulting in severe hyperglycemia
  •  This induces osmotic diuresis that leads to volume depletion and dehydration that characterize the ketoacidotic state.  Glucagon activates the ketogenic process and thus metabolic acidosis.
  • Symptoms & signs  Nausea  Vomiting  Excessive thirst  Frequent urination  Weakness  Ketone / Fruity smelly breaths  Hyperventilation  Confusion  Dry skin  Abdominal pain
  • Diagnosis  Ketonuria or ketonemia is demonstrated  Dipstick method for hyperglycemia  Centrifugation blood for ketonemia ?  Arterial blood gas analysis
  • Investigations  Urea & Electrolytes, Blood glucose, Plasma bicarbonate  Arterial blood gases to assess the severity of acidosis  Urinalysis for ketones  ECG
  • Treatment Replace lost fluid & electrolytes suppressing high blood sugar & ketone production with insulin  Fluid replacement  Insulin therapy  Potassium  NaHCO3 ….?
  • Prevention  Manage diabetes yourself  Monitoring blood sugar levels  Adjust insulin dose as needed  Check urine for ketone levels  Be prepared to act quickly
  • References  Kumar & Clark;Clinical Medicine  Davidson;Clinical medicine  Harper’s illustrated biochemistry
  • Groups 13-14
  • • Have a considerably reduced life expectancy • 70%- due to cardio vascular diseases • Followed by 10% -renal failure • Pathophysiology • Non enzymatic glycosylation of protains • Polyoyl pathway • Abnormal microvasculr pathway • Other factors • Haemodynamic changes
  • • Complications 1.Macrovascular Hypertension Smoking Lipid abnormalities 2.Microvascular Daibetic eye disese Diabetic kidney Diabetic neuropathy The diabetic foot Infections Skin & Joints
  • Diabetic Retinopathy • Impairment of loss of vision • Due to damage to blood vessels of retina • Cause of long standing diabetes Cataract Glucoma
  • Diabetic nephropathy • Important cause of morbidity mortality • Among the most common causes of the end stage renal failure • Management is frequently different & benefits of prevention are substantial
  • Diabetic neuropathy • Usually causing weakness & numbness • Symptoms are depended on nerves which damage • Most commonly affects legs
  • Complications on foot  Main cause of the AMPUTATION is diabetes mellitus  Why it will end up with amputation ????  Diabetes………. 1) Narrow & hardening the blood vessels Poor circulation Less ability to fight with infections & healing also slow Foot ulcer Gangrene
  •  2) Damage the nerves  Loss of sensation (peripheral neuropathy)  Injuries cannot be noticed  Susceptible for infections  3) Damage to the nerves controlling oil & moisture  Skin dryness  Easy to getting cracks  Susceptible for infections
  •  4) Affects joints Making them stiffer  Charcot’s joints
  • Effects of diabetes to blood vessels Diabetes mellitus Part of plaque Glucose Travel through circulation Cholesterol Breakage of plaque Lodge in a vessel Deposit in damaged of brain (STROKE) vessels Loss of blood supply to Atheroma ( in damaged inner layer) part of brain atherosclerosis Diameter of blood vessels Blood flow
  • Effect of diabetes to heart  Diabetes mellitus  Atherosclerosis Blood glucose In peripheral Blockage of vessels coronary vessels blood flow blood supply Cardiac muscle to part of failure heart Heart has to pump (cardiomyopathy) more forcefully Ischemic heart disease hypertension Heart attack
  • GROUP 15-16 DIAGNOSIS of
  • DIAGNOSIS OF DIABETES If patient complains of symptoms suggesting diabetes  Test urine for GLUCOSE & KETONES  Random Blood Glucose (normal <200mg/dL, 11.1mmol/L)  Fasting Blood glucose (FBG) if FBG>7.0mmol/l, 126mg/dL-DIABETES if (6.1 <= FBG < 7.0)mmol/l or (110 <= FBG < 126) mg/dL IMPAIRED FASTING GLUCOSE (IFG)  Oral Glucose Tolerance Test (OGTT)  HbA1C This can be utilized as an assessment of glycaemic control in a patient with known diabetic  other tests - Fructosamine test , Ketone body analysis, microalbuminuria test
  • URINE TESTS
  • BENEDICT’S TEST  To assess urine sugar level  To 5ml Benedict’s solution add 8-10 urine drops,  Boil and allow to cool then observe color change. Color change % of sugar blue Nil Clear green 0.1 Turbid green 0.3 Green & Yellow 0.5-1.0 Yellow 1.0 Orange 2.0 Brick red >2.0 Maltose, galactose, , sucrose & drugs which contain aldehyde groups such as Aspirin, Penicillin, Vitamin C, antibiotics (+)ve results • detects only blood sugar levels >180mg/dL
  • DIPSTICK METHOD • A plastic strip coated with reagents • Reagent strip measure glucose level using glucose oxidase method. GLUCOSE OXIDASE GLUCOSE H2O2 (Change the color of the indicator)
  • BLOOD TESTS
  • Random blood glucose level • Measure the blood glucose level other than post prandial stage or fasting. • If it is above 11.1mmol (200mg/dl) considered as diabetes. • GLUCOMETER • For rapid diagnosis of blood glucose levels (capillary blood )
  • Fasting Plasma Glucose After 12hr fasting measure the blood glucose level in venous blood. 4 mmol/L 6.1 7.0 80 mg/dL mmol/L mmol/L 110 126 mg/dL mg/dL Hypoglycemi Normal Impaired (Hyperglycemic) c Fasting Diabetes Glucose
  • OGTT (Oral Glucose Tolerance Test)  Unrestricted carbohydrate diet for 3 days before test  8 Hour overnight fasting is required.  75g of glucose in 300ml of water is given orally within 5 minutes.  Measure plasma glucose BEFORE and 2 hours AFTER the glucose load. Time Non Diabetic Diabetic Impaired Glucose _ Tolerance Fasting(0 <6.1mmol/l >7.0mmol/l 6.1-7.0mmol/l min) (110mg/dl) (126mg/dl) (110-126mg/dl) 120min <7.8mmol/l >11.1mmol/l >7.8-11.1mmol/l (140mg/dl) (200mg/l) (140-200mg/dl)
  • HbA1C  Measure the glycated hemoglobin proportion which indicates the glycaemic condition  Glycosylation of hemoglobin α [glucose]  This can reflect the glycaemic control of the patient over 2 to 3 months  For every 1% increase of theHbA1c indicate 35mg/dl incease of blood glucose levels. 4.5% – 6.5 % Reference range HbA1c > 8% Poor control
  • HbA1 Mean plasma glucose c % mg/dl 6 135 7 170 8 205 9 240 10 275 11 310 12 345
  • Fructosamine Test  Fructosamine = glycosylated plasma proteins, mainly albumin  Indicate previous 2-3 week glyceamic control  Impaired in patients with anemia , hemoglobinopathies & pregnancy.
  • DIAGNOSIS OF COMPLICATIONS OF DIABETES  Diagnosis of Diabetic Neuropathy Lower limbs  Peripheral pulses  Tendon reflexes  Perception of vibration sensation, light touch and proprioception Feet  Callus skin indicating pressure areas  Nails  Need for podiatry  Ulceration  DeformityDiabetic Nephropathy
  • Diagnosis of Diabetic Nephropathy Microalbuminuria test  In normal people Albumin excretion =30mg/day  In kidney damage > 300mg/day  In diabetic nephropathy ; Albumin excretion =30-300mg/day microalbuminuria
  • Diagnosis of Diabetic Retinopathy Eye examination  Visual acuities (near and distance)  Ophthalmoscopy (with pupils dilated)  Digital photography
  • Group 17 & 18
  •  Diet is an essential part of the management of diabetes  Diet is based on healthy eating principles
  • Reasons for diet •Weight control •Blood glucose control •Prevention and management of short-term and long-term complications of diabetes
  • Basic Principles of Diabetic Diet •Ensure regular meals • Base meals on starchy carbohydrates • Aim for more fruit and vegetables • Cut down on sugar and sugary foods • If in doubt read food label • Encourage relatives to bring low sugar foods •Reduce salt
  • Eat starchy foods regularly  Bread  Potatoes  Rice  Cereals  Plantain  CHO –to form 45-60% of total energy [cereals,vegetables,legumes] better use foods which has low glycaemic index
  • Eat fruit and vegetables  Fresh  Frozen  Tinned  Dried  Juice  Encourage food rich in antioxidants - vitamins
  • Reduce protein intake  Restriction of protein intake to 0.6 -0.8 g/ kg/ day  Replace red meat with chicken ,fish or vegetable protein  To contribute 10-20% of total energy
  • • Aim for low sugar diet –Not a sugar free diet –Instead of sweet cakes/ biscuits offer fruit loaf, plain biscuits, teacakes  Cut down on sugar and sugary foods: • Use low sugar foods – Use drinks labeled diet, low calorie or sugar- free – Choose diet or ‘light’ yoghurts instead of low-fat or whole yoghurts • Use sugar free/ low sugar - jelly, custard, rice pudding as dessert ideas
  • Nutrition Claims – Sugar ‘No added Sugar’ – No sugar from any source added ‘Low Sugar’ – No more than 5gs sugar/100gs ‘Reduced Sugar’ – 25% less sugar than regular product FREE SUGER – do not exceed 50g per day
  • Choose more high fibre foods To help maintain blood glucose levels and cholesterol levels Helps to maintain a  Fruit healthy gut  Vegetables  Pulses • Wholegrain cereals  Oats • Wholemeal bread • Brown rice  FIBERS – 40g per day or more half of fiber should be soluble
  • Reduce animal or saturated fat intake  Use low fat milk  Use low fat spread instead of butter  Use oil high in unsaturated fat, eg olive oil, rapeseed oil
  • Use less fat in cooking  Dry-roast  Microwave  Steam  FAT - should not exceed 30 % of total energy restrict cholesterol to 300mg or less per day
  • Choose the right sort of fat SATURATED MONO- POLY- UNSATURATED UNSATURATED • Full fat dairy produce (eg • Olive oil • Sunflower oil cheese, butter, (products) • Rapeseed oil full cream milk) • Oily fish • Groundnut oil • Biscuits • Savoury snacks • Lard • Hard vegetable fat
  • Nutrition Claims – Fat ‘Low Fat’ - . 3g Fat/ 100g or 100mls ‘Less than 5% Fat’ - . 5g fat/ 100g Reduced Fat’ – 25% less fat than similar products
  • Reduce salt intake • Cut down on added salt • Use alternatives • Look out for reduced/low sodium foods, eg bread • Avoid salt substitutes • SODIUM – restrict to 6g per day
  • Alcohol • Alcohol in moderation can be included, no more than: – 1-2 units/ day for women – 2-3 units/ day for men • Never give alcohol on an empty stomach • Remember to use ‘diet’ mixers •Caution with sweet liqueurs
  • Special diabetic foods  Not recommended  May contain more fat or energy than other foods  May be low in fibers  Has sorbitol – may cause diarrhoea  Excessive fructose may be used - Fruit sugar (fructose) when used excessively as a sweetener will still affect blood sugars in the same way as normal sugar!!
  • If Residents Overweight • Weight loss is desirable –via exercising • Encourage to cut down on fatty foods e.g. chips, pastry, crisps, biscuits, cheese and fried foods • Encourage low-fat food options e.g. semi-skimmed milk, low-fat spread • Offer fruit/ low fat yoghurt as a dessert • Snacks not essential
  • If residents malnourished • Encourage small frequent meals and low sugar puddings and snacks: – Glass of milk/ milky drinks – Crackers and cheese – Toast, butter and reduced sugar jam – Breakfast cereals, nuts – low fat yoghurt or low sugar milk pudding – Plain biscuits, fruit cake, kurakkan bread,
  • Recommended food meals for a diabetic patient Breakfast –chickpea 1 cup or green gram 1 cup or bread two slices with polsambol 1 tsp. Lunch – Rice two cups , Vegetables 6 tablespoons , green leaves ½ cup, fish or chicken 1 piece, fruit 1 serving Dinner – Rice 1 cup, vegetable 3 tablespoons, Dhal 3 tablespoons, Fruit 1 serving
  • Key Points • Ensure regular meals • Base meals on starchy carbohydrates • Aim for more fruit and vegetables • Cut down on sugar and sugary foods • If in doubt read food label • Encourage relatives to bring low sugar foods
  • Group 19-20
  •  CANNOT CURE. But can prevent.  Kathmandu declaration- life cycle approach for prevention & care of DM. o Primary prevention o Secondary prevention
  • THANK YOU!