WHAT IS DIABETES ?

DIABETES

Diabetes is chronic metabolic disorder that prevents the body to utilize glucose completely or partially. It is characterized by raised glucose concentration in the blood and alterations in carbohydrate, protein and fat metabolism. This can be due to failure in the formation of insulin or liberation or action.

CAUSES OF DIABETES

IDDM (Insulin dependent diabetes mellitus) :

Genetics : The inheritance of human IDDM is polygenic. It has been estimated that

over 50% of the heritability is contributed by the HLA class 2 nd genes(chromosome 6).

Environmental factor : Infections: Infections cause a non- specific outpouring of catabolic

hormones which antagonise insulin action and then may trigger the onset of disorder.

The virus may trigger an autoimmune reaction in the pancreatic islets and

this impairs insulin secretion and ultimately destroys the beta cells.

Acute stress: The body releases adrenaline, noradrenaline, and cortisol hormones that raise blood glucose levels to provide a quick source of energy for coping with stress

In acute cases of stress blood glucose levels may rise and in extreme cases diabetic ketosis and coma also may result .

Diet: Wheat and milk protein have the strongest diabetogenic effect and one evidently capable of triggering the string of events which result ultimately in destruction of pancreatic islet insulin secreting cells.

Immunological factors :IDDM is a slow autoimmune disease. IDDM is associated with other autoimmune disorders.

NIDDM ( Non insulin dependent diabetes

mellitus) Genetics : NIDDM is commonly associated with obesity , hypertension , and

hyperlipidemia . It Occurs in subjects who are obese insulin- resistant accompanied by

impaired beta cell function. It represents a combination of major and minor genes affecting insulin

secretion, insulin action , and obesity.

Environmental factors : life style: NIDDM is associated with people who are obese and

underactive usually they over eat. Obesity probably acts as a diabetogenic factor through increasing

resistance to the action of insulin. Age : it is principally a disease of the middle aged and elderly.

Abdominal fat : people with high waist / hip ratio has greater risk of diabetes than people with a similar amount of fat distributed peripherally.

This probably relates to the insulin insensitivity which is caused by a high flux of free fatty acids in the portal circulation, because intra- abdominal fat cells can release fatty acids very rapidly.

Pregnancy : During normal pregnancy the level of plasma insulin is raised by the action of placental hormones thus placing burden on the insulin secreting cells of the pancreatic islets.

The pancreas may be unable to meet these demands in women genetically predisposed to develop both types of diabetes.

Insulin resistance : Insulin resistance may be due to an abnormal insulin molecule, an

excessive amount of circulating antagonists and target tissue defects.

The last is the common cause of insulin resistance in NIDDM and seems to be the predominant abnormality in those with more severe hyperglycemia.

INSULIN Insulin a hormone produced by

the beta cells of the pancreas that is necessary for the use or storage of body fuels.

FUNCTIONS OF INSULIN

In addition to its role of regulating glucose metabolism, insulin also

Stimulates lipogenesis Diminishes lipolysis s Increases amino acid transport into cells Modulates transcription Altering the cell content of numerous mRNAs Stimulates growth DNA synthesis Cell replication

INSULIN AND COUNTER REGULATORY HORMONE

Optimal control of diabetes requires the restoration of normal carbohydrates, protein, and fat metabolism.

Insulin is both anti catabolic and anabolic and facilitates cellular transport.

In general , the counter regulatory hormones have the opposite effect of insulin .

EFFECTS CARBOHYDRATES PROTEIN FAT

Anti catabolic(prevents breakdown)

Decrease breakdown and release of glucose from glycogen in the liver

Inhibits protein degradation diminishes gluconeogenesis

Inhibits lipolysis prevent excessive production of ketones and ketoacidosis

Anabolic (promote storage )

Facilitates conversion of glucose to glycogen for storage in liver and muscle

Stimulates protein synthesis

Facilitates conversion of pyruvates to free fatty acids stimulating Lipogenesis

Transport Activates the transport system of glucose in to muscle and adipose cells

Lower blood amino acids in parallel with blood glucose level

Activate lipoprotein lipase, facilitating transport of triglyceride into adipose tissue

ACTION OF INSULIN ON CARBOHYDRATES, PROTEIN , FAT METABOLISM

INSULIN THERAPY

When the islets of langerhans are unable to produce insulin it must be supplied by injection.

Persons with type 1 diabetes depend on insulin to survive and with

type 2 diabetes, insulin may be needed to restore glycemia to near normal.

Insulin has four properties : action , concentration, purity, and source.

These properties determine its onset, peak , and duration.

TYPES OF INSULIN AND THEIR ACTIONINSULIN ONSET PEAK DURATION

Short acting insulin (clear) Lispro Regular

5-15 minutes30-45minutes

30-75 minutes2-3 hours

2-3 hours4-6 hours

Background insulin (cloudy) NPH (neutral protamine hagedorn)LENTE ULTRALETE

2-4 hours2-4 hours3-5 hours

4-10 hours4-10 hours 8-14 hours

10-18 hours10-18 hours 18 hours

Premixed insulin70/30 or 50/50 60 minutes 2-12 hours Up to 18

hours

TYPES OF INSULIN

Regular and Lispro insulin: Short -acting Regular insulin needs to be taken 30 to 45 minutes before eating. Lispro insulin, an analogue with two amino acids reversed in position. Starts to

work very quickly. So it should be taken immediately before eating.

Both insulins may be used in combination with a background or intermediate

–acting insulin, may also be used independently during acute illness , in insulin pumps , and in multiple daily injection regimen .

Background or intermediate–acting insulins: It include NPH, LENTE AND ULTRALENTE Their appearance is cloudy. And their onset ,peak, duration are similar. Ultralente is a slightly longer-acting insulin than the intermediate –acting

insulins.

Premixed insulins:

70/30 which is 70% NPH and 30% regular 50/50 which is 50% NPH and 50 % regular

Human or highly purified animal insulin are now standard and contain less than 1ppm of impurities.

They are associated with fewer insulin antibodies, less insulin allergy. The source of insulin is important because it affects the speed of

absorption, peak, and duration of action. Animal insulin come from the pancreas of the cows and pigs. Human insulin has been produced synthetically. Human insulins are generally absorbed more rapidly, peak earlier,

and have a shorter duration time than animal insulins. A major advantage of human insulin is that it produce fewer

antibodies and as a result, can also be used for insulin treatment.

TYPES AND TIMING OF INSULIN REGIMEN

A short –acting and background insulin

• Given twice a day • The breakfast dose

consist of about one third regular and two third NPH

A short acting and background insulin

• Prebreakfast a short –acting insulin presupper and background insulin such as NPH, at bedtime.

Intensive insulin regimen

• It consist of multiple daily injection or insulin infusion pump therapy .

A short- acting insulin is given before meals to provide bolus insulin replacement.

A background insulin is given once a twice a day. These types of regimens allow increased flexibility in the type and

timing of meals. The amount of short-acting insulin can be adjusted based on

composition of meals.

INSULIN INFUSION PUMP THERAPY

It provide basal short-acting insulin pumped continuously by a mechanical device in micro amounts through a subcutaneous catheter that is monitored 24 hours a day .

Boluses of the short-acting insulin are then given before meals. Pump therapy requires a motivated person who is willing to do a minimum

of four blood glucose test per day. Keep blood glucose and food records and learn the technical features of

pump usage. Pump therapy is also more expensive than other insulin regimen.

DOSE: 35% Before breakfast 25% before lunch and dinner 15% before bed time

In addition to closer control of blood glucose levels, use of the insulin pump is reported to lower elevated level of serum cholesterol and triglycerides and to permit greater flexibility in timings of meals.

Genetic influence

Insulin resistance

Environmental influence •Deficiency of nutrients•Excessive calorie intake •Low physical activity level

Hyperinsulinemia

Decreased HDL choleste

rol

Increased uric level

Increased LDL cholest

erol

Increased

plasma triglycer

ides

Glucose

intolerance

Increased

lipogenesis

Increased blood pressur

e

Gout Atherosclerosis

Diabet

es

Hypertensi

on

Obesity

Pathaphysiology of insulin resistance

Metabolic syndrome A collection of health risks, including excess fat in the abdominal region, high blood pressure, elevated blood triglycerides , low high- density lipoprotein cholesterol and high blood glucose that increases the chance of developing heart disease , stroke, and diabetes, the condition is also known by others names including syndrome x , insulin resistance syndrome ,dysmetabolic syndrome.

HYPERINSULINEMIA OR SYNDROME X

Syndrome x refers to a clusters of metabolic disorders, including type 2 diabetes, hypertension and dyslipidemia and often include obesity.

A major factor in syndrome X is insulin resistance, which is cellular resistance to insulin.

Resistance to insulin mediated to glucose uptake may be more common.

Factors that have a positive impact on insulin : Exercising Reducing calorie intake Reducing body weight

A defensive nutrition plan for middle-aged adults emphasizes food that supply glucose to the cells at a steady rate and moderate insulin demands.

One useful tool for measuring the rate at which foods provide glucose to the blood and then stimulate insulin release is the glycemic index .

COMPLICATIONS

Without effective insulin hyperglycemia occurs, which can lead to both the short term and long term complication of diabetes mellitus.

Short term or acute complication: 1) Hyperosmolar hyperglycemic nonketotic syndrome 2) Hyperglycemia/ diabetic ketoacidosis 3) Hypoglycemia 4) Hyperglycemia after hypoglycemia 5) Dawn phenomenon

HYPEROSMOLAR HYPERGLYCEMIC NONKETOTIC SYNDROME

HHNK syndrome is defined as a extremely high blood glucose level, absence or only small amounts of ketones and profound dehydration.

Patient who have HHNK syndrome have sufficient insulin to prevent lipolysis and ketosis.

This condition occurs rarely, usually in older patients with type 2

diabetes. Clinical manifestation Hypotension Profound dehydration Tachycardia Variable neurological signs

TREATMENT: Hydration Small doses of insulin

HYPERGLYCEMIA/DIABETIC KETOACIDOSIS

It is characterized by severe disturbance in carbohydrate, protein and fat metabolism.

These ketones split into the urine the reliance on urine testing for ketones

DKA is characterized by elevated blood glucose level and the presence of ketones in the blood and urine.

Symptoms: polyuria polydipsia hyperventilation dehydration fatigue

TREATMENT: Supplemental insulin Fluid and electrolyte replacement Medical monitoring

Acute illness such as flu , colds, vomiting, and diarrhea. If not manage appropriately can lead to the development of DKA.

HPOGLYCEMIA Hypoglycemia is a common side effect of insulin therapy.

SYMPTOMS: Shakiness Sweating Palpitation Hunger

Hypoglycemic symptoms are related to neuroglycopenia

Headaches Confusion Lack of coordination Blurred vision Anger Seizures Coma

CAUSES

Medication errors Excess insulin or oral medication Inadvertent or deliberate errors in insulin doses Improper timing of insulin in relation to food intake Intensive insulin therapy Inadequate food intake Omitted or inadequate meals or snacks Delayed meals or snacks Unplanned activities Alcohol intake

TREATMENT 15 grams of carbohydrate commercially available glucose

tablets .

Parents, roommates , and spouses should be taught how to mix , draw up , and administer glucagon.

Patients need to be reminded of the need to treat hypoglycemia , even in the absence of symptoms

HYPERGLYCEMIA AFTER HYPOGLYCEMIA Hypoglycemia followed by “ rebound” hyperglycemia is also called the

somogyi effect. This phenomenon originates during hypoglycemia with the secretion

of counter regulatory hormones hepatic glucose production is stimulated thus raising blood glucose levels.

If rebound hyperglycemia goes unrecognized and insulin doses are increased, a cycle of over insulinization may result.

DAWN PHENOMENON The amount of insulin required to normalize blood glucose levels

during the night is less in the predawn period (from 1 to 3 am ) than at dawn (4 to 8 am )

The rise in blood glucose levels may be increased if insulin level declines between predawn and dawn or if hypoglycaemia occurs during the predawn period.

Blood glucose level is monitored at bed time and at 2 to 3 am to identify the dawn phenomenon.

Taking intermediate acting insulin at bed time or substituting it with a longer-acting insulin may also be effective.

Long term complications

Micro vascular diseases

Retinopathy

Nephropathy

Macro vascular diseasesCoronary artery diseaseCerebrovascular disease

Peripheral vascular disease

Neuropathy

MACROVASCULAR DISEASES

Macro vascular disease result from changes in the medium to large blood vessels. In this blood vessel walls thicken, and become closed by plaque that adheres to the vessel walls . Eventually blood flow is blocked.

Coronary heart disease , peripheral vascular disease , cerebrovascular disease

Lipid abnormalities are one of the risk factors contributing to accelerated atherosclerotic vascular disease .

Generally , total cholesterol and LDL cholesterol are comparable between persons with diabetes and the general population.

Patients with type 2 diabetes have smaller , more dense LDL particles, which increase atherogenecity .

Elevated plasma triglyceride and very low density lipoprotein cholesterol levels and lower HDL cholesterol level.

Coronary heart disease

• Chest pain • Dyspnea• Orthopnea• Paroxysmal nocturnal

Peripheral vascular disease

• Foot ulcers • Pain in buttock, thigh,

Cerebrovascular disease• Transient blindness, • dysarthria, or• unilateral weakness

SYMPTOMS

TREATMENT

It is based on LDL cholesterol levels. With CHD, PVD, OR CVD , Medical nutrition therapy and drug therapy is initiated.

When LDL cholesterol levels exceed 100mg/dl , with a goal of reducing this value , MNT is initiated.

Drug therapy is appropriate at LDL cholesterol levels of 130mg/dl or higher.

MANAGEMENT

Diet and exercise are important in managing obesity, hypertension , and hyperlipidemia.

Use of medications to control hypertension and hyperlipidemia Smoking cessation is essential Control of blood glucose levels Patients may require increased amounts of insulin or may need to

switch from oral antidiabetic agents to insulin during illness.

MICROVASCULAR DISEASES Micro vascular complications of diabetes affect small blood vessels

and nerves of the body.

Retinopathy Neuropathy Nephropathy

RETINOPATHY The eye pathology refer to as diabetic retinopathy is caused by changes in the

small blood vessels in the retina, the area of the eye that receives images and sends information to the brain.

Nearly all patients with type I diabetes and more than 60% of patients with type II diabetes have some degree of retinopathy after 20 years.

Changes in the micro vasculature include micro aneurysms, intra retinal hemorrhage, hard exudates, focal capillary closure.

There are three main stages of retinopathy:

Nonproliferative retinopathy Preproliferative retinopathy Proliferative retinopathy

Nonproliferative retinopathy It is the earliest stage of retinopathy where structural changes began

to occur in various structures of the eye. It is divided into three stages mild, moderate and severe.

Mild NPDR is characterized by microaneurysms The residue of protein and lipid components that leak from the blood

vessels are present. Intra-retinal hemorrhage appearing as dots or flame shapes and soft

exudates or ‘cotton wool spots’, areas of infraction in the nerve fiber layer of the retina.

Moderate NPDR It is characterized by microaneurysms, dot and blot hemorrhages and

exudates. The retinal veins becomes dilated and intra retinal micro vascular

abnormalities which appear as a clusters of micro aneurysms and hyper cellular vessels develops.

Severe NPDR: It is characterized by hemorrhages and microaneurysms in all of the

retina, IRMA in one, and venous beading in another quadrants signify high for development of PDR.

Preproliferative retinopathy In this retinopathy there are more wide spread vascular changes and

loss of nerve fibers. 10-50% of patients with preproliferative retinopathy will develop

proliferative retinopathy within a short time.

PROLIFERATIVE RETINOPATHY It is characterized by the proliferation of new blood vessels growing

from the retina into the vitreous. These new vessels are prone to bleeding.

The visual loss associated with proliferative retinopathy is caused by the vitreous hemorrhage or retinal detachment.

The vitreous is normally clear, allowing light to be transmitted to the retina.When there is a hemorrhage, the viterous becomes clouded and cannot transmit light resulting in loss of vision.

Another consequence of vitreous hemorrhage is that resorption of the blood in the vitreous leads to the formation of fibrous scar tissue.

Clinical manifestations Retinopathy is a painless process. Blurry vision secondary to macular edema occurs in some patients.

Symptoms: Floaters or cobwebs in the visual field. Sudden visual changes including spotty or hazy vision or complete

loss of vision.

Medical management For advanced cases , the main treatment of diabetic retinopathy is

argon laser photo coagulation. The laser treatment destroys leaking blood vessels and areas of

neovasclarization. For patients at increased risk for hemorrhaging, pan- retinal photo

coagulation may significantly reduce the rate of progression to blindness.

It is characterized by albuminuria, hypertension, and progressive renal insuffiency.

It can lead to end stage renal disease, a serious condition in which a patient’s survival depends on either dialysis or kidney transplantation.

Characteristics Decrease in glomerular filtration rate Increase in glomerular capillary pressure

Clinical manifestations Proteinuria Fluid retention

Nephropathy:

SIGNS AND SYMPTOMS Weight gain ,peripheral edema , and pulmonary edema Elevated blood urea nitrogen (BUN) and creatinine levels Fatigue and shortness of breath Uncontrolled hypertension Uremia due to accumulation of metabolic wastes GI manifestations : anorexia, nausea, vomiting Neuromuscular disturbance : fatigue, muscle cramps, seizures,

coma Hematologic symptoms: anemia fatigue, decreased white blood

cell count , increased risk of infection.

TREATMENT HbA1c<7% Control blood pressure Appropriate diet Manage kidney infections Avoid nephrotoxic drugs Test regularly for microalbuminuria Smoking cessation

NEUROPATHY Damage to the nerves that allow feeling sensation, diminished

transmission of nerve impulses that affect muscle function and sensory perceptions in various parts of the body.

Autonomic dysfunction Diabetic foot, ulceration, amputation

Types of diabetic neuropathy Distal symmetric sensorimotor Diabetic autonomic Diabetic proximal Focal neuropathy

DISTAL SYMMETRIC SENSORIMOTOR

Most commonly legs and foot are affected . Nerve damage in the feet can result in loss of foot sensation,

increasing foot problems.

Symptoms: Tingling Numbness Burning sensation and pain

Peripheral neuropathy leads to Small fiber damage Large fiber damage Motor nerve damage

Prevention: Examine your foot daily Apply lotion on dry feet Wear proper fitting footwear, corns should never be cut and keep them

clean.

DIABETIC AUTONOMIC NEUROPATHY It commonly affects the digestive system especially the stomach,

blood vessels, urinary system and sex organs. Its affects on Upper GI Intestinal Bladder Sexual dysfunction Cardiovascular

DIABETIC PROXIMAL NEUROPATHY

It is usually causes pain in one side in the thighs, hips or buttocks It can also leads to weakness in legs.

Treatment Medication and physical therapy Keep blood glucose level under control

FOCAL NEUROPATHY

It affect specific nerve , most often in the head , legs causing muscle weakness or pain.

symptoms Double vision , pain in eye Severe pain in lower back, legs, chest Abdominal pain

DIABETIC FOOT Foot ulcers are one of the main complication of DM. With damage to the nervous system, a person with diabetes

may not be able to feel his or her feet properly. Normal sweat secretion & oil production that lubricates the skin

of the foot is impaired These factor together can lead to abnormal pressure on the

skin, bones, and joints of the foot during walking and can lead to breakdown of the skin of the foot.

Sores may develop. Damage to blood vessels and impairment of the immune

system from diabetes makes it difficult to heal these wounds. Bacterial infection of the skin connective tissues, muscles and

bones can occur. These infection can develop into gangrene.

FEET SHOULD BE LABELED AS HIGH RISK IF:

If any deformity ids observed. Sensory examination revels loss of sensation. Absence of foot pulses. Previous history of ulcer.

FOOT CARE DO’S AND DONT’S FOR PATIENT

DO DO NOT

Inspect feet daily using mirror Walk barefoot

Wash feet daily in the tepid water Smoke

Apply lotion to the feet after drying

Expose to extreme temperature

Have your feet check at each clinical visit

Use chemical agents e.g. corn plaster to treat corns or calluse

Inspect foot wear daily for detects /foreign bodies, change footwear often

Wear new foot wear for more than a hour or two at a time

THANKYOU