Diabetes Mellitus

Diabetes Mellitus

A multisystem disease related to:

Abnormal insulin production Impaired insulin utilizationBoth abnormal production & impaired

utilization

Diabetes Mellitus

Maori & Pacific Islanders are twice as likely to be diagnosed as European/Pakeha

Leading cause of heart disease, stroke, adult blindness, & non-traumatic lower limb amputations

Normal Insulin Metabolism

Insulin produced by β cells in the islets of Langerhans of pancreas

Normally insulin is released in small increments continuously into bloodstream (basal rate)

Increase in release (bolus) when food ingested

Normal Insulin Metabolism

Insulin facilitates normal glucose range of 3-8mmol/L

Insulin promotes glucose transport from the bloodstream across the cell membrane to the cytoplasm of the cell

Counter-Regulatory Hormones

Glucagon, adrenaline, growth hormone & cortisol work to oppose the effects of insulin

Hormones work to increase blood glucose levels by stimulating glucose production and decreased movement of glucose into cells

Insulin Secretion

↑ Insulin after Meals

Stimulates storage of glucose as glycogen in liver & muscles

Inhibits gluconeogenesis (formation of glycogen from fatty acids & proteins rather than carbohydrates)

Enhances fat deposition in adipose tissue

Increases protein synthesis

Type 1 Diabetes Mellitus

Formerly known as “juvenile onset” or “insulin dependent” diabetes

Most often occurs in people under 30yrs of age

Peak onset between ages 11 and 13Represents 10-20% of all persons with

diabetes

Type 1 DM

Results from:Progressive destruction of pancreatic β

cells due to an autoimmune process in susceptible people

Auto-antibodies cause a reduction of 80-90% of normal β cell function before hyperglycaemia and other manifestations occur

Causes of Type 1 DM

Genetic predisposition & exposure to a virus

Related to human leucocyte antigens (HLAs)

When individual with certain HLA type is exposed to viral infection, the β cells of pancreas are destroyed

Onset of Type 1 DM

Manifestations develop when pancreas can no longer produce insulin

- Rapid onset of symptoms- Present at ED with ketoacidosis

Onset of Type 1 DM

Polydipsia (excessive thirst)Polyuria (excessive urinary output)Polyphagia (excessive eating)Recent & sudden weight loss

Type 2 DM

Accounts for 90% of patients with DMIncidence ↑ with age – 50% are over 55

yrsCan occur in children & adolescents80-90% of patients are overweight↑ incidence in Maori & Pacific Islanders

Type 2 DM

Pancreas continues to produce some endogenous (self-made) insulin

Insulin produced is either insufficient or poorly utilized by the tissues

3 Major Metabolic Abnormalities in DM Type 2

1. Insulin Resistance- Body tissues do not respond to action

of insulin- Results in hyperglycaemia

3 Major Metabolic Abnormalities in DM Type 2

2. Impaired glucose tolerance (IGT) (prediabetes

- Occurs when the alteration in β cell function is mild

Blood glucose levels are higher than normal but not high enough for a diagnosis of diabetes

3 Major Metabolic Abnormalities in DM Type 2

3. Inappropriate glucose production by liver

- Instead of liver regulating the release of glucose in response to blood levels, it does so in a haphazard way

- Only a minor factor in Type 2

Gestational Diabetes

Develops during pregnancyDetected at 24-28 weeks of gestation↑ risk for caesarian delivery, peri-natal

death, & neonatal complicationsMost have normal glucose levels at 6

weeks postpartum

Secondary Diabetes

Results from another medical condition or due to the treatment of a medical condition that causes abnormal blood glucose levels

- Cushing syndrome- Hyperthyroidism- Parental nutrition- Usaully resolves when underlying condition

is treated

Clinical ManifestationsType 1 DM

Onset rapid & manifestations are usually acute

Polyuria- When blood glucose ↑, the amt of

glucose filtered by glomeruli of kidneys exceeds amt reabsorbed by renal tubules. This results in glycosuria & large losses of water in urine

Clinical ManifestationsType 1 DM

PolydipsiaResults from the intracellular dehydration

that occurs as blood glucose levels rise and water is pulled out of body cells

PolyphagiaResult of cellular malnourishment when

insulin deficiency prevents using glucose for energy

Clinical ManifestationsType 1

Weight lossBody cannot utilize glucose & turns to

other energy sources such as fat & protein

Weakness & fatigueBody cells lack needed energy from

glucose

Clinical ManifestaionsType 2 DM

Non-specific symptomsFatigueRecurrent infectionsProlonged wound healingVisual changes

Acute Complications of DMDiabetic Ketoacidosis

Caused by profound deficiency of insulinMost likely to occur with Type 1Caused by illness, infection, inadequate

insulin dosage, undiagnosed Type 1 DM, poor self-management & neglect

Diabetic Ketoacidosis

When circulating supply of insulin is insufficient, glucose cannot be used properly for energy

Body breaks down fat stores as secondary source of fuel

Ketones are by-products of fat metabolism that can cause serious problems when they are excessive in the blood

Ketones alter pH balance causing metabolic acidosis

Clinical Manifestaions of Ketoacidosis

Dehydration – poor skin turgor, dry mucous membranes, tachycardia and orthostatic hypotension

Lethargy & weakness Flushed, dry skin Abdominal pain, nausea & vomiting Rapid deep breathing Acetone on breath (sweet, fruity odour) Elevated blood sugar Ketones in blood & urine

Hypoglycaemia

Low blood sugar levelsOccurs when there is too much insulin in

proportion to available glucose in the blood

Causes blood glucose level to drop to less than 3.5mmol/L

HypoglycaemiaClinical Manifestations

Confusion, irritability Diaphoresis Tremors Hunger Weakness Headaches Visual disturbances Can progress to loss of consciousness,

seizures, coma & death

Causes of Hyper & Hypoglycaemia

Hyperglycaemia Too much food Too little or no

diabetes medication Inactivity Emotional, physical

stress Poor absorption of

insulin

Hypoglycaemia Alcohol intake with

food Too little food Too much diabetic

medication Diabetes medication

or food taken at wrong time

Clinical Manifestations

Hyperglycaemia ↑ blood glucose ↑ in urination ↑ appetite Weakness, fatigue Blurred vision Glycosuria Nausea & vomiting Abdominal cramps Progression to DKA

Hypoglycaemia Blood glucose < 2.8mmol/L Numbness of fingers, toes,

mouth Tachycardia Emotional changes Headache Nervousness, tremors Unsteady gait, slurred

speech Hunger Changes in vision Seizures, coma

Chronic ComplicationsAngiopathy

Blood vessel diseaseAccounts for majority of deaths among

patients with DMMacrovascular or microvascular

complications

Macroangiopathy Cerebrovascular Disease

-TIAs & strokesIncidence twice as frequent in diabeticsHypertension major risk factorRisk highest for femalesStrokes more serious & higher mortality

rates

MacroangiopathyHeart Disease

CAD, atheroscleotic changes → ↓ O2 & nutrient supply to myocardium

More severe and more affected vesselsMIs have higher mortality rate &

experience CHF, shock & arrhythmias

MacroangiopathyPeripheral Vascular Disease

Intermittent claudication, absent pedal pulses & ischaemic gangrene - ↑ incidence in diabetics

Diabetes cause of more than 50% of non-traumatic amputations

Trauma to lower limb with resultant ulceration, infection & poor wound healing

Microvascular Complications

Result for thickening of the vessel membranes in the capillaries & arterioles in response to conditions of chronic hyperglycaemia

Complications are specific to diabetes Mainly affect eyes (retinopathy), the kidneys

(nephropathy) and the nervous system (neuropathy)

Clinical manifestations occur 10-20 years after onset of diabetes

Diabetic Retinopathy

Process of microvascular damage to retina as a result of chronic hyperglycaemia

Most common cause of new cases of blindness

Cataracts are also common

Diabetic Nephropathy

Microvascular complication associated with damage to the small blood vessels that supply the glomeruli of the kidneys

Diabetic Neuropathy

Nerve damage that occurs because of metabolic derangements associated with DM

Approx 60-70% of pts with diabetes have some degree of neuropathy

Most common type is sensory neuropathy which leads to loss of protective sensation in lower extremities and increases risk of complications that result in limb amputation

Neuropathic Ulcers

Useful Website

http://www.diabetes.org.nz/about/