Diabetes 2010
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Transcript of Diabetes 2010
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/