Diabetes mellitus is a multisystem disease related to abnormal insulin production or impaired insulin utilization. It commonly affects Maori and Pacific Islanders at higher rates and is a leading cause of various health complications. The two main types are type 1, characterized by a lack of insulin production, and type 2, characterized by insulin resistance or impaired insulin utilization. Both can lead to acute complications involving abnormal blood sugar levels and chronic complications affecting blood vessels and various organs over time if not properly managed.

1. Diabetes Mellitus

2. Diabetes Mellitus
 A multisystem disease related to:
 Abnormal insulin production
 Impaired insulin utilization
 Both abnormal production & impaired
utilization

3. 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

4. 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

5. 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

6. 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

7. Insulin Secretion

8. ↑ 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

9. 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 13
 Represents 10-20% of all persons with
diabetes

10. 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

11. 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

12. Onset of Type 1 DM
 Manifestations develop when pancreas
can no longer produce insulin
- Rapid onset of symptoms
- Present at ED with ketoacidosis

13. Onset of Type 1 DM
 Polydipsia (excessive thirst)
 Polyuria (excessive urinary output)
 Polyphagia (excessive eating)
 Recent & sudden weight loss

14. Type 2 DM
 Accounts for 90% of patients with DM
 Incidence ↑ with age – 50% are over 55
yrs
 Can occur in children & adolescents
 80-90% of patients are overweight
 ↑ incidence in Maori & Pacific Islanders

15. Type 2 DM
 Pancreas continues to produce some
endogenous (self-made) insulin
 Insulin produced is either insufficient or
poorly utilized by the tissues

16. 3 Major Metabolic Abnormalities in
DM Type 2
1. Insulin Resistance
- Body tissues do not respond to action
of insulin
- Results in hyperglycaemia

17. 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

18. 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

19. Gestational Diabetes
 Develops during pregnancy
 Detected at 24-28 weeks of gestation
 ↑ risk for caesarian delivery, peri-natal
death, & neonatal complications
 Most have normal glucose levels at 6
weeks postpartum

20. 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

21. Clinical Manifestations
Type 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

22. Clinical Manifestations
Type 1 DM
Polydipsia
 Results from the intracellular dehydration
that occurs as blood glucose levels rise
and water is pulled out of body cells
Polyphagia
 Result of cellular malnourishment when
insulin deficiency prevents using glucose
for energy

23. Clinical Manifestations
Type 1
Weight loss
 Body cannot utilize glucose & turns to
other energy sources such as fat &
protein
Weakness & fatigue
 Body cells lack needed energy from
glucose

24. Clinical Manifestaions
Type 2 DM
 Non-specific symptoms
 Fatigue
 Recurrent infections
 Prolonged wound healing
 Visual changes

25. Acute Complications of DM
Diabetic Ketoacidosis
 Caused by profound deficiency of insulin
 Most likely to occur with Type 1
 Caused by illness, infection, inadequate
insulin dosage, undiagnosed Type 1
DM, poor self-management & neglect

26. 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

27. 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

28. Hypoglycaemia
 Low blood sugar levels
 Occurs 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

29. Hypoglycaemia
Clinical Manifestations
 Confusion, irritability
 Diaphoresis
 Tremors
 Hunger
 Weakness
 Headaches
 Visual disturbances
 Can progress to loss of
consciousness, seizures, coma & death

30. Causes of Hyper & Hypoglycaemia
Hyperglycaemia Hypoglycaemia
 Too much food  Alcohol intake with
 Too little or no food
diabetes medication  Too little food
 Inactivity  Too much diabetic
 Emotional, physical medication
stress  Diabetes medication
 Poor absorption of or food taken at
insulin wrong time

31. Clinical Manifestations
Hyperglycaemia Hypoglycaemia
 ↑ blood glucose  Blood glucose < 2.8mmol/L
 ↑ in urination  Numbness of
 ↑ appetite fingers, toes, mouth
 Weakness, fatigue  Tachycardia
 Blurred vision  Emotional changes
 Glycosuria  Headache
 Nausea & vomiting  Nervousness, tremors
 Abdominal cramps  Unsteady gait, slurred speech
 Progression to DKA  Hunger
 Changes in vision
 Seizures, coma

32. Chronic Complications
Angiopathy
 Blood vessel disease
 Accounts for majority of deaths among
patients with DM
 Macrovascular or microvascular
complications

33. Macroangiopathy
Cerebrovascular Disease
-TIAs & strokes
 Incidence twice as frequent in diabetics
 Hypertension major risk factor
 Risk highest for females
 Strokes more serious & higher mortality
rates

34. Macroangiopathy
Heart Disease
 CAD, atheroscleotic changes → ↓ O2 &
nutrient supply to myocardium
 More severe and more affected vessels
 MIs have higher mortality rate &
experience CHF, shock & arrhythmias

35. Macroangiopathy
Peripheral 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

36. 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

37. 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

38. Diabetic Nephropathy
 Microvascular complication associated
with damage to the small blood vessels
that supply the glomeruli of the kidneys

39. 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

40. Neuropathic Ulcers

41. Useful Website
 http://www.diabetes.org.nz/about/