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Diabetes mellitus is

A group of diseases characterised by hyperglycemia due to defects in insulin secretion, insulin action, or both


The pancreas is

Comprised of exocrine and endocrine tissue
Exocrine = digestive enzymes
Endocrine = insulin production from the Islets of Langerhans

alpha cells =secrete glucagon,
beta cells = secrete insulin,
delta and polypeptide cells


Alpha cells

secrete glucagon


Beta cells

secrete insulin


Types of diabetes

Type 1 (formerly Insulin Dependant Diabetes Mellitus)

Type 2 (formerly non – Insulin Dependant Diabetes Mellitus)

Gestational Diabetes- glucose intolerance with onset during pregnancy


Type 1 diabetes

Presents in under 30 years of age
Almost complete lack of insulin or severe lack of
Autoimmune Cause?
Patients commonly lean
Could be genetically linked
Sometimes triggered by Viral infection


Diabetes risk factors

family history
environmental factors
high blood pressure


Functions of insulin

Enables glucose to enter cells to be metabolised for energy
Stimulates storage of glucose in the liver and muscle (as glycogen)
Signals the liver to stop the release of glucose
Enhances storage of dietary fat in adipose tissue
Accelerates transport of amino acids from dietary protein into cells
Inhibits the breakdown of stored glucose, protein, and fat

When carbohydrates, fats and proteins are eaten, insulin promotes cellular transport and storage of all these nutrients


Classifications of diabetes

Pre diabetes (impaired glucose intolerance)
Type 1 diabetes (ex juvenile onset/IDDM)
Latent Autoimmune Diabetes of Adults (LADA)
Type 2 diabetes (NIDDM)
Gestational diabetes (during pregnancy)
Diabetes associated with other conditions/syndromes
Pancreatic & hormonal disorders (diabetes insipidus)
Corticosteroid & hormone drug induced


Type 1 diabetes

Insulin producing pancreatic beta cells are destroyed by a
?autoimmune process in genetically predisposed persons possibly after an environmental trigger (? virus)
Requires insulin, as little or no insulin is produced
Leading to high post prandial blood glucose
If high enough – “leaks” into urine
Onset is acute (often after a long pre-acute build up)
Before 30 years of age
5–10% of persons with diabetes


Type 2 diabetes

Combination of decreased sensitivity to insulin (insulin resistance) and impaired beta cell function (decreased insulin production) 90–95% of person with diabetes
More common in persons over age 30 and in the obese
Slow, progressive glucose intolerance/decreased tissue sensitivity
Treated initially with diet and exercise
Oral hypoglycemic agents/insulin may be required


Clinical manifestations of type 1&2

The‘Three Ps’
Polyuria (osmotic effect of glucose)
Polydypsia (osmotic effect of glucose)
Polyphagia (from cellular malnourishment)

Fatigue/weakness/vision changes
Tingling/numbness in hand & feet/dry skin
Skin lesions/wounds slow to heal & recurrent infections
Type 1 may have sudden weight loss
Type 2 may not present with these symptoms


Diagnostic findings

Fasting blood glucose level (BGL) equal to or greater than 7.0 mmol/L (repeated)
Postprandial BGL equal to or greater than 11.0mmol/L (repeated)

Glycosylated haemoglobin (HbA1C)
Method of assessing elevated blood glucose over time
Equal to or greater than 6.5% (48mmol/mol) (repeated)
Gold standard, though inaccuracies possible

Gerontologic considerations:
Elevation of blood glucose is common after 50 yrs of age


BGL management targets

4.0–6.0 mmol/L (fasting for Type 1)
6.0-8.0 mmol/L (fasting for Type 2)
4.0-8.0 mmol/L (post-prandial for Type 1)
6.0-10 mmol/L (post-prandial for Type 2)


HbA1C management targets

Less/= to 7 (53 mmol/mol)
Variable in certain groups
Tested bi-annually (or every 3 – 6 months for Type 1s)


Diabetes management

With intensive management/decrease in overall complications
Though intensive management also increases hypoglycemic episodes
Patient education is actively required

Prevent wide fluctuations of BGLs
Provide optimal nutrition/all essential food groups
Meet energy needs/maintain a reasonable weight
Low GI foods
Plan with diabetic nutritionist/dietician
Patient education/teaching is essential
Type 1s - insulin & diet must be “integrated”

Planned and consistent
Lowers blood glucose & cardiovascular risk/aids in weight loss
If on insulin need to adjust accordingly/post exercise hypo
Monitor with BGLs regularly


Pharmacological management

Type 1 required/Type 2 often needed
Complex/S & B table 36.1
Type 2 (BD or weekly)
Oral hypoglycaemics
Biguanide (Metformin)
? Combination of two different types
+ Antihypertensives + lipid lowering agents


Nursing management

Newly diagnosed/long term complications/other issue
Interdisciplinary care
Outpatient management
Diabetic educators/specialist knowledge
Individualised care
Patient knowledge base

Take usual insulin/medication
Monitor more regularly (2 – 4 hrly)
Monitor ketonuria
Report hyperglycaemia (? 16 mmol/l)
? Require supplemental insulin
Don’t be alone
If D & V – maintain liquids/glucose
Emergency care
Fasting patients/special pre-op instructions


Long term complications of diabetes

Macrovascular complications
Accelerated atherosclerotic changes
Coronary artery disease
Cerebrovascular disease
Peripheral vascular disease

Microvascular complications
Diabetic retinopathy
Dementia (20% increase/1point high BGL)

Neuropathic changes
Peripheral neuropathy
Autonomic neuropathies

Sexual dysfunction


Acute complications of diabetes

Hyperglycemia Complex management
Diabetic ketoacidosis (DKA)
Hyperglycemic hyperosmolar nonketotic syndrome (HHNS), (hyperosmolar nonketotic coma)
(hyperglycemia hyperosmolar syndrome [HHS])



Abnormally low blood glucose level
Variable ( 3.3mmol/L)
Causes include:
Disrupted routine
Too much insulin (oral hypoglycemic agents)
Too little food
Excessive physical activity


Manifestations of hypoglycaemia

Adrenergic symptoms:
weakness/sweating/tremors/tachycardia/ palpitations/nervousness/hunger

Central nervous system symptoms:
inability to concentrate/ headache/confusion/slurred speech/numbness of lips and tongue/irrational or combative behaviour/double vision

Severe hypoglycemia may cause:
disorientation/seizures/loss of consciousness
abrupt & unexpected/or predictable


Management of Hypoglycaemia

Treatment must be immediate (with staff assist call)
Rule of 15
Give 15 g of fast-acting, concentrated carbohydrate
glucose tablets/juice or regular soda (not diet soda)
candies/honey or syrup
Retest blood glucose in 15 minutes/Repeat if no improvement
MET call after 2 – 3 treatments
If next meal over 15 mins away
Consider longer acting carb (sandwich/milk/fruit/bisc & cheese)
If the patient cannot swallow or is unconscious:
IMI glucagon/50% glucose solution IV
On emergency Cart
If no improvement consider other causes


Management of DKA

S & S
Dehydration, increase in urine output
Dry mucous membranes
Tachycardia, orthostatic hypotension, lethargy and weakness
Abdominal pain with nausea and vomiting
Kussmaul respirations (attempt to reverse metabolic acidosis)
Raised BSL > 14 mmols/L and ketones in urine
Frequent checking of BSL and ketones in urine
Continue medications
Encourage fluids
May need Insulin Infusion


Hyperosmolar hyperglycaemia non- ketotic syndrome

Occurs with Type II diabetes – prevents DKA but not enough to prevent severe hyperglycaemia
Blood sugar climbs high before problem is recognized
Coma, hemiparesis, aphasia, seizures
Treatment is similar to DKA
Will need insulin infusion


Pharmacological therapy

Insulin Therapy and Insulin Preparations
Insulin Regimens-
conventional regimen
intensive regimen
Complications- allergic reactions, lipodystrophy, resistance, hyperglycaemia

Timing of administration
Blood Glucose Levels
Types of Insulin – rapid onset, short acting, intermediate, long-acting
Long acting – Lantas Solostar
Short acting - Regular insulin - actrapid
Rapid acting - lispro, novorapid
Intermediate –Protophane
Routes of administration



acts as a mimic to normal pancreatic response to blood glucose levels – a continual low secretion of insulin to deal with the body’s metabolism of glucose and a rise in insulin concentration following a meal with carbohydrate, enabling the body to cope with the consequent rise in blood glucose.


Quick acting insulin

works rapidly, lasts, 4-6 hrs a clear solution


Intermediate and long acting insulin

sustained action, lasts up to 12 hrs – 24 hrs, a cloudy solution


Nutritional management

Providing all essential food constituents
Meeting energy needs
Maintaining a reasonable weight
Preventing wide fluctuations in BSL
Decreasing lipid levels to reduce risk of macrovascular disease
Reducing alcohol intake
Meal planning – eating out, timing of insulin, reading food labels, adjustments for illness and exercise


Foot ulceration in diabetes

Precipitating, Predisposing, Prolonging
Repeated minor trauma/major trauma to foot.
Peripheral neuropathy:
Sensory neuropathy
Motor neuropathy
Autonomic neuropathy


Foot health advice - daily check

Examine feet daily for blisters, cracks and/or breaks in skin, swelling, bruising, colour changes or abnormalities.

If a problem occurs seek advice immediately from GP, nurse or podiatrist. Cover any breaks in the skin with a clean dry dressing


Foot care

Wash feet regularly.

Always dry feet thoroughly after bathing, drying
between toes to prevent moisture build up.

If skin is dry apply moisturiser each day to affected
areas. Do not apply between toes as this causes
moisture build up.

Avoid corn plasters or verruca treatments as they
contain acids which damage the skin.


Why is there a need for education?

Life-long, self-care condition.
Intense anxiety following diagnosis ()  thirst for knowledge
Obsessive behaviour; ritualistic adherence to regimes adverse  affect on quality of life
Conversely, anger, denial, despair  avoidance of self care.
Adoption of the sick role - abdication of responsibility

monitoring techniques - BGSM, urinalysis, correlation with medication

Complications - risk avoidance,  prognosis

Transcultural issues - communication, healthy eating / lifestyle guidelines vs. cultural / religious expectations / norms


Patient education

Assess prior knowledge and build on this using health promotion strategies
Assess lifestyle, encourage compliance with therapy
Patient centred care / patient negotiated goals / involve NOK
Written & verbal information to patient & family (format?)
Role of MDT:-
Ward staff & MDT inc.
Diabetic specialist nurses
Diabetes Australia
Psychosocial impact of DM (employment, driving, social activities, a chronic disorder)


Patient self management

Exercise & activity
Glucose and urine testing / monitoring
Management of medication (oral hypoglycaemics)
Management of insulin & injection techniques / devices, site rotations
Management of illness / emergencies