Week 12 Flashcards
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 age race high blood pressure weight
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
- 0–6.0 mmol/L (fasting for Type 1)
- 0-8.0 mmol/L (fasting for Type 2)
- 0-8.0 mmol/L (post-prandial for Type 1)
- 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
Dietary:
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”
Exercise:
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
Insulin Type 1 required/Type 2 often needed Individualised Complex/S & B table 36.1 Syringes/pens/pumps Complications Exenatide Type 2 (BD or weekly) Oral hypoglycaemics Biguanide (Metformin) ? Combination of two different types \+ Antihypertensives + lipid lowering agents
Nursing management
Contextual 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
Nephropathy
Dementia (20% increase/1point high BGL)
Neuropathic changes
Peripheral neuropathy
Autonomic neuropathies
Sexual dysfunction
Acute complications of diabetes
Hypoglycemia
Hyperglycemia Complex management
Diabetic ketoacidosis (DKA)
Hyperglycemic hyperosmolar nonketotic syndrome (HHNS), (hyperosmolar nonketotic coma)
(hyperglycemia hyperosmolar syndrome [HHS])
Hypoglycaemia
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
Variable
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
Insulin
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 Factors: 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.
Diabetologist
Diabetic specialist nurses
Dietician
Diabetes Australia
Psychosocial impact of DM (employment, driving, social activities, a chronic disorder)
Patient self management
Hypoglycaemia Hyperglycaemia Diet Exercise & activity Glucose and urine testing / monitoring Management of medication (oral hypoglycaemics) Management of insulin & injection techniques / devices, site rotations Management of illness / emergencies
