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)
