Diabetes Mellitus Flashcards
Diabetes Mellitus Definition
The urine in DM is sweet (‘mellitus’ - sweet) due to the failure of insulin to clear glucose from the blood into cells.
DM is characterised by chronically elevated glucose. A diagnosis of DM can be made in the absence of intercurrent illness with a random glucose of >11.1mmol/L or >7mmol/L fasting, without the need for a formal oral glucose tolerance test (OGTT).
Diabetes Mellitus Types
Type I DM
- Juvenile onset
- Late Autoimmune Diabetes of Adults (LADA)
Type II DM
- Maturity onset diabetes of the young
- Gestational diabetes
Other Causes
- Diseases of exocrine pancreas
- > Pancreatitis
- > Cystic fibrosis
- Endocrinopathies
- > Acromegaly
- Drug-induced
- > Corticosteroids
- Infection
- > CMV
- > Congenital rubella
Diabetes Mellitus Type I and Type II Presentation
Type I DM
- Polyuria
- Polydipsia
- Loss of Weight
- Ketosis
Type II DM
- Asysmptomatic / complications eg MI
Diabetes Mellitus Investigations
BGLs
Fasting
- DM >= 7.0mmol/L
- Impaired Glucose 7.0-6.0mmol/L
- Normal < 6.0mmol/L
Random
- DM >= 11.1mmol/L
- Impaired Glucose 11.1 - 5.5mmol/L
- Normal < 5.5mmol/L
Oral Glucose Tolerance Test
- > = 11.1mmol/L
- Impaired Glucose 11.1-7.8mmol/L
- Normal < 7.8mmol/L
OGTT Procedure
Oral Glucose Tolerance Test
- Fast overnight
- Then drink 300mL with 75g of glucose solution.
- Measure blood glucose levels 2 hours afterwards
HbA1c Significance
HbA1c above 7.0 is indicative. It measures the levels of glycated Hb which is proportional to the longer term (120 days/4 monthly) plasma glucose concentration
Diabetes Mellitus Management Overview
The targets for management of DM is a blood glucose of 4-6mmol/L (fasting) and 6-8mmol/L (postprandial)
Pre-diabetes: 5-7% weight loss can slow the progression to diabetes but there is no long-term evidence on pharmacological options, none are recommended
Diabetes Mellitus Type I Management
Treatment centres on replacement insulin
- Intermediate-acting insulin or long-acting (bedtime)
AND - Short acting or very-short acting (given pre-prandially)
- Mixed insulin: short-acting + intermediate (once daily)
- Continuous infusion: very-short acting infusion pump
Diabetes Mellitus Type II Management Overview
Initially diet and exercise are indicated, more advanced disease requires oral diabetic drugs and eventually insulin will be required.
Early Diabetes Mellitus Type II Management
Early disease requires:
- Lifestyle intervention (diet & exercise) - 2-3 month trial
Advanced Diabetes Mellitus Type II Management
Metformin, an oral diabetic drug, is common to start on. If targets are not met with maximal doses a sulfonylurea may be added.
If dual therapy is unsuccessful, then insulin therapy should be started. Most with DMII will eventually need insulin therapy even after many years of successful oral therapy
Diabetic Medication Types
MSIAITS
- Metformin
- Sulfonylureas
- Incretin-based therapies
- – Dipeptidyl peptidase-4 (DDP-4) Inhibitors
- – Glucagon-Like Peptide - 1 (GLP-1) receptor agonist
- Acarbose
- Insulin
- Thiazolidinediones
- Sodium-glucose co-transporter 2 inhibitors
Diabetes Mellitus Complications
Macrovascular
- Ischaemic heart disease
- Cerebrovascular disease
- Peripheral vascular disease
Microvascular
- Retinopathy
- Nephropathy
- Neuropathy
Life-threatening Diabetes Mellitus Presentations
- Diabetic Ketoacidosis
- Hyperosmolar Hyperglycaemic State (HHS)
Diabetic Ketoacidosis Pathophysiology
DKA is a function of severe insulin deficiency and elevated glucagon, this starves cells of energy and requires the production of energy by GNG (and lipolysis) producing ketone bodies. These ketones have a low pH and leads to metabolic acidosis.
Insulin is needed to promote glucose utilisation, but the level needed to suppress lipolysis is only 1/10 of that. Hence it is rarer for DKA to occur in DM type II. However, increased secretion of glucagon occurs in infection, infarction and severe illness, which can tip the balance.
Diabetic Ketoacidosis Presentation
- Hyperglycaemia
- Polyuria
- Polydipsia
- Hyperventilation
- Dehydration
Diabetic Ketoacidosis Management
- Oral rehydration
- Insulin replacement
- Potassium replacement
HHS Definition
Hyperosmolar Hyperglycaemic State
Characterised by profound hyperglycaemia, hyperosmolality and dehydration without significant ketoacidosis occurring primarily in DM type II patients.
Hyperosmolar Hyperglycaemic State Pathophysiology
A precipitating factor such as infection, infarction and severe illness, causes a relative insulin deficiency but it is high enough to suppress lipolysis ketogenesis.
Hyperosmolar Hyperglycaemic State Presentation
- Hyperglycaemia
- Polyuria
- Polydipsia
- Dehydration
Hyperosmolar Hyperglycaemic State Management
- Oral rehydration
- Insulin replacement
- Potassium replacement
As per DKA but prognosis is much worse due to older age and increased comorbidities
Diabetes Mellitus Check-up Routine
Every 3-6 months - Symptoms and SMBG results - HbA1c - BP - Weight +/- waist circumference - Foot exam (mod to high risk) Every year - Lipids - Urine for microalbumine (ACR) - Creatinine / eGFR - Foot exam (low risk) - Review --- Diabetes education --- Diet, exercise --- Medications - Autoimmune screen for thyroid and coeliac disease - Type 1 Every 2 years - Eye review
Mechanism of Metformin
- Reduces hepatic GNG
Mechanism of Sulfonylureas and Generic Names
- Increase insulin secretion by direct stimulation of beta-cells
- Gliclazide, glipizide
Mechanism of Incretin-based therapies and Generic Names
Incretin hormones (GLP-1 and GIP) stimulate insulin release and reduce glucagon secretion. Two types of drugs
Dipeptidyl peptidase-4 (DDP-4) Inhibitors
- Increase incretin produced in the gut following food ingestion
- Linagliptin
Glucagon-Like Peptide - 1 (GLP-1) receptor agonist
- Synthetic analogues of GLP-1 causing increase insulin, decrease glucagon and small reduction in appetite
- Exenatide
Mechanism of Acarbose
- Alpha-glucosidase inhibitor. Reduces the breakdown of complex carbohydrate in the gut and thus reduces the carbohydrate absorption and hence insulin requirements
Mechanism of Thiazolidinediones and Generic Name
- Reduce peripheral insulin resistance
* Rosiglitazone
Mechanism of Sodium-glucose co-transporter 2 inhibitors
- Reduce glucose reabsorption in the kidneys
