Diabetes Mellitus (DM)
Definition
Lack or reduced effectiveness of endogenous insulin
(Diabetes = siphon, overflowing; Mellitus = honey; Insipidus = without taste)
**Think of DM as a vascular disease**
Aetiology
Type 1 DM (T1DM)
Type 2 DM (stronger genetic influence than T1DM)
Other causes
Pathogenesis
T1DM
Destruction of pancreatic B cells -->
T2DM
INC glucose intake/ INC insulin resistance/ DEC insulin secretion -->
Common
Insufficient insulin --> INC blood glucose --> polyuria --> polydipsia --> glucose bind with proteins --> schiff base formed (reversible) --> advanced glycation end products (AGE) formed --> cell damage
Clinical Features
Sx
Signs
***Also look for Sx and signs of complications (look below)***
Investigations
Bedside
Bloods
Diagnosis
Any of:
Management
Conservative:
Medications:
NOTE: DPPV4/ GLP1 does not cause weight gain and hypoglycaemia
NOTE: Consider Statins and anti-hypertensives if indicated
Complications
Macrovascular
Others
Source
OHCM 8th Ed
Toronto Notes 2012http://www.racgp.org.au/your-practice/guidelines/diabetes/3-screening,-risk-assessment,-case-finding-and-diagnosis/34-diagnosis-of-diabetes/
www.uptodate.com
Lack or reduced effectiveness of endogenous insulin
(Diabetes = siphon, overflowing; Mellitus = honey; Insipidus = without taste)
**Think of DM as a vascular disease**
Aetiology
Type 1 DM (T1DM)
- Autoimmune destruction
- Trauma
- Pancreatitis
Type 2 DM (stronger genetic influence than T1DM)
- Obesity
- Lack of exercise
- Alcohol
Other causes
- Steroids
- HIV drugs
- Newer antipsychotics
- Thiazides
- Cushing's disease
Pathogenesis
T1DM
Destruction of pancreatic B cells -->
T2DM
INC glucose intake/ INC insulin resistance/ DEC insulin secretion -->
Common
Insufficient insulin --> INC blood glucose --> polyuria --> polydipsia --> glucose bind with proteins --> schiff base formed (reversible) --> advanced glycation end products (AGE) formed --> cell damage
Clinical Features
Sx
- Polyuria
- Polydipsia
- LOW
Signs
- Ketoacidosis (usually T1DM)
- Hyperglycaemia
- Metabolic syndrome (T2DM)
***Also look for Sx and signs of complications (look below)***
Investigations
Bedside
- Fundoscopy, ECG, urine dipstick (ketones - T1DM usually, glucose)
Bloods
- Random BGL, fasting BGL, Oral glucose tolerance test (gold std), HbA1C
- T1DM: serum anti-GAD AB, islet cell ab
Diagnosis
Any of:
- Classic sx (polyuria/dipsia/phagia, wt loss, blurred vision, nocturia, ketonuria) + random BSL >/= 11.1 mmol/L
- At least 2 occasions of:
- FBSL (fasting = >8hours) >/= 7.0mmol./L
- OGTT (75g glucose + 2h) >/= 11.1mmol/L
- HbA1c >6.5%
Management
Conservative:
- T2DM: Lifestyle changes (slows progression by 58%)
- S moking: cease
- N utrition: 50% carbs, 20% protein, 30% fats
- A lcohol: 2 std drinks
- P hysical: 30 min/d, 5x/w
Medications:
- HbA1c <9%: Metformin (Biguanides = inc insulin sensitivity)
- HbA1c >/=9%: MUST commence Metformin + other antihyperglc/ insulin
- Symptomatic/ T1DM: Insulin +/- Metformin (0.5-0.7 IU/kg)
- Others:
- Sulfonyluria = insulin secretagogues
- TZD = insulin sensitiser (binds to PPAR-gamma)
- Acarbose = alpha glucosidase inhibitor (inhibit GI absorption of GI) (C/I; IBD)
- DPP -IV inhibitors (-gliptins) = stop anti-incretins. Incretin stimulate insulin release
- Glucagon-like Peptide (GLP)-1 analogue = stimulate insulin release
NOTE: DPPV4/ GLP1 does not cause weight gain and hypoglycaemia
NOTE: Consider Statins and anti-hypertensives if indicated
Complications
Macrovascular
- Stroke
- Heart diseases
- PVD
- Eyes (Cataracts, glaucoma)
- Renal (glomerulus)
- Peripheral Neuropathy
- Erectile dysfunction
- Gastroparesis
- Loss of sensation (***foot ulcers***)
Others
- Hypoglycaemia (T1DM)
- DKA (T1DM)
- Hyperosmolar hyperglycaemic state (HHS) (T2DM)
- Shin spots (glycosylation of tissue proteins)
- Cataracts
- Infections (due immune dysfunction, eg damage neutrophil function)
Source
OHCM 8th Ed
Toronto Notes 2012http://www.racgp.org.au/your-practice/guidelines/diabetes/3-screening,-risk-assessment,-case-finding-and-diagnosis/34-diagnosis-of-diabetes/
www.uptodate.com