Diabetes mellitus

Diabetes mellitus

Type 1 Diabetes


Pathology:                    Absolutelack of insulin secretion > impaired glucose metabolism

Autoimmune destruction of β pancreatic islet cells


Aetiology:                     Primary90% associated with HLD-DR3/4, peak age of onset <25years

                                          Secondarydue to destruction of pancreas


Symptoms:                   Polyuria,polydipsia, weight loss, lethargy, blurred vision, thrush


Signs:                              Acute: Low BMI, dehydration, “peardrop”/fruity odour on breath

Chronic:peripheral neuropathy, decreased vision, lack of hypo awareness


Investigations:          Bloods: Plasma glucose, serum ketones, anti-GADand islet cell antibodies, c-

peptide –ve as noendogenous insulin production

Venous Blood Gas: pH and bicarbonate


Treatment:                  Insulin replacement


Regular follow-up


Complications:          DKA, retinopathy,nephropathy, neuropathy, PVD, Cardiovascular disease, Autonomic dysfunction(postural hypotension, gastroparesis)


Prognosis:                    Dependson good control. Likely to limit life expectancy by 10-20 years.




Impaired  glucose tolerance


Fasting  glucose




Oral  glucose tolerance test




Figure 5.1 Diagnostic Glucose Values For Diabetes Mellitus








Type2 Diabetes

Pathology:                    Relative insulin deficit andresistance to insulin action


Aetiology:                     Genetics+ environment (high density food intake, obesity, lack of exercise, chronic pancreatitis,Cushing’s). Peak incidence 50 years


Symptoms:                   Maybe asymptomatic initially, recurrent infections, polyuria, polydipsia, weightloss, HHS


Signs:                              HighBMI, central obesity, acanthosis, foot ulcers, visual defects


Investigations:          Bloods: Plasma glucose, serum ketones, U&E,HbA1C

VenousBlood Gas: pH and bicarbonate


Treatment:                  Lifestyle measures: Diet, exercise,smoking cessation, patient education

                                          Medical: Sulphonylurea,biguanides, glitazones, GLP-1 analogues, and DPP-4

inhibitors, using astepwise approach.

                                          Surveillance: Regularfollow-up and HbA1c tomonitor glycaemic control and



Complications:          Cardiovasculardisease, DM retinopathy, DM nephropathy, DM neuropathy, peripheral vasculardisease


Prognosis:                    Canbe life limiting due to 4-fold increase in cardiovascular disease, 10-20 yearreduction in life expectancy



Text Box: 	Common Oral Anti-Diabetic Drug Classes
Metformin: 1st line in obese patients BMI >25. Improves sensitivity to insulin, does not cause 
 hypoglycaemia. SEs: nausea, lactic acidosis (monitor renal function)
Gliclazide: 1st line in non-obese patients. Stimulates insulin release. SEs: hypoglycaemia
Rosiglitazone: improves sensitivity to insulin. SEs: weight gain, fluid retention, deranged LFTs
	Glucosidase Inhibitors
Acarbose: prevents intestinal sugar absorption. SEs: flatulence
Text Box: Worked Example
•	A 54 year old male cyclist was hit by a car; the impact caused him to fall and hit his head on the kerb. When the ambulance crew arrived he was alert, speaking clearly and obeying all commands. GCS was 15; E4, V5, M6.  
•	During transfer to the hospital he became less responsive and on arrival to A&E he opened his eye to voice, speech was incomprehensible and he would only withdraw from painful stimulus.  
•	GCS was calculated as 9; E3 V2 M4



















Figure 5.2 Common Oral Anti-Diabetic Agents

Join Shiken For FREE

Gumbo Study Buddy

Explore More Subject Explanations

Try Shiken Premium
for Free

14-day free trial. Cancel anytime.
Get Started
The first 14 days are on us
96% of learners report x2 faster learning
Free hands-on onboarding & support
Cancel Anytime