Treatment of Diabetes pt2 Flashcards
List the 3 causes of hyperglycaemia in T2DM
- impaired insulin secretion
- receptor and pos receptor defects
- increased hepatic glucose secretion
Explain LADA , its frequency, signs and features
- latent autoimmune diabetes in adult hood
- 6-10% of T2DM
- lack of metabolic syndrome features associated with normal T2DM
- poor glucose control with oral agents and patient looses weight
- background autoimmune disease
- behaves like type 1 diabetes
- Anti-GAD antibodies attacking B cells
Give an example of steroid induced diabetes cause
- Cushing’s disease : cortisol excess due to tumour secreting TH
Explain MODY , its frequency and features
- maturity onset diabetes of the young
- rare , genetic form
- could respond to other treatments that insulin
Diagnostic criteria of T1DM
- DKA
- rapid weight loss
- BMI < 25
Diagnostic criteria of T2DM
- HbA1C > 48 ( 2 times 3m apart )
- Fasting plasma glucose > 7
- Random plasma glucose > 11.1
Is HbA1c used fro T1DM diagnosis
no
When can HbA1c not be used for diagnosis
- increased cell turnover ( pregnancy )
- anaemia
- haemoglobinopathies
- rapid blood glucose level rise ( illness, drugs )
What does an HbA1c less than 48 show
- can still have type 2 diabetes
- 42-47 is at high risk
What is the target HbA1c based on
- based on the individual
- usually between 53 to 48
What type of management is used for T2DM (6 factors)
- multifactorial management
1- education
2- lifestyle ( smoking, alcohol)
3- control BP (antihypertensive )
4- statin for increase lipids
5- Anti-platelet ( aspirin ) for micro and macro vascular issues
6- control blood glucose (Metformin )
Non-pharmacological management of T2DM
- education
- dietician
- podiatrist ( foot care )
- retinal photography
What to look out for in DM
K- kidneys
E- eyes
V- vascular
I- infection
N- neuropathy
S- skin
What is the list of drug treatments for DM ( 8 ) - good luck
1- Biguanides ( metformin )
2- Sulfonylureas ( Gliclazide)
3- Glucagon like peptide (liraglutide, exanitide )
4- Dipeptidylpeptidase IV inhibitors ( sitagliptin)
5- Sodium-glucose cotransport2 inhibitor (dapagliflozin )
6- Thiazolidineodiones (pioglitazone)
7- Meglitinides ( repaglinide)
8- aGlucosidase inhibitors (acarbose)
Choice of therapy for a diabetic patient
- Lifestyle measures for everyone
- if HbA1c is greater than 48 then start on monotherapy metformin ( first-line)
- Alternatives if metaformin is not tolerated
What medications should people with high risk of CVD or CKD be using (specify )
- GLP-1 RA or SGLT2 inhibitors
- patients with CVD risk GLP-1 RA
- SGLT2 inhibitors for patients with HF , CKD , microalbuminuria
Adverse effects of SGLT2 inhibitors
- feet swell
- increase risk of amputation
Describe MOA of metformin ( 3)
1- activates liver AMP kinase reducing liver glucose output
2- Increases liver, muscle and fat cell sensitivity to insulin
3- Enhances glucose peripheral uptake and utilization ( sensitizes peripheral tissue )
What is a key advantage of metformin
enhances natural insulin signal so unlikely to cause hypoglycaemia on its own
Metformin adverse effects
- weight loss
- GI adverse effects (nausea, wind, diarrhoea )
- rare : lactic acidosis
How to minimize metformin adverse effects
- start with low dose with meals (once or twice a day)
- can switch to modified release if still getting adverse effects ( more expensive )
What happens if kidney function goes down while patient is on metformin ? At wha level will we have to stop metformin
- stop metformin due to risk of lactic acidosis
- stop if serum creatinine is above 150 and GFR is less than 30
Why is metformin used in patients with adequate renal function
- the cardioprotective gains outweigh lactic acidosis concert if patient has mild to moderate liver dysfunction or cardiac impairment
MOA of Sulfonylureas ( SU ). give example drug
1 - bind to sulfonylurea receptor , closing ATP K+channels
2- decrease in K efflux increases Ca influx
3- Beta cell depolarizes and insulin releases
- ex : Gliclazide
