Osce questions

OSCE QUESTION

TYPES OF MODY AND TYPE TO WHICH THIS PARTY BELONGS TO?

MODY stands for “Maturity-onset diabetes of the young” and was given that name in the past because it acted more like adult type of diabetes (Type 2 Diabetes) but was found in young people. MODY limits the body's ability to produce insulin, but is different than the juvenile type of diabetes (Type 1 Diabetes).

There are now at least 14 different known MODY mutations. They include GCK, HNF1A, HNF4A, HNF1B, INS, NEURO1, PDX1, PAX4, ABCC8, KCNJ11, KLF11, CEL, BLK, and APPL1.

The key features of MODY are:

• Being diagnosed with diabetes under the age of 25.

• Having a parent with diabetes, with diabetes in two or more generations.

• Not necessarily needing insulin.




Probably my patient belong to MODY type 2 because of little glycemic deterioration with no micro vascular complications
.

 

Learning points
LEARNING POINTS:
* I have learnt different types of diabetes and the clinical methods available to detect them on admission.

* I have learnt how to take different negative history and to arrive upon a differential diagnosis in our case.

* I have learnt about different types of ataxia and ponits to differentiate them clinically.

* I have learnt about the complications of dengue and the role of a teritiary care hospital in its management.

*I have learnt about different modalities of treatment available for portal hypertension and their pros and cons.

2)What is the mechanism of action of insulin at cellular level?

Insulin acts on a glycoprotein- tyrosine kinase receptors on the cell membrane and it binds to the alpha subunit which leads to phosphorylation of beta subunit.

This leads to transport of GLUT RECEPTORS on to the cell membrane which in-turn transports glucose into the target cell( adipocyte and muscle cell);

Gluconeogenesis is inhibited and glycogenesis is stimulated in the liver cell with the action of insulin on it;

All these leads to decrease in the blood sugar hence it usage in hyperglycaemic state;

3)How do you differentiate a patient clinically on the bedside whether the patient is type1 or type 2 diabetic?

In type 1 diabetics the beta cells are 100% destroyed and hence supplemenation with secretagogues(hypoglycaemic drugs) would not benefit the patient clinically whereas in type 2 diabetics almost 10-30% of beta cells are functional hence we can boost them up with secretagogues and increase the production of insulin in the patient making him clinically well( reduction in the blood sugar appropriately according to dose adjustment).