OSCE AND LEARNING POINTS

OSCE QUESTION AND ANSWERS:

1) 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;

2)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).

3) what are the different types of MODY in type 2 diabetics?

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 1Diabetes).

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

 HNF4A

GCK

HNFIA

IPFI

HNFIB

MODYI

MODY2

MODY3 MODY4

MODYS

Neonatal hyperinsulinism, early onset, normal renal threshold, macrosomia (common), prolonged neonatal hypoglycemia (20%)

Mildly elevated fasting glucose, little glycemic deterioration with age, low prevalence of microvascular complications (retinopathy, proteinuria

Early onset, low renal threshold, progressive

hyperglycemia with age. Microvascular complications may develop over time

Extremely rare, presents ni range from impaired glucose tolerance to NIDDM. May impair digestive functions of pancreas

Severe kidneydisease, pancreatic hypoplasia, female reproducave ordan aonormaldes

Extremely rare, early onset ofNIDDM Extremely rare

May impair pancreatic digestive functions

extremely rare

Mya cause neonatal diabetes, antibody-negative DM,I and MODY

extremely rare

Frequently causes neonatal diabetes. Rarely causes MODY with mild hyperglycemia

diabetes in two or

more

generations.

• Not necessarily needing insulin.

Table 2. Clinical Presentation of Familial Diabetes in Different Gene Mutations

Type of

Familial Clinical

Gene Diabetes Presentation

NEURODI

MODY6 KLFI

MODY7 C EL

MODY8 PAX4

MODY9 INS

MODY OI

BLK ABCC8

MODYII

N o M O D Y name assigned

DMI: type1diabetes melitas; MODY: oynet-stmiurat dioafbthetes:gnuoy NIDDM: non- insulin-dependent diabetes muetils.

Soucre: References 2,,6 7.

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

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.