Interactive Case Discussion Diabetes

8/4/2019 Interactive Case Discussion Diabetes

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Interactive Case

DiscussionBy:

Mohd Safwan

Siti Noor Atikah


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Mr. A 32 years old Malay male teacher Single

Presents himself to clinic as he worried about his weight andhealth. He had been persistently gaining weight for last 2years as he gained 18kg throughout those years.


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Discussion Points 1

What further history would you elicit from

this patient?


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Further history

He was chubby since secondary school, which it was a boys school,he doesnt have problem with his friends though he quite frequently

teased by his friend due to his appearance.

The problem started during his university time, he got difficulty in

mingle around with his other female colleagues as he was not

confident about his appearance.

He found himself difficult to approach lady for a date even, because

of the issue and end up single until now.


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Further history

No polyuria, polydipsia, polyphagia, weight loss, nocturia, fatigue

and altered vision. He tried to lose his weight many times before but found difficult to

be persistent and ultimately give up.

Both her parents are overweight and diabetic.

Doesnt smoke or taking alcohol.


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Further examination findings

Well looking obese man BP : 118/80mmHg

Antropometric measurements;

Weight 100kg

Height 170cm

BMI kg/m2

Waist to hip circumference

ratio

34.6


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How to diagnose?

Discussion Points 2


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Commonsymptoms:

PolyuriaPolydipsiaTirednessWeight loss


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Capillary Blood

Glucose:

5.7mmol/L


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Fasting Venous Plasma

Glucose:

6.7mmol/L


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OGTT

FPG:7.2 mmol/L

2 Hours PPG:

12 mmol/L


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Discussion Points 3

Summarize his current problems.

How would you manage this gentleman

now?

What is his target blood sugar?

How to use the insulin injection?


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Futher assess:

Risk factor andDM complication

Cardiovascular

Respiratory

Abdominal

Relevant

Examination


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HbA1c: 7%

TG:

HDL:LDL:

Albuminuria

Creatinine/BUNUrine microscopy

ECG

Normal

In this patient:


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Summary of his Problem:

1. He is obese.

2. Having difficulty in exercise as hardly to

do it persistently and ultimately give up.

3. Also having difficulty in diet control.

4. With family history of diabetes mellitus


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Management of diabetes

mellitus


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PLIMS

Patient education

Lifestyle modification

Investigation

Medication/Drug therapy

Safety netting/Follow up

Principle of management


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Patient education

Educator consist of doctor, nurse, assistant

medical officer, health education officer,

dietitian and others.

Objectives:

1. To reassure and alleviate anxiety.

2. To understand the disease, its management

and complication.

3. To promote compliance and self-care.


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Content:

Diet Exercise

Medication

Stop smoking, alcohol Complications (acute and chronic)

Self-care/self blood glucose monitoring

(SBGM)/foot care Psychosocial adaptation to diabetes

(occupation)


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Lifestyle modification

Physical activity

Medical nutrition therapy (MNT):

Prevention of diabetes1. Weight loss

2. Balanced diet

3. Take high fibre diet


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Management of diabetes

1. Meal timings should be regular &synchronised with medication time actions.

2. Diet consist of carbohydrate from cereal,

fruits, vegetables, legumes, and low fat orskimmed milk.

3. Limit intake of saturated fatty acids, trans-

fatty acids, and cholesterol to reduce risk ofCVD.

4. Reduced sodium intake


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Investigation

Venous plasma glucose

- fasting plasma glucose (FPG)

- random plasma glucose (RPG)- Oral glucose tolerance test (OGTT)


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Assessment of cardiovascular risk and end organ

damage:- blood pressure

- glycosylated haemoglobin (HBA1c)

- BMI

- lipid profile- renal profile

- urine analysis particularly for albuminuria

- ECG- eye; visual acuity & fundoscopy

- feets; pulses & neuropathy


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Drug management and Follow Up


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Oral Anti-Diabetic (OAD) Agents

1. Biguanides (metformin)

Does not stimulate insulin secretion, but lowers blood glucose by decreasing

hepatic glucose production.

Lower plasma glucose up to 20% as 1st line drug treatment esp. in

overweight/obese patient.

Should not be used in ptn with impaired renal function, liver cirrhosis, CCF,

recent MI, or any other condition that cause lactic acid accumulation.

2. -glucosidase inhibitors (AGIs) (acarbose)

Act at the gut epithelium to reduce the rate of digestion of polysaccharidesin the proximal small intestine by inhibit -glucosidase enzymes.

Should be taken with meals.


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DPP-4

enzymeprevent

breaks down

GLP-1

&GLP

insulin

glucose

glucagon

DPP-4 inhibitor

_

= glucose

3. Dipeptidyl peptidase-4 (DPP-4) inhibitors (sitagliptin)

Act by inhibit DPP-4 enzyme. This enzyme break downs the incretins

GLP-1 and GIP that are released in response to meal. By preventingGLP-1 and GIP inactivation, insulin will increase and glucagon is

suppressed. This drives blood glucose levels towards normal.


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4. Insulin secretagogues Sulphonylureas (Sus)

SUs lower plasma glucose by increasing insulin secretion.

Major SE is hypoglycemia, but 2nd generation Sus (glimepiride, gliclazide

MR) cause less risk of hypoglycemia & less weight gain.

Taken 30 min before meal.

Insulin secretagogues Non-Sus or Meglitinides

Short acting insulin secretagogues which lower plasma glucose by

increasing insulin secretion, they bind to different site within the SU

receptor.

Taken 10 min before meal.

5. Thiazolidinediones (TZDs)

Act by increasing insulin sensitivity of muscle, adipose tissue, & liver to

endogenous & exogenous insulin (insulin sensitizer)


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Insulin therapy


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Thank you

Interactive Case Discussion Diabetes

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