Details about Diabetes Mellitus

•  Dr.K.T.S
•   Diabetes, Harmonal Disorders
• on Jun, 19, 2013
•  No Comments.

Details about Diabetes Mellitus

While we discuss the details about diabetes,here the definition “A COMPLEX DISORDER OF CARBOHYDRATE,FAT AND PROTEIN METABOLISM THAT IS PRIMARILY A RESULT OF A RELATIVE OR COMPLETE LACK OF INSULIN SECRETION BY THE BETA CELLS OF PANCREAS OR OF THE DEFECTS OF INSULIN RECEPTORS”.

Classification of Diabetes

A. IDDM 10-15% (Type I)

B. NIDDM 85-90% (Type II)

Obese (80%) Nonobese (20%)

C. Maturity onset diabetes of young (MODY)

D. Secondary diabetes

1.Cirrhosis, Chronic pancreatitis, Haemo-chromatosis

2. Endocrine disease : – Cushing’s disease, acromegaly

3. Drug induced:- Thiazides, Steroids

4. Insulin receptor abnormality

5. Congenital lipo dystrophy

6. Acanthosis nigricans

7. Associated with genetic syndromes: Down syndrome, Klinefelter syndrome, Turner syndrome, muscular dystrophies, Friedreich’s ataxia, DIDMOAD (diabetes insipidus nd mellitus, opticatrophy, and deafness.

E.Gestational diabetes

F. Impaired glucose tolerance

G. Malnutrition related diabetes

Comparison of Type I and Type II Diabetes

Age	Type I	Type II
	< 30 years	> 40 years
Body weight	Nonobese	Obese
Insulin deficiency	Severe	Moderate
Insulin resistance	Occasional	Always
HLA	DR3 DR4	None
Indentical twins	40% concordant	70-80%
Islet cell antibodies	Frequent	None
Other autoimmuno disease	Present	Nil

 

Risk of  Diabetes Type I (IDDM) and Type II (NIDDM)

 All systems affected

1. CVS : Hypertension, atherosclerosis

2.  CNS :

Coma:

Common                                Uncommon

Hypoglycemic                         Lactic acidosis

Hyperglycemic ketotic             Uremia

Hyperosmolar nonketotic         nonmetabolic causes

Neuropathy

Sensory motor : Acute, chronic

 Autonomic

Arrests (respiratory) during anaesthesis, or resp.

Bladder (neurogenic)

Cardiac denervation

Diarrhoea, Depressant drugs

E(I)mpotence,

Entrapment neuropathy (e.g. Carpal tunnel syn.)

External pressure palsies

Fail of BP (Postural)

Gustatory sweating

Mononeuropathy

Spontaneous mononeuropathy e.g. cranial nerve

Palsy (Usually 3^rd and 6^th)

Proximal motor neuropathy (Diabetic amyotrophy Esp. quadriceps)

Renal          :  Nephropathy : Microalbminuria,Persistent albminuria,Uremia

Pulmonary   :  Tuberculosis more common

Liver            :  Hepatomegaly

Occular        :  Cataract, errors of refraction, retinopathy

Skin             :   Pyogenic infections

Joints          :   Charcot’s neuropathic

 Sex              :    Impotence,Reduction of fertility and early Menopause in females

Characteristics of diabetic 3rd Nerve palsy

Precipitous onset

Painful

Pupillary sparing

Probably reflects microvascular disease of vasa vosorum

 Prognosis

Diplopia usually improves within 12 months.

Chronic Complications of Diabetes

A.  Microvascular

Retinopathy

Nephropathy

B.  Macrovascular

Coronary artery disease

Cerebro vascular disease

Peripheral vascular disease

C. Neurophathies

Peripheral symmetric polyneuropathy

Mononeuropathies

Autonomic neuropathies

Diabetic amyortophy

D. Foot ulcer

E. Dermopathies

F. Hyperlipidemia

G. Cataract

Clinical Features of Diabetes

Signs and Symptoms	Type – I (IDDM)	Type – II (NIDDM)
Polyuria and thrist	++	+
Weakness	++	+
Polyphagia with weight loss	++	___
Recurrent blurred vision	+	++
Vulvovaginitis or pruritus	+	++
Peripheral neuropathy	+	++
Nocturnal enuresis	++	___
Often asymptomatic	__	++

 Pathogenesis of diabetes

1. Type I diabetes is due to immune destruction of islet cells, probably triggred by viral infection (coxsackie, rubella, mumps, EBV, CMV) in genetically susceptible HLADR₃/ DR₄ (DR₂ is protective)

Prevention is by screening the susceptible in childhood by islet cell anti body titre and providing azathioprine and cyclosporine.

Diagnosis is based on ­islet cell anti body titre, plasma insulin and C peptide (<10mg), ­insulin auto antibodies.

2. Type II diabetes is due to intracellular defect in glucose disposal, insulin receptor antibodies, abnormal insulin structure, defect signaling etc.

It evolves in 3 phases. phases I; euglycemia with increased insulin; phase II postprandial hyper-glycemia with increased insulin level and phase III over  diabetes with decreased insulin (beta cell exhaustion).

Renal glycouria is due to in renal glucose threshold as occurs in pregnancy and young patients. It does not progress to diabetes.

Alimentary glycosuria is due to rapid glucose absorption and is a benign condition; through peak glucose is high it falls to normal after 2 hours.