Diabetes Mellitus

Diabetes Mellitus

Definition

Is a multifactorial disorder caused by diminished insulin action due to its decreased availability or effectiveness in varying combinations.

Types of diabetes:

(based on aetiology)

Type 1: immune mediated or idiopathic

Type 2: insulin resistance /insulin deficiency

Type 3:

  • · genetic syndromes
  • · drug induced
  • · hormonal
  • · malnutrition related etc.

Type 4: gestational diabetes

Diagnosis

With symptoms:

A random blood sugar of >11.1mmol/l (200mg/dl) is diagnostic

Without symptoms:

· WHO (1985)

FBS 2hr PGBS

= or> 7.8mmol/l and/or =or>11.1 mmol/

(140mg/dl) (200mg/dl)

(IGT :FBS <7.8 and PGBS 7.8-11.1)

· ADA (1997)

FBS= or> 7mmol/l

(126mg/dl)

(IFG: 6.1 - 6.9 mmol/l)

WHO (1999)

FBS = or>7mmol/l

(IGT:7-11.1mol/l)

Presentations:

(1) Routine examination

(2) Clinical symptoms:

· Thirst Pruritus vulvae

· Polyuria Balanitis

· Polydipsia Impotence

· Nocturia Changes in vision

· Wt. Loss Parasthesiae

· Tiredness

(3) Ketoacidosis

(4) Symptoms of complications

a) Nephropathy Nodular glomerulo sclerosis

(Kimmelsteil Wilson ) NS

CRF

Proteinuria

Gen. Arteriosclerosis

Pyelonephritis

Symptoms of anaemia

Uraemia

N.S.

b) Retinopathy

I. Simple or background microaneurysms

Blot.hges

Exudates

Cotton wool

Tortuous veins

2. Proliferative retinopathy neovascularization

vitreous haemorrhages

3. Exudative retinopathy macular oedema

macular exudates

Cataract – snow flake in Type I

Accltd. Senile in Type 2

c) Macroangiopathy:

Atheroma in large and medium sized blood vessles

CVD

IHD

PVD

c) Macroangiopathy:

Atheroma in large and medium sized blood vessles

CVD

IHD

PVD

d) Neuropathy:

a. Peripheral neuropathy:

Sensory

Motomotor

? mixed

(Charkot’s neuroarthropathy)

b. Aut. Neuropathy, post. Hypotension

Impotence

Bladder retention

Bowel diarrhoea

Gust sweating

c. Mononeuropathy CTS

Lat.pop

Cervical sp.root

TI

e. Dermopathy: Carbuncles

ulcers

muco cutaneous candidiasis

EVALUATION OF A DIABETIC PATIENT

First visit

History

History

SYMPTOMS OF DIABETES

polyuria, nocturia, polydipsia polyphagia, recent weight loss or weight gain, tingling, numbness or pain in the hands and or feet (night cramps), pruritus, vaginal discharge, balanitis.

DIABETIC HISTORY

Age at which diabetes was detected, duration of disease, family history, previous and current treatment

Drug history (steroids)

PAST HISTORY

HT, Hyperlipidaemia, IHD, stroke, PVD, liver disease,erectile dysfunction.

Smoking, alcohol history, 24 hour dietary recall

EXAMINATION

Anthropometric measures

  • Height
  • Weight
  • Body mass index- Weight in kg / (Height in m)2
  • Waist circumference

Detailed examination

  • Including signs of insulin resistance like acanthosis nigricans, skin tags
  • Signs of Hyperlipidaemia e.g.: xanthelasma, xanthomas.
  • Pay particular attention to cardiovascular system, check blood pressure

Foot examination

  • a must in every diabetic patient – skin, nails, hair, temp, pulses.

Dilated fundoscopy

EVALUATION OF A DIABETIC PATIENT
First visit

What type?

Are there complications?

Any underlying cause?

Risk factors of CAD?

Features of Type 1 diabetes

Early onset

Children/young adults

Generally thin

Not responding to OHAs

C-peptides

Features of Type 2 diabetes

Family history present

Obese or nonobese

Middle aged or elderly

Features of metabolic syndrome

Visceral Fat

Features of Type 3 diabetes

· Iatrogenic

· Endocrine

· Malnutrition

· Pancreatic Diabetes

· Genetic syndromes

Are there complications

· Retinopathy

· Nephropathy

· IHD

· CVD

· PVD

· Skin

· Foot

Nephropathy

· Hypertension

· Proteinuria

· Retinopathy

Ischaemic heart disease

· History

· Hypertension

· Peripheral pulses

· Carotid bruits

· ECG

· Xanthomas

Cerebrovascular disease

· History

· Carotid bruits

Peripheral Vascular Disease

· Peripheral pulses

· Vasomotor changes

· Ulcers

Skin

· Dermopathy

· Ulcers

· Cellulitis

· Necrobiosis diabeticorum

· Mycoses

· Gangrene

Foot

· Curvatures

· Deformities

· Ulceration

· Callosities

· Fissuring

Investigations

FBS and PPBS

HbA1C

Fasting lipid profile

Blood urea and electrolytes

Urine analysis: Ketones, protein, glucose

Urine Microalbumin-

ALT, AST, ALP

ECG

Islet cell antibody/GAD antibody if considering type 1 diabetes

Treatment

To allow the patient to lead a comfortable normal life and to prevent complications

3 methods of treatment:

1. Diet alone 60%

2. Diet and oral hypo. Agts. 20%

3. Diet and insulin 20%

Choice of therapeutic regimes

1. Type I <40 most will need insulin

2. >40 specially obese ones could be controlled on diet alone

3. >40 who fail with diet.

§ Non obese: sulphonylureas

§ Obese: biguanides

Failure: may need insulin

Diet Principles:

a. Total cal. Requirement age, sex, occupation

Actual weight in relation to ideal weight

Economic status

b. Proportion of cals from CHO 60 (instd.of 46%)

Prts 15 (……….. 12%)

Fats 25 (………. 42%)

c. Local availability and preference

d. Foods well spread through out the day

e. Foods should be of high fibre content (slowly digested and absorped)

Oral hypoglycaemic agents

a. Sulphonylureas act by sensitising beta cell to the action of glucose

increase insulin receptors.

Eg. Chlorpropamide

Tolbutamide

Glibenclamide

Glipizide

b. Biguanides . act by reducing hepatic gluconeogenesis

Increasing peripheral utilisation of glucose

Useful in obese diabetics

Danger of lactic acidosis with phenformin

C.Others:repaglinide,acarbose,troglitazone

Oral hypoglycaemic agents

a. Sulphonylureas act by sensitising beta cell to the action of glucose

increase insulin receptors.

Eg.

· Chlorpropamide

· Tolbutamide

· Glibenclamide

· Glipizide

b. Biguanides . act by reducing hepatic gluconeogenesis

Increasing peripheral utilisation of glucose

Useful in obese diabetics

Danger of lactic acidosis with phenformin

C.Others:repaglinide,acarbose,troglitazone

Insulins

Indications:

a. Type I diabetes

b. Type 2 where maximum doses of OHA have failed(sec.OHA failure)-

c. Type 2 younger patients to prevent tissue damage

d. With complications (specially young pts)

Infections

Ketoacidosis

Neuropathy

Foot lesions

e. pregancy

f. glucose toxicity

Types of insulins

Species: purity: Duration:

Bovine conventional Short

Porcine single peak intermediate

Human highly purified long

Rapid-Acting Insulin

Lispro (Humalog)

Insulin Aspart (Novorapid)

These are used as bolus (mealtime) insulin

Short-Acting Insulin

Regular insulin (Actrapid /Humlin R)

Short-acting

Onset of action 30-60 minutes

Duration of action 5-8 hours.

To be taken 20-30 minutes before meals.

Intermediate-Acting Insulin

NPH (Insulatard/ Humulin N) & Lente

Their appearance is cloudy

Onset of action is about 2 hours after injection

Peak effect is from 6-10 hours

Long-Acting Insulin

Detemir (Levemir)

Glargine (Lantus)

peakless delivery over 24 hours.

Clear in solution

Cannot be mixed with other insulin

Usually given at bedtime.

Lower fasting glucose levels and less hypoglycemia

Pre-Mixed Insulin

70/30 means 70% NPH and 30% Regular

50/50 means 50% NPH and 50% regular

Addition of protamine to lispro: used in 75/25 combinations

Protamine to aspart: 70/30 combination (Novomix 30)

Administration:

1. Low dose frequent

2. Sliding scale

3. According to previous blood sugar estimation

Comas in diabetes

1. Hyperglycaemic : Keto acidotic

Non keto acidotic

2. Hypoglycaemic

3. Other metabolic comas:

sec. to diabetes uraemia

Lactic acidosis

4. Other independent causes ex. SAH

Ketoacidosis

Pathogenesis: Pptd by infections

Trauma

Drugs

Non compliance

Clinical: Air hunger Anorexia

Dehydration vomiting

Ketone smell Abd. Pain

Wt loss Low BP

Fatigue

Non ketotic. Usually in elderly

Only dehydration is present

Investigations:

Blood sugar HCO3

Urea PCV

Na, K UFR

pH ECG

Hb

Treatment:

a) Fluids, N. Saline

I lit. first 1/2 hr

I lit next hour

I lit next 2 hrs

Then 500 ml hrly total of 5l.Change to 5% dext. when blood sugar is 10-16 mmol.alternating with N saline

b)Insulin: Sol. Insulin 20 units IV

10 units IM hrly till blood sugar is 13mmol.

Then 10 units SC 4 hrly

c)Potassium: add I.gm(20mmol) to each L of fluid Beginning with second L of N saline

Omit K if S.K is over 6 mmol.

d) HCO3, 100mmol of NaHCO3 if pH is below 7.1 Ppt. In 1 to 1 1/2 hrs if pH is still less than 7.1

e) Gen. Management:

Monitor pulse, BP, CVP urine output.

NG suction

Oxygen

Catheterise bladder

Monitor blood sugar, electrolytes, urea, pH

HCO3 4 hrly

Ppting treat , cause

Mangement of unconcious state

DIC

Hypoglycaemia

Hypo Hyper

by inc. insulin Infection

starvation stress

Exercise Non compliance

Onset: sudden gradual

Clinical:

Drowsy Drowsy

Pupils dilated Normal size

Bounding pulse Low vol. Pulse

BP n. or inc. sys Normal or low

Hydration normal Dehydarated

Breathing normal acidotic

Urine output normal reduced

Fits fits unusual

Abn. Behavior Abn. Behaviour unusual

Lab, Low BS, pH, HCO3, BU



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