DIABETES MELLITUS

ABDUL MUSHIB IBRAHIM

MBBS
UPSM
 Definition

Is a clinical syndrome characterized

by hyperglycemia caused by absolute
or relative deficiency of insulin.

TYPE 1 & TYPE 2

CLINICAL EXAMINATION OF A
PATIENT WITH DIABETES
 OBSERVATION
-Weight loss in Insulin Deficiency.
-Obesity in Type 2 DM
-Mucosal Candidiasis
-Dehydration - Dry Mouth
-Dec Tissue turgor
-Air Hunger-Kussmaul breathing in ketoacidosis
SYMPTOMS OF HYPERGLYCAEMIA
-Thirst,dry mouth-polydypsia
-Polyuria-Nocturia
-Polyphagia- predilection for sweet food.
-Weight loss.
-Blurring of Vision.
-genital Candidiasis-Pruritus Vulvae, Balanitis
-Nausea, headache
-Tiredness, fatigue, lethargy
-Mood changes, irritability, difficulty in
concentrating.
 1-HANDS
1-Prayer Sign:
Type 1 DM is
associated with stiff
joints.

-These Patients also

have:
-Short stature
-Waxy Skin
 HANDS

2-Dupuytren’s Contracture:
Causes nodules or thickening of the skin &
knuckle pads.
3-Muscle wasting

4-Sensory Changes HANDS

NB: Present as features of peripheral
Neuropathy although this is more
common in the lower limbs.
SKIN
 EYES

Examine eyes

1-Visual Acuity

-Distance Vision- Snellen Chart.

-Impaired Visual acuity indicates diabetic eye

Disease such as ratinopathy, maculopathy.
 EYES
2-Lens Opacification

-Look for RED REFLEX using OSP held 30cm from

the eye.
 EYES

3-Fundal Examination
-Dilate pupils with tropicamide & examine with OPS
in a darkened room.
-Note features of diabetic retinopathy.
 INSULIN INJECTION SITE

-Anterior Abdominal Wall

-Upper thigh/buttocks
-Upper outer arms.

Inspect for:
-Bruising
-Lipodystrophy
-Lipohypertrophy
-Erythema (infection)
 LEGS

Look for:

-Muscle Wasting
-Sensory Abnormality
-Hair Loss
-Tendon Reflexes (ankle-
Neuropathy)
 FEET

Look for evidence of:

-Clawing of toes ( feature of
neuropathy)
-Loss of Plantar arch
-Discoloration of Skin (Ischemia)
-Localized Infection-fungal  Between
toes & nails.
-Presence of ulcers
 TYPE 1
-T-cell mediated AUTOIMMUNE disease, involving
the destruction of the Beta cells.

-Classical Symptoms + Hyperglycemia occur when

70-90 % of cells are destroyed.

-is associated with other autoimmune disorders

such as Thyroid Disease, Coeliac Disease, Addison’s
disease, Pernicious Anemia & Vitiligo.
 Type 2
• Resistance to action of insulin on:
liver
Muscle +
Impaired pancreatic Function.
Associated with disorders as:
Central Obesity, HTN, Dyslipdemia Metabolic
Syndrome.
 Comparative Features of:
TYPE 1
• AGE ONSET: Early
• Body Weight: N or Low
• Ketonuria : Yes
• Rapid Death without Insulin:
Yes
• Autoantibodies: Yes
• DM Complication at DX: No
• Family Hx of DM: Uncommon
• Other Autoimmune Diseases:
Common
TYPE 2
• AGE ONSET: > 50 Yrs
• Body Weight: Obese
• Ketonuria : No
• Rapid Death without Insulin:
No
• Autoantibodies: No
• DM Complicatn at DX: 25%
• Family Hx of DM: Common
• Other Autoimmune Diseases:
UnCommon
 INVESTIGATIONS
1-URINE TESTING

-Use of dipsticks
-of urine passed 1-2 hrs after meal.

You are looking for:

3 Things

?
1-Glycosuria
-warrants assessment by blood Testing.
-Disadvantage: Individual variation in renal
threshold.
-common in Pregnancy, Young people.

2-Ketones
-If associated with Glycosuria, Dx of DM is
highly likely.
-also found in Normal people: Fasting,
Strenuous Exercise, Vomiting rapidly,
eating diet high in fat but low in
carbohydrates.

3-Protein
-Testing for albumin.
-only detected if > 300mg/l
-Proteinuria- indicator of the development
of Diabetic nephropathy.
-NB: in absence of UTI
BLOOD TESTING

Glucose:
-venous plasma values -most reliable
for diagnostic purposes.

Measure

a) Fasting Plasma Glucose; < 7.0 mmol/l

b) Random Plasma Glucose: < 11.1 mmol/l

Indications for OGTT

a) Fasting Plasma Glucose; 6.1----7.0 mmol/l

b) Random Plasma Glucose: 7.8---11.0 mmol/l
 How to go about
1-Unrestricted doing a OGTT
carbohydrate 3-Rest for 30
diet for 3 mins.
days.

Preparation Before the Test:

4-Remain
2-Fasted over
seated for the
night for
duration of
atleast 8
the test, with
hours
no smoking.
SAMPLING

Plasma Glucose is measured BEFORE & 2 hours after

a 75 g oral glucose drink.

FASTING 2 HRS –GLUCOSE LOAD

FASTING 6.1-6.9 MMOL/L < 7.8 MMOL/L

HYPERGLYCAEMIA

RESULTS
IMPAIRED GLUCOSE < 7 MMOL/L 7.8-11 MMOL/L
TOLERANCE

DIABETES ≥ 7.0 MMOL/L ≥ 11.1MOL/L

Glycated Haemoglobin

-for diagnosis-uncertain.
-provides measure of glycemic control over a period of
weeks to months.
-Normal 6.5%-7.5 %.

When dx of DM is confirmed, other investigations should

include:

-U/Cr/ E
-Lipids
-LFTS
-Thyroid Function Test
 MANAGEMENT
Adequate Glycemic control can be obtained by:

Diet & Lifestyle Advice: 50%

Oral- Anti Diabetic Med: 20-30 %
Insulin: 20-30%
 Diet & Lifestyle Changes

Aims of Dietary Management:

1-Achieve good Glycaemic Control

2-Reduce Hyperglycemia & avoid Hypoglycemia.

3-Assist with weight management:

Weight Maintaince for Type 1 DM &NON-OBESE

Type 2 DM.
 Weight loss for overweight & Obese type 2
Diabetes.
4-↓ risk of micro-vascular & macro-vascular
complications.

5-Ensure adequate nutritional intake.

LIFE STYLE CHANGES

• Regular Physical Activity

• Healthy Diet
• Reducing Alcohol Consumption.
Refer to Dietitians: Tailored Advice & Nutritional
Plan on account of Patients Age & Lifestyle.
Composition of the Diet
 COMPOSITION OF DIET
CARBOHYDRATE (45-60%)

-Type 1 maintain regular intake in meals throughout

the day. (Traditionally)

-Now-Development of Insulin Analogues, Continuous

Subcutaneous Insulin Infusion has allowed flexibility &
timing of Carbohydrate intake.

-Type 2 Limitation of refined Carbohydrate

 Restriction of total Caloric intake.
Consumption of Foods with low GI is encouraged because:

They produce a SLOW, GRADUAL rise in blood glucose.

EXAMPLES: Starchy foods;

-Basmati rice -Beans

-Spaghetti -Lentils
-Porridge -Noodles
-Granary Bread
FATS
-Consumption of oils & Spreads made from Olives.
-< 10% Saturated Fat , 10-20% Monosaturated
-Should compose < 35% of energy intake.

WHY: CVD

SALT
-Reduce intake to < 6g daily.

FRUITS & VEGETABLES

-5 portions daily.

ALCOHOL
-in moderation
-CI as it suppresses Gluconeogenesis
- Overlooked sources of calories
 Anti-Diabetic Drugs

1-BIAGUANIDES

Metformin

-1st Line therapy

MOA: ↑ insulin sensitivity & peripheral glucose uptake.

DOSES:
-500mg p.c. q 12hrs-gradually increased to 1g q 8 hrs.
ADVANTAGES DISADVANTAGES
• -Doesn’t increase Body - Lactic acidosis
Weight.(Beneficial) - CI in Impaired renal &
Hepatic function,
• -Improves lipid profile Alcoholics, medical
slightly. conditions causing
severe shock ,
Hypoxemia. (Rx with
• -No risk of insulin for the time
Hypoglycemia being)
 Anti-Diabetic Drugs

2-SULPHONYLUREAS

Tolbutamide, Glipizide, Glibenclamide

MOA: ↑ insulin secretion.

INDICATION

-NON Obese patients who fail to respond to dietary measures

alone.

-Dose Response is steepest at low dose.

-Glipizide-few SE

-Daonil-prone to severe hypoglycemia. Avoid in elderly.

 Anti-Diabetic Drugs

3-MEGLITINIDES

Repaglinide

-Can BE + with Metformin.

MOA: directly stimulates endogenous insulin secretion.

DOSES:
-Taken immediately before food.
 Anti-Diabetic Drugs

4-ALPHA-GLUCOSIDASE INHIBITORS

Acarbose, Miglitol

-Can be + with SU.

MOA: delay carbohydrate absorption in the gut.

-Taken with food.

 Anti-Diabetic Drugs

5-THIAZOLIDINEDIONES

Glitatazone

-2nd line with Metformin or 3rd line with Metformin & SU.

MOA: Enhance action of endogenous insulin

-Taken with food.

 Anti-Diabetic Drugs

5-INSULIN
RECOMBINANT
DNA
i)RAPID ACTING :
lispro, Aspart, Glulisine (Analougue) 3 4.5

ii)SHORT ACTING: PROTAMINE

Soluble (regular) 48

iii)INTERMEDIATE ACTING:
ZINC
Isophane (NPH), Lente 7 14

iv)LONG ACTING: Bovine

Ultralente 12 30

v) LONG ACTING:
Glargine, Detemir (Analougue) 18 24
 COMPLICATIONS OF DIABETES
1-Diabetic Ketoacidosis
2-Hypoglycaemia
3-Macro-vascular Diseases
• MI
• Stroke
4-Micro-vascular Diseases
• Diabetic Retinopathy
• Diabetic Nephropathy
• Diabetic Neuropathy
 DIABETIC KETOACIDOSIS
• Medical emergency (in Type 1 DM).

• Established DM: Common presentation is:

InfectionLoss of AppetiteInsulin Stopped.
• Cardinal Biochemical Features:

1-Hyperglycaemia
2-Hyperketonaemia
3-Metabolic Acidosis
HyperglycaemiaCauses Osmotic DiuresisDehydration &
Electrolyte loss:

Na + K+

Loss Is excerbated by Hyperaldosteronism as a

result of ↓ renal perfusion.

-Ketosis results from insulin deficiency,

excerbated by elevated catecholamines 
unrestrained lipolysis.

-When this exceeds the capacity to metabolize

acidic ketones, these accumulate in blood
Metabolic Acidosis Force H+ into cells
Displaces K+.
Every Px is K+ Depleted but Plasma concentration of K+
gives little indication of total body deficit.

AVERAGE LOSS OF FLUID & ELECTROLYTES IN ADULT

DIABETIC KETOACIDOSIS OF MODERATE SEVERITY

WATER: 6L 3L Extracellular
NA+: 500mmol -Replace with Saline
CHLORIDE: 400mmol 3L Intracellular
POTASSIUM: 350mmol. -Replace with Dextrose.
 Clinical Features
Signs
Symptoms

• -Polyuria, thirst • Dehydration

• -Weightloss • Hypotension
• -Weakness • Tachycardia
• • Air Hunger
-N/V
• Cold ectrmities/ peripheral
• -Leg cramps
cyanosis.
• -Blurred Vision • Smell of Acetone
• -Abdominal Pain. • Hypothermia
• Confusion, drowsiness, Coma
(10%)
INVESTIGATIONS

1-Venous blood:
U/E/Glucose/Bicarbonates (<12mmol/L  Severe
Acidosis)

2-Arterial Blood Gases

H+ (More accurate)

3-Urinalysis for Ketones

4-ECG

5-Infection Screen
MANAGEMENT

1-FLUID REPLACEMENT

2-INSULIN

3-POTASSIUM

4-ADDITIONAL PROCEDURES
1-Fluid Replacement

-0.9% Nacl IV
1 L over 30 mins
1 L over 1 hr
1 L over 2 hrs
1 L over 2-4 hrs
-When Glucose Levels < 15mmol/L

Switch to 5% Dextrose, 1 L 8 Hourly.

-Typical requirement is 6L in the 1st 24 hours.
(FR based on clinical response –UO)
2-Insulin

-50 U Soluble Insulin in 50ml 0.9% Saline IV Via Infusion

Pump.

6U/hr initially

3U/hr when Blood Glucose < 15mmol/l.

2U/hr if Blood Glucose < 10mmol/l.

-Aim for fall in Blood Glucose of 3-6mmol/l per hour.

3-POTASSIUM

-None in first liter of IV fluid unless plasma

K+ < 3 mmol/l.

-When < 3.5 mmol/L , give 20mmol/ hr

-When plasma K+ is 3.5-5.0mmol/L, give

10mmol/hr.
4-ADDITIONAL PROCEDURES

-Catherisation if No urine passed after 3 hours.

-Nasogastric tube to keep stomach empty in

unconscious Px or if vomiting is protracted.

-CVP Line if CVS compromised.

-Plasma expender if sys BP < 90mmhg or does not rise

with IV saline.

-Antibiotic if infection is demonstrated or suspected.

-ECG monitoring.
MONITORING IN DIABETIC KETOACIDOSIS

1-GLUCOSE

2-U/E

3-CREATININE

4-BIOCARBONATES

5-BLOOD GASES

THE FOLLOWING SHOULD BE MONITORED HOURLY

-PULSE - BP

-RR - UO

-BLOOD GLUCOSE
COMPLICATION OF DIABETIC
KETOACIDOSIS
1-cerebral Edema

* Caused by -rapid reduction of blood Glucose

-Use of Hypotonics or bicarbonates

-Rx: Mannitol, Oxygen

2-ARDS

3-Thromboembolism

4-Acute circulatory Failure

NON-KETOTIC HYPEROSMOLAR DIABETIC
COMA

-Condition is characterized by severe Hyperglycemia

without hyperketonaemia or acidosis. (M-40%)

-Severe Dehydration & uraemia is common.

-usually affects elderly with undiagnosed Type 2 DM.

-Rx differs from ketoacidosis in 2 respects:

1-Px are sensitive to insulin thus half the dose of insulin

in that used for ketoacidosis should be administered.
(3U/hr)

2-Plasma Osmolality should be measured:

2[ Na+] +2[K+] +[Glucose] + [ Urea]=280-290mmol/L

-The Px should be given 0.45% Saline until Osmolality

approaches Normal & then replace with isotonic solution.
 HYPOGLYCAEMIA
• Blood glucose: < 3.5mmol/L
• Occurs in DM as a result of Rx.
• Often in those with Insulin Therapy +
secretogogues.
• Spontaneous Hypoglycaemia:Non DM pple.
MOST COMMON SYMPTOMS OF HYPOGLYCEAMIA
AUTONOMIC
-Sweating -Hunger
-Trembling -Anxiety
-Pounding Heart
NEUROGLYCOPENIC
-Confusion -Inability to concentrate
-Drowsiness -incoordination
-Speech Difficulty - Irritibilty, Anger
NON-SPECIFIC
-Nausea -Tiredness
-Headache
NB: Symptoms Differ with age.
MANAGEMENT OF HYPOGLYCEMIA

MILD (SELF-TREATED)
-Oral fast acting carbohydrate (10-15g)-Glucose
drinks, Tablets, confectioneries
-Followed with complex carbohydrate snacks.

SEVERE (EXTERNAL HELP REQUIRED)

-If Px is semiconscious, unconscious-parenteral Rx is
required.

•IV 75ml 20% Dextrose (=15g, 0.2g/kg in children) or

•IM Glucogan (1mg, 0.5mg in children)

•If Px Conscious & able to swallow 25g

 LONG TERM COMPLICATIONS OF
DIABETES
Macro-vascular Diseases
• MI
• Stroke
Micro-vascular Diseases
• Diabetic Retinopathy
• Diabetic Nephropathy
• Diabetic Neuropathy
Macrovascular Complications

-Pathological changes associated with atherosclerosis in

DM occurs earlier in life & more extensive & severe then
compared to N population.

-DM amplifies effect of other major cardiovascular risk

factors: Smoking, HTN & Dyslipedimia.

Thus….ANGINA….MI……CARDIAC
FAILURE…..STROKE
Diabetic Microangiopathy
1-DIABETIC RETINOPATHY

-Blindness betn-30-65 yrs.

-HyperG Inc blood Flow endothelial cell proliferation
Capillary closure.

CLINICAL FEATURES OF DIABETIC RATIONOPATHY

-Microaneurysms
-Retinal Haemorrhages
-Exudates
-Cotton wool spots

Loss of Visual Acuity

-unless edema & thickening in macular area.
-Cataract
2-DIABETIC NEPHROPATHY
-most common cause of ESRF.

-Screening : MICROALBUMINURIA

-IDENTIFIES: Nephropathy in Type 1 & 2 DM.

-RISK FACTORS: Inc BP, Poor Glycemic Control, Smoking.

-24 hr Urine 30-300mg/24hrs.

WHO TO SCREEN
-DM 1 PX: annually from 5 yrs of DX.
-DM 2 PX: annually from time of DX

MANAGEMENT
A-Improve BG, BP

BP in DM 1-ACE-I but CI if Nephropathy already.

-Alternatives: Diltiazem, Verapamil
3-DIABETIC NEUROPATHY

-early complication (30%)

-manifested in peripheral nervous system. (Axon)

CLINICAL FEATURES OF AUTONOMIC NEUROPATHY
CARDIOVASCULAR
-Postural Hypotension -Resting Tachycardia
GASTROINTESTINAL
-Dysphagia-atony
-Abdominal fullness, N/V
-Nocturnal Diarrhea +/- Fecal Incontinence
-Constipation-atony
GENITOURINARY
-Difficulty in micturition, urinary incontinence,
recurrent infection due to atonic bladder.
-Erectile dysfunction, Retrograde ejuculation.
VASOMOTOR
-Cold feet-loss of vasomotor function.
-Dependent edema
 THE DIABETIC FOOT
• CME LAST WEEK THURSDAY
HOW TO REVIEW A
PATIENT IN THE
DIABETES CLINIC
HOW TO REVIEW A PATIENT IN THE DIABETES CLINIC

Body Weight & BMI

Urinalysis
-Analyzing Fasting Specimen for: ? ? ?

Biochemistry
-Lipid Profile, renal, liver & Thyroid Function.

Glycemic Control
-HbA1C
-Inspect home blood glucose monitoring record.

BP

SMOKING

EYE Examination

Lower Limbs & feet.

THANK YOU
SALAMAAT

KAMSAMIDA
 REFERANCE
• DAVIDSON’S PRINCIPLES & PRACTICE OF
MEDICINE-PG 795-833.