This segment covers the introduction; classification; signs and symptoms; complications; laboratory investigations pertaining to DM.

2. INTRODUCTION
 From a Greek word meaning ‘To pass through’.
 Group of disorders exhibiting a defective or deficient insulin
secretory response, glucose underutilization, and consequently,
hyperglycaemia.
 Due to Absolute or Relative Insulin deficiency; Insulin resistance.
 Carbohydrate, protein and fat metabolism is affected.
 Long-term complications : Diabetic angiopathies (nephro, neuro
and retino).
 Hyperglycaemia is also caused by over-production of hormones
like glucagon, adrenal hormones or overactivity of Insulinase.
 FBG (3.9 to 5.5 mmol/L or 60 – 90 mg/dl);
RBG (3.9-6.9 mmol/L or 90 – 110 mg/dl);
PPBG (3.9-8.1 mmol/L or 120 – 180 mg/dl).
 Onset : Type-I (20% of cases; early age);
Type-II (80%; occurs later - maturity onset).
 CLASSIFICATION : Primary / Idiopathic DM
Secondary DM

3. Fasting blood
glucose:
Less than or equal to 6.1 mmol/L (110 mg/dL);
2 hours after
eating
(postprandial):
age 50 and younger: <7.8 mmol/L (140 mg/dL);
ages 50-60:<8.3 mmol/L (150 mg/dL);
age 60 and above: <8.9 mmol/L (160 mg/dL)
Random (casual): Levels vary depending on when and how much
you ate at your last meal.
In general:
• before meals or when waking up: 4.4-6.6
mmol/L (80-120 mg/dL);
• at bedtime 5.5-7.7 mmol/L (100-140 mg/dL)

4. CLASSIFICATION
PRIMARY / IDIOPATHIC DM
 Most common; unknown cause.
 Further divided into:
• Type-I DM (Insulin-dependent / IDDM / Juvenile onset)
• Type-II DM (Non- Insulin-dependent / NIDDM / Adult /
Maturity onset)
• Potential DM
• Latent DM
• Gestational DM
• Asymptomatic DM
Type-I DM
- Absolute Insulin deficiency; mostly in people < 40 yrs.
- Exhausted pancreatic β cells can’t produce insulin.
- Unknown cause, but could be due to ….
Immunological destruction of β cells, genetic
susceptibility, viruses, chemicals and environmental
toxins.
- Rapid onset of symptoms

5. Type-II DM
- More common subtype (80%); mostly in people > 40 yrs.
- These days, it can occur at any age.
- Inadequate insulin secretion; Peripheral tissues develop
resistance to insulin.
- Etiology: Hereditary, genetic makeup, obesity, etc.
- Slow onset of symptoms
Note: Type-I and Type-II are collectively called Clinical DM.
Potential DM
- Person w/ normal glucose tolerance but, positive familial
history.
- Age-related occurrence is very high.
- Must have good diet control and avoid precipitating
factors.

6. Latent DM
- Diabetic type of Glucose tolerance without any consistent
elevation of blood glucose level.
Gestational DM
- Temporary elevation of blood glucose level during
gestational period.
- Automatically disappears post-delivery.
Asymptomatic DM
- Glucose tolerance curve resembles a diabetic patient but,
actual clinical symptoms are absent.
- Can occur in the future.

7. SECONDARY DM
 Minor type
 Has definite causes.
 Causes: Pancreatic disorders, Pancreatic damage,
Insulin antagonist (Excess of Growth Hormone).
Insulin secretion inhibited (by epinephrine).
 May or may not be insulin-dependent.

8.  Foods (mainly high carbs) ed Glucose in blood; (used→ ↑ as fuel)
↓
Insulin released
(to counter rising blood glucose levels)
 Insulin regulates glucose uptake from the blood into most cells
(muscle and fat cells, but not CNS cells).
 Roles of Insulin:
a] Regulates glucose absorption from blood (for use as fuel).
b] Stimulates conversion of excess glucose to glycogen (in
liver and muscle).
c] Stimulates cell growth, protein synthesis and fat storage.
 Insulin deficiency / insensitivity of it’s receptors is vital in all forms
of DM.
 Lowered glucose levels → reduced insulin release & reverse
conversion of glycogen to glucose [Mainly controlled by the
hormone Glucagon which acts in an opposite manner to insulin].
PATHOPHYSIOLOGY

9. • Insufficient or deficient insulin / Insulin resistance
↓
Inadequate absorption and storage of glucose
NET EFFECTS
 Persistent high levels of blood glucose
 Poor protein synthesis
 Derangements in carbohydrate, protein and fat
metabolism
 Acidosis

11. CLINICAL FEATURES
 Elevated Blood sugar levels (nil/inadequate/ underutilization
of insulin).
 Glycosuria
 Polyuria / Excessive urination (response to glycosuria;
kidneys excrete additional water to dilute the excess
glucose).
 Polydipsia / Excessive thirst (due to polyuria).
 Polyphagia / Excessive hunger (due to energy loss).
 Weakness and weight loss (excess loss of calories in urine).
 Nausea, blurred vision, drowsiness, RF, opportunistic
infections, easily fatigued.
 Gangrene develops (Amputate affected part – toes, legs).

12. COMPLICATIONS OF DM
 Diabetic ‘pathies’ / angiopathies (retino,
neuro and nephro)
 Atheroscelorsis (incl. peripheral and coronary
blood vessels)
 Hypertension (persistent systolic HTN)
 Hyperglycaemia-induced cataract
 Altered GI function
 Impaired WBC function Immunity→
compromised
 Deep Infections (Diabetic foot ulcers) with
poor healing
 Diabetic and Hypoglycaemic coma

13. DIABETIC RETINOPATHY
 No early warning signs.
 Damage to retina → Blindness.
 Macular edema → blurred vision; can’t read, write, drive
vehicle.
 Proliferative Diabetic Retinopathy (PDR) : New blood vessels
formed at the back, hemorrhage and leak blood and
proteins. Not severe at first (Blood specks or spots vanish
after a few hours). Becomes worse gradually. Person can’t
distinguish light from dark.
 Aneurysms and Brittle blood vessels (Neovascularization)
cause Retinal scarring and detachment.
 Glaucoma and cataracts
 O/E: Cotton wool spots, Flame hemorrhages, Spot
hemorrhages

14. ‘Cottonwool’ spots

15. DIABETIC NEUROPATHY
 Due to diabetic vascular injury to small blood vessels that
supply nerves (Vasa nervorum).
 Limited blood flow to the nerve → nerve damage or death.
 Signs and symptoms :
• Numbness and tingling of extremities (patients are
unaware of injuries to any part supplied by damaged
nerves).
• Dysesthesia (loss of or decreased sensation to a body
part)
• Diarrhea, Muscle weakness, Dysphagia (difficulty in
swallowing)
• Erectile dysfunction, Impotence
• Urinary incontinence.
• Vision changes, Speech impairment
• Facial, mouth and eyelid drooping.
• Dizziness, Fasciculation (muscle contractions).
• Burning (especially in evenings), Electric Stabbing Pains.

16. DIABETIC NEPHROPATHY
 Kimmelstiel-Wilson syndrome
 Inter-capillary glomerulonephritis.
 Progressive kidney disease caused by capillaries’
angiopathy in the kidney glomeruli. Characterized by
nephrotic syndrome and nodular glomerulosclerosis.
 Proteinuria; kidneys lose filtering and cleansing ability
(toxins remain in the body).
 Signs & Symptoms :
• Oedema (initially around the eyes; later - general body
swelling legs are mostly affected); Unintentional weight
gain.
• Urine (foamy appearance or excessive frothing).
• Anorexia, NV, Malaise, Fatigue, Headache.
• Frequent hiccups, Generalized itching.

17. DIABETIC KETOACIDOSIS
 Very severe form of DM complication.
 Occurs in Type-II DM; glucose can’t be used as an energy
source. So, fats are used for energy.
 Excess liberation of FFAs from adipose tissue and hepatic
oxidation → Ketonic body production (Butyric Acid and
Acetoacetic acid) Blood becomes acidic (→ Diabetic
Ketoacidosis)
 Acetone smell in patient’s breath, Ketonaemia, Ketonuria →
Diabetic Coma.
[FFA= Free Fatty Acids]

18. HYPOGLYCAEMIC
COMA
DIABETIC
COMA
Sudden onset
(Insulin Overdose)
Delayed onset (prolonged
illness and lack of insulin)
Sweating, tremors,
headache, mental
confusion
Dehydration, abdominal
pain, vomiting
Moist skin, normal
respiration and slightly
elevated B.P.
Dry skin, low pulse and
low B.P.
No ketonuria Ketonuria

20.  For Blood Glucose levels : Glucometers
 FBS, RBS and PPBS
 Glucose Tolerance Tests (GTT): Oral or I.V.
HbA1c (Glycosylated Hb)
• To identify average plasma glucose conc. over prolonged
time periods.
• Ratio of Glycosylated Hb to total Hb.
• Hb exposed to high plasma blood glucose levels.
• Estimated by : HPLC and Immunoassays.
• Reference range : 4.0 – 5.9% (normal);
< 6.5% (good control);
Higher for DM (> 6.5%).
• Checking blood sugar control in Pre-diabetics;
Monitoring blood sugar control in DM patients.
• Far more revealing information on glycemic behavior than a
fasting blood sugar value.

21. Interpretation of HbA1c test
HbA1c Mean Blood
Sugar (mg/dl)
6 135
7 170
8 205
9 240
10 275
11 310
12 345

22.  Urine tests : Glycosuria, Ketonuria (severity of DM).
 Blood glucose estimation : GTT
Glucose Tolerance Test [ GTT ]
• OGTT is the standard for the diagnosis of Type-II DM.
• 3 days before test, the person should have eaten a diet high
in carbohydrates (150- 200 grams per day).
• Person fasts overnight (8 - 16 hours).
• The morning of the test, the person should not smoke or
drink coffee.
• The FPG is tested.
• Then, the person receives 75 grams of glucose (100 grams
for pregnant women). Usually, the glucose is in a sweet-
tasting liquid that the person drinks.
• Blood glucose levels are measured five times over a period
of 3 hours.

23. RESPONSES AND DIAGNOSES OF OGTT
Normal response:
• all values between 0 – 2 hours < 200 mg/dl
• 2-hour glucose level <140 mg/dl
Impaired glucose tolerance (IGT):
• Fasting plasma glucose < 126 mg/dl
• 2-hour glucose level is between 140 – 199 mg/dl
Diabetes:
• 2 diagnostic tests done on different days show high blood glucose
levels
• fasting glucose > 126 mg/dl; 2 hour levels > 200 mg/dl
Gestational diabetes:
• For 100g OGTT, a fasting plasma glucose > 95 mg/dl;
• 1-hour glucose level > 180 mg/dl, 2-hour glucose level of > 155
mg/dl, or 3-hour glucose level > 140 mg/dl

24. Health Screening
 Height, weight and B.P. measurements
 Thyroid examination
 Examination of hands, fingers, feet, and toes for
circulatory abnormalities
 Blood tests for fasting blood sugar, HbA1c and cholesterol
 Family history of diabetes, cardiovascular disease, and
stroke.
 Prior infections and medical conditions
 A list of current medications, including: Prescription
medications, OTC medications, Vitamins and herbal
supplements

25. Health Screening (contd’.)
 Smoking history, including encouragement to stop smoking (if
applicable).
 Signs of complications with pregnancy.
 Eating and exercise habits
 Vision abnormalities, to check for eye health issues
 Urination abnormalities, which can indicate kidney disease.

26. TO BE CONTINUED…