Diabetes mellitus is a chronic condition characterized by high blood glucose levels due to insufficient insulin production or resistance. The document discusses the structure and function of insulin, glucose metabolism, classification and complications of diabetes. It describes key complications like diabetic ketoacidosis, retinopathy causing vision loss, nephropathy potentially leading to kidney failure, neuropathy with nerve damage, and foot complications risking amputation. Management involves lifestyle changes, medications, and treatments like laser photocoagulation for retinopathy.

1. DIABETES MELLITUS
QURATULAIN MUGHAL
ISRA UNIVERSITY
BATCH IV
DOCTOR OF PHYSICAL THERAPY
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2. Introduction
• Diabetes mellitus (DM) is a syndrome of chronic
hyperglycaemia due to relative insulin deficiency,
resistance, or both.
Insulin structure and secretion:
• Insulin is the key hormone involved in the storage and
controlled release within the body of the chemical energy
available from food.
• synthesized in the beta-cells of the pancreatic islets.
• After secretion, insulin enters the portal circulation and
is carried to the liver, its prime target organ.
• About 50% of secreted insulin is extracted and degraded
in the liver; the residue is broken down by the kidneys.
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3. GLUCOSE METABOLISM
• Blood glucose levels are closely regulated in
health and rarely stray outside the range of 3.5–
8.0 mmol/L (63–144 mg/dL), despite the
varying demands of food, and exercise.
• The principal organ of glucose homeostasis is
the liver, which absorbs and stores glucose (as
glycogen) in the postabsorptive state and
releases it into the circulation between meals to
match the rate of glucose utilization by
peripheral tissues.
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4. Glucose production
• About 200 g of glucose is produced and utilized each day.
• More than 90% is derived from liver glycogen and hepatic gluconeogenesis,
and the remainder from renal gluconeogenesis.
Glucose utilization
• The brain is the major consumer of glucose.
• Its requirement is 1 mg/kg bodyweight per minute, or
100 g daily in a 70 kg man.
• Glucose uptake by the brain is obligatory and is not
dependent on insulin, and the glucose used is oxidized
to carbon dioxide and water.
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5. CLASSIFICATION OF DIABETES
• primary (idiopathic)
• Secondary
• polygenic forms known as type 1 and type 2
diabetes.
• immune-mediated diabetes (type 1)
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7. DIABETIC COMPLICATIONS
1. Diabetic Ketoacidosis
2. Diabetic Retinopathy
3. Diabetic Nephropathy
4. Diabetic Neuropathy
5. Diabetic Foot
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8. 1. Diabetic Ketoacidosis
• Diabetic ketoacidosis is the hallmark of type 1
diabetes.
• Ketoacidosis is a state of uncontrolled catabolism
associated with insulin deficiency
Ketone bodies
• three water-soluble molecules.
1. Acetoacetate
2. beta-hydroxybutyrate
3. Acetone
• they are produced by the liver from fatty acids
during periods of low food intake (fasting).
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9. Clinical features of diabetic
ketoacidosis
Symptoms Signs
• Polyuria, thirst
• Weight loss
• Weakness
• Nausea, vomiting
• Blurred vision
• Abdominal pain, leg cramps
• Dehydration
• Hypotension (postural or
supine), tachycardia
• Cold extremities/peripheral
cyanosis
• Air hunger (Kussmaul
breathing)
• Smell of acetone
• Hypothermia
• Confusion, drowsiness, coma
(10%)
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10. Diagnosis of pre-diabetes
• ‘impaired fasting glucose’ (IFG; fasting plasma
glucose 6.1–6.9 mmol/L)
• ‘impaired glucose tolerance’ (IGT; glucose 7.8–
11 mmol/L 2 hrs after 75-g oral glucose drink).
Management:
• Initially: metformin(glucophage)
• For last stage: Thiazolidinediones.
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11. 2. Diabetic Retinopathy
• Diabetic retinopathy (DR) is a common cause of
blindness in the long term complications.
Pathophysiology:
• Hyperglycaemia increases retinal blood flow and
metabolism, and has direct effects on retinal
endothelial cells, resulting in impaired vascular
autoregulation.
• This leads to chronic retinal hypoxia, which
stimulates production of growth factors and causes
new vessel formation and increased vascular
permeability.
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12. Clinical features
1. Dot haemorrhages or microaneurysms:
Hyperglycaemia increases retinal blood flow
and metabolism, and has direct effects on
retinal endothelial cells, resulting in impaired
vascular autoregulation. This leads to chronic
retinal hypoxia, which stimulates production of
growth factors and causes new vessel formation
and increased vascular permeability.
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13. 2. blot haemorrhages
• Round and regular shaped.
• Leakage of blood into deeper retinal layer.
3. Hard exudates
• Exudation is the characteristic feature of DM.
• Tiny large patches are formed which are vary in
size.
• The plasma leak from the retinal capillary due to
damage.
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14. 4.Cotton wool spot
• White spots are seen in retina due to arteries
occlusion which causes ischemia.
• It found in combination with uncontrolled
hypertension.
5. Intra-retinal microvascular anomalies (IRMA):
• spidery vessels
6. Neovascularisation:
• Fine tufts of vessels forming arcades on the
retinal surface, later extending forwards on to
the vitreous.
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15. 7. Rubeosis iridis
• New vessels formed at the surface of iris.
• It can secondary to glaucoma.
• The vessels compress, block and drainage
obstruction.
Treatment
• Retinal photocoagulation: Laser
photocoagulation is eye surgery using a laser to
shrink or destroy abnormal blood vessels in the
retina.
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16. 3. Diabetic nephropathy
• Important cause of morbidity and mortality rate.
• Kidney damage due to poor glycaemic control
and cause renal failure.
• Following changes occur in nephron:
1. Hyperfilration
2. glomerular capilaries HTN
3. Nephrosclerosis if thickening of the glomerular
basement membrane.
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17. Sign and symptoms
• Frequent urination
• Lack of appetite
• Paddle edema
• Nausea
• Vomiting
• Headache
• Malaise
• Echy skin
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Treatment
ACE inhibitors provide greater protection and
equal BP reduction

18. 4. Diabetic neuropathy
• Diabetes can damage peripheral nervous system
more as compare to CNS.
• The following varieties of neuropathy occur:
a) symmetrical sensory polyneuropathy
b) Asymmetrical motor diabetic neuropathy
(diabetic amyotrophy)
c) Mononeuropathy
d) Autonomic neuropathy
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19. a. symmetrical sensory
polyneuropathy
• This can be symptomatic or asymptomatic.
• The most common signs are diminished
perception of vibration distally, ‘glove-and-
stocking’ impairment of all sensorymodalities,
and loss of tendon reflexes in the legs.
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20. b. Asymmetrical motor diabetic
neuropathy (diabetic amyotrophy)
• This presents as severe, progressive weakness
and wasting of the proximal muscles of the legs
(occasionally arms), accompanied by severe
pain, hyperaesthesia and paraesthesia.
• There may also be marked loss of weight
(‘neuropathic cachexia’) due to chronic illness.
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21. c. Mononeuropathy
• Nerve compression palsies commonly affect the
median nerve and lateral popliteal nerve (foot
drop).
• Most commonly affected are the 3rd and 6th
cranial nerves (causing diplopia), and femoral
and sciatic nerves.
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22. d. Autonomic neuropathy
• Postural hypotension
• Dysphagia
• Difficulty in maturation
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23. 5. The diabetic foot
• Frequent site of lesions on foot.
• DM foot care is necessary.
• Can lead to amputation due to gangrene.
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24. Relationship of etiological factors and clinical
features
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25. REFERENCES
• KUMAR AND CLARK
• DAVIDSON’S
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