Diabetes Mellitus-I

Dr. Anmar AL-TAIE

• Diabetes Mellitus (DM) is a chronic condition, characterised by hyperglycaemia
due to impaired insulin secretion with or without insulin resistance.

Aetiology
• There is a strong association between type 2 and obesity, with obesity causing
insulin resistance.
• Central obesity, where adipose tissue is deposited intra-abdominally rather than
subcutaneously, is associated with the highest risk.

Differences between Type 1 and Type 2 Diabetes

Clinical Manifestations
• Polyuria (increased urine production, particularly noticeable at night).
• Fatigue due to an inability to utilize glucose.
• Marked weight loss because of the breakdown of body protein and fat as an
alternative energy source to glucose.
• Blurred vision caused by a change in lens refraction.
• A higher infection rate, especially Candida, and urinary tract infections due to
increased urinary glucose levels.

Type 1 DM
• The symptoms mentioned earlier are usually extreme and of recent (days or
weeks) onset.

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Type 2 DM
• Many patients have an insidious onset of hyperglycaemia, with few or no classic
symptoms.
• Obese individuals, whose diabetes may be detected only after glycosuria or
hyperglycaemia is found accidentally.
• Recurring infections, as UTI, chest, soft tissue, are common because sustained
hyperglycaemia can result in severe impairment of phagocyte function, and raised
glucose levels provide a growth medium for bacteria.
• Generalised pruritus and symptoms of vaginitis, due to candidal infection, are
frequently the initial complaints of women with type 2 diabetes.
Diagnosis
• Underlying symptoms.
• An oral glucose tolerance test with a fasting serum glucose concentration ≥7.0
mmol/L or serum glucose concentration ≥11.1 mmol/L 2 h after 75 g anhydrous
glucose.
• At least one additional glucose test result, on another day with the value in the
diabetic range, is essential, either fasting or from the 2-h post-glucose load.
Diabetic ketoacidosis (DKA)
• It occurs because absence of insulin causes extreme hyperglycaemia, normally
associated with type 1 diabetes, rarely with type 2.
• Ketone bodies, acetoacetate and hydroxybutyrate are formed in increased amounts
and released into the circulation.
• Weakness is increased by potassium loss, caused by urinary excretion, and
vomiting due to stimulation of the vomiting centre by ketones, and catabolism of
muscle protein.
• Ketoacidosis exacerbates dehydration and hyperosmolarity by producing anorexia,
nausea, and vomiting.
• Metabolic acidosis causes stimulation of the medullary respiratory centre, giving
rise to Kussmaul respiration (deep and rapid breathing) to correct the acidosis.
• The patient's breath may have the fruity odour of acetone (ketones) commonly
described as smelling like pear drops or nail varnish remover.

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Precipitating Factors
• Omission of insulin dose • Trauma or myocardial infarction
• Acute infection

Diagnosis
• Demonstration of hyperglycaemia and metabolic acidosis with the presence of
ketones.
• Urinalysis will show marked glycosuria and ketonuria.
• A blood glucose test strip usually shows a blood glucose level of more than 22
mmol/L.
• Laboratory measurement of WBCs (raised but correlates with the ketone body
level), glucose, urea, creatinine, electrolytes, and venous bicarbonate should be
carried out.
• The serum sodium level is low due to the osmotic effect of glucose draining water
from the cells and diluting the sodium.
Treatment of DKA
• Fluid volume expansion (0.9% sodium chloride)
• Correction of hyperglycaemia and ketones by infusion of insulin.
• Prevention of hypokalaemia, and identification and treatment of any associated
infection.
Long-Term Diabetic Complications
Macrovascular Disease
1. Cardiovascular Disease (IHD, MI and Cerebrovascular disease or stroke)
• Most common cause of death in people with type 2 DM
• The risk is increased if nephropathy, smoking, hypertension, and dyslipidaemia is
present and is associated with metabolic syndrome and insulin resistance.
• Silent myocardial infarction (infarction with no symptoms) due to cardiac
autonomic neuropathy.

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2. Peripheral Vascular Disease (PVD)
Microvascular Disease
1. Retinopathy
• It is the leading cause of blindness in people under the age of 60.
• It is symptomless until the disease is far advanced.
• Regular screening should undertaken.
• Tight glycaemic control to prevent and delay the progression of retinopathy.
• When retinopathy is detected early, sight may be saved by laser photocoagulation.
• In advanced cases, surgery may be required.
2. Nephropathy
• The kidneys become enlarged, and the glomerular filtration rate (GFR) initially
increases.
• If nephropathy progresses, the GFR starts to decline.
• Serum creatinine and GFR (eGFR) can be used to estimate renal function.
• The presence of nephropathy is indicated by the detection of microalbuminuria
(small amounts of albumin present in urine).
• If higher amounts of albumin are detected, this is termed proteinuria (or
macroalbuminuria) and signifies more severe renal damage which may progress to
end-stage renal disease and require dialysis.
• Microalbuminuria is defined as an albumin: creatinine ratio (ACR) greater or equal
to 2.5 mg/mmol (men) and 3.5 mg/mmol (women).
• Proteinuria may be defined as an albumin: creatinine ratio greater than 30 mg/mmol
or albumin concentration greater than 200 mg/L.
• Albumin in the urine increases the risk of cardiovascular disease.
• Tight control of both glycaemic levels and blood pressure reduces the risk of
developing nephropathy.
• ACE inhibitors and/or ARBs are the treatments of choice to provide renal protective
effects additional to their antihypertensive effects. They delay the progression to
proteinuria in patients with microalbuminuria.

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 3. Peripheral Neuropathy
• It is a progressive loss of peripheral nerve fibres resulting in nerve dysfunction.
• Diabetic neuropathies are characterized by sensory, motor, and autonomic
symptoms.
• Diabetic proximal motor neuropathy is rapid in onset and involves weakness and
wasting, principally of the thigh muscles.
• Muscle pain is common and may require opiate analgesia.
• Autonomic neuropathy is diabetic impotence, diarrhea, bladder dysfunction as loss
of bladder tone with a large increase in volume.
• Gastroparesis causes vomiting and delayed GI transit and variable food absorption,
causing difficulty in the insulin-treated patient.
• Autonomic neuropathy may cause dry skin and lack of sweat and contribute to
diabetic foot problems.
Macro- and Microvascular Disease Combined
• Infected diabetic foot ulcers account for diabetes-related hospital bed-days and are
the most common non-trauma cause of amputations.
• It develops due to sensory and autonomic neuropathy, PVD and hyperglycaemia.
• Poor foot care and poorly controlled diabetes are also contributory factors.
• There are three main types of foot ulcers: neuropathic, ischaemic and
neuroischaemic.
• Neuropathic ulcers occur when peripheral neuropathy causes loss of pain sensation.
• Ischaemic ulcers result from PVD and poor blood supply causing a reduction in
available nutrients and oxygen required for healing.
• Most ulcers have elements of both neuropathy and ischaemia and are termed
neuroischaemic.
• Diabetic foot ulcers are prone to infection, the most common pathogens being
staphylococci and streptococci.
• Wounds with an ischaemic component are commonly infected with anaerobic
organisms.

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