Diabetes mellitus is a clinical syndrome characterized by high blood glucose levels. The presentation discusses types of diabetes including type 1, type 2, and gestational diabetes. Complications of diabetes include diabetic neuropathy, where high blood sugar can damage nerves throughout the body. Diabetic neuropathy can cause numbness, pain, and other symptoms and is classified as somatic or autonomic neuropathy. Proper management of diabetes includes lifestyle modifications, oral medications, insulin therapy, and treatment of complications to prevent further issues.

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MISCELLANEOUS DISEASE

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PRESENTER
DR. SHIREEN MANSOOR

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Learning objectives
 DIABETES MELLITUS
 DIABETES NEUROPATHY
 DIABETIC FOOT

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DIABETIC MELLITUS

7. DIABETES MELLITUS
• Diabetes mellitus is a clinical syndrome characterized by an increase in plasma blood glucose
(hyperglycaemia).
• The incidence of diabetes is rising. Globally, it is estimated that 366 million people had
diabetes in 2011 (approximately 8.3% of the world population, or 3 new cases every 10
seconds), and this figure is expected to reach 552 million by 2030.
• The effects of diabetes mellitus include long–term damage, dysfunction and failure of various
organs.
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8. Types of Diabetes
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• Type 1 Diabetes Mellitus
• Type 2 Diabetes Mellitus
• Gestational Diabetes

9. Functional Anatomy & Physiology
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 REGULATION OF INSULIN SECRETION:
Insulin is secreted from pancreatic β cells into the portal circulation
in response to glucose and other nutrient. It reduces blood glucose
level.
Only antidiabetic hormone secreted in body.
REGULATION OF GLUCAGON SECRETION:
Pancreatic α-cells of islets of Langerhans that secrete glucagon.
Glucagon has opposite effects of insulin, stimulate Glycogenolysis.
BLOOD GLUCOSE HOMEOSTASIS:
Blood glucose concentration is maintained within narrow range.
Glucose homeostasis reflects a balance between the entry of
glucose into the circulation from the liver and intestine and the
uptake of glucose by peripheral tissues, particularly muscle and
brain.

10. Type 1 diabetes
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Caused by autoimmune destruction of insulin-
producing cells (β cells) in the pancreas, resulting
in absolute insulin deficiency.
 Type 1 diabetes develops when the body’s
immune system destroys pancreatic beta
cells, the only cells in the body that make the
hormone insulin that regulates blood
glucose.
 This form of diabetes usually strikes children
and young adults, although disease onset can
occur at any age.

11. Type 2 diabetes
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Characterised by resistance to the action of insulin
and an inability to produce sufficient insulin to
overcome this ‘insulin resistance’
Was previously called non-insulin-dependent
diabetes mellitus (NIDDM) or adult-onset
diabetes
It usually begins as insulin resistance, a
disorder in which the cells do not use insulin
properly. As the need for insulin rises, the
pancreas gradually loses its ability to produce
insulin.

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13. Gestational Diabetes
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 A form of glucose intolerance that is diagnosed in some women
during pregnancy.
 During pregnancy, gestational diabetes requires treatment
to normalize maternal blood glucose levels to avoid
complications in the infant.
 After pregnancy, 5% to 10% of women with gestational
diabetes are found to have type 2 diabetes.

14. ETIOLOGICAL CLASSIFICATION
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 Type 1
Immune Mediated, Idiopathic
Type 1 diabetes is a T cell-mediated autoimmune disease involving destruction of
the insulin-secreting β cells in the pancreatic islets.
 Type 2
• Genetic defects of β-cell function
• Genetic defects of insulin action
• Pancreatic disease (e.g. pancreatitis)
• Excess endogenous production of hormonal antagonists to insulin
• Drug-induced e.g. corticosteroids, thiazide diuretics, phenytoin)
• Uncommon forms of immune-mediated diabetes
• Wolfram’s syndrome – diabetes insipidus, diabetes mellitus, optic atrophy, nerve
deafness; Friedreich’s ataxia; myotonic dystrophy

15. Presenting Complain Of DM
Hyperglycaemia
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• High blood glucose.
• Symptoms: Thirst, Fatigue, Blurred Vision, Polyuria, Headache,
Blurred vision.
• Type 2 DM patient can be asymptomatic or present with chronic
fatigue or malaise.
• Typical type 2 diabetes occurs increasingly in obese young
people.
• Older patient may have evidence of autoimmune activity
against B cells, a slowly evolving variant of type 1
diabetes(LADA).

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17. Diabetic Emergencies
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Diabetic Ketoacidosis:
Medical emergency that principally occurs in people with type 1 diabetes. It occurs when
the body starts breaking down fat at a rate that is much too fast. The liver processes the fat
into a fuel called ketones, which causes the blood to become acidic.
The cardinal biochemical features of DKA are:
Hyperglycemia
Hyperketonaemia
 Metabolic acidosis
Treatment:
• Insulin
• Fluid Replacement
• Potassium
• Bicarbonate.

18. Hyperglycaemic Hyperosmolar state
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• Hyperglycaemic hyperosmolar state (HHS) is characterised by severe
hyperglycaemia, hyperosmolality, and dehydration in the absence of
significant hyperketonaemia or acidosis.
• HHS, hyperglycaemia usually develops over a longer period (a few days to
weeks), causing more profound hyperglycaemia and dehydration.
• It typically affects elderly patients, but is seen increasingly in younger adults.
• Common precipitating factors include infection, myocardial infarction,
cerebrovascular events or drug therapy (e.g. corticosteroids).

19. Hypoglycaemia
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Blood glucose level less than 70mg/dL, occur as a result of treatment with insulin.
Symptoms Of ANS: Hunger, anxiety, sweating, palpitation, trembling.
Symptoms of neuroglycopenia:speech difficulty, drowsiness and poor cordination.
Treatment depends on its severity and on whether the patient is concious.
Oral fast acting carbohydrate, carbohydrate snacks is sufficient.

20. TESTING
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• URINE TESTING
o Testing the urine for glucose with dipsticks is a common screening procedure for
detecting diabetes.
o Ketone bodies can be identified by the nitroprusside reaction, which measures
acetoacetate, using either tablets or dipsticks.
o Ketonuria may be found in normal people who have been fasting or exercising
strenuously for long periods,
o Standard dipstick testing for albumin detects urinary albumin at concentrations
above 300 mg/L, but smaller amounts
• BLOOD TESTING
o Glucose
o Protein

21. Management of Diabetes
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Type 1: Urgent insulin therapy and prompt referral to a specailist.
Type 2: Advice about Dietary and lifestyle modification, followed be oral antidiabetic
drugs/insulin if needed.
Drugs to reduce Hyperglycemia:
Biguanides
sulphynylureas
TZDs(Thiazolidinediones)
Alpha-glucosidase inhibitors

22. Insulin Therapy
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In most patients, insulin is injected subcutaneously
several times a day into the anterior abdominal wall,
upper arms, outer thighs and buttocks.
s. It is removed mainly by the liver
and also the kidneys, so plasma insulin concentrations
are elevated in patients with liver disease or renal failure

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24. Life Style Modification
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• Undertaking regular physical activity
• Achieve adequate glycemic control
• Maintain adequate nutritional intake
• Reducing alcohol consumption
• Many people with type 2 diabetes require dietary advice for achieving weight loss, to
include caloric restriction and, in particular, reduced fat intake.

25. COMPLICATIONS
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Microvascular / Neuropathic level Macrovascular
Impaired vision Myocardial ischemia
Renal failure Myocardial infarction
Sensory loss Transient ischemic attack
Pain stroke
Motor weakness claudication
Ulceration ischemia
Arthropathy
Postural hypotension
Gastrointestinal problems

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DIABETIC
NEUROPATHY

27.  Nerve damage that can occur if you have diabetes.
 High blood sugar (glucose) can injure nerves throughout your body
 About 30% of patients with type 1 diabetes have developed diabetic nephropathy 20 years
after diagnosis
 Most common causes of end-stage renal failure in developed countries
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Diabetic Neuropathy

28. • Diabetic neuropathy causes substantial morbidity and increases mortality.
• Diagnosed on the basis of symptoms and signs, and after the exclusion of other causes of
neuropathy
• Affects between 50 and 90% of patients with diabetes, and of these, 15–30% will have
painful diabetic neuropathy (PDN).
• Like retinopathy, neuropathy occurs secondary to metabolic disturbance
• Prevalence is related to the duration of diabetes and the degree of metabolic control.
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Diabetic
Neuropathy(cont.)

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SIGNS & SYMPTOMS
• Pain
• Poor circulation
• Numbness or tingling in your fingers, toes, hands, and
feet
• Sharp pains or cramps.
• Increased sensitivity to touch

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CLASSIFICATION DIABETES NEUROPATHY
Somatic (peripheral)
• Polyneuropathy
• Symmetrical, mainly sensory and distal
• Asymmetrical, mainly motor and proximal (including amyotrophy)
• Mononeuropathy (including mononeuritis multiplex)
Visceral (autonomic)
• Cardiovascular
• Gastrointestinal
• Genitourinary
• Sudomotor
• Vasomotor
• Pupillary

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Symmetrical sensory polyneuropathy
• frequently asymptomatic.
• most common clinical signs are diminished perception of
vibration sensation distally
• loss of tendon reflexes in the lower limbs.
• In symptomatic patients, sensory abnormalities are
predominant.

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Symmetrical sensory
polyneuropathy(cont.)
Symptoms include
• paraesthesiae in the feet (and, rarely, in the hands)
• pain in the lower limbs (dull, aching and/or lancinating
• worse at night, and mainly felt on the anterior aspect of the
legs)
• burning sensations in the soles of the feet
• cutaneous hyperaesthesia
• an abnormal gait (commonly wide-based), often associated
with a sense of numbness in the feet.

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Asymmetrical motor diabetic neuropathy
• Also known as ( Diabetic amyotrophy )
• presents as severe and progressive weakness and
wasting of the proximal muscles of the lower
(and occasionally the upper) limbs.
• accompanied by severe pain, mainly felt on the
anterior aspect of the leg, and hyperaesthesia
and paraesthesiae.
• Tendon reflexes may be absent on the affected
side(s).

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Autonomic neuropathy
• not associated with peripheral somatic neuropathy.
• Parasympathetic or sympathetic nerves may be predominantly
affected in one or more visceral systems.
• Within 10 years of developing overt symptoms of autonomic
neuropathy, 30–50% of patients are dead, many from sudden
cardiorespiratory arrest.
• Patients with postural hypotension (a drop in systolic pressure
of 30 mmHg or more on standing from the supine position)
have the highest subsequent mortality.

35. Clinical features of autonomic neuropathy
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Cardiovascular
• Postural hypotension
• Resting tachycardia
• Fixed heart rate
Gastrointestinal
• Dysphagia, due to oesophageal atony
• Abdominal fullness, nausea and vomiting, unstable
glycaemia, due to delayed gastric emptying (‘gastroparesis’)
• Nocturnal diarrhoea
• Fecal incontinence

36. Clinical features of autonomic neuropathy
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Genitourinary
• Difficulty in micturition, urinary incontinence, recurrent
infection, due to atonic bladder
• Erectile dysfunction and retrograde ejaculation
Sudomotor
• Nocturnal sweats without hypoglycaemia
• Gustatory sweating
• Anhidrosis; fissures in the
feet

37. Clinical features of autonomic neuropathy
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Vasomotor
• Feet feel cold, due to loss of skin vasomotor responses
• Dependent oedema, due to loss of vasomotor tone and
increased vascular permeability
Bullous formation
Pupillary
• Decreased pupil size
• Resistance to mydriatics
• Delayed or absent reflexes to light

38. MANAGEMENT
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Pain and paraesthesiae from peripheral somatic
neuropathies
• Intensive insulin therapy (strict glycaemic control)
• Anticonvulsants (gabapentin, pregabalin, carbamazepine,
phenytoin)
• Tricyclic antidepressants (amitriptyline, imipramine)
• Other antidepressants (duloxetine)
• Substance P depleter (capsaicin – topical)
• Opiates (tramadol, oxycodone)
• Membrane stabilisers (mexiletine, IV lidocaine)
• Antioxidant (α-lipoic acid)

39. MANAGEMENT
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Postural hypotension
• Support stockings
• Fludrocortisone
• NSAIDs
• α-adrenoceptor agonist (midodrine)
Diarrhoea
• Loperamide
• Broad-spectrum antibiotics
• Clonidine
• Octreotide
Atonic bladder
• Intermittent self-catheterisation

40. MANAGEMENT
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Excessive sweating
• Anticholinergic drugs (propantheline, poldine, oxybutinin)
• Clonidine
• Topical antimuscarinic agent (glycopyrrolate cream)
Gastroparesis
• Dopamine antagonists (metoclopramide, domperidone)
• Erythromycin
• Gastric pacemaker; percutaneous enteral (jejunal) feeding
Constipation
• Stimulant laxatives (senna)

41. MANAGEMENT
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Erectile dysfunction
• Phosphodiesterase type 5 inhibitors (sildenafil, vardenafil,
tadalafil) – oral
• Dopamine agonist (apomorphine) – sublingual
• Prostaglandin E1 (alprostadil) – injected into corpus
cavernosum or intra-urethral administration of pellets
• Vacuum tumescence devices
• Implanted penile prosthesis
• Psychological counselling; psychosexual therapy

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DIABETIC FOOT

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DIABETIC FOOT
• Foot is the frequent site of complications in
patients with diabetes.
• Tissue necrosis in the feet is a common reason
for hospital admission in diabetic patient.

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ETIOLOGY
Aetiology of diabetic foot is :
• Due to trauma
• Peripheral neuropathy
• Ischemia

45. CLINCAL FEATURES OF DIABETIC FOOT
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NEUROPATHY ISCHEMIA
SYMPTOMS NONE
PARAESTHESIA
PAIN
NUMBNESS
NONE
CLAUDICATION
REST PAIN
STRUCTURAL DAMAGES ULCER
SEPSIS
ABSCESS
OSTEOMYELITIS
DIGITAL GANGRENE
CHARCOT JOINT
ULCER
SEPSIS
GANGRENE

46. Stages of diebetic
ulcer
• Grade 0 : No ulcer a high risk foot.
• Grade 1 : Superficial ulcer involving the full skin thickness but not underlying tissues.
• Grade 2 : Deep ulcers, penetrating down to ligament and muscles, but no bone
involvement or abscess formations.
• Grade 3 : Deep ulcers with cellulitis or abscess formation, often with osteomyelitis
• Grade 4 : Localized gangrene
• Grade 5 : Extensive gangrene involving the whole foot
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MANAGEMENT
• Antibiotics
• If gangrene is localized or extensive Surgical amputation will be done

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Care of the Diabetic Foot
Preventive advice to all diabetic patients includes:
• Inspect feet every day
• Wash feet every day
• Moisturize skin if dry
• Cut or file toenails regularly
• Change socks or stockings every day
• Avoid walking barefoot
• Check footwear for foreign bodies
• Wear suitable, well-fitting shoes
• Cover minor cuts with sterile dressings
• Do not burst blisters
• Avoid over-the-counter corn/callus remedies

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