Diabetes mellitus type II

1. SOEPEL
Diabetes mellitus type II
Abdul Waris Khan
Dept: Internal medicine

2. SOEPEL
• Subjective: A 48 years old female presented to
ER with blurring of vision and numbness in the
feet and legs.
• H/O presenting illness: she is known to be
diabetic for 15 years and the glycaemic control
is poor.

3. • Objective: physical exam
• Evaluation: Complication of DM, MS
• Plan: CBC, FBG, HbA1c, OGTT
• Elaboration: management of DM &
complications
• Learning goals: Complications of DM type-II

4. Definition
• Type 2 diabetes mellitus (NIDDM) consists of
an array of dysfunctions characterized by
hyperglycemia and resulting from the
combination of resistance to insulin action
and/or inadequate insulin secretion.

5. Epidemiology
• Type 2 diabetes is relatively common in all populations enjoying an
affluent lifestyle.
• The four major determinants are:
– increasing age,
– obesity,
– ethnicity
– family history.
• In poor countries diabetes is a disease of the rich, but in rich
countries it is a disease of the poor, obesity being the common
factor.
• 25–50% of patients already have some evidence of vascular
complications at the time of diagnosis.

6. • The onset may be accelerated by the stress of
pregnancy, drug treatment or coexisting illness.
• The overall prevalence within the UK is 2–3%, and
the lifetime risk is around 15%.
• Type 2 diabetes is 2–4 times as prevalent in
people of South Asian, African and Caribbean
ancestry who live in the UK.
• Obesity increases the risk of type 2 diabetes 80–
100 fold.

7. • Type 2 diabetes is associated with central
obesity, hypertension, hypertriglyceridemia, a
decreased HDL cholesterol.
• Insulin resistance is strongly associated with
many of these variables, as is increased
cardiovascular risk

8. Aetiology
• Exact cause is unknown, but following maybe responsible:-
• Genetics:
– Identical twins of NIDDM have almost 100% chance of developing
diabetes. About 25% of patients have first degree relative with NIDDM
• Environmental factors:
– lifestyle, overeating when specially combined with obesity acts as
diabetogenic factor (increasing resistance to action of insulin)
• Pancreatic pathology:
– Reduction of insulin secretion cells
– Resistance to insulin action
– delayed insulin secretion in response to oral glucose

9. Clinical features
• Most patients are asymptomatic
• May present with lethargy, delayed wound
healing, visual blurring, infections pruritus vulvae
or balanitis.
• Complications may be the first presenting
feature:
– Infections
– Deterioration of vision

10. Investigations

12. Complications
• The major cause of death in treated patients is
due to cardiovascular problems (70%)
followed by renal failure (10%) and infections
(6%).
• The duration and degree of hyperglycaemia
play a major role in the production of
complications.

13. Complications of DM
Macrovascular Microvascular

14. Macrovascular
• The central pathological mechanism in
macrovascular disease is the process of
atherosclerosis, which leads to narrowing of
arterial walls throughout the body.
– Stroke
– Coronary artery disease
– Peripheral vascular disease

16. Microvascular
• Small blood vessels throughout the body are
affected but the disease process is of
particular danger in three sites:
• Retina
• Renal glomerulus
• Nerve sheaths.

17. Retinopathy
• Diabetic retinopathy increases with the length
of diabetes, 20% will have retinal changes
after 10 years, rising to 80% after 20 years.
• In type 2 diabetes the progression is much
slower and initially in the macular and
paramacular region. These changes are
associated with macular oedema and
consequent loss of vision.

20. Nephropathy
• Clinical nephropathy secondary to glomerular
disease usually manifests 15–25 years after
diagnosis of diabetes and affects 25–35% of
patients diagnosed under the age of 30 years.
It is the leading cause of premature death in
young diabetic patients.

21. The earliest functional abnormality in the diabetic kidney is renal
hypertrophy associated with a raised GFR and is related to poor
glycaemic control.
As the kidney becomes damaged by diabetes, the afferent arteriole
(leading to the glomerulus) becomes vasodilated to a greater extent
than the efferent glomerular arteriole. This increases the
intraglomerular filtration pressure, further damaging the glomerular
capillaries and leading to mesangial cell hypertrophy.
This process eventually leads to glomerular sclerosis.
The initial structural lesion in the glomerulus is thickening of the
basement membrane. Associated changes result in disruption of the
protein cross-linkages which normally make the membrane an
effective filter.
In consequence, there is a progressive leak of large molecules
(particularly protein) into the urine.

23. Neuropathy
• Diabetes can damage peripheral nervous tissue in a number of
ways. The vascular hypothesis postulates occlusion of the vasa
nervorum as the prime cause. Since hyperglycaemia leads to
increased formation of sorbitol and fructose in Schwann cells,
accumulation of these sugars may disrupt function and structure.
• The earliest functional change in diabetic nerves is delayed nerve
conduction velocity; the earliest histological change is segmental
demyelination, caused by damage to Schwann cells.
• In the early stages axons are preserved, implying prospects of
recovery, but at a later stage irreversible axonal degeneration
develops.

24. • The following varieties of neuropathy occur:
• Symmetrical mainly sensory polyneuropathy (distal)
• Acute painful neuropathy
• Mononeuropathy and mononeuritis multiplex
• (a) cranial nerve lesions
• (b) isolated peripheral nerve lesions
• Diabetic amyotrophy (asymmetrical motor diabetic neuropathy).
• Autonomic neuropathy.

25. Symmetrical mainly sensory polyneuropathy
• This is often unrecognized by the patient in its
early stages.
• Early clinical signs are loss of vibration sense, pain
sensation and temperature sensation in the feet.
•
• At later stages patients may complain of a feeling
of ‘walking on cotton wool’ and can lose their
balance when washing the face or walking in the
dark owing to impaired proprioception.

26. Acute painful neuropathy
• A diffuse, painful neuropathy is less common.
• The patient describes burning or crawling pains in the feet,
shins and anterior thighs.
• These symptoms are typically worse at night, and pressure
from bedclothes may be intolerable.
• It may present at diagnosis .
• It usually remits spontaneously after 3–12 months if good
glycemic control is maintained.

27. Mononeuritis and mononeuritis multiplex
(multiple mononeuropathy)
• Any nerve in the body can be involved in diabetic
mononeuritis; the onset is typically abrupt and
sometimes painful.
• Isolated palsies of nerves to the external eye
muscles, especially the third and sixth nerves, are
more common in diabetes.
• Full spontaneous recovery is the rule for most
episodes of mononeuritis over 3–6 months

28. Diabetic amyotrophy
• This condition is usually seen in older men with diabetes.
Presentation is with painful wasting, usually asymmetrical,
of the quadriceps muscles or occasionally in the shoulders.
• The affected area is often extremely tender.
• Diabetic amyotrophy is usually associated with periods of
poor glycaemic control and may be present at diagnosis.
• It often resolves in time with careful metabolic control of
the diabetes.

29. Autonomic neuropathy
• Asymptomatic autonomic disturbances can be
demonstrated on laboratory testing in many
patients, but symptomatic autonomic neuropathy
is rare. It affects both the sympathetic and
parasympathetic nervous systems and can cause
disabling postural hypotension.
– Cardiovascular system
– GIT system
– Bladder involvement
– Male Erectile dysfunction

30. References
• Kumar and Clarks clinical medicine 7th edition
• Emedicine.medscape.com