cmp presentation b6 - 2013
TRANSCRIPT
7/29/2019 CMP Presentation B6 - 2013
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Complications of Type II Diabetes
Lucinda
Helena
Rosie
Soumya
David (Thomas)
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Aims
> Summarise the complications of diabetesmellitus.
> Describe pathophysiology of select
complications.> Describe some treatments available.
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Treatments
● Leg stenting
● Hypertensive drugs
● Retinal LASER surgery – damage control
● Cataract surgery
● Endarterectomy
●
Metformin;● Formerly Tolbutamide
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Diabetic Retinopathy
Damage to the retina of the eye.
On-going inflammation and vascularremodelling may occur over periods of
time where the patient is not fully aware of
the extent of the disease.
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●Almost invariably asymptomatic untilpatient has catastrophic intraocular sight-threatening haemorrhage.
●
Retinopathy is treatable.●Symptoms of more advanced stages of the disease:
●
Floaters● Distortion
● Blurred vision
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Stages of Diabetic Retinopathy:1 - Background Retinopathy
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Stages of Diabetic Retinopathy:2 - Maculopathy
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Stages of Diabetic Retinopathy:3 - Pre-Proliferative Retinopathy
IRMA
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Stages of Diabetic Retinopathy:4 - Proliferative Retinopathy (PDR)
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CARDIOVASCULAR
COMPLICATIONS> Coronary heart disease is recognized to be the cause of deathfor 80% of people with diabetes, however, the NHS states thatheart attacks are largely preventable.
> Both type 1 and type 2 diabetics are at greater risk of developing heart disease.
> Serious cardiovascular disease may develop in diabetics beforethe age of 30 (does NOT only affect the middle-aged and elderly).
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Symptoms include:• Pain in the chest• Shortness of breath•
Arrythmias• Swelling of ankles
Complications are macrovascular,revolve around atherosclerosis andinclude:
• Ischaemic heart disease• Stroke• Peripheral Vascular Disease
• Hypertension• Myocardial Infarctions
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There are several ways in which cardiovascularcomplications can be increased by diabetes.
1) Increased VLDL’s cause increased blood
coagulation by activation of factor VII.
2) Impaired Endothelial Function
Effects:• Reduced release of NO, therefore greater
arterial contraction and reduced blood flow.• Increased platelet aggregation due to lack of
NO.•
• May be caused by:• Effects of increased VLDL’s• Osmotic effects of glucose• Modification of LDL’s
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3) Modification of Lipoproteins
As well as collagen, LDL can also be glycated non-
enzymatically.
This leads to cross-linking of LDL to matrix protein in thearterial intima.
Therefore causing deposition of LDL.
Macrophages in atherosclerotic plaque accumulate lipids asthey can recognize modified lipoproteins:
They have receptors for AGEP’s called RAGE
Leads to the uptake and accumulation of modified
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4) Proliferation of Smooth Muscle Cells
Part of development of atherosclerosis due to:
• Activation of macrophages (which take upLDL’s)
• Release of chemokines and growth factorsfrom macrophages
5) Hyperinsulinaemia
In some Type 2 diabetics this may also have
independent effects which enhance atherosclerosis.
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People with diabetes and signs of coronary heart diseasewill be advised to make lifestyle changes such asstopping smoking, eating a healthy, balanced diet
and incorporating physical activity into their lives.
In general, severity can be controlled by tight control of blood glucose.
Medication may also be prescribed. Common medicationsfor treating heart disease include:
• ACE inhibitors
•
Calcium channel blockers• Statins
• A low dose of aspirin
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Neuropathy
Cause:
- pressure; ischemia; metabolic abnormalities
Types:
-pressure palsy; mononeuropathies; diffusesensory and autonomic polyneuropathy
Mechanisms:
- polyol pathway; protein glycation;
altered intracellular redox potential
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Protein glycation in nerves
• AGE in endothelial cells of endoneural microvessels
• Decrease cytoskeletal activity, induced protein
aggregation in cytoplasm, alter ligands for cellsurface receptors
• AGE modified peripheral nerve myelinsusceptible to phagocytosis leading to
demyelination• Glycation of extracellular matrix proteins
impairs regeneration
•
Oxidative stress compounds actions
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Over activity of PolyolPathway
• Sorbitol and fructose accumulate in cells withincreased glucose
• Sorbitol and fructose diffuse slowly
•
Osmotic effects damage nerve cells
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Effects• Distal symmetrical sensory and autonomic
neuropathy• Disabling pain from paraesthesia
• Focal neuropathies
•
Autonomic neuropathy:• Diarrhoea/gastroparesis
• Postural hypotension
• Respiratory arrest
• Cardiovascular
(early vagal; later sympathetic denervation)
Gustatorysweating
Urinary retention
Impotence
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Umbrella term for….•
Diabetic foot ulceration• Diabetic foot infections• Neuropathic• osteoarthropathy of the foot
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PVD + neuropathy + developinginfections + decreased ability to
clear infections = severe footproblems (e.g. infection, gangrene,amputation)
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Aetiology
• Foot ulcers due to ischemia &/or
neuropathy
•
Sensory deficits and application of abnormal forces
• Initiating injury (e.g. thermal trauma, ill
fitting shoes)
• Weak skin
•
Defective healing
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Charcot foot“A neuro-arthropathic processwith osteoporosis, fracture, acute inflammationand disorganisation of foot architecture”
Slight trauma fracture of a weakened bone
increased on adjacent bones gross destruction
persisting deformity increased risk of secondary
ulceration.
• Limb threatening or life threatening
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Summary
● Multiple complications arise from poorlycontrolled diabetes mellitus.
● Pre-dominantly PVD –
Micro/Macrovascular Disease● Co-morbidities
● Controlled, reduced morbidity and
mortality, but not to level of normalpopulation (Type II)
● Prevention of complications – lower blood
glucose.
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Any Questions?