CMP Presentation B6 - 2013

7/29/2019 CMP Presentation B6 - 2013

http://slidepdf.com/reader/full/cmp-presentation-b6-2013 1/27

Complications of Type II Diabetes

Lucinda

Helena

Rosie

Soumya

David (Thomas)



Aims

> Summarise the complications of diabetesmellitus.

> Describe pathophysiology of select

complications.> Describe some treatments available.



Treatments

● Leg stenting

● Hypertensive drugs

● Retinal LASER surgery – damage control

● Cataract surgery

● Endarterectomy

●

Metformin;● Formerly Tolbutamide



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.



●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



Stages of Diabetic Retinopathy:1 - Background Retinopathy



Stages of Diabetic Retinopathy:2 - Maculopathy



Stages of Diabetic Retinopathy:3 - Pre-Proliferative Retinopathy

IRMA



Stages of Diabetic Retinopathy:4 - Proliferative Retinopathy (PDR)



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).



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



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



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



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.



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



Neuropathy

Cause:

- pressure; ischemia; metabolic abnormalities

Types:

-pressure palsy; mononeuropathies; diffusesensory and autonomic polyneuropathy

Mechanisms:

- polyol pathway; protein glycation;

altered intracellular redox potential



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



Over activity of PolyolPathway

• Sorbitol and fructose accumulate in cells withincreased glucose

• Sorbitol and fructose diffuse slowly

•

Osmotic effects damage nerve cells



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



Umbrella term for….•

Diabetic foot ulceration• Diabetic foot infections• Neuropathic• osteoarthropathy of the foot



PVD + neuropathy + developinginfections + decreased ability to

clear infections = severe footproblems (e.g. infection, gangrene,amputation)



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



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



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.



Any Questions?

CMP Presentation B6 - 2013

Documents

Transcript of CMP Presentation B6 - 2013