Diabetic retinopathy: signs of symptoms and causes

2021-01-25 12:00 AM

Symptoms of diabetic retinopathy are very important and need to be monitored carefully. The more severe the degree of diabetic retinopathy at diagnosis, the higher the risk of disease progression.

Describe

Diabetic retinopathy is a general term to describe eye diseases caused by complications of diabetes. Some of the terms and causes overlap with hypertensive retinopathy and share the same target path. In general, diabetic retinopathy can be divided into categories such as tables.

No progressive retinopathy

Cotton secretions

Retinal oedema, congestion, produces white, round, or patchy images.

Nodules and bleeding stains

Large, red dot, the boundary may or may not be clear.

Hard secretions

Lipids build up in the retina forming waxy white or yellow patches.

Micro aneurysm

Separate red circle spots.

Progressive retinopathy

Neoplasm of vessels from the papillary region or from existing blood vessels

Macular oedema

Thickening and oedema of the macula (can be seen at any stage of the disease including proliferative or non-proliferative retinopathy).

Board. Changes in diabetic retinopathy.

Causes

Diabetes.

Hypertensive retinopathy can cause a number of similar complications.

Mechanism

The mechanism behind these changes is complex and is currently not well known. Chronic hyperglycemia is thought to be the main driver of diabetic retinopathy, which starts with a series of changes that ultimately lead to two major medical conditions:

Vascular permeability changes - blood vessels rupture or just "leak".

Retinal anemia is associated with vascular neoplasm.

These changes are related to the visual field, macular oedema, and diabetic proliferative retinopathy.

However, there are many different diseases that contribute to the progression of these two conditions.

Element

Consequence

Chronic hyperglycemia.

High blood sugar disrupts the retinal blood flow regulation - leading to increased blood flow, increased pressure in the retinal blood vessels. The vasomotor are synthesized, resulting in increased capillary permeability and macular oedema. Contributes to the production of sorbitol.

Sorbitol.

Sorbitol is a metabolite product of glucose. Excess sorbitol alters cell-damaging osmosis and changes other protein structures - leading to increased vascular permeability.

End products of the glycosylation process.

Excess glucose binds to amino acids and proteins inactivating important enzymes and altering cellular proteins, forming oxidative radicals, and causing inflammatory responses. Hence blood vessel damage and anemia. In addition, glucose is attached to collagen causing microvascular complications.

Endothelial growth factor (VEGF).

VEGF is caused by a lack of tissue oxygen in the retina and can cause a rupture of the blood-retinal barrier, leading to macular oedema. VEGF is also a major factor in creating new blood vessels in proliferative retinal damage.

Inflammatory reaction.

The adhesion of leukocytes to the capillary walls impedes the flow of blood, aggravating the lack of tissue oxygen. May cause rupture of the blood-retinal barrier and macular oedema.

Micro thrombosis.

Lead to retinal capillary blockage, anemia, and capillary secretion. The secretion phenomenon stimulates many growth factors including VEGF.

Another factor.

Pigmentation - The factor is derived from the epithelium.

Growth Factor and IGF-1.

Oxidative radicals.

Board. Mechanisms and factors that influence diabetic retinopathy.

Mechanism of diabetic retinopathy

Figure. Mechanism of diabetic retinopathy

Meaning

Symptoms of diabetic retinopathy are very important and need to be monitored carefully. The more severe the degree of diabetic retinopathy at diagnosis, the higher the risk of disease progression; That further confirms the importance of blood sugar control. Hypertrophic retinopathy and macular oedema are treatable in most cases prior to blindness, suggesting that symptom detection and control is important in any case.

Image of a microaneurysm in diabetic retinopathy without proliferation. 

Figure. Image of a microaneurysm in diabetic retinopathy without proliferation. 

Small hemorrhagic spots, microaneurysms, hard secretions (lipids), fern-shaped corneal ulcers, retinal microvascular abnormalities, and macular oedema. B Angiogram of fundus fluorescence retina is shown in figure A. Aneurysms are hyper-fluorescent spots, but hemorrhagic nodules do not increase fluorescence. The avascular area in the fovea is only minimally enlarged.

Non-proliferative retinopathy with hemorrhagic lesions, splinter hemorrhages, and cotton secretions.

Figure. Non-proliferative retinopathy with hemorrhagic lesions, splinter hemorrhages, and cotton secretions.

Diabetic retinopathy is heavily proliferated with cotton secretions, retinal microvascular abnormalities, and venous bleeding.

Figure. Diabetic retinopathy is heavily proliferated with cotton secretions, retinal microvascular abnormalities, and venous bleeding.

The changes related to diabetic retinopathy are seen in:

Most patients have had type 1 diabetes for more than 20 years.

80% of patients have type 2 diabetes over 20 years.

After 10 years, progressive retinopathy is found in 50% of type 1 diabetics and in 10% of type 2 diabetics.

The clinician can assess the patient's vision to assess the danger of retinopathy. The points found are:

Macular oedema is rarely detected by a non-specialist.

Using fundoscopy, the patient's pupils dilated with a specificity of 53-69% when the worker was a non-specialist and the specialist up to 91–96% with a PLR of 10.2.

Studies suggest that the symptoms of diabetic retinopathy are difficult to detect by a doctor who is not an ophthalmologist.

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