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Diabetes Complications – Symptoms & Cause

1. Diabetes Complications, as a Chronic Disease

Diabetes Complications can be a direct cause of death. Diabetes mellitus refers to a group of diseases that affect how your body uses blood sugar (glucose). Glucose is vital to your health because it’s an important source of energy for the cells that make up your muscles and tissues. The conclusion is that the prognosis in diabetes is burdened by complications and that these complications are still very dangerous to health and life.

1.1 – Microangiopathy

Microangiopathy is defined as the pathological process that is specific to diabetes, which takes place within the capillary system and in the smallest arteries and veins. It involves degenerative changes in the capillaries, especially within the retina and kidneys”.

It is a disease that affects the smallest blood vessels, i.e. microcirculation.

In the course of the disease, initially, there are morphological changes (mainly in the thickening of the basal membrane of tissue capillaries) and then functional capillaries (the permeability of the capillary walls increases, blood flow and intravascular pressure increase, blood viscosity increases, and the function of platelets and vascular endothelium increases). Functional changes appear before the organ changes that are the result of microangiopathy. Three pathogenetic mechanisms are of fundamental importance in the pathogenesis of microangiopathy: metabolic, hemodynamic, and genetic factors.

 1.2 – Diabetic Retinopathy

 Diabetic retinopathy is one of the main complications of microangiopathy, as it most often manifests itself by damaging the blood vessels of the eye’s retina. The changes it causes develop in direct proportion to the duration of Diabetes Complications and its type. Hyperglycaemia and hypertension play a major role in the pathogenesis. The processes leading to an increase in oxidative stress and the excessive production of growth factors are also important. The process of retinopathy is quite rapid, with veins initially dilating the retina, then the walls of small arterioles are damaged with subsequent formation of microaneurysms. Another element is the closing of the lumen of the arterioles before the retinal capillaries. As a result, neovascularization develops, i.e. the formation of new pre-retinal and blood vessels within the optic nerve. Weakened vessels burst, creating bloody effusions also into the retina. This process leads to deeper and deeper eye damage, up to irreversible blindness.

1.3 – Diabetic nephropathy

Diabetic nephropathy manifests as progressive glomerulopathy, manifested by proteinuria, nephrotic syndrome, and later symptoms of chronic renal failure. This complication is the result of damage to the glomerular capillaries of the kidneys, which leads to damage to the renal parenchyma. The pathogenesis of nephropathy includes many causal factors, but the most important are metabolic, hemodynamic, and genetic factors. The undiagnosed and untreated complication may be the cause of patient death

1.4 – Cardiac microangiopathy

Long-term diabetes causes degenerative changes not only in the capillaries and small vessels of the retina or kidneys but also in the whole organism. If a complication affects the heart, cardiac microangiopathy develops. Capillaries and arterioles of the heartless than 100 nm in diameter are involved.

1.5 – Nervous microangiopathy.

The possibility of developing nervous microangiopathy in people with type 2 diabetes is as possible as other microangiopathies. In chronically ill people, microangiopathy-dependent changes in the brain and other parts of the nervous system can be detected. These changes are analogous to those in the area of ​​small vessels of the kidneys, retina, and heart. They are responsible for small cerebral infarctions, the cavernous state of the brain, subcortical infarcts, and other scattered post-infarction in the area of ​​the cerebellum or brain stem.

1.6 – Diabetic macrovascular disease

Diabetic macrovascular disease describes a group of diseases characterized by organ damage resulting from degenerative changes in medium and large arteries. The clinical forms of diabetic macrovascular disease are ischemic heart disease, stroke, and lower limb obliterating atherosclerosis. The process of vascular damage is associated with the coexistence of hyperglycemia, hyperlipidemia, hyperinsulinemia, insulin resistance, oxidative stress, and chronic inflammation.

 1.7 – Diabetic foot syndrome

 Diabetic foot syndrome develops as a result of changes in the blood vessels and damage to nerve fibers (neuropathy). The formation of these changes is favored by poor Diabetes Complications control. Initially, vascularization changes, atherosclerosis develops, hardened arterioles, and the arteries become obstructed. Microangiopathy of the foot tissues develops, soft tissues and bones are ischemic, necrotic foci (infected or not infected) are formed. Then there are changes in the foot innervation.

1.8 – Neuropathy causes loss or Impairment of innervation:

Neuropathy causes loss or impairment of innervation: Sensory (loss or weakening of the sensation of pain, temperature, touch, vibration), motor (foot muscle tension and movement are impaired, muscle atrophy), autonomic (impaired blood flow through the foot), and joint trophic disorders. In an advanced process, changes occur in the skin, which becomes pale, thin, dry, easily cracked, and inelastic. Hair loss, nail growth is disturbed, calluses and necrotic foci appear until deep ulceration and infection develop. Often there are bone changes, atrophy, necrosis, or serious deformation. This complication leads to injuries and permanent disability usually ends with amputation.

Diabetic neuropathy refers to a wide variety of clinical syndromes including damage to the brain, peripheral nerves, and the autonomic system. These injuries develop as a result of degenerative processes dependent on microangiopathies, such as ischemia, infarcts, or microinfarcts, and as a result of metabolic disorders in the nervous tissue. In the course of neuropathy, the peripheral nervous system may be damaged in any of its segments.

2.  Hypoglycemia (hypoglycemia)

Hypoglycemia is also known as hypoglycemia. It is a condition in which the concentration of glucose in the blood (other than the portal vein ) falls below the standard. Full symptomatic hypoglycemia usually develops at levels below 2.2 mmol / L (40 mg / dL). However, symptoms onset earlier, at concentrations below 2.8 mmol / L (50 mg / dL). In long-term diabetics, these values ​​may increase, and hypoglycemia may be the direct cause of death.

2.1 – The symptoms of low blood sugar are:    

  • Trembling (e.g. of the hands)
  • Dizziness
  • Increased sweating
  • Feeling hungry
  • Headache
  • Pale skin
  • Sudden changes in mood or behavior, such as crying for no apparent reason
  • Awkward or jerky movements
  • Fainting
  • Attention problems, confusion
  • Tingling around the mouth hyperglycemia

2.2 – Hyperglycemia is in contrast to hypoglycemia high blood sugar

A sugar level that is too high is when the fasting glucose level is above 110 mg% and after a meal is above 160 mg%. At concentrations above 250 mg%, ketoacidosis may also occur, manifested by the presence of ketone bodies in the urine, a by-product of the body’s energy production from fats. The most common reason is poorly controlled diabetes. In people with Diabetes Complications, this can be due to insufficient insulin, overeating, insufficient physical activity, illness, infection, injury, or surgery. Hyperglycaemia can lead to diabetic coma.

2.3 – The symptoms of hyperglycemia are:  

  •  Thirst
  • Sleepiness
  • Apathy
  • General Fatigue
  • Shallow Breathing
  • Vomiting
  • Headaches
  • The Last Stage – Coma


  1. https://www.diabetes.org/diabetes/complications
  2. https://www.cdc.gov/diabetes/library/features/prevent-complications.html

prevention diabetes complications


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Written by Dr. Ozair (CEO of SignSymptom.com) as physician writers are physicians who write creatively in fields outside their practice of medicine.

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