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Diabetic complications
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There are many complications of diabetes, which can be divided into acute complications and chronic complications. Acute complications mainly include diabetic ketoacidosis (more common in 1 diabetes, and type 2 diabetes can also occur under stress) and diabetic hyperosmotic nonketotic coma (more common in type 2 diabetes). Chronic complications accumulate in various tissues and organs of the whole body, mainly including large blood vessels (such as cardiovascular and cerebrovascular diseases, kidneys and limb blood vessels), microvessels (such as diabetic nephropathy and diabetic retinopathy) and neuropathy (such as autonomic nerves and somatic nerves).
Diabetic patients with long course of disease and poor control are often accompanied by various complications or complications, and various infections are obviously complications; Ketoacidosis may be a serious manifestation of the deterioration of the disease; Pathology based on microangiopathy, such as nephropathy, fundus lesions and neuropathy, is an important chronic complication of diabetes. However, although macrovascular diseases, such as atherosclerosis, cardio-cerebral nephropathy and hypertension are closely related to diabetes, they can also be seen in non-diabetic patients. Whether it is a complication needs specific analysis.
(A) diabetic ketoacidosis and coma
(2) Diabetic nonketotic hyperosmotic coma
(III) Diabetic lactic acidosis
(4) The following people are common in infection:
1. Skin infections such as tinea corporis, pyogenic infections such as onychomycosis, tinea pedis, furuncle and carbuncle are very common, and sometimes lead to sepsis.
2. Tuberculosis, especially tuberculosis, once it occurs, spreads quickly and widely. The lesions are mostly exudative diehard pneumonia, which is easy to become empty. The incidence rate is 3 ~ 5 times higher than that of ordinary people, and fluctuates with the control of tuberculosis.
3. Urinary tract infection, in which pyelonephritis and cystitis are the most common, sometimes accompanied by fungal vaginitis, is difficult to control, and must be carried out at the same time as strict control of diabetes to achieve better curative effect. Necrotizing renal papillitis is rare in China.
4. Gallbladder, cholangitis, gallstones, periodontitis, gingival abscess and sinusitis.
(5) Cardiovascular disease has become the most serious and prominent problem among patients with this disease, accounting for more than 70% of the death causes of diabetic patients. The basic pathology is arteriosclerosis and microangiopathy. The incidence of atherosclerosis is much higher than that of ordinary people, which occurs earlier, progresses faster and is more serious. The incidence of cardiovascular diseases in domestic diabetic patients is lower than that reported abroad, especially myocardial infarction, angina pectoris and gangrene of limbs. The relationship between the pathogenesis of this group of diseases and the disease has not been clarified. Metabolic disorders such as lipids and mucopolysaccharides, especially the increase of blood drug concentrations such as triglycerides and cholesterol, and the decrease of HDL2-2 and ch, are often more serious than those in diabetic patients or non-diabetic patients, suggesting that lipid metabolic disorders in diabetes are an important factor in the pathogenesis of arteriosclerosis. In addition to coronary heart disease, diabetic cardiomyopathy has also received attention in recent years. 1 case in our hospital died of acute heart failure complicated with cardiogenic shock. No myocardial infarction was found in pathological anatomy, but the thrombus in coronary artery blocked most of the lumen, accompanied by extensive myocardial lesions (focal necrosis), which may be related to myocardial microvascular lesions. From the examination of cardiovascular autonomic nerve function, it is found that vagus nerve function is damaged in the early stage and tachycardia is easy to occur. In the later stage, sympathetic nerve may also participate in the formation of a transplanted heart similar to that without neuromodulation, leading to painless myocardial infarction, severe arrhythmia and frequent cardiogenic shock. Many cases of sudden death due to acute heart failure have been found in our hospital, so they are called diabetic heart disease, including diabetic cardiomyopathy, diabetic cardiovascular autonomic neuropathy and/or hypertension and atherosclerotic heart disease. Although it is still controversial at present, the WHO Diabetes Expert Group and most scholars have realized that noninvasive tests can be used to help early diagnosis in clinic, such as echocardiography, radionuclide examination of left heart function, myocardial imaging of dipyridamole radionuclide and R-R interval of electrocardiogram. Traumatic examination such as cardiac catheterization coronary angiography is more helpful for diagnosis. Animal experiments with BB rats, streptozotocin and alloxan further prove that the earliest manifestation of diabetic heart disease is myocardial damage. See pathology, its mechanism needs to be studied. The pathogenesis of microangiopathy includes many factors, such as hemorheological changes, high perfusion, high filtration, thickening of microvascular basement membrane, increased blood viscosity, abnormal coagulation mechanism and so on. In recent years, the microcirculation disturbance and non-enzymatic glycosylation of various plasma and tissue proteins, such as glycosylated hemoglobin HbA 1C, glycosylated lipoprotein, glycosylated collagen and increased production of free radicals, are closely related to the accumulation of advanced glycation end products (AGE), tissue damage and hypoxia.
(6) Diabetic nephropathy in a broad sense can include:
1. Diabetes-specific
(1) Diabetic glomerulosclerosis is nodular, diffuse and exudative.
(2) Diabetic renal tubular nephropathy.
2. Renal arteriosclerosis in diabetic patients (unique to non-diabetic patients).
3. Renal infection (unique to non-diabetic patients).
⑴ Pyelonephritis: ① Acute, ② Chronic.
(2) Necrotizing papillitis.
Typical diabetic nephropathy, more common in adolescents (type I), the incidence of about 2? Many years later, five years later, it is more certain. About 75% of patients suffered from this disease more than 20 years ago, so it is positively related to the length of the course of disease and is the main cause of death of type I patients. From modern renal transplantation, it is found that only two years after normal renal transplantation, the pathological changes such as hyaline arteriole suggest typical diabetic nephropathy. Pathological electron microscopy showed that the glomerular basement membrane was thickened and the matrix increased and expanded, which was closely related to the disorder of glucose metabolism. Human diabetic nephropathy can be divided into the following three groups.
Nodular type was first described by Kimmelstiel-Wilson in 1936, so it was later called Kimmelstiel-Wilson nodule (or syndrome) or nodular capillary diabetic glomerulosclerosis. In the anatomical records of 17% ~ 36% diabetic patients, it was found that the diameter around glomerular capillaries was 20 ~ 100? M's spherical nodules, containing PAS-positive glycoprotein, lipid and hemoglobin, form a reticular layered structure, showing onion-like multilayer fibrous reticular lesions, dyed red and glassy; Under the electron microscope, it can be seen that the substance in the basement membrane of the matrix is piled up or nodular, with hyaline degeneration in the late stage, telangiectasia in the early stage and occlusion in the late stage.
Diffuse type is characterized by thickening of capillary wall, eosin deposition on basement membrane, positive PAS staining, early lumen expansion, late lumen narrowing and finally occlusion. Because of the thickening of basement membrane, permeability and charge change are affected, microalbuminuria often leads to clinical proteinuria, and cells and casts are found by routine urine examination. This type can coexist with nodular type.
The exudative type is the least common, which appears after the above-mentioned type II lesions and begins with the deposition of transparent and crimson fibrin-like substances in the glomerular capsule cavity, which contain triglycerides, cholesterol and mucopolysaccharides and adhere to the surface of Bowman's capsule. Among the three types, diffuse type is the most specific for diabetes, and the other two types can also be seen in other diseases, especially exudative type.
The patient is asymptomatic at the earliest, and there is no albumin excretion in the urine, or; ; When the dosage is 500mg/d, the routine examination of urine protein is positive, and edema and renal insufficiency may appear clinically. By stage V, the patient is already in the stage of renal insufficiency or failure, accompanied by various manifestations of uremia.
(VII) Neuropathy can involve any part of the nervous system, collectively referred to as diabetic neuropathy. From the lesion site, pathogenesis, clinical manifestations and other aspects, it is classified as follows. ：
1. Peripheral neuropathy
(1) Symmetric peripheral neuropathy (also known as diabetic neuropathy).
(2) Asymmetric peripheral neuropathy (also known as unilateral neuropathy and multiple unilateral neuropathy).
⑶ Nerve root lesions.
2. Cranial neuropathy
3. Vegetative neuropathy (also called autonomic visceral neuropathy).
4. Spinal cord injury
(1) Diabetic myelopathy (also known as diabetic pseudotuberculosis).
⑵ Acute vascular syndrome, myelomalacia.
5. Diabetic neuropathy In the early stage of infantile neuropathy, the mother has no symptoms and signs, but only electrophysiological abnormalities. For example, 1980, about 90% of the newly diagnosed patients in our hospital have abnormal motor nerve conduction velocity, and most of them are asymptomatic.
Symmetric neuropathy has a slow onset and can involve peripheral nerves, including femoral nerve, superficial femoral nerve, sciatic nerve, sural nerve, median nerve, radial nerve, ulnar nerve and supralaryngeal nerve. Generally, the lower limbs are heavier than the upper limbs, and the distance between the long nerve and the sensory nerve is far away. Therefore, sensory disturbance is the main symptom in the early stage, including symmetrical calf or lower limb pain, burning pain or heartache, and sometimes severe pain such as amputation, which is more obvious at night, or chief complaint. Distribution, such as socks and gloves, has numbness, burning pain, acupuncture pain or the feeling of stepping on a cotton pad, such as insects crawling, ants walking, or electric shock, sometimes accompanied by hyperalgesia, and even the lid can't stand being pressed (needs support). After a long time, motor nerves are also involved, and muscle tension is often reduced, especially the muscles inside and outside the pelvis, such as psoas, gluteus, quadriceps femoris, hamstring and scapula. The lower limbs are often weak, it is difficult to stand and walk, and the upper limbs cannot be held high and rotated outwards. Hyperreflexia in the early stage and disappeared in the later stage. In severe cases, foot disease or even complete paralysis occurs, accompanied by muscle atrophy and ankle edema. All these symptoms are similar to beriberi. If diabetes can be controlled as soon as possible and actively treated, the motor nerve symptoms and conduction velocity of this group of patients can be easily relieved or returned to normal, but the long-term curative effect is poor, and some cases have an acute onset. In particular, unilateral nerves or muscles near the pelvic cavity and shoulders are more involved, including myalgia, tenderness, emaciation and weakness, and sensory disturbance. But the prognosis is good. Using insulin pump for 6 weeks can effectively treat peripheral neuropathy. The earlier the treatment, the better the prognosis. Diabetes was strictly controlled in our hospital for an average of 7.2 months, and most of them can recover after improvement.
Cranial nerve involvement is rare, and the third and sixth pairs are more common in one side. In addition to ophthalmoplegia, diplopia, ptosis, retrobulbar pain and ipsilateral headache are more common in patients over 50 years old with long-term onset, but they can recover in about 2 ~ 3 months if they can be treated early.
When autonomic nerve is involved, the pupil's light reflection disappears and contracts irregularly, but the adjustment is normal; Hyperhidrosis in the upper body and less sweating in the lower body; Postural hypotension (late manifestation), the heart rate increases faster and slower when standing up from the lying position, but increases faster when resting, often >; ; 90/ min, suggesting that vagus nerve function is impaired; Impotence, reverse ejaculation, male infertility, urinary retention or incontinence, dripping is not clean; Refractory diarrhea, constipation, lower extremity edema, etc. After bladder paralysis, it is easy to cause urinary tract infection, and the future trouble is often very serious.
The pathogenesis of neuropathy is still unclear. There are two groups of theories: metabolism and microvessels. The former can better explain symmetrical lesions, while the latter can explain unilateral lesions. Metabolic theory developed from early sorbitol theory to inositol theory. Recently, it is considered that the deficiency of Na+-K+-ATPase and protein kinase leads to various pathological changes, all of which are related to insulin deficiency and hyperglycemia. After early treatment, motor nerve conduction velocity and clinical symptoms can be recovered. However, inositol therapy is not effective, so it is suspected that glycosylated protein and lipid metabolism disorder may also be related. Microangiopathy that nourishes the nerve in unilateral neuropathy will cause pathological changes, but the two theories can complement each other and compound without contradiction.
Diabetic patients with eye diseases often complain of blurred vision. Of the 374 cases followed up in our hospital, 47% had cataracts, of which 16.5% had severe visual impairment or even blindness. Diabetic cataract is snowy opacity with lens cyst. If it's okay, it won't affect your vision much. For example, if the lens is completely turbid, there is often only light perception, and the latter is rare. More serious is retinopathy, accounting for 35.6%. In this group, the course of disease is less than 5 years in 28%, 6 ~ 10 in 36.4%,1~ 15 in 58.0% and15 in 72.7%. /kloc-is rare in people under 0/8 years old, and then it will increase with the course of disease and age, and the prevalence rate is low in those who are well controlled. It is now recognized that this kind of retinopathy can be divided into non-proliferative phase and proliferative phase. ① There are microaneurysms in the nonproliferative stage, and the capillaries are bag-shaped or spindle-shaped. Fluorescent angiography showed more microaneurysms than fundus examination. If microaneurysms leak, retinal edema can be produced, and deep macular hemorrhage and edema, hard exudation and lipid deposition can be seen. There are clear yellow-white boundaries, irregular exudation foci, piled up in piles and arranged in a ring shape. In addition, cotton-wool spots, dilated veins and twisted beads can be seen, suggesting severe retinal ischemia. ② Proliferative retinopathy is caused by the proliferation of many new blood vessels and fibrous tissues after vitreous hemorrhage, which can lead to retinal detachment, decreased vision, severe pain during initial hemorrhage of eyeball, followed by dark clouds and sparks in visual field, often causing blurred vision and even blindness.