Extensive and detailed clinical highlights on Diabetes Mellitus - atp skin care products
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A slender organ located next to the first part of the small intestine.
The pancreas that synthesized and secreted hormones.
More simply, it appears in the form of many small cell clusters called Langerhansor islands.
About 1 million islands.
The pancreas, the island, is considered relatively pale.
In the dark sea
Tissue staining of exsecretion.
Secretion of insulin. Islet cells.
The number of other endocrine cells in the body.
Not randomly distributed.
Island, surrounded by the "shell" of alpha and delta cells. islets cells.
Hormones can enter the blood circulation.
Although the island only includes 1-flow. glucagon.
Diabetes refers to the excretion of a large amount of sweet urine. âx80x9csweetâx80x9d.
Treatment is not ideal.
DM is marked by elevated blood sugar.
Chronic elevated blood sugar changes in different systems and organs of patients.
About 6000 tons of weight. Two sulfur bonds
Blood concentration of blood sugar
Promote the charge of glucose into the cell. (e. g. secretion.
Secretions are still fragile. transporter;
The concentration of glucose in B cells increased.
De-polarization and inflow of calcium outside the cell.
Vomiting of insulin
Contains secreted particles.
Conversion into a change in membrane conductivity.
Glucose in B cells seems to activate calcium as well.
Involved in insulin secretion.
It is easy to observe the release of insulin throughout an animal or person.
Each 100 ml is associated with a very low level of insulin secretion. dramatically.
It soon ran out badly. immediately.
There is also the transcription of insulin genes and the translation of their mRNA. blood sugar?
Michael Jackson? of a musician? metabolism.
It has an important impact on protein and mineral metabolism.
Many organs and tissuesacids).
The important target organs of insulin action are :-liver-muscles-adipocytes.
The brain and blood cells did not respond to insulin.
It is then absorbed into the blood.
Promote the absorption, utilization and storage of glucose by the human body.
The effect of insulin on glucose metabolism varies from target tissue to target tissue. include:1.
Promote the entry of glucose into muscle, fat and several other tissues. 2. glycogen . 3.
From glycogen (sugar decomposition) and from Amino
(Sugar generation ). As a result -well-
It should be meaningful, taking into account the above mechanisms. ceases.
Fatty acids of energy.
In the short term, this is provided from the sugar dollar reserve. active.
Below normal range.
Insulin and protein metabolism: 1.
Through the plasma membrane2.
Insulin stimulates protein synthesis. 3.
Insulin inhibitors of protein hydrolysis.
Fat and carbohydrates are closely intertwined.
Insulin also has an important effect on fat metabolism.
The effects of insulin on lipid metabolism include the following aspects: 1.
Promote the synthesis of fatty acids in the liver. 2.
The fatty acid is released by the hydrolysis of glycerin triacid. fat-sparing effect. tissue.
Insulin and nucleic acid metabolism: 1.
The formation of ATP, DNA and RNF. Other effects: 1.
Intracellular flow of potassium, phosphate and magnesium in the heart. 2. hypoglycemia).
The role of insulin can be reduced :-Sugar generation; -
Enter the blood from the digestive tract; -
Insulin resistance ); -: inhibits Î²-
Stimulate the secretion of glucose and hormone; -: Stimulation Î ±-by tissues; -
Stimulating the secretion of cortisolSecretion of cells; -
Inhibit the formation of fat from carbohydrates.
Little or no production at all (due to beta-vandalism
Through inflammation, autoimmune processes, or surgery ).
Insulin is produced but it does not work. next levels:-glycemia; -
The hormone that activates the original insulin (converted into insulin), and there is no enzyme; -insulin). chronic (long-. I.
Vascular complications of diabetes: 1.
Kidney disease; complications; 2) retinopathy;
Vascular complications of lower limbs. 2.
Coronary heart disease; major vascular complications;
2) vascular complications of lower limbs. II.
Diabetic Neuropathy: 1) Central (cerebral ); 2) peripheral;
(Visceral dysfunction ). The long-of DM.
There is a causal relationship with metabolic control level. retinopathy.
Causes of blindnessg.
Retinal detachment or bleeding ).
Type 2 DM patients at diagnosis.
Some degree of retinal diseasedilated. I.
Micro-aneurysm, hard and soft secretions ). II.
Edema and/or bleeding ). III.
The sign of this complication is the new blood vessel. e.
In low perfusion areas.
The retina is detached, the glass is bleeding, etc. poor. blind).
It is not clear whether it is related to retinal development.
Lipid, in particular, has been implicated. nephropathy.
Renal disease syndrome before the development of hematuria.
30-50% of patients with type 1 DM and a small proportion of patients with type 2 DM.
Histological injury of DM
Diabetic kidney disease in MogensenI. .
It is characterized :-
Increased circulation of kidney blood; -
(> 140 ml/min ); -
Mast kidney; -
Normal white urine ( 500 mg/day ); -
Normal or decreased renal function; -
Persistent high blood pressure)V. . .
It is characterized by signs of chronic renal failuredecreased GFR; -
High blood pressure; -
Increase of serum insides; -
Signs of poisoning
Affected (microvascular disease ).
Vascular complications of lower limbs. I. .
(Changes can only be found when the instrument is inspected. )II. . examination. )III. .
Characterized by trophyc changes: dry skin, dry skin
Ulcer and necrosis.
) Coronary heart disease. 1. same age. 2.
Non-diabetic patients are of the same age. 3.
To make matters worse, if there is a ketone poisoning or other complications of the DM. 4.
Not typical form (no pain ). 6.
Male: female = 1:1 (non-diabetic = 10:1 ). neuropathy.
Classification of diabetic neuropathy. I. and others. II.
(Radicloud neuropathhy ).
There are three types of Radicul neuropathy :-
Hyporeflexia, reduced reaction touch, burning of heel and sole.
It becomes shrinking, dry and cold, and hair loss may stand out.
Reactions to touch and pain can easily lead to burns and ulcers in the legs and toes. ); --
Super feeling; thigh;
It is common to lose weight. ); -
Abnormal root distribution. ). III.
Send a nerve signal to the proper muscles.
Like you do with your arms and legs, consciously control them. think about it.
Relax the muscle tissue.
What can hinder normal functions. :-
There is no bowel movement in the body of the esophagus. ); -
Vomiting, early satiety, stomach swelling, abdominal pain. ); -
Diarrhea, constipation, poor absorption and incontinence; :-
Arterial contraction); -involvement). :-
Dysfunction will have a profound impact on the quality of life.
Nerves that control bladder function.
Get up at night and often urinate or leak urine (incontinence ). .
Urinate and do not empty at all (keep ). .
Earlier than those without diabetes.
Do not intend to urinate, resulting in leakage of urine. infections.
Nerve or infection.
Men with diabetes range from 20 to 85%.
Persistent inability to erect is strong enough for sexual intercourse. erection.
Men with erectile dysfunction also suffer from undiagnosed diabetes.
Male erectile dysfunction without diabetes.
10 to 15 years earlier than men without diabetes. vessel disease.
Drugs, psychological factors, smoking and lack of hormones.
The doctor on this is the first step to getting help. conditions.
Medical examinations and tests may help to identify the cause.
Blood sugar control and hormone levels will be checked.
Change your life.
Check the erection while sleeping. ejaculation.
Nipple, not working properly.
A section of the body.
The body does not damage the bladder when urinating.
Ejaculate, or may be aware of this if there is a fertility problem.
His urine may be cloudy.
Reveal the presence of semen.
Related to retrograde ejaculation
Surgery or taking some pressure medicineintercourse.
Discomfort is likely to reduce sexual response or desire.
Drugs, certain prescriptions and excessesthe-
The problem of women. response.
Sexual response may decrease or disappear.
Orgasm can be produced.
Feet with no signs of edema or infection.
The longitudinal arch is wider, flipped, rotated and leveled.
The damage of the sensation of the pain body. Diabetic foot.
Neuropathy and infection.
Diabetic foot is divided :-ischemic; -neuropathy; -mixed. of long-
Adequate metabolic control.
Diabetic kidney diseasediabetes;
Non-additive retinal diseases :-times); -lovostatin); -trental); -
Vitamin B, A, E, PP; -anticoagulants;
Or proliferation of retinal diseases: light coagulation treatment.
Diabetic kidney disease1) low-
(The Daily protein content is less than 40g );
Inhibitor of ACF (renitec;
Treatment of hypertension; Transplant.
Vascular complications of lower limbsin foot care;
Nail exposure, weakened pulse, deformity;
Improve blood circulation.
1) the treatment of neuropathy includes preparation
Fatty acid (Berlition, Espa-liplipon, Tiogama), aldose enzyme inhibitor (sorbinil), multivitamin, Bento sodium,
(Inductotermia, magnitozerotherapy, etc ).
Several types of Visceral neuropathy :-
Go for surgery.
These methods have advantages and disadvantages.
Psychotherapy to reduce anxiety or solve other problems may be necessary. option. -
This improves muscle tension in the neck of the bladder. insemination. -
The specific problems and causes depend on the bladder.
It is called regular urination. urine.
Complete emptying of the bladder in the lower abdomen is also helpful.
Is the main problem that medicine or surgery can help. -, or insulin-
Absolute reduction in insulin
Individuals are prone to ketone disease under basic conditions.
It is usually when young, but it can happen at any age.
Take insulin every day to survive.
The pathogenesis of type 1 DM includes: 1.
The individuals with diabetes are HLA DR3, DR4 or DR3/DR4;
Provide protection for the development of type 1 DM ); 2. Disease process. 3.
Ultimate clinical onset of type 1 diabetes.
Type 1 DM development (Flier, 1986) I.
Genetic tendency or change of immunityÎ²-cellsII.
Environmental factors. III.
Cell destructionInsulinitisIV. of Î²-cells. V.
Obvious diabetes. VI. Total Î²-
Cell destructionÎ²-or non-insulin-
Accounting for 95-90% of the population with diabetes. gene locus.
Role in the development of disease.
The antibody destroys normal insulin, or changes in the insulin receptor ).
Clinical differences between type 1 and type 2 diabetes. 1. 2.
The beginning of the disease; 3. 4. 5. 6. 7. 8.
Season of disease onset: frequent autumn-9.
Connection to HBA10.
Insulin and C-levels11.
Cells: present in 80-12. 13. 14. Spreading: 10-1. 2. 3. 4. 5.
Weight: 80-obesity6. 7. 8. 9.
Connection to HBA10.
Insulin and C-levels
Peptide: Normal level often. 11.
Class B antibiotics12. 13. 14. Spreading: 80-1999)I.
Type 1 ofDM (destruction-
Mainly resulting in insufficient absolute insulin ):-autoimmune; -idiopathic. II.
No insulin resistance ). III.
Other specific types :-
-Genetic defectscells function; -
Genetic defect of insulin action-
Pancreatic disease; pancreatectomy;
Endocrine disease; -drug exposures; -
Infection and other diseasesIV.
Diabetes is defined as the first diagnosis of elevated blood sugar during pregnancy.
Diabetes can be type 1 or type 2 diabetes. mother.
Diet adjustment and insulin therapy. contrindicated. development1.
Factors or pre-disposal factors ):-
Family history of DM positive; -
People with a birth weight of 4, 0 kg or more; -
Women weighing more than 4 and 0 kg: = children born; anamnesis; -
High blood pressure;
Autoimmune disease; furunculosis;
Infection of monnuclear cell2.
Tolerance (potential DM ). 3. of DM. Severity of Dm1
Mild: 1) compensation that can be achieved by diet; is lessthan 8. 4 mmol/l;
Month) glucosurialessthan20 gr. /l (2 %);
Ketone disease does not work; long-be observed. 2.
Moderate: 1) compensation can be achieved by oral hypoglycemic drugs (patients with type 2 DM) or insulin (patients with type 1 DM;
2) serum glucose is 8 faster. 4 to 14. 0 mmol/l; to 40 gr. /l (2 âx80x93 4 %);
Ketone disease occurs; long-
Terminology (chronic) complications can be observed (but the final stage cannot be observed ). 3.
Achieved by insulin or oral hypoglycemic drugs;
2) the concentration of serum glucose is above 14, 0 mg/L;
More than 40 grams of glucose. /l (4 %);
Ketone disease is a common final stage in the long term.
There is a terminology (chronic) complexity.
Compensation stage: 1. Compensation. 2.
Compensation. 3. Decompensation.
Compensation phase. 1.
The patient has new complaints. 2.
The rapid serum glucose level is normal (but can be lower than 8.
Haven â x80 x99 t complicationsandunder11.
Length-0 Milli Moore/L of the patient
Term complications ). 3. absent. 4.
Fluctuations are below 4. 4-5.
5 cents/liter during the day. 5.
No Coma and pre-coma. 6.
Divided into stages of compensation. 1.
Patients may have new complaints. 2.
The serum glucose is almost High. 3.
Expressed in the letter. 4.
Glucose levels fluctuate by more than 4. 4-5.
5 cents/liter during the day. 5.
No pre-coma. 6.
Retirement stage: 1.
There is a coma or pre-coma. 2.