Know about hypoglycemia, lengthiness your life (KISUKARI CHA KUSHUKA)

Hello did you  about  hypoglycemia? 

Hypoglycemia has been  a critical problem in now days, and it has more effects and allot of complications, this may be due to ignorance of people, they fail to manage it, finally it lead to death, Today gammaLOVE  want to make you clear about hypoglycemia, hope after passing through this you will not be the same again even your life span will  increased

( gammaLOVE THE LOVE OF HUMANITY)

 Hypoglycaemia is a clinical situation characterized by a reduction in plasma glucose concentration to a level that may induce
symptoms or signs such as altered mental status and/or sympathetic nervous system stimulation it associate with low plasma glucose level below  50 mg/dL


    EPIDEMIOLOGY of hypoglycemia
 AGE
 o Symptoms of hypoglycaemia are fewer in elderly persons and they frequently appear at a lower threshold of plasma glucose than in younger persons.
  oInsulin-producing tumours:
Gender:
     Reactive hypoglycaemia is reported most frequently by women aged 25-35 years. Other causes of hypoglycaemia are not associated with a gender preference.

The average age of a patient diagnosed with an insulinoma is the early 40s but cases have been reported in patients ranging from birth to age

 80 years.

Incidence:
The true prevalence of hypoglycaemia with blood sugar levels below 50 mg/dL generally occurs in 5-10% of people presenting with symptoms suggestive of hypoglycaemia.
The incidence of hypoglycaemia in a population of people with diabetes is very different from that in a population of people without diabetes.


Causes:
1.Drugs:

• Insulin.• Quinine.• Lithium.• Isoniazid. • Methanol.• Salicylates.• Didanosine. • Haloperidol.• Pentamidine.• Trimethoprim.•Chlorpromazine.• Cytotoxic agents.• Thiazide diuretics.• Tricyclic antidepressants.• Oral hypoglycaemics drugs.• Sulphonamides ("sulphur drugs").

• Angiotensin converting enzyme inhibitors.

• Ethanol (including propranolol plus ethanol).

• Organophosphates and carbamate insecticides.

                                         • Disodium ethylenediaminetetraacetic acid (EDTA).

2. Endogenous insulin secretion:

A. Insulin-producing tumours of pancreas:
       Islet cell adenoma or carcinoma (insulinoma) is an uncommon and usually curable cause of fasting hypoglycaemia most often diagnosed in adults.
o Carcinomas account for only 10% of insulin-secreting islet cell tumours.
•Age:
o Insulinomas are uncommon in persons younger than 20 years and are rare in those younger than 5 years.

•Gender: Approximately 60% of patients with insulinoma are female.
Cause:
• It may occur as an isolated abnormality or as a component of the multiple endocrine neoplasia type-1 (MEN-1) syndromes.
• Hypoglycaemia in patients with islet cell adenomas results from uncontrolled insulin secretion, which may be clinically determined during fasting and exercise.

B. Non-beta-cell tumours:
• Hypoglycaemia may also be caused by large non-insulin-secreting tumours, most commonly retroperitoneal or mediastinal malignant mesenchymal tumours. 
• Pathophysiology:
The tumour secretes abnormal insulin-like growth factor-II (large IGF-II), which does not bind to its plasma binding proteins. This increase in free IGF-II exerts hypoglycaemia through the IGF-I or the insulin receptors. 
• Treatment and prognosis: 
The hypoglycaemia is corrected when the tumour is completely or partially removed and usually recurs when the tumour re-grows. 

3. Reactive hypoglycaemia:
A. Idiopathic reactive hypoglycaemia:
Idiopathic reactive hypoglycaemia is an alimentary hypoglycaemia occurring in patients who have had previous upper gastrointestinal surgical procedures such as:

• Vagotomy. • Pyloroplasty.• Gastrectomy.• Gastrojejunostomy.

They allow rapid glucose entry and absorption in the intestine, provoking excessive insulin response to a meal. This may occur within 1-3 hours after a meal.
Very rarely it may occur in patients who have not had GI operations.

B. Congenital enzyme deficiencies reactive hypoglycaemia:
• Galactosaemia.
• Hereditary fructose intolerance.
• Leucine sensitivity of childhood.
In hereditary fructose intolerance and galactosaemia, an inherited deficiency of a hepatic enzyme causes acute inhibition of hepatic glucose output when fructose or galactose is ingested respectively.
Leucine provokes an exaggerated insulin secretory response to a meal and reactive hypoglycaemia in patients with leucine sensitivity of childhood.

4. Fasting hypoglycaemia:
Causes of fasting hypoglycaemia usually diagnosed in infancy or childhood include:
A. Nesidioblastosis:
Incidence:
It is a rare cause of fasting hypoglycaemia in infants and an extremely rare cause in adult.

Cause:
• This condition is characterized by a diffuse budding of insulin-secreting cells from pancreatic duct epithelium and pancreatic microadenomas of such cells.
• Several cases of nesidioblastosis were reported recently after gastric bypass surgery.

B. Inherited liver enzyme deficiencies that restrict hepatic glucose release:

• Phosphorylase. • Glycogen synthetase. • Pyruvate carboxylase.  • Glucose-6-phosphatase.• Fructose 1, 6-diphosphatase.• Phosphoenolpyruvate carboxykinase.

C. Inherited defects in fatty acid oxidation, including that resulting from systemic carnitine deficiency and inherited defects in ketogenesis (3-hydroxy-3-methylglutaryl-CoA lyase deficiency):
• They cause fasting hypoglycaemia by restricting the extent to which non-neural tissues can derive their energy from plasma free fatty acids (FFA) and ketones during fasting or exercise.
• This results in an abnormally high rate of glucose uptake by non-neural tissues under these conditions.

5. Factitious hypoglycaemia:
Secret sulfonylurea use/abuse for an intention of causing self-induced hypoglycaemia can be seen in healthcare workers or in relatives who care for diabetic family members at home.

6. Others:• Artefact.• Starvation.• Pregnancy. • Hypopituitarism.• Renal glycosuria.• Chronic renal failure.• Adrenal insufficiency• Hepatic cirrhosis/failure.• Critical illnesses: o Sepsis with multiorgan failure. o Cardiac, hepatic and renal diseases.• Hormonal deficiencies:  o Glucagons (rare).o Epinephrine (very rare). o Growth hormone (in children).
to sympathetic activation and brain dysfunction secondary to decreased levels of glucose.

DEAR this are symptoms of hypoglycemia
A. Adrenergic symptoms:
They are produced in response to the stimulation of the sympathoadrenal nervous system:
 • Hunger. • Anxiety. • Sweating.• Palpitations.• Tremulousness• Pounding heart.

B. Neuroglycopenic symptoms:
Reduction in cerebral glucose availability can manifest with:
• Tiredness.• Dizziness.• Weakness.• Irritability. • Confusion.• Hallucinations. • Blurred vision.• Coma and death.• Difficulty concentration.• Inappropriate behaviour.• Difficulty with concentration.• Focal impairments e.g. hemiplegia.

C. Asymptomatic:
It is important to note that a patient with repeated hypoglycaemia can have almost no symptoms (hypoglycaemic unawareness). The threshold at which a patient feels the hypoglycaemic symptoms decreases with repeated episodes of hypoglycaemia.
The adrenergic symptoms often precede the neuroglycopenic symptoms and, thus, provide an early warning system for the patient. The primary stimulus for the release of catecholamines is the absolute level of plasma glucose; the rate of decrease of glucose is less important. Previous blood sugar levels can influence an individual's response to a particular level of blood sugar.

For further updates about hypoglycemia i will give you soon.

treatment complication..

(C)gammaLOVE THE LOVE OF HUMANITY