Endocrine pathology endocrine pancreas

Содержание

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ENDOCRINE PANCREAS

ENDOCRINE PANCREAS

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ENDOCRINE PANCREAS

The pancreas consists of two functionally distinct components:
The exocrine pancreas, which

ENDOCRINE PANCREAS The pancreas consists of two functionally distinct components: The exocrine
secretes digestive enzymes into the duodenum
The islets of Langerhans, scattered within the tissues of the exocrine pancreas act together as an endocrine gland.

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CELL TYPES IN THE ISLETS OF LANGERHANS

CELL TYPES IN THE ISLETS OF LANGERHANS

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DIABETES MELLITUS

Abnormal metabolic state characterised by glucose intolerance due to inadequate insulin

DIABETES MELLITUS Abnormal metabolic state characterised by glucose intolerance due to inadequate
action
Type 1 (juvenile onset) due to destruction of Bela cells (probably a result of virus infection and genetic factors); Insulin dependent
Type 2 (maturity onset) due to defective insulin action; treatment by weight reduction and oral hypoglycaemlc agents
Complications include
Accelerated atherosclerosis,
Susceptibility to infections, and
Microangiopathy affecting many organs

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Diagnosis is based on the clinical demonstration of glucose intolerance
Insulin is

Diagnosis is based on the clinical demonstration of glucose intolerance Insulin is
unique, in that it is the only hormone with a hypoglycaemlc effect.
There are live hormones that tend to exert a hyperglycaemic effect
Glucagon,
Glucocorticoids,
Growth hormone,
Adrenaline (epinephrine)
And non-adrenaline (norepinephrine),
The hyperglycaemic effects of these hormones cannot be counterbalanced if there is inadequate insulin action.

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PATHOGENESIS

The actions of insulin are all anabolic, that is, they promote the

PATHOGENESIS The actions of insulin are all anabolic, that is, they promote
laying down of tissue stores from circulating nutrients.
The consequences of insulin deficiency are therefore catabolic, that is, there is breakdown of tissue energy stores.
The major features of diabetes mellitus are:
Inability to utilise, and overproduction of, glucose(hyperglycaemia)
Diminished protein synthesis
Lipolysis resulting in hyperlipidaemia, hence there is rapid wasting and weight loss.

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In hyperglycaemia the renal threshold for glucose conservation is exceeded, so that

In hyperglycaemia the renal threshold for glucose conservation is exceeded, so that
there is osmotic diuresis resulting in polyuria, dehydration and thirst.
Lipolysis may also have serious consequences.
Free fatty acids are converted in the liver to ketone bodies, such as acetoacetate, acetone and beta-hydroxybutyrate.
These dissociate to release hydrogen ions, and a profound metabolic acidosis may ensue.

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The combined result of severe ketosis, acidosis, hyperglycaemia, hyperosmolarity and electrolyte disturbance

The combined result of severe ketosis, acidosis, hyperglycaemia, hyperosmolarity and electrolyte disturbance
is to impair cerebral function, producing diabetic ketoacidotic coma.
This is quite distinct from the hypoglycaemic coma that may also be found in diabetic patients; this is due to insulin overdosage, and has entirely different clinical features.

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CLASSIFICATION

Type 1 (juvenile-onset, insulin-dependent diabetes)
Typically presents in childhood.
The patient usually shows

CLASSIFICATION Type 1 (juvenile-onset, insulin-dependent diabetes) Typically presents in childhood. The patient
the catabolic effects and is prone to develop ketoacidosis.
The central defect is inadequate insulin secretion by the beta cells of the pancreas, and this can be corrected only by the life-long administration of exogenous insulin.

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Postmortem examination of the pancreas in patients who had recently developed type

Postmortem examination of the pancreas in patients who had recently developed type
1 diabetes but died from other causes (e.g. road traffic accident) shows lymphocytic Infiltration of the islets with specific destruction of the beta-cells.
There are three major theories concerning the aetiology of these changes:
Autoimmune destruction,
Genetic factors and
Viral infection.

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Autoimmune destruction. The majority of patients have circulatory antibodies to several different

Autoimmune destruction. The majority of patients have circulatory antibodies to several different
types of islet cell.
Genetic factors. As with other ‘organ-specific' autoimmune diseases, there is an association with certain HLA types. It seems that environmental factors also play a role.
Viral infection. Titers of antibodies to viruses such as Coxsackie B types and mumps are elevated in some patients developing this type of diabetes 

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Type 2 (maturity-onset, non-insulin-dependent diabetes)
is more common than type 1 and

Type 2 (maturity-onset, non-insulin-dependent diabetes) is more common than type 1 and
usually presents in middle age, being commonest in the obese.
Patients are not prone to ketoacidosis, but occasionally develop a non-ketotic coma in which there is extreme hyperosmolarity of the plasma.
Insulin secretion is normal or increased and the central defect may therefore be a reduction in the number of cell surface receptors for insulin.

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Type 2 (maturity-onset, non-insulin-dependent diabetes)
Genetic factors clearly play an important part in

Type 2 (maturity-onset, non-insulin-dependent diabetes) Genetic factors clearly play an important part
the aetiology of type 2 diabetes.
Treatment is usually by weight reduction coupled with orally administered drugs that potentiate the action of insulin.

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Secondary diabetes
Hypersecretion of any of the hormones that tend to exert a

Secondary diabetes Hypersecretion of any of the hormones that tend to exert
hyperglycaemic effect may cause glucose intolerance.
Thus Cushing's syndrome, phaeochromocytoma, acromegaly and glucagonomas may cause secondary diabetes.
Generalized destruction of the pancreas by acute and chronic pancreatitis, haemochromatosis and occasionally, carcinoma may cause insulin deficiency.

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COMPLICATIONS

The commonest complications are seen in blood vessels.
Atheroma, often ultimately severe

COMPLICATIONS The commonest complications are seen in blood vessels. Atheroma, often ultimately
and extensive, develops at an earlier age than in the non-diabetic population. Small blood vessels show basal lamina thickening and endothelial cell proliferation (diabetic microangiopathy), frequently causing retinal and renal damage.
About 80% of adult diabetics die from cardiovascular disease, while patients with longstanding diabetes, especially type 1, frequently develop serious renal and retinal disease.

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TUMOURS

Less common than pancreatic adenocarcinoma
Present with endocrine effects and may be

TUMOURS Less common than pancreatic adenocarcinoma Present with endocrine effects and may
malignant
Insulinoma: causes hypoglycaemia
Glucagonoma: causes secondary diabetes and skin rash
Adenomas and carcinomas derived from the islet cells are quite rare.

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Insulinoma
Insulinoma is the commonest islet cell tumour and produces hypoglycaemia through hypersecretion

Insulinoma Insulinoma is the commonest islet cell tumour and produces hypoglycaemia through
of insulin.
During hypoglycaemic attacks, the patient develops confusion, psychiatric disturbances and possibly coma. Diagnosis is urgent because hypoglycaemia may produce permanent cerebral damage.
Other islet cell tumours are very rare, but include somatostatinomas and tumours secreting vasoactive intestinal peptide (VIP), which leads to watery diarrhoea.

TUMOURS

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Gastrinomas : Although gastrin is usually produced in the G-cells of the

Gastrinomas : Although gastrin is usually produced in the G-cells of the
stomach, tumours of the G-cells, called gastrinomas, most commonly originate in the pancreas.
Islet cell tumours and gastrinomas may occur as part of one of the MEN syndromes , most commonly MEN type 1.
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