FUNCTION/DYSFUNCTION OF ENDOCRINE PANCREAS

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FUNCTION/DYSFUNCTION OF ENDOCRINE PANCREAS. Diabetes. Anatomy of the pancreas: Both an exocrine and endocrine organ Cells with exocrine function release an alkaline fluid containing sodium bicarbonate and enzymes → pancreatic duct → small intestine
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FUNCTION/DYSFUNCTION OF ENDOCRINE PANCREASDiabetesAnatomy of the pancreas:
  • Both an exocrine and endocrine organ
  • Cells with exocrine function release an alkaline fluid containing sodium bicarbonate and enzymes →
  • pancreatic duct → small intestine
  • Pancreatic “juice” aids in breakdown and digestion of food in the small intestine
  • Pancreatic exocrine cells = acinar cells
  • Endocrine Function :
  • Cells of the Islet of Langerhans synthesize and release hormones into the circulation.
  • Hormones travel through the bloodstream to target tissues (especially liver and muscle)
  • At the target cells, hormones bind specific receptors and cause cell changes that control metabolism
  • Pancreatic endocrine cells regulate carbohydrate, fat, protein metabolism:
  • Alpha cells – secrete the hormone glucagon
  • Beta cells – secrete the hormones insulin and amylin
  • Delta cells – secrete the hormones gastrin and somatostatin
  • F cells - secrete hormone pancreatic polypeptide
  • Beta Cells
  • Synthesize pre-proinsulin, a protein
  • This is cleaved by enzymes →proinsulin, then cleaved again → insulin
  • Insulin is the biologically active hormone that is released into the bloodstream
  • Insulin secretion is controlled through several mechanisms:
  • Chemically – high levels of glucose and amino acids in the blood
  • Hormonally – beta cells are sensitive to several hormones that may inhibit or cause insulin secretion
  • Neurally – stimulation of the parasympathetic nervous system causes insulin to be secreted.
  • Insulin secretion is decreased by:
  • Decreased blood glucose concentration
  • Increased blood insulin concentration
  • Sympathetic stimulation
  • Insulin
  • Transported through the blood to target tissues where it binds to specific receptors
  • The binding of insulin to target cells:
  • Acts as a biochemical signal to the inside of the cell
  • Overall, cell metabolism is stimulated
  • There is increased glucose uptake into the cell
  • Regulation of glucose breakdown within the cell
  • Regulation of protein and lipid breakdown within the cell
  • Blood glucose is decreased because insulin causes glucose to leave the bloodstream and enter the metabolizing cells.
  • With the exception of brain, liver and erythrocytes, tissues require membrane glucose carriers.
  • Disorder ‑ Diabetes mellitus
  • The single most common endocrine disorder – group of glucose intolerance disorders
  • Incidence is estimated at 1-2% of the North American population
  • Many of these cases are undiagnosed
  • Diabetes mellitusHistorically ‑ distinguished by weight loss, excessive urination, thirst, hunger Excessive urination = polyuria Excessive thirst = polydipsia Excessive hunger = polyphagiaModern characterization is by hyperglycemia and other metabolic disordersModern classifications (Table17.7)
  • Type 1 or IDDM ‑ Insulin Dependent Diabetes Mellitus
  • Type 2 or
  • NIDDM ‑ Non‑Insulin Dependent Diabetes Mellitus
  • Other Types of Diabetes Mellitus
  • GDM ‑ Gestational Diabetes Mellitus
  • Type 1 or IDDM
  • Accounts for 10% all DM in the Western world
  • ~10-15% have parent or sibling with the disease
  • Peak age of diagnosis = 12 years
  • Genetic/environmental/autoimmune factors destroy beta cells
  • Believed abrupt onset – now immunomarkers and preclinical symptoms have been discovered
  • Disequilibrium of hormones produced by islets of Lagerhans : low insulin and high glucagon
  • Ratio insulin/glucagons apparently controls metabolism of glucose and fats.
  • Clinical Manifestations:Glucose in urine- Because when insulin is not present, glucose is not taken up out of the blood at the target cells.So blood glucose is very highly increased → increased glucose filtered and excreted in the urine (exceeds transport maximum)Clinical Manifestations:Weight loss - Patient eats, but nutrients are not taken up by the cells and/or are not metabolized properlyOsmotic diuresis results in fluid lossLoss of body tissue by metabolism of fats and proteinsPolyuria, polydipsia, pholyphagia
  • Ketoacidosis
  • Fats and proteins are metabolized excessively, and byproducts known as ketone bodies are produced. These are released to the bloodstream and cause: Decreased pH (so increased acidity)
  • Compensations for metabolic acidosis
  • Acetone given off in breath
  • Treatment1. Administer insulin May be of animal or human origin Cannot be given orally Patient must monitor their blood glucose concentration and administer insulin with the correct timing2.Control diet
  • Carbohydrates should make up about 55-60% of patient’s total calories
  • Fats should make up <30% of patient’s total calories
  • Proteins should make up about 15-20% of patient’s total calories
  • 3. Monitor exercise
  • Remember: muscles are a target tissue of insulin, and metabolize much glucose for energy
  • Sometimes exercise →irregular blood glucose levels So diabetic patients should be monitored when they are exercising
  • Other:
  • Pancreatic transplant – so far not successful
  • Experimental therapies – not as successful as hoped
  • Type 2 or NIDDM
  • More common than IDDM, often undiagnosed
  • It has a slow onset
  • Most common in those > 40 years, though children are being diagnosed more regularly
  • May be genetic
  • Obesity is the greatest risk factor for this disease
  • And is related to increased incidence in children
  • NIDDM → insulin resistance in target cells
  • See decreased β cell responsiveness →
  • Decreased insulin secreted by β cells
  • Also abnormal amount of glucagon secreted
  • These effects may be due to:
  • Abnormally functioning β cells
  • Decreased β cell mass,
  • or a combination of the two
  • 3. Target cell resistance to insulin
  • Due to:
  • Decreased number of insulin receptors
  • Postreceptor events may be responsible
  • Cells “burn out” and become insensitive
  • Clinical manifestations
  • Overweight, hyperlipidemia common (but these are precursors, not symptoms)
  • Recurrent infections
  • Visual changes, paresthesias, fatigue
  • Treatment
  • 1. Weight loss
  • 2. Appropriate diet (see IDDM above)
  • 3. Sulfonyl ureas
  • stimulate βcells to increase insulin secretion
  • Works only when β cells are still functioning
  • → An enhancement of insulin’s effect at target cells
  • 4. Exercise - promotes weight loss
  • Gestational Diabetes
  • Due to increased hormone secretion during pregnancy
  • Seen if patient has predisposition
  • If previous or potential glucose intolerance has been noted
  • Important ‑ increased mortality risk for mother, child
  • Complications of Diabetes Mellitus
  • Acute:
  • Hypoglycemia = rapid decrease in plasma glucose = insulin shock
  • Neurogenic responses – probably due to decreased glucose to hypothalamus.
  • Symptoms include:
  • Tachycardia, palpitations, tremor, pallor
  • Headache, dizziness, confusion
  • Visual changes
  • Treatment : provide glucose (I.V. or subcutaneous if unconscious)Observe for relapseKetoacidosis – involves a precipitating event:
  • Increased hormones released w/ trauma  increased glucose produced by the body’s cells
  • This “antagonizes” the effects of any glucose present 
  • Increased ketones in blood
  • Acid/base imbalance
  • Polyuria, dehydration Electrolyte disturbances
  • Hyperventilation (Kussmaul – deep, gasping)
  • CNS effects
  • Acetone on breath
  • Treatment: ‑ low dose insulinAlso, administer fluids, electrolytesChronic Complications of DM
  • Neuropathies = nerve dysfunctions → slowing of nerve conduction. In these patients, see:
  • Degeneration of neurons →Sensory, motor deficits →Muscle atrophy, paresthesias
  • Depression
  • G.I. problems, as muscle motility decreased
  • Sexual dysfunction
  • Microvascular disease – chronic diabetes w/ improper glucose metabolism → thickening of the basement membrane of capillaries, particularly in the eye and the kidney. As the capillary changes in this way, → Decreased tissue perfusion
  • So ischemia → hypoxia
  • In the eye – the retina is metabolically quite active, so hypoxia here is a big problem
  • So see:
  • Retinal ischemia→
  • Formation of microaneurisms, hemorrhage, tissue infarct, formation of new vessels, retinal detachment
  • In the kidney – diabetes is the most common cause of end‑stage renal disease
  • Injured glomeruli (glomerulosclerosis)
  • In these patients, see:
  • Proteinuria (protein is excreted into the urine) → Generalized body edema, hypertension
  • Macrovascular disease – atherosclerosis Plaque formation increases→
  • Increased risk of coronary artery disease, so increased risk of myocardial infarction
  • Increased risk of congestive heart failure
  • Stroke
  • Peripheral vascular disease
  • why diabetic patients face problems with their lower legs and feet
  • Increased risk of infections
  • Related Search
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