Download Southwest Ontario Regional Base Hospital Program

Southwest Ontario
Regional Base Hospital Program
Diabetes Review
Diabetes Review
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Objective: To better the understanding of the diabetic patient
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To discuss the anatomy and physiology of the pancreas and how its
hormones work to maintain normal glucose metabolism
To discuss the pathophysiology as a basis for the signs and symptoms,
patient assessment, and patient care of diabetic emergencies for
hypoglycemia, hyperglycemia, and non-ketotic hyperosmolar coma
Pancreas
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The pancreas plays an important role in the absorption and use of
carbohydrates, fat, and protein
The pancreas is the principal regulator of blood glucose concentration
The pancreas is located in the retroperitoneal cavity to the right side of the
duodenum, and extends to the spleen on its left side
The pancreas has exocrine and endocrine functions
The exocrine glands (containing ducts), have acini which produce pancreatic
amylase which is a digestive enzyme that enters the small intestine
The endocrine glands (ductless), contain the pancreatic islets (islets of
Langerhans), which produce hormones glucagon and insulin
Pancreas continued:
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The islets of Langerhans contain 500000 to 1000000 islets dispersed
among the ducts and acini of the pancreas
The beta cells secrete an average of 0.6units/kg of insulin
The alpha cells secrete glucagon
Some cells contained as well (delta cells), have questionable effects.
Some help in the secretion of somatostatin which inhibits the release
of HGH
Nerves from both divisions of the autonomic nervous system
innervate the pancreatic islets
All islets are surrounded by a developed capillary network
Insulin and Glucagon
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Insulin:
Released by the beta cells when blood glucose levels rise
• The primary function is to increase glucose transport into the cells,
increase glucose metabolism, increase liver glycogen levels, and to
decrease blood glucose concentration to normal levels
• Insulin will antagonize the effects of glucagon
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Glucagon:
Released by the alpha cells when blood glucose levels fall
• The primary functions of glucagon are to increase blood glucose
levels through stimulation of the liver and to stimulate breakdown of
other substances for glucose utilization
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Glycogenolysis and Gluconeogenesis
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Glycogenolysis is defined as the conversion of glycogen to glucose.
Gluconeogenesis is defined as the breakdown of all other elements
(except glycogen) for conversion into glucose for energy.
Diabetes Mellitus Pathophysiology
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A decrease or absence of insulin secretions by the cells in the islets of
Langerhans in the pancreas. Insulin, which is a hormone, is required
to facilitate glucose into the body cells for energy. Glucose is to large
of a molecule to cross the cell membrane on its own.
Excess glucose is lost through the urine. Cells are then forced to
metabolize fats and proteins (our other 2 main food sources in
addition to carbohydrates). This metabolism of fats leads to
production of ketone bodies and acids causing acidosis.
Normal Digestion:
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Food is eaten
Digestion begins in the stomach
Simple sugars are broken down in the small intestine
Normal digestion continued:
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Simple sugars enter the bloodstream
Insulin is released by the pancreas
Sugar enters the body cells with the aid of insulin
Diabetic digestion:
Food is eaten
Digestion begins in the stomach
Simple sugars are broken down in the small intestine
Simple sugars enter the bloodstream
Little or no insulin is released by the pancreas
The sugar stays in the bloodstream and is eliminated in the urine
Diabetic digestion continued:
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When sugar does not enter the body cells, the patient feels tired and
weak. Sugar is then released from its stored sources in an attempt to
provide energy to the body (gluconeogenesis). Fatty acids and
acetone develop from the breakdown of stored fat. Fatty acids
accumulate in the blood and urine which may lead to diabetic
ketoacidosis or non-ketotic hyperosmolar coma
Type I Diabetes (insulin dependant)
Also known as juvenile diabetes
No insulin is released by the pancreas
The beta cells my have been destroyed by a virus or destroyed by the
bodies own immune system
The patient must take daily doses of insulin
Type I Diabetes continued:
When insulin levels are low the body will metabolize fats and proteins.
The breakdown of fats will cause the formation of ketone bodies and
a subsequent acidotic state resulting in ketoacidosis
• The blood glucose levels are increased however the glucose cannot
enter the cells
• Patients may present with:
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Hypoglycemia (insulin shock)
Hyperglycemia, diabetic ketoacidosis (diabetic coma)
Type II Diabetes Mellitus (non insulin dependent diabetes)
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Also known as juvenile diabetes
Little insulin produced by the pancreas (may be normal)
Can be associated with obesity, a decrease in the number of insulin
receptors, or a decrease in glucose utilization
Controlled by weight reduction and reducing carbohydrate intake with
the use of oral diabetic medications
Diabetic ketoacidosis does not develop, however non-ketotic
hyperosmolar coma may develop
Blood glucose levels are increased but the glucose is unable to enter
the cells
Patients may present with hyperglycemia, or non-ketotic
hyperosmolar coma
Type III Diabetes Mellitus (gestational diabetes)
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Diabetes that develops during pregnancy
Cannot be managed with oral drugs as they will cross the placenta
membrane into the fetus (lipid soluble)
Must be controlled with insulin if diet alone cannot control (lipid
insoluble)
Often disappears post delivery; may remain as Type II
Babies from diabetic mothers tend to be large (11-14lbs) which may
complicate delivery
Pathophysiology of Hyperglycemia
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Insulin deficit: insulin deficient
severe infections
excessive sugar intake
Glucose cannot enter the cells fast enough causing the cells to
become glucose deficient
Prolonged hyperglycemia results in various complications:
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Kidney damage
Nerve cell damage
Retinal damage (blindness)
Circulatory system damage (poor circulation pH abnormalities)
Cells burn fats and proteins to produce energy; a byproduct of the
metabolism of fat are ketone bodies (ketoacidosis) resulting in a state of
metabolic acidosis
Assessment of Hyperglycemia
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Signs and symptoms of Diabetic Coma:
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Confusion, disorientation
Dim vision
Deep red lips
Normal or decreased blood pressure
Vomiting
Red, hot, dry skin
Fever
Sunken eyes
Sweet or fruity odour on breath (ketone bodies)
Intense thirst
Rapid, deep breathing
Intense abdominal pain
Frequent urination
Management of Hyperglycemia
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Primary exam
Manage and maintain airway
Important history questions
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Have you eaten today?
Have you taken your insulin/pills today?
Have you been ill recently?
Blood glucose exam
The patient needs IV fluids and insulin
Cardiac monitor
Vitals
Oxygen
Pathophysiology of Hypoglycemia
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Insulin excess
Insulin overdose
Insufficient carbohydrate intake
Excessive exercise, stress or exertion without adequately
replacing lost sugars
Glucose enters the cells too rapidly causing the amount of
blood glucose to decrease
Brain cells require a constant supply of glucose which is not
available
Brain injury may quickly result
This is a true emergency; the patient requires glucose
Signs and symptoms of Hypoglycemia
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Dizziness
Fainting
Double vision
Drooling from mouth
Normal blood pressure
Pale, cool, diaphoretic skin
Normal or rapid pulse
Tingling in hands and feet
Headache
Convulsions
Apathy and irritability
Absence of thirst
Normal or shallow breathing
Occasional hunger
Extreme weakness
Tremors
General muscle weakness
Management of Hypoglycemia
Primary exam
• Manage and maintain airway
• Important history questions
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Have you eaten today?
Have you taken your insulin today?
Have you been exercising or over exerting yourself today?
Blood glucose exam
The patient needs glucose
O2
Cardiac monitor
Vitals
Administration of D50W, Glucagon or Oral Glucose if blood glucose
is less than 4.0mmol/L or less than 3.0mmol/L(than 2 years of age)
Note: Hypoglycemia can be caused by problems other than
diabetes (alcohol, drug overdoses, hypothermia)
Management of Diabetes (by patient):
Diet and exercise
• Insulin: human, beef, pork
• Insulin pens and pumps
• Oral hypoglycemic medications (glyburide, metformin,
glucophage)
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Future Management:
Pancreas transplants ( 1 successful transplant in
Ontario), beta cell transplants, artificial beta cells,
nasal insulin spray
References:
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Greg Skomash, Paramedic Program Coordinator St.Clair
College Windsor Campus, Emergency Care AM 110 notes
1997/1998
Mick J. Sanders, Mosby’s Paramedic Textbook Revised
Second Edition, Adapted from chapter 30 pgs. 944-958
Mick J. Sanders, Mosby’s Paramedic Textbook Revised Third
Edition, 2007, Adapted from chapter 32 pgs. 851-862