3. ANATOMY AND PHYSIOLOGY
• Directly or Indirectly effects almost every cell, organ, and function of the
body.
• Controls and regulates all of the bodies systems.
• Made up of Hypothalmus, Pituitary gland, parathyroid gland, thymus,
thyroid gland, pancreas, and gonads.
• Secretion of hormones causes cellular reactions throughout the body.
4. ORGANS THAT ACT LIKE GLANDS
• Heart
• Atrial natriuretic hormone
• Placenta
• Human chorionic gonadotropin
• Kidneys
• Renin
9. DIABETES MELLITUS
• An inability to sufficiently metabolize glucose.
• The body either does not produce sufficient amounts of insulin OR the body
does not respond to the effects of insulin.
• Causes harm to kidneys, circulatory system, eyes.
• Can also cause CVA’s, Hypertension, and neuropathy.
10. TYPE 1 DIABETES MELLITUS
*USED WITH THE
EXPRESS WRITTEN
CONSENT OF PMD
BISHOP*
11. TYPE 1 DIABETES MELLITUS
• Known as Insulin Dependent Diabetes
• The body develops autoantibodies that attacks the pancreas
• Beta cells in the Islet of Langerhans create insulin
• Eventually the pancreatic beta cells can not produce enough insulin
• Type 1 diabetics require insulin injections
12. TYPE 1 DIABETES MELLITUS
• Assessment
• Determine if the patient is compliant with managing their diabetes
• If the patient has an altered mental status, suspect hypoglycemia
• Assess for signs of sores or infections
• Patients may have a history of hypertension, CHF, renal failure, Coronary
artery disease, etc.
• Vision changes, dizziness, bleeding, or sores in the mouth
13. TYPE 1 DIABETES MELLITUS
• Management
• Insulin injections
• Some patients will have implanted insulin pumps
15. TYPE 2 DIABETES MELLITUS
• The body cannot produce enough insulin or is unable to utilize the insulin
created
• The most common form of diabetes mellitus
• Associated with physical inactivity and obesity
• 8.5% of the worlds population is considered to be Diabetic
16. DIABETES TYPE 2
• Assessment
• New onset weakness in the diabetic patient should be considered an AMI until
proven otherwise
• Patients may present with Fatigue, Nausea, Thirst, Blurred vision, etc.
17. TYPE 2 DIABETES MELLITUS
• Management:
• Exercise and healthy eating habits
• EMS can help reinforce the importance of healthy habits
19. GESTATIONAL DIABETES
• Not associated with the pancreas, but is a Glucose intolerance
• 40-60% increased risk of developing into type 2 diabetes
• Blood glucose can cross the placenta barrier
• Causes increased insulin production by the fetus
• Large babies, difficult deliveries, and can lead to Cesarean’s
21. HYPOGLYCEMIA
• Normal Blood Glucose Levels 60-120mg/dl
• Hypoglycemia occurs when levels drop to 45mg/dl or less
• Can be experienced by both type 1 and type 2 diabetics
• Loss of consciousness or alerted mental status requires immediate
intervention
• Can lead to coma and death if untreated
22. HYPOGLYCEMIA
• Type 1 diabetics: too much insulin
• Type 2 diabetics: body is not using insulin effectively
• Body's first line of defense against hypoglycemia is to suppress insulin
production
• Second line of defense is catecholamine release, causing tachycardia and
diaphoresis, and cortisol
• Cortisol release leads to increased BGL
23. HYPOGLYCEMIA
• Assessment
• Blood glucose <60mg/dl
• Develops rapidly over time, from minutes to hours
• Altered mentation, confusion, irritability, incoordination
• Cool, clammy skin
• Tachycardia
24. HYPOGLYCEMIA
• Do not allow a history of hypoglycemia keep from ruling out other causes of
comatose
• The longer a patient remains comatose the more brain is damaged
• D50 is contraindicated in CVA with normal BGL’s
• Hypertonic properties of D50 can cause increased cerebral edema
25. HYPOGLYCEMIA
• Management:
• Immediately increase blood glucose levels
• Least invasive to most
• Patients capable of swallowing may be encouraged to eat in order to normalize
glucose levels
• If patient is altered provide IV dextrose
27. HYPERGLYCEMIA AND DKA
• High blood glucose levels
• Early signs are excessive and frequent thirst and urination
• Defined as BGL >160mg/dl
• Caused by excessive food intake, illness, infection, emotional distress,
insufficient insulin dosages, etc
• Can also be caused by “Dawn phenomenon” and Somogi effect
28. HYPERGLYCEMIA AND DKA
• Hyperglycemia puts strain on the cardiovascular system, kidneys and other
end organs
• Can cause renal failure, CHF, retinopathy, coronary artery disease, and
neuropathy
• Diabetic ketoacidosis BGL >350mg/dl
• Hyperosmolar Hyperglycemic Syndrome >600mg/dl
29. HYPERGLYCEMIA AND DKA
• DKA/HHS primarily associated with type 1 diabetics
• Body can not use the glucose available and turns to fat to produce energy
• Metabolizing fat produces acids and ketones as waste products
• Produces a “fruity” breath odor
• Body attempts to compensate for acidosis with Bicarbonate and increased
respiratory rate
31. HYPERGLYCEMIA AND DKA
• Assessment
• Progresses slowly over 12 to 48 hrs with level of consciousness deteriorating
gradually
• Patient may admit to excessive thirst, urination, nausea or vomiting, warm
and dry skin, abdominal pain
• Patients can be tachycardic, feverish, hypocapnic and have “fruity” breath odor
• Seldom comatose
• Respiratory rate and tidal volume increased (Kussmaul respirations)
32. HYPERGLYCEMIA AND DKA
• Management:
• Prehospital goal is to begin the rehydration process
• Correct electrolyte imbalances and acid base abnormalities
• IV fluids and monitor cardiac rhythm
• Treatment with insulin should be administered at the hospital
34. HYPEROSMOLAR HYPERGLYCEMIA
SYNDROME
• Occurs primarily in type 2 diabetics
• Most patients have severe dehydration and focal or global neurologic
deficits
• AMI is frequently associated with HHS
• Develops in diabetics that have a secondary illness that leads to reduced
fluid intake
35. HYPEROSMOLAR HYPERGLYCEMIC
SYNDROME
• Assessment:
• Unlike DKA, HHS do not experience ketoacidosis
• Most patients have a history of type 2 diabetes, 30% of patients however do not
have a diabetes history
• Patients may be drowsy and lethargic, delirious or comatose, have seizure like
activity, visual disturbances, and sensory deficits
• ASSESS THE PATIENT NOT THE NUMBERS!!!
36. HYPEROSMOLAR HYPERGLYCEMIC
SYNDROME
• Management:
• Treating dehydration and altered mental status
• ABC’s
• IV fluid bolus
• Patients may receive up to 1-2 L in the first hour of treatments and need up to
10 L or more possibly
38. PANCREATITIS
• Inflammation of the Pancreas
• Acute and chronic
• Caused by Gallstones and chronic alcohol abuse
• Acute Pancreatitis results from years of alcohol abuse in younger patients
• Chronic pancreatitis destroys the Pancreas and leads to a loss of all
endocrine and exocrine function
49. ADRENAL MEDULLA
• Both nerve and gland cells
• Sympathetic Nervous System
• Release of epinephrine and norepinephrine
50.
51. ADRENAL CORTEX
• Secretes three steroids:
• Glucocorticoids (including cortisol)
• Mineralocorticoids (including aldosterone)
• Androgenic Hormones- same effects of gonads
52.
53. DISORDERS OF THE ADRENAL
GLANDS
• Cushing’s syndrome- too much
• Addison’s disease- not enough
54. OTHER ENDOCRINE EMERGENCIES
• Primary Adrenal Insufficiency
• Addison Disease
• Atrophy or destruction of both adrenal glands
• Deficiency of all steroid hormones produced by these glands
55. OTHER ENDOCRINE EMERGENCIES
• Secondary Adrenal Insufficiency
• Lack of ACTH
• Patients who abruptly stop taking corticosteroids
• Corticosteroid withdrawal is most common cause of Addisonian crisis
• Chief indicator of a crisis is shock
• Unrecognized and untreated can be lethal
56.
57.
58. OTHER ENDOCRINE EMERGENCIES
• Cushing Syndrome
• Caused by an excess of cortisol production
• Changes many body systems
• Bones become weaker and more prone to fracture, muscle weakness and loss of
muscle fibers
• “Moon face”, easily bruised, weight gain, acanthosis of the neck, etc are all
signs of Cushing syndrome
• Management is with decreased levels of cortisol in the body
