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Pathophysiology of Diabetes Mellitus

KEY VOCABULARY 
The following terms will be used during this lesson:

·        Conscious - patient is awake and responds to stimuli appropriately

·        Coma - patient is not aroused by external stimuli

·        Diabetes mellitus - endocrine disorder characterized by inadequate insulin production by beta cells in the islets of Langerhans in the pancreas

·        Endocrine Glands - glands that secrete hormones directly into the blood stream

·        Glucose – source of energy required by cells for normal functioning

·        Hyperglycemia - abnormally high levels of glucose in the blood

·        Hypoglycemia - abnormally low levels of glucose in the blood

·        Hormones - chemical substances released by a gland that control or affect other glands or body systems

·        Insulin – hormone secreted by pancreas which allows cells to use glucose

·        Ketoacidosis - complication of diabetes that occurs from too little insulin production or secretion

·        Oriented - responds appropriately to questions regarding person, place, time, and events (purpose)

Lets Start ...!!!

DIABETES MELLITUS – OVERVIEW

Pathophysiology

·        All cells require glucose for survival
·        Glucose is primarily acquired from the digestion of carbohydrates
·        Starches and complex sugars are converted to the simple sugar          glucose
·        If glucose is not available from the ingestion of carbohydrates the body will break down glycogen (a sugar stored in the liver) or protein in the liver
·        Insulin (a hormone secreted by the beta cells in the pancreas) is necessary to allow glucose to pass from the blood stream into the cells.


 

 

Classifications of diabetes:


Type I:
·        Insulin dependent (IDDM)
·        Onset is usually in adolescence or early adulthood
·        Cause is thought to be a virus that damages the pancreas                  resulting in an inadequate production of insulin
·        Usually “brittle” diabetics (hard to control)
·        Diabetic ketoacidosis is common



Type II:
·        Non-insulin dependent (NIDDM)
·        Use oral hypoglycemic agents
Orinase
                  Tolinase
      Diabinese
      Diabeta
      Dymelor
·        Onset is in older adults
·        Often associated with obesity
·        The cells do respond to the insulin that is available


Complications of diabetes

Acute:
·        Hypoglycemia
·        Diabetic ketoacidosis
·        Hyposmolar, hyperglycemic, nonketotic coma


Chronic:
·        Infections
·        Vascular disease
·        Coronary artery disease
·        Stroke
·        Neuropathies
·        Blindness




PATHOPHYSIOLOGY, SIGNS AND SYMPTOMS, AND FIELD MANAGEMENT OF COMMON DIABETIC EMERGENCIES

Hypoglycemia (insulin shock)
Pathophysiology:
·        Occurs when there is too much insulin in the blood stream.
·        Usually occurs when the diabetic patient takes their insulin and does not eat.
·        Can occur if the diabetic patient eats but is vomiting and the nutrients are not absorbed.

Signs and symptoms:
·        Dizziness/headache
·        Pale, cool, clammy
·        Mental confusion
·        Abnormal behavior
·        Altered LOC
·        Tachycardia is common
·        Strong or bounding pulse
·        Normal BP
·        Shallow respirations


Field management of hypoglycemia
BLS procedures:
·        Maintain airway
·        High flow O2 by mask
·        Left lateral position if unconscious
·        Thorough history to determine to determine possible cause
·        Oral hypoglycemic agent if patient is conscious and has a gag reflex
·        Transport
·        Assist with ALS procedures

ALS procedures:
·        Advanced airway management prn
·        Venous access
·        Monitor
·        Glucometer
·        Dextrose 50% if blood glucose < 80
·        Glucagon 1 mg.  May be ordered if unable to obtain venous access and glucose <80
·        Transport

Hyperglycemia (Diabetic Coma)
Pathophysiology:
·        Insulin levels are inadequate to meet the body’s needs. 
·        Glucose cannot be utilized by the cells and it accumulates in the       bloodstream. 
·        The excess sugar begins to spill over into the urine. 
·        As the sugar is excreted it takes excessive amounts of water with it  resulting in serious dehydration. 
·        Ketones and acids are produced as cellular glucose depletion continues. 
·        Ketoacidosis is a serious complication that can result in coma and death.


Signs and symptoms:
·        Increased hunger
·        Increased thirst
·        Altered LOC
·        Kussmauls respirations
·        Hypotension
·        Weak, rapid pulse
·        Fruity odor on breath
·        Frequent urination

Field management of hyperglycemia
BLS Procedures
  • Maintain Airway
  • High flow O2 by mask
  • Left lateral position if comatose
  • Shock position if hypotensive
  • Thorough history to determine possible causes
  • Assist with ALS Procedures

ALS Procedures
  • Advanced airway prn
  • Venous access (large bore)
  • Glucometer
  • Fluid challenge if hypotensive
  • Transport



 
 



















INITIAL ASSESSMENT AND FOCUSED HISTORY AND DETAILED PHYSICAL EXAMINATION OF DIABETIC PATIENTS

Initial Assessment
1).  Assess environment:  (may need to manipulate the environment)
·        Safety of rescuers and environment
  • Environmental factors
    • Medications (may offer clues to past medical history)
    • Witnesses (may help to explain circumstances)

 
 








2).  Airway:   determine responsiveness and patency of airway
  • Unconscious patients may need assistance to maintain and protect their airway

3).  Breathing:  assess the rate and quality of respirations
  • Rapid shallow breathing may be indicative of hypoglycemia
  • Rapid deep (Kussmauls) breathing may be indicative of hyperglycemia

4).  Circulation:  palpate for pulse noting rate/rhythm/quality
  • Rapid bounding pulses may indicate hypoglycemia
  • Weak thready pulses may indicate hyperglycemia

5). Skin signs:  assess color, temperature and moisture
  • Pale, cool, moist skin and delayed capillary refill are due to peripheral vasoconstriction
  • If signs of poor perfusion, consider placing patient supine

 
 







6).  Assess Neurological Status:  
·        Assess level of consciousness using the GCS, and neuro deficits
·        Hyperglycemia and hypoglycemia both result in altered LOC
·        Assess thoroughly for “AEIOUTIPS”

7).  Determine chief complaint:

 
 







Focused History and Detailed Physical Examination
1).  Elicit history of chief complaint or problem
  • Emesis may indicate they have been vomiting recently
  • Check for refrigerated medications (insulin)

 
 






2).  Elicit personal history (HAM)
  • H   medical history/under a doctors care
  • A   allergies/age
  • M   medications-current over the counter and prescription

3).  Vital Signs
  • Blood Pressure - hypotension may indicate hyperglycemia
  • Pulses - cardiac dysrhythmias are commonly seen, assess rate
  • Respirations - assess rate, rhythm, and quality
  • Pupils – pupillary size and reaction to light


4).  Special Questions
  • Helps to determine the possible cause of the problem
  • Duration of symptoms
·          Hypoglycemia is often rapid onset
·          Hyperglycemia is often slow inset
  • Recent infections often disrupt the insulin-glucose balance and result in hyperglycemia
  • Compliance with medication and diet
  • Oral hypoglycemic agents are typically long acting and may result in recurring hypoglycemia if glucose levels are not carefully monitored


5).  Pertinent Body Check:
  • Medical or minor trauma—perform body check pertinent to chief complaint
 
 







Head to Toe Examination:
  • Look for associated injuries
  • If altered LOC look for “AEIOUTIPS”

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