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CCRN®/PCCN® Review Course - Day 2 ©TCHP Education Consortium, September 2003, Rev. December 20151
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CCRN/PCCN Exam Review:The Endocrine System
Tom Scullard MSN RN CCRN
Endocrine System
• 4% of both the PCCN and CCRN Examination
Functions of the Endocrine System
• The glands of the endocrine system and the hormones they release influence almost every cell, organ and function of the body
Anatomy and Physiology
• General Functions– Growth and development
– Metabolism
– Fluid and electrolyte balance
– Acid-Base balance
– Reproduction
Anatomy and Physiology
• Eight endocrine glands– Pituitary– Thyroid– Parathyroid– Adrenal– Pancreas– Thymus– Pineal– Gonads
Pituitary (Master Gland)
• Key hormones secreted include:– Growth Hormone
– Thyrotropin
– Antidiuretic hormone
CCRN®/PCCN® Review Course - Day 2 ©TCHP Education Consortium, September 2003, Rev. December 20152
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Pancreas
• Islets of Langerhans: Secretes glucagon and insulin
• Alpha cells produce glucagon
• Beta cells produce insulin
• Delta cells produce somatostatin
Pancreas
• Glucagon: Stimulates glycogenolysis, gluconeogenesis
• Released due to decrease in blood glucose, high protein feeding, catecholamines, exercise, starvation
• Excess: Hyperglycemia• Deficiency: Hypoglycemia
Pancreas
• Insulin: enables glucose to move into the cell, aids in storage of glycogen, inhibits lipolysis
• Released due to a rise in blood sugar, gastrin, ACTH
• Excess: hypoglycemia• Deficiency: hyperglycemia
Endocrine
Patient Care Problems
#1 - Acute Hypogycemia
• G M is a 32 yo lawyer who was recently diagnosed with type 2 diabetes. After collapsing at work this morning, he is transported to the ER. His wife stated he followed his diet diligently, and had recently started an ambitious exercise program, going to the gym mornings before work. He’s been testing his blood sugars, but was too rushed this am and did not.
Hypoglycemia: Pathophysiology
• Definition:Blood sugar < 50 mg/dl
• Too much insulin in relation to the amount of glucose
• Sympathetic nervous system stimulation
• Rise in counterregulatory hormones, gucagon, epinephrine, cortisol, GH
CCRN®/PCCN® Review Course - Day 2 ©TCHP Education Consortium, September 2003, Rev. December 20153
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Hypoglycemia: Causes
• Decreased food intake
• Excessive insulin dose
• Increased physical activity
• Renal failure/Hepatic insufficiency
• Pentamidine therapy: Tx; Pneumocystis carinii
Hypoglycemia: Assessment
• Adrenergic(sympathetic) stimulation; Irritability, diaphoresis, pallor, cool skin, tachycardia, hunger
• Neuroglycopenic stimulation, HA, slurred speech, agitation, confusion, staggering gait, seizures, coma
Treatment: Hypoglycemia
• Replace glucose: Oral intake of 10-20 grams of carbohydrates
• IV glucose: D50 IV (Peds D25), may need repeating
• Prevent injury, seizure precautions
• Frequent vital signs, cardiac monitoring
• Identify and treat cause of hypoglycemia
Diabetic Ketoacidosis DKA
• Definition: Hyperglycemic crisis associated with metabolic acidosis and elevated serum ketones
• Pathopsysiology– Insufficient insulin, glucose cannot move into the
cell which leads to hyperglycemia– Hyperglycemia causes an osmotic diuresis– Diuresis causes glucosuria, dehydration, and
electrolyte imbalance
DKA: Pathophysiolgy
• Breakdown of glycogen is activated
• Gluconeogenesis is stimulated
• Impaired glucose uptake by adipose tissue causes triglyceride synthesis and liberation of free fatty acids
• Fatty acids enter liver, leading to ketoacidosis
DKA: Causes
• Undiagnosed type I DM
• Illness or infection
• Not taking prescribed insulin
• Trauma or Surgery
• Pancreatitis
• Too many calories
• Drugs: Prednisone, HCTZ, Dilantin, Epinephrine
CCRN®/PCCN® Review Course - Day 2 ©TCHP Education Consortium, September 2003, Rev. December 20154
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DKA: Assessment
• Nausea, abdominal pain,
• Weakness, fatigue, HA
• Polydipsia, polyuria, polyphagia
• Flushed, warm, dry skin
• Vision changes
• Tachycardia, orthostatic hypotension
• Change in LOC
DKA: Assessment
• Decreased CVP, RAP,PAP,CO
• Kussmaul’s respiratory pattern
• Acetone (fruity) odor to breath
• Glucose: 300-800 mg/dl
• Sodium: Variable based on hydration
• Potassium: High at first, then decreases
DKA: Assessment
• Serum Ketones: Elevated
• Urine: Positive for glucose and ketones
• Serum Osmol: elevated 295-330 mOsm/L
• Metabolic acidosis– pH less than 7.30
– HCO3 less than 15
– Paco2 less than 35 mm Hg
DKA: Treatment
• Rapid replacement of fluid deficit
• Correct electrolyte imbalances
• Usually total body K+ is severely depleted but serum levels show normal level or hyperkalemia because an intracellular to extracellular shift occurs due to acidosis
DKA: Treatment
• Normalize serum glucose level gradually
• Insulin therapy (often a loading dose~0.15 U/kg, followed by continuous drip~0.1 U/kg/hr )
• Do not drop serum glucose by more than 100/mg/dl/hr to avoid hypoglcemia, hypokalemia, and cerebral edema
DKA: Treatment
• Insulin infusion is decreased to 3-5 U/hr when serum glucose < 250 mg/dl and discontinued 1-2 hours after SQ insulin
• SQ insulin is started when BS is less than 250 mg/dl; pH >7.2; HCO3 >18 mEq/L
CCRN®/PCCN® Review Course - Day 2 ©TCHP Education Consortium, September 2003, Rev. December 20155
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Hyperglycemic Hyperosmolar Nonketotic Syndrome: HHNK
• Definition: Hyperglycemic crisis associated with hyperosmolality and severe dehydration in the absence of ketoacidosis
• Pathophysiology:– Relative insulin deficiency which leads to
hyperglycemia which leads to osmotic diuresis, electrolyte imbalance
– Sufficient insulin is present to inhibit gluconeogenesis, thus no ketoacidois
HHNK: Causes
• Infections
• Burns
• Trauma
• Renal Disease
• Alcohol
• Pancreatitis
• Drugs: Prednisone, HCTZ, Lasix, Dilantin, Betablockers, Thorazine
HHNK: Assessment
• Severe dehydration
• Hypotension and tachycardia
• Tachypnea
• Polyuria, polydipsia, and polyghagia
• Tachycardia, orthostatic hypotension
• Decreased CVP, RAP, PAP, CO/CI
• Vision changes
HHNK: Assessment
• Glucose: 600-2,000 mg/dl
• Sodium: normal or elevated
• Postassium: decreased
• Serum osmolality: > 330 mOsm/L
• Normal pH or slightly acidotic
• Urine: glucose + Ketones –
• No abdominal pain
HHNK: Treatment
• Rapid replacement of fluid deficit
• Serum Na, K and Blood Pressure to guide fluid selection
• Correct serum glucose level gradually
• Correct electrolyte imbalance
#2 - Case Study
• JJ is a 19 year old male, freshman at college and living in a dorm with a roommate. After a 2 day course of the flu, according to his roommate, he is found unresponsive in his bed. He is slightly flushed and dry, RR rapid and deep, and his HR is 148. Medics checked his finger-stick blood sugar: “High”- in the ER his blood sugar was 790
CCRN®/PCCN® Review Course - Day 2 ©TCHP Education Consortium, September 2003, Rev. December 20156
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DKA Vs HHNK
Type of DMBlood SugarKetosis and pHAnion GapRespiration/OdorOsmolaityPotassiumBunFluid Deficit
Diabetes Insipidus: DI
• Definition: Impaired renal conservation of water, due to decrease in ADH or inappropriate response to ADH
• 3 Forms:– Neurogenic (central)
– Nephrogenic
– Psychogenic (rare)
DI: Pathophysiology
• Inability to concentrate urine
• Insufficient ADH secretion causes immediate excretion of large volumes of dilute urine…leads to increased plasma osmolality
• Profound ADH deficiency; > 12L/day urine
• Serum ADH level decreased; <1pg/ml
DI: Causes
• Pituitary or Hypothalamic tumor
• Cranial trauma (basilar skull fracture)
• Cranial surgery
• Stroke
• Drugs; Lithium, Dilantin, and alcohol
DI: Assessment
• Polyuria, polydpsia, nocturia
• Weight loss, dehydration
• Hypotension, tachycardia
• Low urine osmolality (50-200)
• Urine sp. Gravity <1.005
• Increased serum osmolality (>300)
• Sodium > 147 mEq/L
DI: Treatment
• Maintain fluid and electrolyte balance
• Administration of synthetic ADH
• Synthetic ADH– Aqueous vasopressin (Pritressin) , IV-IM-SQ
– Vasopressin tannate, IM-SQ
– ADH Analogs
DDAVP (Desmopressin), IV-SQ-Intranasally
CCRN®/PCCN® Review Course - Day 2 ©TCHP Education Consortium, September 2003, Rev. December 20157
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Syndrome of Inappropriate Antiduretic Hormone: SIADH
• Definition: Impaired renal excretion of water due to excess of ADH or an increased renal responsiveness to ADH
SIADH: Pathophsiology
• ADH secretion continues despite low serum osmolality, failure of Negative feedback system
• Result: Inability to secrete a dilute urine, fluid retention and dilutional hyponatremia
• Plasma ADH >5 pg/ml
SIADH: Neurogenic Causes
• Pitutitary tumor
• CNS trauma or infection
• Stroke: thrombotic or hemorrhagic
• Guillain-Barre’ syndrome
• Nonmalignant pumonary disease
• Oat cell lung CA
SIADH: Nephrogenic Cause
• General anesthetics
• Narcotics
• Barbiturates
• Thiazide diuretics
• Tricyclic antidepressants
• Acetominophen
SIADH: Assessment
• Anorexia, N/V, weight gain
• Tachpnea, HTN, JVD
• Increased CVP,RAP, PAP
• Sodium < 120 mEq/L
• Bun decreased
• Serum osmolality < 280
• Urine sp. Gravity > 1.030
SIADH: Treatment
• Treatment is based on underlying cause and the patient’s response to symptoms
• Restricting fluid intake to 500-1000ml/day
• Severe hyponatremia may see 3% sodium chloride IV gtt
• Loop diuretic may be used to reduce the risk of heart failure
CCRN®/PCCN® Review Course - Day 2 ©TCHP Education Consortium, September 2003, Rev. December 20158
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#3 – Case Study
• Mack S. was involved in a MCC 2 days ago, and suffered a traumatic brain injury along with other injuries. He had a ventriculostomy placed, and is being kept sedated, is intubated. The past 2 hours, his nurse is noticing an increase in urine output > 200cc/hr. The other red flag is that the urine is watery, clear, very pale.
DI vs SIADH
Serum ADH
Urine Output
Urine sp. Gravity
Urine Osmolality
Serum Osmolality
Serum sodium
CVP
CCRN®/PCCN® Review Course - Day 2 ©TCHP Education Consortium, September 2003, Rev. December 20159
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CCRN®/PCCN® Review Course - Day 2 ©TCHP Education Consortium, September 2003, Rev. December 201510
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