images have been removed from the powerpoint slides in ...€¦ · anatomy and physiology •...

CCRN®/PCCN® Review Course - Day 2 ©TCHP Education Consortium, September 2003, Rev. December 20151

Images have been removed from the PowerPoint slides in this handout due to copyright restrictions.

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



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



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



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



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



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



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



#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

images have been removed from the powerpoint slides in ...€¦ · anatomy and physiology •...

Documents