Page 1 Endocrine/Hematology/Gastrointestinal/ Renal/Integumentary Study Guide for the CCRN®
Obviously, if it covers five different topics, there is a lot to know to be successful at answering this type of question. About 20% of the exam covers these areas, so use this study guide to help you know what to study. Remember, you’ll not only need to know the construction of the various systems, but explicitly how they function and, especially, how to care for a patient whose condition is critical and who has problems with any of these body functions.
The endocrine system is responsible for maintaining and regulating numerous hormones and bodily systems. While the most common endocrine disease is diabetes, many other conditions can cause dysregulation across the bodily system. Review the following critical conditions and the role the nurse plays in monitoring for and managing these.
Acute hypoglycemia, otherwise known as hyperinsulinism, is classified by a blood glucose less than 50-60 mg/dL. This is often complicated by symptoms varying in severity. Seizures, changes in consciousness, lethargy, vomiting, myoclonus, respiratory distress, hypothermia, diaphoresis, and cyanosis can all be central nervous system symptoms of acute hypoglycemia. The adrenergic system may also be affected and result in symptoms of diaphoresis, tremor, tachycardia, palpitations, hunger, and anxiety.
There are several possible causes of acute hypoglycemia. Pancreatic islet tumors or hyperplasia can affect how much insulin is produced in the body, driving down blood glucose levels. In patients with diabetes mellitus, overdosing insulin correction or not maintaining appropriate dietary measures can also quickly drop blood sugars. Genetic defects, infections, sepsis, and drug or alcohol overdose may also impact the body’s blood glucose regulatory system.
Treatment for acute hypoglycemia involves correcting the blood glucose to a more normal range and treating insulin regulatory problems. Some patients may need medication to block or suppress insulin production. Medications such as diazoxide (Hyperstat®) and somatostatin (Sandostatin®) can be used to control the amount of insulin being released in the body. Diazoxide (Hyperstat®) works by inhibiting insulin release, whereas somatostatin (Sandostatin®) works by suppressing insulin production. Glucose and glucagon are often used to provide an instantaneous blood glucose elevation.
Patients with acute hypoglycemia need to be acutely monitored for persistent symptoms and lowered blood glucose levels. What may acutely increase a patient’s blood glucose may not maintain their levels if the underlying problem (insulin production/release) is not also addressed. Nurses should especially monitor their patients for central nervous and cardiopulmonary changes, as hyperinsulinism may cause damage to these systems, resulting in neurologic impairment if not corrected.
Acute hyperglycemia most commonly occurs in patients with diabetes (type I, type II, and gestational). In acute illness, patients may also have difficulties with hyperglycemia due to dysfunction of their insulin production or absorption due to other underlying conditions or extreme stress response.
Acute hyperglycemia can be diagnosed by repeated testing of a patient’s blood glucose level, both fasting and non-fasting, or by way of long-term glucose regulation (hemoglobin A1C). If checking a patient’s blood glucose when fasting, levels greater than 130 mg/dL are concerning for hyperglycemia. In non-fasting patients, levels that exceed 180 mg/dL will be considered hyperglycemia. Many patients will also have their hemoglobin A1C tested. Levels greater than 5.7% are considered to be abnormal. Levels 5.7-6.4% on two or more occasions is considered to be diagnostic for prediabetes. If the levels 6.5% or higher on two different tests, this is considered diagnostic for diabetes.
Symptoms of acute hyperglycemia include polyuria, polydipsia, polyphagia, blurred vision, headache, and fatigue. If left untreated, the hyperglycemia could develop into more serious conditions, such as diabetic ketoacidosis or hyperglycemic hyperosmolar nonketotic syndrome, which are discussed later in this study guide.
Hyperglycemia must be addressed to prevent long-term changes to the body. These changes can cause other chronic, debilitating conditions such as cardiovascular disease, neuropathy, kidney damage/failure, diabetic retinopathy, cataracts, poor circulation and healing, and infections. Treatment for hyperglycemia usually results in the use of insulin or other medications. Medications such as metformin, sulfonylureas, meglitinides, thiazolidinediones, and others may be prescribed. Patients should also be educated on healthy diet, physical activity, and weight loss measures to help control their blood sugars.
Diabetic ketoacidosis occurs in the event of poorly controlled diabetes mellitus, as an exacerbation of stress, or an acute illness in a patient with diabetes mellitus. In ketoacidosis, the body cannot metabolize glucose due to inadequate insulin levels. The body then looks to the breakdown of fat for energy. This process leads to ketone creation. The body can only use so many ketones, so excess ketones are released through the urine (ketonuria) and through respiration (Kussmaul’s respirations).
Diagnosis and Symptoms
Acute care nurses should be aware of diabetic ketoacidosis in previously known and unknown diabetics. Diabetic ketoacidosis is generally the presenting factor in children with Type I diabetes. Untreated illness can lead to severe reactions, such as cardiac arrhythmias, lethargy, hypotension, coma, and possibly death. Other symptoms include CNS depression, fluid imbalance, dehydration, chest pain, nausea/vomiting, appetite loss, abdominal pain, and confusion.
In a patient with diabetic ketoacidosis, the nurse can anticipate the patient’s blood glucose will exceed 250 mg/dL. The patient will also have decreased sodium and increased potassium levels before treatment. This will inverse following treatment. Arterial blood gas results will show metabolic acidosis with a pH less than 7.3 and \(HCO_3\) less than 18 mEq/L. A urinalysis will show elevated glucose and ketones.
Treatment of diabetic ketoacidosis focuses on fluid resuscitation and slow lowering of the patient’s blood glucose. 1-2 liters of isotonic fluids are recommended to be given within the first hour. This is followed by up to 8 liters of that fluid within the first 24 hours. As the patient’s potassium begins to decrease, potassium may be added to the fluids. This generally occurs when the patient’s potassium falls below 5 mEq/L.
Continuous intravenous insulin will be initiated beginning at 0.1 unit/kg/hour. This usually does not exceed 5-7 units per hour. The goal of treatment is to reduce the blood glucose slowly, between 50-75 mg/dL per hour. Nurses should monitor for rebound hypoglycemia, and dextrose may be added to the fluids once the patient’s blood glucose decreases to less than 200 mg/dL.
The combination of insulin and fluid resuscitation can quickly decrease a patient’s potassium. If the patient’s potassium level falls below 3 mEq/L, the insulin infusion should be stopped and potassium corrected prior to reinitiation of insulin. Since sodium and potassium have an inverse relationship, the patient’s sodium level should be monitored as well. The patient may have to be decreased to fluids with 0.45 normal saline if the patient’s levels become greater than 150 mEq/L. Magnesium supplementation should be prescribed if the patient’s magnesium levels decrease, as magnesium prevents the uptake of potassium.
Patients in acute diabteic ketoacidosis are often managed in the intensive care unit due to the close monitoring needs and frequent medication/drip changes. Some patients may require mechanical ventilation due to vomitus aspiration, ARDS, or respiratory alkalosis. As the patient’s electrolytes and arterial blood gas results normalize, the patient may be transitioned to a step-down or general medicine unit. These patients will likely need extensive education to help prevent future episodes of diabetic ketoacidosis throughout their hospital stay.
Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNK)
Hyperglycemic hyperosmolar nonketotic syndrome, or HHNK, is a condition when a patient’s increased blood sugars last so long their body starts to have osmotic diuresis. In some texts and updates, the abbreviation HHNK has been changed to HHS. For the purposes of this section, we will refer to hyperglycemic hyperosmolar nonketotic syndrome as HHNK. This can occur in patients with and without a history of type 2 diabetes. Hyperglycemia causes fluid shifts within the cells to help the body maintain an osmotic equilibrium. When the hyperglycemia is not corrected, this process continues until hypernatremia occurs due to glucosuria and dehydration. The hypernatremia increases the osmotic pull from the tissues, causing adverse symptoms and HHNK. Patients with HHNK have enough insulin to prevent the breakdown of fats that would normally result in ketoacidosis.
HHNK is most common in people between the ages of 50-70 years old. While patients may have had an elevated blood glucose for a long period of time, HHNK often results as an imbalance that occurs after an acute illness, medications, or dialysis. Illnesses such as strokes and cardiac events make these patients with chronic hyperglycemia more likely to develop HHNK. Thiazide medications are also known to contribute to this condition.
Patients with this condition will likely present with symptoms of polyuria, dehydration, hypotension, and tachycardia. More severe symptoms include changes in mental status, seizures, and hemiparesis. Several labs may be obtained. Essential laboratory tests include glucose, sodium, osmolality in both urine and blood, and BUN/Creatinine. While HHNK is not the same as diabetetic ketoacidosis, the treatment is extremely similar. The patient with HHNK will be initiated on an insulin drip with slow correction of hyperglycemia. Electrolytes will be monitored closely for imbalances and treated appropriately. The patient will also have replacement fluids for rehydration.
Nurses should monitor patients for rebound hypo- or hyperglycemia and begin education on ways to prevent this from occurring in the future.
Diabetes insipidus (DI) is a condition that is classified by a deficiency of antidiuretic hormone (ADH). ADH is also known as vasopressin. ADH/vasopressin is a hormone that works by maintaining peripheral vascular resistance, increases arterial blood pressure, and determines water reabsorption in the kidneys. When this hormone is absent or deficient, the body struggles to regulate the body’s osmolality.
DI usually develops as secondary to other conditions. Head trauma, primary brain tumor, meningitis, encephalitis, metastatic tumors, or surgical removal/irradiation of the pituitary gland may all cause DI. Rarely, patients may experience congenital nephrogenic diabetes insipidus, which results due to the absence or renal tubule response rather than decreased ADH production.
Symptoms of DI include polydipsia and polyuria. Patients with this condition may have a water deprivation test performed to determine the body’s urine output despite withholding fluids. Patients with DI will exceed 250 mL/hr of urine output in this test. When water/liquid is not deprived, a patient with DI may drink 2-20 liters or more of fluid a day. Other diagnostic labs for DI include:
- Elevated serum sodium levels
- Increased BUN
- Decreased ADH levels
- Decreased urine osmolality (<200 m0sm/kg)
- Decreased urine specific gravity (<1.005)
- Increased serum osmolality
Treatment for DI focuses on correcting the body’s fluid regulation. Vasopressin tannate provides the body with the decreased or absent ADH/vasopressin and may be given either intramuscularly or subcutaneously and lasts up to 72 hours per dose. Desmopressin acetate (DDAVP) helps patients to regulate fluid output and may be given via oral medication 2-3 times a day. One potential adverse reaction with DDAVP includes water intoxication, which can occur with medication overdose. Make sure to monitor the patients on this medication closely for neurologic status changes. Finally, some fluid deficits may be corrected with hypotonic solutions. This therapy must be conducted slowly, decreasing serum sodium levels no faster than 1 mEq/hr, to prevent cerebral edema.
Syndrome of Inappropriate Secretion of Antidiuretic Hormone (SIADH)
The pituitary gland plays an important role in how the body processes fluids. If there is an increase in secretion (hypersecretion) of the posterior pituitary gland, syndrome of inappropriate secretion of antidiuretic hormone (SIADH) can occur. With the increase in hormones from the posterior pituitary gland, the kidneys begin to reabsorb fluid from the body. This in turn causes fluid retention and dilutional hyponatremia. Patients will have extremely concentrated urine due to the decreased fluid processing through the kidneys and draining into the bladder.
There are many potential causes of SIADH. This includes neurologic disorders of the CNS, surgical manipulation of the brain, trauma, and tumors. Lung disorders such as pneumonia and pneumothorax may precipitate SIADH. SIADH may also result from adverse reactions to vincristine, phenothiazines, tricyclic antidepressants, and thiazide diuretics. Monitor patients on these medications closely to increase early detection of symptoms.
Symptoms and Diagnosis
Common symptoms of SIADH include edema, dyspnea, anorexia, nausea/vomiting, irritability, and abdominal discomfort. If left untreated, symptoms may progress into stupor and seizures due to hyponatremia. If suspected, a patient’s urine specific gravity, sodium, and serum osmolality should be checked. Diagnosis can be made if a patient’s serum sodium is less than or equal to 130 mEq/L, urine output less than 3 mL/kg/hr, urine specific gravity greater than 1020, and urinary sodium concentration greater than 20 mEq/lit.
In patients with SIADH, fluid excess should be managed by limiting the patient’s fluid intake to less than 800 mL/day for many patients. In patients with concern for cerebral vasospasms or subarachnoid hemorrhage, fluid restriction is less appropriate. Using 3% hypertonic saline may be used instead in these cases to prevent brain swelling and preserve perfusion. Medications such as furosemide (Lasix®) may be used to prevent fluid retention. This may be used in addition to oral salt tablets to maintain appropriate serum sodium levels. Vasopressin receptor antagonists may be used to provide regulation of vasoconstriction and ACTH release. While there are many supportive measures for correcting SIADH, ultimate correction occurs with treatment of the underlying condition when applicable.
Nurses must keep close observation of patients with SIADH. Strict monitoring of intake and output should be implemented to ensure a patient is making urine at least 0.5-1 mL/kg/hour. Overhydration should be avoided in patients to prevent further reuptake of fluid and resultant decreased sodium levels. Seizure precautions should be initiated to help prevent harm in the event of a hyponatremic seizure event.