Endocrine/Hematology/Gastrointestinal/Renal/Integumentary Study Guide for the CCRN
Obviously, if five different topics are covered, 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.
Adrenal insufficiency is a critical medical condition that occurs when cortisol production in the body is significantly decreased or absent. Adrenal insufficiency can quickly progress to adrenal crisis, which, if left untreated, is fatal.
Four types of adrenal insufficiency have been identified. Glucocorticoid-induced adrenal insufficiency occurs when there is an acute interruption or withdrawal of long-term corticosteroid therapy. It is the most common cause of adrenal insufficiency. Addison’s disease, noted by autoimmune destruction of the adrenal gland, is the most common primary cause of adrenal insufficiency. Secondary adrenal insufficiency can develop when the pituitary gland is compromised and unable to produce ACTH to stimulate cortisol release from the adrenal glands. Tertiary adrenal insufficiency involves dysfunction of the hypothalamus and subsequent disruption of the ACTH release process.
Adrenal insufficiency can go unnoticed until it becomes a crisis. Many patients will present to an emergency department or critical care unit in acute shock, unresponsive to IV fluids or vasopressors. Earlier symptoms of this condition are vague and include weakness, fatigue, decreased appetite, and weight loss. Late symptoms include hypotension, cardiovascular collapse, and neurologic changes.
Diagnostic labs can identify electrolyte imbalances including hyponatremia, hypoglycemia, hyperkalemia, hypercalcemia, decreased ACTH levels, elevated creatinine, low aldosterone, high renin, and elevated TSH levels. Treatment of any underlying cause is crucial to recovery. Treatment includes administration of hydrocortisone (given as an initial bolus followed by daily or more frequent dosing), IV fluid resuscitation, correction of hypoglycemia, and slow correction of hyponatremia.
Patients must understand that long-term corticosteroid medication cannot be abruptly stopped. Any withdrawal of these medications must be done in slowly tapered increments.
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 of 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 two to three 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.
Diabetes mellitus (DM) is a chronic illness that affects numerous patients. Patients may be admitted to critical care units due to complications with this illness or present with diabetes as a comorbid illness that impacts, and often complicates, medical therapies for other dominating illnesses.
Type 1 DM is often referred to as juvenile diabetes. It is most often diagnosed in early childhood following failure of the pancreas’s ability to produce insulin. Symptoms often develop quickly and include polydipsia, polyphagia, polyuria, new onset bedwetting, unintended weight loss, irritability, fatigue, and vision changes.
Blood tests to aid in the diagnosis of type 1 DM include random blood glucose screening, fasting blood glucose testing, and hemoglobin A1C. A random blood sugar greater than 200mg/dL with associated symptoms is highly indicative of diabetes. A fasting blood glucose greater than 126mg/dL and/or hemoglobin A1C 6.5% or higher on two separate tests are also indicative of diabetes. Patients with acute onset or exacerbation of type 1 DM can develop diabeteic ketoacidosis. This condition is discussed later in this guide. To help distinguish between type 1 and type 2 DM, labs are completed to help identify any presence of autoantibodies and urinalysis is performed to determine ketonuria (less common in type 2 DM).
Treatment of type 1 DM focuses on insulin therapy, a regulated diet (low-carb), and exercise. Treatment is lifelong. Patients will need to have their blood sugars monitored and corrected frequently. Patients may use insulin injections, basal rate pumps, or closed-loop insulin delivery. Review the common insulin types and indications for use including short-acting (regular) insulin, rapid-acting insulin, intermediate-acting (NPH) insulin, and long-acting insulin.
Type 2 DM is an acquired, chronic condition related to the inability of the body to metabolize glucose due to insulin resistance or decreased insulin production. It generally develops in adulthood. Risk factors for type 2 DM include obesity, sedentary lifestyle, abdominal fat distribution, family history, race (African American, hispanic, American Indian, and Asian American), age greater than 45, prediabetes, and gestational diabetes.
Type 2 DM affects almost every system in the body. It can increase a patient’s risk for heart disease, atherosclerosis, renal failure, vision changes, nerve damage, hearing loss, infection, and neurologic changes. It can also complicate therapy plans for other illnesses as patients with type 2 DM often have decreased healing ability and are at increased risk for infection.
Treatment of type 2 DM often focuses on prevention of disease prior to medication or insulin. Patients can reduce their risk for type 2 DM by exercising regularly; eating healthy low-carb, low-fat, well-balanced meals; and losing weight. If preventive measures are not enough, patients may be prescribed oral medications such as Metformin (Glucophage®) to help decrease the body’s resistance to naturally produced insulin. Insulin therapy may be added if previous measures are not effective in reducing blood glucose and hemoglobin A1C levels.
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 1 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 the 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. One to two liters of isotonic fluids are recommended to be given within the first hour. This is followed by up to eight 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 five to seven 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.
Acute hyperglycemia most commonly occurs in patients with diabetes (type 1, type 2, 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 of 5.7-6.4% on two or more occasions is considered to be diagnostic for prediabetes. If the levels are 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.
Hyperosmolar Hyperglycemic State (HHS)
Hyperosmolar hyperglycemic state, or HHS, is a condition when a patient’s increased blood sugars last so long their body starts to have osmotic diuresis. 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 HHS. Patients with HHS have enough insulin to prevent the breakdown of fats that would normally result in ketoacidosis.
HHS is most common in people between the ages of 50-70 years old. While patients may have had elevated blood glucose levels for a long period of time, HHS 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 HHS. 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 HHS is not the same as diabetetic ketoacidosis, the treatment is extremely similar. The patient with HHS 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.
Acute hypoglycemia, otherwise known as hyperinsulinism, is classified by a blood glucose level 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 closely 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.
The thyroid is responsible for hormone secretion and regulation. If too much or too little thyroid hormones circulate the system, complications can incur.
Hyperthyroidism is caused by an overactive thyroid when the thyroid produces too much thyroxine (T4). It can be caused by a variety of conditions including thyroiditis, Graves’ disease, cancerous lesions, and benign enlargement of the thyroid. Patients at increased risk for hyperthyroidism include women, those with a family history of Graves’ disease or other hyperthyroid conditions, and those with chronic illness.
Symptoms of hyperthyroidism can be non-specific and include unintentional weight loss, tachycardia, abnormal heart rhythm patterns, increased appetite, tremor, nervousness, sweating, heat sensitivity, increased bowel motility, goiter, thinning skin, brittle hair, and fatigue. Patients with Graves’ disease may develop Graves’ ophthalmopathy where protrusion of the patient’s eyeballs occur as tissues behind the eyes swell. Eyes may become dry, reddened, swollen, and uncomfortable. Patients may experience light sensitivity, blurred vision, and reduced eye movement. Patients who smoke are more at risk for this development.
Diagnosis of hypothyroidism combines the use of medical history, physical exam, and blood work. Patients will have thyroxine (T4) and thyroid-stimulating hormone (TSH) levels drawn. Elevated T4 and low or absent TSH levels indicate a hyperactive thyroid. To help identify the underlying cause of hyperthyroidism, patients may undergo a radioiodine uptake test, thyroid scan, and/or thyroid ultrasound.
Treatment of hyperthyroidism includes correction of the underlying cause. If the thyroid is enlarged, oral radioactive iodine can be used to help shrink the thyroid. Anti-thyroid medications, such as methimazole (Tapazole®) and propylthiouracil, can be used to reduce thyroid hormone secretion. These medications can cause liver failure and death in some patients. Beta blockers may be used to help manage the symptoms of hyperthyroidism including tremor and heart rate abnormalities. Finally, thyroidectomy may be indicated if hyperthyroidism cannot be managed with alternative therapies.
Hypothyroidism is caused by an underactive thyroid. It can occur spontaneously or as a result of autoimmune disease (Hashimoto’s thyroiditis), over-treatment of hyperthyroidism, thyroid surgery, radiation therapy, or medication (lithium). Less common causes of hypothyroidism include pregnancy, iodine deficiency, and pituitary disorder. Risk factors for hypothyroidism include being a woman, age greater than 60, family history, autoimmune disorder, radiation to neck or thyroid, and thyroid surgery.
Early symptoms of hypothyroidism may be subtle and include fatigue and weight gain. If not recognized or treated, hypothyroidism can progress with symptoms of cold sensitivity, constipation, dry skin, thinning hair, muscle aches, weakness, joint pain, depression, and impaired memory. Patients may also have increased cholesterol levels, peripheral neuropathy, and myxedema.
Lab work is commonly used to diagnose hypothyroidism. Thyroid-stimulating hormone (TSH) and thyroxine (T4) levels can help determine the function of a patient’s thyroid. In hypothyroidism, patients will likely have an elevated TSH and low T4.
Treatment of hypothyroidism focuses on correction of thyroid hormone levels and resolution of any underlying disease. Patients will often be prescribed the synthetic thyroid hormone levothyroxine (Levothroid®). Patients should be educated on dietary recommendations including the limiting of soy and fiber as excess of one or both can decrease the absorption of thyroid hormones.
Syndrome of Inappropriate Antidiuretic Hormone Secretion (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 antidiuretic hormone secretion (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.
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