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Midterms Examination Reviewer

Oct 03, 202420 min read

Pointers to Review

  • Diabetes Mellitus: pp. 1488 - 1530
    • HbA1C Testing
    • Insulin Administration
    • Complications: Hyperglycemia, Hypoglycemia, Diabetic Ketoacidosis (DKA), Diabetic Retinopathy, Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNKS)
  • Pituitary Disorders: pp. 1449 - 1452
    • Symptom of Inappropriate Antidiuretic Hormone: p. 1452
    • Diabetes Insipidus: p. 1451
  • Parathyroid Disorders: pp. 1470 - 1473
    • Hyperparathyroidism: pp. 1470 - 1472
    • Hypoparathyroidism: pp. 1472 - 1473
  • Adrenal Disorders: pp. 1474 - 1483
    • Pheochromocytoma: pp. 1474 - 1476
    • Adrenocortical Insufficiency (Addison’s Disease): pp. 1477 - 1479
    • Cushing’s Syndrome: pp. 1479 - 1482
    • Primary Aldosteronism: pp. 1482 - 1483
  • Increased ICP: pp. 2000 - 2004
  • Head Injury: pp. 2055 - 2060
  • Cardiovascular Accident: pp. 2031 - 2050
  • Spinal Injury: pp. 2070 - 2081

Diabetes Mellitus (pp. 1488 - 1530)

HbA1C Testing

Insulin Administration

Complications

  1. Hyperglycemia
  2. Hypoglycemia
  3. Diabetic Ketoacidosis (DKA)
  4. Diabetic Retinopathy
  5. Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNKS)

Pituitary Disorders (pp. 1449 - 1452)

Symptom of Inappropriate Antidiuretic Hormone (p. 1452)

  • Definition: failures in negative feedback mechanisms result in overproduction of ADH, resulting in fluid retention and subsequent dilutional hyponatremia. Urine is concentrated. This may be caused by lung disorders or malignant cancers that produce ADH. Direct stimulation by medications can result in SIADH.
  • Clinical Manifestations: fluid retention, weight gain, dilutional hyponatremia, concentrated urine
  • Diagnostic Examination: ---
  • Management:
    • Medical: often self-limiting; treatment is focused on etiology. Restrict fluid intake, potentially with paired diuretics. Hypertonic NaCl (3%) may be given IV for patients with severe hyponatremia.
    • Nursing: I&O monitoring, weighing, urine and blood chemistry, and neurologic status is monitored. Supportive measures are taken.

Diabetes Insipidus (p. 1451 - 1452)

  • Definition: A rare disorder of deficient ADH production due to hypothalamic or pituitary injury.
  • Clinical Manifestations: polyuria, polydipsia
    • Enormous daily urine output greater than 250 mL per hour with very low specific gravity of 1.001 to 1.005.
  • Diagnostic Examination:
    • Fluid Deprivation Test, withholding fluids for 8 to 12 hours until 3% to 5% of body weight is lost. If the urine being produced is still dilute, and fluid loss continues, DI is suspected. The test is terminated if tachycardia, excessive weight loss, or hypotension occurs.r
    • Serum Studies: ADH testing in plasma shows deficiency.
    • Trial Desmopressin
  • Management:
    • Medical: long-term HRT of ADH (Desmopressin), fluid balance, and correcting underlying etiologies.
      • Desmopressin causes vasoconstriction, and therefore should be used cautiously for patients with CAD.
      • Previous management techniques are not effective for nephrogenic DI. Thiazide diuretics, mild salt depletion, and prostaglandin inhibitors (indomethacin, aspirin) are used instead.
    • Nursing:
      • On-going physical assessment: dehydration, I&O, client education for HRT with return demonstrations

Parathyroid Disorders (pp. 1470 - 1473)

Four glands situated on the posterior aspect of the thyroid gland, producing parathormone, responsible for controlling calcium through bone deposition/resorption, GI absorption, and Kidney absorption. Phosphorus is lowered by parathormone. Excess serum calcium and phosphorus may result in calcium phosphate precipitation in body tissues.

Hyperparathyroidism: pp. 1470 - 1472

  • Definition: excess parathormone production characterized by bone decalcification and the development of renal calculi containing calcium.
    • Primary Hyperparathyroidism: onset most common between 60 to 70 years of age, more common in women, and rare in children less than 15 years of age, multiplying ten-fold by 65 years of age.
    • Secondary Hyperparathyroidism occurs in patients with chronic kidney failure and “renal rickets” as a result of phosphorus retention, and parathyroid stimulation/secretion.
  • Clinical Manifestations:
    • 50% of patients are asymptomatic.
    • Apathy, fatigue, muscle weakness, nausea, vomiting, constipation, hypertension and cardiac arrhythmias may occur, all attributable to hypercalcemia.
    • Anywhere between irritability to psychoses can result as the calcium acts on the brain and nervous system; higher calcium concentrations reduce nerve excitability.
    • A major complications of hyperparathyroidism is nephrolithiasis, found in 15% to 20% of newly diagnosed patients. It may result in pyelonephritis and kidney injury.
    • Demineralization of the bones or bone tumors (from overgrowth of osteoclasts) result in skeletal pain/tenderness, pain on weight bearing, pathologic fractures, deformities, and shortening of stature.
  • Diagnostic Examination:
    • Persistent elevation of serum calcium levels
    • Radioimmunoassays reveal an elevation of parathormone concentration, and can differentiate primary hyperparathyroidism from malignancy as a cause of hypercalcemia.
    • Imaging (Ultrasound, MRI, Thallium Scan), and fine-needle biopsy can evaluate parathyroid functioning and localize parathyroid cysts, adenomas, or hyperplasia.
  • Management:
    • Medical:
      • Surgical: Parathyroidectomy used when hypercalcemia is marked. Mild forms can allow for delaying of surgery.
      • Hydration: increased fluid intake prevents renal calculi formation. 2000 mL or more is recommended.
      • Mobility and Weight-bearing reduce the amount of calcium resorbed from bones.
      • Diet and Medication: restrict calcium. Protein and antacids may be used if GI was involved (peptic ulcer). Constipation is offset by dieting (physical activity, stool softeners, prune juice, fluid intake)
    • Nursing:
      • Educate the clients; family may believe the symptoms to be psychosomatic, and clients may be frustrated or depressed.
      • Postoperative:
        • Monitor for airway patency, dehydration, immobility, and diet.
        • Monitor for development of tetany, an early postoperative complication.
        • Mild transient hypocalcemia may occur, but functioning of the remaining parathyroid tissue often compensates adequately. Regular laboratory testing for calcium levels is recommended.
  • Complication: Hypercalcemic Crisis is an elevation of serum calcium over 13 mg/dL, resulting in neurologic, cardiovascular, and kidney symptoms that can be life-threatening.
    • Hydration maintains fluid output and promotes calcium excretion. Large volumes of isotonic IV saline is given. Monitor for edema and fluid overload and stop infusion if noted.
    • Calcitonin is used to reduce bone resorption and promote renal excretion of calcium.
    • Other medications that may be used in emergencies: cytotoxic agents, dialysis, corticosteroids with calcitonin, or bisphophonates.

Hypoparathyroidism: pp. 1472 - 1473

  • Definition: abnormal parathyroid development, destruction, or vitamin D deficiency results in inadequate secretion of parathormone. The most common cause is a subtotal thyroidectomy. Hyperphosphatemia and hypocalcemia occurs. Decreased renal resorption of calcium results in decreased phosphate excretion in urine.
  • Clinical Manifestations:
    • Low calcium levels increase irritability of the neuromuscular system and contributes to the chief symptom: tetany; general muscle hypertonia with tremors and spasmodic or uncoordinated contractions.
      • Latent Tetany: Numbness, tingling, and cramps, complaints of stiffness of hands and feet.
      • Overt Tetany: bronchospasms, laryngeal spasms, carpopedal spasms, dysphagia, photophobia, arrhythmias, and seizures.
    • Anxiety, depression, potential delirium
  • Diagnostic Examination:
    • Chvostek Sign: positive if tapping the facial nerve anterior to the ear and and just in front of the parotid gland results in spasming or twitching of the mouth, nose, and eye.
    • Trousseau Sign: positive if carpopedal spasm is induced by a blood flow occlusion to the arm for 3 minutes with a blood pressure cuff.
    • Serum phosphate is increased, and calcium is low.
    • Increased density of bone is noted during x-ray. The subcutaneous or paraspinal basal ganglia of the brain may be calcified.
  • Management:
    • Medical: increase the serum calcium level to 9 - 10 mg/dL and provide symptomatic care.
      • Calcium, magnesium, and calcitriol (or ergocalciferol) are used. Thiazide diuretics reduce urinary calcium excretion.
      • IV Calcium Gluconate is used if hypocalcemia and tetany occur after a thyroidectomy. If immediate effect is not noted, sedative agents such as pentobarbital may be given.
      • Respiratory distress may occur due to neuromuscular irritability. Provide a mechanical ventilator or tracheostomy, and prepare bronchodilators.
      • After normal calcium levels are reached, diet should include high calcium, but not high phosphorus. Milk, milk products, and egg yolk are high in phosphorus and therefore restricted. Supplementation with oral calcium salts (e.g., Calcium Gluconate) may be used. Aluminum hydroxide gel or aluminum carbonate after meals bind phosphate and promote its excretion.
    • Nursing:
      • Detect hypocalcemia in postoperative clients who underwent a thyroidectomy, parathyroidectomy, or radical neck dissection. Anticipate tetany, seizures, and respiratory difficulties.
      • Prepare IV Calcium Gluconate for emergency cases. If cardiac disorder, arrhythmias, or digitalis is present, calcium gluconate is given slowly and cautiously.
      • Calcium and Digitalis act to increase systolic contraction, and potentiate each other’s action. Fatal arrhythmias may arise when unmanaged. Cardiac patients require continuous monitoring.
      • Patient Education for disease processes and treatment.

Adrenal Disorders (pp. 1474 - 1483)

Divided into two adrenal glands on top of each kidney, with two distinct endocrine glands: the adrenal medulla, and the adrenal cortex.

  • Adrenal Medulla: secretes catecholamines (epinephrine/adrenaline as 90% of its secretions; norepinephrine) as stress response, contributing to the fight-or-flight response.
  • Adrenal Cortex: secretes steroid hormones: glucocorticoids (mainly cortisol), mineralocorticoids (mainly aldosterone), and sex hormones (mainly androgens).
    • Glucocorticoids: glucose metabolism; more glucocorticoids results in a higher glucose serum level.
    • Mineralocorticoids: electrolyte metabolism, acting on the renal tubular and GI epithelium to increase sodium absorption in exchange for potassium or hydrogen ion excretion. The main hormone for long-term sodium balance is aldosterone.
    • Sex Hormones: mainly androgens (male sex hormones). They often have little effect, but excess results in virilization in women, feminization in men, or precocious puberty in children (androgenital syndrome)

Pheochromocytoma: pp. 1474 - 1476

  • Definition: A rare, often benign, tumor originating in the chromaffin cells of the adrenal medulla (90%) or extra-adrenal chromaffin tissue (10%). Onset is 40 to 50 years old. 10% are malignant, 10% are bilateral. There is a high incidence in family members, and all first-degree relatives should be alerted and screened for the tumor.
  • Clinical Manifestations:
    • Typical triad: headaches, diaphoresis, palpitations in the patient with hypertension. Cardiovascular disturbances are common.
    • Pheochromocytoma may be paroxysmal; attacks last from seconds to hours, and produce extreme anxiety, tremors, and weakness. Headaches, vertigo, blurring of vision, tinnitus, air hunger, and dyspnea may occur. Other symptoms include polyuria, nausea, vomiting, diarrhea, abdominal pain, and a feeling of impending doom.
    • Orthostatic hypotension occurs in 70% of patients with untreated pheochromocytoma.
  • Diagnostic Examination:
    • Suspected in sympathetic nervous system overactivity with associated with hypertension.
    • Five Hs: hypertension, headache, hyperhidrosis (diaphoresis), hypermetabolism, and hyperglycemia.
    • Urine and plasma catecholamine levels are the most direct and conclusive tests for adrenal medulla overactivity.
      • 24-hour urine sample with food restrictions (coffee, tea, bananas, chocolate, vanilla, aspirin, etc.) can be analysed for catecholamines and catecholamine metabolites. A sample taken 2 to 3 hours after an attack can be used.
      • Blood sample taken after 30 minutes of rest in a supine position, with a butterfly needle, scalp vein needle, or venous catheter inserted 30 minutes before collection (to catecholamine secretion related to venipuncture).
    • If inconclusive, a clonidine suppression test can be done (antiadrenergic medication); if clonidine does not suppress catecholamines, pheochromocytoma is indicated.
    • Imaging (CT, MRI, UTX) can localize the pheochromocytoma. MIBG (I131-metaiodobenzylguanidine) scintigraphy is catecholamine-producing specific and noninvasive.
  • Management:
    • Medical:
      • Surgical: definitive treatment is adrenalectomy where a tumor is present. However, surgical treatment is high risk for this population. Stored catecholamines may be released during manipulation of the tumor, resulting in a hypertensive crisis.
      • During an attack, bed-rest with head elevation is prescribed for hypertension.
      • Control hypertension: alpha-adrenergic blockers, beta blockers, calcium channel blockers, or even catecholamine-synthesis inhibitors.
      • Postoperatively, corticosteroid HRT may be required for bilateral adrenalectomy or initially after a unilateral adrenalectomy.
      • Postoperative hypotension and hypoglycemia may result from withdrawal of catecholamines. Monitor for these changes. Monitor urine and plasma catecholamines and its metabolites.
    • Nursing:
      • Monitor for recurrence if not all tissue was removed: glucose levels, fluid and electrolyte balance, arterial pressures, and ECG changes. Maintain IV access for fluid and medications.
      • Educate the patient about measuring blood pressure and HRT.

Adrenocortical Insufficiency (Addison’s Disease): pp. 1477 - 1479

  • Definition: dysfunction of the adrenal gland feedback loop results in insufficient steroid production. Most cases are caused by autoimmune disorders. Tuberculosis and histoplasmosis may also result in direct adrenal gland destruction. This may also result from adrenalectomy and some medications. Long term use of corticosteroids and sudden cessation of exogenous adrenocortical hormone therapy can also result in insufficiency.
  • Clinical Manifestations:
    • Increased excretion of sodium, chloride, and water; increased retention of potassium (decreased mineralocorticoids)
    • Hypoglycemia, muscle weakness, lethargy, GI symptoms e.g. anorexia, weight loss, nausea and vomiting (decreased glucocorticoids)
    • Increased ACTH (in an attempt to increase steroid secretion) results in hyperpigmentation, especially around the knuckles, knees, and skin folds.
    • An Addisonian Crisis may occur, where severe hypotension, cyanosis, fever, nausea, vomiting, and signs of shock develop. Exertion may result in circulatory collapse, shock, and death if untreated.
  • Diagnostic Examination:
    • Early-morning serum cortisol and plasma ACTH differentiate primary adrenal insufficiency (increased ACTH) from secondary adrenal insufficiency and normal adrenal function.
  • Management:
    • Medical:
      • Circulatory Shock: restore circulation, fluids, and corticosteroids. Hydrocortisone is administered IV followed by 3 to 4 liters of NSS or D5W. Vasopressors may be used if hypotension persists.
      • Antibiotics can be given if an infection is causing a crisis.
      • Initiate oral intake as soon as tolerated, exchanging IV intake with oral intake.
      • Lifelong corticosteroid and mineralocorticoid replacement may be required if the adrenals do not regain function.
      • Additional salt in the diet to replace losses from vomiting or diarrhea.
    • Nursing:
      • Assess patient fluid balance and blood pressure, skin changes (color, turgor), weight changes, muscle weakness, fatigue, and other stressors.
      • Monitor for addisonian crisis: shock, hypotension, rapid/weak pulses, tachypnea, pallor, extreme weakness.
      • Management for addisonian crisis: fluid, glucose, electrolyte, and corticosteroid replacement. Vasopressors may be required.
      • Restore fluid balance: encourage adequate dietary consumption.

Cushing’s Syndrome: pp. 1479 - 1482

  • Definition: excessive presence of adrenal hormones; most commonly due to corticosteroid medications, but can occur from hyperplasia, or tumors.
  • Clinical Manifestations:
    • Arrest of growth, obesity, and musculoskeletal changes occur. Glucose intolerance is present due to elevated blood glucose levels.
    • Buffalo-hump appearance of the neck and supraclavicular areas, heavy trunk, and thin extremities.
    • Hypertension and heart failure result from excess water retention from aldosterone.
    • Virilization of women; hirsutism, breast atrophying, amenorrhea, clitoral enlargement, voice deepening.
    • Visual changes as a result of pressure on the optic chiasm from a growing tumor (if it is the cause).
  • Diagnostic Examination:
    • Serum cortisol, urinary cortisol, and low-dose dexamethasone suppression tests. At least two should be entirely abnormal to diagnose Cushing’s syndrome.
      • Serum cortisol is usually diurnal (6 AM to 8 AM > 4 PM to 6 PM). If this variance is lost, results are abnormal.
      • 24-hour urine collection should return cortisol levels three times higher than normal.
      • Dexamethasone should suppress cortisol levels.
  • Management:
    • Medical:
      • Tumor excision if caused by tumors; if on the pituitary, a transsphenoidal hypophysectomy is done. Radiation may also be effective. Adrenalectomy is done if the disease is primary.
      • Adrenal enzyme inhibitors may be used to reduce hyperadrenalism if tumors cannot be eradicated.
      • Inadequate adrenal function can be caused by treatment. Temporary replacement therapy may be required for several months until compensation.
      • If caused by exogenous corticosteroids, tapering or removal of the medication is attempted. Alternate-day therapy decreases Cushing’s and allows recovery of the adrenal glands.
    • Nursing:
      • Maintain adequate cardiac function: hypertension, hypokalemia
      • Risk for Injury
      • Risk for Infection
      • Impaired skin integrity
      • Disturbed body image
      • Manage complications

Primary Aldosteronism; Conn Syndrome (pp. 1482 - 1483)

  • Definition: excess of aldosterone, the salt-saving hormone.
  • Clinical Manifestations:
    • Hypertension is most prominent.
    • Urine volume is excessive (polyuria), but is dilute. Serum becomes concentrated, contributing to polydipsia.
    • Hypokalemia may occur as potassium is excreted to retain sodium. Hypokalemia produces variable muscle weakness, paralysis, cramping, fatigue, and decrease serum calcium levels, resulting in positive Chvostek and Trousseau signs, paresthesia, and tetany.
  • Diagnostic Examination:
    • Plasma aldosterone concentration (PAC) and plasma renin activity (PRA)
  • Management:
    • Medical:
      • Total Laparoscopic Adrenalectomy
      • Administration of corticosteroids, fluids, and other agents to maintain blood pressure postoperatively. Replacement of corticosteroids is lifeline if removal was bilateral.
      • Glucose levels are maintained through IV fluids, insulin, and diet modifications.
      • If adrenal involvement is bilateral, medical treatment is preferred over surgical treatment.
      • Spinorolactone, first-line drug for hypertension. Monitoring should be maintained.
    • Nursing:
      • Frequent assessment for adrenal insufficiency, crisis, or hemorrhaging.

Neurologic Dysfunction

Increased ICP (pp. 2000 - 2004)

  • Definition: ICP is normally 0 to 10 mmHg, and 15 mmHg at most for normal cases. Most commonly elevated due to head injury.
  • Clinical Manifestations:
    • Impaired neural function, initially manifested as altered LOC, later on by abnormal respiratory and vasomotor responses. Pupillary dysfunction is noted. Restlessness, confusion, and drowsiness are neurologically significant. This progresses to stupor then to a coma. Brain death may be evaluated if no confounding factors are known and the coma is profound and irreversible.
    • Decortication, decerebration or flaccidity may occur.
    • Changes in VS: Cushing’s triad (1) hypertension, widening pulse pressure as systolic BP increases, (2) bradycardia, (3) irregular breathing, and elevated temperature.
    • Complications:
      • Brain Stem Herniation: brain tissue presses down on the brain stem, restricting blood flow, leading to irreversible brain anoxia and brain death.
      • DI: neurologic DI results from decreased ADH secretion.
      • SIADH: neurologic SIADH results from increased ADH secretion.
  • Diagnostic Examination:
    • Imaging (CT, MRI, Angiography, PET, SPECT)
    • Transcranial Doppler
  • Management:
    • Medical:
      • Monitor ICP and Cerebral Oxygenation: Invasive monitoring is necessary (ventriculostomy, intraventricular catheter, subarachnoid bolt, epidural or subdural catheter, fiberoptic transducer-tipped catheter).
      • Decrease ICP: decrease cerebral edema (osmotic diuretics), CSF volume (draining CSF), or cerebral blood volume.
        • Cerebral edema can be reduced with Mannitol, an osmotic diuretic, or hypotonic saline (3%) that draws out fluids from the cerebral tissue into the serum. Fluid restriction also aids in reducing edema. Fevers affect cerebral edema, and therefore should be controlled. Antipyretics, a hypothermia blanket, etc. may be used.
        • CSF volume reduction is done through continuous drainage. A ventriculoperitoneal shunt (VP Shunt) connects the ventricles into the peritoneum to facilitate drainage. Monitor effectiveness and infection after insertion of shunt.
        • Decompressive hemicraniectomy: removal of bone to allow for expansion of the brain. It may be replaced once problems are resolved.
      • Maintain cerebral perfusion: cardiac output may be manipulated for brain perfusion. Fluid volume changes and inotropic agents (dobutamine, norepinephrine) improve cardiac output.
      • Pharmacology:
        • Anticonvulsants: Phenytoin (Dilantin); prevent seizures
        • Antipyretics, Muscle Relaxants: Acetaminophen (Tylenol) and Diazepam (Valium) to reduce temperature.
        • Blood Pressure Medications: Beta-Blockers (Propanolol) to maintain cerebral perfusion.
        • Corticosteroids: Dexamethasone (Decadron) reduces cerebral edema.
        • Hyperosmotic Agents: Mannitol (Osmitrol) induces diuresis, drawing fluids out from the brain. IVF is hypertonic to avoid promoting cerebral edema.
    • Nursing:
      • Maintain breathing: ensuring patency, removing secretions, and auscultation is done. Coughing can lead to increased ICP, and hypoxia results in cerebral edema.
        • Breathing can be impaired due to increased ICP: Cheyne-Stokes respirations manifest from pressure on the frontal lobe or deep midline structures.
        • Mechanical Ventilation may be required.
      • Optimizing cerebral tissue perfusion: reduce factors contributing to ICP. Maintain elevation of the head to reduce ICP. Extreme hip flexion and neck flexion and extreme rotation of the head increase ICP.
      • Maintain body temperature: shivering increases ICP. Fever increases cerebral edema.
      • Monitor electrolytes, acid-base, and I&O.
      • Maintain Negative Fluid Balance: limit intake to 1200 mL/day. Monitor fluid balance; catheterization is used to assess fluid balance. A urine output of 200 mL or more for two hours may indicate onset of neurologic DI.

Head Injury (pp. 2055 - 2060)

  • Definition: trauma to the skull, resulting in damage to the brain. Often from falls, vehicular accidents, and assault. Immediate complications include cerebral bleeding, hematomas, uncontrolled ICP increase, infections, and seizures. Changes in personality or behavior may occur, and cranial nerve deficits are produced depending on the area involved.
    • Open Head Injuries: scalp lacerations, fractures of the skull, interruption of the dura mater.
    • Closed Head Injuries:
      • Concussion: temporary loss of consciousness; widespread and microscopic jarring of the brain within the skull.
      • Contusions: localized, macroscopic, and “bruising” type of injury. Noticeable loss of function is noted. Coup-contra coup involvement. Bruising occurs, and the brain stem may swell and tear.
      • Fractures: hairline (a line, no splintering and distortion), depressed (crushed portion of skull), compound (break in skin, splintering of bone), comminuted (fragmentation)
        • Basilar skull fracture: a fracture on the base of the skull. This manifests as rhinorrhea and otorrhea from CSF leakage, raccoon eyes (ecchymosis around the eye), and battle’s sign (ecchymosis behind the ear). On a pillow, a “halo ring” is formed by a stain of CSF with blood in the center.
  • Clinical Manifestations: most symptoms result from increased level of consciousness. CSF drainage is checked (otorrhea, rhinorrhea)
  • Diagnostic Examination:
  • Management:
    • Medical:
      • Craniotomy: removal of tumor, relieve ICP, remove blood clots, or control hemorrhage. This may be (a) supratentorial, (b) infratentorial, or (c) transsphenoidal.
      • Alternative: craniectomy and cranioplasty
    • Nursing: maintain patent airway, ventilation, V/S, neuro checks, complication (Increasing ICP, Seizures, Hyperthermia)
      • Observe for CSF Leak: halo ring appearance of stains. If observed, instruct patient not to blow the nose, elevate the head of bed by 30 degrees, observe for infection (meningitis), place cotton ball on ear to absorb otorrhea, and gauze pad at the bottom of the nose for rhinorrhea.
      • Prevent complications of immobility.
      • Check for signs of infection.
      • Postoperative Positioning:
        • Supratentorial positioning: neutral neck alignment and side-lying or supine. Avoid operative side.
        • Infratentorial positioning: maintain straight neck alignment; no flexion to avoid tearing suture. Position patient on either side, not supine.
        • Transsphenoidal positioning: nasal packing, instruct patient to avoid blowing the nose. Provide oral care and keep head of bed elevated.

Seizures (p. 2017)

  • Definition: abnormal, sudden, excessive, uncontrolled electrical discharge of neurons within the brain that may result in alteration of consciousness, motor, or sensory ability, and/or behavior. Epilepsy is a chronic disorder characterized by recurrent, unprovoked seizure activity, in which 75% of cases are idiopathic.
  • Clinical Manifestations:
    • Generalized Seizures
      • Grand Mal; Major Motor Seizures: may be preceded by an “aura”. These have tonic and clonic phases, and are the most dramatic form of seizures.
        • Tonic phase involves stiffening, eye-rolling, and glottis closure. Incontinence and loss of consciousness may occur. 20 to 40 seconds.
        • Clonic phase involves jerking movements that taper off. Mucus production is increased.
        • Postictal period includes confusion and drowsiness.
      • Akinetic Seizure: organic brain damage results in sudden loss of postural tone and loss of consciousness.
      • Myoclonic Seizure: brain damage, may be precipitated by tactile or visual sensations. Brief flexor muscle spasm and myoclonic jerks occur.
      • Petit Mal; Absence Seizure: nonorganic brain damage; similar to daydreaming. Sudden onset, with twitching or rolling of eyes. Lasts a few seconds and is frequent. Common in preschoolers.
      • Febrile Seizure: most common in children, usually not resulting in brain damage. Also tonic-clonic, similar to grand mal seizures. Seizure abates when temperature is controlled.
      • Status Epilepticus: prolonged seizures with minimal postictal stages or without regaining consciousness.
    • Partial/Focal Seizures
      • Simple Partial Seizure: limitation to one hemisphere of the brain, with no loss of consciousness. This may be motor, sensory, or autonomy.
      • Complex Partial Seizure: begins in the anterior temporal lobe, then spreading to both hemispheres. This impairs consciousness and may be preceded by an “aura”.
  • Diagnostic Examination:
    • Differential:
      • Blood studies: rule out lead poisoning, hypoglycemia, infection, or electrolyte imbalances.
      • Lumbar Puncture: rule out infection or trauma
      • Imaging (Skull X-rays, CT Scan, Head Ultrasound, Brain Scan, Arteriogram) to detect pathologic defects
      • EEG to detect abnormal wave patterns that can specify a type of seizure.
  • Management:
    • Medical:
      • Surgery: if caused by a tumor, hematoma, or epileptic focus.
      • Phenytoin (Dilantin) is the drug of choice for generalized tonic-clonic (grand mal, febrile) and partial seizures.
        • Side effects include gum hyperplasia (swollen, tender), growth of facial and body hair, enlarged or rough facial features, acne, and skin.
        • Pregnancy Drug Category D: risk to the baby, but with benefits may outweigh the risk.
        • May be taken with a potentiator: phenobarbital. Seizure thresholds and spread/electrical discharge is inhibited.
      • Carbamazepine is used for some seizures. It reduces abnormal excitement in the brain.
      • Benzodiazepines: Diazepam (Valium) slows the CNS and reduces muscle spasms and convulsions.
    • Nursing:
      • Protect from injury: use side rails, loosen tight clothing, positioning
      • Keep airway open: side-lying, suction excess mucous production
      • Documentation: preictal aura, nature of ictal phase (symmetry, responses to stimuli, LOC, respiratory pattern), and postictal response (amount of time to orient to time and place; sleepiness).
    • First Aid: do not restrict the patient. Loosen neckwear, remove anything in their mouth, and turn them on their side. Cushion the patient’s head.

Cardiovascular Accident (pp. 2031 - 2050)

Spinal Injury (pp. 2070 - 2081)

Disorder

  • Definition:
  • Clinical Manifestations:
  • Diagnostic Examination:
  • Management:
    • Medical:
    • Nursing:

OBE MIDTERMS COVERAGE Hyperthyroidism Thyroid Storm Acute pancreatitis Pancreatic CA Gallstones Obesity Liver Cirrhosis Body Mechanics Hyperinsulism Meniere’s disease Abdominal assessment Eye medication DM Bowel/Gastric Bypass Surgery Hypothyroidism PUD UGIB Hepatic encephalopathy Hyperparathyroidism Glaucoma Hepatitis B Multiple sclerosis Seizures SIADH Chron’s disease Anatomy of the eye Retinopathy Osteoporosis Routine eye examination Osteomyelitis Retinal detachment Fracture of the ulna and radius Parkinsons Phenytoin levodopa Conjunctivitis Examination of the ear Hearing loss Otitis external Rheumatoid arthritis Head trauma Hypophysectomy Acute gastritis Osteoarthritis Subdural hematoma Caloric test Arthrogram Thrombotic stroke Subarachnoid hemorrhage Gastric CA Appendicitis

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