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The Anatomy of a Neuron Dendrites - receive information, respond to signals from other neurons, responds to external stimuli (pain,

, pressure) Cell Body - decides how to respond to information received from the dendrites, produces the action potential- an electrical output signal of the neuron Axon - carries electrical signals from the cell body to destination. Axons can be very long (some in your body are 3 feet) and are usually bunded together into nerves Synapses (Synaptic Terminal) - at the end of the axon, they transmit signals to other neurons. A chemical, known as a neurotransmitter, is released at the synapse in response to an action potential. These terminals may communicate with glands, muscles, or other neurons. Myelin - a special insulating sheath on some axons, interrupted by "naked" areas called nodes. Structures of the Brain: Medulla (also called medulla oblongata) 1 - continuous with spinal cord 2 - contains ascending & descending tracts that communicate between the spinal cord & various parts of the brain 3 - contains 3 vital centers: cardioinhibitory center, which regulates heart rate respiratory center, which regulates the basic rhythm of breathing vasomotor center, which regulates the diameter of blood vessels Pons 1 - Bridge connecting spinal cord w/ brain & parts of brain w/ each other 2 - contains pneumotaxic center (a respiratory center) Thalamus 1 - Relay station for nearly all sensory impulses (except olfaction) Hypothalamus 1 - Control of Autonomic Nervous System 2 - Reception of sensory impulses from viscera

3 - Intermediary between nervous system & endocrine system 4 - Control of body temperature 5 - Regulation of food intake 6 - Thirst center 7 - Part of limbic system (emotions such as rage and aggression) 8 - Part of reticular formation Reticular formation 1 - portions located in the spinal cord, medulla, pons, midbrain, & hypothalamus 2 - needed for arousal from sleep & to maintain consciousness Cerebellum 1 - functions in coordination, maintenance of posture, & balance Cerebrum 1 - largest portion of the human brain 2 - consists of 2 hemispheres divided by a fissure 3 - includes cerebral cortex, medullary body, & basal ganglia: Cortex: outer 2 - 4 mm of the cerebrum consists of gray matter (cell bodies & synapses; no myelin) 'folded', with upfolded areas called gyri & depressions or grooves called sulci consists of four primary lobes Medullary body: the 'white matter' of the cerebrum; consists of myelinated axons Basal ganglia: masses of gray matter in each cerebral hemisphere important in control of voluntary muscle movements

Limbic System 1 - consists of a group of nuclei + fiber tracts 3 - Functions: aggression, fear, feeding, sex (regulation of sexual drive & sexual behavior) The left hemisphere is thought to control language and mathemathics. The right hemisphere is the center for spatial perception, music and creativity. FOUR PRIMARY LOBES The frontal lobe is concerned with higher intellectual functions, such as abstract thought and reason, speech (Broca's area in the left hemisphere only), olfaction, and emotion. Voluntary movement is controlled in the precentral gyrus (the primary motor area). The parietal lobe is dedicated to sensory awareness, particularly in the postcentral gyrus (the primary sensory area). It is also concerns with abstract reasoning, language interpretation and formation of a mental egocentric map of the surrounding area. The occipital lobe is responsible for interpretation and processing of visual stimuli from the optic nerves, and association of these stimuli with other nervous inputs and memories. The temporal lobe is concerned with emotional development and formation, and also contains the auditory area responsible for processing and discrimination of sound. It is also the area thought to be responsible for the formation and processing of memories. Reflex- rapid (and unconscious) response to changes in the internal or external environment needed to maintain homeostasis Reflex arc - the neural pathway over which impulses travel during a reflex. The components of a reflex arc include: 1 - receptor - responds to the stimulus 2 - afferent pathway (sensory neuron) - transmits impulse into the spinal cord 3 - Central Nervous System - the spinal cord processes information 4 - efferent pathway (motor neuron) - transmits impulse out of spinal cord 5- effector - a muscle or gland that receives the impulse from the motor neuron & carries out the desired response Dorsal Root ( Sensory); Ventral Root (Motor) ascending tracts transmitting sensory information; the descending tracts transmitting motor information Cerebrospinal fluid- is produced by the choroid plexus, in the interior fluid spaces of the brain (ventricles)

II. Middle, vascular layer (also known as the uveal tract) Choroid- a thin, pigmented membrane containing blood vessels that supply eye tissues Ciliary body: the anterior continuation of the choroids containing muscles that change the shape of the lens to focus the vision. Iris- the central extension of the ciliary body consisting of two muscles and central opening, the pupil, which constricts and dilates to regulate the amount of light entering the eyes interior (constricts with strong light and near vision, dilates with dim light and far vision. Aqueous humor- watery fluid filling the eyes anterior chamber that serves as a refracting medium and maintains the hydrostatic intraocular pressure (IOP) Lens- a biconvex crystalline body located behind the pupil that changes shape for accommodation (focusing). Vitreous humor A jellylike substances filling the posterior cavity behind the lens, acting as a refractive medium and maintaining the shape of the eye. III. The inner, neural layer- the retina- contains layers of the nerve cells, including the rods and cones, that translate lightwaves into neural impulses of transmission to the brain EAR STRUCTURES External ear- structures include the auricle, external auditory canal, and tympanic membrane, also called eardrum. T he auricle and external auditory canal receive and direct sound waves to the tympanic membrane Middle ear- known as the tympanum , is an air- filled cavity in the temporal bone. It contains three small bones (malleus, incus, and stapes) The inner ear, known as labyrinth, is the portion of the ear that consists of the cochlea, vestibule, and semicircular canals. DIAGNOSTIC TEST Electroencephalogram (EEG) records the electrical activity of the brain. Using electrodes, this noninvasive test gives a graphic representation of brain activity. Nursing actions: Determine the ability to lie still, reassure that electrical shock wont occur. Withhold medications that may interfere with the results (such as antianxiety, anticonvulsants) and caffeine for 24 to 48 hours before the procedure. Computed tomography (CT) scan- used to identify brain abnormalities, used to identify intracranial tumors and other brain lesions. Nursing actions: Note for allergies to iodine, seafood, and radiopaque dyes, if dye will be used. Make sure that written, informed consent has been obtained.

Magnetic resonance imaging (MRI)- uses magnetic and radio waves to create a detailed visualization of the brain and its structures. Nursing actions: Be aware that patients with pacemakers, surgical, and orthopedic clips, or charnel shouldnt be scanned including jewelry and metal objects. Determine the patients ability to lie still. Administer sedation as prescribed. Lumbar puncture (LP)- a needle is used to collect CSF from the lumbar subarachnoid space. This allows measurement of CSF pressure. Nursing actions: Determine the patients ability to lie still in a flexed, lateral, recumbent position. Make sure that written informed consent has been obtained. ICP is a contraindication. After the procedure, keep the patient flat in bed, as directed (from 20 minutes to a few hours). Electromyography (EMG)- uses electrodes to graphically record the electrical activity of a muscle at rest and during contraction. Nursing actions: explain that the patient must flex and relax the muscles during the procedures. Explain that the patient will feel some discomfort but not pain. Myelography- an injection of rradiopaque dye by LP followed by fluoroscopy allows visualization of the subarachnoid space, spinal cord, and vertebrae. Skull x-rays give a radiographic picture of the head and neck bones. Positron emission tomography (PET) involves injection of a radioisotope, allowing visualization of the brains oxygen uptake, blood flow, and glucose metabolism. Glasgow Coma Scale- a method of assessing a clients neurological condition. A scoring system based on a scale of 1 -15 points. (MOtor responses - 6, Verbal responses- 5, Eye opening- 4). The lowest point is 3. Eye opening is the most important indicator. Visual actuity test- measures clarity of vision using a letter chart (Snellens) placed 20 feet (6 m) from the patient. Acuity is expressed in a ratio that relates what a person sees at 20 feet to what the patient can see at feet. Extraocular eye muscle testing- checks for parallel alignment of the eyes, muscle strength, and cranial nerve function. Tonometry test- measures intraocular fluid pressure using an applation tonometer or an airpuff tonometer. Auditory acuity test- gives a general estimating of a patients hearing. It assess the patients ability to hear a whispered phrase or ticking watch. Otoscopic examinations- use an otoscope to visualize the tympanic membrane. Audiometry- measures the patients degree of deafness using pure- tone or speech methods. MAJOR NEUROSENSORY DISORDERS MOTOR NEURONE DISEASE

Motor nerves become damaged and eventually stop working. Therefore, the muscles that the damaged nerves supply gradually lose their strength. The main types of MND are: Progressive muscular atrophy- The small muscles of the hands and feet are usually first affected, but the muscles are not stiff. Progressive bulbar palsy- The muscles first affected are those used for talking, chewing, and swallowing (the bulbar muscles). Amyotrophic Lateral Sclerosis (ALS)- commonly known as Lou Gehrigs disease, is a progressive, degenerative disorder that leads to decreased motor function in the upper and lower motor neuron systems. The muscles tend to become stiff as well as weak at first. Certain nerve cells degenerate, resulting in distorted or blocked nerve impulses. Nerve cells die and muscle fibers have atrophic changes resulting in progressive motor dysfunction. KEY SIGNS AND SYMPTOMS Awkwardness of fine finger movements, dysphagia, fatigue, muscle weakness in the hands and feet KEY TEST RESULTS Creatinine kinase level is elevated. Electromyography (EMG) shows decreased amplitude of evoked potentials. KEY TREATMENTS Symptomatic relief KEY INTERVENTIONS Assess neurologic and respiratory status. Assess swallow and gag reflexes. Monitor and record vital signs and intake and output. Devise an alternate method of communication, when necessary. Suction the oral pharynx, as necessary. BELLS PALSY Is a weakness (paralysis) that affects the muscles of the face. It is due to a problem with the facial nerve. It usually affects one side of the face, but rarely both sides are affected.

KEY SIGNS AND SYMPTOMS Inability to close eye completely on the affected side, pain around the jaw or ear, unilateral facial weakness Key test results EMG helps predict the level of expected recovery by distinguishing temporary conduction defects from a pathologic interruption of nerve fibers. KEY TREATMENTS Moist heat Corticosteriod: prednisone (Deltasone) to reduce facial nerve edema and improve nerve conduction and blood flow. KEY INTERVENTIONS During treatment with prednisone. Watch for adverse reactions, especially GI distress and fluid retention. If GI distress is troublesome, a concomitant antacid usually provides relief. Apply the heat to the affected side of the face, taking care not to burn the skin. Massage the patients face with a gentle upward motion two or three times daily for 5 to 10 minutes, or have him massage his face himself. When hes ready for active exercises, teach him to exercise by grimacing in front of a mirror. Arrange for privacy at mealtimes; Offer psychological support. Give reassurance that recovery is likely within 1 to 8 weeks. ENCEPHALITIS AND MENINGOENCEPHALITIS Encephalitis is inflammation of the brain parenchyma, often caused by viral infections but also by other pathogenic organisms and occasionally by other conditions, e.g. toxins, autoimmune disorders. Meningoencephalitis is an inflammatory process, most often due to viral infection, involving both the brain and meninges. KEY SIGNS AND SYMPTOMS Meningeal irritation (stiff neck and back) and neuronal damage (drowsiness, coma, paralysis, seizures, ataxia, and organic psychoses)

Positive Kernigs sign- pain resistance when the patients leg is flexed at the hip or knee while hes in a supine position and Brudzinskis sign- flexion of the hips and knees in response to passive flexion of the neck. Sudden onset of fever, headache, vomiting KEY TEST RESULTS Endotracheal intubaion and mechanical ventilation Nasogastric tube feedings or total parenteral nutrition Anticonvulsants: phenytoin (Dilantin), Phenobarbital (Luminal) Analgesic and antipyretics: aspirin or acetaminophen (Tylenol) to relieve headache and reduce fever Diuretics: furosemide (Lasix) or mannitol (Osmitrol) to reduce cerebral swelling Corticosteroid: dexamethasone (Decadron) to reduce cerebral inflammation and edema KEY INTERVENTIONS During acute phase of illness Assess neurologic function often. Observe the patiens mental status and cognitive abilities. Maintain adequate fluid but avoid fluid overload. Measure and record intake and output accurately. Carefully position the patient and turn him often. Assist with range-of-motion exercises. Maintain a quiet environment. Darken the room. TRIGEMINAL NEURALGIA Neuralgia means pain coming from a nerve. In TN you have sudden, and usually severe, pains coming from one or more branches of the trigeminal nerve. The second and third branches are the most commonly affected. Therefore, the pain is usually around your cheek, jaw or both. The pain is stabbing ("like electric shocks"), piercing, sharp, or knife like. It usually lasts a few seconds but can last up to two minutes. The pain can be so sudden and severe that you may jerk or grimace with pain. KEY SIGNS OR SYMPTOMS

Searing pain in the facial area. KEY TEST RESULTS Observation during the examination shows the patient favoring (splinting) the affected area. To ward off a painful attack, the patient commonly holds his face immobile when talking. He may also leave the affected side of his face unwashed and unshaven or protect it with a coat or shawl. KEY TREATMENTS Anticonvulsants: carbamazepine (Tegretol) or phenytoin (Dilantin) may temporarily relieve or prevent pain. Microsurgery for vascular decompression Key interventions Observe and record the characteristics of each attack, including the patients protective mechanisms. Provide adequate nutrition in small, frequent meals at room temperature. If the patient is receiving carbamazipine , watch for cutaneous and hematologic reactions (erythematous and pruritic rashes, urticaria, photosensitivity, leucopenia, aplastic anemia, thrombocytopenia) If the patient is receiving phenytoin, watch for adverse effects, including ataxia, gingival hyperplasia. Advise the patient to place food in the unaffected side of his mouth when chewing, to brush teeth and rinse his mouth often, and see a dentist twice a year to detect cavities. The blood supply to the brain comes mainly from four arteries - the right and left carotid arteries, and the right and left vertebrobasilar arteries There are two main types of stroke: Ischemic- This common form of stroke is usually caused by blood clot in an artery which blocks the flow of blood. Hemorrhagic- A damaged or weakened artery may 'burst' and bleed: KEY SIGNS AND SYMPTOMS Fever, headache, mental impairment, seizures, coma, nuchal rigidity, vomiting KEY TEST RESULTS

CT scan reveals intracranial bleeding, infarct (shows up to 24 hours after the initial symptoms), or shift of midline structures Digital subtraction angiography reveals occlusion or narrowing of vessels. MRI shows intracranial bleeding, infarct, or shift of midline structures. KEY TREATMENTS Anticoagulants: heparin, warfarin (Coumadine) Anticonvulsants: phenytoin (Dilantin) Glucorticoid: Dexamethasone (Decadron) Thrombolytic therapy: tissue plasminogen activator given within the first 3 hours of an ischemic stroke, to restore circulation to the affected brain tissue and limit the extent of brain injury, KEY INTERVENTIONS Take v/s every 1 to 2 hours initially and q 4 hours when the patient becomes stable. Elevate the head of the bed 30 degrees Conduct a neurologic assessment q 1-2 hours initially. SPINAL CORD INJURY Usually result from traumatic force on the vertebral column. Necrosis and scar tissue form in the area of the traumatized cord. The prime directive is always consider the possibility of spinal injury, especially if: Major trauma Suggestive mechanism of injury Spinal pain or neurological symptoms/signs Altered consciousness Elderly or severe arthritic disease KEY SIGNS AND SYMPTOMS Loss of bowel and bladder control, paralysis below the level of injury, paresthesia below the level of the injury KEY TEST RESULTS

CT scan shows spinal cord edema, vertebral fracture, and spinal cord compression MRI shows spinal cord edema, vertebral fracture, and spinal cord compression. KEY TREATMENTS Flat position, with neck immobilized in a cervical collar Maintenance of vertebral alignment through Crutchfield tongs and Halo brace. Surgery for stabilization of the upper spine such as insertion of Harrington rods. Atianxiety agent: lorazepam (Ativan) Glucocorticoid: methyprednisolone (Solu- MedroL) given as infusion immediately following injury (improves neurologic recovery when administered within 8 hours of injury). H2- receptor antagonists: cimitidine (Tagamet), ranitidine (Zantac) Laxative: bisacodyl (Dulcolax) KEY INTERVENTIONS Assess neurologic and respiratory status. Assess for spinal shock. Check for autonomic dysreflexia (sudden extreme rise in blood pressure). Provide skin care. PARKINSON'S DISEASE (PD) Is a chronic (persistent) disorder of part of the brain. It mainly affects the way the brain coordinates the movements of the muscles in various parts of the body. A small part of the brain called the substantia nigra is mainly affected. This area of the brain sends messages down nerves in the spinal cord to help control the muscles of the body. Messages are passed between brain cells, nerves, and muscles by chemicals called neurotransmitters. Dopamine is the main neurotransmitter that is made by the brain cells in the substantia nigra and it is deficient. KEY SIGNS AND SYMPTOMS Pill- rolling tremors, tremors at rest, masklike facial expression, shuffling gait, stiff joints, dyskinesia, cogwheel rigidity, stooped posture. KEY TEST RESULTS

EEG reveals minimal slowing of brain activity KEY TREATMENTS Antidepressant: amitriptyline (Elavil) Antiparkisonian agents: levodopa (Larodopa), carbidopalevodopa (Sinemet), benztropine (Cogentin). KEY INTERVENTIONS Assess neurologic and respiratory status. Reinforce gait training Reinforce independence in care. MYASTHENIA GRAVIS A neuromuscular disorder that is marked by weakness of voluntary muscles. Is characterized by a disturbance in transmission of nerve impulses at neuromuscular junctions. This transmission results from a deficiency in release of acetylcholine or a deficient number of acetylcholine receptor sites. The fault is is due to a problem with the immune system. Myasthenia gravis is an 'autoimmune disease'. The immune system normally makes antibodies (special proteins) to attack bacteria, viruses and other 'germs'. In people with autoimmune diseases, the immune system makes antibodies against part or parts of the body. The fault is due to a problem with the immune system. Myasthenia gravis is an 'autoimmune disease'. The immune system normally makes antibodies (special proteins) to attack bacteria, viruses and other 'germs'. In people with autoimmune diseases, the immune system makes antibodies against part or parts of the body. KEY SIGNS AND SYMPTOMS Dysphagia, drooling, muscle weakness and fatgability (typically, muscles are strongest in the morning but weaken throughout the day, especially after exercise), profuse sweating KEY TEST RESULTS EMG shows decreased amplitude of evoked potentials. Neostigmine (Prostigmin) or edrophonium (Tensilon) test relieves symptoms after medication administrationa positive indication of the disease. KEY TREATMENTS

Anticholinestrease: neostigmine (Prostigmine), pyridostigmine (Mestinon) Glucocorticoids: prednisone (Deltasone), dexamethasone (Decadron), corticotrophin (ACTH) Immunosuppresants: azathioprine (Imuran), cyclophosphomide (Cytoxan) KEY INTERVENTIONS Assess neurologic and respiratory status. Assess swallow and gag reflexes. Watch the patient for choking while eating MULTIPLE SCLEROSIS Is a progressive disease that destroys myelin in the neurons of the brain and spinal cord. Degeneration of the myelin sheath results in patches of sclerotic tissue and impairs the ability of the nervous system to conduct motor nerve impulses. KEY SIGNS AND SYMPTOMS Nystagmus, diplopia, blurred vision, optic neuritis, weakness, paresthesia, impaired sensation, paralysis KEY TEST RESULTS CT scan eliminates other diagnosis such as brain or spinal cord tumors. MRI eliminates other diagnoses such as brain or spinal cord tumors. KEY TREATMENTS Plasmapheresis (for antibody removal) Cholinergic: bethanechol (Urecholine) Glucocorticoids: prednisone (Deltasone), dexamethasone (Decadron), corticotrophin (ACTH) Immunosupressants: cyclophosphosphomide (Cytoxan), methotrexate (Folex) Skeletal muscle relaxants: Baclofen (Lioresal) KEY INTERVENTIONS Assess changes in motor coordination, paralysis, or muscular weakness and report changes. Encourage the patient to express feelings about changes in body image. Establish a bowel and bladder program.

Maintain activity, as tolerated (alternating rest and activity). HUNTINGTON'S DISEASE is associated with cell loss within the basal ganglia and cortex. It is inherited as an autosomal dominant disease and leads to progressive choreic movements and dementia. KEY SIGNS AND SYMPTOMS Dementia (can be mild at first but eventually disrupts the patients personality) Gradual loss of musculoskeletal control, eventually leading to total dependence. KEY TEST RESULTS Positron emission tomography detects the disease. Deoxyribonucleic acid analysis detects the disease. KEY TREATMENTS Antidepressant: Imipramine (Tofranil) to help control choreic movements. Antipsychotics: Chlorpromazine (Thorazine) and haloperidol (Haldol) to help control choreic movements. Supportive, protective treatment aimed at relieving symptoms (because Huntingtons disease has no known cure) KEY INTERVENTIONS Provide physical support by attending to the patients basic needs, such as hygiene, skin care, bowel and bladder care, and nutrition. Look for signs of suicide. Control the patients environment to protect him from suicide or other self- inflicted injury. Pad the side rails of the bed but avoid restraints. GUILLAIN-BARR SYNDROME An autoimmune disorder causing demyelination and axonal degeneration, causing an acute, ascending and progressive neuropathy characterised by weakness, paraesthesia, and hyporeflexia. In severe cases, muscle weakness may lead to respiratory failure. Severe autonomic dysfunction may also occur. KEY SYMPTOM Muscle weakness (ascending from legs to arms)

KEY TEST RESULTS A history of preceding febrile illness (usually a respiratory tract infection) and typical clinical features. CSF protein level begins to rise, peaking in 4 to 6 weeks. The CSF white blood cell count remains normal but, in severe disease, CSF pressure may rise above normal. KEY TREATMENTS Anticoagulants: heparin , warfarin Corticosteroid: prednisone (Deltasone) Endotracheal intubation or tracheotomy if the patient has difficulty clearing secretions; possibly mechanical ventilation. I.V. fluid therapy Nasogastric tube feedings or parental nutrition Plasmapheresis KEY INTERVENTIONS Watch for ascending sensory loss, which precedes motor loss. Also monitor v/s and LOC Assess and treat respiratory dysfunction. Use a respirometer with a mouthpiece or a facemask for bedside testing. Obtain ABG measurements Begin respiratory support at the first sign of dyspnea (in adults vital capacity < 800 mL) or decreasing partial pressure of arterial oxygen. If respiratory failure becomes imminent, establish an emergency airway with an endotracheal tube. Establish a strict turning schedule; inspect the skin for breakdown, and reposition the patient q 2 hours. If aspiration cant be minimized bty diet and position modification, expect to provide NGT. Apply antiembolism stocking and give prophylactic anticoagulants, as needed. Encourage adequate fluid intake (2 qt or 2L/ day), unless contraindicated. EPILEPSY (SEIZURE)

Seizure is a short episode of symptoms caused by a burst of abnormal electrical activity in the brain. Epilepsy means that you have had repeated seizures. If you have a single seizure, it does not necessarily mean that you have epilepsy. Status epilepticus refers to continued seizure activity, a medical emergency treated with medications. Seizures are divided into two main types I. Generalized- These occur if the abnormal electrical activity affects all or most of the brain. The symptoms tend to be 'general' and involve much of your body. There are various types. A tonic-clonic seizure (grand mal)- With this type of seizure your whole body stiffens, you lose consciousness, and then your body shakes (convulses) due to uncontrollable muscle contractions. Absence seizure (petit mal)- With this type of seizure you have a brief loss of consciousness or awareness. There is no convulsion, you do not fall over, and it usually lasts only seconds. Absence seizures mainly occur in children. A myoclonic seizure is caused by a sudden contraction of the muscles which cause a jerk. A tonic seizure causes a brief loss of consciousness, and you may become stiff and fall to the ground. An atonic seizure causes you to become limp and collapse, often with only a brief loss of consciousness. II. Partial- these type of seizures the burst of electrical activity starts in, and stays in, one part of the brain. Therefore, you tend to have localized or 'focal' symptoms. Simple partial seizures- You may have muscular jerks or strange sensations in one arm or leg. Complex partial seizures- These commonly arise from a temporal lobe (a part of the brain) but may start in any part of the brain. Therefore, this type is sometimes called 'temporal lobe epilepsy'. You may fiddle with an object, or mumble, or wander aimlessly. KEY SIGNS AND SYMPTOMS Aura- a sensation that warns the client of the impending seizure. Loss of motor activity or bowel and bladder function, or loss of consciousness during the seizure.

Prodromal signs, such as mood changes, irritability, and insomia. KEY TEST RESULTS A brain scan (usually an MRI or CT scan) can show the structure of different parts of the brain. EEG (ElectroEncephaloGram), blood tests KEY TREATMENT Anticonvulsants: phenytoin (Dilantin), IV diazepam (Valium), and Phenobarbital sodium (Luminal) as prescribed to stop the seizure. KEY INTERVENTION Maintain patent airway (do not force the jaws open). Prepare to suction. Administer oxygen. Note the time and duration of the seizure If the client is standing, place the client on the floor and protect the head and body. Do not restrain the client. Prevent injury during the seizure. Remain with the client. Turn the clients head to side. Instruct to avoid alcohol, excessive stress, and fatigue. ACUTE HEAD INJURY Results from a trauma to the head, leading to brain injury or bleeding within the brain. Effects of injury may include edema and hypoxia A head injury is classified by brain injury type: fracture, hemorrhage, or trauma. KEY SIGNS AND SYMPTOMS Disorientation to time, place, or person Unequal pupil size, loss of papillary reaction (if edema is present) KEY TEST RESULTS Computed tomography (CT) scan shows hemorrhage, cerebral edema, or shift of midline structures. Magnetic resonance imaging (MRI) shows hemorrhage, cerebral edema, or shift of midline structures. KEY TREATMENTS

Cervical collar (until neck injury is ruled out) Anticonvulsant: phenytoin (Dilantin) Barbiburate: pentobarbital (Nembutal) if unable to control intracranial pressure (ICP) will diuresis Diuretics: mannitol (Osmitrol), furosemide (Lasix) to combat cerebral edema Dopamine (Intropin) or phenylephrine (NeoSynephrine) to maintain cerebral perfusion pressure above 50 mm Hg (if blood pressure is low and ICP is elevated) Glucocorticoid: dexamethasone (Decadron) to reduce cerebral edema Histamine2 (H2)-receptorantagonists; ranitidine (Zantac), famotidine(Pepcid), nizatidine Axid) Mucusoal barrier fortifier: sucralfate (Carafate) Posterior pituitary hormone: vasopressin (Pitressin) if patient develops diabetes insipidus KEY INTERVENTIONS Assess neurologic and respiratory status. Observe for signs of increasing ICP (greater than 20 mm Hg for more than 10 minutes) to avoid treatment delay and prevent neurologic compromise. TRIAD (Late signs): widened pulse pressure ( increased systolic BP), bradypnea, bradycardia. Decorticate (flexor)- indicates a nonfunctioning cortex. Client flexes one or both arms on the chest and may stiffly extend the legs. Decerebrate (extensor) posturing- indicates a brainstem lesion. Client stiffly extends one or both arms and possibly legs. Elevate the head of the bed 30 to40 degrees as prescribed. Instruct to avoid straining and Valsalva maneuver. Monitor and record vital signs, intake and output, hemodynamic variables, ICP, cerebral perfusion pressure, specific gravity, laboratory studies, and pulse oximetry. Check for signs of diabetes insipidus (low urine specific gravity, high urine output) Allow a rest period between nursing activities. CATARACTS Are cloudy (opaque) areas that develop in the lens of an eye. The lens should normally be clear but if you develop cataracts the affected lens becomes like 'frosted glass'. There are different types of cataracts.

a. Age-related cataract ('senile cataract') b. Congenital cataracts (present at birth) KEY SIGNS OR SYMPTOMS Dimmed or blurred vision, poor night vision; yellow, gray, or white pupil KEY TEST RESULT Ophthalmoscopy or slit-lamp examination confirms the diagnosis by revealing a dark area in the normally homogeneous red reflex. KEY TREATMENT Extracapsular extraction or intracapsular lens implant KEY INTERVENTIONS Provide a safe environment for the patient. Modify the environment to help the patient meet his self-care needs (for example, by placing items on the unaffected side). ALLERGIC CONJUNCTIVITIS Conjunctivitis means inflammation of the conjunctiva. The conjunctiva is the thin 'skin' that covers the white part of the eyes and the inside of the eyelids. Causes of Conjunctivitis: Infection, allergy, irritant KEY SIGN AND SYMPTOMS Excessive tearing, itching, burning, mucopurulent KEY TEST RESULT Culture and sensitivity tests identify the causative bacterial organism and indicate appropriate antibiotic therapy. KEY TREATMENTS Antiviral agents: Acyclovir (Zovirax), if herpes simplex is the cause. Corcosteroids: Dexamethasone (Maxidex) Mast cell stabilizer: cromolyn (Opticrom) for allergic conjunctivitis Topical antibiotics: according to the sensitivity of the infective organism (if bacterial)

KEY INTERVENTIONS Teach proper hand- washing technique. Stress the risk of spreading infection to family members by sharing washcloths, towels, and pillows. Warn against rubbing the infected eye, which can spread the infection to the other eye and to other persons. Apply warm compresses and therapeutic ointment or drops. Dont irrigate the eye. Have the patient wash his hands before he uses the medication, and use clean washcloths or towels. Teach the patient how to instill eyedrops and ointments correctlywithout touching the bottle tip to his eye or lashes. GLAUCOMA Is characterized by abnormally high IOP (Normal: 12- 21 mm Hg) that damages the optic nerve and other intraocular structures. Inadequate drainage of aqueous humor from the canal of Schlemm or overproduction of aqueous humor. The aqueous humour drains out from the eye into the bloodstream through the sieve-like trabecular meshwork.

There are different types of glaucoma. a. Primary open angle glaucoma (also called chronic glaucoma)- This develops slowly so that any damage to the nerve and loss of sight is gradual. There is a partial blockage within the trabecular meshwork. This restricts the drainage of aqueous humour. The term 'open angle' refers to the angle between the iris and sclera which is normal, in contrast to: b. Acute angle closure glaucoma where the angle is narrowed. Obstructed by anatomically narrow angles between the anterior iris (thickened or bulging) and the posterior corneal surface. In this condition there is a sudden increase in the pressure within one eye. The eye quickly becomes painful and red. c. Congenital glaucoma (buphthalmos) is present from birth (inherited as an autosomal recessive trait). Initial manifestation: Tunnel vision (loss of peripheral vision), gun-barrel vision. Macular degeneration: Loss of central vision KEY SIGNS AND SYMPTOMS Chronic open- angle glaucoma: initially asymptomatic Acute angle- closure glaucoma: Acute ocular pain, blurred vision, dilated pupil, halo vision

KEY TEST RESULTS Opthalmoscopy shows atrophy and cupping of optic nerve head Tonometry shows increased IOP. Gonioscopy reveals if angle is open or closed KEY TREATMENTS Chronic open- angle glaucoma: Alpha agonist: brimonidine Beta- adrenergic antagonists: timolol (Timoptic) Acute angle- closure glaucoma: Cholinergic agent:pilocarpine Laser iridectomy or surgical iridectomy if pressure doesnt decrease with drug therapy. KEY INTERVENTIONS Assess eye pain and administer medication as prescribed. RETINAL DETACHMENT Is the separation of retina from the choroid, It occurs when the retina develops a hole or tear and the vitreous seeps between the retina and choroid. KEY SIGNS AND SYMPTOMS Painless change in vision (floaters and flashes of light) With progression of detachment, painless vision loss may be described as a veil, curtain or cobweb that eliminates part of visual field. KEY TEST RESULTS Indirect opthalmoscope shows retinal tear or detachment. Slit- lamp examination shows retinal tear or detachment. KEY TREATMENTS Scleral buckling to reattach the retina KEY INTERVENTIONS Postoperatively instruct the patient to lie on his back or on his unoperated side. Discourage straining during defection, bending down, and hard coughing, sneezing, or vomiting.

MENIERE'S DISEASE The inner ear includes the cochlea and semicircular canals in which there is a system of tiny fluid filled channels called the labyrinth. The labyrinth is lined with cells which send messages of sound and balance down nerves to the brain. It is thought that a build up of fluid in the labyrinth from time to time causes the symptoms. It usually affects adults, men slightly more often than women, between ages 30 and 60. This disorder may also be called endolymphatic hydrops. KEY SIGNS AND SYMPTOMS TRIAD: Sensorineural hearing loss, severe vertigo, tinnitus KEY TEST RESULTS Audiometric studies indicate sensorineural hearing loss and loss of discrimination and recruitment KEY TREATMENTS Restriction of sodium intake to less than 2 g/ day Anticholinergic: atropine (may stop an attack in 20 to 30 minutes) Antihistamine: diphenyhydramine (Benadryl) for severe attack KEY INTERVENTIONS If the patient is in the facility during the attack Advise the patient against reading and exposure to glaring lights. Keep the side rails of the patients bed up. Tell him not to get out of bed or walk without assistance. Instruct the patient to avoid sudden position changes and any tasks that vertigo makes hazardous Before surgery If the patient is vomiting, record fluid intake and output and characteristics of vomitus. Administer antiemitics as necessary, and give small amounts of fluid frequently. After surgery Tell the patient to expect dizziness and nausea for 1 to 2 days after surgery.

OTOSCLEROSIS Is a condition that affects the stapes, one of the tiny bony ossicles in the middle ear. To have normal hearing, the ossicles need to be able to move freely in response to sound waves. What happens is that abnormal bone material grows in and around the stapes. The cause of otosclerosis is not known. KEY SIGNS AND SYMPTOMS Progressive hearing loss, tinnitus KEY TEST RESULT Audiometric testing confirms hearing loss. KEY TREATMENTS Stapedectomy and insertion of prosthesis to restore partial or total hearing. KEY INTERVENTIONS Develop alternative means of communication ENDOCRINE SYSTEM HORMONES SECRETED BY THE MAIN ENDOCRINE GLANDS MAJOR DIAGNOSTIC TESTS FASTING BLOOD GLUCOSE- measures plasma glucose levels following a 12-14 hour fast. NURSING ACTIONS: Withhold and fluids for 12-to14 hour before the fasting sample is drawn. Withhold insulin until the test is completed. 2- HOUR POSTPRANDIAL GLUCOSE TEST- a blood sample is used to analyze the bodys insulin response to carbohydrate ingestion. NURSING ACTIONS: Provide the patient with a 100 g carbohydrate diet before the test and then ask him to fast for 2 hours. GLUCOSE TOLERANCE TEST (GTT)- uses blood and urine samples to measures carbohydrate absorption. NURSING ACTIONS: Provide with high carbohydrate diet for 3 days. Instruct tto fast for 10 to 16 hours before the test GLYCOSYLATED Hb testing- provides information about average blood glucose levels during the preceding 2 to 3 months. This test is used to evaluate the long-term effectiveness of diabetes therapy ADRENOCORTICOTROPIC HORMONE (CORTICOTROPIN) STIMULATION TEST- analyzes blood samples for cortisol.

DEXAMETHASONE SUPPRESSION TEST- involves administration of dexamethasone, is used to analyze blood sample for serum cortisol. URINE VANILLYLMANDELIC ACID- is a quantitative analysis of urine collected over 24 hours to determine the end products of catecholamine metabolism (epinephrine and norepinephrine). NURSING ACTIONS- Restrict foods that contain coffee, tea, and chocolate for 3 days before the test. BMR TEST- is an indirect, non-invasive measurement of oxygen consumed by the body during a given time and evaluates caloric expenditure in a 24- hour period. ULTRASONOGRAPHY- allows visualization of thyroid, pelvis, and abdomen through the use of reflected sound waves. CLOSED PERCUTANEOUS THYROID BIOPSY- uses the percutaneous, sterile aspiration of a small amount of thyroid tissue for histologic evaluation. NURSING ACTIONS: Withhold foods and fluids after midnight. THYROID UPTAKE- also called radioactive iodine uptake or RAIU measures the amount of radioactive iodine taken up by the thyroid gland in 24 hours. NURSING ACTIONS: Instruct not to ingest iodine- rich foods for 24 hours before the test. Discontinue all thyroid hormone and cough medications 7 to 10 days before the test. THYROID SCAN- gives visual imaging of radioactivity distribution in the thyroid gland. NURSING ACTIONS: Instruct to stop consuming iodized salt, iodinated salt substitutes, and seafood 1 week before the procedure. Remove dentures, jewelries that may interfere with imaging. SULKOWITCHS TEST- analyzes urine to measure the amount of calcium being excreted. BLOOD CHEMISTRY TEST, HEMATOLOGIC STUDY KEY TEST RESULT Blood chemistry reveals decreased hematocrit (Hct); decreased haemoglobin (Hb), cortisol, glucose, Na, Cl, and aldosterone levels, and increased BUN and K level. Fasting blood glucose reveals hypoglycemia. BMR is decreased. KEY TREATMENTS In adrenal crisis, I.V. hydrocortisone given promptly along with 3 to 5 L saline solution. Glucocorticoids: cortisone (cortone), hydrocortisone Mineralocorticoid: fludrocortisone (Florinef)

KEY INTERVENTIONS Be prepared to administer I.V. hydrocortisone and saline solution promptly if the patient is in adrenal crisis. Administer I.V. fluids Dont allow the patient to sit up or stand quickly. KEY TEST RESULTS Blood chemistry shows increased triiodothyronine (T3), T4, and free thyroxine levels and decreased TSH and cholesterol levels. Radioactive iodine uptake (RAIU) is increased. KEY TREATMENTS Radiation therapy, thyroidectomy, Iodine preparations: K iodide (SSKI), radioactive iodine. Antithyroid agents: methimazole (Tapazole), propylthiouracil High- protein, high carbohydrate, high calorie diet; restricting stimulants such as caffeine Adrenergic- blocking agents: propanolol (Inderal) KEY INTERVENTIONS Assess cardiovascular status. Provide skin and eye care. Administer I.V. fluids; weigh the patient daily. Provide postoperative nursing care. Provide rest periods to reduce metabolic demands. Provide a quiet, cool environment due to sensitivity to heat. KEY TEST RESULTS Blood chemistry shows decreased T3, T4, free thyroxine, and Na levels and increased TSH and cholesterol levels. RAIU is decreased. Cretinism- characterized by severe congenital hypothyroidism KEY TREATMENTS

High fiber, high protein diet, low calorie Thyroid hormone replacement: levothyroxine (Synthroid), liothyronine (Cytomel) Stool softener: docusate Na (Colace) KEY INTERVENTIONS Avoid sedations; administer to 1/3 the normal dose of sedatives or narcotics. Check for constipation and edema. Force fluids. Provide a warm environment because of sensitivity to cold. GOITER (SWELLING OF THE THYROID) Is an enlarged thyroid gland. A goiter can mean that all the thyroid gland is swollen or enlarged, or one or more swellings or lumps develop in part or parts of the thyroid. Endemic goiter usually results from inadequate dietary intake of iodine such as malnutrition. KEY SIGNS AND SYMPTOMS Single or multinodualr, firm, irregular enlargement of the thyroid gland Dizziness or syncope when the patient raises his arms above his head (Pembertons sign) Dysphagia CAUSE SPORADIC: ingestion of large amount of goiterogenic foods (contain agents that decreases thyroxine production) e.g. cabbage, soybeans, peanuts, peaches KEY TEST RESULTS Laboratory test reveal high or normal thyroid- stimulating hormone (TSH), low serum thyroxine (T4) concentrations, and increased iodine 131 uptake. KEY TREATMENTS Subtotal thyroidectomy Thyroid hormone replacement: levothyroxine (Synthroid) Small doses of iodine (Lugols or K iodide solution) for goiter resulting from iodine. KEY INTERVENTIONS

Measure the patients neck circumference. Also check for the development of hard nodules in the gland. Provide preoperative teaching and postoperative care if subtotal thyroidectomy is indicated. ACROMEGALY Are chronic progressive diseases that occur when the pituitary gland produces too much GH, causing excessive growth. Acromegaly develops slowly (after epiphyseal closure, causing bone thickening and transverse growth) and gigantism develops abruptly (before epiphyseal closure and causes proportional overgrowth of all tissue. KEY SIGNS AND SYMPTOMS Prognathism (projection of the jaw) becomes marked and may interfere with chewing. Enlarged supraorbital ridge, thickened ears and nose, paranasal sinus enlargement, thickening of the tongue GIGANTISM Abrupt, excessive growth in all parts of the body KEY TEST RESULT Plasma human growth hormone (HGH) levels measured by radioimmunoassay typically are elevated. However, because HGH secretion is pulsatile, the results of random sampling may be misleading. KEY TREATMENTS Surgery to remove the affecting tumor (transphenoidal hypophysectomy) Thyroid hormone replacement therapy after surgery: levothyroxine (Synthroid) Corticosteroid: Cortisone (Cortone) Inhibitor of HGH release: Bromocriptine (Parlodel) KEY INTERVENTIONS Provide the patient with emotional support. Perform or assist with ranged of motion (ROM) exercises. Keep in mind that this disease can also cause inexplicable mood changes. Reassure the family that these mood changes result from the disease and can be modified with treatment.

After surgery, diligently monitor v/s and neurologic status. Be alert for alterations in level of consciousness, pupil equality, or visual acuity as well as vomiting, falling pulse rate, and rising blood pressure Check blood glucose often. Measure I & O hourly, watching for large increases. DIABETES INSIPIDUS Stems from a deficiency of ADH (vasopressin) secreted by the posterior lobe of the pituitary gland. Decreased ADH reduces the ability of distal and collecting renal tubules in the kidneys to concentrate urine, resulting in excessive urination, excessive thirst, and excessive fluid intake. KEY SIGNS AND SYMPTOMS Polydipsia (consumption of 4 to 40 L/day) Polyuria (greater than 5 L/day) KEY TEST RESULTS Urine chemistry shows urine specific gravity less than 1.004, osmolarity 50 to 200 mOsm/ kg, decreased urine pH, and decreased Na and K levels. KEY TREATMENTS I.V. therapy: hydration (when first diagnosed, intake and output must be matched mL to mL to prvent dehydration), electrolyte replacement Antidiuretic hormone replacement: vasopressin (Pitressin) KEY INTERVENTIONS Assess fluid balance Monitor and record v/s, I & O (urine output should be measured q 1 hour when 1st diagnosed), urine specific gravity (check q 1 to 2 hours when 1 st diagnosed), and laboratory studies. Administer I.V. fluids DIABETES MELITUS Occurs when the level of glucose (sugar) in the blood becomes higher than normal. There are two main types of diabetes.

Type 1 diabetes - This is also known as juvenile, early onset, or insulin dependent diabetes. It usually first develops in children or young adults. Illness usually develops quite quickly, over days or weeks, as the pancreas stops making insulin. It is treated with insulin injections and a healthy diet. Type 1 diabetes is thought to be an 'auto-immune' disease. Type 2 diabetes- This is also known as maturity onset, or non-insulin dependent diabetes. Type 2 diabetes usually develops after the age of 40 (but sometimes occurs in younger people). It is more common in people who are overweight or obese. With Type 2 diabetes, the illness and symptoms tend to develop gradually (over weeks or months). This is because in Type 2 diabetes you still make insulin (unlike Type 1 diabetes). However, you either do not make enough for your body`s needs, and/or the cells in your body are not able to use it properly. This is called 'insulin resistance'. KEY SIGNS AND SYMPTOMS Polydipsia, polyphagia, polyuria KEY TEST RESULT Fasting blood glucose level is increased ( 126 mg/dl) 2- hour postprandial blood glucose level shows hyperglycemia (> 200 mg/dL) KEY TREATMENTS Antidiabetic agents: insulins and oral agents, such as tolbutamide (Orinase), chlorpropamide (Diabinase), glipizide (Glucotrol) KEY INTERVENTIONS Assess acid- base and fluid balance Monitor for signs of hypoglycemia (vagueness, slow cerebration, dizziness, weakness, pallor, tachycardia, diaphoresis, seizures, and coma), ketoacidosis (acetone breath, dehydration, weak or rapid pulse, Kussmauls respirations), and hyperosmolar coma (polyuria, thirst, neurologic abnormalities, stupor). Be prepared to administer I.V. fluids, insulins, and, usually, K replacement for ketoacidosis or hyperosmolar coma. Monitor wound healing. Maintain the patients diet.

Provide meticulous skin and foot care. Patients with diabetes are increased risk for infection from impaired leukocyte activity. Foster independence PHEOCHROMOCYTOMA Functioning tumor of the adrenal medulla that secretes excessive amount of epinephrine and norepinephrine. Occurs most commonly between ages 25-50 Key signs and symptoms Severe headache, apprehension, palpitation, profuse sweating, nausea, HPN, tachycardia, vomiting, hyperglycemia, dilation of pupils, cold extremities Key test results Increased plasma levels of catecholamines Elevated urinary catecholamines and urinary vanillylmandelic acid (VMA) levels Key treatments Adrenalectomy ( removal of one or both adrenal glands) Key interventions Provide high- calorie, well- balanced diet; avoid stimulants such as coffee, tea. Promote rest; decrease stressful stimuli.