Midterm Exam Study Guide

28. Phenytoin ...Also know what increases the risk for toxicity while on this med.

(used in tonic-clonic or focal seizures) watch the gums: will enlarge and easily bleed (called gingival hyperplasia....teach about good mouth care may cause bone marrow suppression (watch platelets and WBCs) tell patient to watch for rash or Steven-Johnson's Syndrome and to REPORT it to their doctor immediately don't give with milk or antacids (interferes with absorption) 10 to 20 mcg/mL

What are clinical manifestations of meningitis?

-Initially headache and fever will be present (fever tends to remain high throughout course of illness) -Neck immobility (stiff and painful neck, nuchal rigidity is usually an early sign) -Positive Kernig's sign -Positive Brudzinski sign -Photophobia (extreme sensitivity to light) -Rash (skin lesions develop ranging from a petechial rash, to large areas of ecchymosis) -Disorientation and memory impairment headache, fever, light sensitivity, nausea, vomiting, respiratory changes, and signs and symptoms of increasing intracranial pressure, such as changes in pupillary reaction to light, behavior, or level of consciousness.

What is nuchal rigidity?

A third sign used to diagnose meningitis is called nuchal rigidity. Nuchal rigidity is an inability to flex the neck forward due to rigidity of the neck muscles.

P.D. also has dysphagia. Before allowing him to eat, which action should you take first? a.Check the patient's gag reflex. b.Request a soft diet with no liquids. c.Place the patient in high-Fowler's position. d.Test the patient's ability to swallow with a small amount of water.

Answer: A Rationale: Before initiation of feeding, assess the gag reflex by gently stimulating the back of the throat with a tongue blade. If a gag reflex is present, the patient will gag spontaneously. If it is absent, defer the feeding and begin exercises to stimulate swallowing. To assess swallowing ability, elevate the head of the bed to an upright position (unless contraindicated) and give the patient a small amount of crushed ice or ice water to swallow.

P.D. is diagnosed with a thrombotic stroke. Over the next 72 hours, you plan care with the knowledge that he: a.is ready for aggressive rehabilitation. b.will show gradual improvement of the initial neurologic deficits. c.may show signs of deteriorating neurologic function as cerebral edema increases. d.should not be turned or exercised to prevent extension of the thrombus and increased neurologic deficits.

Answer: C Rationale: Ischemic stroke symptoms may progress in the first 72 hours as infarction and cerebral edema increase.

As one of your clinical assignments, you are assisting an RN with health screening at a health fair. Which individual is at greatest risk for experiencing a stroke? a.A 46-year-old white female with hypertension and oral contraceptive use for 10 years b.A 58-year-old white male salesman who has a total cholesterol level of 285 mg/dl c.A 42-year-old African American female with diabetes mellitus who has smoked for 30 years d.A 62-year-old African American male with hypertension who is 35 pounds overweight

Answer: D Rationale: Option D: This individual has five risk factors: age, African American, male, hypertension, and overweight. Option A: This individual has two risk factors: hypertension and oral contraception use. Option B: This individual has two risk factors: male and increased cholesterol level. Option C: This individual has three risk factors: African American, diabetes mellitus, and smoking. Nonmodifiable risk factors include age, gender, ethnicity/race, and family history/heredity. Stroke risk increases with age, doubling each decade after 55 years of age. Two- thirds of all strokes occur in individuals >65 years. Strokes are more common in men, but more women die from stroke than men. Because women tend to live longer than men, they have more opportunity to suffer a stroke. African Americans have a higher incidence of stroke as well as a higher death rate from stroke than whites. A family history of stroke, a prior transient ischemic attack, or a prior stroke also increases the risk of stroke. Modifiable risk factors are those that can potentially be altered through lifestyle changes and medical treatment, thus reducing the risk of stroke. Modifiable risk factors include hypertension, increased cholesterol, elevated blood lipid levels, heart disease, smoking, excessive alcohol consumption, obesity, sleep apnea, metabolic syndrome, lack of physical exercise, poor diet, and drug abuse. The early forms of birth control pills that contained high levels of progestin and estrogen increased a woman's chance of experiencing a stroke, especially if she also smoked heavily. Newer, low-dose oral contraceptives have lower risks for stroke except in those individuals who are hypertensive and smoke. Other conditions that may increase stroke risk include migraine headaches, inflammatory conditions, and hyperhomocystinemia. Sickle cell disease is another known risk factor for stroke.

14. Patient who have a stroke involving the right cerebral hemisphere will display what kind of changes?

CREATIVE SIDE! tends to be impulsive and to move quickly •Stroke on right side of brain is more likely to cause problems in spatial-perceptual orientation short attention span Left side weakness: Hemiplegia Impairment in creativity: arts and music Confused on date, time, place Cannot recognize faces or the person's name Loss of depth perception Trouble staying on topic when talking Can't see things on left side: LEFT SIDE NEGLECT (unilateral neglect)(Ignores left side of body) Trouble with maintaining proper grooming Emotionally: not going to think things through....very impulsive Poor ability to make decisions and assessing spatial qualities....shapes Denial about limitations Not able to read nonverbal language or understand the hidden meaning of things Very short attention span

What is the cushing triad?

Cushing's Triad: LATE SIGN...herniation of the brain stem Increased systolic blood pressure (widening pulse pressure: increase in SBP and decrease in DBP), decreased heart rate, and abnormal breathing EMERGENCY SIGN OF IMPENDING DEATH

8. Know the difference between decerebrate and decorticate positioning. Don't just know what the picture looks like but also how is it described in word form.

Decerebrate or decorticate posturing Decorticate (flexor posturing): brings upper extremities to the core of the body (middle)adduction and flexion of arms, leg rotated internally, feet flexed Decerebrate: (Extension posturing): extends upper extremities from the body *worst of the two (remember all the E's in decerebrate and think EXTEND arms)adduction and extension of arms with pronation, and feet flexed

32. Patients on who take MAOI medications should avoid what kinds of food?

Educate about limiting foods with tyramine: hypertensive crisis aged cheese smoked or cured meats (pepperoni, bacon, hot dogs) fermented food beer

17. What is homonymous hemianopsia? (Keep in mind how you would intervene in regards to a patient. Whether they are ambulating or eating etc. Knowing just the definition is not good enough.)

Hemianopia: limited vision in half of the visual field (pending patient teaching information)

4. What is a normal ICP reading or level? pg 1315

ICP: 5-15 mmHg (>20 mmHg...needs treatment)

16. What are ways to facilitate safe eating post stroke with diagnosed dysphagia. (In other words would having the patient lay flat be a good idea? No. So sitting upright would be one way to facilitate safety during meal times.)

If he's tired, your patient may have more difficulty swallowing. Wait 30 minutes, then reassess his alertness before performing the test. * Have suction equipment immediately available. * Minimize environmental distractions and position him upright in a chair or elevate the head of the bed 60 to 90 degrees. * Assess his mental status and make sure he can voluntarily cough, clear his throat, and swallow saliva before proceeding with the test. If he's managing his oral secretions, offer him small bites of ice chips or sips of water from a cup or a teaspoon. Observe him carefully before, during, and after each offering for cough, drooling, voice change (especially a wet or gurgling quality), and swallowing difficulty. Stop the test immediately if any of these occur and notify his health care provider. * If he can swallow without his voice or breathing sounding wet, and without choking or coughing, proceed with a soft diet, then if tolerated to a regular diet as ordered. * If he has difficulty tolerating water, try giving him thickened liquid (the consistency of honey) by spoon and try pureed semisolids. Observe him for choking or coughing. If tolerated, proceed with a pureed or thickened liquid diet as ordered until he's formally evaluated by a speech-language pathologist or place him on N.P.O. status based on your observations. * Provide diligent oral care to all patients with dysphagia, including those who are N.P.O. * Don't offer semisolids, liquids, or solids (including oral medications) to a patient who can't swallow saliva or voluntarily cough and clear his throat. * Don't leave the patient unattended during the test. * Don't administer sedatives and hypnotics, if possible, because they can impair the cough reflex and swallowing.

15. Patient who have a stroke involving the left cerebral hemisphere will display what kind of changes?

LOGICAL SIDE! Aphasia slow performance Both memory and judgment impairment very cautious in making judgments Right side Hemiplegia Aphasia (trouble formulating words and comprehending them) Aware of their limits...experiences depression, anger, frustration Trouble understanding written text Can't write (agraphia) Impaired math skills Memory intact Issues with seeing on the right side

2. Osmitrol. (Your info should contain information such as what is it how does it work when given to a patient, side effects, electrolytes to monitor if it applies etc)

Mannitol: it's a concentrated type of sugar When this drug enters the blood it is very concentrated and it draws water that is pooling in the brain back into the blood. This type of diuretic is filtered through the glomerulus and not reabsorbed through the renal tubules, and because of this it creates an osmotic pressure that will pull water and electrolytes (sodium, chloride) from the blood (won't be reabsorbed) and be excreted out. Watch for fluid overload (water intoxication) and depletion. •Plasma expansion •Osmotic effect •Monitor fluid and electrolyte status

Meningitis

Meningitis is a clinical syndrome characterized by inflammation of the meninges, the three layers of membranes that enclose the brain and spinal cord. These layers consist of the following: ADVERTISEMENT Dura - A tough outer membrane. Arachnoid - A lacy, weblike middle membrane. Subarachnoid space - A delicate, fibrous inner layer that contains many of the blood vessels that feed the brain and spinal cord. Anatomically, meningitis can be divided into inflammation of the dura (sometimes referred to as pachymeningitis), which is less common, and leptomeningitis, which is more common and is defined as inflammation of the arachnoid tissue and subarachnoid space. Pathophysiology Most cases of meningitis are caused by an infectious agent that has colonized or established a localized infection elsewhere in the host. The organism invades the submucosa at these sites by circumventing host defenses (eg, physical barriers, local immunity, and phagocytes or macrophages). Invasion of the bloodstream and subsequent seeding is the most common mode of spread for most agents. Meningeal seeding may also occur with a direct bacterial inoculate during trauma, neurosurgery, or instrumentation. The blood-brain barrier can become disrupted; once bacteria or other organisms have found their way to the brain, they are somewhat isolated from the immune system and can spread. When the body tries to fight the infection, the problem can worsen; blood vessels become leaky and allow fluid, WBCs, and other infection-fighting particles to enter the meninges and brain;this process, in turn, causes brain swelling and can eventually result in decreasing blood flow to parts of the brain, worsening the symptoms of infection. Replicating bacteria, increasing numbers of inflammatory cells, cytokine-induced disruptions in membrane transport, and increased vascular and membrane permeability perpetuate the infectious process in bacterial meningitis. Causes Causes of meningitis include bacteria, viruses, fungi, parasites, and drugs (eg, NSAIDs, metronidazole, and IV immunoglobulin [IVIg]). Bacteria. S pneumoniae, a gram-positive coccus, is the most common bacterial cause of meningitis. Viruses. Enteroviruses account for of the majority of cases of aseptic meningitis in children; the nonpolio enteroviruses (NPEVs) account for approximately 90% of cases of viral meningitis in which a specific pathogen can be identified; the mumps virus is the most common cause of aseptic meningitis in unimmunized populations, occurring in 30% of all patients with mumps. Fungi. Cryptococcus neoformans is an encapsulated, yeastlike fungus that is ubiquitous; Coccidioides immitis is a soil-based, dimorphic fungus that exists in mycelial and yeast (spherule) forms; lastomyces dermatitidis is a dimorphic fungus that has been reported to be endemic in North America (eg, in the Mississippi and Ohio River basins). Parasite. Angiostrongylus cantonensis, the rat lungworm, can cause eosinophilic meningitis (pleocytosis with more than 10% eosinophils) in humans; Gnathostoma spinigerum, a GI parasite of wild and domestic dogs and cats, may cause eosinophilic meningoencephalitis; Gnathostoma spinigerum, a GI parasite of wild and domestic dogs and cats, may cause eosinophilic meningoencephalitis. Clinical Manifestations Only about 44% of adults with bacterial meningitis exhibit the classic triad of fever, headache, and neck stiffness. Fever. The patient presents with fever at first, which ultimately grow worse. Seizures. As bacterial meningitis progresses, patients of any age may have seizures (30% of adults and children; 40% of newborns and infants). Neck stiffness. The patient feels stiffness of the neck as part of the triad of symptoms. Positive Kernig's sign. When the patient is lying with the thigh flexed on the abdomen, the leg cannot be completely extended. Positive Brudzinski's sign. When the patient's neck is flexed, flexion of the knees and hips is produced; when the lower extremity of one side is passively flexed, a similar movement is seen in the opposite extremity. Neurologic symptoms. Patients with subacute bacterial meningitis and most patients with viral meningitis present with neurologic symptoms developing over 1-7 days. High-pitched cry. Infants may present with high-pitched crying. Lethargy. An infant may appear only to be slow or inactive, or be irritable. Photalgia (photophobia). Discomfort when the patient looks into bright lights. Assessment and Diagnostic Findings The diagnostic tests in patients with clinical findings of meningitis are as follows: Lumbar puncture. In general, whenever the diagnosis of meningitis is strongly considered, a lumbar puncture should be promptly performed; examination of the cerebrospinal fluid (CSF) is the cornerstone of the diagnosis. CT scan. A screening computed tomography (CT) scan of the head may be performed before LP to determine the risk of herniation. Blood studies. In patients with bacterial meningitis, a complete blood count (CBC) with differential will demonstrate polymorphonuclear leukocytosis with a left shift. Chest radiography. As many as 50% of patients with pneumococcal meningitis also have evidence of pneumonia on initial chest radiography. Cultures and bacterial antigen testing. The utility of cultures is most evident when LP is delayed until head imaging can rule out the risk of brain herniation, in which cases antimicrobial therapy is rightfully initiated before CSF samples can be obtained. Serum procalcitonin testing. increasing data suggest that serum procalcitonin (PCT) levels can be used as a guide to distinguish between bacterial and aseptic meningitis in children. Medical Management Management of the patient includes: Crystalloid infusion. If the patient is in shock or hypotensive, crystalloid should be infused until euvolemia is achieved. Seizure precautions. If the patient's mental status is altered, seizure precautions should be considered, seizures should be treated according to the usual protocol, and airway protection should be considered. IVT and oxygen administration. If the patient is alert and in stable condition with normal vital signs, oxygen should be administered, intravenous (IV) access established, and rapid transport to the emergency department (ED) initiated. Pharmacologic Management Begin empiric antibiotic coverage according to age and presence of overriding physical conditions. Sulfonamides. Trimethoprim and sulfamethoxazole work together to inhibit bacterial synthesis of tetrahydrofolic acid. Tetracyclines. Tetracyclines inhibit protein synthesis and, therefore, bacterial growth by binding with 30S and possibly 50S ribosomal subunits of susceptible bacteria. Carbapenems. Carbapenems inhibit bacterial cell wall synthesis by binding to penicillin-binding proteins; carbapenems, including meropenem, can be used for the treatment of meningitis. Fluoroquinolones. Fluoroquinolones inhibit bacterial DNA synthesis and, consequently, growth by inhibiting DNA gyrase and topoisomerases, which are required for replication, transcription, and translation of genetic material. Glycopeptides. Vancomycin inhibits bacterial cell wall synthesis by blocking glycopeptide polymerization; it is indicated for many infections caused by gram-positive bacteria. Aminoglycosides. Aminoglycosides primarily act by binding to 16S ribosomal RNA within the 30S ribosomal subunit; they have mainly bactericidal activity against susceptible aerobic gram-negative bacilli. Cephalosporins, 3rd generation. Third-generation cephalosporins are less active against gram-positive organisms than first-generation cephalosporins are; they are highly active against Enterobacteriaceae, Neisseria, and H influenzae. Antivirals. Antiviral agents interfere with viral replication; they weaken or abolish viral activity; they can be used in viral meningitis. Systematic antifungals. Antifungal agents are used in the management of infectious diseases caused by fungi. Vaccines, inactivated. Inactivated bacterial vaccines are used to induce active immunity against pathogens responsible for meningitis. Corticosteroids. The use of steroids has been shown to improve overall outcome for patients with certain types of bacterial meningitis, such as H influenzae, tuberculous, and pneumococcal meningitis. Osmotic diuretics. Mannitol may reduce subarachnoid-space pressure by creating an osmotic gradient between CSF in the arachnoid space and plasma. Loop diuretics. Furosemide is a loop diuretic that increases the excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule. Anticonvulsants. Anticonvulsants are used to help aggressively control seizures (if present) in acute meningitis, because seizure activity increases ICP. Nursing Management Nursing management of the patient with meningitis include the following: Nursing Assessment Assessment of the patient with bacterial meningitis include. Neurologic status. Neurologic status and vital signs are continually assessed. Pulse oximetry and arterial blood gas values. These values are used to quickly identify the need for respiratory support. Nursing Diagnosis Based on the assessment data, major nursing diagnoses include: Risk for Infection related to contagious nature of organism. Acute Pain related to headache, fever, neck pain secondary to meningeal irritation. Impaired Physical Mobility related to intravenous infusion, nuchal rigidity and restraining devices. Activity Intolerance related to fatigue and malaise secondary to infection. Risk for Impaired Skin Integrity related to immobility, dehydration, and diaphoresis. Risk for Injury related to restlessness and disorientation secondary to meningeal irritation. Interrupted Family Process related to critical nature of situation and uncertain prognosis. Anxiety related to treatment and risk of death. Nursing Interventions Important components of nursing care include the following measures: Assess neurologic status and vital signs constantly. Determine oxygenation from arterial blood gas values and pulse oximetry. Insert cuffed endotracheal tube (or tracheostomy), and position patient on mechanical ventilation as prescribed. Assess blood pressure. (usually monitored using an arterial line) for incipient shock, which precedes cardiac or respiratory failure. Rapid IV fluid replacement may be prescribed, but take care not to overhydrate patient because of risk of cerebral edema. Reduce high fever to decrease load on heart and brain from oxygen demands. Protect the patient from injury secondary to seizure activity or altered level of consciousness (LOC). Monitor daily body weight; serum electrolytes; and urine volume, specific gravity, and osmolality, especially if syndrome of inappropriate antidiuretic hormone (SIADH) is suspected. Prevent complications associated with immobility, such as pressure and pneumonia. Institute infection control precautions until 24 hours after initiation of antibiotic therapy (oral and nasal discharge is considered infectious). Inform family about patient's condition and permit family to see patient at appropriate intervals. Evaluation Expected patient outcomes include: Avoidance of injury. Avoidance of infection. Restoration of normal cognitive functions. Prevention of complications. Discharge and Home Care Guidelines After hospitalization, the patient at home should: Activities. Alternate rest and activity to conserve energy. Diet. Consume safe, clean, and healthy foods. Asepsis. Promote simple infection control procedures at home. Infectious process. Identify signs and symptoms of an infectious process and report to the physician promptly. Documentation Guidelines The focus of documentation in patients with bacterial meningitis are: Client's description of response to pain. Acceptable level of pain. Prior medication use. Current physical findings. Client's understanding of individual risks and safety concerns. Availability and use of resources. Current and previous level of function. Effect on independence and lifestyle. Results of laboratory and diagnostic tests. Mental status pr cognitive evaluation results. Plan of care. Teaching plan. Response to interventions, teaching, and actions performed. Attainment or progress towards desired outcomes. Modifications to plan of care.

Seizures

Seizures NCLEX Review What are seizures? Seizures occur when abnormal electrical signals are being rapidly fired for neurons in the brain. This can happen throughout the brain affecting both sides (generalized seizure) or being located in a specific area of the brain (partial or focal seizure). Seizures can occur in anyone (children and adults) due to a severe acute condition, such as a high fever, illness (especially central nervous system types like bacterial meningitis), hypoglycemia, acid-base imbalances like acidosis, alcohol withdraw, brain tumor etc. Once the condition is corrected the seizures tend to stop. However, some patients can experience epilepsy. Epilepsy is where the patient has frequent seizures due to a chronic condition of some type like congenital brain defect, stroke, traumatic brain injury, long-lasting effects of an infection etc. Simplified Patho of Seizures In the brain, our neurons are tasked with handling and transmitting information. There are two types of neurons I want to discuss. These are excitatory and inhibitory neurons. Just like their name says, excitatory neurons produce "an action" or cause "excitement" by releasing a neurotransmitter called glutamate (this is an excitatory neurotransmitter). Inhibitory neurons "stop an action" or cause inhibition by releasing an inhibitory neurotransmitter called GABA. ***For seizure activity not to occur in a healthy brain, there needs to be a proper balance between these two types of neurons. If there is an imbalance of excitatory neurons vs. inhibitory neurons seizures will occur. For example, if there is not enough GABA (remember this is the inhibitory neurotransmitter) being released, too much excitation will occur leading to seizure activity. The reason I cover this is to help you understand how some of the anti-seizure drugs work to treat seizures. For instance, barbiturates stimulate GABA receptors which help control excitation and decreases seizure activity (more about medications below). Types of Seizures **remember these types for exams, especially their characteristics, expected duration, post ictus phase etc. Generalized: seizure is affecting both parts of the brain Tonic-clonic (formerly called grand -mal): most common type of generalized seizureMay experience AURA (warning a seizure is about to happen)Loses consciousness (at risk for injury)Will experience a tonic phase: body stiffens (may bite inside of the cheek or tongue....may see blood leaving mouth with foaming of saliva), breathing stops followed by cyanosis)Then a clonic phase: recurrent jerking (spasm and relaxation back-to-back) of extremities (patient may have incontinence of stool or/and urine)Usually lasts no more than 3 minutes.....at risk for status epilepticus with this type of seizure****if greater than 5 minutes or having multiple seizures in a row...activate emergency response team (will need immediate treatment to stop seizure (more on this in the nursing interventions)Post ictus (duration: hours to days): this is the recovery period: patient will feel very tired, extremely sore from muscle stiffening and jerking, can't remember what happened. Tonic seizure: (stiffening of the body....risk for falling) or Clonic seizure: (jerking....can be symmetrical or asymmetrical ) Absence Seizure (formerly called petit-mal) Most common in pediatric patients and Hallmark is a staring like stateIt will be like the child is just daydreaming but can't be snapped out of it....can go unnoticed by others for a while because it short and the child won't remember it. The person will look confused and won't be able to talk during the even. Very short.....seconds Post Ictus: immediate...doesn't remember staring off Atonic (drop attacks): "A" means without and when you put the word tonic after it the meaning is: WITHOUT MUSCLE TONEThe patient goes limp and falls if standing or slumps over if sitting...at risk for head injury (may need helmet) Usually not aware during event....post ictus: immediate...regains consciousness Myoclonic: Quick duration of jerking of the muscles Patient usually aware and conscious (this is what makes it different from a clonic seizure) Very short....few seconds Focal (also called partial): affects a specific part of the brain Two types: know the main differences which is that with focal onset aware (simple partial) the patient is AWARE of their surroundings but with focal impaired awareness (complex partial) the patient is NOT aware of their surroundings AND will have motor symptoms called automatisms. Focal Onset AWARE (simple partial): symptoms vary depending on where the seizure is located It tends to be a small area of a lobe...but patient is AWARE...example: occipital region the person may have vision changes Also sometimes called an aura too because it can happen right before focal impaired awareness (complex partial) Focal Impaired AWARENESS (complex partial): alternation in awareness and has motor symptoms Temporal lobe most commonly involved Focal onset aware (aura) can happen before it Automatisms present: this is where they are performing an action without knowing they are doing it like lip smacking, rubbing hands together, or grasping for something that isn't there Stages of Experiencing a Seizure We can divide how a person experiences a seizure into stages (it varies depending on the seizure type, so remember that) Prodromal: when symptoms start to appear prior to the big event (hence seizure) can start days before a seizure happens mood changes (depression, anger, issues sleeping, anxiety, GI and urinary issues etc.) Aura: doesn't happen with all types happens at the very beginning of the seizure (what type: focal seizures OR in a tonic-clonic seizure) happens within seconds to minutes before a seizure many times it gives the patient time to prepare self for seizure. As the nurse (if you are present) help the patient lay down onto their side with a pillow under the head. Symptoms vary among patients but can include: sudden weird smell or taste, déjà vu feeling, feeling anxious like something bad is about to happen, altered vision (lights or spots in vision) or hearing (hallucination type sounds or increased ability to hear sounds), dizzy (different for every person), inability to speak etc. Ictus: (word means seizure) this is the actual seizure Usually lasts anywhere from 1 to 3 minutes Time the seizureseizures greater than 5 minutes or if the patient starts having seizure back-to-back, the patient may be experiencing status epilepticus (will need medical care and medication to make the seizure stop...it will unlikely stop on its own) Post Ictus: (after the seizure) brain is going to rest and recover from the seizure usually last hours to days (tonic clonic).....for some patients it is immediate (absence) may feel extremely tired, sleepy, confused, headache etc. Nursing Interventions for Seizures Assess risk factors for seizure (remember any patient can experience this if any of the causes mentioned above are presenting...you want to be prepared. If risk factors present initiate seizure precautions: Seizure precautions may include:at bedside have suction and oxygen readyIV access (to given anti-seizure medication, if needed)padded side railspillow under head (to protect head)bed in the lowest positionremove objects that can cause injury (remove any restrictive clothing or items the patient may be wearing....eye glasses etc. ) Assess if your patient has a history of seizures in the past and if so what type of seizure, ask if the patient experiences prodromal signs and symptoms or an aura before the seizure, how long does the seizure last? If patient is able to report prodromal or aura....help patient prepare by getting the patient in a safe position by lying down on their side. What to do when your patient has a seizure? Protect patient if they are standing-up or sitting down by: gently lying the patient down and turning them onto their side. WHY? This helps prevent the tongue from covering the airway and helps saliva and blood drain from the mouth. DO NOT restrain patient or try to hold the patient down Protect their head and extremities (pillow and bed pads will help with this) DO NOT put anything in the patient's mouth Remove anything that can impede breathing or break (eye glasses, tight clothing etc. ). ****Questions to be asking yourself during the seizure**** Note the time it started and time it stopped (VERY IMPORTANT: if greater than 5 minutes or another seizure happens...THINK: status epilepticus and activate the emergency system response team. You will notify the MD of the seizure regardless because the seizure needs to be investigated....is the patient's drug level for anti-seizure medications too low? When the seizure started what was the patient's behavior right before and during it? (did they cry out, become confused, report an aura, become unconscious) and the characteristics of the body movements (if any) presented at the beginning and throughout the seizure.....stiffening of the whole body or just the extremities and then jerking or just jerking, was it on just one side or both sides of the body....be sure to be as detailed as possible...this helps the healthcare team determine what type of seizure this was and what treatment may be needed Did the patient become incontinent of urine or stool? Oxygen status (cyanosis present) Your role during the Post Ictus stage: Note the time the seizure stopped and how the patient is behaving afterwards: Are they tired (let them sleep and rest), confused, can't think or talk, have a headache (ask where it is located and pain rating), has any injuries (some patienst may bite their tongue or cheek) Maintain airway (suction, administer oxygen) If a tonic-clonic seizure, the patient will be very sleepy, won't remember what happened. Assess vital signs and neuro status: pupils, reflexes, is patient confused or oriented Clean patient if incontinence was experienced. Document and report it to the physician... is this your patient's first seizure, are they on anything for seizures (is drug level not therapeutic....may need to draw a drug level if ordered by MD) EEG may be ordered: What's an EEG?: assesses brain activity Painless Hold seizure medications or medications that are stimulants or depressants prior to EEG (these medications can prevent the proper assessment of abnormal brain waves associated with a seizure) No caffeine products (a stimulant) 8 hours before Can eat before Make sure patient's hair is clean (needs good attachment to scalp) Different types of EEGs: some patients will need to experience sleep deprivation before the test by not sleeping the night before the test or only part of the night....always ask about this Education to patient about factors that can trigger a seizure: "Stop Seizure" Stress Trauma to the head Overexertion Period, pregnancy (hormones) Sleep depravation Electrolyte and metabolic issues (hypoglycemia, dehydration, acidosis) Illness (high fever) VisualiZation disturbances (strobe lights, certain smells or sounds) Under medicated with seizure med (remind patient importance of taking and coming to office visits to get drug levels drawn) Recreational drugs ETOH use Medications/Treatments Medications treat based on type of seizure: Barbiturates: Phenobarbital (used tonic-clonic or focal seizures & status epilepticus) stimulates GABA receptors & this helps inhibitory neurotransmission side effects: drowsiness, uncoordinated movements (ataxia) etc. watch for: respiratory depression and hypotension drug level 15 to 40 mcg/mL Hydantoins: Phenytoin (used in tonic-clonic or focal seizures) watch the gums: will enlarge and easily bleed (called gingival hyperplasia....teach about good mouth care may cause bone marrow suppression (watch platelets and WBCs) tell patient to watch for rash or Steven-Johnson's Syndrome and to REPORT it to their doctor immediately don't give with milk or antacids (interferes with absorption) 10 to 20 mcg/mL Benzodiazepines: absence seizures, tonic clonic, focal Diazepam or Lorazepam: status epilepticus (fast acting) Very drowsy, tolerance can develop where it isn't as effective, impair liver (monitor liver studies) Reversal agent: Flumazenil (*used with extreme caution due to its risks) Valproates: Valproic Acid all types....monitor liver, WBC and platelets, GI issues Other treatments: surgery: to remove an area of the brain that is causing the seizure....example: focal seizures that arise from temporal lobe (temporal lobectomy) Meds not working: placement of a vagus nerve stimulator: an electrical device that sends electrical signals to the vagus nerve Ketogenic diet (used in pediatric patient who have epilepsy): high fat, low carb, diet....used when seizures not controlled by medication

What does CPP mean?

The cerebral perfusion pressure (CPP) is the pressure needed to ensure blood flow to the brain. CPP is regulated by two balanced opposing forces: Mean arterial pressure (MAP) is the driving force that pushes blood into the brain. Intracranial pressure (ICP) is the force that keeps blood out

11. Know how to calculate CPP. (We did this in class with the equation on the board for finding the MAP before Plugging it in to find the CPP). Know your interventions after if there needs to be any. You may be asked to calculate CPP but after you have done that you may be asked what action you perform next if you note that it's high.

To calculate CPP you need to know that: CPP=MAP - ICP *cerebral perfusion pressure is EQUAL to the mean arterial pressure MINUS intracranial pressure So, to calculate it you need to know the patient's BP and ICP: Let's give it a try! BP: 108/72 ICP: 13 Right now we have: CPP= MAP - 13 First, we need to figure out the MAP (mean arterial pressure)...this is the pressure within a patient's arteries during one cardiac cycle. Formula for MAP: SBP + 2(DBP) = MAP 3 *systolic blood pressure PLUS (diastolic blood pressure which is multiplied by 2) and then DIVIDED by 3. 72 x 2 = 144 144 + 108 = 252 252/3 = 84 MAP = 84 CPP= 84 -13 CPP= 71 It is normal....<60 mmHg: brain is not being perfused and as the MAP starts to equal the ICP the CPP will fall.

24. Parkinson's Disease. Know pathoetiology, manifestations, drugs, diagnostic tests, pt teaching, goals of care.

What is Parkinson's Disease? It's a neuro disease that gradually starts to affect movement. What is happening in Parkinson's disease to cause movement to become affected? The dopaminergic neurons in the part of the brain called substantia nigra have started to die. Significance of this area? This area is part of the basal ganglia which is part of the midbrain that controls movements. What is the role of these dopaminergic neurons? They release the neurotransmitter dopamine, which allows us to have accuracy with movement. Therefore, if they are dying this will lower the amounts of dopamine available to our body for normal movement. Why is there the signs and symptoms of tremors, rigidity etc.? Normally in the nervous system there is a balance between acetylcholine (an excitatory neurotransmitter) and dopamine (an inhibitory neurotransmitter). Therefore, the loss of dopamine leads to more acetylcholine being able to produce more excitatory affects to the neurons in the basal ganglia and this leads to overstimulation.....tremors, rigidity (increased cholinergic activity) etc. Key Points about Parkinson's Disease The disease tends to occur in older age 60+ (however it can affect younger people...example: Michael J. Fox was diagnosed with PD at the age of 29). There is currently no cure (there are medications to relieve signs and symptoms). Signs and symptoms are subtle (some patients don't notice them at first) and they will become worse overtime. Signs and symptoms may present on one side or one extremity and progress to the others overtime. Signs and Symptoms of Parkinson's Disease Mainly motor symptoms: affects how the patient is able to move Tremors at rest (most common): hands, arms, legs (even lips and tongue)... improves with movementPill-rolling: tremors of the hands and fingers....looks like the patient is rolling a pill between fingers and hands. Stiffness of extremities (arms DON'T swing with gait).... akinesia: inability to move the muscles voluntarily...."freeze up"Shuffling of gait (extremities can freeze while walking)Cogwheel rigidity: when moving the patient's arms passively toward the body they jerk or push back slightlyBradykinesia: movements are slow, difficulty swallowing (drooling), Face mask-like: expressionless Coordination issues.....so the patient will stoop to compensate. Issues with the muscles used for chewing food, swallowing, and speaking: soft or slurred speech, problems swallowing (aspiration) Other signs and symptoms that are non-motor: Depression Constipation: digestion slows down Loss of smell Nursing Interventions for Parkinson's Disease What is going on? Safety issues (balance coordination, swallowing, freezing episodes can lead to falls) Psychosocial issues (low self-esteem, loses ability to care for self, depression, isolation) Digestion issues/nutrition issues Side effects and teaching with medications Safety Issues: Patient needs to wear low heel shoes and avoid rubber soles (they tend to stick to the floor and can cause tripping). The soles should be smooth (not slick). For balance: move slowly when changing positions...rubber tip cane that is single point can help. Education on how to deal with freezing episodes (some patients have them and they can occur randomly). For example, it can occur in the legs, and it feels like the shoes suddenly become stuck to the ground and they can't move. Try to change direction of movement....rather then continue going to the side go forward. Use cane or walker with a laser...it provides a laser line on the floor that will help the patient find a landmark for when freezing episode happens and helps the patient coordinate their next step. Consciously lift the legs (as in marching) with each step or pretend they are walking over an object. DON'T push through the freeze up. Use handrails in bathroom and shower, elevated toilet seat, non-slip shoes and socks, removes rugs and make sure pets are away from feet etc. Psychosocial Issues: autonomy very important! Help them with locating utensils for eating, cooking etc..... there are special types of cookware for PD like spoons, forks, bowls, knives to maintain autonomy isolation: local support groups with other people who have PD exercise Don't stress patient about activities or hurry them...stress increases symptoms....wait for medication to peak so the most dopamine will be the most available. Dress patient in shirts without buttons or zippers...easy to put on...replace articles of clothing with Velcro and shoes that don't have to be tied. Digestion/Nutrition: Avoid taking antiparkinson's medication (Carbidopa/Levodopa) with a high protein meal (meats, eggs, dairy, beans) because they interfere with how the body can absorb the medication (makes medication less effective). At risk for weight loss because of the struggle with swallowing, chewing, depression, and hard to feed self due to rigidity Needs foods that are soft, easy to swallow, and chew...speech therapy to evaluate...recommend consistency of fluids Prevent constipation: drink plenty of fluids 2 L per day (unless contraindicated) with high fiber foods....example fresh fruits and vegetable and stool softner per MD order Assess last bowel movement and bowel sounds along with palpation of abdomen. Medications for Parkinson's Disease (side effects and teaching) NO cure but medications can help make signs and symptoms more manageable Carbidopa/Levodopa (combination)....most common "Sinemet": adds more dopamine to the brain Carbidopa helps to prevent levodopa from being broken down in the blood before it enters the brain (hence more enters the brain) and lessens the side effect of nausea and when levodopa enters the brain it turns into dopamine Education: takes up to 3 weeks to notice a decrease in symptoms when beginning treatment don't be alarm if body fluids turn a dark color after long term usage the drug may wear off before next dose and cause signs and symptomsEntacapone "Comtan": a COMT can be prescribed to help decrease this from happening Don't take with MAO inhibitors....hypertensive crisis!! Don't take with high amounts of food or supplements with Vitamin B6: decreases effectiveness Avoid taking with high protein foods like cheese, milk, meat etc...decreases the amount of drug absorbed (competes with protein in the small intestines) Side effects: nausea, involuntary movements Ropinirole "Requip": stimulates dopamine receptors ....dopamine agonists: helps with improving movement Side effects: drowsiness major side effect (educate NOT to take when about to drive, cook, or operative machinery etc.) Amantadine (antiviral: prevents influenza A...antiparkison as well): helps with symptoms by stimulating dopaminergic activity in the CNS Anticholinergic: Remember acetylcholine (causes cholinergic activity) is exceeding dopamine, which is producing an excitatory affect on the neurons. Therefore, ANTIcholinergics can be prescribed to decrease these effects. These medications are usually for younger adults who have extreme tremors and avoided in older adults because for the side effects. Benztropine "Cogentin": blocks acetylcholine by decreasing rigidity, saliva (drooling), improved movements NOT for people with GLAUCOMA!! Education: never abruptly stop taking (increases signs and symptoms seen in Parkinson disease), dry mouth (sugar less candy or gum), NO alcohol. MAO Inhibitor Type B (Monoamine Oxidase Inhibitor Type B): Rasagiline "Azilect": increases dopamine by stopping the activity of MOA...improvement of symptoms Educate about limiting foods with tyramine: hypertensive crisis aged cheese smoked or cured meats (pepperoni, bacon, hot dogs) fermented food beer COMT Inhibitors Entacapone "Comtan" (catechol-O-methyltransferase inhibitors) used with levodopa/carbidopa to prevent the "wearing off" of the drug before the next dose is due....blocks COMT enzyme that will break down the levodopa in the blood to allow it to last longer.

Increased Intracranial Pressure (ICP) (Ch 35)

What is increased intracranial pressure? It's where pressure inside the skull has increased. This is a medical emergency! Intracranial pressure is the pressure created by the cerebrospinal fluid and brain tissue/blood within the skull. It can be measured in the lateral ventricles. What is a normal ICP: 5-15 mmHg (>20 mmHg...needs treatment) Pathophysiology of Increased Intracranial Pressure The skull is very hard and is limited on how much it can expand when something inside the skull experiences a change that leads to increased pressure. Inside the skull are three structures that can alter intracranial pressure: brain cerebrospinal fluid (CSF) blood To understand the patho of increased intracranial pressure, you must understand the Monro-Kellie hypothesis. It deals with how ICP is affected by CSF, brain's blood, and tissue and how these structures work to maintain cerebral perfusion pressure (CPP). In a nutshell, this hypothesis says that if the volume of one of these structures increases, the others must decrease their volume to help alleviate pressure. When there is an increase in intracranial pressure, the body can temporarily compensate for it by shifting CSF to other areas of the brain or spinal cord (or decrease it production), and alter blood volume going to the brain through vasocontriction, but if the pressure is continuous it is unable to compensate. Intracranial pressure fluctuates and this can depend on many factors like: person's body temperature oxygenation status, especially CO2 and O2 levels body position arterial and venous pressure anything that increase intra-abdominal or thoracic pressure (vomiting, bearing down etc.) For the brain to receive proper nutrients to work it must receive a certain about of cerebral blood flow. This is the amount of blood flowing to the brain's tissue. It does this by altering the cerebral perfusion pressure via vasoconstriction or vasodilation. For example, if carbon dioxide levels are abnormally high (>45) vasodilation occurs, which allows more blood volume to enter the brain. However, this is not good if a patient has increased ICP because this will further increase the ICP. Cerebral perfusion pressure can become compromised during increased intracranial pressure. Therefore, there must be a sufficient cerebral perfusion pressure so that the brain is properly maintain. What is a normal CPP? 60-100 mmHg NOTE: When CPP falls too low the brain is not perfused and brain tissue dies. If the patient's mean arterial pressure (MAP) starts to fall to the patient's ICP, then the cerebral perfusion pressure will drop. Therefore, maintaining a sufficient MAP is essential. So How is CPP calculated? Equation: CPP= MAP - ICP You need to know the following: BP: 90/42 ICP: 19 First, the MAP must be calculated: MAP= Diastolic BP x 2 + SBP divided by 3 42 x 2 = 84 84 + 90 = 174 ....divided by 3= 58 (MAP) 58-19= CPP 39....very low...normal 60-100 mmHg -What can cause an increased pressure within the skull that leads to increased intracranial pressure? injury (head trauma) increased in cerebrospinal fluid hemorrhage (hemorrhagic stroke...aneurysm bursts) hematoma (subdural and epidural...bleeding in between structures in the brain) hydrocephalus: buildup of CSF in the brain...normally flows through the brain and spinal cord and enters the bloodstream (blocked, too much is made) tumor: putting pressure on brain encephalitis (inflammation of brain tissue) or meningitis (inflammation of membrane covering spinal cord and brain) -What happens with increased intracranial pressure? Limited cerebral blood flow due to decreased cerebral perfusion from building pressure in the brain. The brain is getting squeezed and this leads to ischemia. All of this can lead to swelling and edema, which will eventually (if not treated) lead to herniation or displacement of the brain. The displacement of the brain can compress important areas of the brain like the brain stem (specifically medulla and vagus nerve). When CPP falls too low the body tries to increase systolic blood pressure to make more blood go to the brain, but this makes things worst!! During this time the arteries will start to dilate because of the retention of carbon dioxide. This causes more blood to flow to the brain but this will compress veins and limit blood flow to the heart. Hence, leading to more swelling and even more ICP. As all this progresses the patient's signs and symptoms will start to become worst. Therefore, it is essential to know the EARLIEST signs and symptoms (mental status changes) of increased ICP. Signs and Symptoms of Increased ICP "Mind Crushed" Mental Status Changes ***Very earliest!! remember this for exam!! (restless, confused, problems performing normal movements and responding to questions) Irregular breathing (slow down of respirations and irregular...cheyne-stokes...hyperventilation then apnea cyclic)*late Nerve changes to optic and oculomotor nerve: double vision, swelling of optic nerve (papilledema), pupil changes (decreased, increased, or unequal size), abnormal doll's eyes: oculocephalic reflex...in an unconscious patient open the eyes and move the head from side to side....if eyes don't move in the opposite direction but stay fixed this is a very bad sign....indicates brain stem damage Decerebrate or decorticate posturing or flaccid Decorticate (flexor posturing): brings upper extremities to the core of the body (middle)adduction and flexion of arms, leg rotated internally, feet flexed Decerebrate: (Extension posturing): extends upper extremities from the body *worst of the two (remember all the E's in decerebrate and think EXTEND arms)adduction and extension of arms with pronation, and feet flexed Cushing's Triad: LATE SIGN...herniation of the brain stem Increased systolic blood pressure (widening pulse pressure: increase in SBP and decrease in DBP), decreased heart rate, and abnormal breathing Increased SBP (due to body trying to get more blood to the brain...thinks it's helping) -> Baroreceptor reflex (parasympathetic responds by dropping the heart rate to decrease the blood pressure and there may be compression of the vagus nerve due to compression from the swelling in the brain -> The compression on the medulla of the brain leads to abnormal respirations cheyne-stokes Reflex positive Babinski (toe fan out...abnormal) Unconscious LATE Seizures Headache Emesis (vomiting) without nausea projectile Deterioration of motor function (hemiplegia)...weakness on one side of the body Nursing Interventions for Increased Intracranial Pressure Focus on preventing further increase ICP and monitoring ICP (if monitoring device inserted) "PRESSURE" Position head of bed: 30 to 45 degree (helps blood return to heart), proper alignment of head (midline) NO flexion of neck (decreases venous return) or hips (increases intra-abdominal/thoracic pressure)...watching moving around in bed Respiratory: Prevent HYPOXIA and HYPERCAPNIA! When blood oxygen levels drop or carbon dioxide levels increase, vasodilation occurs and this increases intracranial pressure. monitor blood gases, oxygen level, suctioning as needed only (no longer than 15 seconds...increase ICP) hyperoxygenated before and after mechanical ventilation to keep PaCO2 low 30-35 WHY? Vasoconstriction to help decrease ICP by decreasing blood flow....keep the PEEP low...increases intrathoracic pressure Elevated temperature PREVENT this! Monitor temperature If patient is unconscious best to take tympanic, temporal or rectal route NOT orally or axillary....Why is there a risk for hyperthermia? Patient may have damage to the hypothalamus, infection, dehydration etc....a high temp. increases ICP, cerebral blood flow, and metabolic needs of the patient Can give antipyretics per MD order, remove extra blankets, decrease room temperature, cool baths...prevent shivering (increases metabolic needs and ICP) Systems to monitor: Glasgow Coma Scale neuro checks per protocol ventriculostomy (external ventricular drain): monitors ICP. It's a catheter inserted in the area of the lateral ventricle to assess ICP and drains CSF during increased pressure readings.monitor for ICP levels greater than 20 mmHg and report to MD.....patients with increased ICP are not a candidate for lumbar puncture....risk of brain herniation. Straining activities AVOIDED: vomiting, coughing, sneezing, Valsalva, agitation (keep environment calm), avoiding restraints as necessary Unconscious patient care: avoid over sedating with narcotic or sedatives, lung sounds and suction as needed, immobile (skin breakdown, monitor nutrition, at risk for renal stones, constipation, passive range of motion with extremities) nutrition, eye care with solutions and ointments, maintain GI tubes for feeding (monitor residuals....poor gastric emptying more than 100 ml), blood clot formation (SCDs, passive range of motion), talk to the patient as you would a conscious patient Rx: Barbiturates: to help decrease brain metabolism and BP which in turn decreases ICP, Vasopressors/IV fluids or antihypertensive to maintain SBP greater than 90 but less than 150, anticonvulsants meds, hyperosmotic drugs (leads to the next point of edema management)....... Edema management: dehydrating the brain (must be done carefully...watching blood pressure and renal function) Mannitol: it's a concentrated type of sugar When this drug enters the blood it is very concentrated and it draws water that is pooling in the brain back into the blood. This type of diuretic is filtered through the glomerulus and not reabsorbed through the renal tubules, and because of this it creates an osmotic pressure that will pull water and electrolytes (sodium, chloride) from the blood (won't be reabsorbed) and be excreted out. Watch for fluid overload (water intoxication) and depletion. FVO: signs and symptoms of heart failure, pulmonary edema (lung and heart sounds) monitor renal function, UOP, electrolytes not for patients with cerebral hemorrhage or anuria (no urine output) patient will report dry mouth and thirsty...provide mouth care watch fluids (IV, oral), UOP, I and O's (retention of urine?) More edema management meds that may be ordered: loop diuretics to remove fluid from brain and maintain a negative fluid balance....corticosteroids

Multiple Sclerosis (MS)

What is multiple sclerosis (MS)? It's an autoimmune disease that affects the myelin sheath of the central nervous system (CNS). This leads to inflammation and scarring of the nerve, which causes a decrease in nerve transmission. This is why many patients experience sensory and motor problems. Quick Facts about Multiple Sclerosis: It's an autoimmune condition, which means the immune system is actually attacking the myelin sheath found on the nerve. It affects the nerve cells in the brain and spinal cord, and this leads to many sensory and motor type problems. Symptoms vary among patients because different areas of the central nervous system are affected.For example, if the patient has lesions (damage to the myelin sheath)in the cerebellar area, the patient may experience tremors, dysarthria (issues with articulating words...muscles for speech aren't working well), ataxia (trouble controlling body movements), and cognitive issues.Furthermore, if the nerve to the eyes (optic nerve) is being affected the patient will have vision issues like blurry vision or blindness in one eye etc. Women tend to be affected more than men, and MS seems to show up in the age category of 20-40s. Symptoms can appear and then disappear. This is the most common form of MS where signs and symptoms come and go called: relapsing-remitting multiple sclerosis (RRMS) Exact cause is not totally known There is currently no cure, but there are lifestyle changes and medications that can improve signs and symptoms. How is Multiple Sclerosis Diagnosed? Diagnosing (takes time): the neurologist has to assess several things because there is not one test that can diagnose it: Assessing patient's symptoms...may need to rule out other diseases MRI to assess for lesions in the brain and spinal cord Lumbar puncture: assesses spinal fluid for specific proteins called oligoclonal bands (which are immunoglobulins). If these are present it shows there is inflammation in the CNS. Evoked potential studies (sends electrical signals to the CNS and sees the response). Pathophysiology of Multiple Sclerosis You have to understand the anatomy and physiology of the nerve cell (neuron) in the central nervous system. Dendrites: receive the signal needed to create some type of action. This signal goes down to the: Soma: (which means body) and this structure helps pass on the signal it just received from the dendrites to the rest of the neuron. Then the signal goes down and passes where the soma of the neuron and axon connect at the axon hillock. Then the signal goes down this long area known as the axon. For the axon to be able to deliver this signal properly to either another neuron, muscle, or gland, it must be nicely be insulated and protected by the myelin sheath, which is made up of Schwann cells. These cells consist of fats and proteins. ****This is our problem with MS (the myelin sheath has experienced demyelination).....so guess what?! The signal is NOT being transmitted properly to the area that the nerve supplies!! After the signal leaves the axon in a healthy neuron it goes to the axon terminal (the end of the axon) where it synapses (where a nerve signal passes) with another neuron, muscle or glands to cause an action of some type. So, in MS we're talking about the nerve cells in the CNS, which is our BRAIN and SPINAL CORD.....because of this we can expect to finding sensory type problems (touch, vision), coordination, emotional, cognitive, and bowel/bladder issues For sign and symptoms let's divide them by category. Remember signs and symptoms vary in patients depending on where the lesions have occurred due to demyelination. Signs and Symptoms of Multiple Sclerosis Emotionally and cognitive: drained (feel weak), fatigued, depressed, trouble articulating speech (issues swallowing), mood swings, trouble thinking (focusing, solving, keeping thoughts etc.) Sensation issues: involuntary tremors, spasms (painful and strong), clumsiness (leads to unintentional injury), numbness/tingling (face and extremities) electric shock sensation that travels down the body when moving head or neck in various position called "Lhermitte's sign" dizzy, muscles hard to move (stiff)....affects coordination (cerebellum area) unable to be aware of body positon (proprioception) when eyes are closed....Romberg's Sign...patient puts feet together and closes eye...this causes them to sway Vision: nystagmus (issues with controlling eye movement), optic neuritis (early) double vision...blurry vision or vision is gray (dull colors), blindness in one eye, and seeing dark spots in vision, painful when moving eyes Elimination (nerves are affected that control the bladder/bowel and their sphincters): can't hold urine....overactive bladder (incontinence) leads to nocturia problems urinating...hesitancy leads to retaining urine (at risk for UTI's and renal stones) bowel: constipation/diarrhea or incontinence Early signs and symptoms of MS include: vision issues, tingling numbness, weakness, dizziness, balance issues, bladder problems, cognitive issue...issues speaking, weakness, spasms ****Symptoms can get worse due to heat called Uhthoff's sign. Heat can be from the weather, physical exercise etc. Nursing Interventions for Multiple Sclerosis Nursing considerations: safety (vision, coordination, decrease perception with pain), RRMS (most common form of MS)....preventing symptoms from worsening, bladder and bowel issues, medications What is multiple sclerosis (MS)? It's an autoimmune disease that affects the myelin sheath of the central nervous system (CNS). This leads to inflammation and scarring of the nerve, which causes a decrease in nerve transmission. This is why many patients experience sensory and motor problems. Quick Facts about Multiple Sclerosis: It's an autoimmune condition, which means the immune system is actually attacking the myelin sheath found on the nerve. It affects the nerve cells in the brain and spinal cord, and this leads to many sensory and motor type problems. Symptoms vary among patients because different areas of the central nervous system are affected.For example, if the patient has lesions (damage to the myelin sheath)in the cerebellar area, the patient may experience tremors, dysarthria (issues with articulating words...muscles for speech aren't working well), ataxia (trouble controlling body movements), and cognitive issues.Furthermore, if the nerve to the eyes (optic nerve) is being affected the patient will have vision issues like blurry vision or blindness in one eye etc. Women tend to be affected more than men, and MS seems to show up in the age category of 20-40s. Symptoms can appear and then disappear. This is the most common form of MS where signs and symptoms come and go called: relapsing-remitting multiple sclerosis (RRMS) Exact cause is not totally known There is currently no cure, but there are lifestyle changes and medications that can improve signs and symptoms. How is Multiple Sclerosis Diagnosed? Diagnosing (takes time): the neurologist has to assess several things because there is not one test that can diagnose it: Assessing patient's symptoms...may need to rule out other diseases MRI to assess for lesions in the brain and spinal cord Lumbar puncture: assesses spinal fluid for specific proteins called oligoclonal bands (which are immunoglobulins). If these are present it shows there is inflammation in the CNS. Evoked potential studies (sends electrical signals to the CNS and sees the response). Pathophysiology of Multiple Sclerosis You have to understand the anatomy and physiology of the nerve cell (neuron) in the central nervous system. Dendrites: receive the signal needed to create some type of action. This signal goes down to the: Soma: (which means body) and this structure helps pass on the signal it just received from the dendrites to the rest of the neuron. Then the signal goes down and passes where the soma of the neuron and axon connect at the axon hillock. Then the signal goes down this long area known as the axon. For the axon to be able to deliver this signal properly to either another neuron, muscle, or gland, it must be nicely be insulated and protected by the myelin sheath, which is made up of Schwann cells. These cells consist of fats and proteins. ****This is our problem with MS (the myelin sheath has experienced demyelination).....so guess what?! The signal is NOT being transmitted properly to the area that the nerve supplies!! After the signal leaves the axon in a healthy neuron it goes to the axon terminal (the end of the axon) where it synapses (where a nerve signal passes) with another neuron, muscle or glands to cause an action of some type. So, in MS we're talking about the nerve cells in the CNS, which is our BRAIN and SPINAL CORD.....because of this we can expect to finding sensory type problems (touch, vision), coordination, emotional, cognitive, and bowel/bladder issues For sign and symptoms let's divide them by category. Remember signs and symptoms vary in patients depending on where the lesions have occurred due to demyelination. Signs and Symptoms of Multiple Sclerosis Emotionally and cognitive: drained (feel weak), fatigued, depressed, trouble articulating speech (issues swallowing), mood swings, trouble thinking (focusing, solving, keeping thoughts etc.) Sensation issues: involuntary tremors, spasms (painful and strong), clumsiness (leads to unintentional injury), numbness/tingling (face and extremities) electric shock sensation that travels down the body when moving head or neck in various position called "Lhermitte's sign" dizzy, muscles hard to move (stiff)....affects coordination (cerebellum area) unable to be aware of body positon (proprioception) when eyes are closed....Romberg's Sign...patient puts feet together and closes eye...this causes them to sway Vision: nystagmus (issues with controlling eye movement), optic neuritis (early) double vision...blurry vision or vision is gray (dull colors), blindness in one eye, and seeing dark spots in vision, painful when moving eyes Elimination (nerves are affected that control the bladder/bowel and their sphincters): can't hold urine....overactive bladder (incontinence) leads to nocturia problems urinating...hesitancy leads to retaining urine (at risk for UTI's and renal stones) bowel: constipation/diarrhea or incontinence Early signs and symptoms of MS include: vision issues, tingling numbness, weakness, dizziness, balance issues, bladder problems, cognitive issue...issues speaking, weakness, spasms ****Symptoms can get worse due to heat called Uhthoff's sign. Heat can be from the weather, physical exercise etc. Nursing Interventions for Multiple Sclerosis Nursing considerations: safety (vision, coordination, decrease perception with pain), RRMS (most common form of MS)....preventing symptoms from worsening, bladder and bowel issues, medications Preventing symptoms from getting worse: Watch the heat (keep room cool, avoid heating blankets, pads etc.), avoid infection, stressful events, and getting too tired...overexertion (pace out activities and take time to have many rest periods) Very important to maintain regular exercise as tolerated...not too much because it can exacerbate symptoms (swimming...water aerobics, ...keeps energy and mood level up) Use assistive devices to help with walking and preventing injury (toileting and showering) when symptoms are presenting, clutter free environment, especially when vision affected or experiencing vertigo, scan environment if experiencing blindness in one eye or dark spots Consult SLP (helps with speech if speech is slurred or hard to understand, difficult swallowing), PT (exercises, assistive devices), support groups with others who have MS Bladder and bowel: make accessibility to bathroom easy due to overactive bladder, may need to learn how to self-cath if retaining urine, plenty of fluids to prevent stasis of urine and to keep it from becoming too concentrated 1-2 L, high fiber to prevent constipation...stool softeners Medications for Multiple Sclerosis **Medications vary depending on what symptoms the patient is having...medications treat symptoms.... don't cure disease Beta interferon: decreases the number of relapses of symptoms by decreasing inflammation and the immune system response ....risk of infection because decreases WBC Drug Names: Avonex (interferon beta 1a), Rebif, Betaferon Corticosteroids: for relapses of symptoms...methylprednisolone (solu-medrol), prednisone Bladder issues: Oxybutynin: anticholinergic that helps with an overactive bladder...relaxes bladder to prevent contractions Bethanechol: cholinergic that helps with completely emptying the bladder by helping bladder contract fully. Fatigue: Amantadine (antiviral and antiparkinson but has CNS effects. This helps improve fatigue in MS patients....another drug Modafinil (CNS stimulant) Spasms: baclofen (skeletal muscle relaxants that act centrally), diazepam Tremors: propranolol (beta blocker), isoniazid (antibiotic used to treat infection, especially TB...helps with certain tremors in MS) Watch the heat (keep room cool, avoid heating blankets, pads etc.), avoid infection, stressful events, and getting too tired...overexertion (pace out activities and take time to have many rest periods) Very important to maintain regular exercise as tolerated...not too much because it can exacerbate symptoms (swimming...water aerobics, ...keeps energy and mood level up) Use assistive devices to help with walking and preventing injury (toileting and showering) when symptoms are presenting, clutter free environment, especially when vision affected or experiencing vertigo, scan environment if experiencing blindness in one eye or dark spots Consult SLP (helps with speech if speech is slurred or hard to understand, difficult swallowing), PT (exercises, assistive devices), support groups with others who have MS Bladder and bowel: make accessibility to bathroom easy due to overactive bladder, may need to learn how to self-cath if retaining urine, plenty of fluids to prevent stasis of urine and to keep it from becoming too concentrated 1-2 L, high fiber to prevent constipation...stool softeners Medications for Multiple Sclerosis **Medications vary depending on what symptoms the patient is having...medications treat symptoms.... don't cure disease Beta interferon: decreases the number of relapses of symptoms by decreasing inflammation and the immune system response ....risk of infection because decreases WBC Drug Names: Avonex (interferon beta 1a), Rebif, Betaferon Corticosteroids: for relapses of symptoms...methylprednisolone (solu-medrol), prednisone Bladder issues: Oxybutynin: anticholinergic that helps with an overactive bladder...relaxes bladder to prevent contractions Bethanechol: cholinergic that helps with completely emptying the bladder by helping bladder contract fully. Fatigue: Amantadine (antiviral and antiparkinson but has CNS effects. This helps improve fatigue in MS patients....another drug Modafinil (CNS stimulant) Spasms: baclofen (skeletal muscle relaxants that act centrally), diazepam Tremors: propranolol (beta blocker), isoniazid (antibiotic used to treat infection, especially TB...helps with certain tremors in MS)

What are the manifestations both physiological (Bp HR etc) and behavioral (Irritability etc) of increased intracranial pressure?

When there is an increase in intracranial pressure, the body can temporarily compensate for it by shifting CSF to other areas of the brain or spinal cord (or decrease it production), and alter blood volume going to the brain through vasocontriction, but if the pressure is continuous it is unable to compensate. Intracranial pressure fluctuates and this can depend on many factors like: person's body temperature oxygenation status, especially CO2 and O2 levels body position arterial and venous pressure anything that increase intra-abdominal or thoracic pressure (vomiting, bearing down etc.) Limited cerebral blood flow due to decreased cerebral perfusion from building pressure in the brain. The brain is getting squeezed and this leads to ischemia.

21. Words to know graphesthesia

Xerostomia, bradykinesia, diplopia, dysmetria

An older patient is admitted to the hospital with a urinary infection and possible bacterial sepsis. The family is concerned because the patient is confused and not able to carry on a conversation. Which statement by the nurse is most appropriate? a."Depression is a common cause of confusion in older adults in the hospital." b."It is normal for an older person to have cognitive problems while in the hospital." c."The mental changes are most likely caused by the infection and most often reversible." d."Drug therapy with antipsychotic agents is indicated to slow the progression of dementia."

c."The mental changes are most likely caused by the infection and most often reversible."

The daughter of a patient with early familial Alzheimer's disease (AD) asks how AD is different from forgetfulness. You describe early warning signs of AD, including a.Forgetting a colleague's name at a party b.Repeatedly misplacing car keys or a wallet c.Leaving a pot on the stove that boils dry and burns d.Having no memory of preparing a meal and forgetting to serve or eat it

d.Having no memory of preparing a meal and forgetting to serve or eat it

Know the different types of strokes (Know the pathophysiology of them)

ischemic and hemorrhagic *Ischemic* • result from inadequate blood flow to brain from partial or complete occlusion of an artery Two types of ischemic strokes: -*Thrombotic stroke* - Occurs from injury to a blood vessel wall and formation of a blood clot •Results in narrowing of blood vessel •Most common cause of stroke (60%) •Often associated with HTN and DM •Many times they are preceded by TIA (TIA is a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, but without acute infarction of brain) •develops readily where atherosclerotic plaques have already narrowed blood vessels. Thrombotic strokes are more common in older individuals, especially those with high cholesterol, atherosclerosis, or diabetes. A majority of thrombotic strokes are associated with hypertension or diabetes mellitus, both of which accelerate atherosclerosis •Manifestations of ischemic stroke may progress in the first 72 hours as infarction and cerebral edema increase. -*Embolic* •Occurs when an embolus lodges in and occludes a cerebral artery •Results in infarction and edema of area supplied by involved vessel 2nd most common cause of stroke •Rheumatic heart disease is a cause of embolic stroke in young to middle-aged adults. An embolus arising from an atherosclerotic plaque is more common in older adults. •Warning signs are less common with embolic than with thrombotic stroke. The embolic stroke often occurs rapidly, giving little time to accommodate to an obstructed blood vessel with the development of collateral circulation. The patient usually remains conscious, although he or she may have a headache. The effects of the emboli are initially characterized by severe neurologic deficits, which can be temporary if the clot breaks up and allows blood to flow. Smaller emboli then continue to obstruct smaller vessels, which in turn involve smaller portions of the brain with fewer deficits noted. •The prognosis is related to the amount of brain tissue deprived of its blood supply. Recurrence of embolic stroke is common unless the underlying cause is aggressively treated. tPA (tissue plasminogen activator): for ischemia strokes ONLY not hemorrhagic! •*Hemorrhagic* - Results from bleeding into •Brain tissue itself •Intracerebral or intraparenchymal hemorrhage •Subarachnoid space or ventricles •Subarachnoid or intraventricular hemorrhage -two types of hemorrhagic stroke: *•Intracerebral* - •Bleeding within brain caused by rupture of a vessel •Sudden onset of symptoms •Progression over minutes to hours because of ongoing bleeding •Prognosis is poor with a 30-day mortality rate of 40%-80% •Hypertension is most common cause, other causes include vascular malformations, coagulation disorders, anticoagulant and thrombolytic drugs, trauma, brain tumors, and ruptured aneurysms •Hemorrhage occurs during activity •Sudden onset with progression over minutes to hours *•Manifestations* •Neurologic deficits •Headache •Nausea and/or vomiting •Decreased levels of consciousness •Hypertension *Subarachnoid hemorrhage* - Intracranial bleeding into cerebrospinal fluid-filled space between arachnoid and pia mater •Commonly caused by rupture of a cerebral aneurysm, trauma, or drug abuse Monitor vital signs and neuro status: especially blood pressure (notify MD is hypertensive) airway (difficulty swallowing....at risk for aspiration HOB 30' with suction at bedside) turn every 2 hours with proper alignment and watch for increased ICP (intracranial pressure) during acute stage headache, nausea and vomiting, increased blood pressure and decreased HR and decreased RR, decrease in mental status from baseline, pupils don't respond Diet: evaluated by speech language pathologist may need thicken liquids and mechanical soft foods assist with eating and monitor for pouching of food in cheek (on the affected side). This increases risk of aspiration. Have patient tuck in chin to their chest while swallowing.

31. Which type of headache is characterized as unilateral and throbbing?

migraine

1. What is Brudzinski Sign? What is Kernigs sign?

occurs w/ meningitis. Kernig's is performed by having the supine patient, with hips and knees flexed, extend the leg passively. The test is positive if the leg extension causes pain. The Brudzinski's sign is positive when passive forward flexion of the neck causes the patient to involuntarily raise his knees or hips in flexion.

What are factors that increase Intracranial pressure? ch 56

•Increased ICP can be caused by changes in any of the three components. •Common causes of increased ICP include a mass (e.g., hematoma, contusion, abscess, tumor) and cerebral edema (associated with brain tumors, hydrocephalus, head injury, or brain inflammation). •These cerebral insults, which may result in hypercapnia, cerebral acidosis, impaired autoregulation, and systemic hypertension, increase the formation and spread of cerebral edema. ischema, hematoma, edema.

18. What is the most common and sudden initial manifestations of hemorrhagic stroke (Your book has a scenario with a husband playing a sport who stops and complains to his wife about this manifestation.)

•Initially, patients experience a severe headache with nausea and vomiting, decreased LOC.

12. What would be the point of giving an osmotic diuretic to a patient with ICP?

•Mannitol acts to decrease the ICP in two ways: plasma expansion and osmotic effect. •An immediate plasma-expanding effect reduces the hematocrit and blood viscosity, thereby increasing CBF and cerebral oxygen delivery. • A vascular osmotic gradient is created by mannitol. Thus fluid moves from the tissues into the blood vessels. Therefore the ICP is reduced by a decrease in the total brain fluid content.

7. Know how to calculate CPP. Also know what is.

•Cerebral perfusion pressure (CPP) •The cerebral perfusion pressure (CPP) is the pressure needed to ensure blood flow to the brain. CPP is regulated by two balanced opposing forces: Mean arterial pressure (MAP) is the driving force that pushes blood into the brain. Intracranial pressure (ICP) is the force that keeps blood out •CPP = MAP - ICP •Normal is 60 to 100 mm Hg •<50 mm Hg is associated with ischemia and neuronal death •Effect of cerebral vascular resistance •CPP = Flow x Resistance BP: 108/72 ICP: 13 Right now we have: CPP= MAP - 13 First, we need to figure out the MAP (mean arterial pressure)...this is the pressure within a patient's arteries during one cardiac cycle. Formula for MAP: SBP + 2(DBP) = MAP 3 *systolic blood pressure PLUS (diastolic blood pressure which is multiplied by 2) and then DIVIDED by 3. 72 x 2 = 144 144 + 108 = 252 252/3 = 84 MAP = 84 CPP= 84 -13 CPP= 71 It is normal....<60 mmHg: brain is not being perfused and as the MAP starts to equal the ICP the CPP will fall.

What are the clinical manifestations of ICP?

•Change in level of consciousness •Change in vital signs •Cushing's triad •Ocular signs •Change in level of consciousness •Flattening of affect → coma •Change in vital signs •Cushing's triad (widened pulse pressure, bradycardia, irregular respirations) •Change in body temperature •Compression of oculomotor nerve •Unilateral pupil dilation •Sluggish or no response to light •Inability to move eye upward •Eyelid ptosis •Other cranial nerves •Diploplia, blurred vision, EOM changes ↓ In motor function Hemiparesis/hemiplegia Decerebrate posturing (extensor) Indicates more serious damage Decorticate posturing (flexor) Reflex positive Babinski (toe fan out...abnormal) nconscious LATE Seizures Headache Emesis (vomiting) without nausea projectile Deterioration of motor function (hemiplegia)...weakness on one side of the body