AVSAdvanced Adult Health Fall 2008

Study Guide for Exam #2

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General Study Tips:

1. Exam #2 will cover Advanced Adult Health content presented in Modules 4 and 5.

2. Be sure you have read all the assigned chapters. a. The chapters on assessment of the various systems are not

included below, but information in these chapters is important background information.

b. Be sure you understand lab tests discussed with each disorder and any pre- and post-procedure nursing interventions. Also, what would you teach the patient?

3. Be sure you have listened to or viewed the activities for each week.

4. Have you answered all the learning questions? 5. Did you use the questions at the end of each chapter or on the

Iggy CD-ROM as a self-test? 6. Have you looked up the big words? (See the first page of each

chapter.)7. Did you take a look at the very important Plans of Care

presented through-out the readings? 8. Did you take a look at the charts and tables throughout the

reading?9. Pay close attention to the sections regarding “health

promotion/illness prevention” included with each disorder-important for nurses to know!

10. Have you reviewed the medications discussed in your assigned readings? It is important for you to understand the category or classification drugs. It is important to understand the action of the drugs in each category, the desired effect, the potential adverse effects, and what the nurse needs to know before administering the medication and what to look for after giving the medication. Also, what would you teach the patient about each medication? Note: many of the medications mentioned in the readings have already been studied. A few are mentioned in the review below, but you are responsible for meds studied previously as well. Note: 18% of the NCLEX pertains to medications.

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11. Have you reviewed the “Key Points” at the end of each chapter?

12. Remember A-B-C and safety!

ADVANCED ADULT HEALTH CONTENT - Iggy

Module 4 – GASTROINTESTINAL Chapter 62

o Cirrhosis Chapter 62

o Cirrhosis: is extensive scarring of the liver usually caused by a chronic irreversible reaction to hepatic inflammation and necrosis. Most common cause is alcoholic liver disease and hepatitis C. and united states, worldwide leading causes hepatitis B.

Pathophysiology: is characterized by diffuse fibroids bands of connective tissue that distorts livers normal architecture. Inflammation caused by toxins for disease results and extensive degeneration and destruction of liver cells. As cirrhosis develops that issue becomes nodular which can block bile ducts a normal blood flow throughout the liver in the early stages of disease liver is usually enlarged, firm and hard. As a disease continues deliver sharks and size.

Complicationso Portal hypertension: in the is a persistent

increase in pressure within the portal vein. The results from increased resistance two or obstruction of the flow of blood through the portal vein and it’s tributaries. Can result in ascites, esophageal varices, prominent abdominal veins, and hemorrhoids.

o Ascites: is the accumulation of free fluid within the peritoneal cavity. This results In decrease circulating plasma protein in the blood. When this happens the effective serum colloid osmotic pressure is decreased and the circulatory system. This can cause renal vasoconstriction the triggering the renin angiotensin system. This results in sodium and water retention which perpetuates a cycle of ascites.

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o Bleeding esophageal varices: as a result of portal hypertension blood backs up from the liver and enters the esophageal and gastric vessel that carry it into the systemic circulation. When this happens the fragile thin walled esophageal veins Become distended from increased pressure. Bigger most often in the distal esophagus they can also be present in the stomach. One bleeding they can represent a significant life-threatening medical emergency.

o Coagulation defects: with cirrhosis there is a decrease in the synthesis of bile in the liver, this prevents the absorption of vitamin K.. Without buttoning Kay clotting factors II, VII, IX, and X are not produced insufficient quantities. This abnormality are manifested in prolonged prothrombin times.

o Jaundice: is caused by one of two mechanisms; Hepatocellular jaundice develops because the liver cells cannot effectively excrete bilirubin. Intrahepatic obstructive jaundice results from edema, fibrosis, or starring of the hepatic bile channels and bile ducts, which interferes with normal bile and bilirubin excretion.

o Portal-systemic encephalopathy: is manifested by neurologic symptoms and is characterized by an altered level of consciousness, impaired thinking process, and neuromuscular disturbances. Exact mechanisms are not clearly understood the most likely are the result of shunting of portal venous blood into central circulation so that the liver is bypassed. As a result toxic substances absorbed by the intestines are not broken down and may lead to metabolic abnormalities most significantly a elevated ammonia levels. However donated ammonia levels are not a clear indication of encephalopathy.

Etiology Alcohol: has a direct effect on the liver cells

and causes liver inflammation. Deliver 3

becomes enlarged with cellular degeneration and infiltration by fat leukocytes and lymphocytes. Damage to liver tissue progresses as a result of malnutrition and repeated exposure to alcohol. If alcohol was withheld the fatty infiltration and information is reversible. But if alcohol abuse continues widespread scar tissue formation you and fibrosis infiltrate the liver as a result of cellular necrosis. The man about the whole necessary causes damage varies from person to person.

Other causes: other causes of cihrrossis include viral hepatitis: what does hepatitis C. or hepatitis B. infection. Autoimmune hepatitis: what is a result of the host immune system circulating anybody’s that inflame the liver. Steatohepatitis: you occurs when fat and cholesterol deposits and deliver a causes inflammation. Drug and toxins may also be a cause. Biliary disease: which develops as a result of chronic biliary obstruction, stasis, inflammation, are hepatic fibrosis. Metabolic and genetic causes and cardiovascular which is due to write sided heart failure disease are also causes.

Physical assessment/clinical manifestations: the client may report the following fatigue, significant change in weight, gastrointestinal symptoms, abdominal pain and liver tenderness, and pruritis. You You either symptoms include jaundice, dry skin, rashes, petichiae, echymossis, warm and bright red homes of the hand, bass guitar lesions and peripheral dependent edema of the extremities abd sacrum. You The plan will have abdominal distention. Presence of blood and vomitus or stool. The patient will also have fetor hepaticus or bad breath, women may experience amenorrhea, men may experience testicular atrophy, enlarged breast and impotance due to the inactive hormones and certain diuretics. Continuously monitor neurological functions.

Laboratory and diagnostic studies: the client will have elevated AST, ALT, LDH, and elevated alkaline and phosphatase. Bilirubin levels will be elevated, potassium and albumin levels are decreased and clients with chronic liver disease, PT/INR is prolonged because deliver decreases the synthesis of prothrombin. I like and as low anemia may be present and white blood cells may be decreased. The

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money levels may be elevated and creatinine elevated as well.

Medical management: management includes placing the patient on a low sodium diet to control fluid, the client made beyond fluid restrictions, vitamin supplements including thiamine, folate, are added to ivy fluids because of livers and ability to store vitamins, oral vitamins are given when a patient is not an IV. Patient is usually on diuretics To reduce fluid into prevent cardiac and respiratory impairment. Need to watch the clients electrolytes Like potassium and sodium. The patient may require paracentesis if dietary and drugs failed to control ascites. This procedure is is one the doctor removes in trains the ascites from the paratoneal cavity. And If an infection is present the client is on antibiotics. Patient may receive some come from measures Including raising the head of the bed 30° or what is more comfortable for the patient due to fluid accumulation causing difficulty breathing. Fluid and electrolytes need to be monitored.

Surgical management: surgical management includes creating a shunt to drain the ascitic fluid into the venous system. But all signs need to meet monitored constantly due to increasing vascular volume. That sounds need to be assessed for the presence of crackles. Diuretics and may need to be prescribed the patience weight, abdominal girth, and urine output need to be assessed to to determine the effectiveness of the shunt.

For Bleeding: medical management; the the administration of long lasting beta blockers like inderal to decrease the higher rate in the paddock venous pressure gradient and decreases the chance of bleeding, if bleeding is occurring replacement of esophagogastric balloon tamponade, and blood transfusions are necessary. Surgical management was a last resort, surgical bypass shunting procedures decreased portal hypertension by diverting a portion of the portal fan blood flow from deliver.

Management of encephalopathy: dietary therapy includes a diet high in carbohydrates, moderates that, and high protein. But the client has donated the money levels usually low protein foods and simple carbohydrates are recommended. Drugs available to reduce the money levels include lactulose (excretion in stool), neomycin sulfate, (broad spectrum

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antibiotic to breakdown flora, and diminishing break down of protein decreasing amminia), metronidazole (similar action of neomycin but less toxic to the kidneys)

Nursing interventions:o Hepatitis A: is caused by the hepatitis A virus, which is an

RNA virus. it is spread via the fecal oral route by the oral ingested of fecal contaminants. sources of infection include contaminated water, shellfish cutting contaminated water, and food contaminated by food handlers infected with hepatitis A. Symptoms are similar to gastrointestinal illness And a disease and recovery uneventful.

o Hepatitis B: is caused by the hepatitis B. virus is it doubles shelled article that contains DNA. It is spread through unprotected sexual intercourse, sharing needles, accidental needle stick or injury from a sharp instrument, blood transfusion, hemodialysis, and maternal fetal route. Symptoms include anorexia, N/V, fever, fatigue, right upper quadrant pain, dark during with light school, joint pain, jaundice. But just confirms the disease, most adults to get uptight as B. recover clear the virus from their body and develop immunity. However 10% of the clients do not develop community and become carriers. Carriers can infect others even though they’re not sick and demonstrate no obvious signs of hepatitis B. chronic areas are at higher risk for cirrhosis and liver cancer.

o Hepatitis C: is caused by the hepatitis C. virus is a single stranded are in a virus. Transmission is blood the blood, rate of sexual transmission is very low, an Israeli transmitted from mother to fetus. His most commonly spread by Needle sharing, blood blood products are organ transplants recede before 1992, needle stick injuries, tattoos, and intranasal cocaine use. It is not transmitted by casual contact or entombment household contact. Most individuals are unaware that they have been infected, the viruses asymptomatic and is not diagnosed until many months or years after exposure. Alcoholic use hastens the progression of the disease

Pathophysiology: hepatitis can be a cute or chronic. There are seven types of the hepatitis virus a, B., C., D., E., F., and G.. Liver injury with information can also develop after its poacher to a number of pharmacologic and chemical agents by inhalation, ingestion, and IV administration. May also occur as a secondary infection During the course of infections with other diseases like herpes, varicella zoster, CMV. After its poacher Deliver becomes enlarged and congested with inflammatory cells, lymphocytes, and

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fluid resulting in right upper quadrant pain and discomfort. As these progressions delivers normal Lobular pattern becomes distorted as a result of war widespread inflammation, necrosis, and liver cell regeneration. This process interferes With blood flow into the liver and causes increased pressure within the portal vein, edema of the liver bile channels result in jaundice

How are they similar? Different? Causes of each type of hepatitis Physical assessment/clinical manifestations: the

client may experience abdominal pain, changes in scanner or eye color, joint and muscle pain, constipation and diarrhea, changes of color in urine or the school, fever, lethargy, malaise, N/V, and pruritis. Jaundice and hepatitis results from intra hepatic obstruction and is caused by a diva of the livers bile channel.

Laboratory assessment: presence of hepatitis a, B., C., are usually indicated by a cute elevations and levels of liver enzyme. Levels of ALT, AST, may be elevated. Alkaline phosphatase levels may be normal or elevated, bilirubin levels are elevated inconsistent with the presence of jaundice, elevated levels of bilirubin may also be present in urine. The presence of antibodies associated with hepatitis A, B., and C. Are also present. Immunoglobulin M our present in the blood for 4-6 weeks.liver biopsy: never biopsy is used to confirm the

diagnosis of hepatitis. Characteristic changes help distinguish a virus, drug, toxin, fatty liver, another disease. It’s quite elation is abnormal the biopsy is done using either a CT guided or trains jugular route. Medical management: rest is essential to reduce

delivers metabolic demands and increase its blood supply, treatment is generally supportive. Strict address may be indicated. Aside from physical rest the client also needs emotional and psychological rest. A special diet is usually not required the client should have a diet high in carbohydrates in calories with moderate amounts of fat and protein.Mall and frequent meals are often preferable them three standard meals. Encourage a client select foods that are appealing high energy snacks may be needed. Medication is used sparingly for clients with acute hepatitis to allow the liver to rest. For clients with hepatitis B. and C. the following drugs are common Lamivudine and adefovir dipivoxil are antiviral drugs

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given to destroy the hepatitis B. virus. But these medications can cause renal toxicity and granulocytopenia. Other drugs used are interferons, immunomodulating drugs are also administered. The most common treatment for hepatitis C. is a combination of subcutaneous interferon and oral ribavarin.

Nursing interventions: Teaching: prevention!: a primer focus in any case is

preventing the spread of the infection. For hepatitis transmitted by the fecal oral route careful hand washing and sanitary disposal of feces are important. Than to precautions are used for other forms of transmission. Education is very important, though there’s needs to ensure that prevention of transmission or precautions need to be taking care of once the client is home, if this is not done in the hospital based infection control personnel should be sought. Teach decline in family to observe measures to prevent infection instruct a client to avoid alcohol and check with the health care provider before taking any medications or vitamins supplements or herbal preparations. The client must determine the pattern for rest on the basis of physical tolerance of the increased activity.

Chapter 63Pancreatic Disorders

Acute pancreatitis – serious and at some times life threatening inflammatory process of the pancreas.

Pathophysiology – The exocrine function of the pancreas is responsible for secreting enzymes. Early activation occurs within the pancreas rather than the intestinal lumen and results in the inflammatory process of pancreatitis. Direct toxic injury to pancreatic cells and release of enzymes from the obstructive damage contribute to ductal rupture, allowing spillage of trypsin and other enzymes into the pancreatic parenchymal tissue.

o Lipolysis – hallmark of pancreatic necrosis is enzymatic fat necrosis of the endocrine and exocrine cells caused by lipase. Hypocalcemia occurs.

o Proteolysis – agent that triggers the premature activation of trypsin to trypsinogen. Involves the splitting of proteins by hydrolysis of the peptide bonds leads to thrombosis and gangrene.

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o Necrosis of the blood vessels – elastase is activated by trypsin and causes elastic fibers of the blood vessels and sucts to dissolve.

o Inflammation – occurs when leukocytes cluster around the hemorrhagic and necrotic areas of the pancreas.

Complications o Pancreatic infection (most common cause of death)o Hypovolemiao Jaundiceo Hemorrhageo Acute renal failureo Paralytic ileuso Hypovolemic or septic shocko Pleural effusiono Acute respiratory distress syndromeo Atelectasiso Pneumoniao Multiorgan system failureo DICo DM transient hyperglycemiao Coagulation defects (DIC) may result in death

History o Ask about abdominal pain and whether the pain occurs

when ingesting alcohol or eating high fat mealso Ask about medical problems known to cause pancreatitis

(PUD, renal failure, vascular disorders, hyperparathyroidism, hyperlipidemia and recent viral infections)

o Excessive ETOH particularly in men is the most frequent cause of acute pancreatitis

Physical assessment/clinical manifestations o ABDOMINAL PAIN that localizes in the epigastrium, has a

sudden onset, usually in mid-epigastric area or left upper quadrant and radiates to back, left flank or left shoulder. Described as BORING (feeling that it is going through the body). Pain is worse when supine and relieved by fetal position.

o Generalized jaundice o Cullen’s sign (gray-blue discoloration of the abdomen and

periumbilical area)o Turner’s sign – gray-blue discoloration of the flanks caused

by pancreatic enzyme leakage to cutaneous tissue from peritoneal cavity.

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o Respiratory complications – left lung pleural effusion, atelectasis, pneumonia

o Shock – significant changes in vital signs (hypotension and tachycardia). Result from pancreatic hemorrhage, excessive fluid volume shifting, or toxic effects of abdominal sepsis.

Laboratory and diagnostic studies o Cardinal diagnostic tests:

Elevated amylase, lipase, trypsin, elastase Amylase – levels increase within 12-24 hrs and

remain for 3-4 days Lipase – more specific, levels remain elevated for up

to 2 wks Trypsin – accurate for acute pain

o Radiographic test Abdominal xray – shoes gas filled duodenum

(supports dx) CXR – pleural effusion CT – RELIABLE DIAGNOSIS OF ACUTE PANCREATITIS MRI and US to confirm CT

Medical management o Fasting – rest the pancreas and reduce pancreatic enzyme

secretiono Drug therapy –

PCA pump – demerol DOC (causes less incidence of spasm of the smooth musculature of the pancreatic ducts and the sphincter of Oddi)

Mild pancreatitis – pain gone in 2-4 days Severe acute panc – pain lasts 2 weeks Anticholinergics (atropine), glucagons, calcitonin,

histamine receptor antagonist (Zantac), and protease inhibitors indicated to decrease vagal stimulation, decrease GI motility, inhibit pancreatic secretions. These drugs cause unwanted side effects and have not been proven to alter clinical outcome

Antibiotics – for acute necrotizing pancreatitis (cefuroxime, ceftazidime, primaxin)

Endoscopic Retrograde Cholangiopancreatography ECRP – if pancreatitis was caused by gallstones, an ECRP with sphincterectomy (opening of the sphincter of Oddi) may be performed on urgent or emergent basis. If not successful, surgery is required.

Surgical management – usually not indicatedo Laparoscopic cholecystectomy o Pre-op care

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o Client is in pain and inhibits the learning process. Reinforce postoperative reminders

o Client having external drainage of the pseudocyst need to expect to have a pancreatic drainage tube and explain its care

o Operative procedureso Pseudocystojejunostomy or pseudocystogastrostomy

performed to drain a pseudocyst into the jejunum or stomach.

o Post-opo Client having MIS (minimally invasive surgery) spend less

time in hospitalo Sump drain is usually inserted. Make sure it is functioning

indicated by the presence of a hissing noise from the lumen

o Provide meticulous skin care and dressing changes. o Monitor for the first signs of redness or skin irritation

because pancreatic enzyme drainage is excoriating to the skin.

o Skin barriers (stoma wafers) applied around the drainage tubes

o Collaborate with ET (Enterostomal) therapist to promote skin initegrity

Nursing interventions including pain o main focus is pain management o Administer analgesics via IV route, rather than IM if

possibleo Administer analgesics around the clock to prevent peaks

and troughs not prn.o Correct misconceptions client or family may hold regarding

analgesics (addictions and overdose)o Use pain control measures before pain becomes severeo help client assume fetal position for pain reliefo if NG tube in place, oral hygieneo lower client’s anxiety and pain by explaining procedureso Nutrition interventions o NPO early stage of pancreatitiso Antiemetics prno Severe pancreatitis NPO 7-10, needs TPN or TEN. TEN

produces fewer episodes of glucose elevationo When food is tolerated offer small, frequent moderate to

high-carb, high-protein, low fat meals. Bland (little spice)o Avoid GI stimulants and caffeine containing foods (coffee,

cola, chocolate) ETOH

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o Ensure supplements to increase caloric intakeo Fat soluble vitamins and other vitamin and mineral

replacements

Teaching o Client will be weak from acute illness and need to confine

activity to one floor, limit stair climbing and other strenuous activity until strength is regained.

o Education begins as soon as acute episodes of pain are over.

o Abstain from ETOH to prevent further attackso If ETOH is consumed, pain will be experienced and further

autodigestion of the pancreas will lead to chronic pain.o Notify health care provider if acute abdominal pain or

biliary tract disease (jaundice, clay-colored stool or darkened urine) occurs INDICATES COMPLICATIONS OR DISEASE PROGRESSION

Chronic pancreatitis Pathophysiology - progressive, destructive disease of

thepancreas, characterized by remissions and exacerbations. Usually develops after repeated episodes of alcohol induced acute pancreatitis. May also be associated with chronic obstruction of the common bile duct.

Types o Chronic calcifying pacreatitis – protein plugs the ducts and

lead to ductal obstruction, atrophy and dilation. Inflammatory process causes fibrosis of the pancreatic tissue. Cystic sacs, contain enzymes and pancreatic secretions. Organ becomes hard and firm as a result of acinar cell atrophy.

o Chronic obstructive pancreatitis – develops from inflammation, spasm, and obstruction of the sphincter of Oddi. Inflammatory and sclerotic lesions occur in the head of the pancreas, around the ducts, causing obstruction and backflow of pancreatic secretions

Pathologic changes – Decreased output of pancreatic secretions and bicarb (=acidosis) Fat malabsorption – causes weight loss and muscle wasting Protein malabsoprtion causes “starvation edema” of feet, legs

and hands Frank diabetes mellitus is caused by loss of pancreatic enzyme

function Pulmonary complications – pleuritic pain, pleural effusions,

pulmonary infiltrates Pancreatic ascities

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ARDS in the ill client

History/Physical assessment ( only dx is tissue biopsy) Abdominal pain – continuous burning or gnawing dullness

with periods of acute exacerbations. Pain is intense and relentless

Abdominal tenderness Ascites Possible left upper quadrant mass (if pseudocyst or abscess is

present) Respiratory compromise manifested by adventitious or

diminished breath sounds, dyspnea or orthopnea Steatorrhea, clay-colored stools Weight loss Jaundice Dark urine Polyuria, polydipsia, polyphagia (diabetes mellitus)

How might findings differ from acute? Abdominal pain description is different. No Cullen’s or Turner’s sign in chronic pancreatitis. No steatorrhea in acute pancreatitis

Medical management Avoid ingesting irritating substances that cause pain Analgesia – opioid (Demerol) and non-opioid tried b/c of

dependency Enzyme replacement – Pancreatin, pancrelipase

o Given with meals or snacks to aid in digestion and absorption of fat and protein

o Take immediately before or during meals with glass of water.

o Pancreatin (donnazyme) should not be broken crushed or chewed (enteric coated)

o Administer pancreatin after antacid or H2 blockers (decreased pH deactivates the drug)

o Mix powder form in applesauce or fruit juice o Don’t mix with food containing protein (dissolves food into

watery substance)o Wipe clients lips with wet towel to prevent skin irritation

from enzymeso Don’t be an idiot and inhale the powder formo Record number and consistency of stools per dayo Follow up on scheduled lab testing (pancrelipase can cause

increase in uric acid levels) Insulin therapy

o Clients on TPN are susceptible to labile glucoseo May require regular insulin additiveso Check FBS every 2-4 hrs

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Other Drugso Zantac – histamine receptor antagonist to decrease gastric

acid Diet therapy –

o TPN or TENo 4000-6000 calories a dayo clients often limits food intake to avoid recurrent paino foods high in fat are avoided (they increase diarrhea)

Surgical therapy – o Not a primary interventiono Indicated for intractable abdominal pain, incapacitating

relapses of pain and complications (abscess or pseudocysts)

o Incision and drain pseudocysto Laparoscopic cholecystectomyo Sphincterectomy of pancreatic duct sphincter to enlarge ito Laparoscopic pancreatectomy (resection of the distal

pancreas)o Pancreas transplant (few cases)

Nursing interventions including teaching – relief of pain, prevention of recurrence of attacks, prevention of complications, and nutritional support are principle interventions.

o Limit activity to one floor until strength is regainedo Toilet facilities must be easily acceptable b/c of chronic

steatorrheao Don’t drink caffeine or ETOHo Eat bland, low fat frequent mealso Adhere to pancreatic enzyme replacement o Report foul smelling frothy, fatty stools, abdominal

distention and cramping (pancreatic enzymes may need to be increased!)

o Use smoothing emoillient or skin barrier b/c of frequent stools

o Keep skin clean and dry

Module 5 – NEUROLOGY Chapter 46

o Spinal Cord Injury Pathophysiology (mechanisms, levels, extent): one

sufficient force is applied to the spinal cord damage results in neurologic deficits. The spinal cord injuries can be divided into primary and secondary mechanisms of injury. Primary mechanisms of injury

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include hyperflexion (which occurs when the head is suddenly and forcefully accelerated forward), hyper extension ( when the head is suddenly accelerated and deaccelerated) usually from all rear end accident. Rotation (when head is turned beyond normal range). Penetrating (when the spine is penetrated by a bullet or knife or other for object). Secondary injuries include neurogenic shock, vascular insult, hemorrhage, ischemia, and fluid and electrolyte imbalance. The patient with an incomplete spinal cord lesion As preservation of the mixed pattern of motor sensory and reflex functions.

Physical assessment/clinical manifestations: first priority is assessing the respite or a pattern and ensuring inadequate airway. Client is an assessed for indications of intra abdominal hemorrhage or bleeding around the fracture site. GCS is used to assess the clients level of consciousness. The level of injury is the lowest neurologic segment with intact or normal motor and sensory functions. You need to assess the patience Level of sensation, motor abilities, and cardiovascular assessment for Brady cardia hypotension and hypothermia. The patience G. I. and GU as well as musculoskeletal also need to be assessed for deficits.

Quadriplegia (tetraplegia, quadriparesis) involve all four extremities has seen with the cervical cord injury.

Paraplegia, paraparesis: involve only the lower extremities as seen in lower thoracic in lumbosacral injuries or lesions.

Spinal shock: occurs immediately after injury as a result of disruption in the communication pathways between a promoter neurons and lower motor neurons. This condition is characterized by flacid paralysis, loss of reflex activity below the lesion, Brady cardia, paralytic ileus, and hypotension. May last from a few days to several months. It’s reversal is indicated by the return of reflex activity.

Autonomic dysreflexia: is characterized by severe hypertension, Brady cardia, severe headache, nasal stuffiness and flushing, blurred vision sweating and nausea. Interventions include PlayStation and sitting position, call doctor, Loosen tight clothing.

Neurogenic shock: Medical and surgical management: interventions

include the immobilization for injuries, positioning, drug therapy to control blood pressure like dextran,

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atropine for bradycardia and dopamine surgery includes eight decompress of laminectomy-placement of the halo, watering and controlling the patients airway providing assistance is needed promoting self-care, monitoring and urine output.

Nursing interventions: assess the clients respite or a status, bottles every four hours, neuro assessment every four hours give pain medications as prescribed, prevent complications of immobility, assessed bladder and all functions, monitor nutrition status including a calorie count, and assess physiological status.

Teaching: patient needs to be taught about mobility and activities of daily living in Asia needs to learn to move around with with any disabilities patient is to begin rehab for strength training as well as occupational therapy. Balint latter retraining need to be implemented in shown to the patient in the family. He’s a client is family about the name purpose dosage timing of medication and side effects. Change the client about changes in sexual and sexuality.

Chapter 48 o Stroke

Pathophysiology: when blood supply to to the brain is disrupted preventing blood flow and the removal of metabolic waste carbon dioxide lactic acid. And in the close of stroke a skinny occurs in the brain tissue supplied by the effected artery and brain dysfunction results. Ischemia leads to hypoxia, anoxia, and hypoglycemia. Depending on the site of the disruption effects of signs and symptoms.

Risk factors: respect is include hypertension, diabetes, heart disease, elevated cholesterol, increased clotting time, ilicit drug use especially cocaine, obesity, A-fib.

Ischemic stroke: is caused by the occlusion of a cerebral artery by either thrombus (plaque formation) are or an embolus (clots that break off and travel to the cerebral artery).

Hemorrhagic stroke: vessel integrity is interrupted and bleeding occurs into the brain tissue or spaces surrounding the brain (ventricular, subdural, subarachonoid).

Aneurysm: Is an abnormal ballooning or blister on the involved artery that results in hemorrhagic stroke.

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TIA: also called silent stroke is a brief interruption in cerebral blood flow possibly resulting from cerebral vasospasm spasm, or transient systemic arterial hypertension. Usually lasts a few minutes To fewer than 24 hours.

Stroke risk screening (figure 48-3): History/Physical assessment/clinical manifestations:

Obtain history of clients activities when stroke began, note the exact time, and obtain medical history. Symptoms of them embolic or hemorrhagic stroke have a sudden onset, where as thrombotic stroke are more gradual. Ischemic strokes occur while sleeping, where hemorrhagic occur during activity. But analysts of current medications including over the counter, illegal drug use, and herbal supplements. Meds that can contribute to stroke includes anticoagulant, aspirin, vasodilators, and illegal drug use as well as products containing ephedra, or herbal products that affect blood clotting.

Left versus right hemisphere stroke symptoms: the right hemisphere is more involved with visual, spatial awareness, and propioperception. A person who has a stroke involving the right hemisphere is unaware of any deficits, maybe disoriented to time and place, personality changes include impulsivity and the poor judgment. Left hemisphere is a center for language, mathematics skills, and analytic thinking. It left him a sphere stroke results aphasia (unable to inderstand language) alexia(unable to read) agraphia ( difficulty to write) persons with left hemisphere strokes tend to be slow and cautious.

Motor changes: When deficits are found on one side of the body the stroke is occurring on the opposite side of brain. In the brain stem or cerebellum is affected the client may experience hemiparesis, quadraparesis, or ataxia.

Sensory changes: sensory examination evaluates the patients response to touch and painful stimuli, in addition to diminish motor functions decrease in station typically occurs on the affected side of the body. The client who has had a stroke may also be unable to write

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comprehend reading material use an object correctly or carry out a purposeful motor activity. Evaluate for indications of neglect syndrome Which is evident with strokes in the right cerebral hemisphere. This client usually is sitting in a wheelchair meaning to the left with the arm caught in the wheel. Another typical sign As a client who washes for dresses on the one side of the body the other side they are not aware of. The says the patience of visual ability And note any visual discrepancies.

Diagnostic studies: no definitivelab tests confirm the presence of a stroke. The patient may have elevated hematocrit, hemoglobin levels with a major stroke in the body attempt to compensate for lack of oxygen to the brain. An elevated white blood cell count may indicate the presence of infection. Blood and the CSF fluid is indicative of a subarachnoid hemorrhage. CT and CT ngiography assist in differential diagnosis of a stroke. The reason for this can use to initially detect the presence of the hemorrhage. Aneurysms is large enough may be identified. For a client with an ischemic or occlusive stroke this game is usually negative initially, after the first 24 hours changes are present. An MRI may also assist in the diagnosis. To assist in the termination of a cardiac cause of a stroke The doctor may request and EKG.

Medical management: for an occlusive stroke TPA needs to be given within the first three hours of symptoms. Catheter directed TPA must be given within six hours of symptoms.

Measures to prevent increased ICP: the first sign of ICP. Is decreased level of consciousness. Extreme hip and neck flexion must be avoided. Also avoid clustering of nursing procedures, have a procedure spaced out over a longer period of time. Hyper oxygenating the patient before suctioning is appropriate. A quiet environment is particularly important for the client experiencing a headache which is common with an aneurysm or increased IC P. the lights and the clients are and should be turned down, monitor vital signs every four hours. The patient’s blood pressure will be slightly higher to select a cerebral tissue perfusion.

Surgical management: the surgical procedure depends on the cause of the stroke. Endarterectomy is the most common surgical procedure to prevent stroke and patience with

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recurrent T. I. A’s or carotid stenosis. The plaque is removed from the inner lining of the carotid artery, the goal is to open the artery enough to reestablish the blood flow. Extracranial-intracranial bypass the surgeon performs a craniotomy and bypasses the blocked artery by making a graft or a bypassed from the first artery to the second. Is procedures that was blood flow around the block artery And we established blood flow to be involved area. Management of atriovenous malformation is interventional therapy to include abnormal arteries were veins and prevent bleeding from vascular lesions. This procedure may be performed to include the vessel surrounding an aneurysm. The Physician and surgeon Mike are catheter into the carotid artery and reads it to the vessel to be embolized the physician then injects an embolic agent. Management of aneurysms during the surgery the aneurysm is clipped or oracle and was placed on the base of the aneurysm to prevent blood from entering the area that the aneurysm does not have a knack and maybe wrapped with muscle, Muslin, or a plastic coating to reinforce the wall and prevent both RE bleeding. A less invasive method is interventional radiology for a small, catheter is directed to the aneurysm specially designed wire quarles our advanced into the aneurysm which helps to seal the area with a clot.

Nursing interventions: passive range of motion exercises at least every two to three hours for the involved extremity. One able to patient may perform these exercises on their own. Effective extremity a need splitting to prevent contractures consult with physical therapy to determine most appropriate splinting technique and client positioning. Placement of compression stockings or pneumatic compression boots to prevent formation of DVT’s. Clients with the right hemisphere brain damage to that we have difficulty with visual perception or spatial perception, and problems with depth and distance perception, because of these problems caregiver should help the client adapt to these disabilities are using frequent verbal and tactile cues and by breaking down tasks into discrete steps. Always approached a client from the unaffected side which should face the door of the room. Patience with the left hemisphere stroke Generally have memory deficits and may show significant changes in the ability to carry out a simple

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task. To assist with memory problems reorient the client to the month year day of the week and circumstance around in hostile admission. Establish a routine schedule that is structured repetitions and consistent as possible. Provide information and a simple concise manner a step by step approach is often most effective. Maintain a safe environments are the clientele times unilateral collect occurs more commonly impatience have right cerebral stroke.

The clients affected side and teach the client to touch and use both sides of the body when dressing remind the client to trust the effect inside first. World communications occurs when the stroke of facts the Broccas an area of the frontal lobe they’re unable to speak. When damage occurs in the Wernicks area of the tempoparietal region, they are unable to understand spoken and written words. The patient needs to see a speech language pathologist also mode of communication need to be established with the client, and have family and significant others and staff repeat the name of objects on a routine basis. The client may have difficulty swallowing saw foods may need to be prescribed that the patient is able to swallow. The client may be in content of urine and school because of altered level of consciousness, impaired innervation, and the inability to communicate a bladder and bowel training program can be implemented.

Meds Thrombolytic therapy: dissolves a cerebral artery inclusion three EST blood flow and prevent cerebral infarction. Recombinant tissue plasminogen activator (rt-PA[retavase]) hemorrhage hemorrhagic hemorrhagic stroke, and recent myocardial infarction, increased PTT time, anticoagulant therapy, and pregnancy. The patient must receive this medication within three hours of onset of symptoms. Catheter directed TPA or rt-PA can be initiated within six hours.Anticoagulants: in the used to treat strokes as controversial and depends on the health care providers preference. Principal drugs include an aspirin, heparin, low molecular weight heparin (lovenox), and warfarin (Coumadin). Baseline PTT times are valuing it before initiating heparin therapy. Is contraindicated in clients who have ulcers, uremia, or hepatic failure. Teaching: teaching includes the medication

schedule, ambulation and transfer skills, communication skills, safety precautions, dietary

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management, activity levels, and self-care levels. Clients must know to take respect medication to prevent another stroke and to keep blood pressure under control. Teach the client and family in the name of the drug, dosage, timing of administration, and how to take it and possible side effects.

Prevention: Care after stroke the

o Traumatic Brain Injury: occurs as a result of an external force applied to the head and brain causing disruption of physiologic stability local a, a decline of injury, as well as globally elevations and ICP and potentially dramatic changes in blood flow with and into the brain . Forced produced by a blow to the head is a direct injury, where as a force applied to another body part with a rebound affected the brain is an indirect injury.

Open head injury: occurs when there is a skull fracture or when the skull is pierced by penetrating object. Fractures include a linear fracture which is a simple clean break, depressed fracture for bone is pressed in word, open fracture the scalpers lacerated creating an opening to brain tissue,comminuted fracture involves fragmentation of the bone with depression into brain tissue.

Closed head injury: is a result of blunt trauma the integrity of the skull is not violated is more serious of the two types of injury and damage to the brain tissue depends on the degree and mechanism of injury. And mild concussion is characterized by a brief loss of consciousness, Diffuse axonal injury is related to high speed acceleration and deceleration as with automobile accidents. A contusion is a bruising of the brain Tissue and is most commonly found that the side of the impact (Coup) or on the opposite side of the impact (contra coup). Laceration The actual tearing of the court will surface vessels which may lead to hemorrhage insignificant cerebral edema and information this is more serious than a condition.

Types of force: and acceleration injury is caused by an external force contacting the head as suddenly placing the head and motion. Decelleration injury occurs when the head is moving and it suddenly stops or hits a stationary object.

Secondary responses and insults: includes me neurological damage that occurs after the initial

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injury. These injuries increase morbidity and mortality after head trauma. Most common as ICP.

Increased ICP: Is the leading cause of death from head trauma and clients who reached the hospital alive. It occurs when compliance no longer takes place in the brain cannot accommodate further volume. As it increases cerebral perfusion decreases leading to tissue hypoxia, serum PH level, an increase in carbon dioxide. But the condition remains and treated the brain may herniated downward ports the brain stem or laterally within the hemisphere causing injury.

Hemorrhageo Epidural: results from arterial bleeding

into the space between the dura in the inner table of the skull. Maybe characterized by presence of lucid interval that lasts for minutes during which time the client has awakened talking, this follows a momentary unconsciousness that occurs within minutes of the injury. This can progress to elevated ICP you.

o Subdural: results from Venous bleeding into the space beneath the Dura and above the arachnoid. Bleeding from a century occurs more slowly than from an epidural hematoma and mares a slower development of symptoms. Subdural hematomas had the highest mortality rate.

o Intracerebral hemorrhage: is the acumulation of blood within the brain tissue caused by the tearing a small arteries and veins and to sub cortical white matter. The brain stem have a ridge occurs as a result of direct trauma, or torsion injuries to the brain stem.

History/physical assessment/clinical manifestations: you attending an accurate history from a client may be difficult you do the injury and presence of amnesia. You Obtained from rescue workers you nature of the injury, loss of consciousness, any changes in consciousness, if drugs or alcohol are related. You determine whether the client experience in usage seizures before or after the injury and if he has a history of seizures. First priority

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in assessment is airway and breathing patterns observation of chest wall movement and assessment of lung sounds are important. Vital signs need to be assessed for impaired auto regulation. The more serious the injury the more severe the impact on the new regulation. Cushing reflects a late sign of increased I C. P.. Hypovolemic shock is usually due to entrap domino bleeding or bleeding into the soft tissue area around major fractures. Patients level of consciousness needs to be assessed, note any changes of deterioration. Assess the patience pupils and visual. Assess for bilateral responses to avoid missing lateralizing signs. In deterioration and motor function or the development of abnormal posturing An indicator of IC P.

Diagnostic studies: ABG’s I analyzed for oxygen and carbon dioxide levels. You Xray is in C. T. scanning of the cervical spine install are done to rule out fractures and dislocations.

Medical and surgical management: assess vital signs at least every one to two hours based on client security. Position the client to avoid extreme flexion or extension of the neck And maintain the head and midline neutral position. Hyperventilation of the patient during the first twenty hours after the injury is avoided due to possible increase ICP. Blood guesses are monitored at least twice a day. A client with increased ICP should be observed when suctioned. Osmotic diuretics are used to treat cerebral edema but pulling water out of extracellular space. Opioid medications may be used with the delay to clients to decrease education. Neuro muscular blocking agents may also be used

Nursing interventions: for all clients with a head injury are directed toward preventing or detecting increased IC. P., promoting fluid and electrolyte balance, and monitoring the effects of treatments and medications.

Teaching Prevention: that you need to be taught about

different measures to prevent head injuries like wearing of the helmet, wearing seat belts, etc..

Minor head injury: a patient who has a minor head injury need to know that post concussion syndrome may occur. Symptoms of the syndrome include but not limited to personality changes, irritability, headaches, dizziness,

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restlessness, nervousness, insomnia, memory loss, and depression.

Care after traumatic brain injury: the goal of rehabilitation is to maximize the clients ability to return to his or her highest level of functioning.

o Brain Tumors Complications of brain tumors: cerebral edema

results from changes in capillary endothelial tissue permeability which allows plasma to seep into the extracellular spaces. This leads to increased intracranial pressure. A tumor may also have stopped the flow of CSF are displacement of lateral ventricles by expanding lesions that can also increase ICP. This is known as hydrocephalus. Pituitary dysfunction may occur as a tumor compresses the pituitary gland and causes the syndrome of inappropriate antidiuretic hormone or diabetes insipidous.

General definitions, characteristics of you Benign: you are associated with a favorable outcome

however they may be malignant by virtue of their location. these tumors may undergo is the histologic changes and become malignant.

malignant (primary): cancerous requires treatment but has not spread

metastatic tumors (secondary): cancer cells that can travel from the long breast: and pancreas to the brain be the blood and lymphatic system. The cancer spreading to other parts of the body. Assessment of

cerebral tumors: headache, vomiting unrelated food intake, changes in visual acuity, hemiparesis or hemiplegia, hypokinesia, hyperparesthesia, seizures, aphasia, and changes in personality or behavior.

Brain stem tumors: hearing loss, facial pain and weakness, dysphagia, decreased gag reflex, nystagmus, hoarseness, ataxia, dysarthia. Diagnostic studies: ex rays cat scan MRI. Post-operative nursing care of client undergoing

craniotomy: is to monitor the client to detect changes in status and to prevent or minimize complications especially I see P.. Assess your logic in vital signs every, assessing EKG for dysrhythmias, and perform range of motion exercises to all extremities, encourage coughing and the breathing every two hours reply compression stockings until

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patient is able to walk. Elevated that only 30° or as tolerated to promote venous drainage from ahead. The client NPO for 24 hours. Monitor the dressing for signs of drainage and infection, monitor lab values including CBC, electrolyte levels, ABG’s, monitor ventilator settings and ensure the patient receives is medications.

Module 5 – SENSORY Chapter 50

o Cataracts An opacity of the lens that distorts the image

projected onto the retina Types

o Age related- usually >65o Traumatic-usually blunt trauma,

penetrating blows, overexposure to excessive heat, xrays or radioactive material

o Toxic-after ingestion of or exposure to certain chemicals such as extended use of corticosteroids, chlorpromazine, or miotic agents

o Associated- seen with other diseases, such as diabetes mellitus, Hypoparathyroidism, Down syndrome, and atopic dermatitis

o Complicated-develops as a result of ocular disorders such as retinitis pigmentosa, glaucoma and retinal detachment

Pathophysiology With aging, the lens gradually loses water and

increases in density. This increased density occurs as older lens fibers are compressed and new fibers are produced in the outer layers. Lens proteins dry out and form crystals. As the density of the lens increases, it becomes opaque with a painless loss of transparency.

Nursing Assessment Client history

o Ageo History of traumao Exposure to radioactive materials or xrayo Current medical problems (DM, Down’s)o Medication history

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o History of intraocular disease Assess for:

o Early signs Blurred vision Decrease in color vision: blue,

green and purple appear greyo Late signs

Diplopia Reduced visual acuity progressing

to blindness Presence of white pupil Anxiety and fear

Operative procedures Two extraction procedures

o Extracapsular: removal of the anterior portion of the capsule

o Intracapsular: removal of the lens completely within the capsule

Pre-operative nursing careo Consento Teach about procedureo Stress importance of eye drop

administration several times a day for 2-4 weeks, may need to arrange for care if pt cannot self admin gtts

o IV may be started preop to give Diamox to reduce intraocular pressure

o Meds given preop to dilate pupils, induce paralysis of eye, local anesthetics(injection)

Post-operative nursing careo Antibiotics given subconjuctivally, may

contain a steroid, also (TobraDex—tobramycin and dexamethasone)

o Wear dark sunglasses in bright lit environments until pupil responds to light

o Mo ay have mild itchingo Eyes may appear bloodshoto Cool compresses to help decrease

swellingo Avoid aspirino

Discharge teachingo Usually discharged 2 hours post opo Avoid activities that may increase

intraocular pressure

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Bending from the waist Sneezing, coughing Blowing the nose Straining to have a BM Vomiting Sexual intercourse Keeping the head in a dependent

position Wearing tight shirt collars

o Best vision will not be present until 4 to 6 weeks post op

o Avoid getting eyes wet in the shower 1 week postop

o Light housekeeping is ok, but vacuuming should be avoided for several weeks because of forward flexion and jerky movements required

o Teach to recognize complications and report to health care provider

Sharp, sudden pain in the eye Bleeding or increased discharge Lid swelling Decreased vision Flashes of light or floating shapes

o Glaucoma Pathophysiology

Intraocular pressure increases (norm 10-21 mm Hg) which leads to ischemia and nerve tissue death, tissue damage may be painless, and may result in blindness

Primaryo Usually bilateral and asymptomatico Reduced outflow of aqueous humor

through the chamber angle. Because the fluid cannot leave the eye at the same rate it is produced, IOP gradually increased

o Causes Aging Heredity Central retinal vein occlusion

Secondaryo Causes

Uveitis Iritis Neovascular disorders Trauma

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Ocular tumors Degenerative disease Eye surgery

Angle-closureo Less common, sudden onseto Medical emergency

Which situation is emergent?o Angle closure

Non-surgical management Drug therapy to reduce IOP

o Papillary constriction Pilocarpine

o Inhibition of aqueos humor Beta blockers

Timoptic-reduces aqueous humor without causing papillary constriction

Carbonic anhydrase inhibitiors Diamox Propine

Surgical management Laser surgery

o Nursing care Inform client of procedure and

expected outcomes Discharge teaching

o Arrange for transportation home, as driving is prohibited immediately post op

o An ocular steroid may be prescribed

o Reevaluate IOP one hour after surgery and prior to discharge

Chapter 52o Meniere’s Disease

Pathophysiology, symptoms Non-surgical management

Make slow head movements Limit dietary salt and fluid to reduce

endolymphatic fluid Stop smoking (smoking causes blood vessel

constriction) Drug therapy

o Mild diureticso Antihistamineso antiemetics

Surgical management

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Last resort because of hearing loss as a result of surgery

Labyrinthectomy-removal of the labyrinth or resection of the vestibular nerve

Endolymphatic decompression-less drastico Small tube placed to drain excess fluido Improves vertigo , better hearing

retention than with labyrinthectomy

MENTAL HEALTH CONTENT - TOWNSEND

SCHIZOPHRENIA Townsend – Chapter 14

o Nature of the disorder (p. 272)- “disturbances in thought processes, perception, and affect invariably result in a severe deterioration of social and occupational functioning.” Symptoms usually occur in late adolescence or early adulthood. Four phases…

o Types of schizophrenia Paranoid- delusions of persecution, grandeur and

auditory hallucinations related to a single theme. Individual is often tense, suspicious, and guarded, and may be argumentative, aggressive, or hostile.

Schizoaffective – schizo behaviors with a strong element of symptoms assoc. with mood disorders (depression or mania). Dx is defined by the presence of schizo symptoms

Brief psychotic disorder – sudden onset of psychotic symptoms that may or may not be preceded by severe psychosocial stressor. Client may experience emotional turmoil, overwhelming perplexity, or confusion.

(including substance-induced) – hallucinations and delusions directly associated with the physiological effects of a substance. See Table 14-2 for substances that may cause psychotic disorders.

o Content of thought - Delusions: false personal beliefs that are inconsistent

with the client’s personal or cultural background.

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(persecution, grandeur, reference, control or influence; somatic or nihilistic delusion).

Religiosity - obsessions of religious ideas and behavior.

Paranoia - suspiciousness of others and of their perceived actions and intentions.

Magical Thinking- thoughts or behaviors have control over specific situations or people.

o Form of thought - Associative looseness : speech that shifts from one

idea to another. Individual is unaware that topics are unconnected.

Neologisms: invention of new words Concrete Thinking : regression to an earlier level of

cognitive development. Clang Associations : choice of words are goverened

by sound (rhythmic). Word Salad : words strung together randomly without

logical connection. Circumstantiality : individual unable to reach the

point of communication because details are lost. Tangentiality: Client never gets to the point of the

communication. Mutism: inability or refusal to speak Perservation : repetition of the same word or idea in

response to different questions.

o Perception Hallucinations, may be auditory, visual, tactile,

gustatory, or olfactory Illusions : misperceptions or misinterpretation of

external stimuli.

o Affect – behavior assoc. with feeling state or emotional tone.

Inappropriate: emotional tone incongruent with circumstances.

Bland or Flat Affect : lack of emotional tone/ expressions.

Apathy : disinterest in the environment.

o Sense of Self - individual feeling of uniqueness. Echolalia: repetition of words. Identification and imitation: take on the form of

another persons behavior Depersonalization: feelings of unreality

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o Volition – impairment in the ability to initiate goal-directed activity

Emotional Ambivalence: difficulty satisfying human relationship

Impaired interpersonal functioning and relationship to the outside world: invasion of personal space of others resulting in impaired social functioning

Autism: fantasy world verses real Deteriorated Appearance: decrease in the personal

hygiene and self-care activities.

o Psychomotor behavior Anergia: lack of energy Waxy Flexibility: body parts are placed in bizarre or

uncomfortable positions. Posturing: inappropriate or bizarre positions. Pacing and rocking: slow, rhythmic, backward and

forward swaying of the trunk from the hips, usually when sitting

o Associated features Anhedonia: inability to experience pleasure Regression: retreat to an earlier level of

development.

o Positive symptoms - reflect excess of distortion of normal functions (normal brain structures).

Hallucinations Delusions Disorganized thinking/speech Disorganized behavior – disheveled appearance,

inappropriate sexual behavior, restless, agitation, waxy flexibility

o Negative symptoms - reflect loss of normal function (usually show structural brain abnormalities).

Affective flattening Alogia (poverty of speech)

Brief empty responses, decreased fluency and content of speech

Avolition/apathy Can’t initiate goal directed activity Little or no interest in work or social activity Impaired grooming/hygiene

Anhedonia Absence of pleasure in social activities Diminished sexual interest

Social isolation 31

o Care plan for client with schizophrenia A. Disturbed Thought Process; Ineffective Coping, related

to inability to trust others AEB delusional thinking and suspiciousness of others.

Convey acceptance of client’s need for false belief, and indicate that you do not share the same belief.

Do not argue or deny the belief. (i.e. reasonable doubt) Reinforce and focus on reality. Talk about real events

and people. Use the same staff as much as possible, be honest and

keep promises. Avoid physical contact and laughing and gestures that

the client can not hear.

B. Disturbed Sensory Perception, auditory related to panic anxiety AEB hearing voices, inappropriate responses, and disorientation.

Observe client for signs of hallucinations. Avoid touching the client without warning. Acceptance of the hallucination will encourage the client to

share with you. Do not reinforce the hallucination. Help the client realize the connection between the anxiety

and hallucinations. Try to distract the client from the hallucination by doing

crafts, playing a board game, etc.

C. Social Isolation related to inability to trust AEB withdrawal.

Accepting attitude by making brief, frequent contacts. Show unconditional support.

Offer to be with client during group activities that she may find difficult or frightening.

Give recognition and positive reinforcement when client voluntarily interacts with others.

o Psychopharmacology (290-291) Antipsychotic Drugs : neuroleptics or major

tranquilizers. Rx of acute or chronic phase of schizo. Side effects: dry mouth, blurred vision, EPS, orthostatic hypotension, GI upset, decreased libido, retrograde ejaculation, NMS.

Antiparkinson Drugs : to conteract the EPS. Other:

Reserpine (dopsmine receptor antagonist) produces severe depression. RARELY used.

Lithium (suppress episodic violence) not adequate by itself

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Carbamazepine (not adequate by itself) Valium (control positive psychotic symptoms) , Propranolol (to control temper).

o Treatment modalities: Individual psychotherapy, group therapy, behavior therapy, social skills training, Milieu, and family therapy. Pages 287-290Primary focus is to decrease anxiety and increase trust.Group therapy is effective in reducing social isolation (less productive in inpatient settings)Social dysfunction is a hallmark of schizophrenia so social skills training is importantMileu therapy emphasize group and social interaction, rules and expectations are mediated by peer pressure for normalization of adaptation.Family therapy has very positive outcomes.

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