adv med surg studyguide

7/27/2019 Adv Med Surg Studyguide

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Adv Med Surg Studyguide

1. Hypoproliferative Anemiaa. Iron deficiency anemia

i. Clinical manifestations1. Smooth, sore tongue2. Brittle, rigid nails3. Angular cheliosis (cracks at corners of mouth)

ii. Medical mgt1. Determine cause2. Supplemental iron

b. Folic acid deficiencyc. Megoblastic anemia

i. B-12 relatedd. Iron deficiency anemia

i. Nursing mgt1. Teaching is r/t supplemental iron

a. Take on empty stomach w/ OJi. Food (esp dairy) interferes w/ absorption

b. Reverse-taper i. Allows body to adjust

c. Increase intake of vitamin Ci. Contributes to absorption

d. High fiber intake, stool softenersi. Whole grains, veges

1. Prevents constipationii. Supplement causes darkening of the stooliii. Liquid prep can stain teeth

e. Anemias in renal diseasei. Erythropoietin

1. Decreased production of RBCs2. Treatment: supplement w/



a. Epogenb. Procrit

ii. Folic acid1. Removed from circulation during dialysis

2. Treatment: supplementsa. Folic acid and B-12 are important for the synthesis of DNAf. Megaloblastic anemias

i. Deficiencies1. Folic acid2. Vit B12

ii. Clinical manifestations1. Smooth, sore, red tongue2. Mild diarrhea3. Neurologic SX

a. B12 TX will help w/ the myelin sheath

Anemia Type Causes Manifestations Populations at risk

Iron deficiencyanemia

(low Fe, ferritin,reticulocytes)

Iron intakeIron loss

Iron requirements

Pica, cheliosis,smooth & red

tongue, brittle,spoon-shapednails, fatigue

Preggers, infants,teens,

Chronic conditions



Vitamin B12

deficiency

(low B12,MCV)

Lack B12

Absorption failure,

chronic gastritis,loss of pancreaticsecretions

Jaundice, neuro,smooth sore beefy

red tongue,diarrhea

VegetariansChron’s Dx

GastroectomyPernicious Anemia

Folic AcidDeficiency

Anemia (lowfolate,MCV)

Lack folic acid, Pallor, progressiveweakness& fatigue,

shortness of breath,

Alcoholics, Celiac Dx,Pregnancy, TPN

therapy, older adults

2. Hemolytic Anemiaa. Sickle Cell

i. Inherited disorder 1. Need to carriers to develop sickle cell

ii. Crystal-like abnormal hemoglobin shape1. Change precipitated by hypoxia

iii. Clinical manifestations1. Anemia

a. Sickle cell lifespan 10-12 days



b. Jaundicei. d/t cells getting stuck in the biliary

c. thrombosisi. occlusions caused by sickled cells

1. occlusion of RBCs happen at joints where sickle RBCs aggregateii. vaso-occlusiveiii. Risk for amputation d/t poor perfusion

1. Need to hydrate them so they can adequately perfuseiv. Sickle cell crisis

1. Sickle (vaso-occlusive)a. Severe pain

i. Necrosisb. Organ dysfunctioin

i. Spleen, lungs, CNS

c. Aplastici. Rapid decrease in Hgb level1. Associated human parvovirus infection

d. Sequestrationi. Collection of sickled cells in organs

1. Autospenectomye. Medical mgt

i. PBSCTii. Hydroxyurea

1. Chemo agentiii. RBC transfusioniv. Supplementsv. IV hydration

vi. O2 therapy2. Nursing interventions

a. Managing paini. Morphine, NSAIDsii. Positioning

1. Support and elevate affected joints



b. Preventing and managing infectioni. Give IV antibiotics and monitor

a. Risk increased d/t impaired circulationb. Tissue destructioin

c. Interference w/ immune responseii. Monitor iii. Antibiotic administration

c. Crisis happens more w/ kids d/t activity level – they want to get out and play and thatcan send them into sickle cell crisis

3. Transfusionsa. Blood transfusion administration steps

i. 19 guage cath at the minimumii. Signed consentiii. Assess for previous

iv. Use Y tubingv. Follow facility protocol regarding IDvi. Pre-transfusion responsibilities:

1. Usually takes 2 nurses to verify blood once brought to the unit2. Verify prescription, test donor and recipient blood for compatibility3. Examine4. Check expiration date5. Inspect blood for discoloration, gas bubbles, cloudiness6. **Have a limited time to infuse blood: w/in 4 hours!

b. Adverse transfusion reactioni. STOP transfusion immediatelyii. Infuse normal salineiii. Notify healthcare provider iv. Collect blood and urine specimens and send to blood bank along w/ remaining blood product.v. Get a new line! Do not throw away old tubing – send back to blood bank

c. Transfusion reactionsi. Febrile reaction

1. Recipient antibodies react to donor WBCs2. Manifestations



a. Hypersensitivity reactionsi. Recipient antibodies react to donor ii. Uritacaria, flushing, itchingiii. SX can occur during or after transfusion

iv. Treat w/ Benedrylv. Most of the time its d/t PT getting the wrong bloodi. Flushing, burning in veins, HA, itching, chills, eventually will develop lumbar

pain and chest pain, tachycardic, dyspnea,b. Febrile (most common)

i. Usually noted less than 15 min after transfusion initiatedii. Leukocyte-poor blood can be given to prevent reaction to future blood

transfusions (doesn’t have a lot of WBCs in bag)1. For people who have had a reaction to blood in the past. Need to have

leukocyte-poor blood

c. Hemolytic reactioni. ABO incompatibilityii. Patho: breakdown and agglutination of RBCs causing capillary blockageiii. Release of free hemoglobin into circulationiv. Renal tubule blockage

d. Other blood transfusion complicationsi. Circulatory overloadii. Electrolyte imbalancesiii. Transmission of infectious diseases

4. Guidelines for assissting with percutaneous liver biopsya. Pre-procedure guidelines

i. Check coagulation related labs1. PT, PTT: if it’s way out of whack, they won’t do the biopsy. Platelet count2. Verify consent3. Explain procedure4. Obtain baseline VS

b. Post-procedure guidelinesi. First 2-3 hours

1. Positioning



a. Right side w/ pillow under costal margini. To add more pressure

b. Client should avoid strainingc. Monitor VS

i. Q 10-15 min the 1

st

hour ii. Q 30 miniii. Monitor for bleeding

d. Discharge instructionsi. Avoid heavy lifting for 1 weekii. Should be on bedrest for the most partiii. Need to get the clotting factors in check

5. Ascitesa. Accumulation of fluid in peritoneal space

i. Contributing factors

1. Portal HTNa. Vasodilationb. Blue lines on belly is d/t engorgement

i. Need to measure their abdominal girth often to assess if ascites is getting worse2. Increased aldosterone levels

a. Increased Na and H2O retention by the kidneys3. Increased lymphatic flow4. Decreased albumin levels

a. Third spacingi. May hang albumin

5. Self-perpetuating6. Clinical manifestations

a. Increased abdominal girthb. Weight gainc. SOBd. Discomforte. Varicose veins along abdominal wall (dilated veins)

i. Caput medusa7. Medical mgt



a. Sodium restrictionb. Diureticsc. Bedrestd. Paracentesis

i. The nurse gathers the tubing, labelsii. We label it and it’s sent to the lab to culture itiii. Remove no more than 2 L at a time to r/d risk of BP issues and also to keep

electrolytes in check.iv. TIPS

1. Transjugular intrahepatic portosystemic shunt2. The most important thing to remember before having an abdominal

paracentesis is to EMPTY THEIR BLADDER. If they say they can’turinate, scan them and straight-cath them.

6. Esophageal Varices (1128-1129)a. Dilated veins that are prone to rupture

i. Bleeding associated w/ mortality1. Only 50-70% survive 1st episode2. Mortality rate decreases w/ subsequent episodes

b. Clinical manifestationsi. Hematemesisii. Melenaii i. Shock

c. Assessment and DX findings (1129)i. Endoscopy

1. Prophylactic to see where the bleed is happeninga. Treatment of varices before they ruptureb. Every 2 years for at-risk clients

2. Diagnostica. Identify source of bleeding

i. May be gastric ulcers (30%)3. Post-procedure care

a. NPO until gag reflex returnsb. NPO if further procedures are indicated



d. Medical mgti. Pharm therapy (1132)

1. Treatment of active bleedinga. Selective vasoconstrictors

i. Vasopressin (drip)1. Contraindicated in PTs w/ CAD2. Do not give to HTN PTs

ii. Somatostatiniii. Sandostatin (octreotide) drip

b. Prevention of 1st bleeding episodei. Beta blockers – to prevent a first bleeding

1. Inderal (propranolol)2. Corgard (nadolol)

c. Medical mgti. Balloon tamponade (looks like a tampon put in their throat)

1. It’s a “band-aid”a. Rebleeding rate is 60-70%

ii. Endoscopic therapies (1131)1. Injection sclerotherapy

a. Causes thrombus formation and sclerosis2. Variceal banding (kinda like a lap band)

a. Similar to clipping an aneurysm7. Hepatic encephalopathy and coma (1133)

a. CNS depressioni. d/t increased serum ammonia levels

b. Clinical manifestationsi. Mental status/LOC changesii. Asterixis

1. Flapping tremor of the handsiii. Constructional apraxia

1. Inability to reproduce simple drawingsiv. Coma (last stage)

1. One of the most common causes of death associated with liver disease.



c. Medical mgti. Decrease serum ammonia levels

1. Cephulac (lactulose)a. Changes gut pH

i. Prevents absorption of ammonia from gut to blood2. IV Glucosea. Decreases protein level by prevention of muscle wasting

3. Antibiotic (ATB)a. Decreases number of ammonia-producing gut bacteria

4. Restrict protein intakea. Looking at risk v. benefit

ii. Daily monitoring or ammonia level8. Hepatitis B virus (1141-1144)

a. Bloodborne transmission (viruses)i. Spread thru blood-borne pathways

1. Unprotected sex2. Blood transfusion3. Hemodialysis4. From mom to baby during birth

ii. Prevention1. 3 series shot

a. Healthcare workers should getiii. Won’t get hep D unless you have hep B

b. Incubation period 1-6 monthsc. S/SX

i. Insidious and variable1. May occur w/ or w/out SX2. May develop arthralgias, rash.

d. Med mgti. Minimize infectivity, liver inflammation and decrease SX.ii. Pharm

1. Antiviral agentsa. Lamivudine (Epivir)



b. Adefovir (Hepsera)c. Oral nucleoside analogs for chronic Hep B in the USd. Proteins are restricted.

9. Hepatic cirrhosis (1146-1149)

a. End-stage hepatic diseaseb. Normal tissue replaced by fibrous tissue resulting in dysfunctionc. Causes

i. Prolonged alcohol abuse is the #1 causeii. Viral hepatitis (hep b or hep c)iii. Chronic biliary obstruction

1. Very uncommond. Complications

i. bleeding1. transfusion

a. PRBCb. Plasma (FFP)c. Coagulation factors

ii. Hepatic encephalopathyiii. Fluid volume excess

1. Peritoneal cavity at full capacity2. Heart failure d/t increased resistance

a. Pulmonary edema3. Treatment

a. Decrease circulating volumei. Diureticsii. Fluid restriction

b. Position client to maximize gas exchangei. Usually high fowlers doesn’t work w/ these PTs d/t breathing issues

10.Plan of nursing care: The patient with impaired liver function (1153-1154)a. Nursing interventions

i. Encourage PT to verbalize reactions and feelings about changesii. Assess PTs and fam’s previous coping strats.iii. Assist and encourage PT to keep up appearance



iv. Assist PT in identifying short-term goalsv. Encourage and assist PT in making decisions about care

vi. Identify w/ PT resources to provide addl’ supportvii. Assist PT in identifying previous practices that may have been harmful to self

11.Cancer of the Liver (1158)a. Primary liver tumor i. Arise from hepatic tissue

1. Usually d/t cirrhosis2. Rare in the US

b. Liver metastasisi. Most common primary sites

1. GI2. Breast3. Lungs

ii. Typically occurs via portal circulationc. Clinical manifestations

i. Continuous dull ache in the right upper quadrant, epigastrium, or back.ii. Anorexia/weight lossiii. Anemia/weaknessiv. Other manifestations depend on location

1. Jaundice2. Ascites

d. Medical management (1159)i. Essentially palliative

1. Radiation therapy2. Chemotherapy3. Percutaneous biliary drain placement4. Other nonsurgical TX

ii. Surgical mgt1. Mainly for primary tumors when confined to 1 lobe2. Not often used for metastasis3. Cirrhosis decreases success rate of surgical intervention

a. Interferes w/ regeneration of liver tissue after surgery



12.Cholielithiasisa. Clinical manifestations

i. May be silent, w/ no pain or mild GI SX.1. SX may be acute or chronic

a. Epigastric distressi. Feeling of fullnessb. abdominal distentionc. vague pain in RUQ

i. SX may follow a meal rich in fried or fatty foodsii. Elevated serum bilirubin level

1. Jaundice2. Pruritis3. Dark urine and gray stool

a. d/t no bilirubin going into stollb. bilirubin is excreted by kidney rather than bowel

iii. Complications1. Gangrene2. Perforation

a. Leads to peritonitisi. Board like abdomen

3. Empyemaa. Little sacks of pusb. Sternal painc. Labored breathing; increased resps.

b. Medical mgti. The major objectives of medical thereapy are to reduce the incidence of acute episodes of gallbladder

pain and cholecystitis by supportive and dietary mgt and, if possible, to remove the cause of cholecystitis by pharmacologic therapy, endoscopic procedures, or surgical interventions.

ii. Pharmacologic1. Actigall (ursodeoxycholic acid)

a. Dissolves small stones composed of cholesteroli. Usually takes 6-12 months

b. Inhibits synthesis and secretion of cholesterol



c. Dosage is weight based – strict weight checksi. Low fat diet, decrease cholesterol

iii. Medical mgt1. Nutritional and supportive therapy

a. Avoid dietary fat2. Non surgical intervention

a. Edoscopic proceduresi. ERCPii. Most important assessment after procedure is the gag reflex

1. Must be NPO for the procedure2. If gag reflex is not back, DO NOT FEED THEM!

13.ERCPa. Complications

i. Bleeding – especially w/ esophageal varaiciesii. Peritonitis

1. Tender, rigid abdomen2. Fever 3. Other GI SX

iii. Often leads to septicemia and septic shock14.Laparoscopic cholecystectomy

a. 80-90% are removed this wayb. Less invasive reduces risk of infectionc. Compared to open procedure

i. Decreased incidence of complications (less surgical risk)ii. Less painiii. Quicker recovery (1 week until no restrictions)

d. Abdominal cavity is insufflated w/ CO2 to improve visualization of structuresi. PT c/o pain in right shoulder

e. May convert to open procedure if necessary15.The patient undergoing surgery for gallbladder disease

a. Usually same day surgeryb. Week prior to surgery, preadmission occurs

i. PT told to avoid smoking to enhance pulmonary recovery postop, and avoid resp issues.



ii. Avoid aspirin and other agents (OTC and herbals) that can alter coagulation and other bio-chemicalprocesses.

c. Post-opi. Avoid turning w/out assistance

1. Splint affected side and take shallow breaths to prevent pain during position changesa. Use a pillow or binder over the incision to help reduce pain during position changes.

ii. Encourage deep breaths and coughing q hour to expand lungs fully and prevent atelectasis.iii. Begin light exercise (walking) immed.iv. Avoid lifting >5 lbs for 1 weekv. Resume normal diet

1. If PT had fat intolerance prior to surgery, gradually add fat back into diet.vi. Analgesics PRNvii. F/U w/ doc 7-10 days after discharge

16.Acute Pancreatitisa. Cause

i. Gallstonesii. Alcohol abuseiii. Infection (less common)

b. Pathoi. D/t activation of pancreatic enzymes while still inside the organ

1. Pancreatica. Necrosisb. Hemorrhage increases risk of infectionc. Pain radiating to back

i. PTs sit similar to COPD PTii. Pain brought on by food

1. PT is placed NPO when admitted2. Avoid alcohol3. Avoid fatty foods

c. Formsi. Mild

1. Characterized by edema and inflammation confined to the pancreas.



2. Normal function returns w/in 6 monthsii. Severe

1. Systemic complications w/ organ failurea. Such as pulmonary insufficiency w/ hypoxia, shock, renal failure, and GI bleeding

2. May result in death (2-10% of cases)d. Complications

i. Hemorrhage1. Transfusion, fluids

a. May give platelets to stop hemorrhage2. Monitor VS, Hgb

ii. Imbal. nutrition – less than body requirements (r/t to increased metabolism demand associated w/acute illness and fever)

1. TPNa. Monitor serum glucose

2. Daily weightiii. Impaired gas exchange

1. Semi-fowler’s2. Incentive spirometry3. Cough and deep breathe4. Monitoring

a. RR and O2sativ. Hypovolemiav. Hemorrhage

vi. Acute renal failurevii. Acute resp failureviii. Pancreatic necrosisix. Paralytic abcess and pseudocystsx. Diabetes mellitusxi. Hypovolemic or septic shock

17.Chronic pancreatitisa. Inflammatory disorder characterized by progressive destruction of the pancreas. As cells are replaced by

fibrous tissue with repeated attacks of pancreatitis, pressure with the pancreas increases. Results inobstruction of the pancreatic and common bile ducts, and the duodenum.



b. Manifestationsi. Recurrent attacks of severe upper abdominal and back pain accompanied by vomitingii. Weight loss

c. Medical mgti. Analgesics

1. Nonopioid, antioxidantsii. Glucose mgt

1. Insulin2. Oral antidiabetic agts

iii. Pancreatic enzyme replacement – DO NOT CRUSH!!!iv. Surgery may be an option

1. May need to do a cholesectomyv. Octeotide to stop bleeding especially w/ variaces

vi. May give H2 blockers, Proton pump inhibitors (Tagamet and zantac), octreotide for hemorrhagevii. IV fluidsviii. Low-fat dietix. NG tube suction to remove gastric secretions

18.Tumors of the head of the pancreasa. 60-80% of pancreatic tumors occur in the head of the pancreasb. Obstruct common bile duct where the duct passes thru the head of the pancreas to where the duct passes

thru the head of the pancreas to join the pancreatic duct and empty at the ampulla of Vater into theduodenum.

c. Contributing factorsi. Cigarette smokingii. Exposure to toxinsiii. High fat and meat intakeiv. Chronic pancreatitis

d. Clinical manifestationsi. Jaundiceii. Clay-colored stoolsiii. Dark urineiv. Abdominal discomfort or painv. Pruritus



vi. Anorexia and weight lossvii. Malaise

e. Diagnosingi. ERCP identifies the causeii. Collections of specimensiii. CT, MRI, ultrasoundiv. Glucose tolerance test

1. Identify degree of damage to islet cellsf. Medical mgt

i. Before surgery1. Liver and pancreatic function studies2. High protein diet along with pancreatic enzymes3. Adequate hydration4. Correction of Prothrombin deficiency w/ vit K

a. (synthesis of vitamin K)ii. Analgesics

1. Nonopioid2. Antioxidants

iii. Radiation therapyiv. Chemotherapyv. Surgery

1. Pancreaticoduodnectomy (“Whipple’s procedure)a. For tumors of the head of the pancreas

19.Increased ICP clinical manifestationsa. Early changes

i. LOCii. Mental statusii i. Speechiv. Pupil responsev. Extraocular movement

vi. Unilateral weaknessvii. HA

b. Late changes



i. Abnormal posturing1. Decerebrate – towards the core2. Decorticate – opposite

ii. Comaiii. VS (cushings triad)iv. Respiratory patternv. Projectile vomiting

vi. Loss of brain stem reflexes1. Gag, cough, corneal, swallow, pupil, will have “doll’s eyes,” periorbital edema, will become

flaccidc. Complications

i. Brain stem hernationii. Diabetes insipidus

1. Results from decreased secretion of antidiuretic hormone (ADH)a. Excessive urine outputb. Decreased urine osmolalityc. Serum hyper osmolarity

2. Therapiesa. Fluidsb. Electrolyte replacementc. Vasopressin (desmopressin) (DDAVP therapy)

iii. Syndrome of inappropriate antidiuretic hormone (SIADH)1. Results from increased secretion of ADH.

a. PT becomes volume overloadedb. Low urine output

c. Serum sodium concentration becomes dilute.2. Treatment

a. Fluid restriction (<800 mL/day with no free water)b. In severe cases, careful admin of a 3% hypertonic saline solution may be therapeutic.

20.Medical managementa. Decreasing cerebral edema

i. Administration of colloid solutions1. Mannitol



a. Can cross thru the blood-brain barrier 2. Fluid restriction

a. Monitor I & O3. Reducing CSF/IC blood volume

a. Ventriculostomy (common in peds – shunts going into the abdominal cavity)4. Controlling fever

a. Admin of antipyretic meds like Tylenolb. Cooling blanket (bear huggers)

5. Reducing metabolic demandsa. Barbituratesb. Paralytics (drugs that will paralyze the PT and machines control the PT)

21.Intracranial surgery nursing interventionsa. Maintaining cerebral tissue perfusionb. Regulating tempc. Improving gas exchanged. Managing sensory deprivation

i. Periorbital edema1. Impaired vision is a late sign

e. Enhancing self-imagei. Facial/periorbital edemaii. Hair shaved over operative area

f. Managing potential complicationsi. All standard postoperative concernsii. Bleeds, suture site, drainage (serousanguious)

22.Guidelines for seizure care

a. During seizurei. Provide privacy if possibleii. Ease PT to the floor if possibleiii. Protect head to prevent injury w/ a padiv. Loosed constrictive clothingv. If PT is in bed, remove pillows and raise siderails

vi. If aura precedes the seizure, insert an oral airway to reduce risk of PT biting tongue or cheekvii. Do not attempt to pry open jaws that are clenche



viii. Do not restrain PTix. If possible, place PT on side to prevent aspiration

b. After seizurei. Keep PT on one sideii. Typically a period of confusion after a grand maliii. Short apneic period may occur during or immed after a generalized seizureiv. Reorient PT to environment on awakeningv. If PT becomes agitated after seizure, use persuasion and gentle restraint to assist him or her to stay

calm23.Status epilepticus

a. Series of generalized seizures w/out full recovery between attacks. It’s a medical emergency!i. Increased metabolic demand

1. Energy expended during convulsionsii. Hypoxia and venous congestion

1. Irregular resps d/t convulsions2. May lead to irreversible brain damage

iii. Precipitating factors1. Subtherapeutic medication level is the #1 cause2. Fever and infection

24.Headachea. Primary HA

i. One for which no organic cause can be identified.1. Types

a. Migraines, tension type, cluster ii. Migraine manifestations

1. Phasesa. Prodrome (hours to days before)b. Aura (usually lasts <1 hour)c. HA (varies from 4 to 72 hours)d. Recovery

2. Severe, incapacitating HA3. Photophobia4. N/V



5. May be preceded by visual disturbancesa. Aura

6. May be preceded by other SXa. Mild confusion, drowsiness, dizziness

7. Duration 4-72 hoursa. In the prodromal phase

b. Cluster HA manifestationsi. Excruciating pain

1. Unilateral2. Eye and orbit initially

ii. Radiates to facial and temporal regioniii. Affected side

1. Tears2. Nasal congestion3. Duration 15 minutes4. May occur up to 8 x per day

c. HA preventioni. Prevention

1. Avoid triggersa. stimulationb. stressc. foods

i. caffeineii. chocolateiii. tyramine

iv. Chinese foodii. Medical mgt

1. Preventative therapya. Medication taken routinely (prophylactic)

i. Imitrex1. Do not stop abruptly

ii. Abortive therapy1. Meds taken at or prior to onset



a. NSAIDSb. Tylenolc. Tryptivans

i. Imitrex2. Ischemic stroke

a. CVA or brain attack is a sudden loss of function resulting from disruption of the bloodsupply to a part of the brain.

b. Most common typei. Caused by thrombus

1. Forms at site of atherosclerotic plaque2. Infarction distal to site3. Degree of damage depends on size of vessel

ii. May resolve in an hour: TIAc. Risk factors

i. Nonmodifiable1. Age >552. Gender

a. More frequent in males3. Race

a. Incidence in Af Amer is double than in caucasionsii. Modifiable

1. HTN (esp uncontrolled HTN)a. More significant than all the othersb. d/t weakening the blood vessels

2. Atrial fib

3. Hyperlipidemia4. Diabetes5. Smoking6. Obesity7. Alcohol abuse8. Living in the stroke belt

a. AL, AK, GA,KY, LA, TN, MSi. d/t southern cooking



25. Ischemic Stroke medical mgta. Pharm (prophylactic)

i. Anticoagulants – know INR range!!1. Atrial fib

a. Coumadinii. Platelet aggregation inhibitors

1. Plavix (prevents platelets from sticking together)iii. Statins (cholesterol reduction)

1. Watch out for rhabdomylosis2. Take at night

iv. Anti HTN medsb. Surgical

i. Carotid endarterectomyii. Removal of clot

26.Thrombolytic therapya. Administration must begin over 1 hour b. IV administration over 1 hour c. Only used for ischemic stroke verified by CT scand. Contraindications

i. Risk for bleeding1. INR>1.7 (Coumadin)2. Platelet count <100,0003. PT >15

ii. HTN1. SBP >185

2. DBP >110iii. Seizure activityiv. HX of intracranial disease

1. Neoplasm, AVM, ICHv. Other recent intracranial pathology

1. Stroke, brain injury, intracranial surgery27.Therapy for patients with ischemic stroke not receiving T-PA

a. Anticoagulant administratiin (IV heparin or low molecular-weight heparin)



b. Interventions include:i. Measures to reduce ICP

1. Administering osmotic diuretic (mannitol)2. Maintaining PaCO2 w/in range of 30-353. Position to avoid hypoxia

28.Ischemic stroke nursing interventionsa. Improving mobility and preventing joint deformities

i. Flexion/adduction contractures1. Extremity positioning as directed2. Spints3. Use of prone position

a. 15-30 mins several times a day4. ROM exercises5. Early ambulation

ii. Preventing shoulder pain

1. Turning/transfringa. Assist on unaffected side

2. Positioning3. Sling4. ROM exercises5. Pharm therapy

a. NSAIDSiii. Enhancing self-care

1. Avoid neglect of affected side2. Assistive devices

iv. Managing sensory-perceptual difficulties1. Visual stim on unaffected side2. Use head-turning

v. Assisting w/ nutrition1. Speech therapy

a. Swallowing difficulties2. Modified consistency3. Enteral tube



a. Monitor their glucose4. Attaining bowel and bladder control

a. Intermit catchb. Scheduled toiletingc. Fiber, fluids

5. Improving thought processesa. Cognitive, behavior, emotionalb. Multidisciplinary mgt

6. Improving communicationa. Speech therapyb. Written schedulec. Communication boardd. Speak slowly to cliente. Avoid multi-step instructions

7. Maintaining skin integrity

a. Reposition q 2 hoursb. Skin clean/dry

8. Improve fam copinga. Encourage use of avail. Supportb. Communicate realistic expectations

29.The patient with a hemorrhagic strokea. Assessment

i. Nerologic1. Decreased function is earliest sign of deteriorating condition

a. Glasgow coma scale

ii. Cardiovascular 1. VS, color, pulses

iii. Respiratory1. VS, O2 sat, color, lung sounds

b. Interventionsi. Optimize cerebral tissue perfusion

1. Implementing aneurysm precautions2. Absolute bedrest



3. Minimize stimulation4. Measures to manage ICP

c. Monitoring and managing potential complicationsi. Vasospasm

1. HA2. Change in LOC3. Prophylactic meds

a. Calcium channel blockers w/ spasm4. Seizures

a. Seizure precautionsb. Prophylactic meds

5. Hydrocephalusa. Acute

i. Ventriculostomyb. Subacute

i. VP shunt (ventriculoperitoneal)c. Rebleeding

i. HA, signs of Increased ICPii. Manage BP

6. Hyponatremiaa. Occurs in 30% of SAH casesb. Serum sodium level <135c. Treated w/ hypertonic fluidsd. PT may be evaluated for

i. SIADH

ii. Cerebral salt-wasting syndrome

adv med surg studyguide

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