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554 exam 1


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What determines what organs and tissues can be donated?
The medical condition at time of death.
Does Ohio have an organ donor registry?
Yes - maintained by BMV.
Even if a donor has indicated their wishes on a donor card, they should...
...tell their fmaily and loved ones of their wishes.
What is the perspective of the major religions on organ donation?
Approve. It is either considered the greatest gift or a matter of individual conscience.
Which religions do not allow organ donation>
Shinto (Japanses) b/c of evil spirits.
Roma (gypsies) b/c for 1 yr. spirit stays on earth and needs all parts to get to the next life.
Is there a cost to the family for organ donation?
No, but funeral expenses are still their reponsibility. However, funeral homes should not charge the family extra, this expense s/b charged to the OPO.
Can someone with cancer received an organ?
No, b/c rejection medicine makes cancer grow very quickly by suppressing the immune system.
What is brain death?
-legal declaration of death
-complete & irreversible loss of brain & brainstem fxn
-can be Dx in full-term newborns older than 7 days
-TOD is documented when brain death is declared
-if patient is potential organ donor, physiologic mgmt & mech. vent. is maintained until organ recovery
What is cardiac death?
-patient has no cardiac or resp. activity
-tissues are acceptable(rarely organs)
-body must be kept cool
-removal is within 24 hrs of death
-OR for surgical recovery of tissues
-corneal donation does not require surgical suites
When does countdown begin?
at "crossclamp"
-heart/lung - 4-5 hrs.
-kidney - 48-72 hrs.
How are organs matched to recipients?
HLA marker (there are no difference between races)
What happened in organ transplant in 1961?
Azathioprine - a rejection inhibitor drug
What happened in organ transplant in 1983?
Cyclosporine - immunosuppressant drug
What happened in organ transplant in 1986?
United Network for Organ Sharing (UNOS) receives a federal contract to operate the Organ Procurement and Transplantation Network (OPTN)
What happened in organ transplant in 1998?
Routine Notification Legislation required all hospital deaths be reported to the OPO; trained requesters can approach family; hospital must have aggreement w/OPO, tissue and eye bank, hospital must allow OPO to complete record reviews of all hospital deaths
Why is it important to build a working relationship with the donor's fmaily?
-to work with family for bereavement
-to get complete med/soc Hx
What is first person consent legislation?
It allows the OPO to proceed with donation, w/o the family's consent, if deceased has so indicated in a donor registry.
What does the OPO do?
Links donors with recipients.
Who makes up the donor team?
-procurement team
-transplant coordinatorys
-OPO personnel
-tissue typing lab
-serology lab
-transplant surgeon
-transplant teams from other centers
Who makes up the transplant team?
-clinical transplant coordinators
-transplant physicians
-transplant surgeons
-financial coordinators
-social workers
How long does an organ donation case take?
24 hours - start to finish
*medical interventions to maintain body after brain death b/c very unstable.
Who are the members of UNOS?
every transplant hospital, tissue matching labs, all organ procurement organizations, voluntary health and professional societies, transplant patients, ethicists, and advocates.
What does UNOS do?
United Network for Organ Sharing
-promotes, facilitates, and scientifically advances organ procurement and transplantation
-adminsters a national location system
-coordinates transplant policy development and compliance
*every case is reviewed and monitored
Reasons people choose not to donate:
-unsure what their religion says
-fear that the ER staff won't work as hard to save you
-think they're too old
-think they're too ill
-fail to understand that brain death=death
-fear of additional expense
-fear of mutiliation of body
-fear of unfair or unethical organ allocation
-fear that it contributes to loved one's suffering
-cultural background fosters mistrust of medical system
-option never offered to family
Reasons donation option is not offered to the family
-brain death unrecognized or undeclared
-process viewed as time consuming
-lack of available resources to test/confirm brain death
-staff unaware of legal framework, inst. policy
-donation viewed as compounding family grief
-staff uncomfortable
Who determines the suitability of an organ donor?
-NOT the physicial or hospital
Why do families say no to organ donation?
-believed loved one can recover from brain death
-feel they did not have enough privacy when donation discussed
-religious objections
-desire to have the body buried whole
-system isn't fair
-interviewer/requestor was insensitive
-feel they were not given enough information
-feel they were not given enough time to decide
Not "harvest" but
Not "life support" but
mechanical ventilation
What are the steps in the donation process?
1.identification & referral
4.donor maintenance
5.surgical recovery
Donation: Step 1
identification and referral
-potential donor ID'd by hospital personnel
-referral to local OPO
-preliminary evaluation by OPO for donor suitability
-brain death declaration by physician (=TOD on death certificate)
Donation: Step 2
-serology testing for transmissible diseases
-more in depth evaluation for organ suitability for transplant
*process ongoing throughout
Donation: Step 3
-coroner/medical examiner release
-death explained to family (by hospital personnel)
-time allowed for family to understand reality of death (Do not approach family before death)
-donation option introduced/discussed by OPO - informed consent
-consent forms signed and witnessed
Donation: Step 4
Donor Maintenance
-stabilize hemodynamic functions
-maintain viability of organs
-recipients id'd and transplant teams mobilized
Donation: Step 5
Surgical Recovery of Organs and Tissues
-OR procedure for organ recovery- sterile environment
-procurement and preservation
-tissue recovery follows organ recovery in sterile environment
-eye/cornea recovery follows in clean environment
-possibel autopsy and then body is release for funeral
What is the nurse's role in donation?
-early recognition of potential donor
-referral to the OPO
-ensure the family's legal right to be offered the option of donation
-serve as donor & family advocate
-understand the medical/legal aspects
-comfort & support the family
=assist in management of the donor
Donor MGMT goals:
-hemodynamic stability - organ perfusion
-maintain patent airway
-optimal tissue oxygenation
-fluid & electrolyte balance
-prevent infection
-prevent complications
How is brain death determined?
-known COD
-irreversible condition
-body temp>90F
-absence of barbituate/CNS depress.
-pupils fixed, no reaction to light
-absence of brainstem reflexes
-no spontaneous mvmts. in response to external stimuli
-no reflex activity (except spinal)
-Sx persist
-apnea in the presence of hypercapnia CO2>60
Typical problems in brain death
alteration in perfusion r/t hypothalmic dysfxn
-fluid & lyte imbalance
-hypotension, dysrhythmias

alteration in oxygenation r/t pulmonary complications
-apnea requiring a vent (potential for infection, aspiration, atelectasis)
-neurogenic pulmonary edema
Criteria for allocation of organs:
-HLA tissue type
-size, height, weight
-time on wait list
-severity of illness
Nursing Care of the Transplant Patient and Family:
Psychosocial factors

anxiety, coping(ineffective), family process(altered), fear, hoplessness, non-compliance, self-concept disturbance, family grieving, spritual distress, fear

knowledge deficit, powerlessness, altered role, altered sex, impaired social, social isolation, sleep pattern disturb., altered thought processes

chronic illness, mult. hosp., end of life issues, waiting, loss of independence, finances, euphoria vs. depression, guilt, re-established roles, body image changes, compliance
Nursing Care of the Transplant Patient and Family:
Immunosuppression factors
Rejection - the process by which the immune system of the host (recipient) becomes sensitized against and attempts to eliminate the foreign antigens of the donor organ.
-varies with each patient

goal of immunosuppression
-to control host's natural response to prevent clinically significant rejection
Nursing Care of the Transplant Patient and Family:
Organ specific factors
Nursing Care of the Transplant Patient and Family:
pre-op factors
peri-op factors
post-op factors
Considerations for eligibility for a transplant
-Hx of metastatic cancer
-social/emotional support
-financial ability to pay for meds
-emotional ability to be compliant w/post op regime
-active infection
-presence of mult. diseases
Primary rejection
-always present to some degree
-host develops antibodies to the donor antigens
Hyperacute rejection
-occurs when the recipient has previously been sensitized to the donors antigens and the body immediately responds.
-graft loss within hours
Acute rejection
clinically significant rejection, requires adjustment in the immunosuppressant meds.
chronic rejection
rejection that can occur weeks, months, or even years after the transplant
-characterized by gradual loss of organ function
Immunosuppressant Medications
azathioprine (Imuran)
corticosteroids (Prednisone)
cyclosporine (sandimmune)
tacrolimus (FK 506)
Mycophenolate (MMF)
anti-lymphocytes (atgam)
problems with immunosuppressants
-powerful drugs w/many side effects
-method of fighting infection in body is suppressed
-recipients must avoid exposure to infectious agents
Major causes of chronic renal failure leading to kidney transplant
-congenital (polycystic kidney)
-connective tissue (lupus)
-hypertensive vascular disease
-infections (pyelonephritis)
-metabolic disorders (DM)
-obstructive uropathy (stones)
Major causes of end stage liver disease leading to liver transplant
-advanced chronic liver disease (post necrotic cirrhosis)
-metabolic liver disease
-nonresectable hepatic malignancies
-hepatic failure w/encephalopathy
Major causes of end stage heart disease leading to health transplant
-coronary artery disease, atherosclerosis in the coronary arteris with MI
-congenital diseases
-valvular diseases
Major causes of end stage lung disease leading to lung transplant
-obstructive lung disease (emphysema)
-restrictive lung disease (pulmonary fibrosis)
-infectious lung disease (cystic fibrosis)
-pulmonary vascular disease (primary pulmonary HTN)
Major causes of end stage pancreatic disease leading to pancreas transplant
DM type 1
What are the causes of hepatitis?
viral, alcohol, drugs, toxins, hepatobiliary blockages.
What are the phases of viral hepatitis?
flu-like Sx, malaise, fatigue, fever, N&V, diarrhea
(5-10 days after start of flu-like Sx)
pruritis - bile is not excreted
clay-colored stool
brown urine
absense of flu-like Sx
bilirubin drops
liver enzymes drop
pain subsides
*usually takes 2-3 weeks
Types of Viral Hepatitis
A - fecal/oral
B - B/BF,
C - B/BF
D - B/BF
E - fecal/oral
spordaic or epidemic
water, food, people, shellfish
benign, self-limiting, 2 mos.
vaccine (expensive)
virus shed in stool for 2 wks
states: acute, chronic, fulminant, carrier
health care workers, IVDA, dialysis, mult. sex partners, male to male
damages liver and is a primary risk factor for cancer
vaccine: 3 doses=lifetime immunity
primary worldwide case of chronic hep., cirrhosis, liver ca.
Sx often mild and not recognized until the secondary effects ocur
No vaccine
rare in US
only in people who already have HBV
can increase the severity of HBV and it's longterm effects
No vaccine
fecal contam of H2O
Young adults
Fulminant and fatal to pregnant women (rapid, deadly)
No vaccine
Rare in US
Common in SE Asia, Africa, Central America
Chronic Hep.
-follows HBV, HCV, HDV
-few Sx - malaise, fatigue, hepatomegaly, icterus
-leads to cirrhosis, liver ca. and liver transplants
Fulminant Hep.
rapid and deadly
can proceed to liver failure in 2-3 weeks
usually related to HBV,HDV
Toxic Hep.
from substances that damage the liver:
alcohol-necrosis of the hepatocytes w/inflammation of the liver progressing to cirrhosis
drugs-acetaminophen directly damages hepatocytes, (halothane, chloroform)
carbon tetrachloride, benzene
What is the max. Acetaminophen an adult can have in one day?
4000 mg. in 24 hrs.
hepatobiliary hep.
results from cholestasis: biliary blockage (blockage of bile inflames the liver) secondary to cholelithiasis
-cholecystitis: gall stone blocking the hepatic duct (oral contra., allopurinol)
Tx: remove the stone and reestablish blood flow
Dx tests
Lab studies
-liver fxn tests: ALT, AST, GGT, LDH, Bilirubin

Liver Antigen Studies - ids viral antibodies

Liver Biopsy
to differentiate hep, cirr, and liver ca.
Hep. Lab studies
ALT - alanine aminotransferase - released by damageg liver cells >1000 IU/L (acute)

AST - aspartate aminotransferase - release by damaged liver cells
20-100X normal

ALP - Alkaline phosphatase - released by damaged liver cells, elevated

GGT - gamma-glutamyltransferase - increase hep. & obstr. biliary disease

LDH - lactic dehydrogenase - LDH5 indicates liver damage.

Serum Bilirubin (conj. & unconj.) elevated
Medications for Hep.
prevention- vaccines
HAV 2 doses of inactivated virus
HBV 3 doses of recombinant
(serologic testing for immunity)

post-exposure prophylaxis - immune globulin or HBIG if household or sexual contact
HAV single dose within 2 wks. of exposure
HBV HBIG and HBV vaccine

most acute viral hep. no Tx
Medication for acute HCV
interferon alpha to reduce risk of chronic HCV
(also given to chronic HBV & HCV)
Hep. Tx and Complementary Therapy
bedrest, nutrition, avoid alcohol & toxins
recovery can take 2-3 weeks
milk thistle
licorice root (can cause HTN, fluid & lyte imbalance)

hospital and home-based care
Health promotion and teaching
-discuss hygeine
-teach dangers of sharing needles
-teach safe sex
-get vaccine if high risk
-teach post exposure prophhylaxis if exposed
-health Hx: Sx & duration, high risk behaviors, known exposure, review current meds (OTC, toxins)

VS, color of sclera & skin, abd. contour & tenderness, color of stool & urine
Nursing Dx Hep: Risk for Infection
-standard precautions & meticulous handwashing

HAV, HEV w/fecal incontinence
-use contact isolation along w/standard precautions

encourage prophylacting treatment for food handlers or child care workers
Nursing Dx Hep:
Nutrition<body requirements
Ineffective Health Maintenance
Disturbed Body Image
Nursing Interventions Hep:
energy mgmt
increase calories & nutrients
self-direction of care
social support, confidentiality
progressive, irreverisble
end stage of chronic liver disease leading to liver failure
10th leading COD in US
What is liver's fxn?
1.metabolism - protein, CHO, fat, steroids, & most drugs
2.synthesis - blood proteins, albumin, clotting factors, Vit. K
3.detoxification - alcohol, toxins, converts ammonia to urea (excess ammonia can cause coma)
4.bile production - helps absorb fats - glycogen, mineral & fat-soluble vitamins
cirrhosis pathophysiology
functional liver tissue destroyed and replaced by fibrous scar tissue
metabolic functions are lost
nodules and constrictive bands form that disrupt blood and bile flow
normal portal venous system is interrupted leading to PORTAL HTN with increased pressure
Types of Cirrhosis
Alcoholic Cirrhosis
Laennec's - end result of alcohol causing metabolic changes in the liver (fatty liver)
Biliary Cirrhosis
biles is obstructed within the liver
Post-hepatic Cirrhosis
from chronic HBV or HCV or unknown causes
Manifestations of cirrhosis
p. 587
enlarged, tender liver
dull aching in RUQ
anorexia, weight loss
diarrhea or constipation

ascites, jaundice
gynecomastia, infertility
neurologic changes
edema, hematology changes
Complications of cirrhosis
Portal Hypertension
Esophageal Varices (hemorrhage)
Hepatic Encephalopathy
cirrhosis: portal hyptertension
- shunts blood to collateral veins such as esophagus, rectum, and abdomen, leads to ascites and splenomegaly
complications of cirrhosis: ascites
caused by decrease serum proteins (hypoalbuminemia) and aldosterone
complications of cirrhosis: esophageal varices
thin-walled veins that form due to portal HTN. Can rupture causing massive hemorrhage.
complications of cirrhosis: hepatic encephalopathy
Increased ammonia, build-up of narcotics, analgesics, tranquilizers.
complications of cirrhosis: hepatorenal syndrome
renal failure with azotemia (excess nitrogenous wates products in blood), sodium retention, oliguria, HTN
*may be precipitated by GI bleed, aggressive diuretics
Dx tests for cirrhosis
Lab tests
liver fxn tests, CBC, platelets, PT, INR, PTT (coagulation tests)
Bilirubin, lytes, glucose, magnesium, calcium, phosphorus, serum albumin, serum ammonia

Abdominal ultrasound

Upper endoscopy (esophagascopy) to look for varices

Liver biopsy - to distinguish from hep or liver ca, but may be deferred if PT>3 seconds
Medications for cirrhosis
diuretics: lasix, aldactone (spiranolactone - K sparing diuretic)

laxatives: lactulose (cause diarrhea to clear out ammonia)

anti-infectives: neomycin (clear the bowel of ammonia producing bacteria)

ferrous sulfate, folic acid, Vit. K, antacids, serax

benzodiazepine - anti anxiety not met. by liver but excreted by kidney for pain

corgard and imdur together - vasodilator to reduce portal HTN
Tx for cirrhosis
packed RBCs, fresh frozen plasma, or platelets

supportive: rest, monitor for bleeding, elevate legs

dietary: limit NA & fluids, protein if ammonia is high
add vitamin supplements

Treat alcohol withdrawal
Paracentesis for ascites
-aspiration of fluid from pertoneal cavity
-relieves respiratory distress from increased abdominal pressure
-often give albumin & FFP during and after for BP & replace proteins
-small amounts daily or large volume
-monitor vital signs & for bleeding
-teach patient to avoid lifting, straining, and watch for bleeding

*P. may be done under USN
lay on R side to compress paracentesis area

- may make ammonia buildup - watch neuro status
Tx for esophageal varices
sandostatin or octreotide IV to reduce bleeding
-blood products to stabilize
-endoscopy - band or sclerosis
-balloon tamponade w/Sengstaken-Blakemore tube
-transjugular intrahepatic portosystemic shunt (TIPS)
-liver transplant
Assessment of cirrhosis
Health Hx
-current manifestations
-alcohol use or IVDA
-previous hepatitis/liver
-prescription, OTC drugs

-VS, mental status, color & condition of skin, edema, abd. shape, tenderness, liver size, bowel sounds, bowel movements, telangeictasis
Nursing Dx for cirrhosis
-Excess fluid volume
-Disturbed thought processes
-Ineffective health maintenance
-Ineffective protection
-Skin integrity
Interventions for cirrhosis
-daily wt., urine, sp. gravity
-neuro status, bleeding
-promote rest
-lifestyle changes
-bleeding precautions
-pruritis, poor cap refill
Liver Cancer
-primary is uncommon in US
-r/t alcoholic cirrhosis, HBV, HCV
-tumors or infiltrating nodules
-tumors grow fast and metastasize
-malaise, anorexia, wt.loss, FUO, abd. fullness, RUQ pain & mass
-signs of liver failure - die in 6 mos.
Liver Cancer, Dx
by CT scan, MRI, liver biopsy

*lay on R side q2h to reduce risk of bleeding
Liver Cancer, Tx
-Surgery, if tumor is isolatable
-Radiation can shrink tumor, reduce pain and pressure
-Chemotherapy-into artery
-pain control priority-hospice
Liver Trauma
blunt or penetrating
causes bleeding, hematoma, shock
can be Dx by peritoneal lavage
Tx: surgery (if small, obeservation only)
-give IV fluids, RBCs, FFP and platelets
-monitor VS
-monitor urine output (at least 30 cc/hr)
Liver Abscess
-bacterial or protozoal
-health tissue destroyed leaving necrosis, exudate, blood
-E.Coli common
-happens after liver biopsy sometimes
-sudden onset: fever, malaise, vomiting, hyperbilirubinemia, RUQ pain

Ex: peritonitis from infection from peritoneal dialysis
Acute Pancreatitis:
Interstitial edematous pancreatitis
inflammation & edema
Necrotizing Pancreatitis:
Interstitial edematous pancreatitis
more severe
leads to inflammation
-complication of gallstones (in women) and alcoholism (in men)
Manifestations of Acute Pancreatitis
-abrupt onset: pain epigastric & abdominal radiating to back
-abdominal distension, rigidity, decreased bowel sounds, N&V
-tachycardia, hypotension, fever, cold clammy skin, jaundice
-Turner's sign(flank bruising)
-Cullen's sign(bruising around umbilicus)
Compl. of Acute Pancreatitis
-depletion of intravscular volume leading to Acute tubular necrosis (ATN) and Acute renal failure (AFN)
-ARDS-acute respiratory distress syndrome
-pancreatic necrosis
-pancreatic pseudocysts & abscess
Pancreatic Necrosis can lead to...
infected mass-->shock-->multisystem organ failure
Pancreatic pseudocysts & abscess can lead to...
rupture and peritonitis

*they require surgery

Peri-surgical care: huge amt. of NG drainage (1000 cc/hr), make sure IV is at least 30 cc/hr to prevent dehydration
Chronic pancreatitis
-gradual destruction-irreversible
-alcoholism - US
-malnutrition - world
-10-20% idiopathic

insoluble proteions calcify & block ducts & flow of pancreatic juices

leads to inflammation & fibrosis of parenchyma, losing exocrine fxn., endocrine fxn (DM)
Manifestations of Chronic Pancreatitis
-recurrent pain (drug depenedency)
-wt. loss, anorexia, N&V, malabsorption
-flatulence, constipation, steatorrhea
Compl. of Chronic Pancreatitis
-malnutrition, malabsorption, peptic ulcer disease
-development of pseudocyst, abscess, or stricture of CBD
-new onset DM
-increased risk for P. cancer
-narcotic addiction
Chronic Pancreatitis: Dx
Lab Tests
-amylase, rise with 2-12 hrs. to 2 to 3X normal; returns to normal in 2-4 days
-lipase, rise and stay elevated for 7-14 days
-trypsinogen Up in acute, may be decreased in chronic
-WBC is decreased
-CT scan, USN
-ERCP endoscopic retrograde cholangiopancreatography
Percutaneous fine need aspiration biopsy
Chronic Pancreatitis:
analgesics (maybe not morphine b/c causes spasms of sphincter of Oddi)
-demerol or hydromorphone
-tagamet, zantac, prilosec
-octreotide or sandostatin given IV to suppress enzyme production
-pancrealipase - endogenous source of pancreatic enzymes
-antibiotics as indicated
Chronic Pancreatits:
NPO (no ice, no swabs)
keep on top of pain
NG to low suction
IV replacement fluids, TPN
Foley to monitor urine output
monitor VS
monitor other complications
*When amylase normal & bowel sounds are present, no pain, may start diet slowly
Chronic Pancreatitis:
-gall stones endoscopy, or lap cholycystectomy
-drain large pseudocysts either surgically or percutaneously
-peritonitis requires large open exploration
chronic Pancreatitis:
Nursing Dx
-ineffective breathing pattern
-deficient fluid volume
-imbalance nutrition<body req.
-altered mental status
Chronic Pancreatitis:
-relieve pain
-check PaO2
-third spacing - watch urine output
-weigh, TPN, monitor stools, NG output
-r/t fluids, VS, alcohol WD
Pancreatic Cancer
-common site: head of pancreas, blocks bile through CBD--> jaundice, clay stools, dark urine, pruritis.
*may be surgically resectable by Whipple's procedure(bypass CBD)
-Ca. of body causes pain by pressing on celiac ganglion when pt. eats or is supine
-Ca. of tail - no Sx
-85% is not Dx until Ca is advanced
Cerebrovascular Disorders
TIA transischemic attack
CVA cerebrovascular accident, stroke
-ischemic (thrombotic, embolytic)
-hemorrhagic (intracerebral bleed)
CVA: manifestations: motor deficits
tetraplegia (quadriplegia)
hemiparesis (L or R)
hyptonic (absence of tone)
spasticity (increased tone)
CVA: sensory perception
hemianopia (homonymous) - loss of 1/2 field of vision, one or both eyes
agnosia - can't say name of familiar obj.
-neglect syndrome - don't notice affected side
CVA: communication disorders
speech center - dominant hemisphere - left side
Dysarthria - disturbance in muscular control of speech
Aphasia - expressive, receptive, global, Wernicke's(inappropriate)
CVA: Cognitive & Behavior Changes
change in LOC (cerebral edema)
emotional lability
loss of self control
decreased tolerance of stress
intellectual changes
CVA: elimination & swallowing
loss (full or partial) of sensation for bladder
changes in bowel elimination
dysphagia-choking, drooling, aspirating
CVA: Dx tests
CT scan
doppler studies
lumbar puncture
CVA: Medications
focus on prevention, affect platelet aggregation
ACUTE CVA: Medications
-t-PA - only ischemic and within 3 hours onset of Sx (not hemorrhagic)
-Calcium channel blockers-prevent vasospasm
-Steroids-prednison, decadron
-supportive-rest, monitor neuro status, VS, BP often kept>160 systolic
-physical/occupational/speech therapy
-surgical - carotid endarterectomy to prevent
ACUTE CVA: Nursing care
24-72 hrs. post stroke
(severity of stroke determines care)
-airway - give O2, monitor O2 sat
-neuro checks q 1-2 hrs., change in LOC
-VS- arrythmias, hypothermia
-urine output - diabetes insipidus from ADH involvement from pituitary
-seizure precautions
-repositon q2hrs. ROM joints, muscles
-observe for swallowing impairment
CVA: Nursing care: emotional needs
-assume pt. can hear
-provide aphasic with support, speech Tx
-provide alternative means of communication
-emotional support
-fmaily support
-pastoral care
hemorrhagic strokes
-intracranial hemorrhages
-arterial-venous malformation (2% of all strokes)
Manifestations of ruptured aneurysms
-often asymptomatic
-may have small leakages: mild headache, N&V, pain in neck & back
-prodromal: headache, eye pain, visual distubances, dilated pupil
-rupture: explosive headache, LOC decreased, N&V, stiff neck, photophobia
Compl. of ruptured intracranial aneurysm
vasospasm (give nimitop)
hydrocephalus (increased CSF)
Aneurysm: Dx, Tx
CAT scan
lumbar puncture

meds: amicar-Calcium channel blocers, anticonvulsants, stool softeners, analgesics

surgery: craniotomy for clipping
Aneurysm: Nursing Care
quiet, dark, room
HOB 30-45 degrees
limit visitors and stress
prevent constipation, straining
monitor VS, BP in range
avoid blowing nose, coughing, flexing neck
Spinal cord injuries
-defined by vertebral level
-classifications: complete, incomplete, cause of injury, level of injury
-syndrome classification
central, anterior, posterior, Brown-Sequard (bullet), Horners
Spinal cord injuries: manifestations
-vary according to injury level
-also by amount of tissue damage
-can affect all systems: movement,sensation,perception,sexual functioning, elimination
Compl. of Spinal cord injuries
spinal shock (neurogenic shock): bradycard., decreased BP, lost ANS (parasymp. is dominant)-->severe orthostatic hypotension

upper & lower motor neuron deficits - FLACCID

autonomic dysreflexia - lack of control of ANS
brady, hypo -->then hypertension,profuse sweating above lesion; pale & cold below
Spinal cord injuries:Meds
methylprednisone - reduce inflam.
vasopressors- dopamine
hydrogen ion blockers-pepcid
stool softeners, laxatives
Spinal Cord: stabilization/surgery
-cervical collar (philadelphia collar)
-Gardner-Wells Tongs (attached to skull, weighted for traction)
-Halo external fixator device
-Decompression laminectomy
-spinal fusion with fixator rods
Spinal Cord Injury:
-log roll: hold neck, HOB up 30 degrees
-pin care (infection)
-monitor resp.
-monitor for Autonomic Dysreflexia
-monitor neurogenic bladder - signs of hypotension-->staight cath

*C1-C4 nerves serve diaphragm -->means pt will need vent.
Spinal Cord Injury:
emotional aspects
lifestyle changes
denial and anger
sexual dysfunction
low self esteem
Herniated Intervertebral Disk
-herniated (slipped)
severe pain: sciatica
limited mobility (cervical, lumbar)
Dx: xray, CT, MRI, myelogram
Meds: muscle relax.
Conservative treatment
Sx: laminectomy, spinal fusion, furaminotomy (enlarge foramen), microdiskectomy
Spinal Cord Tumor
benign or malignant
primary or metastatic
classified by tissues they arise from
Spinal Cord Tumor: manifestations
according to location
level of occurrence
type of tumor
spinal nerves involved

pain, motor, and sensory involvement

Tx: inject meds. into disk, narcotics, epidural steroids

Surgical: (see herniated disk)

Mean Arterial Pressure
Cardiac Output
CO X SVR = at least 70 mmHg
strove volume X heart rate 4-8 L/min.(measured w/echo., swan-ganz. temp. change system)
Cardiac Index
to take into consideration the size of the person
divide CO/body surface area
2.8 to 4.2 L/min.
Arteriole determinants of SVR (systemic vascular resistance)
SNS - baroreceptors
adrenal cortex - epi, norepi
RAA system - decrease in renal perfusion->renin release->A1 become A2 in lungs by ACE ->vasoconstriction
ANP - vasodilation
adrenomedullin - vasodilation
vasopressin (ADH) - water retent./vasoconstriction
local factors - inflam. mediators, metabolites
Primary factors affecting BP
arteriosclerosis (hardening of arteries)
atherosclerosis (plaque)
Primary HTN
essential HTN: risk factors
-mineral intake
-insulin resistance(type 2)-> increase atherosclerosis-> increase BP
-excess alcohol
Primary HBP: Manifestations
-headache (back of head and neck)
-Sx of other organ damage, nocturia, N&V, confusion
-visual - retina exam shows damage
Primary HBP: lifestyle modifications
-diet/lose weight
-stop smoking
-limit alcohol use
-physical activity
-stress reduction
-compliance with med. regimen
Anti HTN Drugs
-alpha blockers (osin)
-ACE inhibitors (pril)
-beta blockers (ol)
-Ca channel blockers (pine, cardizem, verapamil)
-centrally acting sympatholytics, suppress SNS
-vasodilators (hydroclorothiazide, spiranolactone)
Primary HTN: nursing issues
health maintenance
nutrition imbalance
sedentary lifestyle
BP monitoring
medication issues
Secondary HTN: why?
cardiac reasons (coarctation of the aorta)
renovascular(renal artery stenosis)
endocrine(pheochromocytoma-tumor of adrenal gland)
neurologic(high spinal cord lesion)
drug use(cocaine, meth., oral. contra.)
ALL HTN: Dx tests
lab tests: BUN, creatinine, UA, Urine protein
toxicology screen
radiology: IVP, chest xray
USN of kidneys
CT of renal system, chest area, abd (to look for pheo.)
HTN crisis
immediate treatment(<1 hr)
prevent cardiace, renal and vascular damage to reduce morbidity, mortality

Malignant HTN (cerebral edema)
HTN emergencies: Tx
avoid rapid decrease (<25% over minutes to hours)
goal: 160/100 w/in 2-6 hrs.
IV push: hydralazine, vasotec, labetolol, cardene
IV drip: nitropresside, nitrogl., esmolol (in conj. w/ART line)
teach to take meds to avoid future episodes

*if too fast, shock, vasospasm, MI
Thoracic Aortic
Abdominal Aortic

Aortic Dissection: plaque pulls wall of artery away from other layer
Thoracic Aortic Aneurysm
10% of aneurysms - marfan's
often asymptomatic, substernal pain, neck, back pain, dyspnea, cough
surgery if 6 cm. in size
Dissecting Aortic Aneurysm
anywhere in aorta but often in ascending or descending aortic arch. Sudden excruciating pain. Dissection can go into aortic valve, other major arteries.
Abdominal Aortic Aneurysms
atherosclerosis, HTN, age>70, smoking
asymptomatic, pulsating mass found
-pain varies: severe indicates impending rupture
sluggish blood flow->emboli occlude peripheral arteries

Rupture: death 50% before reaching hospital
10-20% survive surgery
Popliteal & Femoral aneurysms
atherosclerosis,, bilateral, more common in men
intermittent claudication(leg cramps after exercise)
thrombosis, embolism, gangrene-> amputation

pop.: pulsating mass behind knee
femoral: groin, may rupture
Aneurysms: Dx tests
chest xray - PA & lateral
12 lead EKG
abd. renal USN
trans-esophageal echocardiogram (TEE)
CT scan w contrast dye
dissecting aneurysm: meds
beta blockers, other anti HTNs
nipride drip
Ca channel blockers
avoid hyperstat or apresoline->make dissection worse
constant monitoring of VS, urine output, hemodynamics(w/swan ganz), arrythmias
Aneurysms: Surgery
Thoracic or Dissecting
requires thoracotomy and cardiac bypass
Aneurysms: Surgery
midline abd. incision, endovascular with a stent
Aneurysms: Surgery
incision with grafts bypasses, atherectomies, embolectomy

*w/fem. tib.-> lower leg may have formed collateral circulation
Aneurysm: Nursing care Post-op
VS & Cardiac Rhythm
monitor urine output (renal artery may shut down)
monitor ecchymosis, edema
monitor peripheral pulses
check for decrease in motor function or sensation; change in neuro status
increased pain in abd., back, groin
monitor labs - esp. HgB & HCT
observe skin for breakdown
paralytic ileus
mesentery artery stenosis

*diarrhea directly post surgery->necrotic bowel
Aneurysms: pre-op
bedrest w/legs flat, stress free environment
avoid strain while BM
VS, beta blockers to lower BP
Sx of impending rupture: emergent
back pain, thoracic, difference in BP in both arms, loss of peripheral pulses, drop in HCT, feeling of impending doom
Peripheral Artery Disease:
Peripheral Artery Disease:
-atherosclerosis->ischemia->collateral circulation
Sx: weak, absent pulse, cyanosis, mottling, cold extremity, paresthesias, neuro changes.

-comes from somewhere else(heart w/A.Fib)
Sx: same

-piece of arterial wall breaks off & blocks artery

*have 1-2 hrs. to remove clot w/surgery or drug Tx before permanent damage
Peripheral Artery Disease:
heparin (IV)
intra-arterial thrombolytics - urokinase t-PA.

*risk of bleeding
Peripheral Artery Disease:
Thrombectomy - immediate, within 4-6 hrs.
Peripheral thrombectomy using a fogarty cath.
abdominal laparotomy - caused by a mesenteric thrombosis
Thromboangiitis Obliterans
(Buerger's Disease)
occlusive, small vessel inflamed and spasm causing clots
risk factor: smoking
risk for tissue damage->gangrene
severe pain, claudication or rest

Tx: stop smoking
good foot care (podiatric)
trental, Ca channel blockers, pain meds
surgical bypass, amputation
intense vasospasm in fingers & toes
can go along w/collagen diseases such as scleroderma or RA
female, 20-40, congenital
digits turn blue-white-red
severe pain
keep extremities warm
vasodilators, steroids
Disorders of Venous Circulation
venous thrombosis (thrombophelbitis)->Virchow's Triad:
stasis of blood
vessel damage
increased coagulability

DVT: orthopedic surgeries have 50% risk; air travel
DVTs: Sx and complications
redness, tenderness, swelling, dull aching pain, cyanosis, edema, positive homan's

compl. chronic venous insufficiency
PE (commonly missed)
Dx tests
venous doppler studies

spiral CT
lung scan
DVTs & PEs: Meds
heparin IV->lab PTT 60-70 sec.
(immediate effect, lasts 1hr.)
protamine sulfate is antidote

heparin SubQ->PTT not usually watched, onset 1hr

low molecular weight heparin - lovenox, fragmin, PT & PTT not affected

coumadin - interferes w/vit. K clotting, labPT and INR
antidote is Vit. K IV slow
DTVs & PEs: prevention
SCDs, Foot pumps
elevate legs 15-20 degrees when in bed
walk - avoid sitting or standing
dont cross legs
watch tight socks cutting in below knees
DVTs & PEs: surgery
thrombectomy - for DVT ledged in the large (femoral) vein

venacaval filter(Greenfield filter) - most commonly used, inserted into the inferior vena cava opens and traps emboli
Chronic Venous Insufficiency
inadequate venous return
often occurs after DVT
stasis ulcers develop - edema, itching ,cyanosis, necrotic centers, drainage, brown pigment, leathery but fragile

Tx: of ulcers, drsg. changes, surgical excision with skin grafts

*Arterial ulcers: look more white, red, shiny
Varicose Veins
people in standing occupations (caucasian women)
occur in deep veins
force of gravity affects valves
-lack of leg exercise - walk

Surgery: ligation & stripping
sclerosing therapy
enlarged lymph nodes
Choosing a transplant donor:
HLA - tissue antigens close to recipient as possible decreases potential for rejection

Allografts - living donors of human tissue (bone marrow, blood, kidney)

Cadaver organs - brain dead, <65, free of disease, malignancy, infection(hepatitis)

*also look at size of organ and recipient
These tissues do not require HLA testing for transplant
heart valves
blood vessels, fascia for grafts
bone, cartilage
transplant recipients: long-term care
on anti-rejection meds for life
drugs can cause renal failure
renal trans. avoid contact sports
HTN, high cholesterol still does damage
Which organs reject fastest
liver and heart
What are signs of organ rejection
pain at the site
weight gain (edema)
increased WBCs
Transplants: long-term effects
risk for infection (esp. lung->pneumonia)
heart or heart/lung must undergo biopsies regularly
assess for graft rejection early
*increased sedimentation rate, chills, fever, malaise
Transplants: Psychological effects
anxiety r/t
-someone died for you

-active listening
-teach stress reduction, relaxation
-encourage return to active life, volunteer
Intracranial Disorders
(Altered cerebral fxn):
Altered level of consciousness
arousal - RAS reticular activating system needs to fxn.

cognition - recognize people, talk

metabolic - acid/base, renal fxn, cardiac fxn, DM-hyper/hypo glycemic

drugs - phenylbarbitol, OD (tox screen)
Altered LOC
Tox screen
BS screen

*done in most traumas
Motor responses:
follows commands
withdraws purposefully (pinch finger)
withdraws deep pain only (nail bed pressure)
-decorticate(better)-bring hands across chest
-decerebrate(worse)-hand down, out; feet cross

*posturing occurs with cerebral edema
Coma states:
full recovery
recovery with residual effects
minimally conscious
irreversible coma (persistent vegetative state)
locked in state
brain death
Brain Death
no motor reflexes present
pupils fixed and dilated
absent occular(corneal) reflexes (no blinking)
flat EEG
Angiography shows no blood flow (wait till phenobarb. clears)
no cough, gag, or cornea
bring CO2 up to 60 to see if they breathe
intracranial disorders:
Dx test
lab tests (to look for potential cause, ex: hypoglycemia, dehydration)
tox screen
Radioisotope brain scan
lumbar puncture
cold caloric (cold water in ear)
Intracranial disorders: Meds/support
correct glucose
naloxone (narcan)
thiamine (warnecke's encephalopathy w/alcoholism)
support BP
support airway - vent
nutritional - tube feeds
intracranial disorders:
Nursing Care
positioning (low fowlers; may see reverse trendelenberg)
skin inspection
fmaily support
potential donor
Increased intracranial pressure
decreased LOC
sluggish pupils
call MD

temp. fluctuations
fixe pupils
Cerbral Edema:
interferes with
autoregulatory fxn
normal Insane Clown Posse is 5-15
What is Cushing's Triad?
signs that the brain will herniate (right before brain death)

irregular resp.
increased pulse pressure (140/60: 140-60=80 too high)
Brain Herniation
brain tissue pushes through the tentorial notch
pressure on medulla and ints centers of respiration and VS control
coma, altered resp. fixed pupils, posturing
continues - resp/card arrest
Brain Herniation: Meds
to decrease cerebral edema
-osmotic diuretics (mannitol)
-diuretics (lasix)

acetaminophen (pain)
carafate, pepcid (stress ulcers)
barbituate coma (decrease temp/seizures)
ICP monitoring
intracranial - into brain
subarachnoid bolt or screw
intraventricular drain
central perfusion pressure (pressure in brain needs to be 60 mmHg to perfuse brain)
ICP: Nursing Care
VS, neuro checks - trends
CO2 low for 24-36 hrs
HOB up 30 degrees
no foot boards (it increases pressure if feet against)
quiet environment - music
family support
monitor for infection of ICP site
Seizure Disorders:
partial (jacksonian)
-absence (petit mal)
Status Epilepticus
Seizure Disorders:
-one side

-looks like inattention
-airway, protect head, side-laying, short apnea, post-ital (sleepiness)

seizure's don't stop; life threatening
Seizure: Dx
neuro exam
skull xrays
lumbar puncture
blood studies
Seizures: Meds
anticonvulsants: dilantin, phenobarb

give lowest dose
CNS side effects
lab drug levels
liver fxn

dilantin needs good gum and oral care b/c gum hypoplasia

benzodiazepine-ativan, valium IV
Seizure: Nursing Care
prevent injury
observe: where it started & time
did client lose LOC
what happened right before?
extra movements?
clonic phase?
Care During Status Epilepticus
-save pt. from hypoxia, acidosis, hypoglycemia, hyperthermia, exhaustion
-50% dextrose IV
-IV valium, ativan q10 minutes
-dilantin IV or phenobarb.
-IV fluids (0.9NS)
-transfer to ICU
Seizure: surgery
continuous EEG
locate and do ablation on area causing seizures
Mechanisms of traumatic Brain Injury
blunt (close head)
acceleration injury
deceleration injury
acceleration-deceleration (coup-contracoup) - shaken baby
deformation injury
Skull fractures
closed (dura)
linear - most commone
comminuted - depressed
basilar - combination - if dura disrupted, CSF leak from nose or eat
-Battle's sign: bruise behind ear
-Raccoon eye

*halo test: fluid on 4/4 pink ring around yellow, its CSF
has glucose in it
Traumatic Brain Injury: Tx
depressed usually requires surgery

open CSF leaks-potential for infection

*pt. do not blow nose, but don't inhibit sneeze
Diffues or Focal Brain Injuries
epidural hematoma
subdural hematoma
intracerebral hemorrhage
diffuse brain injury
diffuse axonal injury
Epidural Hematoma
knocked out briefly, come back around, then reduced LOC after
call MD
b/c arterial bleed
Diffues or Focal Brain Injuries:
mortality/morbidity increase with hypotension and hypoxia

ICP monitor
osmotic diuretics
neuro protectant drugs
evacuate hematoma (epidural emergency)
Burr Holes
CNS infections:
bacterial meningitis
viral meningitis
brain abscess
CNS infections:
-nuchal rigidity, fever, irritable, confused
-milder, sensitivity to light
-within brain parenchyma
-pus in brain tissue from infected teeth or sinuses, trauma, neurosurgery

Brain tumors - chemo, rad, surgery: depends on location, size, type
Organizational Theory:
Classical Theory
division of labor
specialization of labor
chain of command
span of control

(like military)
Organizational Theory:
Neo-Classical Theory
humanistic, participative, involved in decisionmaking, relationship building, environment based, hawthorne effect
Organizational Theory:
Contingency Theory
take environment into consideration, know customers, staffing
Organizational Theory:
Chaos Theory
complicated, relationship based, complex issues and change
In organizations...
paradigm shift is a big challenge
Types of organizations

- people s/b managing their own lives - you have to give people the opportunity to fail
-leaders are managing mobility - leaders don’t do things, they see that things are done
Organizational relationships:
vertical: one facility takes on many services
horizontal: several facilities do same kind of service

concentric - stay in same business
Conglomerate, joint venture - different businesses
Organizational Structures

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