Hepatic & Pancreatic disorders

Review of Anatomy and Physiology of the Liver

* * * *

Largest gland of the body

Located upper right abdomen

A very vascular organ that receives blood from GI tract via the portal vein and from the hepatic artery

Performs > 400 functions:

stores many minerals and vitamins, such as iron, magnesium, and the fat-soluble vitamins A, D, E, and K. * protects with Kupffer cells, detoxifies, risk for drug toxicity increases with aging because of decreased liver function. * metabolism of proteins, carbs, fatty acids and triglycerides.

pp. 1179-1180

Liver Structure

* * * * * *

Blood from hepatic portal vein and hepatic artery mi in sinusoids

!he sinusoids empty into central veins" #hich send the blood to the hepatic vein and inferior vena cava

$epatic cells lie along the sinusoids and pic% up chemicals from the blood

!hey modify the blood&s composition

At the bac% end of each hepatic cell" bile is released into a canaliculus

!he bile is carried to the bile duct and then to the gallbladder

Metabolic Functions

* * * * *

'arbohydrate metabolism

Ammonia conversion

Protein metabolism

(at metabolism

)itamin and iron storage

* * * *

Plasma protein synthesis

Bile formation

Bilirubin e cretion

*rug metabolism

Portal

irculation

)enous return from blood vessels of the G+I+ tract , abdominal organs drain into Portal vein

!uestion Is the follo#ing statement !rue or (alse!he ma.ority of blood supply to the liver" #hich is poor in nutrients" comes from the portal vein+ !uestion !ell #hether the follo#ing statement is true or false: !he gall bladder stores bile that has been produced by the liver+

Assessment of the Liver

$istory:

/utrition0 elimination0 drugs0 diseases0 pain0 increased bruising-0 increased bleeding-

Inspection: 1%in discoloration0 .aundice0 rashes0 ecchymosis

" hanges related to aging# p. 1181 Chart 55-1

* *

Percussion: done by $'P

Palpation: light 2 3+45 2 4+5 cms deep

Psychosocial: effect of lifestyle on system , effect of disease on lifestyle

Assessment of Hepatic $ysfunction

* * * * * * *
$epatomegaly 8liver enlargement9

Acute or 'hronic

6assive ascites 2 orthopnea

7mbilicus protrusion

'aput medusae 8dilated abdominal veins9

6easuring abdominal girth: p. 1298 Fig. 61-2

DAILY WEIGHTS is the most reliable indicator of fluid retention

Assessment of Hepatic $ysfunction

Asteri%is

* * *

Assess nasogastric drainage" vomitus" and stool for presence of blood

(etor hepaticus 8breath odor9

Amenorrhea

* * * * *

Gynecomastia" testicular atrophy" impotence

Bruising" petechiae" enlarged spleen

/eurologic changes

Asteri is 8liver flap9

'onstructional Apra ia

onstructional Apra%ia

Progressive $epatic :ncephalopathy

*eterioration of $and#riting , Inability to dra# a simple 1tar figure

Liver Function Studies

* * * * * * * *

p. 1299 Table 61-4 below

1erum aminotransferases: A1!" AL!" GG!" GG!P" L*$

1erum protein studies

Pigment studies: direct and indirect serum bilirubin" urine bilirubin" and urine bilirubin and urobilinogen

Prothrombin time

1erum al%aline phosphatase

1erum ammonia

'holesterol

Additional $iagnostic Studies

* * * * *

Liver biopsy

7ltrasonography

'!

6;I

<ther

Hepatic irrhosis

:tiology:

!ypes:

* * * * * *

6ost common cause is malnutrition related to alcoholism Infection Ano ia 6etabolic disorders /utritional deficiencies $ypersensitivity states

* * *

Alcoholic Postnecrotic Biliary

Pathophysiology

6anifestations:

* *

=aundice Portal hypertension 2

* * * *

Liver enlargement Portal obstruction and ascites Gastrointestinal varices :dema

* *

/utritional deficiencies > )itamin deficiency and anemia 6ental deterioration > $epatic encephalopathy or coma

irrhosis of the Liver

* *

/ursing Process: Assessment

(ocus upon onset of symptoms and history of precipitating factors:

* * * *

Alcohol use?abuse *ietary inta%e and nutritional status : posure to to ic agents and drugs Assess mental status

Abilities to carry on A*L?IA*Ls" maintain a .ob" and maintain social relationships

6onitor for signs and symptoms related to the disease including indicators for bleeding" fluid volume changes" and lab data

*iagnoses

Planning Goals may include:

* * * *

Activity intolerance Imbalanced nutrition Impaired s%in integrity ;is% for in.ury and bleeding

* * * * * *

increased participation in activities improvement of nutritional status improvement of s%in integrity decreased potential for in.ury improvement of mental status absence of complications+

Activity Intolerance

* * * * * *

;est and supportive measures

Positioning for respiratory efficiency Imbalanced N t!"t"#n < ygen

* *

I,<

Planned mild e ercise and rest periods

:ncourage patient to eat

Address nutritional status to improve strength

* *

1mall freAuent meals may be better tolerated 'onsider patient preferences

6easures to prevent ha@ards of immobility

*
Impaired s%in integrity

$igh>calorie diet" sodium restriction for ascites

* * * * * *

(reAuent position changes Gentle s%in care 6easures to reduce scratching by the patient

* * *

Protein is modified to patient needs

BProtein is restricted if patient is at ris% for encephalopathy

;is% for in.ury 6easures to prevent falls 6easures to prevent trauma related to ris% for bleeding 'areful evaluation of any in.ury related to potential for bleeding

1upplemental vitamins and minerals" especially B comple " provide #ater>soluble forms of fat>soluble vitamins if patient has steatorrhea

ollaborative Problems&Potential

omplications

* * * * * * *

=aundice

Portal $ypertension

Ascites

:sophageal varices

$epatic encephalopathy

'aundice

Cello#> or green>tinged body tissues" sclera" and s%in due to increased serum bilirubin levels

!ypes

* * * *

$emolytic $epatocellular <bstructive $ereditary hyperbilirubinemia

$epatocellular and obstructive .aundice are most associated #ith liver disease

Hepatocellular & (bstructive 'aundice

1igns , 1ymptoms:

$epatocellular

* * * *

6ay appear mildly or severely ill Lac% of appetite" nausea" #eight loss 6alaise" fatigue" #ea%ness $eadache" chills" and fever if infectious in origin

<bstructive

* * *

*ar% orange>bro#n urine and light clay>colored stools *yspepsia and intolerance of fats" impaired digestion Pruritus

Portal Hypertension

* *

<bstructed blood flo# through the liver results in increased pressure throughout the portal venous system

;esults in:

* *
Ascites

Ascites :sophageal varices

:tiology:

* * *

Portal hypertension resulting in increased capillary pressure and obstruction of venous blood flo# )asodilatation of splanchnic circulation 8blood flo# to the ma.or abdominal organs9 'hanges in the ability to metaboli@e aldosterone" increasing fluid retention

* *

*ecreased synthesis of albumin" decreasing serum osmotic pressure 6ovement of albumin into the peritoneal cavity

Assessment #$ Asc"tes

* *
distended veins" and umbilical hernia

;ecord abdominal girth and #eight daily

Patient may have striae"

* *

Assess for fluid in abdominal cavity by percussion for shifting dullness or by fluid #ave

6onitor for potential fluid and electrolyte imbalances

!reatment of Ascites

Lo#>sodium diet

* * * * *

*iuretics

Bed rest

Paracentesis

Administration of salt>poor albumin

!rans.ugular intrahepatic portosystemic shunt 8!IP19 Dhich diuretic medication #ould most often be used for a patient #ith ascites-

a. b. c. d.

Acta@olamide 8*iamo 9

Ammonium chloride

(urosemide 8Lasi 9

1pironolactone 8Aldactone9

)leeding of *sophageal +arices

* * *

<ccurs in about 3?E of patients #ith cirrhosis and varices

(irst bleeding episode has a mortality of E0F>50F

6anifestations include hematemesis" melena" general deterioration" and shoc%

Patients #ith cirrhosis should undergo screening endoscopy every 4 years+

,reatment of )leeding +arices

* * * * * * *
Blood and blood products

!reatment of shoc%

< ygen

I) fluids0 electrolytes0 and volume e panders

)asopressin" somatostatin" octreotide to decrease bleeding

/itroglycerin may be used in combination #ith vasopressin to reduce coronary vasoconstriction

Propranolol and nadolol to decrease portal pressure0 used in combination #ith other treatment

*ndoscopic Sclerotherapy

*sophageal )anding

)leeding *sophageal +arices - /ursing 6anagement

* * * * * * *

6onitor patient condition freAuently" including emotional responses and cognitive status+ 6onitor for associated complications such as hepatic encephalopathy resulting from blood brea%do#n in the GI tract" and delirium related to alcohol #ithdra#al+ 6onitor treatments including tube care and GI suction+ <ral care Guiet calm environment and reassuring manner Implement measures to reduce an iety and agitation !eaching and support of patient and family

!uestion

Is the follo#ing statement !rue or (alse-

Bleeding esophageal varices result in an increase in renal perfusion+

Hepatic *ncephalopathy and oma

* * *

A life>threatening complication of liver disease+ 6ay result from the accumulation of ammonia and other to ic metabolites in the blood

1tagesHsee ,able ./-0 )elow

Assessment

::G

* * * *

'hanges in L<'" assess neurological status freAuently Potential sei@ures (etor hepaticus 6onitor fluid" electrolyte" and ammonia levels Stage 11 1mpending I 'ontinuing mental changes I 6ental confusion I *isorientation to time" place" or person I Asteri is 8hand flapping9 Stage 1+ omatose I 7nresponsiveness" leading to death in most patients progressing to this stage I 7narousable" obtunded I 7sually no response to painful stimulus I /o asteri is I Positive Babins%iJs sign I 6uscle rigidity I (etor hepaticus 8characteristic liver breath Hmusty" s#eet odor9 I 1ei@ures

Stage 1 Prodromal I 1ubtle manifestations that may not be recogni@ed immediately I Personality changes I Behavior changes 8agitation" belligerence9 I :motional lability 8euphoria" depression9 I Impaired thin%ing I Inability to concentrate I (atigue" dro#siness I 1lurred or slo#ed speech I 1leep pattern disturbances Stage 111 Stuporous I Progressive deterioration I 6ar%ed mental confusion I 1tuporous" dro#sy but arousable I Abnormal electroencephalogram tracing I 6uscle t#itching I $yperrefle ia I Asteri is

Medical Management

* * * * * * *

:liminate precipitating cause

Lactulose to reduce serum ammonia levels

I) glucose to minimi@e protein catabolism

Protein restriction

;eduction of ammonia from GI tract by gastric suction" enemas" oral antibiotics

*iscontinue sedatives analgesics and tranAuili@ers

6onitor for and promptly treat complications and infections

Hepatitis

)iral hepatitis: a systemic viral infection that causes necrosis and inflammation of liver cells #ith characteristic symptoms and cellular and biochemical changes+

* * * * * *

A B ' * : $epatitis G and GB virus>'

/on>viral hepatitisHto ic and drug induced

Hepatitis A 2HA+3

%ana&ement

* * * * * * * * *

(ecal2oral transmission

Prevention

1pread primarily by poor hygiene0 hand>to> mouth contact" close contact" or through food and fluids

* * *

Good hand #ashing" safe #ater" and proper se#age disposal )accine e+g+ $avri 0 )aAta Immunoglobulin for contacts to provide passive immunity

Incubation: 35250 days

Illness may last 42K #ee%s

;is% factors:

* *

Bed rest during acute stage

/utritional support

6ortality is 0+5F for younger than age 40 and 3F 24F for those over age 40

6anifestations: mild flu>li%e symptoms" lo#> grade fever" anore ia" later .aundice and dar% urine" indigestion and epigastric distress" enlargement of liver and spleen

Anti>$A) antibody in serum after symptoms appear %ana&ement

Hepatitis ) 2H)+3

!ransmitted through blood found in saliva" semen" and vaginal secretions0 se ually transmitted0 transmitted to infant at the time of birth

Prevention

)accine: for persons at high ris%" routine vaccination of infants e+g+ :ngeri >B0 ;ecombiva >$B

* * * * *

A ma.or #orld#ide cause of cirrhosis and liver cancer

* * *

Passive immuni@ation for those e posed 1tandard precautions?infection control measures 1creening of blood and blood products

;is% factors:

Long incubation period 2 3 to L months

6anifestations: insidious and variable" similar to hepatitis A

* * *

Bed rest

/utritional support

!he virus has antigenic particles that elicit specific antibody mar%ers during different stages of the disease

6edications for chronic hepatitis type B include: alpha interferon and antiviral agents: !enofovir 8Baraclude90 lamividine 8:pivir90 adefovir dipivo il 8$epsera9

*o not give $epsera or !y@e%a if pt+ has co>infections

Hepatitis

%ana&ement Prevention

!ransmitted by blood and se ual contact" including needle stic%s and sharing of needles

1creening of blood

* * * * * *
* * *

!he most common blood>borne infection

* * * *

Prevention of needle stic%s for health care #or%ers 6easures to reduce spread of infection as #ith hepatitis B Alcohol encourages the progression of the disease" so alcohol and medications that affect the liver should be avoided

A cause of 3?E of cases of liver cancer and the most common reason for liver transplant

;is% factors :

Incubation period is variable

1ymptoms are usually mild

Antiviral agents: interferon and ribavirin 8;ebetol9

'hronic carrier state freAuently occurs

Hepatitis $ <nly persons #ith hepatitis B are at ris% for hepatitis * !ransmission is through blood and se ual contact 1ymptoms and treatment are similar to hepatitis B but more li%ely to develop fulminant liver failure and chronic active hepatitis and cirrhosis

Hepatitis *

* * * *

!ransmitted by fecal2oral route Incubation period 352L5 days ;esembles hepatitis A and is self>limited #ith an abrupt onset /o chronic form

(ther Liver $isorders

/on>viral hepatitis

!o ic hepatitis

1s the following statement ,rue or False4 <nly persons #ith hepatitis B are at ris% for hep *+

*rug>induced hepatitis

*
ancer of the Liver

(ulminant hepatic failure

Primary liver tumors

* * *

(e# cancers originate in the liver 7sually associated #ith hepatitis B and ' $epatocellular carcinoma 8$''9

* *

Liver metastases

* * * *

Liver is a freAuent site of metastatic cancer

6anifestations:

Pain" a dull continuous ache in ;7G" epigastrium" or bac% Deight loss" loss of strength" anore ia" anemia may occur =aundice if bile ducts occluded" ascites if obstructed portal veins

Liver ancer

Liver

ancer

/on>surgical management:

1urgical 6anagement:

* * * * * *

7nderlying cirrhosis" #hich is prevalent in patients #ith liver cancer" increases ris%s of surgery

* * *

!reatment of choice for $'' if confined to one lobe and liver function is adeAuate

Liver has regenerative capacity

6a.or effect of nonsurgical therapy may be palliative

!ypes of surgery

;adiation therapy

* * *

Lobectomy 'ryosurgery Liver transplant

'hemotherapy

Percutaneous biliary drainage

<ther nonsurgical treatments

Liver ,ransplantation

* * *

7sed in the treatment of end>stage liver disease" primary malignant neoplasm of the liver

*onor livers obtained primarily from trauma victims #ho have not had liver damage

*onor liver transported to the surgery center in a cooled saline solution that preserves the organ for up to K hours

Liver ,ransplant

5ursing are of the Patient 6ndergoing a Liver ,ransplantation

* * *

Preoperative nursing interventions

Postoperative nursing interventions

Patient teaching

omplications

* * * * * * *

Acute or chronic graft re.ection

Infection

$emorrhage

$epatic artery thrombosis

(luid and electrolyte imbalances

Pulmonary atelectasis

Acute renal failure

Psychological malad.ustment

Pancreas *%ocrine Pancreas

Acini produce:

* * *

Inactive digestive en@ymes !rypsin inactivator Bicarbonate 8antacid9

* *

!hese are sent to the duodenum #hen it releases secretin and cholecysto%inin

In the duodenum" the digestive en@ymes are activated

,ell whether the following statement is true or false# !he e ocrine pancreas produces insulin+ Assessment of the Pancreas

$istory:

* *

Personal?(amily: medical Personal: diagnostic procedures0 surgical0 high ris% lifestyle habits0 nutrition0 prescribed , <!' meds+

'linical presentation:

* * *

e+g+ <nset of pain: post alcohol" high fat meal =aundice" gray>blue discoloration of trun%

Psychosocial: recent stressful events0 alcoholism

http:??pathology+.hu+edu?pancreas?Basic<vervie#3+php-areaMba

Assessment of the Pancreas

* * *

:ffects of Aging > p+ 33K3 'hart 55>3 8already put in beginning of ;!(9

*iagnostic tests > p. 1'(' - 1'()

Lab assessment 7 Table 62-4

Autodigestion of the Pancreas Biliary ;eflu 1. Gallbladder contracts 2. Bile is sent do#n common bile duct 3. Bloc%age forms in ampulla of )ater: bile cannot enter duodenum 4. Bile goes up pancreatic duct 5. Bile in pancreas disrupts tissues0 digestive en@ymes activated

Activated en@ymes begin to digest the pancreatic cells

* *

1evere pain results Inflammation produces large volumes of serous e udate hypovolemia

* *

:n@ymes 8amylase" lipase9 appear in the blood

Areas of dead cells undergo fat necrosis

'alcium from the blood deposits in them

N $ypocalcemia

Autodigestion in Acute Pancreatitis

Acute Pancreatitis

'omplications :

* * * * *

$ypovolemia $emorrhage Acute %idney failure Paralytic ileus $ypovolemic or septic shoc%

* * * *

Pleural effusion" respiratory distress syndrome" pneumonia

6ultisystem organ failure

*isseminated intravascular coagulation

*iabetes mellitus

Table 62 3 Management of Acute Pancreatitis

* * * * * * * * * *

/P<

/G! drainage

Analgesics 2 <pioids 8P'A9

I) (luid , :lectrolytes replacement

$istamine receptor antagonists , Proton pump inhibitors

Antibiotics for Acute /ecroti@ing Pancreatitis

1urgical management 8if indicated9 to treat cause

hronic Pancreatitis

Progressive destructive disease of pancreas characteri@ed by remissions and e acerbations

$ave signs and symptoms similar to acute pancreatitis

<ften have:

* * *

*igestive problems because of inability to deliver en@ymes to the duodenum Glucose control problems because of damage to islets of Langerhans 1igns of biliary obstruction because of underlying bile tract disorders or duct compression by tumors

hronic Pancreatitis

hart .0-0 8ey Features hronic Pancreatitis

Intense abdominal pain 8ma.or clinical manifestation9 that

* * * *
* * * * *

'linical manifestations 2 *HA+T N,T TA-LE .(-(

Abdominal tenderness Ascites Possible left upper Auadrant mass 8if pseudocyst or
abscess is present9 ;espiratory compromise manifested by adventitious or diminished breath sounds" dyspnea" or orthopnea 1teatorrhea0 clay>colored stools Deight loss =aundice *ar% urine Polyuria" polydipsia" polyphagia 8diabetes mellitus9

Lab tests

Imaging

p. 1326-1327

5onsurgical management# *rug therapy Analgesic administration Pancreatic :n@yme ;eplacement !herapy 8P:;!9: BBpancrelipase Insulin therapy /utrition therapy Pancreatic Abscess

Pancreatic Pseudocyst

* * *

'omplications: hemorrhage" infection" bo#el obstruction" abscess" fistula formation" pancreatic ascites

* * * *

6ost serious complication of pancreatitis0 al#ays fatal if untreated

$igh fever

6ay spontaneously resolve

Blood cultures

1urgical intervention after L #ee%s

*rainage via percutaneous method or laparoscopy

Antibiotic treatment alone does not resolve abscess

Pancreatic ancer

Surgical Management

/onsurgical management:

Preoperative care:

* * *

*rug therapy ;adiation therapy Biliary stent insertion

* *

/G tube may be inserted !P/ typically begun

* *

<perative procedure may include Dhipple procedure

Patients 9ith Hepatic & Pancreatic $isorders

* *

Postoperative care:

Identify cultural influences #hich may affect the development and course of treatment of hepatic and pancreatic disorders

* * * * *

<bserve for complications GI drainage monitoring Positioning (luid and electrolyte assessment Glucose monitoring

Identify community > based resources for patients #ith hepatic and pancreatic disorders

9hipple Procedure !he three anastomoses that constitute the Dhipple procedure: choledocho.e.unostomy" pancreatico.e.unostomy" and gastro.e.unostomy+