Week 7 GI NURS 222 -Student

8/13/2019 Week 7 GI NURS 222 -Student

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Tamra Samson RN

NURS 222


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Hemolytic jaundiceCAUSES- increased breakdown of

RBCs (blood transfusions, sicklecell crisis)

Hepatocellular jaundiceCAUSES-damage in liver

hepatocytes so billirubin leaksfrom out

Obstructive jaundice-obstruction

in liver or biliary duct


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Copyright 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

What is Jaundice?

Yellowish skin color resulting fromincreased bilirubinSome form of alteration in a

persons normal metabolism orobstruction in hepatic or biliaryduct.

Its a symptom not a diseaseBilirubin is either unconjugated

(indirect) or conjugate (direct


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Fig. 44-1


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What does Jaundice look like in thebody?

Dark urine secondary to excessbilirubin being excreted by kidneysStools will be light or clay colored.Pruritus (dry skin) due to bile salts

beneath the skin.


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EtiologyHepatitis A-G

Clinicalmanifestations: nos/s, acute phaseinclude malaise,anorexia, n/v, RUQ

pain, hepatomegaly,Lymph involvement


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Viral hepatitis most common.

Hepatitis A (HAV)- fecal-oral route

Hepatitis B (HBV)- Perinatally, IV drug

use, infectious blood, or body fluid

Hepatitis C (HCV)- Most common IV

drug users.


9/66Copyright 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

Inflammation of liver tissueCytotocic cytokines and killer cells

cause lysis of infected hepatocytes.Liver can regenerate with time if no

complications.

Incubation 15-180 days dependingon what type.


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Collaborative care

Drug therapy

Chronic hepatitis B

-Interferon

Nucleosideanalogs

Chronic hepatitis C

Prevention

Hepatitis A Hepatitis B

Hepatitis C



Diagnostic Studies:AST

ALTGGTSerum/urinary bilirubinProthrombin time (PT) prolonged

because of decreased absorption ofvitamin K in intestine with decreasedproduction of prothrombin by liver.



Nutritional Therapy

High calorie, high protein, highcarbohydrate, low fat diets withvitamin supplements


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Nursing assessment?

Nursing diagnoses?

Planning?



ASSESSMENT:

Passed history of hemophilla,exposure, food or watercontamination, transfusion before1992, IV drug use, etc. Miss use ofacetaminophen, other toxic drugs toliver cells.

Functional lifestyle, relationships,

ETOH, weightloss, RUQ pain.



Objective: physical exam

Nursing Diagnosis: imbalancednutrition, activity intoleranceineffective therapeutic regimenmang. (f/u care



What are some ways a nurse canimplement care for a patient withViral Hepatitis?



One of the leading public healthconcerns.

Only definitive way to distinguishforms of hepatitis is presence ofantigens and antigenic subtyples

Nurses could teach preventionUnderstand the types of HepatitisTypes A and B can be prevented and

treated

Type C-no vaccine


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Nursing implementation

Health promotion

Hepatitis A

Hepatitis B

Hepatitis C

Acute intervention

Jaundice

Rest

Ambulatory and home care

Evaluation


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Autoimmune hepatitisWilsons diseaseHemochromatosisPrimary biliary cirrhosisNonalcoholic fatty liver disease and

nonalcoholic steatohepatitis

Clinical manifestations and diagnosticstudies

Collaborative care


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Autoimmune Hepatitis

Chronic inflammation of liver ofunknown cause.Elevated liver enzymes without viral

antigens (no A, B, C, etc.Thought to be caused by

environmental factors or geneticsTreated with corticosteroids and

immunosuppressive agents.


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Wilsons Disease

Neurologic Disease in the presenceof chronic liver diseaseDiagnosic findings: Kayser-

Fleischer rings (brownish red

colored rings in the cornea) seen ineye exam.

Higher levels of Copper levels

Treatment is eliminating Copper inactive disease.


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Hemochromatosis (HH)

Caused by the increased andinappropriate absorption of dietaryiron.

If untreated damage to organs


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Primary Biliary cirrhosis (PBC)

S/S-Pruritus, diarrhea of pale stools,hepatomegaly.Unclear of etiology: genetic and

environmental factors such as

chemical exposure and infection.95% if those diagnosed are womenTreatment-suppress ongoing liver

damage with Actigall.


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Degeneration and destruction ofliver cells.

Liver tries to regenerateNew cells are abnormal due to

scarring and fibrous tissueResulting in abnormal blood

vessel and bile duct functioning


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Alcoholic Cirrhosis-

Large intake of ETOH causesaccumulation of fat in the liver

Resulting in scarring and impaired

functioning


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Postnecrotic Cirrhosis:

Resulting from viral, toxic orautoimmune hepatitis.Broad band scarring in liver


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Biliary Cirrhosis:

Chronic obstruction of biliaryduct/system and infection

Fibrotic liver with Jaundice


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Cardiac Cirrhosis:

Resulting from severe right sidedheart failure, pericarditis andtricuspid insufficiency.


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What would be some of the earlysigns and symptoms we would seewith Cirrhosis?


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GI symptoms: anorexia, nausea,

vomiting, change in bowel patterns(liver is having difficultymetabolizing carbs, fats, proteins).

Dull heavy pain in right upper

quadrant, epigastric area.Enlarged liver and spleen


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Later Signs and Symptoms?


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Jaundice

Skin lesions (livers inability tometabolize steroid hormones)

Hematologic Problems: anemia,

coagulation disorders,thrombocytopenia.

Endocrine problems-livermetabolizes normally (estrogen,testosterone


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Fig. 44-4


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Fig. 44-6


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ComplicationsPortal hypertension and

esophageal and gastric

varicesPeripheral edema and ascites

Hepatic encephalopathy

Hepatorenal syndrome


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Portal Hypertension-Compression and Destruction of the

portal veins.

What do you think happens as a resultof decreased blood flow?


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Answers:

Increased venous pressureAscitesSystemic hypertensionEsophageal varicesGastric varies


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Fig. 44-8

E h l V i


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Esophageal VaricesAs a result of tortuous veins at the

lower end of the esophagus.Little elastic tissue-fragileVaries are responsible for 80%

variceal hemorrhageBLEEDING VARIES LIFE THREATENING

COMPLICATION OF CIRRHOSIS.

E h l V i


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Esophageal Varices

S k Bl k T b


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Sengstaken-Blakemore Tube

A i & P i h l Ed


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Ascites & Peripheral Edema

Peripheral edema results from PortalHypertension, occurring in anklesand presacral area.

Ascites is serous fluid in peritoneal orabdominal cavity. HTN movesprotein to lymph space.

C ll b ti C f A it


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Collaborative Care for Ascites:

Paracentesis-temp. measurereserved to help with breathing

Peritoneovenous Shunt-reinfusion ofascitic fluid into venous system.

P it Sh t


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Peritoneovenous Shunt

Reinfusion of ascitic fluid into thevenous system.

Tube that runs from the peritoneum

under the SQ tissue into the jugularvein or superior vena cava


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Fig. 44-9


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Fig. 44-11


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Nursing assessmentNursing diagnosesPlanning


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What are some ways we can assess forCirrhosis?


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HistoryHealth patterns r/t: chronic ETOH,

weight loss, n/v, anorexia, darkurine, bowel changes, easy bruising,change is skin color, dull pain in

RUQ or epigastric, sexualdysfunction

Skin changes, abdominal girth size,

foul breath, enlarged liver, speen.


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What would be some nursingdiagnoses?

Imbalanced nutrition


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Imbalanced nutrition

Impaired skin integrity

Excess fluid volume

At risk for Hemorrage

Planning:


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Planning:

Decrease discomfortPrevent complicationsReturn to active living when possiblePrevention in relation to causes:

ETOH, exposure to viral causes.

Hepatic Encephalopathy


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Hepatic EncephalopathyNeuropsychiatric complication ofliver damage.

Ammonia enters systemic circulation

Crosses the blood brain barrier

S/S-confusion, agitation, slurred

speech, respiratory changes, reflexchanges. CLASSIC SIGN: Asterixis


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How would a nurse assess a patientwith asterixis?

Asterixis (flapping tremors)


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Asterixis (flapping tremors)

When asked to hold hand and armsstretched out.the patient can nothold this position shows flexion andextension of the hands.


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What might be the focus of nursingcare for patients with HepaticEncephalopathy?

Provide a safe environment


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Provide a safe environment

Assist with monitoring andmeasures to reduce ammonia levels

Neuro checksGive medications as ordered such as

laxatives to decrease ammonialevels by excretion.

Pancreatitis


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Pancreatitis

Inflammatory process of thepancreas.

Common causes: biliary tract

disease in women, alcoholism inmen.

Less common: trauma, viral, after

surgical procedures

Pathogenic mechanisms:


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Pathogenic mechanisms:

Body responses by activation ofpancreatic enzymes resulting inautodigestive of enzymes.

Injury to pancreatic cells


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What clinical finds might a nursefind in a patient with Pancreatitis?

Left upper quadrant pain could be


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Left upper quadrant pain, could bemidepigastric pain.

Sudden onset: severe, steady,constant pain

Flushing of the skin, dyspnea, n/v,tachycardia,

Guarding of the abdomenDecreased bowel sounds Ileus


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What might be some of the orders anurse would be given in an acutesetting?

Monitoring vital signs more


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Monitoring vital signs morefrequently.

Respiratory distress, lung sounds(retroperitoneal fluid raises thediaphragm)

Monitoring electrolytes


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NPO status with possible NG tube

Mental status changes

Pain management

Week 7 GI NURS 222 -Student

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