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Flashcards in medicine-hepatic disorders Deck (110):

function of liver in relation to metb
what is nec for the proper processes to take place

Takes glucose from portal vein and converts it to glycogen which is stored for later use. Can synthesize additional glucose (gluconeogenesis) from amino acids or protein breakdown or lactate from exercising muscles. When this gluconeogenesis uses protein it has ammonia as byproduct (also produced by bact in intestines). liver converts this ammonia to urea

protein metb-syntheizes all plasma proteins but gamma globulins. Vit K nec for synthesis of prothrombin and some clotting factors

fat-makes bile in hepatocytes and the bile salts help breaks down fatty acids for prod of energy and ketone bodies when strving or uncontrolled DM. Synthesizes cholesterol, lecithin and other lipoproteins

drugs and hormones metb by liver


what does the liver produce

what storage functions does liver have

what excretory functions does liver have

Synthesizing plasma proteins, nonessential amino acids, Vit A and essential nutrients such as iron, Vit D, B12, bile

STORES vit A, B, D and B complex, iron, copper
also glycogen etc

bilirubin (made from hgb) gets conjugate by hepatocytes and becomes bile excreted in stool and can be excreted by urine


where is bile made, stored and conc? when is the bile signalled to release
wat quadrant is this in?
what does biliary sludge possibly lead to

Bile is made in liver & stored & conc in gal bladder. When we eat fatty foods it signals bile duct to open &emulsify fats
liver and gallbladder in R upper quadrant

biliary sludge-tiny stones, sludgy bile that can block the bile duct. With this erosion etc it canleak out into sterile cavityautodigestion that can lead to sepsis


how is liver fx measured

can you rely just on these tests? why?

• Fx measured in terms of serum enzyme activity (serum aminotransferases, alkaline phosphatase, lactate dehydrogenase) and serum concentrations of proteins (albumin and globulins), bilirubin, ammonia, clotting factors and lipids

cant just rely on the tests because other disorders can affect test results


pigment studies: eg bilirubin, urine bilirubin, fecal urobilinogen what do they meas and when would they be abnormal (in gen)

meas ability of liver to conjugate and excrete bilirubin

abn in liver and biliary tract disease and assoc w jaundice clinically


protein studies eg serum albumin, serum globulin

what affects either albumin or globulin

the normal ratio of albumin to globulin is A1.5:G1 or A2.5:G1 how is this affected in chronic liver disease

proteins made by liver

albumins are affected by cirrhosis, chronic hep, edema, ascites

globulins affected by cirrhosis, liver disease, chronic obstr jaundice and viral hep

in chronic liver disease the globulin ratio is higher and albumin dec


how would prothrombin time be affected by liver disease

PTT may be prolonged w liver disease


are serum aminotransferases better for detecting acute or chroni liver disease

which serum aminotransferase is elevated in acohol abuse

when does ALT elevate and what can it be used for
is it specific to liver


alcohol abuse elevates GGT

• ALT inc primarily in liver disorders, might help monitor course of hepatitis or cirrhosis or effects of tx that may be toxic to liver
yes mostly for liver


wwhen does AST elevate and what can it be used for
is it specific to liver

• AST- present in the tissues that have high metabolic activity, so inc if death of tissues of organs such as heart, liver, skeletal muscle and kidneys.
o Although not specific to liver disease, may be high in cirrhosis, hepatitis, and liver cancer


which serum aminotransferase indicates cholestasis and what else is it used for

• GGT- high levels are associated with cholestasis and can also be due to alcoholic liver disease. min value in liver disease is confirming hepatic origin of elevated alkaline phosphatase level


when would cholesterol levels be inc and dec

cholesterol inc in biliary obstr and dec in parenchymal liver disease


what are the major complications of liver biopsy and what must be done and treated before biopy

when would biopsy not be preferred method

how is the biopsy done

• Bleeding and bile peritonitis after liver biopsy are major complications so coagulation studies done before. so do coag studies and treat before the biospy

if there is ascites or coag abn might do other method

can use needle biospy, percutaneous with U/S or transvenously, or laparoscopically


specific nursin considerations for percutaneous needle biopsy

coag studies and blood standing by

have pt breathe deeply a few times and then hold breath at end of expiration. quick iopsy is done


other diagnostics for liver

US, MRI, CT and radioisotpe liver scan, laparoscpoy


liver disease more common in men or women?
most common cause of parenchymal damage?
acute or chronic liver issue more common?

• men 2x more
• Most common cause is from malnutrition, especially r/t alcoholism
• May be acute or chronic. Moreso chronic


most common and significant mnfts of liver disease

why do nutritional def arise

• Most common mnfts: jaundice, portal htn, ascites and varcites, nutritional def, and hepatic encephalopathy

nutritional def, due to inabiity of damamged liver cells to metb certain vitamins


how do parenchymal cells respond to most noxious agents

• Parenchyma cells respond to most noxious agents by replacing glycogen w lipids, producing fatty infiltration w or without cell death or necrosis. Commonly associated w inflammatory cell infiltration and growth of fibrous tissue


why can jaundice occur

what are the types

what is the risk of severe jaundice

• Results from impairment of heptic intake, conjugation of bilirubin, or excretion of bilirubin into the biliary system
• Types of jaundice: hemolytic, hepatocellular and obstr jaundice, and jaundice d/t hereditary hyperbilirubinemia

prolonged jaundice can lead to pigment stones in gallbladder and vv bad jaundice eg 10x normal i risk for brainstem damage


where and why is bilirubin conjugated

in hemolytic jaundice is the bilirubin conjugated or unconjugated. what about fecal and urine biliinogen
are there major mnfts or complic

hepatocytes remove bilirubin from bllod and chemically conjugate it to glucuronic acid that makes it more soluble in aqueous soln then gets carried in bile into duodenum

its mostly unconjugated. • Fecal and urine urobilinogen levels are inc but no bilirubin in urine
not gen major mnfts or complic


hepatocellular jaundice
would serum aminotransferases be affected
does the jaundice cause mnfts? what if its prolonged?

• AST and ALT inc- indicating cellular necrosis

• In prolonged jaundice, cell damage develops so both ypes of jaundice (obstr and hepatocellular) appear together
• May be mildy or severely ill, w lack of appetite, nausea, malaise, fatigue, weakness, and possibly wt loss
• Pt may report- headache, chills, fever


what can cause obstr jaundice

• Maybe caused by the occlusion of the bile duct from a gallstone, an inflm process, a tumor, or pressure from an enlarged organ (liver, gallstone)
• May also involve small bile ducts within the liver
• Intraheptiacobstr from stasis and thickening of bile within the canliculi may occur after ingestion of certain medications (cholestatic agents)
o agents include phenothiazines, antithyroid meds, tricyclic antidepressant agents, androgens and estrogens


what happens in obstr jaundice

how are AST, ALT, GGT Affected?

• bile cannot flow normally into the intestine and become backed up into the lvier substance, it is then reabsorbed into the blood and stains the skin, mucous membranes and sclerae. (whether it is intrahepatic or extrahepatic)

o AST, ALT< and GGt levels rise only moderately but alkaline phosphate and bilirubin are elevated


mnfts of obstructive jaundice

o it is excreted in the urine which becomes deep orange and foamy. Bc of dec amount of bile in the intestinal tract, stools become light or clay coloured
o skin may itch intensely- baths help
o dyspepsia and intolerance to fatty foods may develop bc of impaired fat digestion in the absence of intestinal bile


hereditary hyperbilirubinemia
when does this happen physiologiclly?
names of the syndromes?

benign’ cholestatis jaundice of preg w retention of conjugated bili, prob secondary to unusual sensitivity to hormones of preg
also beign recurrent intrahepatic cholestasis

• Gilberts syndrome is familial disorder char by inc level of unconjugated bilirubin that causes jaundice
Serum bili is inc but everything r/t liver is normal and no hemolysis
caused by inborn errors of biliary metb=
• Dubin-johnson syndrome (chronic idiopathic jaundice w pigment in the lvier)
• Rotors syndrome (chronic familiar conjugated hyperbilirubinema without pigment in the liver)


2 major conseuqences of portal HTN

• two major consequnces: ascites and varices


why is ascites cyclical

-- means it leads to

cirhosis w portal HTN--splanchnic arterial vasodilation--dec in circ blood vol--activation of RAA and SNS and ADH--kindey retains Na and H20--hypervolemia--persistent activation of systems for retention of Na and H20; ascites and edema formation--continued arterial underfilling and the cycle repeats

inc in cap p and obstr of venous blood flow through the damaged liver and vasodilation that occurs in the splanchnic circulation (arterial supply and venous drainage og GI system from distal esophagus to the midrectum including liver n spleen)
• liver cant metb aldosterone so inc sodium and h2o retention- inc intravascular vol, inc lymph flow and dec synthesis of albumin by damaged liver contribute to movement of fluid into peritonral space
• process becomes self-perpetuating- loss of fluis into spaces causes further sodium and water retention by kidney to maintain vascular vol


what does the liver fail to metb that contributes to dev of ascites

aldosterone leads to inc sodium and water retention


how much fluid can be in abd in ascites. is it just water in the peritoneal caivty? what else and how does this affect osmotic P

• large amounts of albumin rich fluid, 15 L or more, may accumulate in peritoneal cavity as ascites
• osmotic p decreases and with inc portal pressure more movement of fluid into peritoneal cavity


mnfts of ascites

what would you see if percusion or if pt was supine

what can you do daily to assess inc of ascites?

• inc abdominal girth and rapid weight gain
• Pt may be short of breath
• striae& distended veins may be visible,
• Umbilical hernias also occur,
• Fluid and electrolyte imbalance

• Percussion of abd- for shifting dullness or by detecting fluid wave fluid wave is likely to be found if large amounts of fluid)
• Flanks bulge in supine
• Daily measurement


medical mgmt of ascites (headings)

Dietary modification:
bed rest
transjugular intrahepatic portosystemic shunts

• spironolactone an aldosterone blocking agent is most often first line therapy. it is K sparing
• oral diuretics such as furosemide may be added but be cautious bc long term- hyponatremia could occur


diet considerations of ascites
if this fails what is next line of tx

• Negative sodium balance to reduce fluid retention
• Might be reduced to 500mg if accumulation is not controlled.
diuretics if not controlled by Na restriction


which diuretic is first line Tx of ascites and why? what might be used in conjunction and what lyte is a concern with this

what is max daily wt loss if pt has ascites

complic and why

• spironolactone an aldosterone blocking agent is most often first line therapy. it is K sparing
• oral diuretics such as furosemide may be added but be cautious bc long term- hyponatremia could occur

• daily wt loss should not exceed 1-2kg w asicites and peripheral edema or .5-.75 kg wout edema

• possibly complications: fluid and lyteimb and encephalopathy (enceph d/t dehydration nd hypovolemia. when K is depleted ammonia inc)


with bedrest is upright pos better for pt with ascites

• upright position is associated with activation of the R-A-A system and SNS
• causes reduced renal glomerular filtration and sodium excretion and dec response to loop diuretics


paracentesis as Tx of ascites
is it commonly done
how much can you take out
what must it be in combo with and why?

now mostly done for diagnostic exam
• Large vol (5-6L) have been shown to be a safe method for treating patients w severe ascites
• This technique in combo w IV infusion of salt poor albumin or other colloid is standard mgmt. the albumin helps correct dec in effective arterial blood vol that leads to NA retention and makes pt more hemodynamically stable after Tx and prevents reaccum of fluid


Transjugular intrahepatic portosystemic shunt (TIPS)
as tx for ascites

• To reduce portal htn, stent inserted to serve as an intrahepatic shunt between the portal circulation and hepatic vein
• Treatment of choice for refractive ascites
• works well to Dec Na retention, improves renal response to diuretic therapy, and preventing reccurence of fluid accum


nursing mgmt of ascites

• Assessment and documentation of I and outs, abd girth, daily weight
• Monitors serum ammonia and e- levels


what is the major risk for pt during paracentesis and therefore what should be meas very frequently

meas BP


what is the most sginificant source of bleed in cirrhosis

esophageal varices


how do varices dev

what other liver complication might they inc risk of

• Develop in majority of patients w cirrhosis
• Varicosities that develop from elevated p in the veins that drain into the portal system
• Prone to rupture and are often the source of massive hemorrhages from the upper Gi tract and the rectum
• Once they form, they inc in size and eventually bleed

the inc bleeding mightinc nitrogen load and ammonia leading to hepatic encephalopathy


what puts pt at risk of hemm from varices

• Factors that contribute to hemorrhage- muscular exertion from lifting heavy objects, straining at stool sneezing, coughing, vomiting, esophagitis irritation of vessels by poorly chewed food, reflux of stomach contents, meds that erode esophageal mucosa or interfere with cell replication


mnfts of varices

if pt is suspected of bleeding from eophageal varix is it gen true

• Hematemesis, melena, or general deterioriation in mental or physical status and often have a hz of alcohol abuse
• S&S of shock

30% of pts are actually bleeding form other source


diagnostics for esophageal varices

• Endoscopy used to identify the bleeding site, along with barium swallow, ultrasonography, CT and angiography


consideration with endoscopy and giving fluids

gag refex must return beore can be done safely


when might portal HTN be suspected

if dilated abd veins and hemorrhoids detected
splenomegaly ad ascites may be present


lab tests for esophageal varices

• May include various liver function tests such as serum aminotransferases, bilirubin, alkaline phosphatase and serum poteins
• Splenoportography, which involves serial or segmental x rays is used to detect extensive collateral circulation in esophageal vessels which indicate varices


medical mgmt of varices

• Usually transferred to ICU for close monitoring
• Signs of hypovolemia are noted
• Volume of circulating blood is estimated and monitored with CVC or pulmonary artery catheter
• BP monitored via an arterial catheter
• O2
• IV fluids with e- and volume expanders
• Transfusion of blood
• Don’t want to overhydrate bc would raise portal pressure and inc bleeding
• Indwelling catheer inserted
• Nonsurgical treatment preferred


pharm for esophageal varices

• Propranolol and nadolol,
• Vasopressin may be intitial mode of therapy in urgent situations bc produces constriction of the splanchnic arterial bed and decreases portal pressure
• Vasopressin constricts distal esophageal and proximal gastric veins, thus reducing the infow into the portal system and portal p
• Somatostatin and octreotide have been reported to be effective in decreasing bleeding from esophageal varices and they lack the vaoconstrictive effects of vasopressin


name of Tx that directly exerts P on esophageal varices to control hemmorhage
how does it work
how is bleeding detected

Balloon Tamponade
• Pressure exerted on the cardia (upper orfice of stomach) and against the bleeding carices by a double ballon tamponade that is inflated with air and might have trction applied
• Tube has 4 opening: gastric aspiration, esophagea aspiration, gastric balloon inflation and esophageal balloon inflation
• Irrigation of the tubing is performed to detect bleeding, if bleeding continues- inflate more. Desired p is 25-40mmHg


max amount of time for balloon tamponade to be in for
what are complications

• No longer than 24 hours
• Displacement of tube and inflated balloon into oropharynx can cause life-threatening obstr of the airway and asphyxiation- may occur if patient pulls tube
• Sudden rupture of airway can cause airway obstr and aspiration of gastric contents into lungs
• Ulceration and necrosis of nose, mucosa of stomach or esophagus may occur if in there too long or inflated too high


nursing interventions for balloon tamponade

freq mouth and nasal care, oral suction. Pt in ICU


aside from balloon or drugs what are other medical Tx for esophageal varices
what is the major risks of each

Esophageal banding therapy (variceal band ligation)
• A modified endoscope laoded with an elastic rubber band is passed through an overtube directly onto the varix to be banded
--dysphagia, ulceration etc

Endoscopic Therapies
• Injection sclerotherapy, a sclerosing agent is injected through a fibreoptic endoscope into the bleeding esophagealvarices to promtote thrombosis and eventual sclerosis
--bleeds, perforation, aspiration pneumonia, esophageal stricture

Transjugularintrahpetic portosystemic shunting
• Can effectively control acut variceal hrmorrhage by rapidly lowering portal p. indicated for pt who rebleed after loharmacologic or endoscopic prphylaxis
--bleed, sepsis, HF, perforation, thrombosis

Surgical mgmt.
• Procedures- direct surgical ligation of varices, splenorenal, mesocaval, and portacaval venous shunts to relieve portal pressure and esophageal transection w devascularization


if surgically performing shunting or other sx for varices the pt has high risk of complications. what are theyÉ

• High incidence of encephalopathy after the surgical shunting proedures

hypovolemic or hemm shock
lyte imbal
metb and resp alkalosis
alcohol withdrawal
bleeding may recur as collateral vessels dev


nursing mgmt of pt with varices

• Vitals. Pay extra attention to BP
• Emotional responses, cognitive status
• Nutritional ad neurologic status.
• Signs of hepatic encephalopathy (from drowsiness and confusion to profound coma)
• Gastric suction if complete rest of eseophagus
• Oral hygiene from thirst
• Vit k from blood loss maybe and transfusions may be given
• Dec anxiety w calm and quiet
• It pt was heavy ETOH user then theres possibility of delirium secondary to alcohol withdrawal


is hepatice ecnecphalopathy reversible
what is it
is it overtlly manifested

• This reversible metb form of encephalopathy can improve w liver fx
is the neuropsychiatric mnft of hepatic failure assoc w portal HTN and shunting of blood from portal venous sys into systemic circulation
• Insidious, subtle onset


patho of hepatic encph

• Hepatic insufficiency may result in encephalopathy d/t inability of liver to detoxify toxic byproducts of metb
• Portal systemic shunting allows elements of portal blood (w toxic substances) to enter systemic circ
• Ammonia is a major etiologic factor as it enters the brain and stimulates GABA which depresses CNS. Ammona inhibits neurotransmission and synaptic regsleep and behav patterns assoc w hepatic encephalopathy


what factors inc risk of hepatic encephalop

• Proteins are largest source of ammonia.
• Ammonia inc from bleeds (like esophageal varices, Gi bleeds), high protein diet, bact infect, septicemia.
• Alkalosis or hypokalemia also inc absorption of ammonia
• Unrelated to ammonia other factors that hep encephalopathy are: excess dieresis, dehydration, infect, sx, fever, meds (sedatives, tranquilizers, analgesics, diuretics thatK loss)…high serum levels of manganese, changes in circulating dopamine and other NTMs.


nursing Dx in order of progression for hepatic enceph

• Activity intolerance, self-care deficit, disturbed sleep pattern, impaired social interaction, ineffective role-performance, risk for injury, imbalanced nutrition, impaired mobility, impaired verbal communication, risk for aspiration, impaired gas exchange, impaired tissue integrity, disturbed sensory perception


mnfts of hepatic encephalop

• Earliest are minor mental changes and motor disturbances..confused and unkempt w altered sleep/moodeg sleep in day and insomnia. These changes are progressive to coma and seizures
• Asterixis flapping tremor of hands occurs in stage II. Get pt to do handwriting sample daily to track. Inability to reproduce a simple figure is constructional apraxia
• In early stages DTRs are hyperactive but as condition worsens the reflexes disappear and extremities get flaccid
• Fetor hepaticus-sweet, slightly fecal odour to breath. Like acetone or old wine.


pt has hepatic enceph what should they be referred for

what EEG findings will they have

liver transplant as it has low survival rate

• EEG shows generalized slowing, inc in amplitude of brain waves and characteristic triphasic waves


which drugs might be given to hep enceph pt and why or how do they work

• Glucose to minimize protein breakdown, vitamins for deficiencies and lyteimbal corrections (esp K)
o benzo antagonists like flumazenil may be given.
• Abxeg Metronidazole that dec levels of ammonia forming bact in colon
• Lactulose is given to dec serum ammonia.


lactulose as tx of hep enceph
how does it work and what to assess

It promotes excretion of ammonia in the stool by 1: making ammonia enter the colon from blood 2: evacuating bowel to dec ammonia absorbed 3: fecal flora changed to orgs that don’t prod ammonia from urea. 2-3 soft stool preferred..this shows the lactulose is working. Monitor this pt closely for dev of watery diarrheal stools (too much lactulose). Also for hypokalemia and dehydration. SE of lactulose are intestinal bloating and cramps


beyond giving drugs what other principles of mgmt for hep enceph

• Other principles of mgmt
o Assess neuro
o Mental status monitored w daily handwriting and arithmetic
o I/O and daily wts
o VS q4
o s/s of Infect of peritoneum and lungs assessed freq and abn reported
o serum ammonia monitored daily
o protein restricted in comatose or those unresponsive to tx. Don’t restrict protein 1g/kg LTerm
o enteral feeds for PSE that’s persistent
o gastric suction, enema, oral Abx to dec absorption of ammonia from GI


why is hep enceph pt at risk of resp compromise

dt depressed LOC in later stages


other mnfts of hepatic disorders (headings)

Edema and bleeding
• Generalized bleeds d/t hypoalbuminemia. Dec prod of clotting factorsinc bruising, epistaxis, Gi bleeds, wounds bleeding
Vitamin def
Metb abn
Pruritus/skin changes


what kind of vit deficiencies might liver pt face
what supplements will they get

• Dec prod of several clotting factors might be d/t dec absorption of vit K. liver cant use vit K to make prothrombin
• Fat soluble Vits A, D, E absorption might be impaired d/tdec bile salt secretion
• All pts w chronic liver disease, esp if ETOH related, will be supplemented with vits A, B, C, K, folic acid


metb abn of liver pt

what results
how are drugs affected

• Abn of glucose etb: might have abn high BG after meal, but hypoglycemia might occur during fasting d/t dec hepatic glycogen reserves and dec gluconeogenesis
• Dec med doses as liver cant metb so well
• Endocrine abn from pormetb of hormones eg ant inactivate Egynecomastia, menstrual irregs, loss of pubic hair, mestrual irreg, disturbances of sual fx and sex char


skin mnfts of alcoholic liver disease

other mnft of skin if biliary obstr

• Spider angiomas-smvascularities resembling spider’s legs. Assoc w cirrhosises from ETOH. Palmar erythema as well

pruritus d/t bile salt retention


what is viral hep

is viral hep easy to transmit

which viral heps are transmitted fecal oral

• Viral hep is systemic viral infectthat has 5 types, ABCDE

• Hep is easily transmitted

A and E


who is leikley to get hep A

how is hep A transmitter. is it from blood

do pts gen recover

how long does it gen last

if pt has jaundice are they infectious

kids and travelers to endemic countries

• HAVcanbe contracted fecal-oral, from food or water, sex (oral-anal). Not gen transmitted via blood

yes, most recover and 0.5% mortality

4-8wks duration

if pt has jaundice they are likely not infecitous as its present only briefly in serum


mnfts of hep A (do we really need to differentiate these tpes)

• May occur without symptoms, Anicteric (without jaundice); flulike illness
• Preicteric: anorexia (often severe), headache, malaise, fatigue, fever
• Icteric: dark urine, jaundice of sclera and skin, tender liver
pt may dev very strong aversion to strong odours


which organs are affected by hep A

how to determine if past or present infect

• Liver and spleen moderately enlarged for few days after onset
• Other than jaundice, few other signs
• May find hep A Ag in stool. Can analyze immunoglobulins to determine if past or present infect


prevention of HAV

is there risk of chronic hep, cirrhosis, hepatic CA

• Handwash, HAV vaccines (Havrix and Vaqta)

HAV and HEV both dont inc the risks of these conditions


nutrition for all viral hep

should they be active

o For all viral hep follow these dietary recomendations: smfreq meals, 2000-3000cal/day, restrict fat, monitor fluid balance, might need enteral feeds if N and anorexia persist, avoid ETOH (for all hep avoid for 6mo after recovery), avoid meds and substances that affect liver fx

• Bed rest then gradual, progressive activity


nursing mgmt of HAV

• Gen at home unless severe
• Nurse helps pt to cope w the fatigue & seek help if health worsens, teach about diet, rest, lab work, avoid ETOH, sanitation to prevent spread


HBV transmission
severity or chance of recovery
what can it progress to

• Mostly transmitted by blood, also in saliva, semen,vag secretions, breaks in skin, mom-infant at birt
• long incubation (up to 160 days) which inc risk of transmission. Majority who contract HBV recover spontaneously in 6mo.
• Mortality up to 10%, 10%carrier state or get chronic hep, hepatocellular injury and inflm or even carcinoma and cirrhosis.


HBV is it always clinically visible
what are mnfts

• Like HAV but lasts 1-6mos
• May be insidious and variable. Can have subclinical episodes

• Arthralgias& rash, decappetitie, dyspepsia, abdm pain, gen aching, malaise, weakness. Potential jaundice accompanied by light colour stools and dark urine. Liver tender and enlarged to 14cm vertically. Spleen palpable. Posterior lymph nodes might be palpable


significance of antigenic particles of HBV

• HBVConsists multiple antigens that each elicit a particular Ab egHHBc,s,e,x and they all arise and are testable at diff times (can gauge progression)


prevention of HBV

screen blood for HBV, r
Active immunization:Hep B vax-universal vaccines often given 4th grade. Should be given to those w HCV. Nurses/others at high riskeg IVDU should get active immunization

Passive immunity:Hep b Immune globulin—indicated for those exposed to HBV who’ve never had HBV and never received HBvaxeg exposed to splash to mucous membrane should get the globulin within hrs to days of exposure or perinatal (infant should get immune globulin within 12hrs of delivery)


medical mgmt of HBV

• Alpha interferon. SE, bone marrow suppression, thyroid dysfx, alopecia, bact infect
• Antivirals: lamivudine and adefovir, oral nucleoside analogs
• Maybe antacids or antiemetics
• Bed rest until symptoms go away
• nutrition. Proteins might be restricted
no ETOH or shellfish


HCV transmission

how do symptoms compare to HBV

is chronic carrier likely

• Transmitted by blood & products, contaminated eqpt eg drug gear, needlestick, sex, inc risk w STD

• Incubation 15-160days. Course similar to HBV & usually just mild symptoms

yes chronic carrier often


Tx of HCV

is there benefit from rest, diet, vitamins

can they have small amounts ETOH

• Interferon & ribavirin (Hemolytic anemia is most common SE)

No benefit from rest, diet, Vitamins

• Sm amounts of ETOH cause progression.


who is at risk of HDV

how is it Dx


• HDV (delta agent) requires hep B surface Ag for replicationonly those w HBV are at risk

• Anti-delta antibodies in presence of HBAg confirms Dx

transmitted: IVDU, dialysis, blood transfusions. sex w hep B t is important mode of transmission between B and D


mnfts of HDV how are they similar to HBV nd how are they different

like HBV except more likely to get fulminant hepchroni active hep& cirrhosis


what is almost always present with HEV.
how is HEV transmitted
what is it gen similar to
is there a chronic state


transmitted feca oral-gen in water

gen resembles HAV

no chronic state


hep G virus and GB virus C. what are they

risk factors similar to what

does it lead to progressive liver disease

two isolates of same virus

risks like hep C

doesnt dev to progressive liver disease


what is nonviral hep

how do meds relate to this

• Certain chemicals have toxic effects eg tetrachloride, phosphorous, chloroform, gold compounds (true hepatotoxins)
• Many meds can induce hep but are only sensitizing


toxic hepatitis how does it present intiially

how to differentiate from viral hep

is recovery likely

• At onset it resembles viral hep

• Do thorough hx to identify cause as Recovery rapid if hepatotoxin removed&exposure was limited but if prolonged then fulminant hepatic failure &pt will die without liver transplant


what is most common cause of acute liver failure

drug induced liver disease

mostly from tylenol


do mnfts of sensitivity to med occur on first day of use only

how do the symptoms present

if you see fever, rash, pruritis what do you do

• Sympt may occur on first day of taking drug or appear months later

• Sympt onset rapid: chills, fever, rash, pruritis, arthralgia, anorexia, nausea; later jaundice, dark urine, enlarged + tender liver

• See fever, rash, pruritis D/C drug immed


what is fulminant hepatic failure

what are intiial symptoms

is this more serious than chronic liver failure

• = clinical syndrome of sudden + severely impaired liver fx in previously healthy person

• Develops w/in 8 weeks of onset of jaundice (first symptom); also see profound anorexia at start

yes, much worse prognosis than liver failure


what causes fulminant hep failure

• Viral hep is common cause
• Others: toxic meds, chemicals, metb disturbances, structural changes


what are the problems that arise in fulminant hep failure

tx of choice

• Accompanied by coag defects, renal failure, lyte disturbances, CV abn, hypoglycemia, encephalopathy + cerebral edema

• Need rapid intervention, transplant


what is the major concern with the ast stage of hepatic encephalopathy

• Edema in brain huge concern w stage 4 encephalopathy. Cause not fully understood (disrupted bbb + plasma leakage into CSF poos) – risk of ICP
o Need ICP monitoring, careful fluid balance + hemodynamic assessments, mannitol, quiet enviro; sedation


what is hepatic cirrhosis and what are the 3 types

• Cirrhosis = chronic disease; liver tissue replaced w diffuse fibrosis  disrupts liver struct + fx
• 3 types:
o Alcoholic cirrhosis – scar tissue surrounds portal areas; most common type
o Postnecrotic: after acute viral, broad bands of scar tissue
o Biliary: scarring around bile ducts; much less common


who is hepatic cirrhosis more likely in and what is most common cause

• Alcohol = the major causative factor; malnutrition also involved

• 2x more men affected; typically 40-60yrs old


hepatic cirrhosis course

• Insidious onset, over 30yrs or so


mnfts of hepatic cirrhosis



vague, from failure to synthesize proteins, clotting factors, those of portal htn
o Intermittent fild fever, vascular spiders, palmar erythema, unexplained epistaxis, ankle edema, vague morning indigestion, flatulent dyspepsia, abd pain, firm enlarged liver, splenomegaly

• Decompensated: ascites, jaundice, weakness, muscle wasting, weight loss, contin mild fever, clubbing of fungers, purpura, sponteous bruising, epistaxis, hoTN, sparse body hair, white nails


with hepatic cirrhosis does the liver shrink with fibrosis then enlarge with fat

no the reverse


aside from compensated and uncompensated mnfts of hepatic cirrhosis what are the major issues

-liver enlargement
-portal obstr nd ascites--leads to indigestion and alt bowel fx
-infection and peritionitis--in absence of source of infect (spontanous bacteria peritonitis dét translocation of intestinal flora)
-GI varies (caput medusae and varices or hemmorhoids)
-edema dt dec albumin prod
-vit def and anemia (chronic gastritis and impaired GI fx lead to anemia) makes pt very tired
-mental deterioration--encephalopathy + poss hepatic coma


what is hepatorenal syndrome and what can cause it

spontanous bacterial peritonitis dét translocation of intestinal flora can cause it
its unresponsive to fluid or diuretic and is char by lack of pathologic changes in kidney with no evidence of dehydration or obstr of urinary tract or any other renal disorder


with hepatic cirrhosis how are lab values affected

• Serum albumin dec, globulin inc
• Alkaline phosphatase, AST, ALT, GGT elevated
• Serum cholinesterase dec
• PT prolonged
• Bilirubin up


how is hepatic cirrhosis diagnosed

what might ABGs show

liver biopsy

ventilation perfusion imbal and hypoxia


medical mgmt of hepatic cirrhosis


• Based on symptoms
• Antacids + H2RA for GI distress
• Vit + nutritional supplements
• K+ sparing diuretics for ascites (this kind chosen b/c limit fluid + electrolyte imbalances)
• Adequate diet + avoidance of alcohol essential
• Cirrhosis can’t be reversed but can be stopped
• Colchicine (anti-inflm used for gout) may help
• Many meds proven to be antifibrotic for tx of cirrhosis: ACE inhibitors, statins diuretics, immunosuppressants,
• ESLD w cirrhosis pt’s use herb milk thistle to treat jaundice + other symptoms – healing + regenerative properties for liver disease


headings of nursing mgmt of pt with cirrhosis

promoting rest
improving nutrition
skin care-
dec risk of injury


why does cirrhosis pt have impaired skin integrity

what to do

d/t subcut edema, immobility, jaundice, itch, susceptibility to skin breakdown and infect

• Freq position changes
• Non-irritating soaps, avoid adhesive tapes
freq skin checks, ROM exercises and elevate edematous limbs


diet and nutrition for cirrhotic pt
high or low protein

• High protein diet if no ascites, edema, or signs of impending hepatic coma
• Supplements: A,B,C,K
• Pt encouraged to eat – small may be better if ascites
• If profound ascites or vom, enteral or parenteral feeding may be necessary
• Folic a + iron to prevent anemia
• If impending coma/encephalopathy, protein stopped
ice collar if nausea
enc fluids for BMs
• Sodium reduction if ascites


why is cirrhotic pt at risk of injury
how to prevent injury
what to assess

alt clottig and LOC
may give Vit K, pad siderails
s/s of shock, stool for blood, emesis,


why might cirrhotic pt have temp?

d/t inflm or hepatitis


what are potential complications of cirrhosis

• Bleeding + Hem
• Hepatic Encephalopathy: monitor deterioration of mental status; lyte levels important as increases risk
• Fluid Vol excess


why does irrhotic pt have risk of FVE

o Liver failure at risk of CV abn d/t inc CO + dec PVR (poss d/t release of vasodilators) hyperdynamic circ state + plasma vol increases (seems like is not entirely understood, see top of 1232 second column)
o Pulm complications also result d/t FVE