Disorders Of The Hepatic System- 20%

Front 1

Demonstrate understanding of Hepatitis -

Types:

Transmission: (way to remember letters with a VOWEL are all feacal/oral)

pathophysiology:

treatment:

Back 1

Pathophysiology:

Hepatitis, meaning like this inflammation of the liver, most commonly comesabout because of a virus. These viruses tend to target the cells in the liver.And when they get in and infect these cells, they tend to cause them to presentabnormal proteins via the MHC class 1 molecules, and at the same time you’vealso got immune cells infiltrating the liver and trying to figure out what’sgoing on, and so the CD8+ (positive) T-cells recognize these abnormal proteinsas a sign that the cells are in danger, and the hepatocytes then go throughcytotoxic killing by the T cells and apoptosis As someone’s hepatitis progresses, we seeclassic symptoms related to immune system mounting an attack such as fever,malaise and nausea additionally patients may also be presented with‘hepatomegaly’ where their liver is abnormally large from inflammation, whichmay also cause pain

types: hep A to E

HAV- (Hepatitis A Virus)

transmission:

the faecal-oral route; thatis when an uninfected person ingests food or water

pathophysiology:

cytotoxic killing-->cell apoptosis-->liver damage

treatment:

Immunization/vaccination

Type:

HBV (Hep B virus)

Transmission:

Via the blood e.g. Childbirth

Intravenous drug abuse

Unprotectedsex

pathophysiology:

cytotoxic killing-->cell apoptosis-->liver damage

treatment:

Antiviral drugs can help fight the virus and slow itsability to damage liver

Type:

HCV

Transmission:

Via the blood e.g. Childbirth

Intravenous drug abuse

Unprotectedsex

pathophysiology:

cytotoxic killing-->cell apoptosis-->liver damage

treatment:

Antiviraldrugs can help fight the virus and slow its ability to damage liver

Type:

HDV

Transmission:

Can only infect a host if that host also have HBV

pathophysiology:

cytotoxic killing-->cell apoptosis-->liver damage

treatment:

Antiviral drugs can help fight the virus and slow itsability to damage liver

Type:

HEV

Transmission:

Feacal/oral

pathophysiology:

cytotoxic killing-->cell apoptosis-->liver damage

treatment:

Antiviral drugs can help fight the virus and slow itsability to damage liver

Front 2

Understandrisk factors, complications, treatment of liver cirrhosis

Back 2

risk factors:

Hepatitis virus- B and C most common

excessive alcohol intake

autoimmune disorders

or

- Alcohol

- Hepatitis B and C

- Fatty liver disease

- Malnutrition

complications:

- Ascites

- Hepatic encephalopathy

- Variceal hemorrhage

- Bacterial peritonitis

- Portal hypertension

treatment:

It’s generally irreversible once it occurs andtreatment generally focuses on preventing progression and complication

Front 3

List themeaning, causes, complications and treatment of portal hypertension-knowpre-intra and post hepatic causes

Back 3

Meaning:

abnormally high blood pressure in the portal venous system

causes:

resistance or obstruction to portal blood flow

Pre-hepatic- causes:

o Thrombosis or narrowing in portal vein

Intra-hepatic causes:

o Cirrhosis, viral hepatitis

Post-hepatic causes

o Inferior Vena Cava (IVC) clots

o Right sided heart failure

complications:

varices

splenomegaly (an enlargment of the spleen)

Ascites

Hepatic Encephalopathy

treatment

Beta blockers to prevent variceal bleed, reduce portalblood flow.

Antibiotics to prevent infection

Front 4

Apply conceptsof management of hepatic encephalopathy - risk factors, clinicalmanifestation, treatment.

Back 4

risk factors:

- Gastrointestinal bleeding

- Increased dietary protein

- electrolyte imbalance

- Alcohol liver disease

clinical manifestation:

subtle change in personality

memory loss

irritability

lethargy

sleep disturbances

pathophysiology:

Liver inflammation-->liver necrosis-->liver fibrosis and scarring-->liver failure-->hepatic encephalopathy-->hepatic coma-->death

treatment:

· Manage precipitating factors

· Correct fluid and electrolyte levels

· Cease any CNS depressant drugs (if the patient is already on these)

· Correct nutritional deficiencies

· Reduction of inflammation

Front 5

Understand thevarious liver function tests - various enzymes and what do their abnormallevels indicate-

example what is bilirubin?

Why is it high in liverdysfunction?

Back 5

example what is bilirubin?

Bilirubin- awaste product from the breakdown of red blood cells. The liver processedbilirubin so it can be excreted in stool.

Why is it high in liver dysfunction?

It can be highin liver dysfunction in severe liver disease which can impair bile flowtherefore affecting Bilirubin’s flow through the liver’s bile ducts.

Front 6

Hepatic TutorialWeek 6

Billy Richards Patient profile Mr Richards a 55-year-old man is admittedto the medical unit where you are working with a diagnosis of cirrhosis of theliver. Upon arrival you show Mr Richards to his room where you then proceedwith admission. Data is as follows: Subjective data •Has had cirrhosis for 12 years•Acknowledges that he had been drinking heavilyfor 20 years but has been sober for the past 2 years•Complains of anorexia, nausea and abdominaldiscomfortObjective dataPhysical examination:•Thin and malnourished•Has moderate ascites•Has jaundice of sclera and skin•Has 4+ pitting oedema of the lower extremities•Liver and spleen are palpableLaboratory values•Total bilirubin: 257 μmol/L (0 – 20 µmol/)•Serum ammonia: 122 μmol/L (10 - 57µmol/L)•AST: 154U/L (0 – 45U/L)•ALT: 169U//L (0 – 45U/L) Critical thinking questions

1. Perform asystematic assessment for Mr Richards

2. What are thepossible causes of cirrhosis? What type of cirrhosis does Mr Richards probablyhave?

3. Describe thepathophysiological changes that occur in the liver as cirrhosis develops.4. List MrRichards’s clinical manifestations of liver failure. For each manifestation,explain the pathophysiological basis.

5. Explain thesignificance of his laboratory results.

6. If MrRichards began to manifest signs and symptoms of hepatic encephalopathy, whatwould you monitor? What measures should be instituted to control or decreasethe ammonia level?

7. Mr Richardsis being closely observed for the possibility of gastrointestinal bleeding. Whyis this considered a possible complication?

8. In the earlystages of cirrhosis, what can be done to control the disease?

9. For thefollowing medications, identify the drug class, mechanism of action,indications, potential side effects and nursing considerations for use inascites:

1. Spironolactone

2. Frusemide

3. Lactulose

4. Nadolol

5. Isorbidemononitrate

6. OxazepamTP

Back 6

1. Perform asystematic assessment for Mr Richards.

Airway – talking (acknowledges heavy drinking)

Breathing – no data available, but talking and norespiratory distress noted

Circulation – no data available, but no distress noted

Disability – no data available

Exposure – jaundice of sclera and skin, 4+ pittingoedema to lower extremities

GIT – liver and spleen palpable

RENAL – no data available, but would want toknow if he is urinating

2. What are the possible causes of cirrhosis? Whattype of cirrhosis does Mr Richards probably have?

Mr Richards’s cirrhosis is likely due to his20-year history of heavy drinking. Based on this history, Mr Richards’scirrhosis is alcoholic cirrhosis.

3. Describe thepathophysiological changes that occur in the liver as cirrhosis develops.

The first change in the liver from excessivealcohol intake is an accumulation of fat in the liver cells. Uncomplicatedfatty changes in the liver are potentially reversible if the person stopsdrinking alcohol. If the alcohol abuse continues, widespread scar formationoccurs throughout the liver. (Try to get students write a flow chart of thepatho)

Liver inflammation-->liver necrosis-->liver fibrosis and scarring-->liver failure-->hepatic encephalopathy-->hepatic coma-->death

4. List MrRichards’s clinical manifestations of liver failure. For each manifestation,explain the pathophysiological basis.

A thin and malnourished state in liverfailure results from the anorexia, dyspepsia, and nausea and vomiting caused byaltered metabolism of carbohydrates, fats, and protein by the liver.Ascites and peripheral oedema develop as aresult of several mechanisms. Portal hypertension causes leakage of proteinsfrom the blood vessels into the lymph spaces in the liver tissue. When thelymphatic system is unable to carry off the excess proteins and water, theyleak through the liver capsule into the peritoneal cavity. The osmotic pressureof the proteins pulls additional fluid into the peritoneal cavity, creatingascites. Hypoalbuminaemia resulting from impaired liver synthesis of albuminalso contributes to ascites and peripheral oedema by decreasing colloidalosmotic pressure. Hyperaldosteronism resulting from impaired liver metabolismof aldosterone also contributes to ascites and oedema by causing increasedsodium reabsorption by the renal tubules. The retention of sodium, as well asan increase in antidiuretic hormone (ADH), causes additional water retention inthe patient with liver failure.

•Jaundice of the sclera and skin results fromfunctional derangement of liver cells and compression of bile ducts byconnective tissue growth that impairs the ability of the liver to conjugate andexcrete bilirubin.

•Hepatomegaly occurs from the fattyinfiltration, inflammatory reactions, and scarring of the liver that occurswith cirrhosis, while splenomegaly occurs as a result of portal hypertensionand congestion of the spleen. 

5. Explain the significance of his laboratoryresults.

Total bilirubin 257 µmol/L—Total (conjugated andunconjugated) bilirubin increases as a result of the liver’s altered ability totake up bilirubin from the blood or to conjugate or excrete it.

Serum ammonia 122 µmol/L—A major source ofammonia is the bacterial and enzymatic deamination of amino acids in theintestines. The ammonia that results from this deamination process normallygoes to the liver via the portal circulation and is converted to urea, which isthen excreted by the kidneys. When the blood is shunted past the liver via thecollateral anastomoses or the liver is unable to convertammonia to urea, large quantities of ammoniaremain in the systemic circulation.

•AST 154 U/L, ALT 169 U/L — Enzyme levels,including alkaline phosphatase, AST, ALT, and GGT, are elevated because of therelease of these enzymes from damaged liver cells.

6. If Mr Richards began to manifest signs andsymptoms of hepatic encephalopathy, what would you monitor? What measuresshould be instituted to control or decrease the ammonia level?

Clinical manifestations of encephalopathy arechanges in neurological and mental responsiveness, ranging from lethargy todeep coma. Changes may occur suddenly because of an increase in ammonia inresponse to bleeding varices or gradually as blood ammonia levels slowlyincrease. In the early stages, manifestations include euphoria, depression,apathy, irritability, memory loss, confusion, yawning, drowsiness, insomnia,agitation, slow and slurred speech, emotional lability, impaired judgment,hiccups, slow and deep respirations, hyperactive reflexes, and a positiveBabinski reflex. Clinical manifestations of impending coma includedisorientation as to time, place, or person. A characteristic symptom isasterixis, or flapping tremors (liver flap). This may take several forms, themost common involving the arms and hands. Other signs include hyperventilation,hypothermia, and grimacing and grasping reflexes. The goal of management of hepatic encephalopathyis the reduction of ammonia formation. This consists mainly of proteinrestriction and reduction of ammonia formation in the intestines. The degree ofprotein restriction is determined by the severity of mental change. The proteinrestriction may range from 0 to 40 g a day.Several measures to reduce ammonia formation inthe intestines are used. Lactulose (Cephulac) may also be used to treat hepaticencephalopathy. In the colon, it is split into lactic acid and acetic acid,which decreases the pH fromto 5.0. The acidic environment discouragesbacterial growth. The lactulose traps the ammonia in the gut, and the laxativeeffect of the drug expels the ammonia from the colon. It is usually givenorally but may be given as a retention enema or via NG tube. Sterilisation ofthe intestines with antibiotics, such as neomycin sulfate, which are poorlyabsorbed from the GI tract, is another method. Neomycin is given orally orrectally. This reduces the bacterial flora of the colon. Bacterial action onprotein in the faeces results in ammonia production. Cathartics and enemas arealso used to decrease bacterial action. Constipation should be prevented. Controlof hepatic encephalopathy also involves treatment of precipitating causes. Thisinvolves controlling GI haemorrhage and removing the blood from the GI tract todecrease the protein in the intestine. Electrolyte and acid-base imbalances andinfections should also be treated.

7. Mr Richardsis being closely observed for the possibility of gastrointestinal bleeding. Whyis this considered a possible complication?

Oesophageal varices are a common complication,occurring in two-thirds to three- quarters of patients with cirrhosis. Thesecollateral vessels contain little elastic tissue and are quite fragile. Theytolerate the high pressure poorly, and the result is distended, tortuous veinsthat bleed easily. Large varices are more likely to bleed. In addition, becauseof compromised liver function, there are alterations in normal blood-clottingmechanisms.

8. In the earlystages of cirrhosis, what can be done to control the disease?

Health promotion for cirrhosis depends on thecause of the cirrhosis. Patients need to be urged to avoid alcohol ingestionand their efforts supported. Adequate nutrition, especially for the alcoholicand other individuals at risk of cirrhosis, is essential to promote liverregeneration. Hepatitis must be identified and treated early so that it doesnot progress to chronic hepatitis.Drugs that are potentially toxic to liver cellsshould also be avoided. Biliary disease must be treated so that the stones donot cause obstruction and infection. The underlying cause (e.g. chronic lung disease)of right-sided heart failure must be treated so that the heart failure does notlead to cirrhosis.

9. For thefollowing medications, identify the mechanism of action, indications, potentialcomplications and nursing considerations for use in ascites:

. Spironolactone

· Potassiumsparing diuretic

· Blocksaction of aldosterone (it is an aldosterone antagonist)

· Helps toreduce ascites (due to reduced reabsorption of sodium), doesn’t increase urineoutput significantly

. Frusemide

· Loopdiuretic (will decrease potassium)· Helps toreduce accumulated fluid

. Lactulose

· Used whenpeople showing symptoms of increased ammonia levels

· Decreasesnitrogenous load by decreasing number of nitrogen forming bacteria in bowel,and increases acidity of colon, converting ammonia into ammonium ion (notabsorbable and gets excreted in faeces)

. Nadolol

· Beta blocker

· Helps tolower hepatic venous pressure and decrease risk of bleeding from varices

. Isorbidemononitrate

· Nitrate –widens blood vessels

· Benzodiazepam

· Used withalcohol withdrawal scale and administered if patient showing signs ofwithdrawal