CA - Cirrhosis Flashcards
Whats Cirrhosis?
liver in RUQ becomes irreversibly scarred from chronic inflammation.
What are the causes of cirrhosis?
- Alcohol-Related Cirrhosis
- chronic alcohol consumption -> micronodular cirrhosis
- associated with fatty liver, hepatitis, and fibrosis
- overtime: fatty liver -> fat cells replace liver cells -> cant perform fxns of liver cell - Viral Hepatitis-Related Cirrhosis
- caused by chronic Hepatitis B, C, or D infections
- progresses to hepatocellular carcinoma (HCC) - Metabolic & Genetic Causes
- Non-Alcoholic Fatty Liver Disease (NAFLD) → A. obesity: gluconeogenesis & insulin resistance -> fat deposited in the liver
B. diabetes
C. metabolic syndrome
- fat cells build up in the liver - Cardiac Cirrhosis
- chronic right heart failure -> passive congestion & liver fibrosis - Biliary cirrhosis
- bile duct inflammation -> cirrhosis
What are the risk factors for Cirrhosis?
causes & risk factors can overlap
- Chronic Viral Hepatitis (Hepatitis B, C)
- Alcoholic Liver Disease
- Hemochromatosis - immune condition: high levels of iron
- Non-Alcoholic Fatty Liver Disease
Carriers of Hepatitis virus may not have acute infection but have cirrhosis. Why?
- Spontaneous reactivation & mutation of the virus
Inactive HBsAg carrier state – presence of HBeAg and non reactive antiHbe, undetectable or low levels of HBV DNA → spontaneous reactivation → multiple or sustained → progressive hepatic damage or hepatic decompensation
Symptoms / Complications of cirrhosis?
NEUROLOGICAL
1. Hepatic encephalopathy (DN)
- liver unable to effectively filter out Ammonia -> pass through BBB & buildup in brain
- Asterixis / Flapping tremor (DN)
- change in mental behaviour -> coma - Peripheral neuropathy
GI
1. Anorexia
- Dyspepsia
- Nausea, vomiting
- Change in bowel habits
- Dull abdominal pain
- Fetor hepacitus
- Esophageal varices & Ascites
- portal hypertension -> fluid in BVs pushed into peritoneal cavity -> ascites
- liver unable to make albumin (keeps fluid within BVs) -> hypoalbuminemia -> ascites & peripheral edema
- portal hypertension -> hematemesis & melena
gastropathy -> melena - Congestive gastritis
SKIN
1. Jaundice
- increased levels of bilirubin in blood unable to be excreted
2. Spider angioma
3. Palmar erthema
4. Purpura
5. Petechiae
6. Caput medusae
Varicose veins -> caput medusae
- increased venous pressure -> dilation of GI veins -> varicose veins -> radiating out from umbilicus = caput medusae
Bleeding & bruising
- liver unable to synthesize clotting factors like prothrombin -> increased PTT, PT, and INR levels
Hematologic
1. Anemia
2. Thrombocytopenia
3. Leukopenia
4. Coagulation disorders
5. Splenomegaly -> 3. leukopenia & 4. thrombocytopenia
- enlarged spleen traps RBCs -> anemia & WBCs -> leukopenia -> increases risk of infections
- traps platelets -> thrombocytopenia -> easy bruising /bleeding
What causes hepatic encephalopathy?
Decreased liver fxn -> ammonia not broken down -> passes through BBB -> HE
What is the main complication of cirrhosis?
Cirrhosis -> fibrosis of liver -> loses elasticity -> blood cant enter the liver -> backflow -> congestion
blood remains in portal vein -> increased BP & hydrostatic pressure -> portal hypertension -> worsens ascites
What causes the characteristic liver changes in Cirrhosis?
- Fibrosis ->
- Architectural distortion = significant deformation of liver ->
- Regenerative/Useless nodule formation that cant perform fxns of normal liver cells ->
- Decreased liver function
What are the clinical manifestations of portal hypertension that are expected as your patient’s cirrhosis progresses?
- Increased pressure in peritoneal capillaries
-> ascites - Portosystemic shunting of blood ->
A. Development of collateral channels ->
- Caput medusae +
- Hemorrhoids +
- Esophageal varices
B. Shunting of ammonia & toxins from the intestine into the general circulation ->
Hepatic encephalopathy
- Splenomegaly ->
- Hypersplenism = breaks down RBCs, WBCs & platelets that are still functioning ->
Anemia + Thrombocytopenia + leukopenia = pancytopenia: RBCs, WBCs & platelets all decreased -> bleeding
- but hypersplenism is not for all cases of spleenomegaly
What are the manifestations of portal systemic shunt?
Portal hypertension -> portal vein backflows to systemic veins -> portal systemic shunt = alternate pathway for blood to flow from portal vein to systemic bloodflow -> too much pressure in portal vein -> blood diverted to collateral channels/smaller veins & enlarge bcs thats not their original purpose -> veins end up in the anus -> haemorrhoids & esophagus -> esophageal varices
What is the condition of the pt if their HBV serology result has HBsAG, Anti-HBc IgM, HBeAg and >20k HBV DNA?
Acute infection/reactivation. - first time
Body has no time to produce antibodies
high viral load -> HBe antigen is positive ->
seroconversion =
no purpose it js happens
not everybody can recover frm infection, mutation can occur
at first body doesnt know its a pathogen
but body will start to make antibodies to fight the pathogen
will create more antibodies over time
before seroconversion - no antibodies but after will have antibodies
What is the condition of the patient if their HBV serology result only has anti-HBs?
Vaccination with immunity
1. No HBsAg bcs virus surface antigen not present anym/died alr
2. Vaccination only provides sufficient dosage to produce antibodies against HepB surface antigen (HBsAg)
What is the condition of the pt if their HBV serology result has HBsAG, anti-HBc IgG, anti-HBe and <20k HBV DNA?
Chronic HBV carrier.
- Antigen of HBs present -> but not enough to trigger formation of antibody
- antibody-HBcore antigen IgG, anti-HBe -> more E&C produced bcs more sensitive to infections and things in the body -> inconclusive result
- Antigen S needs more amt than C&E then = infection
S - antigen on the virus surface
anti HBs - antibody
C - core antigen
E - active virus produces e - viral protein
antibody for e antigen
high e antigen = high viral load
HBeAg negative after the infection
develops antibody
if it mutates smt else can cause high viral load
antibody e still develops
anti hbe is still positive
sometimes even if e decreases pt is well bcs no additional thing to increase viral load
thrs antibody for S, C and E
No HBeAg - not actively producing viral proteins but still hv some bcs its a chronic infection
SO got leftover antibody = anti-HBe
What are the complications of ascites?
- Increased hydrostatic pressure bcs of portal congestion
- Toxins not detoxified enters kidneys -> hepatorenal syndrome -> kidneys unable to filter salt & water -> Salt & water retention by the kidneys
- Decreased colloidal osmotic pressure
due to impaired synthesis of albumin bcs of cirrhosis
- liver produces albumin (retains water in the blood) -> contributes to osmotic pressure of the blood
What is the immediate nursing care for a patient with Liver Cirrhosis?
Assessment
* History of anorexia, dyspepsia, alcohol abuse or exposure to hepatotoxic agent
* Abdomen for pain and liver tenderness, dullness when percussing enlarged liver
* Abdominal girth measurements for baseline data relative to ascites, weight gain
* Skin for presence of jaundice, dryness, petechial, spider angiomas
* Clinical findings of hepatic coma
Plan
* Prevent bleeding
* Maintain skin integrity from jaundice
* Prevent fluid imbalance from ascites
* Maintain optimal nutrition status
Implementation
* Observe for bleeding
* Observe for clinical findings of impending hepatic coma
* Monitor liver function studies, CBC, and renal function studies
* Provide high calorie, protein-restricted diet
* Provide special skin care and keep the patient nails trimmed because pruritus is associated with jaundice
* Maintain semi-fowler’s position to prevent ascites from causing dyspnoea
* Monitor intake and output, abdominal girth, daily weight to assess fluid balance
Evaluation
* Follow dietary regimen
* Maintain fluid balance
* Remain free from injury
What’s the nursing management for ascites?
- Low salt diet
- Weight control and weight management
- I/O charting
- risks for impaired skin integrity for pt who has ascites and peripheral oedema
What is the discharge plan for the patient?
Assessment
* Abdominal girth measurements relative to ascites and weight gain
* Skin for presence of jaundice, dryness
Plan
* Maintain skin integration from jaundice
* Prevent fluid imbalance from ascites
* Maintain optimal nutrition status
Implementation
* Provide high calorie, protein-restricted diet
* Provide special skin care and keep the patient nails trimmed because pruritus is associated with jaundice
* When Mei Ling is resting, maintain her in a semi-fowler’s position to prevent ascites from causing dyspnoea
* Encourage resting to prevent fatigue
* Monitor abdominal girth, daily weight to assess fluid balance
* Allow Mei Ling and her family members to discuss their feelings
* Provide emotional support
Evaluation
* Follow dietary regimen
* Maintain fluid balance
* Remain free from injury
