Exam #5 (chp 58-59) Flashcards
What is cirrhosis?
Cirrhosis is extensive, irreversible scarring of the liver; characterized by fibrotic (scarred) bands of connective tissue
A chronic reaction to hepatic inflammation and necrosis- results in extensive degeneration and destruction of hepatocytes (liver cells).
Develops slowly and is progressive- results in end stage liver disease.
What are common causes of Cirrhosis?
The most common causes of cirrhosis are:
- chronic alcoholism
- chronic viral hepatitis
- autoimmune hepatitis
- NonAlcoholic Steatohepatitis (NASH) (fatty liver)
- Drug and chemical toxins
- Gallbladder disease
- Metabolic/genetic causes
- Cardiovascular disease
What is the pathophysiology of cirrhosis?
As cirrhosis develops, the tissues becomes nodular, the nodules can block bile ducts and blow flow. Impairments in blood flow and lymph flow result from compression caused by excessive fibrous tissue. (Scarring)
Early- the liver is enlarged, firm and hard. Over time the liver shrinks resulting in decreased liver function- results in elevated liver enzymes (AST/ALT)
What are complications associated with cirrhosis?
Compensated cirrhosis: the liver is scarred but can still function.
Decompensated cirrhosis: liver function is impaired, obvious manifestations of liver failure
- portal hypertension
- ascites and esophageal varices
- coagulation defects
- jaundice
- Portal Systemic Encephalopathy (PSE) with hepatic coma
- hepatorenal syndrome
- spontaneous bacterial peritonitis
What is portal hypertension?
(Associated with decompensated cirrhosis)
Portal hypertension is a persistent increase in the portal vein pressure, greater than 5mm/Hg
It results from increased resistance or obstruction of the blood flow through the portal veins and it’s branches.
Can result in ascites, esophageal varices, prominent abdominal veins, and hemorrhoids.
What is splenomegaly?
Spleen enlargement caused by blood flow backing up into the spleen.
Destroys platelets, causing thrombocytopenia (low platelets) and increased r/f bleeding
THROMBOCYTOPENIA is the first sign of liver dysfunction
What is ascites?
Ascites is a collection of free fluid within the peritoneal cavity caused by increased hydrostatic pressure from portal hypertension.
plasma protein collects in the perineal fluid– decreases circulating plasma protein in the blood– in addition, the liver cannot produce albumin properly– the colloid pressure decreases= shift of vascular fluid to the abdomen “third spacing”
Pt may present: hypovolemia and edema
Massive ascites: causes renal vasoconstriction — triggers renin angiotensin system= results in sodium and water retention. (Causes hydrostatic pressure, and more ascites)
What is esophageal varices?
Esophageal varices occurs when fragile, thin-walled esophageal veins become distended and tortuous from increased pressure.
The bleed depends on their size
Occurs most often in the distal esophagus= LIFE THREATENING EMERGENCY
Severe blood loss can occur, leading to hypovolemia shock
Hematemesis- vomiting blood
Melena- black, tarry stools
No precipitating factor, heavy lifting, vigorous physical activity, chest trauma, or dry hard food increase likely hood of bleed
What is portal hypertensive gastropathy?
Portal hypertensive gastropathy is slow gastric mucosal bleeding, which results from chronic slow blood loss, occult positive stools, and anemia.
In patients with cirrhosis, why does biliary obstruction occur?
In patients with cirrhosis, bile production in the liver is decreased
– prevents absorption of fat soluble vitamins (D, E, A, K)
–lack of vitamin K, clotting factors 2,7,9,10 are insufficient
= increase r/f bleed and bruising
Confirmed by coagulation studies (PT/INR, PTT)
What is Jaundice? And how is it caused?
Jaundice is yellow discoloration of the skin, is caused by biliary obstruction.
Patients often report itching (pruritus)
2 types:
Hepatocellular- develops because the liver cells cannot effectively excrete bilirubin
Intrahepatic- results from edema, fibrosis, or scarring of the hepatic bile ducts and channels
What is hepatic encephalopathy? What are early and late Signs and Symptoms?
Hepatic encephalopathy aka Portal-systemic encephalopathy (PSE) is a complex cognitive syndrome that results from liver failure and cirrhosis.
-reversible with early intervention
EARLY: sleep disturbances, mood disturbances, mental status changes, and speech problems
LATE: altered LOC, impaired thinking processes, and neuromuscular problems
What is the proposed mechanism of action for hepatic encephalopathy?
Shunting of the portal venous blood into the central circulation to bypass the liver, substances absorbed by the intestine are not broken down or detoxified and
= cause metabolic abnormalities
ELEVATED AMMONIA AND GABA (gamma-aminobutyric acid)
What are STAGE 1 Hepatic encephalopathy signs and symptoms?
- Subtitle manifestations that may not be recognized immediately
- personality changes
- behavior changes: agitation, belligerence
- emotional Labile: euphoria, depression
- impaired thinking
- inability to concentrate
- fatigue, drowsiness
- slurred or slowed speech
- sleep pattern disturbances
What are signs and symptoms of STAGE 2 hepatic encephalopathy?
- continuing mental changes
- mental confusion
- disorientation of time, place, or person
- Asterixis (hand flapping)
What are STAGE 3 hepatic encephalopathy signs and symptoms?
- progressive deterioration
- marked mental confusion
- stuporous, drowsy but not arousable
- abnormal EEG
- muscle twitching
- hyperreflexia
- Asterixis (hand flapping)
What are signs and symptoms of STAGE 4 hepatic encephalopathy?
- unresponsiveness, leading to death
- Unarousable, obtunded
- No response to painful stimuli
- NO Asterixis
- Positive Babinski’s sign
- Muscle rigidity
- fetor hepaticus (characteristics of liver death– musty, sweet odor)
- Seizures
What are factors that can lead to hepatic encephalopathy in patients with cirrhosis?
High protein diet
Infection
Hypovolemia (decreased fluid volume)
Hypokalemia (decreased potassium)
Constipation
GI bleeding (causing large protein load in the intestines)
Drugs (hypnotics, sedatives, opioids, analgesics, diuretics, illicits)
What is hepatorenal syndrome (HRS)?
Hepatorenal syndrome indicates a poor prognosis for a pt with liver failure, can cause death
Manifested by:
- a sudden decrease in urine output (<500ml/24hr)
- elevated BUN and Cr levels with decreased urine Na+ levels
- increased urine osmolarity
Usually occurs after clinical deterioration following a GI bleed or hepatic encephalopathy
What is Spontaneous Bacterial Peritonitis (SBP)?
Spontaneous Bacterial Peritonitis is a result of bacteria in the ascites fluid and low concentrations of protein
Patients with cirrhosis and ascites may develop acute SBP
Patients with very advanced liver disease have increased susceptibility
Clinical manifestations:
Fever, chills, abdominal pain, and tenderness.
Increased Jaundice and loss of appetite
Dx with ascitic fluid via paracentesis, leukocyte count > 250 need Tx.
QUINOLONES- norfloxacin (Noroxin) drug of choice!
If allergic, use combo-drug Bactrim.
What is the etiology and genetic risks for Hepatitis C?
Second leading cause of cirrhosis and liver failure in US.
Hepatitis C is an infectious blood borne illness, causing inflammation leading to progressive scarring of the liver.
In combination with alcohol, progression speeds up
What is Nonalcoholic Fatty Liver Disease (NAFLD)?
Nonalcoholic Fatty Liver disease is associated with obesity, diabetes type 2, and metabolic syndrome.
Most common cause of liver disease in the world.
Genetic link to: Patatin-like phospholipase domain-containing 3 (PNPLA3)
Hispanics more like to have.
May cause cirrhosis, liver cancer, or liver failure.
What are the statistics of liver disease, according to the American Liver Foundation?
> 30 million have liver disease, 1 in 10 Americans
4 million Americans have Hepatitis C and >1 million have Hepatitis B
12th most common death in US; 28,000 die per year.
What are EARLY assessment findings associated with cirrhosis?
Fatigue
Significant change in weight
GI symptoms, anorexia and vomiting
ABDOMINAL pain and liver TENDERNESS
What are LATE assessment findings associated with advanced cirrhosis?
GI bleeding
Jaundice
Ascites
Spontaneous bruising
(All indicate poor liver function and complications of cirrhosis)
How would you assess the patient for liver dysfunction or failure? And what are interventions associated to these findings?
Jaundice (yellowing skin) or Icterus (yellowing sclera)
Dry skin ; Rashes
Petechiae or ecchymoses
Warm BRIGHT RED palms
Spider angiomas (vascular lesions on the nose, cheek, thorax, and shoulders)
Ascites ; abdominal distention= measure ABDOMINAL GIRTH, measure in supine position, around largest diameter on exhalation. DAILY WTs
Peripheral Edema- extremities and scrotum
Vitamin deficiency (especially fat soluble D,E,A,K)
Hepatomegaly (liver enlargement)
Occult stools or emesis- FOBT or HEMA-CULT
Fetor Hepaticus- fruity or musty distinctive breath odor (CLF/HE)
Amenorrhea or Gynecomastia or Impotence
Asterixis- “Hand flapping” course tremor, rapid nonrhythmic extensions and flexions of wrists and fingers
Agitation ; insomnia ; emotional lability ; euphoria ; depression
Question: A client previously diagnosed with liver cirrhosis visits the medical clinic. What assessment findings does the nurse expect in the client? Select all that apply: A. Ecchymoses B. Soft abdomen C. Moist, clammy skin D. Jaundice E. Ankle edema F. Fever
A. Ecchymoses
D. Jaundice
E. Ankle Edema
What are LAB findings associated with liver disease?
ELEVATED:
- AST/ALT and LDH (due to inflammation)
- Alkaline phosphatase and GGT (caused by bile obstruction)
- Bilirubin, present in the urine (urobilinogen)
- Prolonged PT/INR (decreased prothrombin)
- Ammonia (with advanced Liver disease)
- Creatinine (with deteriorating kidney function)
DECREASED:
- Protein and Albumin (decreased synthesis by liver)
- platelet count (thrombocytopenia)
- RBCs and H&H (anemia)
- WBCs
- Hyponatremia (caused by ascites)
Clay colored stools (cause bile obstruction & decreased bilirubin in urine)
What is assessment IMAGING indicative of liver disease?
Ultrasound of liver: 1st assessment suspected of liver disease to detect ascites, hepatomegaly, and splenomegaly
X-ray: hepatomegaly, splenomegaly, massive ascites
CT scan
MRI
Liver Biopsy- At risk for bleeding
EGD- esophagogastroduodenoscopy of upper GI (complications: esophageal varices, stomach irritation, and ulceration
ERCP- endoscopic retrograde cholangiopancreatography contrast dye into sphincter for stone removal and biopsies.
What are NANDA diagnoses associated with liver disease?
Excessive Fluid volume r/t third spacing
Potential for hemorrhage r/t portal hypertension
Potential for hepatic encephalopathy r/t shunting and increased ammonia
What are interventions related to cirrhosis and liver disease?
Prevent fluid accumulation- fluid restriction, treat ascites-
paracentesis and diuretics- monitor DAILY WT, I/O, abd. Girth, peripheral edema, and electrolyte levels. (Loop diuretics- decreased K and Na)
LASIX and SPIRONOLACTONE
Prevent scratching/itching skin- use COOL water and minimal soap, use lotion
DIET: Low Sodium diet < 2gm, high carb. moderate fat, high protein. Vitamin supplements (with late stage cirrhosis) Banana Bag IVF (thiamine, folate, and multivitamins)
What is Hepatopulmonary syndrome? And what are some interventions to conduct?
Hepatopulmonary syndrome is caused by excessive fluids caused by ascites
Caused dyspnea, as result of intra-abdominal pressure, limiting thoracic expansion
DO:
-Auscultate lungs every 4-8hrs for crackles
-Continuous Pulse Ox
-Elevate HOB to 30 degrees, elevate feet = decreased ankle edema to relieve dyspnea
- Assess BUN, H&H, protein, and electrolytes
(Elevated BUN and hematocrit and decreased protein indicate hypovolemia)
What are cares associated with a Paracentesis?
Ensure Informed consent is received and answer any questions
Obtain VS and Weight and have pt VOID BEFORE procedure
Position with HOB elevated
Measure the drainage- send fluid analysis
Apply dressing to site and assess leakage
Maintain bedrest and Weigh the pt POST-PROCEDURE
What is TIPS?
TIPS is a Transjugular Intrahepatic Portal-systemic Shunt
Is a nonsurgical procedure used to control long-term ascites and to reduce variceal bleeding
heavy IV sedation or general anesthesia
needle through sheath on jugular vein and pushed through liver into the portal vein
Balloon inflated, shunt to keep open.
Doppler to assess blood flow through stent
Question: The nurse is providing teaching for a client scheduled for a paracentesis. Which statement by the client indicates the teaching has been successful?
A. I must not use the bathroom prior to the procedure
B. I must lie on my stomach while the procedure is performed
C. I will not be allowed to eat or drink anything the night before surgery
D. The physician will likely remove 2-3 liters of fluid from my abdomen
D. The physician will likely remove 2-3 liters of fluid from my abdomen.
What are interventions to PREVENT a bleed? What are interventions if bleeding occurs?
best outcome: pt expected to be free of bleeding.
PREVENT bleed and infection:
- screen for esophageal varices
- nonselective Beta blocker: Propanolol (Inderal)
- Prophylactic ABX on admission (infection is a common cause of AVB)
If bleeding occurs: EMERGENCY
-Vasoactive drugs: Vasopressin and Octreotide acetate (Sandostatin)
-monitor VS q 1 hr, check coagulation studies (PT/INR, PTT and platelets)
What are endoscopic procedures used to control a bleeding veins?
Endocscopic Variceal Ligation (EVL): “banding” - apply a small “O” band at the base of the varices to decrease blood supply
Endoscopic sclerotherapy (EST) aka injection therapy - inject sclerosing agent via a catheter, complication mucosal ulceration
What are RESCUE therapies if rebleeding occurs?
Second endoscpoy or TIPS procedure if possible; if not:
balloon tamponade and esophageal stents using a Sengstaken-Blakemore tube
- place through the nose into stomach, balloon inflated, pressure to stop bleed
- pt intubated and on ventilation
- life threatening complications: aspiration, asphyxia, esophageal perforation.
What are interventions for hepatic encephalopathy?
goal: slowing or stopping accumulation of ammonia
Diet changes: moderate protein and fats, simple carbs.
-give brief, simple dietary do and dont
Drug therapy: used sparingly (no opioids, sedatives, or barbiturates)
Lactulose or lactitol: eleminate ammonia via stools, it is sweet, viscous, sticky liquid given PO or NG
- desired laxative effect, 2-3 soft stools per day and decreased confusion
- may report intestinal bloating and cramping
- dehydration and hypokalemia for stools
Nonabsorbable ABX:
Neomtcin or rifaximin - broad spectrum for intestinal antiseptic- destroys normal flora, decreases protein breakdown and ammonia production. Maintenance dose PO or retention enema- potential kidney toxicity, do not use for pts with kidney disease.
Metronidazole (Flagyl) - similar to neomycin, can cause peripheral neuropathy
Vancomycin - long-term use can lead to resistance
ASSESS: LOC and orientation frequently, asterixis (liver flapping) or fetor hepaticus (liver breath).
thiamine supplements and benzos if at risk for alcohol withdrawal.
What is the goal of community-based care for patients with cirrhosis?
Optimize comfort, promote independence, support caregivers, prevent rehospitalization.
End-stage may need hospice
