Liver Flashcards

(47 cards)

1
Q

Biliary System

_____ + ____ = _____ , empties into small intestine (helps digest fats after a meal)

A

Hepatic duct (liver) + cystic duct (GB)=common bile duct

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2
Q

Hepatic Blood Supply

Largest visceral organ~dual blood supply:

The liver can store up to ___ mL blood to use during shock and hypovolemia.

Where does portal HTN occur?

A

portal vein 80% and hepatic artery (20%).

450

Portal hypertension is high blood pressure in the portal vein

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3
Q

Metabolic functions of the liver

A

Able to regenerate, metabolizes drugs (first pass effect: oral meds absorbed from Gi tract, metabolized by liver, may need to be given different route or larger dose),

stores Vit ADEK, maintains blood glucose levels,

synthesizes plasma proteins (albumin),

degrades toxins converts ammonia to urea excreted in urine),

synthesis of fibrinogen and coagulation factors;

Makes bile 600-1200 ml/day

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4
Q

____: bile

_____: slowing or stoppage of bile
______: gallstones
_____: inflammation of gallbladder
_____: gallbladder removal
_____: endoscopic retrograde cholangiopancreatography

A

“chole”
Cholestasis
Cholelithiasis
Cholecystitis
Cholecystectomy
ERCP

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5
Q

Diagnostic Evaluation

A

Liver function tests (LFTs)

Alanine transaminase (ALT): enzyme, an increase indicates liver damage.

Aspartate transaminase (AST): enzyme, an increase indicates liver or muscle damage/disease.

Alkaline phosphatase (ALP): an enzyme in liver, bile ducts, and bone; an increase indicates liver damage or blocked bile duct, or bone disease.

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6
Q

Liver function tests

These enzymes help metabolize ____

Liver function tests may look normal with _____

A

proteins

cirrhosis

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7
Q

Other labs

____: protein, made in the liver; _____ levels with liver damage or disease.

______: protein made by the liver; ____ in liver damage/dz ; monitor ____

______: a substance produced during the normal breakdown of red blood cells. ____ in liver damage/dz and certain anemias.

____: (NH3), a byproduct of amino acid catabolism. _____ with hepatic encephalopathy.

A

Albumin
decreased

Prothrombin time (PT)
prolonged
INR

Bilirubin (Tbili)
Increased

Ammonia
Increased

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8
Q

_____ helps keep your fluid in your bloodstream and binds with hormones and fatty acids

Need ____ for synthesis of PT/Internationalized Normalized Ratio (INR), calculated based on the PT test result, for people who are receiving the anticoagulant warfarin.

Prothrombin time (PT)
is a test that helps evaluate your ability to appropriately form blood clots. When the PT is ____, it takes longer for the blood to clot~
____ risk (TX with blood components: ________).

What is treatment for Coumadin overdose?

A

Albumin

Vit. K

high
hemorrhagic
clotting factors, platelets, plasma. Vit K

Vit. K

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9
Q

Labs help with identifying disease process & stagesFor example…

48 y.o. client with acute hepatitis B: elevated ALT, AST, bilirubin,& HBsAG

10 y.o. client with bone disease: elevated ALP, no liver disease

62 y.o. with end-stage cirrhosis, hepatorenal failure, and encephalopathy: normal ALT*, elevated BUN, creat, elevated ammonia, decreased albumin, prolonged PT

*ALT and AST return to normal when liver cells are no longer able to create an inflammatory response

A
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10
Q

Diagnostic Evaluation continued

Liver biopsy
US
CT
MRI
Endoscopy
Laparoscopy

Liver bx: ____ or ____
US guided helpful to diagnose If lab tests nondiagnostic.

______ complication

Health hx impt:

A

percutaneously or laprascopic.

Peritonitis

med hx, OTC, herbal, hx etoh and drug use (IV), occupational, recreational, travel hx, any exposure to hepatotoxic substances or infectious agents.

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11
Q

Manifestations of Hepatic Dysfunction

A

Jaundice
Portal HTN
Hepatic encephalopathy & coma

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12
Q

Manifestations of Hepatic Dysfunction 1. Jaundice

High levels of ____ in the blood

Jaundice: serum bilirubin levels > ____ mg/dL

Different causes

Can cause :

A

bilirubin in the blood (hyperbilirubinemia)

2-2.5

pruritus, urine bilirubin, and elevated liver function tests

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13
Q

Bilirubin is a substance produced during the normal breakdown of RBC.

It’s a waste product and that’s what causes the color.

Sometimes first sign; affinity for elastic tissues:

Causes:

A

sclera,mucous membranes.

prehepatic (hemolytic anemia)
intrahepatic (hepatitis, cirrhosis), posthepatic ( gallstones)

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14
Q

Types of jaundice:

A

Physiologic (newborn): immature gut, put under light, light absorbed by the skin and changes bilirubin into products which can pass thru urine

hepatocellular urine urobilogen, bilirubin excreted in urine

obstructive jaundice (gall stones : cholelithiasis)

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15
Q

Manifestations of Hepatic Dysfunction
2. Portal HTN

____ blocks the flow of blood through the liver and slows its processing functions portal HTN

Consequences:

A

Scar tissue

Ascites
Esophageal varices

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16
Q

Ascites treatment

A

Low Na diet
Diuretics (spironolactone)
Albumin
May require paracentesis
Nursing management

What kind of diuretic is spironolactone? first line therapy Potassium sparing, antagonizes aldosterone – reduces sodium retention

Why albumin? Increases intravascular fluid

Paracentesis complications? depending on cause…fill right back up, need paracentesis monthly, then weekly…

What is SBP? Spontaneous bacterial peritonitis- infection

Hyperaldosteronism –

Paracentesis- may need ultrasound, have the urinate prior to, may just fill back up

Nursing mgmt.- monitor vital signs (BP may drop), I&O, daily weights, resp. status,
Bedrest helps

Ascites is a result of portal hypertension

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17
Q

Esophageal & gastricvarices
treatment

A

Band ligation (next slide)

Administration of FFP, PRBC, PPI, Vitamin K, lactulose, antibiotics, meds to stop bleeding

Sclerotherapy

Balloon tamponade

Shunting procedures (TIPS)

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18
Q

Bleeding esophageal varices life-threatening!!

Observe for any signs of bleeding from varices, such as:

A

hematemesis & melena, s/symptoms of hypovolmic shock

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19
Q

Endoscopicvariceal ligation (EVL)

20
Q

Manifestations of Hepatic Dysfunction
3. Hepatic encephalopathy & coma

Accumulation of ____

Liver unable to convert ______ to be excreted, crosses the blood-brain barrier

Changes in:

Treat with:

Stages of hepatic encephalopathy table 43-3.

A

neurotoxins

ammonia to urea
Ammonia toxic! Lactulose traps and expels ammonia

neurologic and mental responsiveness, asterixis (flapping tremors) and fetor hepaticus

lactulose (orally, rectally as an enema, or NGT)
Lactulose- lowers ammonia levels. Makes them deficate

21
Q

Other Manifestations of Hepatic Dysfunction

A

Edema and bleeding
Vitamin deficiency
Metabolic abnormalities
Pruritus and other skin changes

22
Q

Hepatitis

An acute or chronic inflammation of the liver resulting in lysis of ______

Causes:

A

infected hepatocytes

Viral (A, B, C, D, E, G and mononucleosis, cytomegalovirus, and rubella)

Autoimmune

Nonviral: toxic and drug-induced hepatitis

23
Q

Clinical manifestations of hepatitis

Acute phase (1-4 mos)

Convalescent phase (2-4 mos)

A

Maybe asymptomatic but period of maximal infectivity!!!!!!!!!!

Malaise, fatigue, anorexia, weight loss, nausea/vomiting, RUQ abdominal pain, taste and smell alterations

headache, low-grade fever, arthralgias, skin rashes

Icteric (jaundice) or anicteric

May have dark urine and/or light or clay-colored stools

Pruritus

Hepatomegaly, lymphadenopathy, and sometime splenomegaly

Convalescent phase (2-4 mos)
Malaise and fatigue
Hepatomegaly

24
Q

Hepatitis A Virus (HAV)

Mode of transmission

S&S

Person at risk

Chronic infection?
Vaccine?

A

HAV is found in the stool and blood of people who are infected. WASH HANDS!

NOT CHRONIC - clears on its own

YES VACCINE

25
Hepatitis B Virus (HBV)
Hepatitis B is spread when blood, semen, or other body fluids from a person infected with the virus enters the body of someone who is not infected. This can happen through sexual contact; sharing needles, syringes, or other drug-injection equipment; or from mother to baby at birth. Mainly blood! Can be chronic Treat with antiviral meds Yes Vaccine
26
Hepatitis C Virus (HCV) causes treatment CDC recommendation: all adults born during 1945-1965 receive one-time testing for Hepatitis C Virus (HCV)
blood transfusions sharing needles & other drug taking equipment mother to baby transmission body piercing tattooing unprotected sex with multiple partners Yes chronic Yes treatment, but expensive NO VACCINE
27
Diagnostic Testing for Hepatitis
Test for specific antigen or antibody to determine form of hepatitis (for example, Anti-HAV IgM is specific for acute infection of HAV) Viral genotype testing done in patients undergoing drug therapy for HBV and HCV Liver function tests
28
All hepitits can become cirrhosis and liver failure
29
Collaborative Care for Acute Hepatitis
Rest Adequate nutrition Avoid alcohol Notification of possible contacts
30
Pharmacologic Therapy for Chronic Hepatitis Goal: Monitor:
Goal: suppress viral replication and prevent complications Monitor for anemia, leukopenia, and depression with drugs
31
Complications of Hepatitis Most patients with acute viral hepatitis recover completely Complications that can occur:
Acute liver failure Chronic hepatitis (some HBV and majority of HCV) Cirrhosis of the liver Hepatocellular carcinoma
32
Autoimmune, Genetic, Metabolic Diseases of the Liver
Autoimmune hepatitis Wilson’s Hemochromatosis NAFLD (nonalcoholic fatty liver disease) and NASH (nonalcoholic steatohepatitis) NASH Increasing with obesity epidemic.
33
Nonviral Hepatitis Toxic Hepatitis Chemicals Early treatment and removal of causative agent No effective antidotes!!!! Signs/symptoms: early (resembles viral hepatitis) to toxic (fulminant hepatic failure)
34
When hepatitis is caused by an autoimmune disorder or drug, it cannot be spread person to person
35
Nonviral Hepatitis Drug-induced
alcohol anabolic steroids tylenol Other meds: isoniazid, halothane, methyldopa, certain antibiotics, antimetabolites, & anesthetic agents; polypharmacy with older adults What is the recommended maximum dosage of acetaminophen recommended in 24 hours? And for patients with known liver disease? 4 g in 25 hr If you have liver issues, no more than 3 g
36
Cirrhosis - - - Progressive disease In clinical notes you will read about “compensated versus decompensated.” How do you interpret that?
Cells attempt to regenerate but are disorganized Diffuse fibrosis forms constrictive bands Formation of nodules and scarring Compensated: When you don't have any symptoms of the disease, you're considered to have compensated cirrhosis. Decompensated: When your cirrhosis has progressed to the point that the liver is having trouble functioning and you start having symptoms of the disease, you're considered to have decompensated cirrhosis
37
Cirrhosis Risk Factors
alcohol malnutrition viral hepatitis biliary obstruction obesity right-sided heart failure
38
Cirrhosis Signs and symptoms early late
Early manifestations: Often no signs until disease is far advanced Fatigue Later manifestations: Jaundice Spider angiomas and palmar erythema Thrombocytopenia, leukopenia, anemia Coagulation disorders (bleeding tendencies) Endocrine problems Peripheral neuropathy So remember all those functions of the liver, these are the s/sx you’ll see as it progresses. 70% of liver could be damaged before you show signs, What lab is elevated with jaundice? Endocrine problems- sex hormones- estrogen or testosterone increases
39
What causes spider angiomas and palmar erythema with cirrhosis? You see how bulging and torturous those vessels are…imagine the esophagus with esophageal varices, hemorrhoids…
Circulating estrogen
40
Cirrhosis Diagnostic Studies
Liver function studies* Liver ultrasound Liver biopsy *ALT and AST return to normal when liver cells are no longer able to create an inflammatory response
41
Cirrhosis Complication
Portal hypertension varices (esophageal, gastric, hemorrhoids, superficial abd. veins) ascites and edema splenomegaly hepatic encephalopathy hepatorenal syndrome
42
Hepatorenal syndrome: Progressive azotemia-increased serum creatinine-oliguria; renal failure can be reversed by ___________
liver transplantation
43
Collaborative Care for Cirrhosis
Goal: slow the progress of cirrhosis, prevent and treat any complications Management of ascites Prevent bleeding and hemorrhage from esophageal and gastric varices Reduction of ammonia formation with hepatic encephalopathy Diet high in calories, high CHO, moderate to low levels of fat; pt with ascites-low-sodium diet; protein restriction rare Initiate appropriate referrals
44
Nursing Care for Patients with Cirrhosis
Dyspnea Fatigue Anorexia, n/v Jaundice, pruritus Edema, ascites Monitor electrolytes (diuretics) Bleeding tendencies Hepatic encephalopathy Fatigue- cluster care Anorexia- food preferences Edema, ascites- heart sounds, daily wights, electrolytes Hepatic encephalopathy- safety
45
Acute Liver Failure fulminant hepatic failure causes: s&s complications treatment
Causes: drugs (acetaminophen), HBV S/sx: change in mentation, jaundice, coagulation abnormalities, encephalopathy Complications: renal failure, cerebral edema, sepsis Treatment People with acute liver failure are often treated in the intensive care unit of a hospital in a facility that can perform a liver transplant, if necessary. Your provider may try to treat the liver damage itself, but in many cases, treatment involves controlling complications and giving your liver time to heal
46
Liver Cancer hepatocellular cancer ___________ most common cause _____ carcinoma is more common than ______ carcinoma Manifestations often _____ Tx: hepatic resection of the tumor, different types of ablation, chemotherapy, or transplantation
Cirrhosis caused by chronic hepatitis C Metastatic primary insidious
47
Liver Transplantation Rigorous pre-surgery screening Performed using both deceased and live donor livers Split liver transplant (peds*) Postop complications Immunosuppressive therapy
Monitor for acute graft rejection (usually between 4 and 10 days after surgery). *Pediatric patients receive partial liver transplant due to size; generally very sick, stay intubated for awhile, may have to go back to surgery to close belly to achieve better approximation of edges.