Liver Disease Flashcards

1
Q

Liver: major metabolic organ (3)

A
  • receives nutrient-rich blood from GI; mix of venous and arterial blood
  • gets nutrients ready for metabolism
  • regulates glucose and protein metabolism
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2
Q

liver metabolism

A
  • protein metabolism: ammonia –> urea, excreted in urine
  • synthesis albumin (transporter), clotting factors
  • break down of fatty acids for energy
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3
Q

liver metabolism (bile, bilirubin)

A
  • bile: removal of waste from blood stream into bile (bilirubin, urea)
  • bile: digestive function (emulsification of fats)
  • bilirubin: from breakdown of Hg, excreted mostly through bile
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4
Q

liver metabolism (drug metabolism)

A
  • drug metabolism: barbiturates, opioids, sedatives, anesthetics
  • mostly drug inactivation by binding of medication with other compound
  • excretion in feces or urine (before reaching blood stream)
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5
Q

liver metabolism (PO meds)

A
  • PO meds: decreased availability in serum if major metabolism by liver before reaching systemic circulation (first pass effect) - IV route
  • morphine, insulin (first pass effect) –. that is why they are given IV/subq
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6
Q

age related changes of the hepatobiliary system (11)

A
  • steady decrease in size and weight of liver, particularly in women
  • decrease in blood flow
  • decrease in replacement/ repair of liver cells after injury
  • reduced drug metabolism
  • slow clearance of hep B surface antigen
  • more rapid progression of hep C infection and lower response rate to therapy
  • decline in drug clearance capability
  • Increased prevalence of gallstones due to the increase in cholesterol secretion in bile
  • decreased gallbladder contraction after a meal
  • atypical clinical presentation of biliary disease
  • more severe complications of biliary tract disease
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7
Q

Liver assessment: health hx (9)

A
  • alcohol***/drug use, hepatotoxic meds
  • exposure to toxins, infection
  • occupation, travel
  • lifestyle, recreational habits
  • PMH, family hx
  • nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH)
  • strongly associated with obesity
  • Increased r/o liver cancer
  • obesity raises ALT, marker of liver damage in children, adolescents
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8
Q

Liver assessment: clinical manifestations

A
  • symptoms: fever, anorexia, edema, personality changes
  • jaundice, pruritus
  • fatigue, weakness, malaise
  • abd pain, increased abdominal girth, hematemesis
  • sleep disturbances
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9
Q

Liver physical assessment (7)

A
  • pallor, jaundice (skin, mucosa, sclera)
  • muscle atrophy, edema, palmar erythema
  • ecchymosis, petechiae. spider angiomas
  • mental status/neurologic changes (recall, memory) (late, severe disease). **Report to provider sudden late changes: possible hepatic encephalopathy **
  • tremor, weakness, asterisks (late, severe disease, report)
  • slurred speech (late, severe disease)
  • palpable liver, abdominal fluid wave (late, severe disease)
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10
Q

Palpating the liver (4)

A

-place left hand under right lower rib cage –> lightly press the abdomen down on the same side –> try to feel for the inferior border of the liver –> healthy liver will not be palpable

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11
Q

Liver Diagnostic evaluation (4)

A
  • liver panel or liver function tests –> * ALT, AST, alkaline phosphatase (more common), bilirubin*, albumin (edema), total protein, serum globulin, lactate dehydrogenase, PT, INR, aPTT (coagulation)
  • lipid panel: LDL, HDL, total cholesterol
  • biopsy
  • US, CT, MRI
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12
Q

May take more than __% tissue damage before abnormal __.

A

70%, LFTs

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13
Q

ALT

A

liver-specific, monitor cirrhosis, hepatitis

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14
Q

AST

A

tissues with high metabolic activity – liver, heart, skeletal muscle, kidney cell damage/death

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15
Q

What is jaundice?

A

bilirubin accumulation in the blood

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16
Q

normal total bilirubin range

A

0.3-1.9 mg/dl

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17
Q

portal hypertension

A

from obstruction of blood flow –> ascites, esophageal varices

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18
Q

portal hon assessment

A

daily weight and abdominal girth measurement

19
Q

ascites (how it happens)

A

increase in capillary pressure, obstruction of venous blood flow through the damaged liver

20
Q

ascites management (3)

A
  • low sodium diet, diuretics (spironolactone), bed rest, paracentesis
  • daily weight loss 1-2 kg
  • monitor for FE imbalances
21
Q

Paracentesis

A
  • larger volume (5-6L) ascites causes respiratory distress
  • concurrent infusion of albumin
  • monitor postparacentesis VS, renal, respiratory
22
Q

Transjugular Intrahepatic Portosystemic Shunt (TIPSS)

A

facilities drainage of engorged liver into vena cava

23
Q

Why does hepatic encephalopathy happen?

A

from increased serum ammonia, dehydration, meds, electrolyte unbalance

24
Q

hepatic encephalopathy clinical manifestations

A

ALOC, motor changes (asterixis)

25
Q

What to manage during hepatic encephalopathy?

A

FE imbalance, serum ammonia level

26
Q

hepatic encephalopathy: lactulose *****

A

promotes ammonia excretion through feces; monitor for soft bowel movements

27
Q

hepatic encephalopathy: Rifaximin

A

better tolerated and works faster than lactulose; also used for travelers diarrhea and IBS. Few and mild side effects

28
Q

hepatic encephalopathy: management (3)

A
  • watery diarrhea: medication overdose
  • monitor VS, FE imbalance, IO, neuro, handwriting, arithmetic, serum ammonia
  • protein intake moderately restricted, avoid foods high in protein
29
Q

Nutritional management of hepatic encephalopathy (5)

A
  • minimize the formation and absorption of toxins, principally ammonia, from the intestine
  • keep daily protein intake between 1.2-1.5 g/kg body weight per day
  • avoid protein restriction if possible, even in those with encephalopathy
  • for patients who are truly protein intolerant, provide additional nitrogen in the form of an amino acid supplement.
  • provide small, frequent meals and 3 small snacks per day in addition to a late-night snack before bed
30
Q

Stage 1 hepatic encephalopathy: clinical symptoms, clinical signs and EEG changes

A

Clinical symptoms –> normal LOC with periods of euphoria and lethargy; reversal of day-night sleep patterns

Clinical signs and EEG changes –> impaired writing and ability to draw line figures. Normal EEG

31
Q

Stage 2 hepatic encephalopathy: clinical symptoms, clinical signs and EEG changes

A

Clinical symptoms –> increased drowsiness; disorientation, inappropriate behavior; mood swings, agitation

Clinical signs and EEG changes –> asterixis; fetter hepatitis. Abnormal EEG with generalized slowing.

32
Q

Stage 3 hepatic encephalopathy: clinical symptoms, clinical signs and EEG changes

A

Clinical symptoms –> stuporous; difficult to arouse; sleeps most of the time; marked confusion; incoherent speech

Clinical signs and EEG changes –> asterixis; increased DTR; rigidity of extremities. EEG markedly abnormal

33
Q

Stage 4 hepatic encephalopathy: clinical symptoms, clinical signs and EEG changes

A

Clinical symptoms –> comatose; may not respond to painful stimuli absence of asterixis; absence of DTR; flaccidity of extremitie. EEG markedly abnormal

Clinical signs and EEG changes –> absence of
asterixis; absence of DTR; flaccidity of extremitie. EEG markedly abnormal

34
Q

Other manifestations of hepatic dysfunction (4)

A
  • edema (low serum albumin- lack of production by liver)
  • Bleeding: Implement fall precautions ***** due to increased risk for bleeding, report any falls to MD
  • vitamin deficiency
  • pruritus
35
Q

esophageal varices (what it is, clinical manifestations, monitor, how to treat) (5)

A
  • profuse bleeding may lead to airway loss and hemorrhagic shock
  • hematemesis, melena, acute clinical deterioration
  • VS, endoscopy, CBC, LFT
  • vasoactive drugs for acute blood loss (IV octerotide)
  • Sclerotherapy (thrombosis), vaticeal banding
36
Q

What is cirrhosis?

A

normal tissue replaced with diffuse fibrosis; decreased liver function

37
Q

most common cause of cirrhosis

A
  • alcoholic –> scar tissue takes place of normal liver
38
Q

What is biliary cirrhosis?

A

scarring around bile duct

39
Q

s/s compensated cirrhosis (10)

A
  • intermittent mild fever
  • vascular spiders
  • palmar erythema
  • unexplained epistaxis
  • ankle edema
  • vague morning indigestion
  • flatulent dyspepsia
  • abd pain
  • firm, enlarged liver
  • splenomegaly
40
Q

s/s decompensated cirrhosis (14)

A
  • muscle wasting
  • ascites
  • jaundice
  • weakness
  • weight loss
  • continuous mild fever
  • clubbing of fingers
  • purpura
  • spontaneous bruising
  • epistaxis
  • hypotension
  • sparse body hair
  • white nails
  • gonadal atrophy
41
Q

Hepatic cirrhosis clinical manifestations (5)

A
  • hepatomegaly, anemia, vitamin deficiency, mental deterioration
  • portal obstruction and ascites
  • Infection and peritonitis (translocation of intestinal flora; * elevated temp is an ominous sign**
  • GI varices (esophageal, rectal, abdominal)
  • edema: reduced plasma albumin
42
Q

Hepatic cirrhosis dx (4)

A
  • liver function tests
  • serum albumin, globulin, AST, ALT, bilirubin, PT, US, CT, MRI
  • liver biopsy
  • ABGs
43
Q

Hepatic cirrhosis medical management (3)

A
  • antacids, H2 antagonists (minimize GI bleeding)
  • vitamins, nutritional supplements, improvement of nutritional status
  • K-sparing diuretics: spironolactone (pts with hypokalemia), triamterene
44
Q

Hepatic cirrhosis medical management –> 2020 study

A

-increased r/o hepatic encephalopathy in patients with cirrhosis prescribed short-term and chronic opioids prescription