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Clin Med - GI > Liver Disease and Alcohol-Related Liver Disease - collins (INCOMPLETE _ DO X slides) > Flashcards

Liver Disease and Alcohol-Related Liver Disease - collins (INCOMPLETE _ DO X slides) Flashcards

1
Q

when is hemoglobin broken down into

A

heme and globin
heme converted to biliviridin

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2
Q

what bilivurdin

A

converted heme that becomes unconjugated bilirubin (bound to albumin - fat soluble)

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3
Q

what are the four phases of bilirubin metabolism

A

production of bilirubin
uptake via liver cells
conjucation with glucuronic acid
transport via bile/urobilinogen

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4
Q

what is hyperbilirubinemia

A

impairment or dysfunction of any of the phases of bilirubin metabolism

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5
Q

what is the accumulation of bilirubin in the body clinically

A

jaundice

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6
Q

what is normal total bilirubin (indirect and direct)

A

0.2 - 1.2 mg/dL

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7
Q

what is normal newborn total bilirubin

A

1.0-12.0mg/dL

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8
Q

what are the lab values that jaundice is apparent around

A

2.5 - 3 mg/dL

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9
Q

what is unconjugated (indirect) hyperbilirubinemia

A

overproduction from hemolysis
impaired uptake secondary to certain drugs
impaired conjugation by glucoronyl transferse

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10
Q

what is overproduction from hemolysis

A

increased supply of unconjugated bilirubin overwhelms the liver

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11
Q

What is the clinical presentation of overproduction of hemolysis

A

sickle cell, hereditary spherocytosis, Rh incompatabiliy, transfusion reaction
normal stool color; urine color normal
increased indirect/unconjugated bilirubin
+ splenomegaly

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12
Q

what are impaired conjugation

A

physiological neonatal jaundice
gilbert syndrome
Crigler-najjar syndrome

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13
Q

what is impaired uptake

A

primarily a result of certain drugs
rifampin, chlecystographic contrast agents
? gilbert syndrome

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14
Q

what is the clinical presentation of impaired uptake

A

light to normal stool; normal to dark urine color
elevated indirect/unconjugated bilirubin
no bilirubin in urine
resolvves with removal of drug

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15
Q

what are the clinical presentations of impaired conjugation

A

light to normal stool; normal to dark urine
elevated indirect/unconjugated bilirubin
no bilirubin in urine

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16
Q

what is physiologica neonatal jaundice

A

fetal bilirubin cleared by mom
immature GT in newborns
develosp around days 2-5 of life in most newborns

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17
Q

what makes unconjugated bilirubin water soluble in physiological neonatal jaundice

A

UV light

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18
Q

what is Gilbert syndrome

A

hereditary disorder
reduced function of GT
episodic jaundice and hyperbilirubinemia
lifelong problem

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19
Q

What is Crigler-Najjar syndrome

A

autosomal recessive inherited GT disorder
partial to complete loss of GT - complete loss - type1, partial loss - type 2
primarily identified in neonates, persists throughout life

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20
Q

what is conjugated (direct) hyperbilirubinemia

A

decreased excretion of bilirubin
primarily a result of obstruction or hepatocellular dysfunction
-hard to differentiate on labs - elevated Alk Phos, elevated AST/ALT with hepatocellular problems

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21
Q

what are examples of hepatocellular dysfunction

A

hepatitis
cirrhosis
biliary cirrhosis
sepsis/infection
post-operative
cholangitis
sarcoidosis
lymphomas
toxns

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22
Q

what are obstructiosn

A

choledocholithiasis
biliary atresia
carcinoma of biliary duct
sclerosis cholantitis
pancreatitis
pancreastic neoplasma

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23
Q

What does liver function testing typically inclued

A

serum bilirubin
serum albumin
ALK phos
ALT/AST
INR (prothrombin time)
+/- urine bilirubin
+/- GGT (gamma-glutamyl tranferase)
+/- 5’-nucleotidase

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24
Q

what is the most common cause of AST/ALT elevation

A

NAFLD

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25
Q

when is AST > ALT

A

Alcohol-related liver injury and cirrhosis

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26
Q

what releases alkaline phosphate

A

gallbladder

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27
Q

what is low serum albumin typically reflective of

A

chronic liver disease/cirrhosis

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28
Q

what is elevated PT/INR reflective of

A

poor hepatocyte function

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29
Q

what are the vitamin K dependent clotting factors

A

10, 9, 7, 2

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30
Q

what is the definitive study for determining cause and severity of liver disorders

A

liver biopsy

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31
Q

when does acute liver failure occur

A

without pre-existing liver disease

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32
Q

what is fulminant ALF

A

development of hepatic encephalopathy within 8 weeks

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33
Q

what is subfulminant ALF

A

hepatic encephalopathy 8 weeks to 6 months after onset

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34
Q

what are the causes of Acute liver failure

A

acetaminophen (APAP) toxicity
idiosyncratic drug reactions

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35
Q

what is the presentation of acute liver failure

A

jaundice
bleeding disorders
encephalopathy / AMS

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36
Q

what are late complications of acute liver failure

A

systemic inflammatory response syndrome (SIRS) - from death of hepatocytes
Multisystem organ dysfunction

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37
Q

what are LFT findings with ALF

A

significant LFT dysfunction
APA - AST/ALT increase (>5000)
Serum amylase
elevated ammonia (NH3) level
elevated PT-INR

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38
Q

what is the treatment for ALF

A

admit to ICU for management of multiorgan failure
culture transplant team

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39
Q

what determines liver transport priority

A

MELD score (age >12)

40
Q

what is progressive hepatocyte dysfunction and accumulation of fatty tissue

A

non-alcohol related liver disease - exists on a continuum

41
Q

what is the continuum of liver disease

A

Normal liver - NAFLD - NASH - cirrhosis

42
Q

What is NAFLD

A

common
hepatic accumulation of fat absent of significant ETOH consumption
M>W
Hispanic > caucaasian > black

43
Q

what is NAFLD strongly correlated with

A

insulin resistance

44
Q

what is NAFLD commonly associated with

A

Metabolic syndrome
Obesity (BMI >30)
T2DM
Dyslipidemia

45
Q

what is the presentation of NAFLD

A

primarily asymptomatic
+/- RUQ discomfort
non-specific constitutional symptoms
+/- isolated hepatomegaly

46
Q

how is NAFLD diagnosed

A

diagnosis of exclusion so must r/o ETOH liver disease

47
Q

what is the treatment of NAFLD

A

no reliable treatments except lifestyle modifications
GRADUAL weight loss
anti-diabetic agents
tx of dyslipidemias

48
Q

What is NASH

A

NAFLD + inflammation and fibrosis
2nd hit hypothesis: NAFLD + secondary insult
also reversible

49
Q

what are risk factors for progression of NASH

A

obesity
older age
non-AA ethnicity
female
DM
HTN
higher AST, ALT, or AST: ALT
worse US

50
Q

what is cirrhosis

A

end stage fibrosis and hepatocyte death

51
Q

what causes cirrhosis

A

viral hepatitis (C&B)
Alcohol
NAFLD
drug toxicity
autoimmune metabolic liver disorder

52
Q

what are the three stages of cirrhosis

A

compensated
compensated with varices
decompensated - ascites, variceal bleeding, encephalopathy, jaundice

53
Q

what are the initial symptoms of cirhosis

A

fatigue
disturbed sleep
muscle cramps
weight loss

54
Q

what are the later symptoms of cirrhosis

A

anorexia, N/v
reduced muscle strength, reduced exercise capacity
abdominal pain
menstrual irregularities (amenorrhea)
ED, loss of libido
sterility
gynecomastia
hematemesis
skin manifestations, vitamin deficiencies, weight loss, chronic wasting, jaundice, FIRM, PALPABLE, NODULAR LIVER

55
Q

what is seen on labs with cirrhosis

A

macrocytic anemia
thrombocytopenia
prolonged PT-INR
AST and ALT elevations
Elevated bilirubin
low albumin
renal dysfunction
elevated BNP/ventricular dysfunction
low cortison
other hormone dysfunction

56
Q

what imaging studies can be used to identify cirrhosis

A

US to asses liver size, for ascites, assess for hepatocellular carcinoma
doppler US to assess patency of hepatic, splenic and portal veins
CT/MRI with contrast to define any nodules
liver biopsy for cirrhotic histology
EGD for varices or UGI bleeding

57
Q

what is the treatment of cirrhosis

A

abstain from ETOH, adequate caloric intake with increased proteins, sodium restriction for fluid retention, vitamin supplementations
HAV, HBV and pnumoccocal vaccines
yearly influenza
Liver transplant is curative

58
Q

what is ascites

A

portal hypertension - third spacing
peritoneal fluid buildup

59
Q

what is diagnostic and therapeutic for ascites

A

paracentesis - lights criteria

60
Q

what are complications of paracentesis

A

bleeding
infection bowel performation

61
Q

what is lights criteria

A

determines if something is transudative or exudative
looks at serum protein, serum LDH and pleural fluid LDH

62
Q

what is the treatment of ascites

A

sodium restriction (<2,000mg/day)
spironolactone + furosemide
Large volume paracentesis (5L)
transjugular intrhepatic portosystemic hunt (TIPS)

63
Q

what is spontaneous bacterial peritonitis

A

infection of peritoneal fluid
causes abdominal pain, icnreasing ascited, fever and progressive encephalopathy

64
Q

how do you diagnose spontaneous bacterial peritonitis

A

culture of ascitic fluid with paracentesis

65
Q

what is the treatment of spontaneous bacterial peritonitis

A

cefotaxime 2g

66
Q

what is hepatorenal syndrome

A

characterized by Azotemia, macroscopic evidence of kidney injury, shock,
see oliguria, hyponatremia, low urinary sodium

67
Q

what is the treatment of hepatorenal syndrome

A

dialysis (modified protocol) and TIPS

68
Q

what is hepatic encephalopathy

A

altered CNS function from toxin buildup - ammonia
spectrum: day-night reversal - coma

69
Q

what is hepatic encephalopathy precipitated by

A

constipation, opioids, hyovolemia, infection

70
Q

what is the characteristic sign of hepatic encephalopathy

A

asterixis

71
Q

what is the treatment of hepatic encephalopathy

A

lactulose or rifamixin to reduce ammonia (excreted in feces)

72
Q

what is esophageal varices

A

dilated submucosal veins secondary to portal HTN
occurs in about 50% of pts with cirrhosis
high mortality rate with acute bleed

73
Q

what are the signs and symptoms of acute UGI bleeding

A

hematemesis or “coffee ground” emesis
melena

74
Q

what is the treatment of esophageal varices

A

fluid resuscitation and blood transfusion
FFP or platelet transfusions
adjunctive vitamin K
prophylactic abx: fluoroquinolones
octreotide for acute bleeding control
endoscopy
portal decompression
BBlockers

75
Q

What is hepatocellular carcinoma (HCC)

A

85% of HCC associated with cirrhosis
hepatitis and ETOH cirrhosis at greatest risk for converstion

76
Q

what are risk factors for hepatocellular carcinoma

A

male
age>55
asian or hispanic ethnicity
+FH
overweight/obese
tobacco use
DM
hypothyroid

77
Q

what is the presentation of hepatocellular carcinoma

A

cachexia, weihgt loss, weakness
suden development of ascites
enlarging liver with palpable amss

78
Q

what is the diagnostic test of choice for HCC

A

biopsy

79
Q

what is the definitive treatment of cirrhosis and complications

A

TRANSPLANT

80
Q

what are absolute contraindications of liver transplant

A

malignancy (except small HCC)
advanced cardiopulmonary disease (except heaptopulmonary syndrome)
sepsis

81
Q

what is the MELD score

A

transplant patients prioritized

82
Q

are HIV and Hepatitis contraindications for liver transplants

A

NO

83
Q

What is the AUDIT - C

A

scoring for alcohol use disorder identification

84
Q

what is the spectrum for Alcohol related liver disease

A

alcohol related steatosis - alcohol-related heapatitis -cirrhosis

85
Q

what are risk factors for alcohol-related liver disease

A

genetics
gender (F>M)
concurrent APAP use
concurrent obestiy
concurrent DM
concurrent HCV

86
Q

what is alcohol related liver steosis

A

reversible with ETOH dicontinuation
presensation similar to NAFLD
fatigue, anorexia, nausea and RUQ abdominal discomfort

87
Q

what are the later lab findings with alchol related liver disease

A

AST: ALT > 2:1 (HIGH SUSPICION if >3:1)
AST rarely above 300, ALT often normal
elevated GGT helps differentiate from other causes of liver dz
elevated alk phos (<3xnml)
thrombocytopenia due to direct toxic effect of ETOH and hypersplenism

88
Q

what imagine is used for diagnosis of Alcohol related liver disease

A

US to evaluate for steatosis
CT or MRI with contrast to rule out other causes
biopsy

89
Q

what is the treatment for fatty liver

A

abstinence from ETOH
-mental health/detox/rehab, psychosocial interventions
-naltrexone
-disulfram (anatbuse)
- improve nutrition
-treat vitamin deficiencies

90
Q

what is the treatment of cirrhosis

A

abstinence from ETOH
mental health, detox/rehab, psychosocial intervention
Naltrexone (avoid disulfram)
slows or halts progression
-improve nutrition, vitamin deficiencies, sodium restriction, regular exercise to prevent muscle wasting

91
Q

what is the definitive treatment of cirrhosis

A

transplant

92
Q

What is alcohol-related hepatitis

A

hepatocyte injury characterized by:
acute or chronic inflammation, fibrosis, parenchymal necrosis

93
Q

what is the presentation of alcohol related hepatitis

A

recent period of heavy drinking followed by:
jaundice, fever, nausea, anorexia, generalized edema, RUQ abdominal pain, tender hepatosplenomegaly

94
Q

what is seen on labs with alcohol related hepatitis

A

same as other alcohol related liver disease
AST:ALT >2:1 (HIGH SUSPICION IF >3:1)
elevated serum bilirubin
leukocytosis with left shift
elevated alk phos, GGT

95
Q

what is the treatment of alcohol related hepatitis

A

abstinence from ETOH
??corticosteroids if severe
alternative: pentoxifylline (PDE inhibitor)

Clin Med - GI (11 decks)

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