LIVER DISEASE AND CIRRHOSIS Flashcards

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1
Q

what is cirrhosis?

A

chronic and severe inflammation of the liver for an extended
period of time. The regenerative capacity of the liver is enormous; however, over a long time,
fibrosis will develop

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2
Q

Causes of cirrhosis

A
  1. alcohol.
  2. primary biliary cirrhosis, 3.sclerosing cholangitis, 4.alpha-1 antitrypsin deficiency,
  3. hemochromatosis, and 6.Wilson disease.
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3
Q

complications of cirrhosis are due to

A

Portal hypertension develops

because of mechanical factors of fibrosis and regenerative liver nodules

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4
Q

clinical presentatiom

A
• Low albumin
• Portal hypertension
• Esophageal varices
• Ascites
• Peripheral edema
• Elevated prothrombin time (prolonged due to loss of ability to synthesize clotting
factors)
• Splenomegaly
• Thrombocytopenia
• Spider angiomata
• Palmar erythema
• Asterixis
• Encephalopathy (possible)
• Jaundice (possible)
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5
Q

Diagnosis of Ascites

A

paracentesis is a sample of the ascitic fluid

obtained by needle through the anterior abdominal wall to exclude infection (SBP)

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6
Q

Spontaneous bacterial peritonitis is

A

idiopathic infection of ascites

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7
Q

Diagnosis of SBP

A

culture of the fluid is

the most specific test

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8
Q

TTT of SBP

A

Cefotaxime or ceftriaxone is the drug of choice for SBP
**the risk of recurrence is 70% per year. Therefore, treat the patient with
norfloxacin or ciprofloxacin daily
**Stop beta blocker
*albumin infusion
will decrease the risk of hepatorenal syndrome

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9
Q

When SAAG ≥1.1, portal hypertension, the cause of ascites is increased hydrostatic pressure

A

When SAAG ≥1.1 and total protein <2.5 g/dL, the portal hypertension is due to
cirrhosis. (liver produces less protein due to decreased function).
• When SAAG ≥1.1 and total protein >2.5 g/dL, heart failure, Budd-Chiari (check JAK2
to work up P. vera)

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10
Q

When SAAG <1.1, it means the ascitic fluid albumin level is high. Cancer and infections generally produce SAAG <1.1.

A

• When SAAG <1.1 and total protein <2.5 g/dL, there is nephrotic syndrome (protein is
lost in urine).
• When SAAG <1.1 and total protein >2.5 g/dL, there is carcinomatosis (think ovarian),
Tb (do peritoneum biopsy, which will have high lymphocytes in ascites, too)

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11
Q

ascites, are managed with

A

1.diuretics
(spironolactone most useful in cirrhosis
2.Furosemide is
commonly added after spironolactone to increase volume removal

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12
Q

furosemide without

spironolactone will lead to

A

hypokalemia, which can cause encephalopathy.

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13
Q

Encephalopathy is managed with

A

lactulose
This converts the NH3 to NH4+, or ammonia to
ammonium
2. rifaximin

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14
Q

HRS is diagnoised by

A

• Increased creatinine >1.5 mg/dL over days to weeks
• Lack of response to albumin infusion for 48 hours (stop diuretics, too)
• Exclusion of other causes of AKI (sepsis); must have normal urine (no blood or
protein)
• Type 1 is more severe with doubling of creatinine in 2 weeks.
• Type 2 is less severe with more gradual increase in creating.

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15
Q

TTT of HRS

A

midodrine, octreotide and albumin

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16
Q

Primary Biliary Cirrhosis is

A

an idiopathic autoimmune disorder (association with other autoimmune diseases, such as Sjögren syndrome, rheumatoid arthritis, and scleroderm)

17
Q

Clinical Presentation.

A

The most common 1.symptoms are fatigue and pruritus

  1. elevated alkaline phosphatase
  2. Osteoporosis and hypothyroidism
18
Q

Diagnosis

A
  1. most common abnormality is elevated
    alkaline phosphatase and gamma glutamyl transpeptidase (GGTP)
    2.total IgM are elevated
    3.most specific blood test is the antimitochondrial antibody.
    4.Biopsy
19
Q

TTT

A
  1. Ursodeoxycholic acid is primary treatment

2. Cholestyramine will help with the pruritus

20
Q

Primary Sclerosis Cholangitis

A

idiopathic disorder of the biliary system most commonly

associated with inflammatory bowel disease (IBD)

21
Q

Clinical Presentation and diagnosis

A

The most specific test for primary sclerosis cholangitis is ERCP or MRCP
2.the antimitochondrial antibody test will
be negativ
3.only liver disease without biopsy

22
Q

TTT

A

endoscopic therapy for strictures; cholestyramine for itching

23
Q

Hemochromatosis is

A

most common inherited genetic diseases. There is an overabsorption of iron in the duodenum

24
Q

clinical presentation

A

• Cirrhosis (most common finding)
• Hepatocellular cancer (15–20% of patients)
• Restrictive cardiomyopathy (15% of patients)
• Arthralgias,
*osteoarthritis
*skin hyperpigmentation, *diabetes, and
*secondary hypogonadism

25
Q

diagnosis

A

1.elevated transferrin saturation >55%
2.Ferritin is
also elevated
3.The most accurate test is a liver biopsy

26
Q

TTT

A
  1. Phlebotomy

2. chelating agents deferoxamine and deferasirox

27
Q

Wilson Disease

A

autosomal recessive disorder leading to a diminished ability to excrete
copper from the body

28
Q

clinical presentation

A

• Copper builds up in the liver, brain, and cornea.
• Basal ganglia dysfunction contributes to the movement disorder which develops.
• Psychiatric disturbance is seen in 10% of patients.
• Kayser-Fleischer rings are found in the eye on slit-lamp examination.
• Tremor and Parkinson’s result in 35% of patients.
*Fanconi syndrome
* Hemolytic anemia

29
Q

Diagnosis

A
  1. The most specific blood test for diagnosis is decreased ceruloplasmin
  2. increased urinary copper.
  3. single most specific test is liver biopsy
30
Q

TTT

A

1.Penicillamine and trientine are copper chelators
2.Oral zinc interferes with copper
absorption