Lecure 5 - Liver 2 Flashcards

1
Q

Presence of hepatic steatosis w/o cause for secondary hepatic fat accumulation?

What two subdivisions?

A

NAFLD

Nonalcoholic Fatty Liver (NAFL)

Nonalcoholic steatohepatitis (NASH)

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2
Q

Most common causes of NAFLD?

A

Obesity
Diabetes
Hypertriglyceridemia (as part of metabolic syndrome + insulin resistance)

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3
Q

Studies indicate an association between NAFLD and what?

A

cholecystectomy

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4
Q

Most NAFLD pts are asymptomatic. However, pts with NASH may complain of what?

A

Fatigue

Malaise

vague RUQ discomfort

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5
Q

Pts w/ NAFLD usually discovered b/c of elevated what?

A

transaminase levels

or incidental finding of hepatic steatosis on abd imaging ordered for another reason

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6
Q

NAFLD lab findings?

in particular, what’s a particular ratio we might be concerned about?

A

elevated transaminases… 1:1 AST/ALT ratio

Elevated ALK PHOS

(hepatic US/biopsy shows sign of steatosis – but we must r/o other causes of fatty liver disease, e.g., alcohol consumption)

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7
Q

NAFLD tx?

Prognosis?

A

Lifestyle changes (diet, exercise, wt. loss, Vit E, insulin sensitizing agents like ***Metformin)

Prognosis = usually benign course (worse prognosis in elderly, diabetic, higher BMI)

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8
Q

Alcohol abuse may lead to steatosis, steatohepatitis, cirrhosis, and hepatocellular carcinoma.

What is seen in roughly 90% of heavy drinkers?

A

Hepatic steatosis

1/3 of patients w/ steatosis will develop steatohepatitis if they continue to drink… 8-20% of pts w/ stetosis will eventually progress to cirrhosis

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9
Q

Alcoholic steatosis (fatty liver)

Typically found incidentally (asymptomatic – though may have hepatomegaly on PE)

What do the labs look like?

A

Elevation of transaminases w/ ratio at 2:1 AST:ALT

Elevated GGT

(referral for US/biopsy if suspected)

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10
Q

Tx for alcoholic steatosis?

A

Abstinence (from alcohol)

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11
Q

Alcoholic steatohepatitis is a progression from?

Classic ssx?

A

Simple steatosis

Jaundice, anorexia, fever, tender hepatomegaly (maybe muscle wasting, abd distension/ascites)

**elevated transaminase w/ 2:1 ratio (AST:ALT)

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12
Q
AST:ALT ration greater than 2:1
elevated serum bilirubin
elevated GGT
leaukocytosis w/ predominance of neutrophils
elevated INR
A

lab findings for alcoholic steatohepatitis

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13
Q

General tx measures for alcoholic steatohepatitis?

A

R/o other causes of acute hepatitis

Obtain US/biopsy

Admit to GI for (alcohol abstinence tx, fluid/nutritional support, infection surveillance, prophylaxis for gastric mucosal bleeding – IV PPI)

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14
Q

Cirrhosis is late stage progressive hepatic fibrosis characterized by?

A

distortion of the hepatic architecture

formation of regenerative nodules

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15
Q

Alcoholic liver disease

Chronic viral hepatitis (hep C, B)

NAFLD

Hemochromatosis

A

Common causes of cirrhosis

A,B,C Not-A, Iron

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16
Q

Cirrhosis can be classified morphologically as?

Which is associated w/ ETOH?

A

mixed, micro, macronodular

MICRONODULAR is associated w/ ETOH

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17
Q

***alcoholic cirrhosis is from chronic alcohol intake… what are the metrics?

A

10 years of 30-50g/day

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18
Q

Progression to cirrhosis significantly increased in patients who have established ___ and continue to ____?

A

Steatohepatitis and continue to consume alcohol

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19
Q

Three stages of cirrhosis?

correlates w/ thickness of fibrous septa

A
  1. Compensated
  2. Compensated w/ varices
  3. Decompensated (ascites, variceal bleeding, encephalopathy, jaundice)
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20
Q

The clinical features of cirrhosis result from?

A

Hepatocyte dysfunction, portosystemic shunting, portal HTN

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21
Q

Features of compensated cirrhosis?

A

May be asymptomatic (most likely)…

Or may present w/ nonspecific ssx such as anorexia, wt loss, weakness, fatigue

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22
Q

Jaundice
Pruritus
Signs of upper GI bleeding (hematemesis, melena, hematochezia)
Abd disention/ascites
Confusion (due to hepatic encephalopathy)

A

DECOMPENSATED cirrhosis

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23
Q

Systemic manifestations of cirrhosis include fatigue, fever, wt loss, muscle wasting… and what else?

A

Decreasing BP/MAP

pts w/ HTN may normalize or even become HOTN

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24
Q

Hyperdynamic circulation in cirrhotic pts means what?

A

decrease in SVR and arterial pressure -> reduction in arterial blood volume -> diminished renal flow stimulates RAAS -> increase HR/CO

25
Q

Abd findings/manifestions of systemic cirrhosis?

A
Ascites (shifting dullness)
Hepatomegaly
Splenomegaly
Caput medusa
Venous hum (Cruvheilhier-Baumgarten murmur)
26
Q

Dermatologic findings of systemic cirrhosis?

A
Jaundice
Spider angiomata
Palmar erythema
Nail changes 
Nail clubbing
27
Q

Muehrcke nails (white linear patches)

Terry nails (pink band just proximal to lunula)

A

Nail findings of systemic cirrhosis

28
Q

Endocrine cirrhosis manifestations in women?

A

Chronic anovulation/amenorrhea/irregular menstrual bleeding

29
Q

Endocrine cirrhosis manifestations in men?

A

Hypogonadism (impotence, infertility, loss of sexual drive, testicular atrophy)

GYNECOMASTIA

30
Q

HEENT signs of systemic cirrhosis?

A

Hepatic fetor (sweet pungent breath)

Parotid gland enlargement

31
Q

Neurlogic ssx of cirrhosis?

A

Hepatic encephalopathy

Asterixis (bilateral/asynchronous flapping motions of outstretched, dorsiflexed hands)

32
Q

Early/compensated cirrhosis may show minimal/no findings….

Later, you might see what?

A

LATer signs of compensated cirrhosis =

Leukocytosis/leukopenia

Anemia

Thrombocytopenia (due to splenomegaly)

33
Q

In cirrhosis, a hepatic panel would show an icnraesed in everyting but?

A

Albumin

(also might see hyponatremia in Serum chemistry)

(NOTE: the slides don’t specifically say thrombocytopenia… BUT yeah, thrombocytopenia in late compensated cirrhosis, so we can assume…)

34
Q

Shrunken, irregular, nodular appearing liver?

A

Cirrhotic liver on US

35
Q

How might you determine the extent of esopahgeal varices and gastropathy in a patient w/ cirrhosis?

A

capsule endoscopy

36
Q

Tx for cirrhosis?

A

Abstinence from ETOH (monitored/in patient)
Dietary consult
Immunizations

(ultimately a liver transplant)

37
Q

Most common cause of ascites?

A

Portal HTN (from liver disease)

Hypoalbuminemia
Chylous/pancreatic/bile ascites
infections/malignancies

38
Q

Primary symptom is bloating/increasing abd girth

(w/w/o abd pn)

W/ this sign… what should you ask?

A

this is ascites

Ask about h/o liver disease, risk factors liver disease (Alcohol abuse? Risk factors for hep? Hx of CA?)

39
Q

PE ssx of portal HTN?

A

Hepatomegaly
Elevated JVP
Large abd wall veins

Signs of liver disease (Muscle wasting, malnourishment)

FEVER = BACTERIAL PERITONITIS

40
Q

Abd paracentesis….

  1. Cloudy?
  2. Milky?
  3. Bloody?
A
  1. cloudy = infection
  2. milky = chyle (malignancy?)
  3. Bloody = traumatic/malignancy

(other studies include WBC, albumin/total protein/culture and gram stain)

41
Q

SAAG is 1.1 g/dL or higher means?

A

portal HTN

42
Q

For treatment of portal HTN as etiology of ascites… we can use?

A

Transjugular Intrahepatic Portosystemic Shunt (TIPS)

diversion of portal blood flow into the hepatic vein

43
Q

Spontaneous BActerial peritonitis?

A

infection of ascitic fluid in absence of intraaddominal source

Strep pneumo
Enterococcus
E. coli
Klebsiella
Strep viridans

(must differentiate from secondary)

44
Q

Ascites
Fever
Abd pn w/o TTP

(abd ttp suggests other source)

A

Spontaneous bacterial peritonitis

45
Q

Most important lab test for spontaneous bacterial peritonitis?

What do you do if you suspect bacterial peritonitis?

A

Most important is evaluation of ascetic fluid via paracentesis (gram stain culture and CBC w/ diff)

If secondary suspected, CT for source of infection

46
Q

Treatment for spontaneous bacterial peritonitis?

Prophylaxis?

A

ADMIT!
3rd gen cephalosporin
Ceftriaxone

Prophylaxis = cipro or TMP-SMX DS

47
Q

Complication of cirrhosis

Represents end stage of a sequence of reductions in renal perfusion

PROGNOSIS IS SUPER POOR…

what is this and what is it characterized by?

A

Hepatorenal syndrome

azotemia in absence of parenchymal renal injury/dz

SrCR of 1.5 mg/dL or higher

48
Q

Therapy for hepatorenal syndrome is improvement of LIVER function… what else should we do?

A

If short liver function improvement is not possible, reverse the acute kidney injury.

ADMISSION TO ICU!

49
Q

Complication of cirrhosis

Systemic build up ammonia

Neuropsychiatric abnormalities

A

hepatic encephalopathy

50
Q
AMS
Sleep pattern inversion
Mood changes (euphoria/depression)
Decreased attention
Imparied short term memory

(late signs = somnolence, confusion, coma)

A

Hepatic encephalopathy

51
Q

Late signs of hepatic encephalopathy?

A

Somnolence (super sleepiness)
Confusion
Coma

52
Q
Asterixis
Bradykinesia
Ataxia
Slurred speech
Hyperactive deep tendon reflees

Nystagmus

A

PE exam findings for hepatic encephalopathy

53
Q

Tx for hepatic encephalopathy?

A

Admission

  • PROTEIN REDUCTION
  • LACTULOSE - reduces ammonia in serum

fluid/electrolyte replacement

pre/probiotics have shown efficacy in improving hepatic encephalopathy

54
Q

MELD score… Model for End Stage Liver Disease

A

Higher = worser

55
Q

Hepatoxic substances?

A

NSAIDs
Acetaminophen
Statins
Abx

Tylenol + Alcohol = potentiation

56
Q

Direct hepatotoxicity is predictiable…

A

dose related severity
latent period after exposure
universal susceptibility

57
Q

Diagram for acetaminophen?

Tx for OD?

A

Rumack-Matthew Nomogram

Tx w/ N-acetylcysteine

58
Q

Toxic liver injury… classified by pathogenesis and pattern of injury… such as?

A

Hepatocellular injury (hepatitis)

Cholestatic injury (non-inflammatory or inflammatory [cholangitis])

Mixed injury

59
Q

Tx for toxic liver injury?

A

DISCONTNUE THE AGENT

Inpatient vs. outpatient depends on severity

Referral to GI/hepatology

Serial LFTs to monitor for nomalization