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NAFLD Flashcards

1
Q

Most common chronic liver disease in many parts of the world

A

Nonalcoholic Fatty liver disease

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2
Q

NAFLD results from

A

When hepatocyte mechanisms for triglyceride synthesis overwhelm mechanisms for triglyceride disposal, leading to accumulation of fat within hepatocytes

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3
Q

Are triglycerides hepatotoxic

A

No

But their precursors and metabolic by products may lead to hepatocyte lipotoxicity

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4
Q

Disease entities under Nonalcoholic Fatty liver diseases

A

Nonalcoholic hepatic steatosis
Nonalcoholic steatohepatitis (NASH)
Nonalcoholic liver cirrhosis and hepatocellular carcinoma

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5
Q

Simple accumulation of triglycerides within hepatocytes in the absence of significant necroinflammation or fibrosis

A

Nonalcoholic hepatic steatosis

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6
Q

Histologically conspicuous hepatocyte death and inflammation

A

Nonalcoholic steatohepatitis (NASH)

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7
Q

Most clinically ominous extreme of disease entities under NAFLD

A

Nonalcoholic liver cirrhosis and hepatocellular carcinoma

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8
Q

NAFLD is associated with

A 
Overweight/ obesity 
Insulin resistance
Diabetes
Hypertriglyceridemia 
Hypertension
Cardiovascular disease
Chronic Fatigue
Mood alterations
Obstructive sleep apnea
Thyroid dysfunction
Polycystic ovary syndrome
Pancreaticsteatosis
Elevated serum uric acid levels
Colonic adenoma
Chronic pain syndrome
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9
Q

Clinical manifestations of NAFLD

A

Most are asymptomatic
Vague RUQ pain or hepatomegaly
Most have features of metabolic syndrome

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10
Q

How to diagnose NAFLD

A

Requires demonstration of increased liver fat in the absence of hazardous levels of alcohol consumption ( <1 drink/day in women <2 drinks/day for men)

Exclusion of other causes of fat accumulation (drugs ) and liver injury (viral hepatitis, autoimmune liver disease, iron/ copper)

Does not require invasive testin

  1. Liver imaging - UTZ as first line test
  2. Blood tests - to exclude other liver diseases
  3. Condifence in diagnosis is increased by identification of NAFLD risk factors
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11
Q

Management of NAFLD is divided into 3 components

A

Specific therapy of NAFLD related liver disease
Treatment of NAFLD-related comorbidities
Treatment of advanced NAFLD complications

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12
Q

Which NAFLD patients are considered for targeted pharmacologic therapies

A

Patients with NASH

Those with features of hepatic fibrosis on liver biopsy

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13
Q

What are targeted pharmacologic therapies for NAFLD

A 
Metformin
Thiazolidinediones 
Vitamin E
Ursodeoxycholic acid 
Omega-3 fatty acids
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14
Q

NAFLD management focuses on treatment to

A

Improve risk factors for NASH

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15
Q

5 aspects of management of NAFLD

A 
Diet and exercise
Statins
Bariatric surgery
Liver transplantation
Monitoring and surveillance
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16
Q

How to advise diet and exercise to an NAFLD patient

A

Moderate calorie restriction - decrease calories by 500- 750 kcal and achieve 7-10 %. Weight loss
Avoid saturated fatty acids and high-fructose corn syrup in diet
Moderate exercise 4-5 times weekly for 30-45 minutes

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17
Q

Used to treat dyslipidemia in patients with NAFLD/ NASH

A

Statins

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18
Q

Beneficial for metabolic syndrome complications in individuals with refractory obesity
Reduces liver fat and likely to reduce NASH progression

A

Bariatric surgery

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19
Q

Is the 3rd most common indication for liver transplantation

A

NAFLD

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20
Q

When is liver transplantation indicated for NAFLD patients

A

End-stage liver disease

And or HCC

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21
Q

Natural course of liver cirrhosis

A

Chronic liver disease -> compensated cirrhosis -> decompensated cirrhosis -> death

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22
Q

What differentiates compensated vs decompensated cirrhosis?

A

The presence of complications

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23
Q

Etiology of Liver Cirrhosis

A

Alcoholic cirrhosis Chronic Viral Hepatitis B and C Autoimmune Hepatitis Nonalcoholic steatohepatitis Biliary Cirrhosis Cardiac cirhosis Inherited metabolic liver diseases- Hemochromatosis, Wilson’s disease Cryptogenic

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24
Q

Complications of Liver Cirrhosis

A

Portal hypertension (varices, gastropathy, ascites, splenomegaly) Hepatic encephalopathy Hepatorenal syndrome Portopulmonary syndrome Hepatopulmonary syndrome Cirrhotic cardiomyopathy Endocrine dynsfunction (adrenal insufficiency, gonadal dysfunction, thyroid dysfunction, bone disease) Malnutrition Coagulopathy (factor deficiency, fibrinolysis, thrombocytopenia) Hematologic (Anemia, thrombocytopenia, neutropenia)

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25
Q

Elevation of hepatic venous pressure gradient > 5 mmHg

A

Portal Hypertension

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26
Q

A significant complicating feature of decompensated cirrhosis

A

Portal hypertension

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27
Q

Development of portal hypertension is usually revealed by these laboratory findings

A

thrombocytopenia splenomegaly development of ascites encephalopathy esophageal varices with or without bleeding

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28
Q

Classification of Portal Hypertension

A

Pre-Hepatic Hepatic Post- Hepatic

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29
Q

Affects the portal venous system before it enters the liver

A

Pre-hepatic

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30
Q

Most common cause of portal hypertension

A

Hepatic

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31
Q

Types of hepatic causes of portal hypertension

A

Presinusoidal Sinusoidal Postsinusoidal

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32
Q

PH: Affects the hepatic veins and venous drainage to the heart

A

Post-Hepatic

33
Q

Pre-hepatic causes of PH

A

Portal vein thrombosis Splenic vein thrombosis Massive splenomegaly (Banti’s syndrome)

34
Q

Hepatic causes of PH: presinusoidal

A

schistosomiasis congenital hepatic fibrosis primary biliary cirrhosis sarcoidosis

35
Q

Hepatic causes of PH: sinusoidal

A

cirrhosis alcoholic hepatitis

36
Q

Hepatic causes of PH: postsinusoidal

A

Hepatic sinusoidal obstruction (venoocclusive syndrome(

37
Q

Post-Hepatic causes of PH

A

Budd-Chiari syndrome Inferior vena cava webs Cardiac causes

38
Q

Complications of Portal Hypertension (3)

A

Gastroesophageal varices
Ascites
Hypersplenism

39
Q

What is the mechanism of gastroesophageal varices secondary to PH

A

Resistance to portal flow leads to increased resistance in portal pressure
decreased splanchnic arteriolar resistance leads to increased splanchnic flow (increase portal blood flow)

40
Q

What is the mechanism of ascites secondary to PH

A

Due to portal hypertension, vasodilation of splanchnic arterial system occurs resulting in

  1. Increased splanchnic pressure due to increase portal venous flow -> ascites
  2. Underfilling of arterial system -> RAAS activation -> hyperaldosteronism -. Na/H2O retention -> ascites
  3. Decreased synthetic function of the liver -> hypoalbuminemia -> decreased oncotic pressure
41
Q

Common feature of patients with cirrhosis and is usually the first indication of portal hypertension

A

Hypersplenism with development of thrombocytopenia

42
Q

Treatment of hypersplenism secondary to PH

A

No specific treatment - splenomegaly

Transfusion with platelet concentrate as necessary during episode of bleeding

43
Q

Primary prophylaxis of gastroesophageal varices

A

Routine screening by endoscopy
Nonselective beta blockers
Endoscopic variceal band ligation

44
Q

Treatment of an acute bleed

Gastroesophageal varices

A

Vasocontricting agents (somatostatin, octreotide)
Balloon tamponade
Endoscopic intervention (sclerotheraphy, variceal band ligation)
TIPS
Surgery

45
Q

Prevention of rebleeding after an initial bleed

Gastroesophageal varices

A

Repeated variceal band ligation
Beta blockers
Portosystemic shunt surgery

46
Q

Small ascites tx

A

Sodium restriction (<2 g of Na /day , avoid canned or processed food)

47
Q

Moderate ascites tx

A

Diuretics with isokalemic dose (100 mg spironolactone and 40 mg furosemide)
Max diuretic dose per day
Spironolactone 100-200 mg/day , increased cautiously to 400-600 mg/day)
Furosemide 40-80 mg /day increased cautiously to 120-160 mg/day

Fluid restriction is not advised unless with severe hyponatremia (<120 mmol/L)

48
Q

Tense ascites tx

A

Initial therapeutic paracentesis

Sodium restriction, oral diuretics

49
Q

refractory ascites tx

A

Avoid NSAIDs ,ACEI, ARBS ,Beta blockers

Add oral midodrine if BP < 90/60

Large volume paracentesis with albumin infusion every 2 weeks

Consider TIPS procedure (may precipitate encephalopathy)

referral for liver transplantation

50
Q

Alteration in mental status and cognitive function occurring in the presence of liver failure

A

Hepatic encephalopathy

51
Q

Encephalopathy is more commonly seen in
A. Acute liver disease
B. Chronic liver disease

A

B. Chronic liver disease

52
Q

Symptoms of hepatic encephalopathy are due to

A

Neurotoxins that are not removed by the liver because of vascular shunting

53
Q

Precipitating events for hepatic encephalopathy

A 
Hypokalemia 
Infection
Increased dietary protein load
Electrolyte disturbances 
GI bleeding
54
Q

Is there a correlation between severity of liver disease and serum ammonia

A

Poor correlation

55
Q

Symptoms of hepatic encephalopathy

A 
Confused
Changes in behavior
Violent
Difficult to manage
Sleepy and difficult to rouse
Asterixis or liver flap 
Cerebral herniation
56
Q

What is asterixis ?

A

Sudden forward movement of the wrist after it is bent back on an extended arm ( cannot be elicited on comatose patients )

57
Q

Is a feared complication of brain edema

A

Cerebral herniation

58
Q

Nutrition for hepatic encephalopathy

A

Protein restriction is discouraged.

Replace animal-based protein with vegetable-based protein in the diet because of more calorie to nitrogen ratio

59
Q

Mainstay of treatment for hepatic encephalopathy

Goal is to promote 2-3 soft stools/day

A

Lactulose

60
Q

Mechanism of action of lactulose

A

Colonic acidification

Catharsis

61
Q

Why does hypokalemia precipitate hepatic encephalopathy

A

Because it causes increased ammoniagenesis (alkaline tide)

62
Q

Adjunctive tx to lactulose

For hepatic encephalopathy

A

Antibiotics

63
Q

What antibiotics are given for hepatic encephalopathy

A

Poorly absorbed antibiotics : neomycin and metronidazole - given alternately to reduce side effects
Rifamixin 550 mg BID - very effective with better safety profile

64
Q

Supportive management of hepatic encephalopathy involves

A

Management / correction of precipitating factors

Zinc supplementation and LOLA (L-ornithine-L-aspartate)

65
Q

Spontaneous infection of the ascitic fluid without an intra-abdominal source, usually in the setting of liver cirrhosis

A

SBP Spontaneous bacterial peritonitis

66
Q

This type of ascitic fluid is particularly susceptible to SBP

A

Iow protein ascitic fluid (<1 g/dL or 10 g/L) because the opsonic activity of ascitic fluid correlates directly with its protein concentration

67
Q

Diuretic sensitive patients with ascites should be preferably treated with

A

Sodium restriction and oral diuretics than serial paracentesis

68
Q

Serial paracentesis disadvantage

A

Removes opsonins while diuresis concentrates opsonins

69
Q

Most common causative organisms of SBP

A

Escherichia coli and other gut bacteria

70
Q

Isolation / growth of >2 organisms from SBP patients should raise suspicion for

A

Perforate viscus ( secondary bacterial peritonitis)

71
Q

Manifestations of SBP

A

Fever
Altered mental status
Elevated WBC
Abdominal pain/ discomfort

72
Q

How to confirm SBP

A

Fluid sample analysis

  1. Absolute neutrophil count > 250 /uL
  2. Positive culture
  3. No evidence of an intra-abdominal surgically treatable source of infection
73
Q

Antibiotics of choice for SBP

A

Cefotaxime 2 g IV q8 x 5 days
Ofloxacin 400 mg PO BID for 8 days
Ciprofloxacin 200 mg IV q12 x 2 days followed by ciprofloxacin 500 mg PO q12 x 5 days

74
Q

Given in combination with cefotaxime. Indicated for SBP.

It has been shown to reduce risk of renal failure and improve survival

A

Intravenous albumin

75
Q

How is IV albumin given

A

1.5 g/kg BW at the time infection is detected (preferably within 6 hours) an 1 g/kg on day 3

76
Q

DOC

History of SBP

A

Norfloxacin 400 mg PO OD until death or liver transplantation

77
Q

DOC for Patients with cirrhosis with GI (variceal) bleeding

A

Norfloxacin 400 mg BID x 7 days or

Ceftriaxone 1 g IV x 7 days

78
Q

DOC for Patients with Cirrhosis and ascites with ascitic fluid total protein <1.5 g/dL and EITHER
A. Liver failure (Child-Pugh score >/=9, total bilirubin >/= 9.3 mg/dL) OR
B. Impaired renal function (serum crea >/= 1.2 mg/dL, BUN >/= 25 mg/dL, serum Na <130 mEq / L)

A

Norfloxacin 400 mg PO OD x 1 year

79
Q

DOC for patients with ascitic fluid total protein <1.5 g/dL

A

Ciprofloxacin. 500 mg PO OD x 1 year

IM (25 decks)

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