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NAFLD Flashcards

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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
Elevation of hepatic venous pressure gradient > 5 mmHg
Portal Hypertension
26
A significant complicating feature of decompensated cirrhosis
Portal hypertension
27
Development of portal hypertension is usually revealed by these laboratory findings
thrombocytopenia splenomegaly development of ascites encephalopathy esophageal varices with or without bleeding
28
Classification of Portal Hypertension
Pre-Hepatic Hepatic Post- Hepatic
29
Affects the portal venous system before it enters the liver
Pre-hepatic
30
Most common cause of portal hypertension
Hepatic
31
Types of hepatic causes of portal hypertension
Presinusoidal Sinusoidal Postsinusoidal
32
PH: Affects the hepatic veins and venous drainage to the heart
Post-Hepatic
33
Pre-hepatic causes of PH
Portal vein thrombosis Splenic vein thrombosis Massive splenomegaly (Banti's syndrome)
34
Hepatic causes of PH: presinusoidal
schistosomiasis congenital hepatic fibrosis primary biliary cirrhosis sarcoidosis
35
Hepatic causes of PH: sinusoidal
cirrhosis alcoholic hepatitis
36
Hepatic causes of PH: postsinusoidal
Hepatic sinusoidal obstruction (venoocclusive syndrome(
37
Post-Hepatic causes of PH
Budd-Chiari syndrome Inferior vena cava webs Cardiac causes
38
Complications of Portal Hypertension (3)
Gastroesophageal varices Ascites Hypersplenism
39
What is the mechanism of gastroesophageal varices secondary to PH
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
What is the mechanism of ascites secondary to PH
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
Common feature of patients with cirrhosis and is usually the first indication of portal hypertension
Hypersplenism with development of thrombocytopenia
42
Treatment of hypersplenism secondary to PH
No specific treatment - splenomegaly | Transfusion with platelet concentrate as necessary during episode of bleeding
43
Primary prophylaxis of gastroesophageal varices
Routine screening by endoscopy Nonselective beta blockers Endoscopic variceal band ligation
44
Treatment of an acute bleed | Gastroesophageal varices
Vasocontricting agents (somatostatin, octreotide) Balloon tamponade Endoscopic intervention (sclerotheraphy, variceal band ligation) TIPS Surgery
45
Prevention of rebleeding after an initial bleed | Gastroesophageal varices
Repeated variceal band ligation Beta blockers Portosystemic shunt surgery
46
Small ascites tx
Sodium restriction (<2 g of Na /day , avoid canned or processed food)
47
Moderate ascites tx
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
Tense ascites tx
Initial therapeutic paracentesis | Sodium restriction, oral diuretics
49
refractory ascites tx
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
Alteration in mental status and cognitive function occurring in the presence of liver failure
Hepatic encephalopathy
51
Encephalopathy is more commonly seen in A. Acute liver disease B. Chronic liver disease
B. Chronic liver disease
52
Symptoms of hepatic encephalopathy are due to
Neurotoxins that are not removed by the liver because of vascular shunting
53
Precipitating events for hepatic encephalopathy
``` Hypokalemia Infection Increased dietary protein load Electrolyte disturbances GI bleeding ```
54
Is there a correlation between severity of liver disease and serum ammonia
Poor correlation
55
Symptoms of hepatic encephalopathy
``` Confused Changes in behavior Violent Difficult to manage Sleepy and difficult to rouse Asterixis or liver flap Cerebral herniation ```
56
What is asterixis ?
Sudden forward movement of the wrist after it is bent back on an extended arm ( cannot be elicited on comatose patients )
57
Is a feared complication of brain edema
Cerebral herniation
58
Nutrition for hepatic encephalopathy
Protein restriction is discouraged. | Replace animal-based protein with vegetable-based protein in the diet because of more calorie to nitrogen ratio
59
Mainstay of treatment for hepatic encephalopathy | Goal is to promote 2-3 soft stools/day
Lactulose
60
Mechanism of action of lactulose
Colonic acidification | Catharsis
61
Why does hypokalemia precipitate hepatic encephalopathy
Because it causes increased ammoniagenesis (alkaline tide)
62
Adjunctive tx to lactulose | For hepatic encephalopathy
Antibiotics
63
What antibiotics are given for hepatic encephalopathy
Poorly absorbed antibiotics : neomycin and metronidazole - given alternately to reduce side effects Rifamixin 550 mg BID - very effective with better safety profile
64
Supportive management of hepatic encephalopathy involves
Management / correction of precipitating factors | Zinc supplementation and LOLA (L-ornithine-L-aspartate)
65
Spontaneous infection of the ascitic fluid without an intra-abdominal source, usually in the setting of liver cirrhosis
SBP Spontaneous bacterial peritonitis
66
This type of ascitic fluid is particularly susceptible to SBP
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
Diuretic sensitive patients with ascites should be preferably treated with
Sodium restriction and oral diuretics than serial paracentesis
68
Serial paracentesis disadvantage
Removes opsonins while diuresis concentrates opsonins
69
Most common causative organisms of SBP
Escherichia coli and other gut bacteria
70
Isolation / growth of >2 organisms from SBP patients should raise suspicion for
Perforate viscus ( secondary bacterial peritonitis)
71
Manifestations of SBP
Fever Altered mental status Elevated WBC Abdominal pain/ discomfort
72
How to confirm SBP
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
Antibiotics of choice for SBP
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
Given in combination with cefotaxime. Indicated for SBP. | It has been shown to reduce risk of renal failure and improve survival
Intravenous albumin
75
How is IV albumin given
1.5 g/kg BW at the time infection is detected (preferably within 6 hours) an 1 g/kg on day 3
76
DOC | History of SBP
Norfloxacin 400 mg PO OD until death or liver transplantation
77
DOC for Patients with cirrhosis with GI (variceal) bleeding
Norfloxacin 400 mg BID x 7 days or | Ceftriaxone 1 g IV x 7 days
78
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)
Norfloxacin 400 mg PO OD x 1 year
79
DOC for patients with ascitic fluid total protein <1.5 g/dL
Ciprofloxacin. 500 mg PO OD x 1 year

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