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Gastroenterology > Liver Disease > Flashcards

Liver Disease Flashcards

1
Q

what are the causes of NAFLD?

A
  • Unknown
  • Associated with metabolic syndromes
  • Associated factors: obesity, hyperlipidaemia, type 2 diabetes, jejunoileal bypass, sudden weight loss/starvation
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2
Q

what are the clinical features of NAFLD?

A 
•	Usually asymptomatic 
•	Hepatomegally
o	Steatosis = greasy, yellow, soft
o	Cirrhosis = bumpy 
•	ALT is usually greater AST 
•	Inceased echogenicity on US
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3
Q

what is the management of NAFLD?

A

lifestyle

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4
Q

what is the spectrum of disease in NAFLD?

A

o Steatosis = fat in liver
o Steatohepatitis = fat with inflammation
o Progress to fibrosis + liver cirrhosis

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5
Q

what is the “first step” in NAFLD?

A

steatosis

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6
Q

how does steatosis occur?

A

o Insulin resistance causes increased fat storage and decreased fatty acid oxidation
o = decreased secretion of fatty acids into bloodsteream, increased synthesis and uptake of free fatty acids from blood
o Causes fat droplets to form + grow in heaptocytes, some of which become large enough for hepatocytes to swell + nuclei

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7
Q

what is the second hit in NAFLD?

A

STEATOHEPATITIS

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8
Q

how does steatohepatitis occur?

A

o Oxidative stress + lipid peroxidation – unsaturated fatty acids react with hydroxyl radical forming water and a fatty acid radical – reacts with non radicals
o Process causes damage of lipid membrane = cell death
o Proinflam cytokine release = TNFa, TGFb, 17B-estradiol
o Presence of Mallory denk bodies = intermediate filaments

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9
Q

what is liver cirrhosis?

A

• consequence of chronic hepatic injury with healing by regeneration and fibrosis

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10
Q

what are the toxin related causes of liver cirrhosis?

A

alcohol

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11
Q

what are the infectious causes of liver cirrhosis?

A

hepatitis B, hepatitis C

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12
Q

what are the autoimmune causes of liver cirrhosis?

A

o Autoimmune chronic acute liver disease
o Primary biliary cirrhosis
o Primary sclerosing cholangitis

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13
Q

what are the metabolic causes of liver cirrhosis?

A

o Non alcoholic fatty liver disease
o Iron overload – haemochromatosis
o Copper overload – Wilson’s disease
o A1-antitrypsin associated liver disease

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14
Q

what are the hepatic venous outflow obstructive causes of liver cirrhosis?

A

o Budd-Chiari syndrome

o Sebere chronic congestive cardiac failure

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15
Q

what are the other causes of liver cirrhosis?

A

o Secondary to prolonged biliary obstruction
o Cystic fibrosis
o Cryptogenic
o Parental nutrition related

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16
Q

what are the consequences of liver cirrhosis?

A
  • Hepatocellular failure
  • Portal hypertension
  • Ascites due to portal hypertension
  • Malignant change: hepatocellular carcinoma
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17
Q

what are the features of hepatocellular failure in liver cirrhosi

A

o Impaired protein synthesis: prolonged prothrombin time and low albumin
o Impaired metabolism of toxins: encephalopathy
o Impaired bilirubin metabolism: jaundice

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18
Q

what are examples of benign liver neoplasms?

A
  • Haemangioma
  • Adenoma
  • Focal Nodular Hyperplasia
19
Q

what are examples of primary malignant liver neoplasms?

A

o Hepatocellular carcinoma
o Fibrolamellar carcinoma
o Cholangiocarcinoma

20
Q

what are examples of secondary malignant liver neoplasms?

A

o Portal spread
o Systemic blood spread
o Direct spread (from gallbladder, stomach, and hepatic flexure of colon)

21
Q

what is the cause of liver hemangiomas?

A

congenital

22
Q

what is the pathophysiology of haemangioma?

A

hypervascular tumour of hepatic endothelial cells of blood vessels

23
Q

what are the clinical features of haemangiomas?

A

usually asymptomatic, small lesions <1.5xn

24
Q

how are haemangiomas diagnosed?

A

US, CT, MRI

25
Q

what is the treatment of haemangioma?

A

no need for treatment

26
Q

what are the causes of focal nodule hyperplasia?

A

congenital arteriovenous malformation, vascular injury

o Associated with osler-weber-rindu + haemangioma)

27
Q

what is the macroscopic features of focal nodular hyperplasia?

A

o Classically – central scar, containing large artery radiating branches to periphery – hyperplastic abnormal response to blood flow

28
Q

what is the pathophysiology of focal nodular hyperplasia?

A

o Benign nodule formation of normal tissue

o All normal liver constituents – including RES and bile ducts

29
Q

what are the clinical features of focal nodular hyperplasia?

A

usually asymptomatic, may cause minimal pain

30
Q

what imaging can be done for focal nodular hyperplasia?

A

US – vary echogenicity, CT, MRI, FNA

31
Q

how is focal nodular hyperplasia managed?

A

none required

32
Q

what are the causes of hepatic adenoma?

A

o Associated with estrogen
 Oral contraceptives and anabolic
 Estrogen binds to estrogen receptors on hepatocytes converting them into hepatocellular adenoma cell
o Genetic disposistion
o Glycogen storing disorders – von gherkes disease (multiple adenomas)

33
Q

what is the pathophysiology of hepatic adenomas?

A

o Benign neoplasm composed of normal hepatocytes, no portal tract, central veins or bile ducts
o Non-functional cells that contain more glycogen and lipids than normal
o Tissue around highly vascularised

34
Q

what are the clinical features of hepatic adenomas?

A

o Usually asymptomatic
o May have RUQ pain
o May present with rupture , haemorrhage or malignant transformation
o Usually in right lobe

35
Q

what are the investigations for hepatic adenomas?

A

o US – filling defect
o CT – diffuse arterial enhancement
o MRI – hypo or hyper intense lesion
o FNA – may be needed

36
Q

what is the management of hepatic adenoma?

A 
o	Stop hormones, weight loss
o	Males = surgical excision
o	Females – image after 6 months
	<5cm or reducing = annual MRI
	>5cm or increased in size = surgery
37
Q

what are the causes of hepatocellular carcinoma?

A 
Liver cirrhosis – secondary to
o	Hep B and hep C
o	Alcohol
o	NAFLD
o	Haemochromatosis
o	PBC
38
Q

what are the risk factors of hepatocellular carcinoma?

A

Alpha-1 antitrypsin deficiency, hereditary tyrosinosis, glycogen storage disease, aflatoxin, drugs – oral contraceptive, anabolic steroids, poryphyria cutanea tarda, male, diabetes

39
Q

what are the types of hepatocellular carcinoma?

A

fibromellar (presents in younger (5-35), non cirrhosis, normal AFP), pseudo glandular, giant cell, clear cell

40
Q

what are the macroscopic appearances of hepatocellular carcinoma?

A

nodular or infiltrate

41
Q

what is the pathophysiology of hepatocellular carcinoma?

A

• Hepatocytes develop mutations that cause them to replicate at uncontrolled rates and/or avoid apoptosis

42
Q

what are the clinical features of hepatocellular carcinoma?

A
  • Present late (masked by cirrhosis)
  • Weight loss and RUQ pain
  • Asymptomatic
  • Worsening or pre-exisiting chronic liver disease
  • Acute liver failure
  • Hard enlarged RUQ mass
  • Liver bruit
43
Q

what are the investigations for hepatocellular carcinoma?

A
  • Serum AFP (Alfa-fetoprotein) – may be raised
  • US
  • Triphasic CT Scan
  • MRI
  • Biopsy
44
Q

what is the treatment of hepatocellular carcinoma?

A
  • Liver transplantation
  • Resection
  • Local ablation (ethanol injection, radiofrequency)
  • Chemoembolisation = TACR
  • Sorafenib – inhibits vase endothelial receptor

Gastroenterology (4 decks)

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