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Liver Flashcards

1
Q

Metabolic functions of the liver

A 
Carbohydrate metabolism - 
Gluconeogenesis
Glycolysis
Glycogenesis
Glycogenolysis
Fat metabolism and synthesis of -
Cholesterol and triglycerides
Lipoproteins
Phospholipids
Ketogenesis (In starvation)
Protein metabolism -
Transamination and deamination of amino acids
Convert amino acids into urea
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2
Q

Hormonal metabolism in the liver

A 
Degradation of - 
Insulin, glucagon, ADH, steroid hormone
Activation -
Deiodination of thyroxine T4 to more active triodothronine T3
Vitamin D3 to 25(OH)D
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3
Q

Storage function of liver

A

Stores vitamin A, D, E, K, B12
Coagulation of factor II, VII, IX and X. protein C & S
Synthesis of plasma proteins (albumin)

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4
Q

Which factors require post translational modifciation by vitamin K dependant - carboxylation

A

2, 7, 9 10

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5
Q

Protective function of liver

A 
Kupffer cells (liver phagocytes) that digest/destroy cellular debris (RBCs) and invading bacteria
Produce immune factors
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6
Q

Detoxification function of liver

A

Endogenous substances - Make sure proteins of haemolyses are detoxified, bilirubin
Exogenous substances - Drugs, alcohol

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7
Q

Where is bile stored between meals

A

Gallbladder, sphincter of Oddi is closed

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8
Q

What stimulates secretion of bile

A

Chyme on duodenum stimulates release of CCK from enteroendocrine or I cells in duodenum sense the presence of lipids. Sphincter of Oddi opens and gall bladder contracts to release bile into the duodenum.

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9
Q

How is bile concentrated

A

By removal of Cl- and water.

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10
Q

Cause of cholelithiasis

A

Excess cholesterol relative to bile results in acids and lecithin being precipitated into micro crystals that aggregates to galls stones

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11
Q

pH of bile

A

Slightly alkaline to neutralize acidic chyme from stomach. Also allows intestinal enzymes to function at their optimum pH.

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12
Q

Primary bile acids vs secondary bile acids

A

Primary bile acids - Cholic and chenodeoxycholic acids

Secondary - Deoxycholic and Lithocholic acids

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13
Q

How is primary bile acid converted to secondary

A

Hepatocytes release primary bile juice into the bile canaliculi which drains into the bile duct via cystic duct. This enters the duodenum. Intestinal bacteria dehydroxylate primary bile acids to form secondary bile acids. These acids are reabsorbed across intestinal wall and taken back to the liver where they can be re-secreted into the bile.

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14
Q

What gives faeces brown appearance

A

Bilirubin, dark urine and pale stool can indicate poor liver function

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15
Q

Composition of bile

A

Bile acids mainly cholic and chenodeoxycholic acid, water and electrolytes, lipids/phospholipids. cholesterol, IgA, bilirubin

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16
Q

Most common pathology of biliary tract

A

Cholelithiasis

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17
Q

Treatment for symptomatic stones

A

Laparoscopic cholecystectomy

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18
Q

Treatment for unimpaired gallbladder function having small/medium sized radiolucent stones

A

Ursodeoxycholic acid

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19
Q

What stones may be radiolucent and not detectable by x-ray

A

Large stone made up of purely cholesterol

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20
Q

How can morphine worsen biliary colic pain

A

Morphine constricts the sphincter of Oddi, increasing intrabiliary pressure and making the pain worse. Atropine may be administered together to make the pain better

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21
Q

Alternatives to morphine in biliary colic

A

Buprenorphine and pethidine

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22
Q

What is biliary colic

A

Gallbladder/gallstone attack is pain due to a gallstone blocking the bile duct

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23
Q

Treatment for relief of biliary spasm

A

Atropine or Glyceryltrinitrate (GTN)

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24
Q

Transporters involved in reabsorption of bile salts

A

Active transport in the ileum by hepatocytes via Na coupled transport. Enterohepatic recycling takes place

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25
Q

What synthesized more bile if too much is lost in faeces

A

Cholesterol

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26
Q

What are bile acid sequestrants

A

Group of resins used to bind to certain components of bile in GI tract. They disrupt enterohepatic circulation of bile acids and prevent reabsorption

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27
Q

Examples of bile acid sequestrants

A

Colesevelam, colestipol and colestyramine. These prevent reabsorption of bile thereby promoting hepatic conversion of cholesterol into bile acid, leading to a lowered plasma cholesterol.

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28
Q

What does hepatic conversion of cholesterol into bile acids cause

A

Increase in LDL-receptor activity of hepatocytes increasing clearance of LDL-cholesterol from plasma

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29
Q

Use of bile acid sequestrants

A

Hyperlipidemia, cholestatic jaundice (depleting cholesterol leads to less cholesterol available to be precipitated out to form gallstones), bile acid diarhoea (eliminate bile acids from body)

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30
Q

Drawbacks of bile acid sequestrants

A

Unpalatable, inconvenient (large doses needed), diarrhoea, deficiency of fat soluble vitamins due to reduced absorption

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31
Q

What does drug metabolism act to do

A

Convert parent drug to more polar metabolites so they aren’t readily reabsorbed by the kidney
Convert drugs to metabolites that are usually pharmacologically less active than parent

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32
Q

Main organ of drug metabolism

A

Liver but GI tract, lungs, plasma have activity too

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33
Q

Aspirin metabolism

A

Possess different type or spectrum of action -

Aspirin has antiplatelet and anti-inflammatory activity whereas its metabolite salicylic acid is anti-inflammatory

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34
Q

Phases of drug metabolism (usual)

A

Phase 1 - Mediated by cytochrome P450 enzyme
A more reactive polar group is added to the parent compound, this can involve oxidation/reduction/hydrolysis
Phase 2 - Conjugation
Adds an endogenous compound increasing polarity

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35
Q

Why do drugs have to be polarized and metabolized

A

Most drugs are lipophilic and difficult for the kidneys to be excreted as they are reabsorbed by the kidney easily. Hence adding a polar group makes excretion of the drug easier.

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36
Q

What are cytochrome (CYP) P450 family of monooxygenases

A

Haem proteins located in endoplasmic reticulum of liver hepatocytes mediating oxidation reductions (phase 1) of lipid soluble drugs

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37
Q

Main gene families of cytochrome P450 monooxygenase

A

CYP1, CYP2 and CYP3

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38
Q

What is hepatic encephalopathy (HE)

A

Decline in brain function due to insuffiiency in detoxification of ammonia to urea resulting in raised ammonia (NH3) levels

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39
Q

Therapeutic option in hepatic encephalopathy

A

Lactulose - Semisynthetic fructose + lactose
Not digested or absorbed in ileum
Breakdown products in colon are acidic - reduce pH
This converts ammonia into ammonium which isn’t absorbed and safely excreted
Antibiotics - Neomycin and Rifaximin
Minimally absorbed kind, suppress colonic flora, inhibit ammonia generation

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40
Q

Solid liver lesions in elderly

A

More likely to be malignant with metastases, more common than primary liver cancer in the absence of liver disease

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41
Q

Solid liver lesions in chronic liver patients

A

More likely to be primary lung cancer than metastases or benign tumours.

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42
Q

Solid liver lesion in non cirrhotic younger patients

A

Haemangioma

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43
Q

What is a hepatic haemangioma

A

Benign tumour of the liver composed of hepatic endothelial cells

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44
Q

Benign tumours of liver

A

Haemangioma
Focal nodular hyperplasia
Adenoma
Liver cyst

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45
Q

Malignant tumour of liver

A 
Hepatocellular carcinoma
Cholangiocarcinoma
Fibrolamellar hepatocellular carcinoma 
Hepatoblastoma
Metastases
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46
Q

What is fibrolamellar hepatocellular carcinoma

A

Form of hepatocellular carcinoma that typically affects young adults, histologically shows laminated fibrous layers between tumour cells

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47
Q

Features of haemangioma

A

Females > males, hypervascular tumour. Usually single, small and well-demarcated capsule. Asymptomatic

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48
Q

Management of haemangioma

A

No treatment needed, no need for fine needle aspiration biopsy. US/CT scan and MRI diagnostic

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49
Q

How does haemangioma show up in a CT scan

A

Lights up with a contrast as it’s a very vascular tumour

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50
Q

Second most common benign tumour of the liver

A

Focal nodular hyperplasia (FNH)

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51
Q

What causes focal nodular hyperplasia

A

Congenital vascular anomaly

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52
Q

Classical presentation of focal nodular hyperplasia

A

Central scar containing a large artery, radiating branches to the periphery

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53
Q

Features of focal nodular hyperplasia (FNH)

A

Asymptomatic usually, rarely grows or bleeds, no malignant potential. More common in young-middle aged females with sinusids, bile ductules and kupffer cells on histology

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54
Q

Treatment for focal nodular hyperplasia

A

No treatment required

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55
Q

Liver disease associated with contraceptive hormones and anabolic steroids

A

Hepatic adenoma, more common in females than males, 10:1 ratio

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56
Q

Clinical features of hepatic adenoma

A

Mainly asymptomatic but may have RUQ pain and may progress to rupture, haemorrhage or malignancy (rare)

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57
Q

Malignant transformation of hepatic adenoma is higher in which gender

A

Males than females

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58
Q

Is the portal tract present in hepatic adenoma

A

No portal tract, central vein or bile duct present in hepatic adenoma

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59
Q

Glycogen storage disease can lead to

A

Formation of multiple adenomas (adenomatosis)

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60
Q

Diagnosis of hepatic adenoma

A

Stop hormones (oral contraceptives/anabolic steroids)
Weight loss
Males - Surgical excision
Females - Imaging after 6 months, if;
<5 cm or reducing in size - annual MRI
>5 cm or increasing in size - surgical excision

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61
Q

What is a simple cyst

A

Liquid collection in a sac lined by an epithelium

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62
Q

Clinical features of a simple cyst

A

Asymptomatic with no malignant potential

If symptomatic, may be related to intracystic haemorrhage, infection, rupture (rare) or compression

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63
Q

Management of simple cyst

A

No follow up necessary, image 3-6 months if in doubt

Surgical resection if symptomatic or uncertain of diagnosis

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64
Q

What causes hydatid cysts

A

Infection due to ingestion of the larvae of the tapeworm - Echinococcus granulosus, not common in the UK

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65
Q

How is diagnosis of hydatid cyst made

A

History, appearance (may be jaundiced, weight loss, abdominal pain), serological testing by detection of anti-Echinococcus antibodies

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66
Q

Cyst commonly found in dogs that consume organs or meat of infected sheep

A

Hydatid cyst

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67
Q

Mangement of hydatid cyst

A

Conservative surgery - Open cystectomy, marsupialization
Radical surgery - Pericystectomy, lobectomy
Drugs - Albendazole

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68
Q

Option for patients unresponsive to surgery for hydatid cyst

A

PAIR - Percutaneous aspiration-injection reaspiration drainage

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69
Q

What can embryonic ductal plate malformation of the intrahepatic biliary tree lead to

A

Formation of numerous cysts through the liver -
Polycystic liver disease
von Meyenburg complex (VMC)
Autosomal dominant polycystic kidney disease

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70
Q

What are von Meyenburg complexes

A

Also known as multiple biliary hamartomas, rare cause of multiple benign hepatic lesions throughout the liver.

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71
Q

What is polycystic liver disease (PCLD)

A

Numerous cysts throughout the liver with liver function preserved. Symptoms depend on size and involves a mutation in PCLD gene - PRKCSH and SEC63

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72
Q

What is autosomal dominant polycystic kidney disease (ADPKD)

A

Renal failure due to polycystic (multiple cysts) in the kidney. Non-renal extra hepatic features and massive hepatic enlargement are common. Due to a mutation in the ADPKD genes - PKD1 and PKD2

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73
Q

One of the most lethal and prevalent monogenic human disorder

A

Autosomal dominant polycystic kidney disease

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74
Q

Examination findings of polycystic liver disease

A

Abdominal pain, abdominal distension, atypical compression of adjacent structures due to voluminous cysts

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75
Q

Management of polycystic liver disease

A

Conservative treatment to halt cyst growth and allow abdominal decompression and ameliorate symptoms

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76
Q

When are invasive procedures called for in polycystic liver disease

A

In selective patient groups such as those with advanced PCLD, ADPKD or liver failure

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77
Q

Pharmacological therapy and polycystic liver disease

A

By somatostatin analogues can relieve symptoms and reduce liver volume

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78
Q

Patient with a abdominal or biliary infection, recent dental procedure. High fever, leucocytosis and RUQ abdominal pain.

A

Liver abscess

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79
Q

Management of liver abscess

A

Empirical broad spectrum antibiotics
Aspiration/drainage percutaneously
Echocardiogram

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80
Q

Management of liver abscess if no improvement

A

Operation - Open drainage or resection

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81
Q

Most common primary liver cancer mostly found in men

A

Hepatocellular carcinoma (HCC)

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82
Q

Cause of hepatocellular carcinoma

A

Hepatitis B, hepatitis C, alcohol, aflatoxins

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83
Q

What are aflatoxins

A

Family of toxins produced by certain fungi found on agriculture crops such as maize, peanuts, corn. Main fungi producing this are Aspergillus flavus and Aspergillus parasiticus

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84
Q

Most common feature of hepatocellular carcinoma

A

Right upper quadrant pain and weight loss

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85
Q

Examination of hepatocellular carcinoma (HCC)

A

Signs of cirrhosis, hard enlarged RUQ mass, rare liver bruit

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86
Q

Where can hepatocellular carcinoma metastasize to

A

Rest of liver, portal vein, lymph nodes, lung, bone, brain

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87
Q

How is hepatocellular carcinoma invstigated for

A

Alfa fetoprotein and ultrasound. Elevation of alfa fetoprotein is seen in 60-80% of patients.

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88
Q

Why is biopsy avoided in diagnosing HCC

A

Biopsy may lead to seeding of cells along the route of resection.

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89
Q

Best treatment for HCC

A

Liver transplant only is single tumour < 5cm or less than 3 tumours less than 3 cm each

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90
Q

When is resection done in HCC

A

Small tumours with preserved liver function, i.e. no jaundice or portal hypertension. Recurrence rate is high

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91
Q

Treatment for patients without resectable livers and advanced liver cirrhosis in HCC

A

Local ablation using percutaneous ethanol injection or radiofrequency. Not a good choice for tumours beside major blood vessels, diaphragm or bile duct. It is a temporary measure and rate of recurrence is high

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92
Q

Palliative treatment for unresectable HCC in patients with early cirrhosis but well compensated

A

TransArterial ChemoEmbolization (TACE), it restricts the tumours blood supply. Chemotherapeutic drugs are injected into the artery supplying the tumour through a catheter. These drugs not only block blood supply but also induce cytotoxicity.

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93
Q

Systemic therapy for HCC

A

Sorafenib -
Kinase inhibitor drug, inhibits vascular endothelial growth factor receptor, platelet-derived growth factor receptor and Raf

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94
Q

Young patient showing typical stellate scar with radial septa showing persistent enhancement on CT scan. Alfa-fetoprotein blood test is normal

A

Fibro-lamellar carcinoma

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95
Q

Treatment options for fibro-lamellar carcinoma

A 
Surgical resection or transplantation. 
TransArterial ChemoEmbolization (TACE) for unresectable tumours
96
Q

Most common site for blood borne metastases

A

Liver

97
Q

Areas of a lobule

A

1.Periportal zone closest to the portal triad. 2.Mid acinar or midzonal and 3.centrilobular or pericentral zone is closest to the central vein

98
Q

Cells of which zone are the most prone to injury

A

Zone 3 - Pericentral

99
Q

Normal progression of liver disease

A

Insult to hepatocytes - Inflammation - Fibrosis - Cirrhosis

100
Q

What is acetaminophen poisoning

A

Paracetamol poisoning, excessive use of paracetamol. Feeling of tiredness, abdominal pain or nausea. Can progress onto a yellowish skin, blood clotting problems and confusion. Can lead to death

101
Q

How can uncomplicated jaundice be treated in a newborn

A

Exposed the undressed infant to filtered sunlight

102
Q

Do all patients with liver disease get jaundice

A

No

103
Q

Is liver disease the only cause of jaundice

A

No

104
Q

Cause of pre-hepatic jaundice

A

Too much haem breakdown due to excess haemolysis. Leads to formation of unconjugated bilirubin

105
Q

Cause of hepatic jaundice

A 
Dead or injured liver cells -
Acute liver injury (virus, drugs, alcohol)
Alcoholic hepatitis
Cirrhosis (decompensated)
Bile duct loss (atresia/PBC/PSC)
Pregnancy
106
Q

What is primary biliary cirrhosis commonly known as now

A

Primary biliary cholangitis

107
Q

Primary biliary cholangitis vs primary sclerosing cholangitis

A

PBC - Slow, progressive autoimmune destruction of the small bile ducts of the liver
PSC - Slow, progressive disease of liver and gallbladder affecting the medium and large bile ducts inside and outside the liver causing sclerosis (hardening)

108
Q

Post hepatic jaundice

A

Bile can’t get into the bowel

109
Q

Cause of post hepatic jaundice

A

Congenital biliary atresia
Gallstones blocking common bile duct
Strictures of common bile duct
Tumours

110
Q

Is cirrhosis reversible

A

No, fibrous bands form separating regenerative nodules of hepatocytes. Hepatic microvasculature is altered causing a loss in hepatocyte function

111
Q

Common causes of liver cirrhosis

A 
Alcohol
Hepatitis B and C
Iron overload
Gallstones
Autoimmune liver disease
112
Q

Why is chronic liver failure inevitable after cirrhosis

A

Hepatic microvasculature is altered causing a reduced blood supply to hepatocytes. Hence the liver can’t detox nor synthesize

113
Q

Why are lower oesophageal varices seen in portal hypertension

A

Lower oesophagus enters portal circulation via the left and right gastric veins to the hepatic portal vein

114
Q

Complications of cirrhosis

A 
Portal hypertension causing - 
Oesophageal varices
Caput medusa
Haemorrhoids
Ascites
Liver failure
115
Q

What causes caput medusae

A

Portal hypertension causes the superficial epigastric vein to become engorged and distended. Paraumbilical vein, which normally closes within one week of birth, becomes recanalised due to portal hypertension

116
Q

Causes of portal hypertension

A 
Liver cirrhosis
Budd-Chiari syndrome
Portal fibrosis
Sarcoidosis
Schistosomiasis
Portal vein thrombosis
117
Q

What is Budd-Chiari syndrome

A

Rare condition, caused by occlusion of hepatic veins that drain the liver to IVC. Presents with classical triad of abdominal pain, ascites and liver enlargement

118
Q

Pathophysiological basis of oedema due to liver failure

A

Reduced albumin synthesis resulting in hypoalbuminemia due to reduction in oncotic pressure. This pulls leads to excess fluid buildup in tissues

119
Q

Pathophysiological basis of haematemesis due to liver failure

A

Ruptures oesophageal varice

120
Q

Pathophysiological basis of purpura and bleeding due to liver failure

A

Reduced clotting factor synthesis

121
Q

Pathophysiological basis of infection due to liver failure

A

Reduced kuffper cell number and function

122
Q

What happens in liver after ingesting alcohol

A

Alcohol causes increased peripheral release of fatty acids, increased synthesis of fatty acids and triglycerides within hepatocytes. The major product of alcohol metabolism, acetaldehyde is mainly responsible for cell injury by formation of Mallory’s hyaline. Fibroblasts also increase synthesis of collagen

123
Q

Is hepatitis reversible

A

Yes

124
Q

Histological difference between alcoholic fatty liver and alcoholic hepatitis

A

Alcoholic fatty liver - Fat vacoules seen in hepatocytes

Alcoholic hepatitis - Mallory bodies and pericellular fibrosis seen, neutrophils and hepatocyte necrosis seen

125
Q

Histology shows fat vacuoles in hepatocyte with collagen (stained blue)

A

Alcoholic fibrosis

126
Q

What stain can be used to see alcoholic cirrhosis clearly

A

Masson’s trichrome - Three colour staining procedure that helps distinguish cells from surrounding connective tissue

127
Q

Non-alcoholic steatohepatitis generally occurs in

A

Patients with diabetes, obesity or hyperlipidaemia

128
Q

Disease pathologically identical to alcoholic liver disease but in non-drinkers

A

Non-alcoholic steateohepatitis (NASH)

129
Q

What kind of hepatitis can Hepatitis viruses cause

A

Interface hepatitis or piecemeal necrosis

130
Q

What is piecemeal necrosis

A

Refers to necrosis that occurs in fragments. It is necrosis of the limiting plates in the liver

131
Q

What is the periportal limiting plate

A

In smaller portal triads, the vessels lie in a network of connective tissue and are surrounded on all sides by hepatocytes. This ring is the periportal limiting plate

132
Q

What is a councilman body

A

It is an apoptotic body, a globule of cells that represents a dying hepatocyte often surrounded by normal parenchyma

133
Q

Mallory bodies vs councilman body

A

Mallory bodies - Intracytoplasmic inclusion and mainly seen in alcoholic hepatitis. Formed by aggregation of cytoskeletal intermediate filaments
Councilman body - Seen in viral hepatitis, complete cell is involved and formed by apoptosis

134
Q

Primary biliary cirrhosis is mainly found in which gender

A

Females (90%), autoimmune

135
Q

Why is biopsy doen in primary biliary cirrhosis

A

To stage the disease

136
Q

Chronic inflammation affecting intra and extra-hepatic bile ducts associated with ulcerative colitis

A

Primary sclerosing cholangitis

137
Q

Primary sclerosing cholangitis is seen more in gender?

A

Male

138
Q

What is haemochromatosis

A

Accumulation of iron in the body

139
Q

Primary vs secondary haemochromatosis

A

Primary - Genetic condition, increase iron absorption

Secondary - Iron overload from diet, transfusion, iron therapy

140
Q

What is hereditary or primary haemochromatosis

A

Inherited autosomal recessive condition causing excess absorption of Iron from intestine, abnormal iron metabolism

141
Q

How does primary haemochromatosis affect the liver

A

Iron is deposited in the liver due to excess absorption and abnormal iron metabolism. This is eventually deposited in portal connective tissue, stimulating fibrosis. This can lead to cirrhosis and predispose to carcinoma if untreated

142
Q

What stain can be used to confirm iron deposition in hepatocytes in primary haemochromatosis

A

Perls stain

143
Q

Inherited autosomal recessive disease of Copper metabolism

A

Wilson’s diseaese

144
Q

Wilson’s disease can lead to accumulation of copper in the eye forming dark rings around the iris called?

A

Kayser-Fleischer rings

145
Q

What protein is deficient in Wilson’s disease

A

Ceruloplasmins, copper-carrying protein

146
Q

Why does Wilson’s disease cause chronic hepatitis and neurological deterioration

A

Due to accumulation of copper in the liver and brain (basal ganglia)

147
Q

What is alpha-1-antitrypsin deficiency

A

Inherited autosomal recessive disorder of production of an enzyme inhibitor. Causes excessive trypsin

148
Q

Hepatocellular adenoma is more common in what gender

A

Females

149
Q

What is chronic liver diseaes

A

Duration of liver disease greater than 6 months

150
Q

What are hepatic stellate cells

A

Pericytes found in perisinusoidal space of the liver also known as space of Disse. They store vitamin A as retinol ester in their cell bodies. During an injury, the amount of vitamin A stored decreases progressively. This activates stellate cells causing secretion of collagen scar tissue.

151
Q

Function of senescent stellate cells

A

Role as liver resident antigen presenting cells to natural killer cells

152
Q

What are hepatic stellate cells also known as

A

Perisinusoidal cells or Ito cells

153
Q

What switches off hepatic stellate cells

A

Tissue inhibitor of metalloproteinase

154
Q

Chronic liver disease vs disease affecting liver that is chronic

A

Chronic liver disease can lead to cirrhosis

155
Q

Non-alcoholic steatohepatitis is also known as

A

Non-alcoholic fatty liver disease

156
Q

Pathogenesis of non-alcoholic steatohepatitis

A

2 hit paradigm -
1st hit - Excess fat accumulation
2nd hit - Intrahepatic oxidative stress, lipid peroxidation, TNF-a, cytokine cascade

157
Q

Investigating simple steatosis

A

Investigate by ultrasound

158
Q

Investigating NASH

A

Investigate by liver biopsy

159
Q

Is primary sclerosing cholangitis autoimmune related

A

Disease showing auto-immune features but cause in unknown. Related to UC

160
Q

How does primary biliary cholangitis present

A

Middle aged woman, asymptomatic/incidental find, may have fatigue/itch without rash or xanthelasma or xanthoma

161
Q

Investigating primary biliary cirrhosis

A

Positive antimitochondrial-antibody test (AMA)
Cholestatic LFT’s
Liver biopsy

162
Q

Treatment of primary biliary cirrhosis/cholangitis

A

Ursodeoxycholic acid - Is a secondary bile acid, produced as a byproduct of intestinal bacteria
Liver transplant

163
Q

Autoimmune hepatitis is also known as

A

Chronic active hepatitis

Lupoid hepatitis

164
Q

Type 1 vs type 2 autoimmune hepatitis affecting population

A

Type 1 - More in children

Type 2 - Any age but often in young adults

165
Q

Presence of LKM-1 antibody suggests what type of hepatitis

A

Type 2 autoimmune hepatitis

166
Q

Antibody found in autoimmune hepatitis type 2

A

anti-liver kidney microsomal antibody (LKM-1)

anti mitochondrial antibody (AMA)

167
Q

Antibodies found in autoimmune hepatitis type 1

A

Autonuclear antibodies (ANA)
Anti-smooth muscle antibody (ASMA)
anti-soluble liver antigen (SLA)

168
Q

Presentation of autoimmune hepatitis

A 
Spider angioma
Jaundice
Scleral icterus
Palmar erythema
Gynaecomastia
Ascites
Encephalopahty
Asterixis 
Hepatomegaly
Splenomegaly
Malaise, nausea, fatigue, lethargy, abdominal pain, anorexia
169
Q

Stigmata of liver disease

A 
Spider angioma
Jaundice
Scleral icterus
Palmar erythema
Gynaecomastia
Ascites
Encephalopahty
Asterixis
170
Q

LFT finsings of autoimmune hepatitis

A

Elevated AST and ALT

Elevated PT

171
Q

Pattern of autoimmune hepatitis

A

Piecemeal necrosis and lobular involvement with interface hepatitis and numerous plasma cells

172
Q

Treatment of autoimmune hepatitis

A

Oral Prednisolone and Azathioprine (immunosuppresant)

173
Q

Dosage of drugs in autoimmune hepatitis

A

Prednisolone - Start at 30mg daily, taper down to 15mg at week 4 and maintain 10mg daily until therapy end
Azathioprine - 50-100mg daily

174
Q

Commonest liver disease in Scandinavia

A

Primary sclerosing cholangitis, more common in men

175
Q

Clinical presentation of PSC

A

Recurrent cholangitis

176
Q

Investigating PSC

A

Imaging

177
Q

Treatment of PSC

A

Maintain bile flow

Monitor for cholangiocarcinoma and colorectal cancer

178
Q

Mutations causing haemochromatosis

A

C282Y or H63D mutations in Human Haemochromatosis Protein (HFE) gene

179
Q

Common presentation of haemochromatosis

A

Bronze diabetic -

Darkening of skin and hyperglycaemia

180
Q

Why does haemochromatosis have a late presentation

A

As the Iron accumulates in the liver showing no symptoms. Takes many years for it to have an effect

181
Q

Clinical presentation of alpha-1-antitrypsin deficiency

A

Lung emphysema,deposition of mutant protein in lungs causing SOB, wheeze and increased risk of infection. May also have COPD, cirrhosis and panniculitis.

182
Q

Mutation found in alpha-1-anti-trypsin deficiency

A

A1AT gene

183
Q

Treatment of A1AT deficiency

A

Supportive management

184
Q

Investigating Budd-Chiari syndrome

A

Ultra-sound of hepatic veins

185
Q

Treatment of Budd-Chiari syndrome

A

Recanalization or TIPS

186
Q

Patients with Budd-Chiari syndrome often have what protein deficiency

A

Protein C and S, increased thrombotic potential

187
Q

Methotrexate and liver

A

Can cause dose dependant progressive fibrosis of liver

188
Q

Treatment for methotrexate liver fibrosis

A

Stop methotrexate

189
Q

What is cardiac cirrhosis

A

Hepatic derangement that occur due to setting of right-sided heart failure. Signs and symptoms of right sided heart failure dominate

190
Q

Deficiency of this affect lung and the liver

A

Alpha-1-anti-trypsin deficiency

191
Q

What organs contribute to portal vein inflow

A

Spleen, distal end oesophagus, stomach, pancreas, small and large intestine

192
Q

Hepatic blood flow direction

A

Liver sinusoids - Central vein - Hepatic vein - Inferior vena cava - Right atrium of heart

193
Q

What is considered portal hypertension

A

Portal vein pressure above 5 - 8 mm Hg

194
Q

2 factors that can cause portal hypertension

A

Increase resistance to portal flow

Increase portal venous inflow

195
Q

Prehepatic cause of portal hypertension

A

Blockage of portal vein before liver due to thromboembolus (Budd-Chiari syndrome or occlusion secondary to congenital portal venous abnormalities)

196
Q

Intrahepatic causes of portal hypertension

A

Presinusoidal - Schistosomiasis or non-cirrhotic portal hypertension
Postsinusoidal - Cirrhosis, alcoholic hepatitis, congenital hepatic fibrosis

197
Q

Compensated vs decompensated liver cirrhossi

A

Compensated is clinically normal and found incidentally on imaging. Portal hypertension may be present
Decompensated cirrhosis is deterioration in liver function in patient with cirrhosis usually leading to development of jaundice, ascites, variceal haemorrhage, hepatic enchephalopathy or infections

198
Q

Most common liver cause of ascites

A

Decrease in albumin synthesis decreasing oncotic pressure

199
Q

Complications of cirrhosis

A

Jaundice, encephalopathy, variceal bleeding, liver failure

200
Q

Treatment of cirrhosis

A

Feed early and quickly as patietns tend to undergo catabolism
Identify and treat infections
Remove or treat cause

201
Q

What vitamin supplementation is mandatory in alcohol excess cirrhosis

A

Vitamin B1 - Thiamine

202
Q

Why should Calcium be administered in cirrhosis

A

Osteoporosis (fragile bone) and osteomalacia (soft bones). 1000mg of Ca supplement and 20 microg of D

203
Q

Cirrhosis due to PBC and PSC can cause deficiency of

A

Fat soluble vitamines - A, D, E, K

204
Q

How can ascites be diagnosed

A

Ultrasound - Dark

Shifting dullness - Percuss on GI examination

205
Q

Treatment of ascites

A 
Improve liver disease
Look for and treat infection
No NSAID
Reduce salt intake
Diuretics - Spironolactone
Paracentesis
TIPS
Transplantation
206
Q

Spironolactone vs Amiloride in ascites treatment

A

Spironolactone (aldosterone antagonist) is more effective than Amiloride (K-sparring loop diuretic)

207
Q

What should be frequently monitored after dose change or paracentesis

A

U&E

208
Q

Infection of ascitic fluid

A

Spontaneous bacterial peritonitis (SBP)

209
Q

Investigating spontaneous bacterial peritonitis

A

Tap in ascites and neutrophil count (>250 cells/mm3)

210
Q

Treatment of spontaneous bacterial peritonitis

A

Antibiotics
Terlipressin for vascular instability
Maintain renal perfusion
Hepatorenal syndrome development

211
Q

Alcohol withdrawal vs encephalopathy flap

A

Alcohol withdrawal gives a tremor whereas encephalopathy gives a liver flap

212
Q

Pathophysiology of hepatic encephalopathy

A

Ammonia is generated in the intestines from diet. This ammonia is metabolised to urea in the liver and excreted out by the kidney in urine.
Portal systemic shunts and liver failure cause a rise in blood ammonia as this ammonia is taken into systemic circulation directly rather than passing through the liver. This affects brain function via astrocytes and disturbs neurotransmitter trafficking.

213
Q

Should protein and energy intake be reduced in encephalopathy

A

No as this may cause more harm by adversely affecting the nutritional status

214
Q

Treatment of encephalopathy

A

Look for cause such as infection, drugs, liver failure or metabolic and treat
Lactulose to reduce transit time - Rifaximin
Small frequent meals and carbohydrate containing late evening snack to reduce fasting period overnight and reduce catabolism
Transplant

215
Q

Pathophysiology of variceal bleeding

A

Increased portal pressure
Increased variceal size
Decreased vessel wall thickness
Increased variceal wall tension

216
Q

Primary prophylaxis for variceal bleeding

A

Non-selective beta-blockers;
Propanolol, Carvedilol
Variceal ligation

217
Q

Treatment for acute variceal bleeding

A 
Resuscitation
Pharmacological therapy
Timing of therapy
TIPS
Transection/shunt surgery
218
Q

Possible endoscopic therapies for variceal bleeds

A

Sclerotherapy or variceal ligation

Variceal ligation preferred due to lower morbidity and quicker eradication

219
Q

What is sclerotherapy

A

Procedure to treat blood vessels or blood vessel malformations by injecting a medicine into vessels to make them shrink

220
Q

What can be done to ‘buy time’ for a TIPS or transfusion

A

Balloon tamponade

221
Q

Drawback of TIPSS

A

Can cause encephalopathy due to formation of porto-systemic shunt. This can lead to ammonia entering the systemic circulation directly, bypassing the liver for conversion to urea and safe excretion

222
Q

What can be used to prioritise liver transplantation

A

United Kingdom Model for End-Stage Liver Disease (UKELD) predicts prognosis in chronic liver disease and is used to prioritise transplants

223
Q

Threshold to be eligible for liver transplant

A

49 or higher on UKELD score unless hepatocellular carcinoma

224
Q

Variant syndromes

A 
Diuretic resistant ascites
Hepatopulmonary ascites
Chronic hepatic encephalopathy
Intractable pruritus
Polycycstic liver disease
Familial amyloidosis
Primary hyperlipidaemia
225
Q

The first sign of jaundice is seen in which organ

A

The eyes

226
Q

Clinically apparent hyperbilirubinemia

A

Jaundice

227
Q

Duration of liver damage to be classified as chronic

A

> 6 months

228
Q

True liver function tests consists of

A

Bilirubin, albumin and prothrombin. These mark liver function

229
Q

What are markers of liver damage

A

Alkaline phosphatase (ALP), Alanine amino transferase (ALT) and Gamma Glutamly Transferase (GGT)

230
Q

Markers of cholestatic problems

A

Alkaline phosphatase (ALP) and Gamma GT

231
Q

Markers of hepatocyte damage

A

Alanine amino transferase (ALT)

232
Q

Not dilated bile duct common cause

A

Drug induced, common cause if Flucloxacillin

233
Q

What can cause abnormal liver function tests

A

Obesity, diabetes, alcohol, drugs

234
Q

Degree of liver dysfunction can be classified via

A

Child-Pugh classification

235
Q

What does high portal pressure and low albumin lead to

A

Ascites

236
Q

Shunting of portal brain affects the brain. Why?

A

Toxins bypass the liver and enter straigth into the systemic circulation.

237
Q

Albumin and plasma volume

A

Low albumin leads to low plasma volume as oncontic pressure is lowered

GI (32 decks)

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