Liver and Friends Flashcards

1
Q

Define liver failure?

A

The inability of the liver to perform its normal function as well as encephalopathy and coagulopathy.
Acute = rapid development of symptoms
Chronic = occurs in the context of cirrhosis

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2
Q

Causes of liver failure?

A
Acute = Hep A/E, EBV, alcoholic hepatitis, hepatic venin thrombosis/blood flow occlusion to the liver
Chronic = alcoholism, Hep B/C, autoimmune hepatitis, haemochromatosis, wilsons disease, NAFLD and A1AD
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3
Q

What is the characterisitic triad seen in Budd-Chiari syndrome?

A

Abdominal pain, ascites, and liver enlargement due to occlusion of the hepatic vein

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4
Q

S&S of acute liver failure?

A

Malaise, Nausea, Anorexia, Jaundice, Confusion, Bleeding, RUQ pain and Hypoglycaemia

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5
Q

Treatment for liver failure?

A

IV glucose, nutritional supplements, transplantation. AVOID drugs with hepatic metabolism e.g. sedatives
TREAT CAUSE

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6
Q

S&S of chronic liver failure?

A

Ascites, jaundice, spider naevi, hepatomegaly, haematemesis, itching, muscle wasting, anorexia, easy bruising, fatigue and confusion

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7
Q

What is fulminant Hepaic failure?

A

Massive necrosis of liver cells leading to severe impairment of liver function

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8
Q

How is fulminant liver failure graded?

A

By how quickly encephalopathy occurs after jaundince onset.
Hyperacute = < 7 days
Acute = 8-28 days
Subacute = 5-26 weeks
The more onset is delayed the lower the risk of cerebral oedema

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9
Q

How is hepatic encephalopathy graded?

A
I = altered mood/behaviour and sleep disturbances
II = drowsniess, confusion and slurred speech
III = liver flap, incoherent speech and restlessness
IV = coma
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10
Q

How does alcohol damage the liver?

A

Alcohol metabolism produces fat in the liver. Large amounts of alcohol = steatosis (the liver becomes swollen with fat). If collagen is layed down around the central hepatic vein = cirrhosis.
The fat surrounding the liver will dissapear on stopping drinking, cirrhosis will NOT.

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11
Q

How can you tell if someone drinks heavily on a blood test?

A

Raised MCV and Gamma GT = heavy drinker

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12
Q

How do you treat alcohol withdrawals?

A

Chlordiazepoxide for withdrawal symptoms, give vitamin K and thiamine. Advise patient to attend group therapy e.g. AA

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13
Q

What is alcoholic hepatitis?

A

As well as fatty changes to the liver there is infiltration by polymorphoneuclear leucocytes and hepatocyte necrosis. If alcohol consumption continues this rapidly develops into cirrhosis

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14
Q

S&S of alcoholic hepatitis?

A

Malaise, anorexia, D&V, tender hepatomegaly, bleeding and ascites (general and non-specific symptoms).
Severe hepatitis = jaundice, coagulopathy and encephalopathy

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15
Q

S&S of alcoholic cirrhosis?

A

Clubbing, spider naevi, dupuytren’s contracture, hepatosplenomegaly, ascites, laukonychia and gynaecomastia
ALSO signs of dependancy may be present e.g. sweating, anxiety, tremours etc. and palmar erythema/dupuytren’s contracture

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16
Q

Causes of Non-Alcoholic Fatty Liver disease?

A

Obesity, T2DM, hyperglycaemia, hyperlipidaemia

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17
Q

Alcohol enhances the effects of what on the liver?

A

Toxic metabolites e.g. paracetamol - makes OD far more severe

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18
Q

What is haemochromatosis?

A

An inherited disorder (but can also be caused by high iron intake and blood transfusions) leading to increased iron absorption. Iron will deposit in the joints, liver, heart, skin, pancreas etc.
It can lead to fibrosis and organ failure

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19
Q

S&S of haemochromatosis?

A

Bronze skin pigmentation, chirrhosis and diabetes mellitus - classic triad
Hepatomegaly, arthralgia, hypogonadism, dilated CM, arrhythmias and osteoporosis

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20
Q

Treatment for haemochromatosis?

A

Venessection 3/4 times a year (chelation therapy e.g. desferrioxamine if not tolerated), low iron diet, avoid vitamin C, HRT/testosterone replacement, treat diabetes

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21
Q

What is Wilson’s disease?

A

Autosomal recessive condition of biliary copper excretion leading to copper depositis in the liver, CNS and cornea

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22
Q

S&S of Wilson’s disease?

A

Kayser-Fleischer rings.
Children = cirrhosis/hepatitis/fulminant liver failure
Young adults = CNS issues e.g. tremour, disarthria, disphasia, dyskinesia adn dementia

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23
Q

Treatment for Wilson’s disease?

A

liver transplant, avoid copper in diet, chelating agents e.g. penicillamine

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24
Q

What is alpha-1-antitrypsin deficiency?

A

An autosomal recessive disorder where alpha-1-antitrypsin is not excreted from the liver correctly, this leads to uncontrolled neutrophile elastase causing emphysema. Its build up within the liver causes inflammation, fibrosis and cirrhosis

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25
Q

What is the most common cause of liver disease in children?

A

Alpha-1-antitrypsin deficiency

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26
Q

Which hepatitis viruses lead to chronic hepatitis?

A

C and B (with or without D)

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27
Q

How does acute hepatitis present?

A

Cholestatic jaundice, tender hepatomegaly, malaise, myalgia, GI upset and RUQ pain

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28
Q

How does chronic hepatitis present?

A

Ascites, jaundice, hepatomegaly, low albumin, portal hypertension and coagulopathy/encephalopathy

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29
Q

Which types of hepatitis are faeco-oral spread and which are blood bourne?

A

A and E = faeco-oral

B, C and D = blood-bourne, also vertically transmissable

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30
Q

S&S of hepatits A infection?

A

Fever, malaise, anorexia, nausea, arthralgia then jaundice, hepatosplenomegaly and adenopathy
OFTEN FROM SHELLFISH

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31
Q

S&S of hepatits E infection?

A

Fever, malaise, anorexia, nausea, arthralgia then jaundice, hepatosplenomegaly and adenopathy
In the immuosuppressed/pregnant this can occasionally lead to chronic hepatitis
OFTEN FROM PIGS

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32
Q

S&S of hepatits B infection?

A

Fever, malaise, anorexia, nausea, arthralgia then jaundice, hepatosplenomegaly and adenopathy - arthralgia and urticaria are more common
In a chronic infection (5-10%) cirrhosis will develop

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33
Q

S&S of hepatits D infection?

A

Fever, malaise, anorexia, nausea, arthralgia then jaundice, hepatosplenomegaly and adenopathy
Can cause acute liver failure and cirrhosis

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34
Q

What are the 2 types of infection that occur with combined hepatitis B and D?

A
Co-infection = Hep B and D infection which is clinically indistinguishable from regular Hep B/D
Superinfection = when a person who has chronic Hep B contracts Hep D, this leads to secondary acute hepatits and comes with high risk of fulminat hepatitis
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35
Q

S&S of hepatits C infection?

A

This tends to be asymptomatic initially. Jaundice, hepatospelnomegaly and flu-like symptoms
Usually develop into cirrhosis (3/4)

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36
Q

How do you treat Hep A/E?

A

Supportive treatment (avoid alcohol) and manage close contacts with vaccine/immunoglobulins - no vaccine for E in Europe

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37
Q

How do you treat Hep B/D?

A
Acute = Supportive treatment (avoid alcohol) and manage close contacts with vaccine/immunoglobulins
Chronic = SC pegulated interferon-alpha 2A to stimulate immune response or life-long nucleoside analogues e.g. tenofovir/entecavir (inhibits viral replication). D may require transplant
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38
Q

How do you treat Hep C?

A
Acute = SC pegulated interferon-alpha 2A with ribavirin or tirple therapy with direct acting antivirals (if mental health SE of ribavirin cant be tolerated)
Chronic = triple therapy with direct acting antivirals and ribavirin
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39
Q

Describe the two types of cirrhossis?

A
Micronodular = even size and development across the liver - due to alcohol or biliary tract disease
Macronodular =  vary in size across the liver - due to chronic viral hepatitis
40
Q

Name 2 complications of liver cirrhosis?

A

Increased risk of hepatocellular carcinoma and portal hypertension

41
Q

Causes of portal hypertension?

A
Pre-hepatic = portal vein thrombosis
Hepatic = cirrhosis/schistosomiasis
Post-hepatic = IVC obstruction/constrictive pericarditis
42
Q

S&S of portal hypertension?

A

Gastro-oesophageal varicies and varices in the rectum. Rupture will lead to haematemesis and melaena

43
Q

What is ascites and what may cause it?

A

The accumulation of >25ml free fluid in the peritoneal cavity.
Causes = local inflammation (peritonitis, abdo infection), low protein (hypoalbuminaemia, malnutrition), low flow ( portal hypertension, Budd-Chiari syndrome)

44
Q

S&S of ascites?

A

Distended abdomen, shifting dullness on percussion, peripheral oedema, mild abdo pain.
Tense ascites = Respiratory distress and difficulty eating

45
Q

What are the 2 types of ascitic fluid?

A
Transudate = transparent as low protein e.g. portal hypertension, HF and Budd-Chiari syndrome
Exudate = high protein e.g. malignancy, peritionits or pancreatitis - THIS IS MORE SEVERE
46
Q

Treatment of ascites?

A

Transjugular Intrahepatic Portosystemic Shunt, spironolactone, ascitic drainage

47
Q

Causes of peritonitis?

A
Primary = ascites or SBP on their own
Secondary = inflammation due to another cause e.g. bile from burst intestine or old clotted blood from burst ectopic pregancy
48
Q

S&S of peritonits?

A

Rigid abdomen, patient lies very still, pain relieved by resting hands on the abdomen.
Pain is initially poorly localised then as disease worsens it will localised

49
Q

Treatment of peritonitis?

A

IV fluids and broadspectrum antibiotics, peritoneal lavage

50
Q

Risk factors for gall stones?

A

Obestity, rapid weight loss, female, fertility, smoking, DM, oral contraceptive pill,

51
Q

What are the types of gall stones - describe them?

A
Cholesterol = large, solitary and caused by high cholesterol concentrations
Pigmented = friable, irregular and caused by haemolysis. Black in haemolytic anaemias, Brown in bile stasis/biliary infection
52
Q

What infections are commonly associated with cholecystitis?

A

Klebsiella, enterococcus and E.coli

53
Q

Treatment for gall stones?

A

Shockwave lithotripsy, basket removal.

Cholesterol stones = simvistatin and ursodeoxycholic acid

54
Q

What is biliary colic?

A

Gall stones blcoking the cystic duct leading to sudden onset, constant and severe RUQ pain with nausea and vomiting

55
Q

What is acute cholecystitis?

A

Gall bladder obstruction leading to its inflammation and often infection. Causes continuous RUQ pain, guarding and rigiditiy, vomiting, fever and local peritonitis

56
Q

What is Murphy’s sign?

A

RUQ tenderness

57
Q

What is ascending cholangitis?

A

Inflammation of the bilairy tree/common bile duct due to gall stone blockage, benign biliary strictures (from surgery) and pancreatic cancer.

58
Q

S&S of ascending cholangitis?

A

Biliary colic pain, fever/rigours, obstructive jaundice, RUQ pain, and itchy skin

59
Q

Treatment of ascending cholangitis?

A

Urgent drainage with ERCP, remove stones with ballon/stenting/crushing and give IV antibiotics

60
Q

What is pancreatits and what causes it?

A

Enzyme mediated auto-digestion of the pancreas due to premature activation of the enzymes.
Idiopathic, Gall stones, Ethanol (alcohol), Trauma, Steroids, Mumps, Autoimmune, Scorpion venom, Hyperlipidaemia, ERCP and Drugs - I GET SMASHED

61
Q

S&S of pancreatitis?

A

Severe epigastric pain radiating to the back and relieved by sitting forward. Anorexia, vomiting, tachycardia, hypotension, oedmea, fever, jaundice, guarding, tetany and Cullen’s/Grey Turner’s signs.

62
Q

What is the scale used to assess severity of pancreatitis?

A

APACHE II

63
Q

Treatment of pancreatitis?

A
Acute = analgesia, IV fluids and nil by mouth (use NGT)
Chronic = analegia, enzyme replacement and alcohol abstience (chronic pancreatitis tends to relapse and remmit)
64
Q

What is systemic inflammatory response syndrome?

A
Sepsis due to a proinflammatory state characterised by any 2 of:
Temp >38 or <36
RR > 20 
HR > 90
WCC >12 or <4
65
Q

Name some common causes of infective diarrhoea?

A
Viral = rotavirus, norovirus, adenovirus and astrovirus
Bacterial = campylobacter jejuni, E.coli, salmonella and shigella spp.
Parasitic = giardia lamblia, entamoeba histolytica and cryptosporidium
66
Q

Which antibiotics can commoly cause C.difficile?

A

Clindamycin, ciprofloxacin, co-amoxiclav and cephalosporins

67
Q

How can we classify hernias?

A
Reducible = can be pushed back into place
Irreducible = can't be pused back, may be incacerated (stuck due to adhesions) or obstructed (stuck due to pressure)
Strangulated = blood supply is cut off, may lead to ischaemia and perforation
68
Q

What is a direct inguinal hernia?

A

The peritoneal sac enters the inguinal canal through the posteroior wall medial to the epigastric vessels.
These reduce easily and rarely strangulate

69
Q

What is an indirect inguinal hernia?

A

The peritoneal sac enters the inguinal canal through the deep inguinal ring lateral to the inferior epigastric vessels.
These strangulate easily

70
Q

Risk factors for an inguinal hernia?

A

Being male, having a chronic cough, constipation, urinary obstruction, heavy lifting, past abdominal surgery and ascites.
The hernia appears in the scrotum

71
Q

What is a femoral hernia?

A

The bowl passes through the femoral canal and presents as a mass in teh upper medial thigh. These are irreducable and strangulate easily.
More common in women

72
Q

What is a incisional hernia?

A

A complication of abdominal surgery where tissue protrudes through a weak surgical scar due to the breakdown of muscle

73
Q

What are the 2 types of hiatus hernia?

A
Sliding = The gastro-oesophageal junction and part of the stomach slide into the chest cavity via the hiatus and lie above the diaphragm - reflux likely
Rolling = The gastro-oesophageal junction remains in teh abdomen but the fundus prolapses through the hiatus - reflux unlikely
74
Q

What may hiatus hernias cause and how can you test for them?

A

GORD - especially in sliding

Barium swallow to test

75
Q

Where is hepatocellular carcinoma likely to metastasise too?

A

Lymph nodes, bones and lungs

76
Q

S&S of hepatocellular carcinoma?

A

Jaundice, acites, large irregular and tender liver, weight loss, fever, fatigue and ache in the right hypochondrium

77
Q

S&S of cholangiocarcinoma?

A

Jaundice, fever, malaise, abdominal pain with or without ascites

78
Q

Treatment for hepatocellular carcinoma?

A

Surgical resection or liver transplant

79
Q

Treatment for cholangiocarcinoma?

A

Non, patients die in <6months

80
Q

Where do secondary liver tumours commonly come from?

A

GI tract, breast and bronchus cancers

81
Q

Causes of cholangiocarcinoma?

A

Parasitic worms, biliary cysts and IBS

82
Q

Causes of hepatocellular carcinoma?

A

HBV, HCV, cirrhosis of any cause

83
Q

Caues of pancreatic adenocarcinoma?

A

smoking, alcohol/coffee/aspirin excess, diabetes, chronic pancreatitis, being a male

84
Q

S&S of pancreatic adenocarcinoma?

A

Acute pancreatitis, anorexia, weight loss.
If head of pancreas = painless obstructive jaundice
Body/tail of pancreas = epigastric pain radiating to the back and relieved by sitting forward

85
Q

Treatment for pancreatic cancer?

A

Mainly palliative e.g. stenting to releive jaundice, opiates and nutritional support. This cancer metastasises very early and has an extremely low 5 year survival

86
Q

What are the main benign liver tumours?

A

Liver hemangioma and hepatic adenoma.
Hemangiomas require no treatment but hepatic adenomas can lead to abdominal pain and intraperitoneal bleeding so surgical resection is required.

87
Q

What type of viruses are the hepatitis viruses?

A
B = DNA
Rest = RNA, D is a partial RNA virus
88
Q

Treatment for alpha-1-antitrypsin deficiency?

A
Lungs = bronchodilators and ICS
Liver = transplant
89
Q

What are the causes of jaundice?

A
Pre-hepatic = malaria and sickle cell disease
Hepatic = Gilbert's syndome, ALD, HCC
Post-hepatic = gall stones, pancreatic cancer and HCC
90
Q

What is seen in the differnt types of jaundice?

A
Pre-hepatic = raised unconjugated bilirubin
Hepatic = dark urine, light stools and raised conjugated AND unconjugated bilirubin
Post-hepatic = dark urine, light stools and raised conjugated bilirubin
91
Q

What are the markers of liver disease and which is most specific?

A

Raised AST and ALT - ALT is more specific

Raised Alkaline Phosphate (ALP) also indicated iver disease with biliary tree disease

92
Q

What can be found in a biopsy of liver cirrhosis?

A

Mallory bodies and neutrophil infiltration

93
Q

What is the screening test for potential alcohol abuse issues?

A

CAGE

94
Q

What are the two types of autoimmune hepatitis?

A
T1 = Increased IgG as well as ASMA and ANA antibodies
T2 = LMKI anibodies
95
Q

What are the differences between PBC and PSC?

A
PBC = autoimmune, affects teh small interlobular bile ducts, affects women more and AMA antibodies are seen
PSC = associated with UC, affexts the intra/extra-hepatic ducts, affects men more and ANA/ANCA antibodies are both seen
96
Q

What is raised in HCC that is a marker of this but also testicular cancer?

A

Alpha-fetoprotien