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Medicine > Liver and Friends > Flashcards

Liver and Friends Flashcards

1
Q

list 4 causes of acute pancreatitis

A

GET SMASHED Gallstones Ethanol (alcohol) Trauma Steroids Mumps/Malignancy Autoimmune Scorpion venom Hyperlipidaemia, hypothermia, hypercalcaemia ERCP and emboli Drugs

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2
Q

describe the pain of acute pancreatitis

A

gradual or sudden severe epigastric/central abdominal pain, radiates to back, may be relieved by sitting forward.

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3
Q

give 3 symptoms and signs of acute pancreatitis

A

pain, vomiting. tachycardia, fever, jaundice, shock, ileus, rigid abdomen ± local tenderness. Cullen’s and Grey Turner’s signs.

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4
Q

what are Cullen’s and Grey Turner’s signs? what causes them?

A

Cullen’s = periumbilical bruising Grey Turner’s = bruising of flanks. due to blood vessel autodigestion and retroperitoneal haemorrhage.

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5
Q

what 2 enzymes would you test for in acute pancreatitis? what would the results be?

A

serum amylase - raised. serum lipase - raised (more sensitive/specific).

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6
Q

what investigations would you carry out in acute pancreatitis?

A

serum amylase and lipase. ABG. CT. AXR.

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7
Q

give 3 criteria in the Modified Glasgow criteria for predicting severity of pancreatitis

A

PANCREAS: PaO2 low Age >55yrs Neutrophilia Calcium - low Renal function Enzymes Albumin Sugar (blood glucose)

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8
Q

how would you medically manage an acute pancreatitis patient?

A

Nil by mouth / NG tube. pethidine (antispasmodic), tramadol (pain relief). prophylactic abx, treat underlying cause.

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9
Q

give 2 early and 2 late possible complications of acute pancreatitis

A

early: shock, ARDS, renal failure, DIC, sepsis, hypocalcaemia. late: pancreatic necrosis, abscesses, bleeding, thrombosis, fistulae.

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10
Q

explain the pathology of chronic pancreatitis

A

inappropriate activation of enzymes within the pancreas - leads to precipitation of protein plugs within duct lumen - forms a point for calcification - duct blockage - ductal hypertension + pancreatic damage - pancreatic inflammation + impaired function

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11
Q

give 3 causes of chronic pancreatitis

A

alcohol, tropical chronic pancreatitis, hereditary, autoimmune, cystic fibrosis, haemachromatosis, pancreatic duct obstruction (stones/tumour), hyperparathyroidism, congenital.

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12
Q

give 3 clinical features of chronic pancreatitis

A

epigastric pain boring through to back - relieved by sitting forward or hot water bottles on epigastrium/back. bloating, steatorrhoea, weight loss, brittle diabetes,

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13
Q

what would you expect serum pancreatic enzymes levels to be in chronic pancreatitis?

A

amylase and lipase are normal

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14
Q

what investigations would you run in chronic pancreatitis?

A

ultrasound + CT.

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15
Q

how would you treat a patient with chronic pancreatitis?

A

NSAIDs and tramdol for abdo pain (amitriptyline for more chronic episodes). lipase + fat-soluble vit supplements. no alcohol, low fat diet. surgery if pain can’t be controlled, or there’s weight loss.

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16
Q

give 2 possible complications of pancreatitis?

A

pseudocyst, diabetes, biliary obstruction, local arterial aneurysm, splenic vein thrombosis, gastric varices, pancreatic carcinoma

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17
Q

describe the 3 different types of gallstones and their causes

A

pigment stones - small, friable, irregular - haemolysis. cholesterol stones - large, often solitary - age, obesity, female sex. mixed stones - faceted (calcium salts, pigment and cholesterol).

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18
Q

what are the 2 risk factors for gallstones become symptomatic?

A

smoking and parity (having given birth).

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19
Q

how does acute cholecystitis develop from an obstruction?

A

obstruction to gall bladder emptying - increased glandular secretion in gall bladder - distension and inflammatory response to retained bile, leads to infection

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20
Q

what special test would you do on examination to confirm cholecystitis?

A

Murphy’s sign - 2 fingers over RUQ + ask patient to breathe in - causes pain and arrest of inspiration as inflamed gallbladder hits your fingers

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21
Q

how would you differentiate the pain of biliary colic from cholecystitis?

A

cholecystitis features an inflammatory component - local peritonism, fever, high WCC

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22
Q

what are the clinical features of acute cholecystitis?

A

epigastric/RUQ pain, referred to R shoulder. vomiting, fever, local peritonism, possibly a gallbladder mass.

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23
Q

what investigations would you perform in cholecystitis?

A

ultrasound - thick walled, shrunken gallbladder, pericholecystic fluid, stones, common bile duct dilation. FBC (high WCC).

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24
Q

how would you treat cholecystitis?

A

nil by mouth, analgesia, IV fluids. cefuroxime. laparoscopic cholecystectomy.

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25
Q

describe the clinical features of chronic cholecystitis

A

chronic inflammation ± colic. flatulent dyspepsia - vague abdo discomfort, distension, nausea, flatulence and fat intolerance.

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26
Q

describe the pain of biliary colic

A

severe, constant, increasing pain in RUQ, can radiate to right shoulder/scapula.

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27
Q

how would you tell that a gallstone had moved to obstruct the common bile duct?

A

obstructive jaundice and cholangitis

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28
Q

what is the triad of symptoms for acute cholangitis?

A

Charcot’s triad - jaundice, fever, biliary colic.

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29
Q

what structure is being obstructed by gallstones if a patient has developed acute cholangitis?

A

common bile duct

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30
Q

what is the gold standard investigation in cholangitis?

A

transabdominal ultrasound - measure CBD dilatation.

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31
Q

how would you treat acute cholangitis?

A

laparoscopic cholecystectomy with IV abx - cefuroxime and metronidazole

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32
Q

list 3 complications of gallstones

A

in gallbladder and cystic duct: biliary colic, acute and chronic cholecystitis, mucocoele, empyema, carcinoma, Mirizzi’s syndrome. in bile ducts: obstructive jaundice, cholangitis, pancreatitis. in gut: gallstone ileus.

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33
Q

what is jaundice?

A

yellowing of the skin, sclerae and mucosae due to increased plasma bilirubin

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34
Q

give 3 causes of unconjugated hyperbilirubinaemia (pre-hepatic jaundice)

A

haemolysis - malaria, DIC. ineffective erythropoiesis. impaired hepatic uptake - drugs (contrast agents, rifampicin), RHF. impaired conjugation - Gilbert’s syndrome, Crigler-Najjar.

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35
Q

what will the urine and faeces look like in conjugated hyperbilirubinaemia (hepatic/post-hepatic jaundice)? why?

A

urine = dark - conjugated bilirubin is soluble, so excreted in urine. Faeces = pale - less conjugated bilirubin enters gut.

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36
Q

give 3 causes of conjugated hyperbilirubinaemia due to hepatocellular dysfunction

A

viruses - hep, CMV, EBC. drugs - paracetamol od, isoniazid, rifampicin, pyrazinamide, statins, sodium valproate. alcohol. cirrhosis. liver metastases/abscesses. haemachromatosis. autoimmune hepatitis. septicaemia. syphilis. alpha1-antitrypsin deficiency. Budd-Chiari. Wilson’s disease. Right heart failure.

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37
Q

give 3 causes of conjugated hyperbilirubinaemia due to impaired hepatic excretion (cholestatic / obstructive jaundice)

A

primary biliary cirrhosis, primary sclerosing cholangitis, drugs, common bile duct gallstones, pancreatic cancer, compression of the bile duct, choledochal cyst

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38
Q

how is hepatitis A spread? what are the risk factors?

A

faecal-oral route. poor sanitation, overcrowding, contaminated food/water. (fish in sewagey water)

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39
Q

what would you find when looking at viral markers for hepatitis A? what other blood test would you perform?

A

Anti-HAV IgM (acute) and IgG (raised for life - carrier). LFTs - AST/ALT are raised

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40
Q

how would you treat hepatitis A?

A

supportive treatment - self-limiting.

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41
Q

how would you prevent hepatitis A?

A

passive and active immunisation (inactivated protein) and good hygiene

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42
Q

what type of virus is hep A?

A

RNA

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43
Q

give 3 symptoms of hep A as well as 2 later signs

A

symptoms: fever, malaise, anorexia, nausea, arthralgia. later signs - jaundice, hepatosplenomegaly, lymphadenopathy.

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44
Q

what type of virus is hep B?

A

DNA

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45
Q

how is hep B spread?

A

blood products - vertical transmission, IVDU, found in semen and saliva - sexual/direct contact.

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46
Q

name 3 of the at-risk groups for hep B

A

IVDUs, their sexual partners/carers, health workers, haemophiliacs, job exposure to blood (morticians), haemodialysis patients, sexual promiscuity, foster carers, staff/residents of institutions/prisons, babies of +ve mothers

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47
Q

what are the clinical features of hep B?

A

resembles hep A - fever, malaise etc - plus arthralgia and urticaria (hives).

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48
Q

what antiviral agents would you give to treat a chronic HBV infection? what would you monitor?

A

interferon alpha, lamivudine, adefovir. monitor HBV levels and platelets.

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49
Q

describe how vaccination is used in hep B

A

passive immunisation is given to non-immune contacts after high-risk exposure. Hep B vaccine given (UK) to children born to +ve mothers, chronic liver patients, haemophilia patients, offered as a travel vaccine, and to healthworkers.

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50
Q

list 2 possible complications of hepatitis B

A

cirrhosis, HCC, fulminant hepatic failure, cholangiocarcinoma, cryoglobulinaemia

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51
Q

what type of virus is hep C?

A

RNA flavivirus

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52
Q

how is hep C transmitted and can the spread be prevented?

A

blood products, mainly IVDU (also transfusions, sexual etc) Can’t prevent spread - vaccination impossible due to rapid change of proteins.

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53
Q

what haematological disorder is associated with hep C?

A

Non-Hodgkin’s lymphoma

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54
Q

give 3 risk factors for progression of hepatitis C to cirrhosis

A

male, older, higher viral load, alcohol use, HIV, HBV

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55
Q

what viral markers would you look for in hepatitis C at 8 weeks?

A

HCV RNA at 8weeks.

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56
Q

if you took a liver biopsy of a hepatitis C patient, what might you see?

A

lymphoid follicles in portal tracts and fatty change

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57
Q

how would you treat a chronic infection with hepatitis C? what major problem should be noted about one of the drugs?

A

serine protease inhibitors (boceprevir, telaprevir) - directly acting antivirals against genotype 1 HCV. combine with: interferon alpha. ribavirin - very teratogenic.

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58
Q

give 3 possible complications of hepatitis C

A

glomerulonephritis, cryoglobulinaemia, thyroiditis, autoimmune hepatitis, PAN, polymyositis, porphyria cutanea tarda

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59
Q

what other virus is needed for hep D to infect someone? why?

A

hep B. hep D is an incomplete RNA that needs hep B for assembly.

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60
Q

how can hepatitis D be prevented?

A

hep B vaccine

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61
Q

how can you test for hepatitis D?

A

test for anti-HDV antibody

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62
Q

what can hep D cause?

A

acute liver failure/cirrhosis

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63
Q

how can you treat a hep D infection?

A

may need liver transplant as interferon alpha has limited success.

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64
Q

what type of virus is hep E? what infection is it similar to?

A

RNA. hep A.

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65
Q

how is hep E transmitted?

A

enterally - contaminated water.

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66
Q

what can you detect in blood and stools to confirm a diagnosis of hep E?

A

hep E RNA

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67
Q

what collagen type is deposited in the liver in cirrhosis?

A

type 1 and 3

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68
Q

what is the difference between macro and micronodular cirrhosis?

A

macronodular - variable nodule size, normal acini within, tends to follow hepatitis. micronodular - uniform involvement of liver and regenerating nodules

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69
Q

if there was alpha-fetoprotein present in the serum of a cirrhosis patient, what would you suspect to be the cause of their cirrhosis?

A

hepatocellular carcinoma

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70
Q

what medications should be avoided when treating cirrhosis?

A

NSAIDs, opiates, sedatives

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71
Q

list 3 causes of cirrhosis

A

*chronic alcohol abuse. *HBV or HCV infection haemachromatosis alpha1-antitrypsin deficiency Budd-Chiari non-alcoholic steatohepatitis autoimmune - primary biliary cirrhosis, primary sclerosing cholangitis, autoimmune hepatitis. drugs - amiodarone, methyldopa, methotrexate.

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72
Q

give 3 clinical features of cirrhosis

A

pruritus jaundice raised LFTs leuconchyia Terry’s nails clubbing palmar erythema hyperdynamic circulation Dupuytren’s circulation spider naevia xanthelasma gynaecomastia atrophic testes loss of body hair parotid enlargement hepatomegaly

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73
Q

list 3 possible complications of cirrhosis

A

hepatic failure - coagulopathy, encephalopathy, hypoalbuminaemia, sepsis, SBP, hypogylcaemia. portal hypertension - ascites, splenomegaly, portosystemic shunt + oesophageal varices. increased risk of HCC.

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74
Q

what investigations would you carry out in cirrhosis? what would you find?

A

bloods - raised bilirubin/AST/ALT/alk phos, low albumin. liver ultrasound and duplex - small liver or hepatomegaly, focal liver lesions, ascites. MRI - big caudate lobe, small islands of regenerating nodules, right posterior hepatic notch. transient elastography scan. ascitic tap for urgent MC&S. liver biopsy - confirms diagnosis.

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75
Q

if a cirrhosis patient presented with ascites, how would you treat this?

A

bed rest, fluid and salt restriction, spironolactone ± furosemide.

76
Q

how would cirrhosis be treated?

A

nutrition, alcohol abstinence, avoid certain drugs. colestyramine for pruritus. treat underlying cause. liver transplant.

77
Q

what are the indications for liver transplant?

A

advanced cirrhosis secondary to - alcoholic liver disease, hepatitis (B, C, autoimmune), primary biliary cirrhosis, Wilson’s disease, alpha1-atintrypsin deficiency, primary sclerosing cholangitis. hepatocellular cancer.

78
Q

what are the contraindications for liver transplant?

A

extrahepatic malignancy, multiple tumours, severe cardiorespiratory disease, systemic sepsis, HIV infection, non-compliance (drug therapy or alcohol abstinence)

79
Q

what immunosuppression would a liver transplant patient be put on?

A

ciclosporin or tacrolimus + azathioprine.

80
Q

what’s the difference between hyperacute and acute transplant rejection?

A

hyperacute - due to ABO incompatibility. acute - T cell mediated, 5-10d post-op, patient feels unwell with pyrexia and tender hepatomegaly - managed by altering immunosuppressives.

81
Q

describe the underlying pathogenesis of primary biliary cirrhosis?

A

serum antimitochondrial antibodies (AMA) cause chronic autoimmune granulomatous inflammation damages interlobular bile ducts causing cholestasis, cirrhosis and portal hypertension.

82
Q

give 2 risk factors for primary biliary cirrhosis

A

family history, frequent UTIs, smoking, past pregnancy, other autoimmune diseases, hair dye/nail polish

83
Q

give 2 signs found in a patient with biliary cirrhosis

A

jaundice, skin pigmentation, xanthelasma, hepatomegaly, splenomegaly

84
Q

what blood test results would you find in a patient with primary biliary cirrhosis?

A

**very high alkaline phosphate - unique to PBC **AMA ab +ve. raised AST/ALT increased Igs.

85
Q

what other investigation, apart from blood tests, might you perform in primary biliary cirrhosis?

A

ultrasound

86
Q

how would you treat primary biliary cirrhosis?

A

ursodeoxycholic acid. vitamin supplements for malabsorption. bisphosphonates for osteoporosis, colestyramine/rifampicin for pruritus.

87
Q

give 3 diseases associated with primary biliary cirrhosis

A

scleroderma, thyroid disease, keratoconjunctivitis sicca, renal tubular acidosis, membranous glomerulonephritis, coeliac disease, interstitial pneumonitis

88
Q

explain secondary biliary cirrhosis

A

destruction of biliary tracts due to prolonged large duct biliary obstruction, caused by gall stones, bile duct stones, sclerosing cholangitis.

89
Q

how would you investigate secondary biliary cirrhosis?

A

US followed by ERCP.

90
Q

what are the CAGE questions?

A

ever felt you should Cut down on your drinking? have people Annoyed you by criticising your drinking? ever felt Guilty about your drinking? ever had an Eye opener to help you get up in the morning?

91
Q

what changes would you see on a liver biopsy of an alcoholic hepatitis patient?

A

fatty change and infiltration by polymorphonuclear leucocytes and hepatocytes in zone 3. Mallory bodies - dense cytoplasm and giant mitochondria.

92
Q

what is “fatty change”?

A

first change in the alcoholic liver - hepatocytes contain microvesicular droplets of triglycerides. reversible, but will progress if alcohol isn’t stopped.

93
Q

what is the path of damage the alcoholic liver follows?

A

fatty change - alcoholic heptatitis - fibrosis - micronodular cirrhosis

94
Q

what are the clinical features of alcoholic hepatitis?

A

SPIDER NAEVI. rapid onset jaundice, nausea, anorexia, RUQ pain, encephalopathy, fever, ascites, tender hepatomegaly

95
Q

how would you manage an alcoholic hepatitis patient?

A

supportive - poss. NG tube. alcohol cessation - IV thiamine and diazepam if needed.

96
Q

what causes hereditary haemachromatosis?

A

autosomal recessive inheritance with a mutation in the HFE gene (chromosome 6). mostly affects middle aged men.

97
Q

what is the defining feature of hereditary haemachromatosis?

A

increased intestinal iron absorption leading to excess iron deposition in organs.

98
Q

list 3 clinical features of hereditary haemochromatosis

A

erectile dysfunction, slate grey skin pigmentation, hepatomegaly, cirrhosis, dilated cardiomyopathy, osteoporosis, diabetes mellitus, hypogonadism

99
Q

what would be the blood test results (iron, ferritin, total iron binding capacity) in hereditary haemachromatosis? what disease is this the same as?

A

increased iron and ferritin, low total iron binding capacity. the same as sideroblastic anaemia.

100
Q

what staining would you use on liver biopsy in hereditary haemachromatosis?

A

Perl’s staining

101
Q

how would you treat hereditary haemachromatosis?

A

venesection - once a week, then a few times a year. desferrioxamine (iron chelator) if can’t venesect. testosterone replacement. low iron diet, screen family members.

102
Q

what is alpha1-antitrypsin?

A

glycoprotein that controls the inflammatory cascade. synthesised in the liver and protects lung tissue from damage by elastase.

103
Q

what diseases does deficiency of alpha1-antitrypsin causes?

A

emphysema, COPD, chronic liver disease and HCC

104
Q

what are the different genotypes you can inherit for alpha1-antitrypsin? which one brings about symptomatic disease?

A

PiMM - normal (M = medium) PiZZ - homozymgous, symptomatic (Z = very slow) PiMZ - heterozygous (slow)

105
Q

give the clinical features of alpha1-antitrypsin deficiency

A

dyspnoea (emphysema), cirrhosis, cholestatic jaundice.

106
Q

how would you diagnose alpha1-antitrypsin deficiency?

A

serum alpha1-AT levels. genotyping. liver biopsy.

107
Q

what stain would you use on a liver biopsy in alpha1-antitrypsin defiency? what would you see?

A

Periodic Acid Schiff - PAS +ve globules.

108
Q

what is the curative treatment of alpha1-antitrypsin deficiency?

A

liver transplant

109
Q

what is Wilson’s disease?

A

autosomal recessive disorder resulting in impaired excretion of copper in bile and faeces, leading to toxic accumulation of copper.

110
Q

what system, apart from the liver, is affected by Wilson’s disease? how does this present?

A

CNS - basal ganglia degeneration, depression, labile emotions, decreased libido, personality changes, tremor, dysarthria, dementia, decreased memory/IQ, delusions

111
Q

what is a Kayser-Fleischer ring?

A

copper deposition in cornea - see in eyes of Wilson’s disease patients

112
Q

what investigations would you carry out in Wilson’s disease? what would they show?

A

slit lamp eye exam. 24h urine copper - excretion high. liver biopsy - increased hepatic copper, hepatitis, cirrhosis. + genetic testing, serum copper/caeruloplasmin.

113
Q

how would you treat Wilson’s disease?

A

lifetime copper chelation - penicillamine. screen siblings (treatment whilst asymptomatic prevents liver damage).

114
Q

name an infective cause of liver failure

A

EBV, hep B and C, yellow fever

115
Q

name a drug cause of liver failure

A

paracetamol OD, halothane, isoniazid

116
Q

name a toxin cause of liver failure

A

carbon tetrachloride, mushrooms

117
Q

name a vascular cause of liver failure

A

Budd-Chiari, venous thrombosis

118
Q

name an inherited cause of liver failure

A

primary biliary cirrhosis, haemachromatosis, autoimmune hepatitis, antitrypsin deficiency, Wilson’s disease

119
Q

name some other causes of liver failure

A

alcohol, fatty liver of pregnancy, malignancy

120
Q

give 4 signs of fulminant hepatic failure

A

hepatomegaly, jaundice, splenomegaly, ‘pear drop’ smell, asterixis (flapping tremor) palmar erythema, clubbing, ascites, pruritus, portal hypertension

121
Q

what is hepatic encephalopathy? explain it

A

a major complication of liver failure: liver fails - nitrogenous waste (ammonia) builds up in circulation - passes to brain - astrocytes clear it by converting glutamate to glutamine - excess glutamine causes an osmotic imbalance - cerebral oedema

122
Q

what might you find on investigating the blood of a patient with liver failure?

A

high bilirubin and aminotransferases. low sodium, albumin, prothrombin, factor V

123
Q

how would you manage a liver failure patient?

A

treat cause. treat complications: seizures - lorazepman. bleeding - vit K. ascites - diuretics. infection - blind abx = ceftriaxone. hypoglycaemia - IV glucose.

124
Q

what tests would you run on ascitic fluid once aspirated?

A

cell count, MC&S, protein/albumin, cytology for malignancy, amylase to exclude pancreatitis.

125
Q

give 3 causes of transudate ascites

A

portal hypertension (cirrhosis). hepatic outflow obstruction. Budd-Chiari syndrome. cardiac failure. tricuspid regurgitation. constrictive pericarditis. Meig’s syndrome.

126
Q

give 3 causes of exudate ascites

A

peritoneal carcinomatosis peritoneal TB pancreatitis nephrotic syndrome lymphatic obstruction

127
Q

what would you find on abdo examination of a patient with ascites?

A

SHIFTING DULLNESS. fullness in flanks.

128
Q

how would you manage a patient with ascites?

A

aspirate for testing. sodium restriction + oral spironolactone ± furosemide.

129
Q

what would you seen on a liver biopsy of a patient with cirrhosis?

A

irregular nodules of fibrous tissues.

130
Q

how would you investigate ascites?

A

paracentesis - investigation and intervention.

131
Q

what would you see on biopsy in primary biliary cirrhosis?

A

bile duct granuloma

132
Q

explain why gynaecomastia can be a feature of liver failure in males

A

failure of liver to eliminate steroid hormones

133
Q

what would you find in the blood of a patient that would indicate they have carrier status for HBV?

A

HBsAg - surface antigen. present 1-6 months after exposure. present for >6 months = carrier status.

134
Q

what would you find in the blood of a patient that has recently (last couple of months) been infected with HBV? what does this mean?

A

HBeAg (e antigen) - present 1.5-3 months after exposure. implies high infectivity.

135
Q

what might you find in the blood of a patient that indicates they have immunity to HBV through having previously been infected?

A

anti-HBc antibody

136
Q

what might you find in the blood of a patient that indicates they have immunity to HBV through having been vaccinated?

A

anti-HBs antibody

137
Q

what blood test would you do on an HBV patient to monitor progress?

A

HBV PCR

138
Q

are most liver tumours primary or secondary?

A

90% are secondary.

139
Q

list some common origins of secondary liver tumours

A

men - stomach, lung, colon. women - breast, colon, stomach, uterus.

140
Q

what are the 5 types of primary malignant liver tumours?

A

hepatocellular carcinoma (HCC). cholangiocarcinoma angiosarcoma hepatoblastoma fibrosarcoma and hepatic GIST

141
Q

list the 5 types of primary benign liver tumours

A

cysts, haemangioma, focal nodular hyperplasia, fibroma, benign GIST

142
Q

list 3 symptoms of liver tumours

A

fever, malaise, anorexia, weight loss, RUQ pain. jaundice - late, apart from in cholangiocarcinoma.

143
Q

list 3 signs of liver tumours

A

hepatomegaly - smooth, or hard and irregular (mets, cirrhosis, HCC). signs of chronic liver disease. jaundice/ascites. abdo mass. bruit over liver = HCC.

144
Q

how would you investigate liver cancer?

A

bloods. US guided biopsy / MRI.

145
Q

what protein is raised in serum in HCC?

A

alpha fetoprotein

146
Q

how would you treat liver metastases? what is the prognosis?

A

mostly palliative treatment - prognosis is often less than 6/12

147
Q

list 3 causes of HCC

A

*HBV. HCV, autoimmune hepatitis, cirrhosis, non-alcoholic fatty liver, aflatoxin, clonorchis sinesis, anabolic steroids.

148
Q

how would you diagnose HCC?

A

4 phase liver CT. MRI. biopsy.

149
Q

how might HCC be treated?

A

resect solitary tumours. liver transplant. percutaneous ablation, tumour embolisation and sorafenib.

150
Q

give 3 causes of cholangiocarcinoma

A

flukes, primary sclerosing cholangitis, HBV, HCV, diabetes mellitus.

151
Q

what breakdown product is raised in the serum of those with cholangiocarcinoma?

A

bilirubin

152
Q

how might cholangiocarcinoma be managed?

A

precutaneous (or via ERCP) stenting of obstruction. surgery not an option.

153
Q

what is the usual prognosis of cholangiocarcinoma?

A

5 months

154
Q

what is the most common benign liver tumour? should it be biopsied?

A

haemangiomas. incidental finding on US/CT - DON’T biopsy.

155
Q

what are hepatic adenomas associated with? when is surgical resection indicated?

A

oral contraceptives, anabolic steroids. only if symptomatic.

156
Q

list some risk factors for pancreatic carcinoma

A

male >60yo smoking alcohol carcinogens diabetes mellitus chronic pancreatitis central adiposity diet high in fat + red/processed meat

157
Q

what is the genetic association seen in pancreatic carcinoma?

A

95% have mutations in KRA52

158
Q

what are the clinical features of carcinoma of the head of pancreas?

A

painless obstructive jaundice (pain late on, radiates to back). pruritus, Courvoisier’s sign (enlarged, palpable gallbladder), central abdo mass, hepatomegaly

159
Q

what are the clinical features of carcinoma of the body/tail of pancreas?

A

abdo pain, weight loss, anorexia, dull ache radiating to back, relieved when sitting forward. polyarthritis, skin nodules

160
Q

what investigations would you carry out in pancreatic carcinoma?

A

transabdominal ultrasound. CT. bloods - Ca19-9 antigen - not specific, but good marker for monitoring progress.

161
Q

how would you manage a patient with pancreatic carcinoma? what is their prognosis like?

A

surgical resection with post-op chemo or palliative endoscopic stents. opiates/radiotherapy for pain. mean survival less than 6/12.

162
Q

how does ursodeoxycholic acid work?

A

reduces cholesterol absorption and is used to dissolve cholesterol gallstones. it’s a bile acid that is present in the body anyway.

163
Q

how does cholestyramine work?

A

binds bile in GI tract to prevent its reabsorption by forming insoluble complexes with bile acids, which are then excreted in the faeces. useful for pruritus in primary biliary cirrhosis/liver failure. also reduces plasma cholesterol levels.

164
Q

what group of patients is at highest risk of developing oesophageal varices? why?

A

cirrhosis patients - portal hypertension causes dilated collateral veins at site of portosystemic anastomoses

165
Q

what is the complication risk with oesophageal varices?

A

that they will cause an acute haemorrhage - life-threatening. the varices protrude into oesophageal lumen so are easily traumatised by passing food.

166
Q

how would you manage a patient bleeding from oesophageal varices?

A

restore blood volume and correct clotting abnormalities - vit K. endoscopic banding, sclerosing or cauterising. vasocontrictors - terlipressin.

167
Q

what patient groups are at greater risk of primary peritonitis?

A

liver disease - spontaneous bacterial peritonitis (SBP). females, immunocompromised, peritoneal dialysis, ascites.

168
Q

give 3 examples of causes of secondary peritonitis

A

perforation of hollow viscus, inflammation of abdo organs, peritoneal dialysis, TB, ischaemia of a hollow viscus, chemical.

169
Q

give 3 symptoms of peritonitis

A

pain, tendenderness, nausea, chills, rigor, dizziness, weakness and inability to move due to pain

170
Q

give 3 signs you might find on examination of a peritonitis patient

A

pyrexia, tachycardia, confusion, guarding, rebound, rigidity, silent abdomen, patient lies very still

171
Q

what investigations would you perform on a patient with peritonitis?

A

CXR - look for free air under the diaphragm. US/CT

172
Q

how would you manage peritonitis?

A

ABCs, abx, surgical repair of perforated viscus.

173
Q

give 2 conditions that predispose to inguinal hernias

A

male sex, chronic cough, constipation, urinary obstruction, heavy lifting, ascites, past abdominal surgery

174
Q

in relation to pubic tubercle, where does an inguinal hernia present?

A

superior and medial

175
Q

what is the difference between a direct and indirect inguinal hernia?

A

indirect - passes through inguinal canal into testicle due to failure in embryonic closure. direct - enters through weak point in the transversalis fascia (the posterior wall of the inguinal canal) - Hesselbach’s triangle.

176
Q

where might a lump from a femoral hernia present in a patient?

A

inner upper thigh, pointing down the thigh

177
Q

where, in relation to the pubic tubercle, is a femoral hernia felt?

A

inferior and lateral

178
Q

give 3 causes of an incisional hernia

A

infection, increased abdo pressure, poor surgical technique, obesity, haematoma

179
Q

what are the 3 types of liver abscess?

A

pyogenic, amoebic or hyatid

180
Q

give 3 causes of pyogenic liver abscess

A

*idiopathic. biliary sepsis portal pyaemia from intra-abdominal sepsis trauma bacteraemia direct extension from e.g. perinephric abscess

181
Q

list the most common causative organisms in liver abscesses

A

E coli, Strep milleri. anaerobes e.g. bacterioides

182
Q

what causes an amoebic liver abscess?

A

spread of entamoeba histolytica from bowel to liver via portal system

183
Q

what is the main GI feature of amoebic liver abscess?

A

bloody diarrhoea

184
Q

what would you see on performing blood investigations on a patient with a pyogenic liver abscess?

A

raised serum bilirubin, normocytic anaemia, raised alkaline phosphatase, ESR, serum B12

185
Q

if you took a stool culture and liver aspiration of an amoebic abscess patient, what would you see?

A

faeces - pus and amoeba trophozoites. liver aspiration - ‘anchovy sauce’ pus

186
Q

how would you manage an amoebic liver abscess?

A

metronidazole. no need to aspirate.

187
Q

how would you manage a pyogenic abscess?

A

percutaneous aspiration under radiological (e.g. US) control. pig tail catheter for continuous drainage. IV metronidazole and cefuroxime.

Medicine (14 decks)

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