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1 - Finals > GI - liver + co. > Flashcards

GI - liver + co. 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

= acute inflammation of pancreas releasing exocrine (secrete via ducts) enzymes causing autodigestion of the organ. activation of proenzymes within duct.

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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.

presents with this + vomiting

typically presents at around 60yo

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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.

shock!

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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 causing 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.

FBC, LFT (AST:ALT >3, raised bilirubin)

hypocalcaemia, hypergylcaemia, raised urea.

plain erect AXR - retroperitoneal shadow = bleed, intestinal obstruction, pancreatic calcifications

CT w/ contrast = diagnostic.

USS shows swollen pancreas +/- gallstones

ERCP

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7
Q

explain the Modified Glasgow criteria for predicting severity of pancreatitis

A

PANCREAS: 3 or more = SEVERE

PaO2 <8kPa

Age >55yrs

Neutrophilia - WCC >15

Calcium - <2mmol/L

Renal function - urea >16mmol/L

Enzymes AST/ALT >200 units

Albumin <32g/L

Sugar >10 mmol/L

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8
Q

how would you medically manage an acute pancreatitis patient?

A

MILD = Nil by mouth / NG tube, manage on general ward. pain relief = pethidine (antispasmodic) or buprenorphine +/- IV benzodiazepines (morphine causes spasms in ampullar). IV fluids, no need to CT. repeat glasgow scores at 24 and 48h + daily bloods and obs. when symps and blood stabilise can restart fluids/food. refer for Rx of gallstones if relevant.

SEVERE = HDU/ITU + CT for necrosis.

if necrosis - aspirate peritoneal fluid for culture and target IV abx.

enteral nutrition (NG tube), early ERCP for gallstones, give O2.

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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 (raising CRP and dynamic CT), pancreatic abscess, ascities, acute pseudo cyst (4W after attack, needs surgery), pulmonary oedema

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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.

typically a 40yo male drinker.

DDX = PANCREATIC CANCER

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12
Q

give 3 clinical features of chronic pancreatitis

A

epigastric painradiating to back - relieved by sitting forward or hot water bottles on epigastrium/back, made worse by eating.

nausea and vomiting.

exocrine dysfuncton - malabsorption, wt loss, diarrhoea, steatorrhoea.

endocrine dysfunction - DM.

differentiate from pancreatic cancer!!!

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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 - there’s no biochemical markers for chronic pancreatitis, and radiology is frequently nromal.

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14
Q

what investigations would you run in chronic pancreatitis?

A

bloods - FBC, U&E, LFT, Ca (cause), amylase (normal), glucose/HbA1c (raisesd)

secretin stimulation test - causes pancreas to release bicarb to neutralise stomach acid, will be positive if >60% exocrine function lost.

malabsorption tests - serum trypsinogen/faecal elastase.

imagine - CT (atrophy, duct dilatation or calcification), *MRCP (magnetic retrograde cholangiopancreatography)

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15
Q

how would you treat a patient with chronic pancreatitis?

A

NSAIDs and tramdol for pain

replace pancreatic enzymes if malabsorption.

alcohol advice

low fat diet

gallstones treatment, diabetes treatment

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16
Q

give 2 possible complications of chronic 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 (10%) - small, friable, radiolucent:

  • black = calcium bilirubinate + mucin, glycoproteins. result of haemolytic conditions.
  • brown calcium bilirubinate + fatty acids = result of stasis and biliary infection (e. coli/klebsiella)

cholesterol stones - 80% of stones in UK - large, solitary, radiolucent

mixed stones (10%) - faceted (calcium salts, pigment and cholesterol).

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18
Q

who gets gallstones?

A

fair, fat, fertile, female and forty.

also - FHx, oral contraceptions, hyperlipidaemia.

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19
Q

what are the different outcomes a gallstone can cause, and give some clinical features for each.

A

biliary colic = RUQ pain

acute cholecystitis = RUQ pain + fever/WCC

ascending cholangitis = RUQ pain + fever/WCC + jaundice - Charcot’s triad.

pancreatitis = jaundice, raised bili, alk phos, GGT - 70% asymptomatic though

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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

what is biliary colic? how does it present, how would you investigate it?

A

most common presentation of gallstones.

due to - temporary obstruction of cystic or common bile duct (jaundice)

pain = sudden onset, epigastric/RUQ, radiation to interscapular region, constant lasting 15 minutes- 24 hours, relieved spontaneously or with analgesia

  • With nausea and vomiting due to GB distension

Ix = USS is 90-95% sensitive for stones
Urinalysis, CXR, ECG for exclusion

will get =jaundice if stone moves to CBD

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22
Q

what are the clinical features of acute cholecystitis?

A

second most common presentation of gallstones - 95% due to stones, they get impacted in cystic duct and there’s an inflammatory response to retained bile.

presentation - continuous epigastric/RUQ pain, referred to R shoulder. vomiting, fever, local peritonism, possibly a gallbladder mass. jaundice if stones in CBD. Murphy’s +ve.

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23
Q

what investigations would you perform in acute cholecystitis?

A

ultrasound - thick walled (>3mm), shrunken gallbladder, fluid or air in GB. dilated CBD >6mm diameter

may do ERCP/MRCP.

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24
Q

management for gallstones/biliary colic/acute cholecystitis - non-surgical v surgical?

A

Non-Surgical:

  • NBM (stops CCK release)
  • parenteral opioids (pethidine) or **PR diclofenac
  • if >24hrs admit, rehydrate IV fluids, consider IV abx (3rd gen cephalosporin)

Surgical:

  • lap chole to remove gallbladder
  • comps - fat intolerance, injury to bile duct
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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 (fat stimulates CCK).

can occur if repeated attacks of acute cholecystitis.

USS shows shrunken gallbladder

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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

what is the triad of symptoms for ascending cholangitis?

A

Charcot’s triad (70%) - RUQ pain + fever/chills + jaundice.

also Reynold’s pentad (20%) - RUQ pain + fever/chills + jaundice + altered mental state + hypotension/tachycardia.

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28
Q

what structure is being obstructed by gallstones if a patient has developed ascending cholangitis? what’s the mechanism? what organisms are involved?

A

common bile duct

bile normally sterile, if CBD is obstructed then flow of bile is reduced –> biliary stasis and infection. infection can also be due to acute cholecystis or ERCP (1%).

organisms = E coli, klebsiella, enterococci

*medical emergency*

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29
Q

what is the gold standard investigation in ascending cholangitis? other Ix?

A

transabdominal ultrasound - measure CBD dilatation.

also - WCC/ESR/CRP/LFT

?sepsis 6

imaging - KUB XR + AUSS + contrast CT (best method), MRCP

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30
Q

how would you treat ascending cholangitis?

A

fluid resus, broad spec abx, correct any coagulopathy,

Rx as sepsis if shocked.

if AKI, shock, DIC etc - emergency endoscopic biliary drainage.

might do laparoscopic cholecystectomy with IV abx - cefuroxime and metronidazole

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31
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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32
Q

what is jaundice?

A

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

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33
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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34
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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35
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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36
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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37
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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38
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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39
Q

how would you treat hepatitis A?

A

supportive treatment - self-limiting.

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40
Q

how would you prevent hepatitis A?

A

passive and active immunisation (inactivated protein) and good hygiene

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41
Q

what type of virus is hep A?

A

RNA

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42
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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43
Q

what type of virus is hep B?

A

DNA

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44
Q

how is hep B spread?

A

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

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45
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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46
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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47
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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48
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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49
Q

list 2 possible complications of hepatitis B

A

cirrhosis, HCC, fulminant hepatic failure, cholangiocarcinoma, cryoglobulinaemia

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50
Q

what type of virus is hep C?

A

RNA flavivirus

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51
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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52
Q

what haematological disorder is associated with hep C?

A

Non-Hodgkin’s lymphoma

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53
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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54
Q

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

A

HCV RNA at 8weeks.

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55
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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56
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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57
Q

give 3 possible complications of hepatitis C

A

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

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58
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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59
Q

how can hepatitis D be prevented?

A

hep B vaccine

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60
Q

how can you test for hepatitis D?

A

test for anti-HDV antibody

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61
Q

what can hep D cause?

A

acute liver failure/cirrhosis

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62
Q

how can you treat a hep D infection?

A

may need liver transplant as interferon alpha has limited success.

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63
Q

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

A

RNA. hep A.

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64
Q

how is hep E transmitted?

A

enterally - contaminated water.

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65
Q

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

A

hep E RNA

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66
Q

what is liver cirrhosis

A
  • diffuse hepatic process with fibrosis and conversion of normal liver architecture to ndoles - final pathway for most liver disease.
  • cytokines activate stellate cells at space of disse. normal matrix replaced by collagen (types 1 and 3) and fibronectin. loss of fenestration/sinusoids –> impaired function

complications:

  • distortion of hepatic vessels –> increased intrahepatic resistance + portal hypertension (causes oesophageal varices, hypoperfused kidneys, increase CO)
  • hepatocyte damage –> impaired liver function and decreased synthesis of clotting factors
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67
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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68
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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69
Q

what medications should be avoided when treating cirrhosis?

A

NSAIDs, opiates, sedatives

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70
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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71
Q

give 3 clinical features of cirrhosis

A

jaundice

hyperdynamic circulation

Dupuytren’s contracture

xanthelasma

gynaecomastia

atrophic testes

loss of body hair

parotid enlargement

hepatomegaly

cutaneous signs = FLAPS = Finger clubbing, Leukonychia, Asterixis (liver flap) Palmar erythema, Spider naevi, Scratch (pruritus)

arise when 80% of parenchyma destroyed so often asymptomatic.

Vauge - fatigue, malaise, anorexia, nausea, wt loss

decompensated - oedema, ascites, bruising, poor memory, bleeding varices, SBP

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72
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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73
Q

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

A
  • LFT = AST+ ALT raised w/hepatocyte damage, GGT raised if alcohol
  • Albumin = low if advanced cirrhosis
  • FBC = bleeding (anaemia), low pltls (hypersplenism), macrocytosis (alcohol)
  • U+E = hepatorenal synd.
  • Red cell folat = low if alcohol
  • Coag screen = increased PT if advanced
  • Ferritin = raised in hereditary haemachromatosis, low in IDA/blood loss
  • Viral screen = hep B/C
  • Non-alcoholic fatty liver disease = fasting glucose, insulin, triglycerides and uric acid levels
  • Metabolic = A1AT level, caeruloplasmin, urinary copper, fasting transferrin saturation
  • Imaging = USS (complications of cirrhosis/fatty change), CXR (elevated diaphragm and pleural effusions - passage of ascites across diaphragm)

**Biopsy = Gold standard for histology - 1) loss of hepatic architecture, 2) bridging fibrosis, 3) nodular regeration

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74
Q

how would cirrhosis be treated?

A

aim to delay progression + treat cause + avoid complications

general - nutrition, alcohol abstinence, exercise (muscle wasting)

avoid certain drugs - beware those hepatically metabolised.

colestyramine/antihistamines for pruritus.

treat underlying cause.

monnitor for oesophageal varices and HCC.

proph. abx (ciprofloxacin if protein <15g/l), vaccinate against hep A, flu, pneumococcus.

liver transplant.

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75
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.

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76
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)

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77
Q

what immunosuppression would a liver transplant patient be put on?

A

ciclosporin or tacrolimus + azathioprine.

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78
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.

79
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.

80
Q

risk factors for primary biliary cirrhosis?

A

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

90% are women - typically 50yo woman, sister had it too.

heavily associated with Sjogrens! and other AI disease

81
Q

how does PBC present?

A

can be asymptomatic

fatigue (80%) - most common! also pruritus and RUQ pain.

cholestatic jaundice

O/E - hepatomegaly, hyperpgimentation, jaundice

82
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.

raised ESR.

TFT - strong association with AI thyroid disease.

83
Q

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

A

ultrasound - rule out obstruction

cholangiography e.g. MRCP to rule out PSC.

liver biopsy for staging.

84
Q

how would you treat primary biliary cirrhosis?

A

ursodeoxycholic acid - slows disease progression.

pruritus - sedating antihistamines or colestyramine.

vitamin supplements for malabsorption.

bisphosphonates for osteoporosis

might immunosuppress (steroids, MTX)

avoid COCP as oestrogens promote cholestasis

85
Q

give 3 diseases associated with primary biliary cirrhosis

A

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

86
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.

87
Q

how would you investigate secondary biliary cirrhosis?

A

US followed by ERCP.

88
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?

89
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.

90
Q

what is “fatty change”?

A

first change in the alcoholic liver - hepatocytes contain microvesicular droplets of triglycerides that accumulate.

reversible, but will progress if alcohol isn’t stopped.

can be non-alcoholic in NAFLD.

other causes = metabolic syndrome (obesity etc), PCOS, HBV/HCV, weird metabolic disorders, medications (amiodarone, tamoxifen, glucocorticoids, methotrexate)

91
Q

what is the path of damage the alcoholic liver follows?

A

fatty change - alcoholic heptatitis - fibrosis - micronodular cirrhosis

92
Q

what are the clinical features of alcoholic hepatitis?

A

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

93
Q

how would you manage an alcoholic hepatitis patient?

A

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

94
Q

what causes hereditary haemachromatosis?

A

autosomal recessive inheritance with a mutation in the HFE gene (chromosome 6) - C282Y (or H63D)

mostly affects middle aged men.

mechanism = increased intestinal absorption of iron leading to accumulation in tissues: liver (fibrosis, cirrhosis, HCC), heart, skin, joints (arthropathy), pancrease (diabetes).

95
Q

list 3 clinical features of hereditary haemochromatosis

A

early - fatigue, weakness, arthralgia, erectile dysfunction

late - skin bronzing (or “slate grey pigmentation”), cirrhosis (liver signs), cardiac arrhytmias, arthropathy esp. in 2nd and 3rd MCPJs

96
Q

what would be the blood test results (iron studies) in hereditary haemachromatosis? other bloods/Ix?

A

iron studies = increased iron and ferritin, low total iron binding capacity. transferrin saturation >45% (lots of iron in blood - specific) - similar results as for sideroblastic anaemia.

  • also do: HFE genetic testing, LFTs, MRI (iron overloaded liver), liver biopsy with Perl’s stain, liver Fibroscan (transient elastography), ECG/ECHO for cardiomyopathy.
  • tests for alternative causses of hyperferittinaemia - inflammation (CRP), alcohol, metabolic syndrome (BP, BMI, glucose, triglycerides)
97
Q

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

A

Perl’s staining

98
Q

how would you treat hereditary haemachromatosis?

A

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

might require transplant.

99
Q

what is alpha1-antitrypsin?

A

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

serine protease inhibitor, controls inflammatory cascades, balances action of neutrophil elastase in lungs.

in A1AT deficiency an abnormal protein is produced which can’t leave so builds up in liver cells, damaging them.

100
Q

what diseases does deficiency of alpha1-antitrypsin causes?

A

emphysema, COPD, chronic liver disease and HCC

101
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)

SERPINA1 gene on chromosome 14.

102
Q

give the clinical features of alpha1-antitrypsin deficiency

A

dyspnoea (emphysema), cirrhosis, cholestatic jaundice.

103
Q

how would you diagnose alpha1-antitrypsin deficiency?

A

serum alpha1-AT levels (low) –> requires phenotyping.

liver biopsy, LFTs

CXR and lung function testing.

104
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.

105
Q

what is the curative treatment of alpha1-antitrypsin deficiency? other Rx?

A

curative = liver transplant - v. extreme.

if asymptomatic - smoking and alcohol advice.

lung symps Rx as for COPD.

liver disease - regular LFTs, treat cirrhosis, screen for HCC.

106
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.

107
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

108
Q

what is a Kayser-Fleischer ring?

A

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

109
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 (low).

liver biopsy shows copper.

liver MRI shows density at basal ganglia.

110
Q

how would you treat Wilson’s disease?

A

lifetime copper chelation (binds copper for excretion in urine) - penicillamine.

zinc compounds can stop absorption of copper.

avoid high copper foods - mushrooms, liver, chocolate, nuts.

monitor liver/kidney function, FBC, clotting.

avoid alcohol and hepatotoxic drugs.

screen siblings (treatment whilst asymptomatic prevents liver damage).

111
Q

name an infective cause of liver failure

A

EBV, hep B and C, yellow fever

112
Q

name a drug cause of liver failure

A

paracetamol OD, halothane, isoniazid

113
Q

name a toxin cause of liver failure

A

carbon tetrachloride, mushrooms

114
Q

name a vascular cause of liver failure

A

Budd-Chiari, venous thrombosis

115
Q

name an inherited cause of liver failure

A

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

116
Q

name some other causes of liver failure

A

alcohol, fatty liver of pregnancy, malignancy

117
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

118
Q

what is hepatic encephalopathy? explain it. how doees it present?

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

presents with confusion, drowsiness, fits etc.

119
Q

what investigations might you do for liver failure, and what would you find?

A
  • FBC = thrombocytopaenia
  • LFT = raised ALT+AST
  • bilirubin = raise
  • ammonia = raised
  • glucose = dangerously low
  • copper studies (if ?wilson’s)
  • paracetamol (if ?OD)
  • creatinine = raised if hepatorenal syndrome
  • PT/INR = raised
  • blood culture/viral serology
  • doppler USS - ascites, occluded hepatic vein if Budd-Chiari
  • CT/MRI liver - check for hepatic anatomy
  • CT head - for cerebral oedema
120
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.

121
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.

75% of ascites is due to cirrhosis!

122
Q

give 3 causes of exudate ascites

A

peritoneal carcinomatosis

peritoneal TB

pancreatitis

nephrotic syndrome

lymphatic obstruction

123
Q

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

A

SHIFTING DULLNESS (if >1500mls)

fluid thrill

abdo discomfort (tense ascites).

presentation = abdo distension, often umbilical hernia (high intra-abdo pressure), weight gain, discomfort & nause if tense ascites, dyspnoea (impaired lung expansion)

124
Q

how would you manage a patient with ascites?

A

monitor abdo girth + weight

treat cause, restrict salt intake.

diuretics - spironolactone best for cirrhosis, monitor for hyperK+

* therapeutic paracentesis +/- plasma expander

* TIPS = transjugular intrahepatic shunt if require frequent paracentesis

complications = SBP in 10-30%, hepatorenal synd.

125
Q

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

A

irregular nodules of fibrous tissues.

126
Q

how would you investigate ascites?

A

LFT - shows cirrhosis

abdo USS (check for Ca ovary, liver mets)

CXR (heart failure, pleural effusion)

paracentesis - investigation and intervention.

127
Q

what would you see on biopsy in primary biliary cirrhosis?

A

bile duct granuloma

128
Q

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

A

failure of liver to eliminate steroid hormones

129
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.

130
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.

131
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

132
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

133
Q

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

A

HBV PCR

134
Q

what are the 3 types of liver abscess?

A

pyogenic, amoebic or hyatid

135
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

136
Q

list the most common causative organisms in liver abscesses

A

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

137
Q

what causes an amoebic liver abscess?

A

spread of entamoeba histolytica from bowel to liver via portal system

138
Q

what is the main GI feature of amoebic liver abscess?

A

bloody diarrhoea

139
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

140
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

141
Q

how would you manage an amoebic liver abscess?

A

metronidazole. no need to aspirate.

142
Q

are most liver tumours primary or secondary?

A

90% are secondary.

143
Q

list some common origins of secondary liver tumours

A

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

144
Q

what are the 5 types of primary malignant liver tumours?

A

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

145
Q

list the 5 types of primary benign liver tumours

A

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

146
Q

list 3 symptoms of liver tumours

A

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

147
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.

148
Q

how would you investigate liver cancer?

A

bloods.
US guided biopsy / MRI.

149
Q

what protein is raised in serum in HCC?

A

alpha fetoprotein

150
Q

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

A

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

151
Q

list 3 causes of HCC

A

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

152
Q

how would you diagnose HCC?

A

4 phase liver CT.
MRI.biopsy.

153
Q

how might HCC be treated?

A

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

154
Q

give 3 causes of cholangiocarcinoma

A

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

aka Klatskin’s tumours.

90% are ductal adenocarcinoma, 10% squamous cell carcionma

usually occurs at bifuurcation of R and L hepatic duct (perihilar region), near ampullar of Vater.

155
Q

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

A

bilirubin rasied (LFTs show cholestatic picture)

tumour markers - CA19-9 and CEA but not AFP.

USS/CT - but MRI optimal.

156
Q

how might cholangiocarcinoma be managed?

A

aggressive surgical resection incl. liver resection +/- transplant.

symptom relief - stents and ERCP.

157
Q

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

A

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

158
Q

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

A

oral contraceptives, anabolic steroids.
only if symptomatic.

159
Q

list some risk factors for pancreatic carcinoma

A

*male >60yo
*smoking
*alcohol

*obesity
*diabetes mellitus
chronic pancreatitis - precursor
*diet high in fat + red/processed meat, low fruit and veg

FHx pancreatic can + familiar cancer syndroms (BRCA1/2, FAP, Lynch, MEN)

160
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 - due to retrograde flow), central abdo mass, hepatomegaly

161
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

162
Q

what investigations would you carry out in pancreatic carcinoma?

A

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

FBC (anaemia of Ca), LFT (for jaundice - raised bilirubin, ALP, GGT), serum glucose (hypergylcaemia).

USS liver, bile duct, pancreas –> tumour mass + dilated bile ducts

abdo CT for diagnosis and staging

163
Q

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

A

Only 10-20% are resectable (often metastatic)

  • Whipple’s procedure (proximal pancreaticoduodenectomy)
  • Distal pancreatectomy for body/tail

Adjuvant chemotherapy 5-FU (flourouracil)

Unresectable: (stage IIB - 4 locally advanced to metastatic)
- Bile duct stent (ERCP) for pruritus/jaundice, palliative chemo/radio

164
Q

try and learn the divisions of abdo aorta (to gut)

A
165
Q

blood supply to spleen etc

A
166
Q

what info can the ALT/AST liver tests give you?

A
  • associated w/hepatocellular damange. ALT more specific for liver.
  • ratio important:

AST:ALT = 1 implies ischaemia

AST:ALT >2.5 = alcoholic hepatitis

AST:ALT <1 = high ALT for hepatocellular damage e.g. paracetamol OD w/hepatocellular necrosis, viral hepatitis, ischaemic necrosis, toxic hepatitis

167
Q

what info do the ALP + GGT LFTs give you? what else is in your standard LFT?

A

ALP + GGT elevated w/ cholestasis

ALP is associated w/cholestasis and malignant hepatocellular damage and marker of bone turnover.

GGT sensitive for alcohol ingestion

also tests albumin, bilirubin, PT

168
Q

what are the three important metabolic causes of liver disease?

A
  1. Hereditary haemachromatosis - deficiency of iron regulatory hormone hepcidin
  2. Wilson’s diseases - hepatolenticular degeneration - accumulation of copper in tissues
  3. Alpha-1 antitrypsin deficiency (A1AT) - affects liver and lungs (emphysema - COPD)
169
Q

explain the roles of hepcidin, transferrin and ferritin in iron absorption

A
  • hepcidin - produced by hepatocytes in response to high iron levels. blocks iron absorption by blocking ferroportin at enterocytes, and reduces iron exit from liver and macrophages (storage sites) in same way.
  • transferrin - binds iron reversibly in blood
  • ferritin - stores iron intracellularly, acute phase protein
170
Q

what 4 things characterise liver failure? what are the different types?

A
  1. hepatic encephalopathy
  2. jaundice
  3. abnormal bleeding
  4. ascites

Classification:

  • fulminant hepatic failure = within 8 weeks of initial illness
  • last onset/subacute FHF = 8-26 weeks
  • chronic hepatic failure = >6/12
171
Q

which clotting factors are produced by the liver? what does this mean in liver failure?

A

factors 2, 7, 9 and 10 are produced alongisde vit K

fibrinogen (factor 1)

also factors 5, 8, 11, 12

means you get abnormal bleeding in liver failure!

172
Q

outline general management principles for liver failure

A
  • consider transplant early (MELD score used to help prioritise transplant lists, there’s also a Child-Turcotte-Pugh classification for severity of cirrhosis)

Specific management:

  • Rx paracetamol OD - N-acetylcysteine
  • ammonia = lactulose + neomycin - traps ammonia in gut
  • IV mannitol if raised ICP
  • manage any AKI, or hypoglycaemia etc
  • bleeding = FFP, platelets, IV vit K
  • ascites = restrict fluid, low salt diet, *diuretics
173
Q

what’s included in the MELD score for liver failure?

A

= model for end-stage liver disease.

BRAIN (mnemonic)

  • Child-Turcotte-Pugh score B/C
  • Bilirubin high
  • Refractory ascites
  • Albumin low <28
  • INR >1.7
  • eNcephalopathy

(Child-Turcotte-Pugh is separate grading system for cirrhosis severity)

174
Q

what is portal hypertension?

A

abnormally high pressure in hepatic portal vein (signif. if hepative venous pressure gradient >10mmHg)

increased vascular resitance/increased blood flow –> raised pressure opening venous collaterals connecting portalto systemic system (GO junct., ant abdo wall, anorectal junct., retroperitoneum)

portosytemic shunts can cause encephalopathy, as toxins can bypass liver

175
Q

how is hepatic encephalopathy graded?

A

0 = minimal changes in memory/intelligence

1 = mild confusion (+/- euphoria, depression, disorder of sleep, decreased attention)

2 = drowsiness, gross deficits in mental ability, inappropriate behaviour

3 = somnolent but rousable, unable to perform mental tasks, marked confusion, occasional fits

4 = coma

176
Q

how do you investigate/manage a patient with hepatic encephalopathy?

A

Ix - serum ammonia, ECG (triphasic waves), MRI/CT for other causes of encephalopathy

Rx - avoid sedatives, diagnose early. decrease nitrogen load (lactulose removes from gut, neomycin lower nitrogen forming gut bacteria)

177
Q

what is hepatorenal syndrome? criteria for diagnosis? Rx?

A

complication of end-stage liver disease (in 40%)/

impaired renal function often precipitated by events lowering BP e.g SBP, GI bleed, penumonia.

criteria is diagnosis of exclusion = cirrhosis w/ascites, Cr >133, no shock, no hypovolaemia, no nephrotoxics

Rx = admit to HDU, monitor UO, treat infections, stop nephrotoxics/diuretics.

give splanchnic vasoconstrictors e.g. terlipression w/ albumin - increases BP and GFR

+/- TIPS to reduce ascites in portal vein.

178
Q

give some causes of portal hypertension divided into:

prehepatic

hepatic

posthepatic

A

prehaptic = portal vein thrombosis, splenic vein thrombosis, extrinsic compression (e.g. tumour)

hepatic = cirrhosis, hepatitis, schistosomiasis, granuloma (sarcoid)

posthepatic = Budd-Chiari, RHF/CCF, constrictive pericarditis

179
Q

what investigations might you do in portal hypertension?

A

AUSS - for liver/spleen/ascites

doppler USS - blood flows

spiral CT - for portal vasculature

endoscopy - for oesophageal varices

portal pressure - by hepatic venous pressure gradient (normal <5, varices >10)

180
Q

management of portal hypertension?

A

management = treat cause +/- liver transplant

beta blocker/nitrates or shunts/TIPS can reduce portal venous pressure

need to use non specific beta blockers e.g carvedilol, propranolol

most important complication = VARICES - life threatening bleed. primary prevention with prophylaxis (non-selective beta blockers)

181
Q

what is Budd-Chiari syndrome? how does it present? Ix/Rx?

A

rare synd. caused by obstruction of hepatic veins.

?genetic basis but also associted with myeloproliferative disorders, hypercoagulable states, TB, tumour.

presents - sudden RUQ pain + rapidly developing ascites (+ hepatomegaly + jaundice +/- renal involvement)

Doppler USS main Ix

Rx - underlying condition. treat ascites. may be due to chronic inferior vena cava thrombosis - begin warfarin.

182
Q

what is autoimmune hepatitis?

A

chronic disease of unknown cause, characterised by hepatocellular inflammation, necrosis and autoantibodies (associated with other autoimmune disease)

hepatocytes express HLA antigens which get attacked by T cells - lymphoid infiltration of portal tract and necrosis.

usually seen in young women.

183
Q

how does autoimmune hepatitis present?

A

often subclinical until full blown cirrhosis.

generic - *nausea, fatigue, myalgia, anorexia, arthralgias, wt loss

endocrine - skin rashes, hirsutism, amenorrhoea, oedema, chest pain (pleuritis)

liver - pruritus + jaundice, URQ discomfort

hepatomegaly, jaundice, splenomegaly, ascites

no real clear pathognomic fx

184
Q

what invetstigations might you do in autoimmune hep and what will they show?

A

LFTs - elevated x10

raised IgG+ve autoantibodies (on autoantibody screen)

serum protein electrophoresis and quantitive Igs (IgG polyclonal hypergammaglobulinaemia)

raised alk phos, low albumin

FBC and blood film

***liver biopsy = most important = interface hepatitis with portal plasma cell infiltrate

185
Q

management of autoimmune hepatitis

A
  • immunosuppression - pred + azathioprine (can cause bone marrow suppression)
  • monitor: 6mthly USS + AFP, liver biopsies
  • hep A/B vaccination
  • liver transplant if end stage

associated w/ : coeliac, IBD, proliferative glomerulonephritis, Grave’s, AI thyroiditis, T1DM

186
Q

list the retroperitoneal structures

A

SADPUCKER

Suprarenal

Aorta/IVC

Duodenum (parts 2+3)

Pancreas

Ureter

Colon

Kidney

Esophagus

Rectum

187
Q

what are the different types of pancreatic cancer?

A

endocrine v exocrine

95% adenocarcinoma

mostly - exocrine, 90% are infiltrating ductal adenocarcinoma @ head/neck/uncinate

90% of periampullary malignancies are pancreatic - better prognosis as present early (obstructive jaundice)

pancreatic cancer has high mortality, early metastasis (liver/peritoneum/lung) and late presentation!

188
Q

explain how pancreatic cancer is staged

A

using multiphase spiral/helical CT. ERCP visualises common bile duct and pancreatic duct using contrast.

  • T1 = limited to pancreas <2cm
  • T2 = limited to pancrease >2cm
  • T3 = beyond pancrease not to coeliac axis or SMA
  • T4 = to coeliac axis or SMA
189
Q

what are the endocrine pancreatic cancers?

A

neuroendocrine tumours

functional (hormone hypersecretion) or non-function (majority e.g. MEN1)

3% of all pancreatic tumours.

mostly insulinomas (90% of these are benign) and gastrinomas (>50%), VIPoma, glucagonoma. (>50% of all types other than insulinomas = malignant)

190
Q

how do the different endocrine pancreatic cancers present?

A
  • Insulinoma: confusion, sweating, dizziness, weakness, hypoglycaemia
  • Gastrinoma: severe peptic ulceration/diarrhoea - Zollinger-Ellison (excess gastrin -> HCl)
  • VIPoma - profuse watery diarrhoea with hypokalaemia and achlorhydria (no HCl)
  • Glucagonoma - DM, weight loss, necrolytic migratory erythema
  • Non-functional - mass effect e.g. jaundice
191
Q

what are the diagnostic criteria for ascending cholangitis?

A

Systemic inflammation (A):

  • Fever/chills/T>38
  • Lab data - elevataed WCC or CRP

Cholestasis (B)

  • jaundice
  • abnormal LFT: raised ALP, ALT/AST, GGT

Imaging (C):

  • biliary dilatation
  • evidence of aetiology: stricture, stone, stent

definitive Dx if one in A+B+C, suspect if A + B/C

192
Q

what is primary sclerosing cholangitis? how does it present?

A
  • chronic inflam. + fibrosis of intra/extrahepatic bile ducts –> multifocal biliary strictures.
  • rare, typical pt 35M, assoc. IBD, HCC, CRC - cause of 10% of all UK liver transplants.

presentation:

  • asymptomatic + abnormal LFT/hepatomegaly
  • jaundice/pruritus
  • RUQ pain
  • fever, wt loss, fatigue, sweats
193
Q

how would you investigate and stage primary sclerosing cholangitis?

A
  • bloods: LFT (raised alk phos/GGT, raised transaminase), raised Igs (IgG, IgM, hypergammaglobulinaemia), p-ANCA autoantibodies.
  • imaging = USS may show bile duct dilatation but MRCP is standard
  • Biopsy to stage using histology: “periductal onion skin fibrosis”
194
Q

how would you manage PSC?

A

treat symptoms + use balloon dilatation for strictures.

pruritus - colestyramine

nutrition - supplement fat soluble vits (DEAK) - should be done for all cholestatic disroders!

avoid alcohol

increased risk of cholangiocarcinoma + CRC, comps incl obstruction, cholangitis, ascites, portal HTN, varices

1 - Finals (15 decks)

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