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HPB Flashcards

1
Q

Causes of acute hepatitis

A

Viral infection: Hep A-E, non-hep
Autoimmune
Drug reactions
Alcohol

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2
Q

Chronic causes

A 
Hep B +/- hep D
Hep C
Autoimmune hepatitis
Alcohol
Hyperlipidaemia (NAFLF)
Drugs (methyldopa/nitrofurantoin)
Metabolic: wilson's disease, alpha-1-antitrypsin deficiency, haemachromatosis
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3
Q

Components of a liver screen

A 
Microbiology: viral screen
Clinical chemistry: ferritin/transferrin, lipids, caeruloplasmin, AFP, alpha-1-antitrypsin
Immunology: autoantibodies
Abdominal USS
Consider Hep A+E, and hep B+D together
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4
Q

Hepatitis A aetiology

A 
RNA picorna virus
Transmitted feco-orally
Incubation: 2-6w
80% asymptomatic
Notifiable disease in UK
Doesn't lead to chronic liver disease, so no carriers
Typically affects children/young adults
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5
Q

Hepatitis E aetiology

A 
RNA calcivirus
Transmitted feco-orally
Epidemics of acute, self-limiting hepatitis
Common in indo-china
Severe disease in pregnant women
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6
Q

Hepatitis B aetiology

A

Hepa-DNA virus
Transmitted in blood, semen, saliva via skin breaks/mucous membranes
Vertical transmission most common
Incubation period: 1-6m
Inner core (HBcAg) surrounded by outer envelope of surface protein (HBsAg)
10% develop chronic disease, 1% develop fulminant liver disease

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7
Q

Hepatitis D aetiology

A

Incomplete RNA virus
Only causes infection in presence of Hep B
Transmitted by bodily fluids, acute/chronic
Can be acquired simultaneously with hep B or later (more likely to develop fulminant liver disease)

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8
Q

Hepatitis C aetiology

A

RNA flavivirus, clinically similar to Hep B
Transmitted via bodily fluids, common in IVDUs
Vertical transmission rare, sexual transmission uncommon

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9
Q

Other viruses that can cause acute hepatitis

A

non A-E infections
CMV
yellow fever
HSV

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10
Q

Acute hepatitis pathology

A

Hepatocytes undergo degenerative changes (swelling + vacuolation) before necrosis + rapid removal
Necrosis maximal in zone 3 (centrilobular) as recieves least oxygenated blood
Scattered/periportal necrosis

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11
Q

Chronic hepatitis pathology

A

Hepatitis >6m
Principle cause of chronic liver disease, cirrhosis, hepatocellular carcinoma
Chronic inflammatory cell infiltrates are present in portal tracts
Loss of definition of the portal/periportal limiting plate, confluent necrosis, fibrosis –> cirrhosis
Severity: Child Pugh score

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12
Q

Serological markers of Hep B infection

A

HBsAg: marker of viral replication/active infection, appears within 6w, disappears 3m after
HBsAb: marker of previous cleared infection/immunisation
HBeAg: marker of a high degree of viral replication (high infectivity)
HBeAb: natural immunity to Hep B
HBcAb IgG: non-specific marker of current/previous infection
HBcAb IgM: infection within last 6 months
HBV PCR: marker of viraemia

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13
Q

Hepatitis immune tolerance/incubation phase markers

A

HBsAg +ve
HBeAg +ve
PCR +ve
transaminases -ve

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14
Q

Acute hepatitis markers

A 
HBsAg +ve
HBeAg +ve
HBcAb IgG +ve
HBcAb IgM +ve 
HBV PCR +ve
HBsAg -ve
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15
Q

Chronic hepatitis markers

A

Acute markers +ve >6m
LFTs less deranged
HBeAg +ve
HBeAb -ve

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16
Q

Natural hepatitis immunity markers

A

HBsAg -ve
HBsAb +ve
HBcAg IgG +ve, IgM -ve
HBeAg -ve, HBeAb +ve

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17
Q

Vaccination to hepatitis markers

A 
Only evidence of surface antibody immunity
HBsAg -ve
HBsAb +ve
HBcAg IgG -ve, IgM -ve
HBeAg -ve, HBeAb -ve
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18
Q

Acute viral hepatitis presentation

A

Pre-icteric: 1-2w prodrome of malaise, arthralgia, headache, anorexia, aversion to cigarette smoke, vague RUQ pain
Icteric: iteric (jaundice), pale stools, dark urine (intrahepatic cholestatic jaundice), pruritis, skin rash, lymphadenopathy, hepato/splenomegaly
Hep A+C: mild/no symptoms
Hep B has more extrahepatic symptoms

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19
Q

Acute alcoholic hepatitis presentation

A

Presents after binge: jaundice, RUQ pain, systemic upset
Signs of chronic liver disease
Discriminant function (DF): bilirubin, prothrombin, hepatic encephelopathy predict survival
AST:ALT>2 suggests alcoholic liver disease

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20
Q

Autoimmune hepatitis presentation

A

Commonly presents as chronic, 40% present as acute hepatitis with jaundice
Non-specific fatigue, arthralgia, fevers, weight loss
Age 15-25 or peri-menopausal
Associated with: primary biliary cirrhosis, primary sclerosing cholangitis, IBD)

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21
Q

Chronic hepatitis presentation

A

Asymptomatic
Complications: cirrhosis may cause symptoms
Diagnosed when serum ALT levels elevated for >6m

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22
Q

Paracetamol overdose pathology

A

Intrinsic hepatotoxin
Conjugated with glucuronide & sulphate at therapeutic doses
A small amount metabolised (oxidised) to form NAPQI
NAPQI immediately conjugated with glutathione due to its toxicity
In overdose, conjugation pathway becomes saturated = large amounts of NAPQI created which overwhelms liver glucothione stores causing cellular damage
Severity is dose-related

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23
Q

Paracetamol overdose presentation

A

Asymptomatic for 24h, maybe anorexia, nausea, vomiting
After 24h: RUQ pain, metabolic acidosis, hypotension, hypoglycaemia, pancreatitis, arrhythmia
Liver damage detectable on bloods >18h
Damage peaks 72-96h: deranged ALT/ALP & INR
Liver failure/acute tubular necrosis & renal failure can occur

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24
Q

Bilirubin metabolism

A

RBCs >120d destroyed in reticuloendothelial system of the spleen
Haem converted to biliverdin then to bilirubin, then bound by albumin (insoluble)
Protein-bound bilirubin taken up by hepatocytes –> conjugated by glucuronyl transferase to bilirubin glucuronide (soluble)
Soluble bilirubin excreted in the bile into the bowel where it is transformed by bacteria to urobilinogen
Urobilinogen exreted in stools, small amount reabsorbed and excreted by kidneys

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25
Q

Normal/jaundice levels of bilirubin

A

Normal upper limit: 25micromol/L

Jaundice: 50micromol/L

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26
Q

Pre-hepatic jaundice pathology

A

2ndary to increased erythrocyte breakdown (e.g. haemolysis/reabsoroption of large haematoma)
Bilirubin not yet been processed by the liver so mainly unconjugated

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27
Q

Cholestatic jaundice pathology

A

Bile outflow obstruction (cholestasis)
Intrahepatic: hepatitis, cirrhosis, neoplasm, drugs, pregnancy
Extrahepatic: gallstones, cholangiocarcinoma, primary sclerosing cholangitis, comgenital atresia of common bile duct, pancreatitis, tumour of pancreatic head
Mainly conjugated bilirubin, can give dark urine
Pale stools as none excreted into GI tract

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28
Q

Hepatocellular jaundice pathology

A

Hepatocyte dysfunction, partial inability to conjugate bilirubin
Mixed conjugated/unconjugated bilirubin in the blood
Causes: hepatitis, cirrhosis, neoplasm, hepatotoxic drugs
If severe: unconjugated hyperbilirubinaemia

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29
Q

Gilbert’s syndrome pathology

A

Congenital lack of gluconyltransferase
7% of population
Transient episodes of jaundice, especially following infection
Serum unconjugated bilirubin raised but LFTs and reticulocytes normal

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30
Q

Jaundice investigations

A

Bloods: FBC, reticulocytes, LFTs, U&Es, clotting, glucose, bilirubin levels
Transaminases most raused in hepatocellular jaundice/intrahepatic obstruction
ALP most raised in extrahepatic cholestasis
Glucose low in liver failure, high in pancreatitis
Urinary urobilinogen/bilirubin
Blood film/Coomb’s test: ?prehepatic jaundice
Viral serology/autoantibodies: ?hepatitis
USS: ?cholestasis cause
MRCP: biliary tree imagina
CT/MRI: demonstrate intrahepatic/pancreatic lesions
Needle biopsy: hepatic pathology

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31
Q

What types of cancer commonly metastasise to the liver?

A

Lung, stomach, colon, breast, uterus

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32
Q

Hepatocellular carcinoma pathology

A

90% of primary liver cancers
Common in China/sub-saharan Africa
Causes: chronic hepatitis, cirrhosis, metabolic liver diseases, aspergillus alfatoxin, parasites, anabolic steroids
Risk greater in males

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33
Q

Hepatocellular carcinoma symptoms and signs

A 
Non-specific fever, malaise, weight loss
RUQ pain
Hepatomegaly
Signs of chronic liver disease/decompensation
Abdominal mass/bruit over liver
Jaundice = late sign
34
Q

Hepatocellular carcinoma investigations

A

Bloods: FBC, LFTs, clotting, hepatits serology, AFP (raised in >50% HCC)
USS/CT to identify lesions/guide biopsy
MRI to distinguish benign/malignant lesions
ERCP/biopsy if cholangiocarcinoma suspected

35
Q

Cholangiocarcinoma pathology

A

Adenocarcinoma arising from biliary tree
10% of hepatic primaries
Present with painless jaundice (like pancreatic cancer)
Chronic inflammation predisposes (e.g. primary sclerosing cholangitis/parasite infestation)
Spreads by direct invasion of liver

36
Q

Benign liver tumour pathology

A

Commonly haemangiomas
Young women on OCP: more likely to be a liver cell adenoma
Found incidentally on CT/USS
Only treated if symptomatic/>5cm

37
Q

Characteristics of liver cirrhosis

A

Destruction of liver cells
Associated chronic inflammation, stimulating fibrosis
Regeneration of hepatocytes to form nodules

38
Q

Liver cirrhosis pathology

A

Fibrosis due to growth factors released from Kupffer cells & hepatocytes
Inflammatory cells due to disease process (e.g. hepatitis) or in response to liver cell necrosis (e.g. alcoholism)
Kupffer cells activated –> form myofibroblasts which secrete collagen
Nodules form due to hepatocyte division/regeneration in response to damage, but don’t have normal vascularisation/bile drainage

39
Q

Liver cirrhosis types

A

Micronodular (<3mm): alcoholic liver damage/biliary tract disease
Macronodular (>3mm): previous hepatitis
Biliary cirrhosis (centred around hepatic bile ducts): primary biliary cirrhosis/primary sclerosing cholangitis

40
Q

Classic history of chronic liver disease

A

Fatigue
Weight loss/anorexia: hepatomegaly = early satiety, central weight gain = ascites
Jaundice
Leg swelling: increased intra-abdominal pressure, low oncotic pressure
Bleeding/bruising: decreased sympathetic function
Itching: bile salt accumulation in peripheral nerves

41
Q

Chronic liver disease signs

A

Nails: leuconychia (low albumin), clubbing
Hands: palmar erythema, Dupytren’s, liver flap
Skin: pigmentation, spider naevi, striae
Feminization: gynaecomastia, testicular atrophy, loss of body hair, 2ndary hyperaldosteronism (activation of RAAS as hypoalbuminaemia = lower circulating volume)
Signs of portal hypertension: caput medusae, hepatosplenomegaly, ascites
Signs of hepatocellular failure: bruising, prolonged clotting
Signs of decompensation: encephalopathy, ascites, jaundice

42
Q

Precipitants of chronic liver disease decompensation

A

Alcohol binge, variceal bleed, hepatotoxic drugs, portal/hepatic vein thrombosis

43
Q

Variables in Child-Pugh score

A 
Gives 1/2 year mortality score in chronic liver disease:
Total bilirubin
Serum albumin
PT/INR
Ascites
Hepatic encephalopathy
44
Q

Investigations to determine severity of cirrhosis

A

Liver function: albumin, INR
Liver damage: LFTs
Complications: U&Es, ABG (hepatorenal/hepatopulmonary syndrome)

45
Q

Investigations to determine type of liver disease

A

Liver screen: viral serology, serum autoantibodies/immunoglobulins, AFP, iron studies (hereditary haemochromatosis), serum copper/caeruloplasmin (Wilson’s disease), alpha-1-antitrypsin
USS & duplex: shrunken/enlarged? splenomegaly? reveral of portal system flow? focal lesions/portal vein thrombosis?
Endoscopy: ?varices
CT/MRI if indicated
Ascitic tap: MCS if infection suspected
Liver biopsy: confirm type/severity of disease

46
Q

Cirrhosis complications

A

Portal hypertension: often symptomatic/hepatosplenomegaly
Ruptured gastro-esophageal varices: 90% will develop over 10y, 1/3 will suffer a bleed
Ascites: severe pain raises suspicion of spontaneous bacterial peritonitis
Encephalopathy: nitrogenous waste build up in circulation –> cerebral oedema when astrocytes attempt to clear it

47
Q

Encephalopathy grading

A

Grade I: altered mood/behaviour, sleep disturbances
Grade II: increasing drowsiness/confusion
Grade III: stupor, incoherence, restlessness
Grade IV: coma

48
Q

Porto-systemic anastomoses

A

Cardia of stomach: gastric/oesophageal varices (left gastric vein)
Anus: rectal varices
Retroperitoneal organs: stomal varices
Paraumbilical veins of anterior abdominal wall: caput medusae

Portal system has no valves so blood can flow in reverse direction

49
Q

Define portal hypertension

A

Portal vein pressure >10mmHg

50
Q

Portal hypertension aetiology

A

Pre-hepatic: portal vein thrombosis (portal pyaemia/prothrombotic states)
Hepatic: cirrhosis, hepatitis, idiopathic non-cirrhotic portal hypertension, schistosomiasis, congenital hepatic fibrosis
Post-hepatic: Budd-Chiari syndrome (obstruction of hepatic veins)

51
Q

Portal hypertension manifestations

A 
Variceal bleeding
Haemorrhoids/caput medusae
Ascites
Splenomegaly
Portosystemic encephalopathy: toxins bypass liver
52
Q

Common causes of splenomegaly

A

Infection: infective endocarditis, bacterial sepsis, EBV, TB, malaria, schistosomiasis
Inflammation: rheumatoid arthritis, SLE, sarcoidosis
Portal hypertension:
Haematological disease: haemolytic anaemia, leukaemia, lymphoma, myeloproliferative disorders

53
Q

Splenomegaly complications

A

Hypersplenism –> pancytopenia, increased plasma volume, haemolysis

54
Q

Bile components and function

A

Bile = cholesterol + phospholipids + bile salts + water + conjugated bilirubin
Function: bile salts emulsify fats in the gut & enterohepatically recycled to be re-secreted into the bile
Presence of fatty acids/amino acids in the duodenum –> cholecystokinin release (CCK) –> contraction of gall bladder & release of bile

55
Q

Types of gallstones +

A

Cholesterol: caused by excess cholesterol secretion into the bile/loss of bile salt content
Risk factors: >age, obesity, high fat diet, rapid weight loss, female, multiparity, pregnancy, OCP, DM, ileal disease/resection, liver cirrhosis

Bile pigment: calcium bilirubinate, form independently to cholesterol stones
Black pigment = haemolytic conditions
Brown pigment = biliary stasis/infection, cause of recurrent gallstones following cholecystectomy

56
Q

Biliary colic/acute cholecystitis pathology

A

Gallstone impaction in gallbladder +/- inflammation

Can lead to mucocele (+ empyema if infected) in obstruction of an empty gallbladder which continues producing mucin

57
Q

Choledocholithiasis pathology

A

Stone impaction in common bile duct: biliary colic if temporary, obstructive jaundice if prolonged
Can predispose to ascending cholangitis/acute pancreatitis

58
Q

Mirizzi’s syndrome pathology

A

Stone impaction in cystic duct/Hartmann’s pouch (at neck of gallbladder) causing extrinsic compression of the common hepatic duct
Leads to obstructive jaundice - dilation of cystic/common bile duct

59
Q

Gallstone ileus pathology

A

Large gallstone erodes through gallbladder lumen creating a fistula into the adjacent duodenum
Can create obstruction if impacts on narrow segment of bowel (terminal ileum)
AXR: signs of small bowel obstruction, visible gallstone, aerobilia

60
Q

Biliary colic presentation

A

Severe constant epigastric/RUQ pain, crescendo characteristic (peak at 2h post-eating due to CCK peak)
Radiate to back, right shoulder, subscapular region
Associated nausea + vomiting
Worst mid-evening to early hours of morning
Systemically well

61
Q

Acute cholecystitis presentation

A

Obstruction of gallbladder –> distension –> highly concentrated retained bile causes 2ndary inflammatory response in gallbladder wall (chemical cholecystitis) + 30% get superadded infection
Same as biliary colic + inflammation component…
Severe localised RUQ pain + guarding & rigidity
Vomiting & systemic upset: fever & leucocytosis
Palpable gallbladder: Murphy’s sign +ve (continuous pressure over gallbladder + inhalation = catch breath at max inhalation point)
Rarely: gallbladder becomes gangrenous and perforates = generalised peritontis

62
Q

Chronic cholecystitis presentation

A

Repeated episodes of inflammation –> fibrosis & thickening of gallbladder wall
Recurrent bouts of abdo pain due to mild cholecystitis
Discomfort/flatulence after fatty meals

63
Q

Common bile duct obstruction presentation

A

Mainly due to choledocholithiasis
Obstructive jaundice & biliary colic
Attacks last hours-days
If obstruction not relieved, chronic back pressure can lead to 2ndary biliary cirrhosis and liver failure

64
Q

Ascending cholangitis presentation

A 
Infection of common bile duct, usually follows obstruction due to choledocholithiasis
Charcot's triad of symptoms...
Obstructive jaundice
High fever +/- rigors
RUQ pain
Liver may have multiple small abscesses
65
Q

Gallstones investigations

A

Bloods: WBC/inflammatory markers (cholecystitis), LFTs (cholecystitis/common bile duct obstruction), amylase (pancreatitis), prothrombin
Abdominal USS: stones in gallbladder (echogenic foci + acoustic shadow), thickened wall (inflammation), increased diameter of duct (obstruction)
MCRP: visualise biliary tree/detect calculi

66
Q

Acute pancreatitis symptoms & signs

A

Gradual/sudden onset severe epigastric pain
Classically radiated to the back & relieved by sitting forwards
Nausea/vomiting is prominent
Tachycardia/shock
Fever
Ileus
Jaundice (30%)
Rigid abdomen
Cullen’s sign: periumbilical discolouration due to peritoneal space haemorrhage
Grey-Turner’s sign: discolouration in the flanks
Bruising signs >48h = poor prognosis

67
Q

Aetiology of acute pancreatitis

A 
I GET SMASHED
Idiopathic (20%)
Gallstones/obstructive lesion (40%)
Ethanol (35%)
Trauma (15%)
Steroids
Mumps/CMV/EBV
Autoimmune: SLE, polyarteritis nodosa
Scorpion venom
Hyper/hypo: hyperlipidaemia, hypercalcaemia, hypothermia
ERCP
Drugs: thiazides, sulphonamides, ACEIs, NSAIDs
68
Q

Acute pancreatitis pathology

A

Leakage of activated pancreatic enzymes into the pancreatic & peripancreatic tissue = acute inflammatory reaction
Common: gallstone damaging ampulla of vater allowing gastric contents up the pancreatic duct activating pro-enzymes
Extensive local tissue necrosis (particularly fat)
Litres of extracellular fluid collect in the gut, peritoneum and retroperitoneum

69
Q

Patterns of lobule injury in acute pancreatitis

A

Periductal necrosis: necrosis of acinal cells adjacent to ducts, due to obstruction

Panlobular necrosis: necrosis of whole acinar lobule, due to drugs/toxins/viruses/metabolic insults, can spread from periductal necrosis

Perilobular necrosis: necrosis of the peripheries of lobules, due to poor vascular perfusion

70
Q

Complications of acute pancreatitis

A

Early: shock (hypovolaemic/septic), ARDS (microthrombi in pulmonary vessels), renal failure, disseminated intravascular coagulation, hypocalcaemia, hyperglycaemia

Late: pancreatic pseudocyst, abscesses, bleeding from elastase eroding a major vessel, thrombosis of splenic/gastroduodenal arteries causing bowel necrosis, fistulae

71
Q

Acute pancreatitis investigations

A

Bloods: baseline FBC, CRP, U&E, LFT, glucose, calcium to assess progression
ALT>3x normal suggests gallstone disease
Raised serum amylase + lipase?
ABG to monitor oxidation and acid-base status
AXR: ?sentinel loop/small bowel ileus/exclude causes
Erect CXR: assess perforations
CT: enlarged pancreas with stranding, abscess, collections, necrosis, pseudocyst
MRCP: visualisation of collections + ductal system
Endoscopic USS

72
Q

Modified Glasgow criteria for prediction of acute pancreatitis prognosis

A 
3 or more +ve factors within 48h onset = severe
PaO2 <8kPa
Age >55y
Neutrophils: WBC >15x10'9/L
Calcium <2mmol/L
Renal: Urea >16mmol/L
Enzymes: LDH >600iu/L, AST >200iu/L
Albumin <32g/L
Sugar: glucose >10mmol/L
73
Q

Metabolic complications of acute pancreatitis

A

Hyperglycaemia, hypocalcaemia, reduced serum albumin, malabsorption leading to reduced vitamin levels

74
Q

Pancreatic adenocarcinoma aetiology

A

> 60y

Associations: smoking, alcohol, DM, chronic pancreatitis, genetic

75
Q

Carcinoma of the head of the pancreas presentation

A

Painless jaundice (obstructive), pain may develop
O/E: obstructive jaundice signs, Courvoisier’s sign/palpable abdominal mass
Hepatosplenomegaly
Ascites
Acute pancreatitis/diabetes?

76
Q

Carcinoma of the body/tail of the pancreas presentation

A

Present late, dull abdominal pain radiating through back, partially relieved on sitting forward
Non-specific B symptoms
Often no physical signs
Acute pancreatits/diabetes?

77
Q

Trousseau’s syndrome

A

Related to pancreatic carcinoma

Thrombosis of superficial/deep leg veins (thrombophlebitis migrans)

78
Q

Pancreatic carcinoma investigations

A

Bloods: FBC, U&E, LFTs (?obstructive jaundice)
CA 19.9 or CEA = non-specific, useful as baseline
Amylase rarely elevated
USS: ?obstruction + duct dilation
CT: pancreatic mass +/- dilated biliary tree +/- hepatic metastases
Endoscopic USS (EUS) +/- biopsy: location, local spread, local lymph node involvement, biopsy
Staging laparoscopy

79
Q

Types of pancreatic malignancy

A 
Ductal adenocarcinoma (head): 60%
Ductal adenocarcinoma (body): 25%
Ductal adenocarcinoma (tail): 15%
Islet cell tumours: <2%
80
Q

Multiple Endocrine Neoplasia (MEN) syndromes

A

Insulinoma: symptomatic hypoglycaemic events (mornings/exertion), gross weight gain, 90% benign
Glucagonoma: often asymptomatic, 2ndary DM may develop
Gastrinoma: Zollinger-Ellison syndrome, oesophagitis, GI ulcers, diarrhoea
Somatostatinoma: DM (insulin release inhibited), achlorrhydria (gastrin release inhibited), gallstones (CCK release inhibited)
VIPoma: vasoactive intestinal peptide release causes profound diarrhoea

CP1 (12 decks)

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