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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
Normal/jaundice levels of bilirubin
Normal upper limit: 25micromol/L | Jaundice: 50micromol/L
26
Pre-hepatic jaundice pathology
2ndary to increased erythrocyte breakdown (e.g. haemolysis/reabsoroption of large haematoma) Bilirubin not yet been processed by the liver so mainly unconjugated
27
Cholestatic jaundice pathology
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
28
Hepatocellular jaundice pathology
Hepatocyte dysfunction, partial inability to conjugate bilirubin Mixed conjugated/unconjugated bilirubin in the blood Causes: hepatitis, cirrhosis, neoplasm, hepatotoxic drugs If severe: unconjugated hyperbilirubinaemia
29
Gilbert's syndrome pathology
Congenital lack of gluconyltransferase 7% of population Transient episodes of jaundice, especially following infection Serum unconjugated bilirubin raised but LFTs and reticulocytes normal
30
Jaundice investigations
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
31
What types of cancer commonly metastasise to the liver?
Lung, stomach, colon, breast, uterus
32
Hepatocellular carcinoma pathology
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
33
Hepatocellular carcinoma symptoms and signs
``` Non-specific fever, malaise, weight loss RUQ pain Hepatomegaly Signs of chronic liver disease/decompensation Abdominal mass/bruit over liver Jaundice = late sign ```
34
Hepatocellular carcinoma investigations
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
Cholangiocarcinoma pathology
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
Benign liver tumour pathology
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
Characteristics of liver cirrhosis
Destruction of liver cells Associated chronic inflammation, stimulating fibrosis Regeneration of hepatocytes to form nodules
38
Liver cirrhosis pathology
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
Liver cirrhosis types
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
Classic history of chronic liver disease
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
Chronic liver disease signs
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
Precipitants of chronic liver disease decompensation
Alcohol binge, variceal bleed, hepatotoxic drugs, portal/hepatic vein thrombosis
43
Variables in Child-Pugh score
``` Gives 1/2 year mortality score in chronic liver disease: Total bilirubin Serum albumin PT/INR Ascites Hepatic encephalopathy ```
44
Investigations to determine severity of cirrhosis
Liver function: albumin, INR Liver damage: LFTs Complications: U&Es, ABG (hepatorenal/hepatopulmonary syndrome)
45
Investigations to determine type of liver disease
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
Cirrhosis complications
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
Encephalopathy grading
Grade I: altered mood/behaviour, sleep disturbances Grade II: increasing drowsiness/confusion Grade III: stupor, incoherence, restlessness Grade IV: coma
48
Porto-systemic anastomoses
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
Define portal hypertension
Portal vein pressure >10mmHg
50
Portal hypertension aetiology
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
Portal hypertension manifestations
``` Variceal bleeding Haemorrhoids/caput medusae Ascites Splenomegaly Portosystemic encephalopathy: toxins bypass liver ```
52
Common causes of splenomegaly
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
Splenomegaly complications
Hypersplenism --> pancytopenia, increased plasma volume, haemolysis
54
Bile components and function
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
Types of gallstones +
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
Biliary colic/acute cholecystitis pathology
Gallstone impaction in gallbladder +/- inflammation | Can lead to mucocele (+ empyema if infected) in obstruction of an empty gallbladder which continues producing mucin
57
Choledocholithiasis pathology
Stone impaction in common bile duct: biliary colic if temporary, obstructive jaundice if prolonged Can predispose to ascending cholangitis/acute pancreatitis
58
Mirizzi's syndrome pathology
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
Gallstone ileus pathology
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
Biliary colic presentation
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
Acute cholecystitis presentation
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
Chronic cholecystitis presentation
Repeated episodes of inflammation --> fibrosis & thickening of gallbladder wall Recurrent bouts of abdo pain due to mild cholecystitis Discomfort/flatulence after fatty meals
63
Common bile duct obstruction presentation
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
Ascending cholangitis presentation
``` 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
Gallstones investigations
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
Acute pancreatitis symptoms & signs
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
Aetiology of acute pancreatitis
``` 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
Acute pancreatitis pathology
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
Patterns of lobule injury in acute pancreatitis
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
Complications of acute pancreatitis
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
Acute pancreatitis investigations
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
Modified Glasgow criteria for prediction of acute pancreatitis prognosis
``` 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
Metabolic complications of acute pancreatitis
Hyperglycaemia, hypocalcaemia, reduced serum albumin, malabsorption leading to reduced vitamin levels
74
Pancreatic adenocarcinoma aetiology
>60y | Associations: smoking, alcohol, DM, chronic pancreatitis, genetic
75
Carcinoma of the head of the pancreas presentation
Painless jaundice (obstructive), pain may develop O/E: obstructive jaundice signs, Courvoisier's sign/palpable abdominal mass Hepatosplenomegaly Ascites Acute pancreatitis/diabetes?
76
Carcinoma of the body/tail of the pancreas presentation
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
Trousseau's syndrome
Related to pancreatic carcinoma | Thrombosis of superficial/deep leg veins (thrombophlebitis migrans)
78
Pancreatic carcinoma investigations
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
Types of pancreatic malignancy
``` Ductal adenocarcinoma (head): 60% Ductal adenocarcinoma (body): 25% Ductal adenocarcinoma (tail): 15% Islet cell tumours: <2% ```
80
Multiple Endocrine Neoplasia (MEN) syndromes
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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