HPB Medicine Flashcards
ACTUTE AND CHRONIC HEPATITIS: Describe the morphology and pathological consequences of acute and chronic hepatitis
Morphology:
Acute hepatitis - ‘lobular disarray’
Chronic hepatitis - Fibrosis, characterised by portal inflammation and necroinflammatory activity and fibrosis
Pathological consequences:
- Progression to cirrhosis
- Decompensated liver failure: Hepatitic encephalopathy, ascites, coagulopathy/bleeding (varices), hepatorenal syndrome (hyponatraemia, elevated creatinine)
ACUTE AND CHRONIC HEPATITIS: Describe the features of drug induced liver injury (including paracetamol overdose)
Paracetamol overdose:
- Elevated liver enzymes (hepatocellular injury due to build up of toxic metabolites)
- Deranged clotting screen (if hepatic synthetic function is disrupted) - INR
- Typically, asymptmatic until 24 hrs after ingestion or develop anorexia/nausea/vomiting
- Symptoms/signs start to develop after 24hrs: RUQ pain, metabolic acidosis, hypotension, hypoglycaemia, pancreatitis and arrhythmias
- Liver damage is not detectable on blood tests until 18 hours after ingestion
- Renal failure, due to ATN, may occur
Features of drug induced liver injury:
- Hepatocellular predominant liver injury
- Elevated AST and ALT
- ALT is more specific for hepatocellular injury
ACUTE AND CHRONIC HEPATITIS: Describe the causes of acute and chronic hepatitis
Acute hepatitis
- DILI (drug induced liver injury)
- Infection e.g. viral
- Acute alcoholic hepatitis
- Autoimmune hepatitis
- Ischaemic hepatitis
Chronic hepatitis
- Infection - viral
- Autoimmune
- Alcoholism
- NAFLD
- Drug induced
- Metabolic conditions e.g. Wilson’s disease, haematochromatosis
- Ischaemic hepatitis (secondary to heart failure)
ACUTE AND CHRONIC HEPATITIS: Discuss the diagnosis and investigation of a patient with jaundice
Diagnostic work up:
- FBC:
- Low plts1
- ?anaemia if bleeding suspected
- LFTs:
- Elevated ALP and gGT suggest obstructive jaundice
- PT and INR (plus albumin)
- Checks synthetic function of the liver
- U&Es
- ?hepatorenal syndrome
- Bilirubin levels:
- Conjugated vs unconjugated
- Unconjugated for pre-hepatic and mixed for hepatic
- Virology: May allow cause to be identified
- Abdominal USS
- Look for bile duct dilatation
- Look for possible cause of obstruction
- ?Pancreatic cancer
- CT CAP - if suspected malignancy
Investigation looks to identify whether jaundice is pre-hepatic, hepatic or post-hepatitic in nature
1: Low plts are seen due to reduced production of TPO and destruction of plts by the spleen (portal hypertension → redistribution of blood and platelets to the spleen)
ACUTE AND CHRONIC HEPATITIS: Outline the clinical presentation of acute and chronic hepatitis including relevant features in the medical history
Features in the medical hx:
- Onset: Acute vs chronic as an indication of the cause
- Associated symptoms
- Jaundice, bleeding, ascites, hepatitic encephalopathy
- Pain - Usually present with mechanical obstruction of the cystic duct or CBD e.g. ?cholelithiasis/cholecystitis. Pain is often absent in pancreatic and biliary malignancies
- Fever - ?cholecystitis
- Fatigue, anorexia, pruritis, weight loss, nausea/vomiting, RUQ pain
- Risk factors for different aetiologies:
- Viral hepatitis: IVDU, tattoos, Sexual Hx - unprotected sex, anoreceptive sexual intercours; Alcohol intake
- Features of other infections: Sore throat and lymphadenopathy in EBV and CMV
- Diet (if ?gallstones)
- Medical conditions that may cause liver damage
- Personal or FHx of autoimmune disease
- Previous episodes of hepatic symptoms
ACUTE AND CHRONIC HEPATITIS: Outline the treatment options for hepatitis due to autoimmunity, hepatitis B or C and paracetamol overdose
Autoimmunity
- Corticosteroids +/- immunosuppressant therapy (dependent upon severity)
- Findings: Raised AST and ALT, elevated serum gamma-globulin (IgG) level
Hepatitis C
- Antiviral therapy
Hepatitis B
- Interferon-alpha
- Antivirals may be considered second line
Paracetamol overdose
- Check for complications - renal failure1, hypoglycaemia, metabolic acidosis
- If < 8 hours since ingestion - activated charcoal
- NAC
- Nausea/vomiting is common following adminsitration. Antiemetic should be considered
- Fluids
1: Renal failure may manifest as loin pain, haematuria or proteinuria. Serum creatinine may also be elevated. ?cause - may be ‘acute’ hepatorenal syndrome
ACUTE AND CHRONIC HEPATITIS: Outline the indications for and dicuss contraindications of liver biopsy in hepatitis
Indications:
- Clinical picture suggestive of hepatitis/fibrosis/cirrhosis without an immediate cause identified
- Viral
- Autoimmune
- AFLD or NAFLD
- Suspected malignancy
- Diagnostic and evaluation of severity
Contraindications for percutaneous liver biopsy:
- Coagulopathy
- INR < 1.5
- Low platelet count
- If so, transjugular biopsy may instead be performed (with FFP)
- Complications include bleeding, bowel perforation and pneumothorax
ACUTE AND CHRONIC HEPATITIS: Be aware of other investigations
- Fibroscan
- Ultrasound
- Blood tests: Clotting, albumin, U&Es (sodium, creatinine), LFTs, platelet count (splenic sequesting)
LIVER NEOPLASMS, ABSCESS AND CYSTS: Compare and contrast the pathology and natural histories of liver neoplasia, abscesses and cysts
LIVER NEOPLASMS, ABSCESS AND CYSTS: Describe the symptoms and signs associated with liver abscess
- RFs for liver abscess present e.g. possible route of infection
- Biliary tract disease, hepatic/biliary intervention, sepsis, DM, malignancy
- RUQ pain
- Fever/chills (swinging fever)
- Hepatomegaly
- Nausea and vomiting
- Non-specific symptoms: Weight loss, fatigue, abdo pain
LIVER NEOPLASMS, ABSCESS AND CYSTS: List the investigations that differentiate neoplasia, abscesses and cysts - outlining their treatment options
LIVER NEOPLASMS, ABSCESS AND CYSTS: Outline the aetiology and pathology of primary and secondary liver neoplasms
Primary Liver Neoplasms
Aetiology:
- Secondary to chronic liver disease/cirrhosis e.g. hepatitis, NAFLD, AFLD, autoimmune, metabolic
- Often remains asymptomatic for long periods, presenting with non-specific symptoms of fatigue, weight loss, anorexia, nasuea and abdo pain. Jaundice and pruritis often develop later on.
Pathology:
- Hepatocellular carcinoma (90%) (AFP)
- Cholangiocarcinoma (10%) - associated with PSC (CA19-9)
- Benign neoplasms include haemangiomas and focal nodular hyperplasia (often related to oestrogen, hence more common in women and those on the COCP)
Secondary Liver Neoplasms
Aetiology:
- 90% of liver neoplasms are metastases
- Commonly from the lung, stomach, colon, breast and uterus
Pathology:
CHRONIC LIVER DISEASE: Define cirrhosis in pathological terms
Cirrhosis: An irreversible pathological result of chronic liver inflammation, which leads to fibrosis and the formation of nodules. There is destruction of hepatocytes.
CHRONIC LIVER DISEASE: Describe the morphology and pathological consequences of cirrhosis
Morphology
- Distortion of the hepatic architecture and dense bands of fibrosis, leading to nodules of hepatocytes
Pathological consequences
- Decompensated Liver failure
- Hepatic encephalopathy, ascites (→SBP), bleeding (sythetic function disruption and varices), hepatorenal syndrome and hepatocellular carcinoma
- Jaundice
- Loss of hepatic synthetic function → bleeding, hypoalbuminaemia
- Hyponatraemia
- Elevated urea and creatinine (due to hepatorenal syndrome)
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CHRONIC LIVER DISEASE: Describe the investigation of a patient with suspected cirrhosis
Bloods
- Clotting: PT/INR, PTT
- Platelet count: Thrombocytopenia is highly sensitive and specific1
- Albumin levels
- LFTs: Reranged LFTs
- U&Es: Hyponatraemia, elevated urea and creatinine may be seen due to hepatorenal syndrome
- AFP: Elevated in malignancy
Imaging
USS: Nodularity, ‘corkscrew’ appearance to the arteries, enlarged portal vein with reduced flow, ascites, splenomegaly
Fibroscan reveals reduced elastisticy
Endoscopy: Diagnostic and therapeutic potential for varices
CT and MRI: Check for neoplasms
Liver biopsy: Confirms diagnosis. Architectural disruption with formation of regenerative nodules.
Investigations to establish possible cause
- Autoantibodies: PBS
- Viral serology
- Serum ceruloplasmin (reduced in Wilson’s disease - excess Cu2+)
- Haemochromatosis: Elevated total iron, transferrin saturation and ferritin with reduced TIBC
1: Thrombocytopenia is resultant of platelet sequestration by the liver
CHRONIC LIVER DISEASE: Discuss how to establish the diagnosis of the cause of cirrhosis
Assessing Severity
- Child-Pugh Score for Cirrhosis
- Uses bilirubin, albumin, INR, ascites ans encephalopathy to assess the severity and prognosis of cirrhosis
- MELD score
- Used every 6/12 to assess patients with cirrhosis
Possible causes and associated investigations
- NAFLD
- Biopsy
- Enhanced Liver Fibrosis (ELF) blood test
- AFLD
- Autoimmune causes
- ANA and anti-smooth muscle Igs raised in autoimmune hepatitis
- PBS - Elevated AMA (anti-mitochondrial antibody)
- Metabolic disease
- Wilson’s disease - Serum ceruloplasmin
- Alpha-1 antitypsin deficiency
- Haemachromatosis - Total iron, TIBC, transferrin saturation and ferritin
- Hepatitis
- HCV IgG = chronic HCV infection
- HBV surface antigen = infection
CHRONIC LIVER DISEASE: Outline the pathophysiology underlying the clinical features of cirrhosis
Hepatic encephalopathy: Due to retention of urea, crosses the BBB
Ascites: Due to hypoalbuminaemia and fluid retention
Asterixis: Due to retention of urea
Hepatorenal syndrome: Reduced renal blood flow leads to RAAS activation, eventually renal perfusion is permanently reduced and AKI results
Thrombocytopenia: Splenic sequestration
Splenomegaly: Due to venous congestion
Bleeding (varices): Reduced synthetic function of the liver and portal hypertension
Jaundice – caused by raised bilirubin
Hepatomegaly – however the liver can shrink as it becomes more cirrhotic
Splenomegaly – due to portal hypertension
Spider Naevi – these are telangiectasia with a central arteriole and small vessels radiating away
Palmar Erythema – caused by hyperdynamic cirulation
Gynaecomastia and testicular atrophy in males due to endocrine dysfunction
Bruising – due to abnormal clotting
Ascites
Caput Medusae – distended paraumbilical veins due to portal hypertension
Asterixis – “flapping tremor” in decompensated liver disease
CHRONIC LIVER DISEASE: Describe the clinical features of complications of cirrhosis and portal hypertension. Outline their management
Clinical features and management
Malnutrition: Regular meals, low sodium with high protein and calorie content
Hepatic encephalopathy:
- Pathophysiology: Ammonia is produced by the breakdown of proteins by intestinal bacteria, it is then absorbed by the gut
- Laxatives - promote ammonia excretion
- Abx - reduced the number of ammonia producing intestinal bacteria
- Nutritional support - low protein diet. May require NG feeding
Portal hypertension
- Beta-blocker - propranolol to reduce portal hypertension
- Varices: Endoscopy +/- banding if required. Haemodynamic stabilisation, terlipressin and abx in acute bleeding
- TIPS (transjugular intra-hepatic portosystemic shunt): Used if medical and endoscopic treatment fails
Hepatorenal syndrome:
- Liver transplant
Ascites:
- Anti-aldosterone diuretics (spironolactone): To reduce Renin driven fluid reabsorption and sodium retention
- Paracentesis (ascitic tap or drain)
- Low sodium diet
- Prophylactic abx to prevent SBP
- TIPs or transplantation for refractory peritonitis
PORTAL HYPERTENSION: Describe portal venous anatomy
Portal venous system: Venous drainage for the alimentary system, carrying nutrient rich blood to the liver.
The portal vein is formed by the union of the splenic vein and the SMV.
Upon entering the liver the portal vein divides into right and left branches.
PORTAL HYPERTENSION: Define portal hypertension and classify its causes
Portal hypertension: Increased back-pressure within the portal system.
Causes:
Pre-hepatic: Portal vein thrombosis or obstruction
Hepatic: Cirrhosis; acute hepatitis; schistomiasis; congenital hepatic fibrosis
Post-hepatic: Compression (e.g. malignancy); Budd-Chiari syndrome- constrictive pericarditis; R sided heart failure
PORTAL HYPERTENSION: Describe the clinical manifestations of portal hypertension
Varices, +/- bleeding
- Oesophageal, periumbilical, rectal
Clinical signs
- Caput medusa
- Splenomegaly
- Haemorrhoids
- Ascites
- Hepatic encephalopathy (toxins bypass the liver via shunt due to increased pressure)
PORTAL HYPERTENSION: Outline the treatment methods available for bleeding oesophageal varices
General management of varices
- Beta-blockers
- Banding
Bleeding varices
- A-E approach, fluid resuscitation
- Pharmacological: Beta-blockers, terlipressin and abx
- Banding
- Balloon tamponade (can be used as a bridge to more definitive treatments)
- TIPS (transjugular intrahepatic portosystemic shunt)
THE SPLEEN: List the common causes of splenomegaly
- Cirrhosis / Portal hypertension
- Lympho-reticular disease: Leukaemia, lymphoma, Hodgkin’s. haemolytic anaemia
- Chronic infection
- Acute infection: IE, EBV
- Inflammation: Including autoimmune diseases: SLE, RA, sarcoidosis
THE SPLEEN: Outline the haematological abnormalities correctable by splenectomy
- Splenic trauma
- Hypersplenism (Describes over active function of the spleen, may be seen in the absence of splenomegaly. Leads to rapid and premature destruction of RBCs)
- Autoimmune haemolysis: Haemolytic anaemia
THE SPLEEN: Discuss the potential causes of splenic rupture
- Trauma
- Pre-existing illness: EBV, haemolytic anaemia, lymphoma, Malaria
THE SPLEEN: Disucss the potential adverse consequences associated with splenectomy and recommendations for preventing overwhelming post-splenectomy sepsis
Adverse consequences
- Immune suppression
Preventing post-spenectomy sepsis
- Life-long abx therapy with penicillin V
- Annual vaccination to protect against meningitis, flu and pneumonia
OBSTRUCTIVE JAUNDICE: Classify intrahepatic and extrahepatic causes of obstructive jaundice and outline underlying pathology
Intrahepatic Causes
- Hepatocellular causes: Viral hepatitis, acute alcoholic hepatitis, parenteral nutrition, intrahepatic atresia
- Medications: COCP, abx, antithyroid
- Pregnancy
- Luminal obstruction: Sickle cell disease, CF, bacterial infection
Extrahepatic Causes
- Biliary tree abnormalities: Cholelithiasis, cholecystitis
- PSC
- Mirizzi syndrome1
- Malignancy: Pancreatic, cholangiocarcinoma, ampullary adenoma
1: Describes compression, and subsequent obstruction, the CBD by extrinsic compression from an impacted stone in the cystic duct
OBSTRUCTIVE JAUNDICE: Describe the clinical features of obstructive jaundice and outline their pathophysiology
Pale stools and dark urine: The largely conjugated bilirubin is water soluble, giving a dark colour to the urine. As the metabolite is unable to enter the GI tract there is loss of ‘colour’ from faeces
Yellow discolouration of the skin and sclera: Bilirubin accumulates in elastin rich tissues preferentially
Pruritis: Resultant of elevated levels of circulating bilirubin
- Treatment includes cholestyramine
OBSTRUCTIVE JAUNDICE: Describe the laboratory and radiological investigation of a patient presenting with obstructive jaundice
Laboratory investigation
- FBC: Hb ?haemolytic anaemia
- LFTs: ALT, AST, ALP, gGT
- Cholestatic sees predominantly ALP and gammaGT elevation
- PT/INR - checking synthetic function of the liver (reduced → hepatic dysfunction)
- Bilirubin - conjugated and unconjugated
- CRP: ?cholecystitis
- Autoantibodies, viral serology for ?hepatitis
- Coombs test and blood films1: ?haemolytic anaemia
Radiological investigation
- USS: Look for duct dilatation
- MRCP: High resolution imaging of the biliary tree
- CT/MRI
Needle biopsy may also be performed
1: Elevated reticulocytes seen in haemolytic anaemia
OBSTRUCTIVE JAUNDICE: Describe the aetiology, morphology and pathological consequences of cholelithiasis
Aetiology:
- Gallstones form in the gall bladder and then migrate into the common bile duct
Morphology:
Pathological consequences:
- Biliary colic (intermittent RUQ pain, worse following meals)
- Cholecystitis (RUQ pain, fever)
- Cholangitis
- Pancreatitis
- Gallstone ileus
- Obstructive jaundice (pale stools, dark urine)
OBSTRUCTIVE JAUNDICE: Discuss the methods of relieving common bile duct obstruction
- ERCP
- Percutaneous transhepatic cholangiography (PTC)
- Cholecystectomy
ACUTE AND CHRONIC GALLBLADDER DISEASE AND CARCINOMA OF THE BILIARY TRACT: List the common types of gallstone and describe their pathophysiology
Types of gallstone
- Cholesterol: Cholesterol supersaturation and impaired gallbladder contractility contribute to the formation of gallstones. Hence, RFs for gallstones include those related to elevaed cholesterol levels
- Pigment: Conditions in which unconjugated bilirubin levels are raised can lead to the formation of pigmented gallstones. They form de novo in bile ducts as a result of stasis and infection.
ACUTE AND CHRONIC GALLBLADDER DISEASE AND CARCINOMA OF THE BILIARY TRACT: Describe the symptoms and signs of biliary colic and contrast with acute cholecystitis
Symptoms and signs of biliary colic:
- RUQ pain, worse after eating
- Nausea/vomiting
- Anorexia
- Obstructive jaundice
- Murphy’s sign negative
Symptoms and signs of acute cholecystitis:
- Fever
- Constant RUQ pain
- RUQ tenderness on palpation
- Nausea/vomiting
- Obstructive jaundice
- Murphy’s sign positive1
1: Murphy’s sign - apply pressure to the RUQ. Ask the pt to inspire. If there is a halt in inspiration, due to pain, gallbladder inflammation is likely.
ACUTE AND CHRONIC GALLBLADDER DISEASE AND CARCINOMA OF THE BILIARY TRACT: List the common tests used in the diagnosis of gallstones
- USS of the biliary tree
- MRCP
- FBC: Normal, with elevated WCC suggesting inflammation
- LFTs: AST, ALT, ALP, gammaGT
- Bilirubin levels
- Serum lipase and amylase (to rule out pancreatitis)
ACUTE AND CHRONIC GALLBLADDER DISEASE AND CARCINOMA OF THE BILIARY TRACT: Describe the symptoms and signs and management of bile duct stones
Symptoms and signs:
- Colicky RUQ pain, worse following meals
- Nausea/vomiting
- Obstructive jaundice
- Dyspepsia, bloating and flatulence are also commonly experienced symptoms
Management:
- ERCP
- Cholecystectomy
ACUTE AND CHRONIC GALLBLADDER DISEASE AND CARCINOMA OF THE BILIARY TRACT: Define the following: Murphy’s sign, Courvoisier’s sign, T-tube and gallstone ileus
Murphy’s sign: Apply pressure in the RUQ, ask the pt to breathe in. If inspiration is hindered by pain then inflammation is likely e.g. cholecystitis.
Courvoisier’s sign: Painless jaundice, in the presence of a palpable gallbladder is unlikely to be due to gallstones. It is likely to be due to an obstructing pancreatic or biliary neoplasm.
T tube: A drainage tube placed in the common bile duct following CBD exploration, cholecystectomy or liver transplant.
Gallstone ileus: Fistula between the biliary tree and dueodenum allows passage of a gallstone into the duodenum, causing small bowel functional obstruction
ACUTE AND CHRONIC GALLBLADDER DISEASE AND CARCINOMA OF THE BILIARY TRACT: List the complications of gallstones and describe the history, physical examination and laboratory findings for each
ACUTE AND CHRONIC GALLBLADDER DISEASE AND CARCINOMA OF THE BILIARY TRACT: Outline the medical management of a patient with biliary colic and acute cholecystitis, including appropriate antibiotic regimen
Medical management of biliary colic
- Analgesia
- Laparoscopic cholecystectomy is the definitive treatment
Medical management of cholecystitis
- Analgesia
- IVI
- Antibiotic therapy: Broad spectrum abx e.g. co-amoxiclav
- Laparoscopic cholecystectomy may be indicated to prevent reoccurence
ACUTE AND CHRONIC GALLBLADDER DISEASE AND CARCINOMA OF THE BILIARY TRACT: Outline carcinoma of the gallbladder, bile duct and ampulla of Vater with regard to presenting symptoms and survival
DIAGNOSTIC STUDIES IN BILIARY TRACT DISEASE: Contrast changes in liver function tests in obstructive and hepatocellular jaundice
Obstructive jaundice:
Elevated conjugated bilirubin, ALP and gammaGT
Hepatocellular jaundice:
Elevated unconjugated bilirubin, AST and ALT
DIAGNOSTIC STUDIES IN BILIARY TRACT DISEASE: List the most common bacteria cultured in acute cholecystitis
- E. Coli
- Enterococci
DIAGNOSTIC STUDIES IN BILIARY TRACT DISEASE: Outline the place of radiological and endoscopic investigation in the diagnosis of obstructive jaundice and in staging of pancreatic cancer
Diagnosis of obstructive jaundice
- Bloods: FBC, CRP, U&Es, LFTs, bilirubin
- US of the biliary tree - look for dilatation, evidence of stones
- MRCP - look for stones
- ERCP may be used to further investigate and to remove stones
- CT CAP to look for evidence of malignancy
Staging of pancreatic cancer
DIAGNOSTIC STUDIES IN BILIARY TRACT DISEASE: Describe the indications for, and risks of, ultrasound scanning, transhepatic cholangiography and endoscopic retrograde cholangiography
ACUTE PANCREATITIS: Describe the clinical presentation of acute pancreatitis
- Epigastric/RUQ pain
- Radiates to back, may be relieved by sitting forward
- Nausea/vomiting
- Fever
- Hyperglycaemia
- Hypocalcaemia
- Elevated CRP
- Jaundice
- Cullen’s sign (periumbilical) or Grey-Turners sign (flanks)
ACUTE PANCREATITIS: Describe the aetiology and pathology of pancreatitis
Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion venom
Hyperlipidaemia, hypothermia, hypercalcaemia
ERCP, emboli, embryo (pregnancy)
Drugs
Pathology: Necrosis of the pancreas leads to release of pancreatic enzymes. Local tissue destruction
ACUTE PANCREATITIS: Classify pancreatitis on the basis of the severity of organ injury
The severity of pancreatitis can be assessed through use of the Modified-Glasglow criteria: Where 3 or more positive factors are detected within 48 hours of pain onset then severe pancreatitis is suggested, urgent transfer to ITU/HDU should be considered.
PaO2 < 8kPa
Age > 55 years
Neutrophils WBC > 15 x109L
Calcium < 2 mmol/L
Renal function - Urea < 16 mmol/L
Enzymes (LDH > 600u/L, AST >200iu/L)
Albumin < 32g/L
Sugar - Blood glucose > 10mmol/L
ACUTE PANCREATITIS: Discuss the management of acute pancreatitis and potential early complications of acute pancreatitis
Management
- Analgesia: Pethidine or morphine
- IVI
- Anti-emetic
- Regular observations
- Insert urinary catheter to monitor fluid output
- Treat the cause if applicable: ERCP for gallstones
- Check for complications
- AKI
- Hypocalcaemia
- Hyperglycaemia
- DIC
- Sepsis
- Shock
ACUTE PANCREATITIS: Outline the investigation of suspected acute pancreatitis, emphasising the timing, interpretation and reliabilty of currently available tests
- Lipase/amylase
- Lipase is more sensitive and specific. It also rises earlier and stays elevated for longer
- Amylase may be normal, even in severe pancreatitis. It is excreted renally so may be elevated in renal failure
- Serum calcium
- Bloods
- FBC: WCC
- LFTs: AST
- U&Es: Serum urea, check for signs of AKI
- LDH
- Albumin
- ABG: Check PaO2
- Blood glucose levels
- AXR
- CT abdo: Standard choice of imaging to assess severity and for complications
ACUTE PANCREATITIS: Discuss the criteria used to predict the prognosis for acute pancreatitis
Modified Glasgow Criteria
ACUTE PANCREATITIS: Discuss the metabolic complications of pancreatitis
- Hypocalcaemia
- Hyperglycaemia - loss of pancreatic endocrine function
- Uraemia - if renal injury occurs
PANCREATIC PSEUDOCYSTS: Define pseudocyst and discuss mechanisms of their formation
Pseudocyst: Fibrosis allows for the formation of cyst, which is filled with enzyme rich fluid, blood and necrotic pancreatic tissue.
Mechanism of formation:
- Complication of acute/chronic pancreatitis
- Gallbladder disease
- Medication toxicity
- Traumatic injury
- Surgical complications
PANCREATIC PSEUDOCYSTS: List and discuss the signs and symptoms and natural history of an untreated pseudocyst
Signs and symptoms
- RUQ/epigastric pain
- Fever
- Diarrhoea
- Nausea/vomiting
- Weight loss
- Jaundice
- May be asymptomatic
Untreated pseudocyst
- Peritonitis - secondary to rupture
- Haemorrhage - if the pseudocyst injures nearby blood vessels
- Obstruction - bile duct, intestines
PANCREATIC PSEUDOCYSTS: Discuss the indications for and sequence of investigations for suspected pseudocyst
Small, not growing or causing symptoms can be monitored.
Larger cysts are more likely to be symptomatic.
Investigations
Cyst fluid analysis:
- Tumour markers: CEA
- Fluid viscosity: Low in pseudocysts and elevated in tumours
- Amylase: High in pseudocysts
Imaging:
- USS
- CT
- MRCP
PANCREATIC PSEUDOCYSTS: Describe the treatment of pancreatic pseudocyst
- Endoscopic drainage of the pseudocyst
- External drainage (if infected)
- Surgical drainage - if growth continues
PANCREATIC NEOPLASMS: Describe the symptoms and signs of pancreatic cancer, dependent upon the location of the tumour within the gland
Head: Obstructive jaundice, weight loss, malaise, symptoms related to endocrine dysfunction (thirst, polyuria, nocturia and weight loss), symptoms related to exocrine dysfunction (steatorrhoea)
