Upper GI Conditions 2 Flashcards
What 2 ducts form the Common Bile duct?
Common Hepatic duct + Cystic duct
What 2 ducts form the Ampulla of Vater?
Common Bile duct + Pancreatic duct
What is CCK released in response to?
Fats, Peptides, AAs in the Duodenum
What does CCK do?
- GB: stimulates GB contraction, relaxation of the Sphincter of Oddi (release of stored bile into the intestine)
- Pancreas: release of digestive enzymes
- Stomach: delayed gastric emptying
What is the most common type of Gallstone?
Cholesterol stones = 80%
>50% cholesterol, less pigment
What are the risk factors for Cholesterol Gallstones?
- Females
- Age
- Obesity
- Parity
- OCP
- Smoking
(4 Fs: Female, 40, Fertile and Fat)
What is the main risk factor for Pigment Gallstones?
Haemolytic anaemia
What are the main clinical features of Gallstones?
- Majority asymptomatic (incidental finding)
- > 90%
- Biliary Colic
- > RUQ pain, radiates to back/shoulder, episodes last between 2-6 hours, they resolve spontaneously and occur after eating fatty food, occurs early at night
- +/- Jaundice
What are the complications of Gallstones?
In the GB and Cystic duct:
- Biliary colic
- Acute + Chronic Cholecystitis
- Empyema
- Perforation
- Carcinoma
- Mirizzi’s syndrome (stone in GB obstructing the CBD and causing jaundice)
In the Bile ducts:
- Obstructive jaundice
- Cholangitis
- Pancreatitis
In the gut:
- Biliary Enteric Fistula (gallstone -> small intestine)
- Gallstone Ileus (biliary enteric fistula -> GB ruptures -> stone obstructing small intestine)
What are the investigations for pts with suspected gallstone disease?
- Blood tests: LFTs (AST, ALT, ALP)
- Abdominal USS
- (MRCP if diagnosis still uncertain)
What is the management of asymptomatic gallstones?
No treatment required!
unless they develop symptoms
What is the treatment of symptomatic gallstones?
- Laparoscopic cholecystectomy (!!!)
- (Open surgery if GB perforation)
- (if declines non-surgical option: dissolution or lithotripsy)
What are the risk factors for Cholangiocarcinoma?
- PSC (strong association)
- Congenital cystic disease (ie. choledochal cysts)
- Biliary-enteric drainage
- Hepatolithiasis
- Thorotrast (contrast)
- Carcinogens: aflatoxins, N-nitroso toxins, etc
What are the clinical features of Cholangiocarcinoma?
- Fever
- Abdominal pain (± ascites)
- Malaise
- Painless Obstructive Jaundice: Increased Bilirubin, Increased ALP, itching
What are the investigations for Cholangiocarcinoma?
- LFTs
- ECRP + Biopsy
What is the management of Cholangiocarcinoma?
- Surgery: Majority unresectable at presentation (70%), and of those that do, majority recur
- Palliate the Jaundice: Stent (percutaneous vs. ERCP)
What genetic disorder increases risk for Ampullary cancer?
FAP !
Familial Adenomatous Polyposis
What us the treatment of choice for Ampullary cancer?
Pancreatico-duodenectomy
similar to pancreatic cancer!
What are the causes of Acute Pancreatitis?
- I GET SMASHED *
- Idiopathic (!!)
- Gallstones (most common) (!!)
- Ethanol (!!)
- Trauma
- Steroids
- Mumps
- Autoimmune (PAN)
- Scorpion venom
- Hyperlipidaemia, Hypothermia, Hypercalcaemia
- ERCP and Emboli
- Drugs
What are the symptoms of Acute Pancreatitis?
- Sudden onset severe Epigastric pain
- > radiates to back, relieved by sitting forwards
- Nausea + Vomiting
What are the signs of Acute Pancreatitis?
- In severe disease*
- Tachycardia, Fever, Shock (hypotension, oliguric)
- Widespread tenderness with guarding (rigid abdomen)
- Periumbilical bruising (Cullen’s sign), or Flanks (Grey Turner’s sign)
- > in severe necrotising pancreatitis due to blood vessel autodigestion + haemorrhage
- Jaundice, Cholangitis
- > if caused by gallstones
What investigations would you do for Acute Pancreatitis?
- Bloods: Serum amylase (!!!), serum lipase (more sensitive and specific for pancreatitis), LFTs, inflammatory markers
- Radiology: Abdominal US (?gallstones!!), contrast-enhanced CT and/or MRI (assesses severity + complications)
Which criteria is used to assess for the severity of Acute Pancreatitis?
Modified Glasgow Criteria!
MNEMONIC: PANCREAS
What is the management of Acute Pancreatitis?
- Conservative and Prophylaxis !!*
- Nasogastric suction
- > prevents risk of aspiration pneumonia
- Baseline ABGs
- Prophylactic abx
- Analgesia
- NG tube -> feeding
- Anticoagulation -> LMWH prophylaxis for DVT
What are the complications of Acute Pancreatitis?
Early:
- Shock
- ARDS
- Hypocalcaemia
- Hyperglycaemia
Late (>1 week):
- Pancreatic Necrosis + Pseudocyst
- Pancreatic Abscess
- Thrombosis
When should you suspect Pancreatic Necrosis development in Acute Pancreatitis?
- Should be suspected in a pt. who has persistent systemic inflammation for 7-10 days after the onset of Pancreatitis
- Confirmed by CT imaging
When should you suspect Pancreatic Pseudocyst development in Acute Pancreatitis?
- CT imaging: collection of fluid in the lesser sac
- Fever
- Mass
- Persistent raised Amylase or LFTs
What is the management of a Pancreatic Pseudocyst?
- may be found incidentally on CT imaging
- May resolve spontaneously
- OR may need drainage (if >6 weeks)
What is the management of Pancreatic Necrosis?
- confirmed by CT imaging
- if infected (clinical deterioration with raised infection markers): EUS + FNA of necrosis
- Pancreatic Necrosectomy
What is the definition of Chronic Pancreatitis?
- Continuous inflammatory disease of the Pancreas
- Characterised by irreversible cellular destruction of the Pancreas
- Typically causes pain and/or permanent loss of function
What are the aetiology of Chronic Pancreatitis?
- Chronic Alcohol abuse (80%)
Rarely:
- Cystic Fibrosis
- Congenital abnormalities: Annular Pancreas, Pancreas Divisum
- Hereditary Pancreatitis
- Hypercalcaemia (increased PTH)
What are the clinical features of Chronic Pancreatitis?
- Epigastric pain:
- > ‘bores’ through to back
- > relieved by sitting forward or hot water bottles on epigastrium/back
- Exocrine insufficiency:
- > weight loss
- > nutritional deficiencies
- > steatorrhoea
- > bloating
- Endocrine insufficiency
- > diabetes
What Investigations would you do for Chronic Pancreatitis?
- Imaging: Contrast-enhanced CT (!!!) (pancreatic calcifications confirm the diagnosis) -> MRCP -> EUS
- Bloods: do NOT check serum Amylase!!, LFTs, HbA1c
- Faecal Elastase
What is the treatment of Chronic Pancreatitis?
- Drugs: analgesia, lipase (Creon), fat-soluble vitamins
- Diet: cessation of alcohol/smoking, low-fat diet, well-balanced diet
- Endoscopic Therapy: ERCP (for stones/strictures of pancreatic duct)
- Surgery: Pancreatectomy (if all else fails)
What are the clinical features of Pancreatic cancer?
- Epigastric Pain -> radiates to back, relieved by sitting forwards
- Painless Obstructive Jaundice (head of pancreas)
- Weight Loss
- Anorexia, Fatigue, Diarhoea/Steatorrhea, N+V
- Thrombophlebitis migrans, Portal HT, Ascites
What are the first line investigations for Pancreatic cancer?
- CT Scan (!!!)
- if still unclear: EUS + Biopsy
What is the treatment of Pancreatic cancer?
Radical
- Resection (pancreatico-duodenectomy
- Whipple’s (head of pancreas)
Palliative:
- of Jaundice: ERCP or Percutaneous stent insertion +/- RFA
- Pain: opiates, RT, coeliac plexus infiltration w bupivucaine (nerve block)
What are the most common causes of Chronic Liver Disease?
- Chronic Hepatitis
- Chronic Cholestasis
- Fibrosis + Cirrhosis
- Others: ie. Steatosis
- Liver Tumours
What are the most common causes of Hepatic Cirrhosis?
- Chronic alcohol abuse (!!!)
- Chronic HBV or HCV infection (!!!)
- Genetic disorders: Haemachromatosis, A1AT deficiency, Wilson’s disease
- Hepatic vein events: Budd-Chiari
- Non- Alcoholic: Steatohepatitis (NASH)
- Auto-immunity: PBC, PSC, Autoimmune Hepatitis
- Drugs: Amiodarone, Methyldopa, Methyltrexate
- Others: Sarcoidosis, Amyloid, Schistosomiasis
What are the clinical examination findings of Chronic Liver Disease?
- Leuconychia
- Clubbing
- Palmar erythema
- Dupuytren’s contracture
- Spider naevi
- Xanthelasma
- Gynaecomastia, loss
of body hair - Hepatomegaly
- Jaundice
- Altered mental status
- Fetor Hepaticus
- elevated JVP
- Abdominal veins
What are the clinical findings for Compensated Chronic Liver Disease?
no symptoms of disease!
Abnormality of LFTs
-> may be routinely detected on screening tests
What are the clinical findings for Decompensated Chronic Liver Disease?
- Jaundice
- Ascites
- Hepatorenal syndrome
- Variceal bleeding
- Hepatic Encephalopathy
What are the 3 clinical presentations of Cirrhosis?
- Compensated Chronic Liver Disease
- Decompensated Chronic Liver Disease
- Hepatocellular Carcinoma
How is the diagnosis of Ascites made?
- Abdominal Distension
- Dullness in the Flanks
- Shifting Dullness
- Umbilical nodule
- (additional signs of Chronic Liver Disease)
- Confirmed by US
What is the management of Ascites?
Diagnostic Paracentesis (!!!) (aka. Ascitic Tap)
- > test for protein + albumin (SAAG) -> >1.1g/dl = high, <1.1g/dl = low
- > WCC + differential
What does a high SAAG value represent?
- > 1.1g/dl -> transudate*
- Portal HT
- CHF
- Constrictive Pericarditis
- Budd-Chiarri
- Myxedema
- Massive Liver mets
What does a low SAAG value represent?
- <1.1g/dl -> exudate*
- Malignancy
- TB
- Chylous Ascites
- Pancreatitis
- Biliary Ascites
- Neprotic Syndrome
- Serositis
What are the treatment options for Ascites?
- Diuretics (!!!) -> 1st line!!
- Large-volume Paracentesis
- TIPS (shunt)
- Aquaretics
- Liver transplantation (if all else fails)
What are the treatment options for Hepatorenal Syndrome?
- Terlipressin (!!!) -> 1st line -> vasoconstricts splanchnic vessels
- Albumin -> volume expansion -> increases effective blood volume
- TIPS -> decreases Portal HT
- Liver transplant -> last resort!
What is the pathogenesis of Hepatorenal Syndrome?
Portal HT -> NO release -> Splanchnic vasodilation -> decreased effective blood volume -> increased RAAS, Vasopressin release, increased SNS output -> increased renal vasoconstriction -> decreased renal blood flow, decreased GFR and Na+ retention
Where is the management of a Variceal Haemorrhage?
- Resuscitate pt.
- Good IV access
- Blood transfusion as required
- Terlipressin (!!)
- Endoscopic Band Ligation (!!) -> EMERGENCY!!
- Sengstaken-Blakemore tube (for uncontrolled bleeding)
- TIPS (if rebleed after banding)
What are the precipitants of Hepatic Encephelopathy?
• GI bleed
-> proteins in blood get metabolised in the gut -> produces NH3
- Infection
- Constipation
- Dehydration
- Electrolyte Disturbance
- Medication esp. sedation
all precipitate an altered mental state -> makes HE worse !!
What are the clinical features of Hepatic Encephelopathy?
- Flap -> Asterixis
- Foetor Hepaticus
What causes Hepatic Encephelopathy?
Build up of toxins due to Chronic Liver Disease -> Liver cannot flush them away so they build up and accumulate in the body -> goes to the brain and causes an altered mental state
What are the management of Hepatic Encephelopathy?
- Treat underlying cause (of CLD)
- Exclude: Infection, Hypoglycaemia, IC Bleed
- > all contribute to reduced conscious levels
- Laxatives: Lactulose (!!), Phosphate enemas
- Broad-spectrum non-absorbed abx.: Rifaximin (!!)
(-> removes the bacteria which are causing NH3 build-up )
What is the most common cause of Hepatocellular Carcinoma?
- Cirrhosis (caused by Chronic Hep B (!!) or Hep C infection)
What are the clinical features of Hepatocellular Carcinoma?
- Decompensation of Liver Disease (ie. Ascites, Varices, HRS, HE, etc)
- Abdominal Mass
- RUQ pain
- Fatigue, Anorexia, Weight loss
- Jaundice
What are the investigations of Hepatocellular Carcinoma?
AFP (tumour marker) + US!
What is the most common cancer in the Lung?
Secondary metastases!
Men: CRC
Women: Breast
What are the treatment options of Hepatocellular Carcinoma?
- Hepatic resection
- Liver Transplant
- Percutaneous Ablation: alcohol, RFA
- Chemo: TACE (Transcatheter arterial chemo-embolisation, Sorafenib
What is the chemical byproduct of alcohol that causes unpleasant symptoms when drinking alcohol?
Acetaldehyde = toxic metabolite
How does alcohol cause Hypoglycaemia?
- Increases NADH formation
- > increases NADH/NAD ratio
- Excess NADH favours the formation of Pyruvate to Lactic Acid
- This results in less Pyruvate available for Gluconeogenesis -> Hypoglycaemia!
How is alcohol metabolised in the Liver?
- Ethanol -> Acetaldehyde (forms NADH)
Excess NADH contributes to…
- Pyruvate -> Lactic acid formation (-> Lactic acidosis)
- Lipogenesis (-> excess lipids)
- It contributes to the Electron Transport Chain where it produces energy
What are the screening tests used for Alcoholism?
CAGE:
- Have you ever felt the need to Cut down?
- Have you been Annoyed by criticism of your drinking?
- Have you felt Guilty about your drinking?
- Do you need an Eyeopener?
score >2 = problematic drinking
FAST/AUDIT:
- FAST score of 3 or more is positive
- If FAST +ve -> complete remaining AUDIT questions to obtain full AUDIT score
What is the weekly recommended intake of alcohol for men and women?
14 units for both men and women
What are the clinical features of Alcoholic Hepatitis?
- Jaundice
- Hepatic Encephalopathy
• Muscle wasting
-> less eating due to increased alcohol consumption
- Infection common
- signs of Decompensated Liver function
What are the investigations of Alcohol-related Liver disease?
- Labs: AST>ALT (2:1) (!!!), raised Gamma GT, raised Bilirubin
- USS Fatty Liver
What are the common complications of Alcoholic-related Liver disease?
- Hepatic Encephaloathy
- Spontaneous Bacterial Peritonitis
- Alcoholic Hepatitis
- Steatosis, Steatohepatitis
What are the clinical features of Spontaneous Bacterial Peritonitis?
Suspect in any pt. with Ascites who deteriorates suddenly
- Abdominal Pain
- Fever, Rigors
- Renal impairment
- Signs of Sepsis, tachycardia, temperature
What is the management of Spontaneous Bacterial Peritonitis?
- Diagnostic Paracentesis (!!!) (aka. Ascitic Tap)
EXUDATE:
- > high WCC (>0.25 x10^9/L) - esp. Neutrophils
- > low protein (<25g/L)
What is the treatment of Spontaneous Bacterial Peritonitis?
- IV abx
- Ascitic Fluid Drainage
- IV Albumin infusion (20% ALBA)
What is the treatment of Alcoholic Hepatitis?
- Supportive
- Treat infection
- Treat HE
- Treat alcohol withdrawal
- Protect against GI bleeding (increased risk)
- Airway protection/ITU
- Oral Steroids (!!) -> only if grading severe (only if >9 on Glasgow Alcoholic Hepatitis score)
- Nutritional (!!): Thiamine (vit B1), frequent feeds, high energy requirements
- > 100% pts w alcoholic hepatitis are malnourished
What are the clinical features of Steatohepatitis (NAFLD)?
- Asymptomatic (25-40% of population -> probably the chief cause of mildly raised
LFTS in the general population) - Raised ALT (ALT > AST)
What are the investigations for Steatohepatitis (NAFLD)?
- Diagnosis of exclusion!*
- Fatty Liver on USS
- Liver Biopsy (gold-standard!)
What are the risk factors for Steatohepatitis (NAFLD)?
- Obesity
- DM
- Hypercholesterolaemia
What is the treatment of Steatohepatitis (NAFLD)?
- Weight Loss
- Exercise
no pharmaceutical treatment available!
What are the functions of the Liver?
• Synthetic Function
-> clotting factors, bile, glucose, albumin, lipids, hormones (IGF-1, angiotensinogen)
• Detoxification
-> of drugs, bilirubin metabolism (conjugation), urea from NH3, breakdown of insulin + hormones
• Immune Function
-> first portal of entry from the gut
• Storage Function
-> stores glycogen, vitamin A, D, B12 and K, copper + iron
What would a raised ALP indicate?
- Obstruction of the bile ducts (ie. ?gallstones)
- Bone disorders (ie. paget’s osetomalacia, fractures, etc)
- Pregnancy (placenta)
- Intestinal disorders (ie. PU, bowel perforation, etc)
- Cancer mets (Liver/bone)
What would a raised AST indicate?
Alcoholic Liver Disease
AST:ALT ratio -> 2:1
What is Gamma GT used for?
- used to confirm Liver source of ALP
(-> if both Gamma GT + ALP raised then it is confirmed biliary disease) - elevated with ALD
- NSAIDs also raise levels
What does low albumin signify?
- Chronic Liver disease
(-> problem w synthetic function of the Liver) - Kidney disorders
- Malnutrition
Why is Prothrombin Time used in LFTs?
- Tells us degree of liver dysfunction
(-> Liver makes clotting factors) - used in scoring systems to decide the stage of Liver disease to decide who needs + gets a Liver transplant
Why is Creatinine used in LFTs?
- Marker of Renal function
- Determines survival from Liver disease
- Critical marker in determining the need for Liver transplant
Why is Platelet count used in LFTs?
Platelets low in Cirrhotic pts. due to…
- Splenomegaly (therefore, an indirect marker of Portal HT), and
- lack of Thrombopoeitin from the Liver (due to liver damage)
At what circulating Bilirubin level is Jaundice detectable?
Detectable when total plasma bilirubin levels exceed 34 µmol/L
What is Jaundice?
Yellowing of the skin, sclerae, and other tissues caused by excess circulating Bilirubin
Describe Bilirubin metabolism
- old/damaged RBCs broken down to Haem + Globin in the Spleen (“RBC’s graveyard”)
- Haem broken down to Bilirubin in the circulation (unconjugated)
- Bilirubin conjugated in the Liver
- unconjugated Bilirubin is reabsorbed via Enterohepatic circulation
- conjugated Bilirubin is metabolised by intestinal lumen bacteria to form stercobilin (excreted in faeces) and urobilin (reabsorbed + excreted in urine)
What causes Pre-Hepatic Jaundice?
Haemolysis
unconjugated bilirubin
What clues in the history would suggest Pre-Hepatic Jaundice?
- History of Anaemia (fatigue, dyspnoea, chest pain)
- Acholuric Jaundice
-> bilirubin is unconjugated and cannot get released into the urine
What clues in the history would suggest Hepatic Jaundice?
- Risk factors for Liver disease (ie. IVDU, drug intake)
- Decompensation (ascites, variceal bleed, HE)
What clues in the history would suggest Post-Hepatic Jaundice?
- Abdominal pain (RUQ, radiates to back/shoulders)
- Cholestasis (pruritus, pale stools, high coloured urine)
(-> due to conjugated bilirubin all coming out in the urine but not able to come out in the stools)
What clues in the examination would suggest Pre-Hepatic Jaundice?
- Pallor
- Splenomegaly
What clues in the examination would suggest Hepatic Jaundice?
- Stigmata of CLD (spider naevi, gynaecomastia)
- Ascites (abdominal distension, shifting dullness)
- Asterixis (Flapping Tremor -> HE!)
What clues in the examination would suggest Post-Hepatic Jaundice?
- Palpable GB (RUQ)
Courvoisier’s sign
What is the usual cause of painful vs. painless obstructive Jaundice?
- painful = indicates gallstone aetiology
- painless = indicates tumours (nb, cancer!!)
What investigations would you do for Jaundice?
- Liver screen: ?type of Liver damage
- > Hep B, C serology, autoantibody profile, caeruloplasmin + copper (Wilson’s), ferritin + transferrin (haemachromatosis), A1AT, fasting glucose + llipids
- Abdominal US (!!!)
- > ?obstruction, ?portal HT, ?cancer
- CT scan (usually requested in 2ary care)
