Chronic Liver Disease, Cirrhosis, Gallstone problems Flashcards

Question

Wilson's disease Ep Ax Px [3]

Answer 1

Ep: presents between childhood and 30y/o (NEVER >56y/o) Ax: autosomal recessive mutation in ATP7B gene on chromosome 13 Px: - mutation in copper transporting ATPase - means there is impaired hepatocyte incorporation into caeruloplasmin and excretion into bile - which results in copper accumulation in liver and later in other organs

Answer 2

* Eyes: corneal Kayser Fleischer rings (may require slit lamp to see) * Neurology: parkinsonism, spasticity, dysarthria, dysphagia, ataxia, asterixis * Psychiatry: depression, dementia, psychosis * Haematology: Coombs’ negative haemolytic anaemia

Answer 3

* Liver: childhood acute hepatitis, fulminant necrosis may occur leading to cirrhosis * Renal: renal tubular acidosis causing osteomalacia * Gynae: recurrent miscarriage * Arthritis: chondrocalcinosis and osteoporosis

Answer 4

<2 weeks | Usually following acute event e.g. acute GI bleed

Answer 5

Gradual decline in renal function | Usually in combination with refractory ascites

Answer 6

Jaundice is yellowish discoloration of the sclera and mucous membrane It is clinically manifest when serum bilirubin > 3mg/dL (51 µmol/L)

Answer 7

Haemolytic jaundice Hepatocellular jaundice Obstructive jaundice

Answer 8

Medical obstructive jaundice - Which is caused by intrahepatic biliary obstruction Surgical obstructive jaundice - Which is caused by extrahepatic biliary obstruction

Answer 9

Calcular obstructive jaundice | Malignant obstructive jaundice

Answer 10

Unconjugated bilirubin high ALT, AST, ALP normal Urine and stool normal

Answer 11

Mixed bilirubin ALT+ AST high ALP mild increase Dark urine

Answer 12

Conjugated bilirubin raised ALT and AST mild increase ALP marked increase Urine dark / pale stool

Answer 13

Haemolysis Gilbert, Crigler Naajar Post-transfusion Drugs

Answer 14

All hepatomegaly causes Drugs, TPN 3 C's Cancer, Cirrhosis, Congestion 3 I's Infection, Inflammation, Infiltration

Answer 15

CBD stone, Cholangitis Cholangiocarcinoma Stricture (iatrogenic) Pancreatic cancer, Liver mets PBC Mirizzi syndrome

Answer 16

Types of stones - Cholesterol gallstones 90% - Bile pigment stones - Mixed gallstones

Answer 17

Biliary colic Acute cholecystitis RF: - Female - Fat - Forty - Fertile - Fair (genetic)

Answer 18

1. Biliary colic: transient obstruction of cystic duct 2. Acute cholecystitis: - persistent cystic duct obstruction traps bile in the gallbladder - causing irritation and increasing pressure - trauma by gallstone stimulates prostaglandin release - inflammation and secondary bacterial infection causing necrosis and perforation (occasionally acalculous)

Answer 19

Biliary colic - RUQ or epigastric pain - 30min to 6h - Sudden, dull, colicky - Worse after meal, fatty foods Acute cholecystitis - Intense RUQ pain - Initially in epigastrium and LLQ, referred to shoulder tip - Previous episodes of biliary colic - Fever, nausea, vomiting

Answer 20

Paplable distended gallbladder Pyrexia Positive Murphy's sign

Answer 21

- palpation of the right subcostal region - produces tenderness which worsens during deep inspiration and causes termination of inspiration - only +ve if does not occur on LHS; can also be elicited during USS - Indicates acute cholecystitis

Answer 22

- Bloods: FBC (WCC up), CRP, amylase (?pancreatitis), LFT showing obstructive picture - Abdo USS - MRCP

Answer 23

NSAIDs, opiates as required Anti-emetic Elective laparoscopic cholecystectomy within 6w of first presentation

Answer 24

NBM, IV fluids, monitoring, analgesia, anti-emetic IV abx - coamoxiclav, metronidazole Laparoscopic cholecystectomy within 1 week Percutaneous cholecystectomy

Answer 25

Elective lap chole: Do within 6w of first presentation Lap chole for acute cholecystitis: - within 72h-1w of presentation

Answer 26

Gallbladder empyema Mirizzi syndrome Acute pancreatitis Bouveret syndrome Gallstone ileus

Answer 27

Gall stone impaction in neck of gallbladder | Causes compression of common bile duct and obstruction jaundice

Answer 28

F>M, >40yo Common bile duct stones Can lead to ascending cholangitis

Answer 29

Symptoms - Fluctuating obstructive jaundice - dark brown urine, pale stools) - NO weight loss Signs - Pale lemon to bright orange jaundice - Scratch marks - Bradycardia - Gallbladder not distended

Answer 30

Charcots triad | Reynolds pentand

Answer 31

o Charcot’s triad: RUQ pain, jaundice, fever/rigors | o Reynold’s pentand: Charcots triad + hypotension and confusion

Answer 32

LFT CRP, ESR (up) Abdo USS MRCP Pancreatico-billiary EUS

Answer 33

- IV antibiotics - ERCP after 24-48h: Endoscopic sphincterotomy + CBD stone extraction - Laparoscopic cholecystectomy

Answer 34

* Typical pt: post-op jaundice if complete, intermittent cholangitis with jaundice if incomplete * Ix: MRCP * Mx: biliary stent or Roux-en-Y pancreatojejunostomy

Answer 35

Cholelithiasis is the presence of gallstones. Choledocholithiasis refers to the presence of one or more gallstones in the common bile duct (CBD).

Answer 36

Bile duct and gallbladder cancer Ep: Eastern Europe, Thailand, Japan and Korea Symptoms: obstructive jaundice, abdominal pain, weight loss, anorexia Signs: - Courvoisiers sign - Sister Mary Joseph nodes - Virchow node

Answer 37

Palpable painless RUQ mass most likely malignancy in biliary tree - unlikely to be gallstones because gall stones are formed over a longer period of time, and this results in a shrunken, fibrotic gall bladder which does not distend easily

Answer 38

Periumbilical lymphadenopathy

Answer 39

``` Adenocarcinoma RF: primary sclerosing cholangitis 1. Abdo USS 2. CT 3. MRCP ```

Answer 40

CA-19-9, CEA, CA125

Answer 41

Surgical resection is only curative option But 80% have inoperable disease so: - palliate w/ biliary stents or chemo

Answer 42

Cholangiocarcinoma Pancreatic ca - head Periampullary tumour

Answer 43

Associations: - HLA-A1, B8 and DR3, autoimmune hepatitis, HIV - Ulcerative colitis: affecting whole colon, IBD often presenting before PSC, although colitis is usually inactive, colorectal malignancy risk much increased Patho: progressive cholestasis and intra and extrahepatic bile duct inflammation and strictures

Answer 44

``` Pruritus Fatigue RUQ pain Ascending cholangitis End stage hepatic failure (severe cases) ```

Answer 45

LFT (bilirubin up, ALP up) Autoab: hypergammaglobulinemia MRCP (beaded appearance, strictures) Liver biopsy (onion skin)

Answer 46

hypergammaglobulinaemia, AMA NEGATIVE but ANA, SMA and ANCA may be +ve

Answer 47

* Medical: LOW dose UROSEOXYCHOLIC ACID (may improve LFTs and protect against colon cancer), CHOLESTYRAMINE for pruritus * Transplant: for end stage disease (recurrence in 30%; worse prognosis if IBD as 30% develop colorectal cancer post-transplant) * Monitoring: annual colonoscopy and USS, cholecystectomy for gallbladder polyps (usually incidental finding on USS and can be left if <1cm but a lot more likely to be malignant in PSC)

Answer 48

bile duct, gallbladder, liver and colon cancers

Answer 49

Ascites is defined as the presence of free fluid within the abdomen; in chronic liver disease it develops due to presinusoidal portal hypertension and is associated with: * Changes in vascular tone: general vasodilatation, raised NO levels. * Sodium retention (and, therefore, water) due to secondary hyperaldosteronism. * Decreased ability to excrete free water due to increased antidiuretic hormone (ADH).

Answer 50

Presentation is either symptomatic (e.g. abdominal distension, breathlessness due to diaphragmatic splinting) or as an incidental finding on ultrasound. On examination, shifting dullness (>–.5L ascites) or a fluid thrill (tense ascites) may be detectable. Key investigations when assessing ascites are: * Abdominal ultrasound with Dopplers to quantify volume, identify appearances of chronic liver disease and portal hypertension, and exclude portal vein thrombosis. * Fluid should be sampled (tapped) and analysed for WCC to exclude spontaneous bacterial peritonitis (SBP), Gram stain, bacterial culture, and albumin and total protein levels. Fluid LDH, amylase, lipids and cytology may be sent dependent upon appearance and putative causes. * Calculate serum albumin ascites gradient (SAAG). SAAG = ascitic fluid [albumin] – serum [albumin]; if ≥1.1 g/L suggests ascites secondary to portal hypertension

Answer 51

The treatment of ascites includes: * Sodium (<90 mmol/day) and fluid restriction (<1.5 L/day). * Diuretics: spironolactone (initially 00 mg/day, but up to 400 mg/day), furosemide may be added. Treatment should target gradual weight loss of 0.5 kg/day (i.e. 500 mL) and patients must be monitored for complications of therapy (hyponatraemia, hyperkalaemia and renal dysfunction). Failure to respond to or inability to tolerate diuretic therapy should trigger consideration of liver transplantation or TIPSS.

Answer 52

Patients with ascites may develop the complication of SBP due to translocation of bowel organisms into ascites, leading to infection of the fluid. Causative organisms are typically bowel flora (e.g. E. coli, Klebsiella sp.), though streptococcal and staphylococcal infections may occur. Fever, abdominal tenderness and an altered mental state SBP must be considered in any patient with ascites with a deterioration in liver function tests. Patients with a low ascitic fluid albumin are at highest risk. Diagnosis is based upon an ascitic fluid WCC >250/mm3 with >50% neutrophils.

Answer 53

Empirical broad-spectrum antibiotics (e.g. piperacillin-tazobactam, ciprofloxacin), after appropriate cultures have been sent. * Renal failure and hepatorenal syndrome (HRS) may develop. Early plasma expansion with human albumin solution (HAS) reduces the risk, if this fails IV terlipressin is used. * Recurrence of SBP approaches 70%, patients surviving an episode should receive antibiotic prophylaxis (lifelong or until liver transplantation). * A single episode confers a poor prognosis and should prompt consideration of transplantation.

Chronic Liver Disease, Cirrhosis, Gallstone problems Flashcards

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