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Year 3 - TCD > Case 3 - HPB > Flashcards

Case 3 - HPB Flashcards

1
Q

What is considered as alcohol excess?

A

14units/wk over 3+ days, no more than 5/day

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2
Q

What are the alcohol withdrawal symptoms and what is their timeline?

A
  • 6-12h: tremor, sweating, headache, craving, anxiety
  • 12-24h: hallucinations
  • 24-48h: seizures
  • 24-72h: delirium tremens
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3
Q

What symptoms are considered in delirium tremens?

A

Confusion, agitation, delusions, hallucinations, tremor, tachycardia, HTN, hyperthermia, ataxia, arrhythmias, seizure

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4
Q

What tool can be used to score the patient on their alchol withdrawal symptoms and guide treatment?

A
  • CIWA-Ar (Clinical Institute Withdrawal Assessment – Alcohol revised)
  • Consider medication for high-risk i.e. ≥8)
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5
Q

What medications can be given in alcohol withdrawal?

A
  • Chlordiazepoxide (benzodiazepine) 5-7days titrate then wean
  • IV high-dose B vitamins (Pabrinex) then
  • Oral thiamine
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6
Q

What is alcoholic liver disease?

A

Alcoholic liver disease results from the effects of the long term excessive consumption of alcohol on the liver.

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7
Q

What are the 3 stages of ALD?

A

1) Fatty liver (steatosis, reversible)
2) Alcoholic hepatitis (inflammation and necrosis)
3) Alcoholic liver cirrhosis (irreversible)

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8
Q

What are the symptoms of ALD?

A
  • Abdominal pain – RUQ
  • Jaundice
  • Hepatomegaly
  • Nausea and vomiting
  • Splenomegaly and ascites may be present
  • Fatigue, lethargy
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9
Q

What are the risk factors for ALD?

A
  • Prolonged heavy alcohol consumption
  • Presence of hepatitis C
  • Female sex
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10
Q

What are the investigations for ALD?

A
  • ALT, AST and ALP (Later on) raised
  • Serum AST/ALT ratio >2
  • GGT elevated
  • Raised bilirubin
  • Raised prothrombin time
  • Decreased albumin
  • Macrocytic anaemia
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11
Q

What might the ultrasound show for ALD?

A
  • Hepatomegaly
  • Fatty liver
  • Liver cirrhosis
  • Liver mass
  • Splenomegaly
  • Ascites
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12
Q

What is the treatment for ALD`?

A
  • Immediate cessation of alcohol use, high protein and nutrition diet.
  • In some cases, glucocorticoids
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13
Q

What is NAFLD?

A

Accumulation of fat in the liver cells with risk of inflammation and cirrhosis

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14
Q

What are the 4 stages of NAFLD?

A

1) NAFLD
2) NASH - non alcoholic Steatohepatitis
3) Fibrosis
4) Cirrhosis

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15
Q

What are the causes of NAFLD?

A
  • Obesity
  • Type 2 diabetes: metabolic syndrome
  • Medication: amiodarone, glucocorticoids, oestrogen
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16
Q

What are the symptoms of NAFLD?

A
  • Often asymptomatic
  • Fatigue and malaise
  • Truncal obesity
  • Hepatosplenomegaly
  • RUQ abdominal pain
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17
Q

What are the investigations of NAFLD?

A
  • AST, ALT and GGT raised
  • Bilirubin raised
  • ALP raised
  • Prothrombin, INR raised
  • Albumin decreased
  • AST
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18
Q

What is the treatment for NAFLD?

A
  • Weight loss, optimise diabetic treatment

- Discontinue responsible medication

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19
Q

What is liver cirrhosis?

A

The result of chronic inflammation and damage to liver cells which can derive from any liver disease.

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20
Q

How is the liver tissue changed in cirrhosis?

A

Liver cells are replaced with scar tissue (fibrosis) and nodules of scar tissue form.

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21
Q

What are the causes of cirrhosis?

A
  • ALD
  • NAFLD
  • Viral hepatitis (B+C)
  • Drugs: amiodarone, methotrexate
  • Alpha-1 antitrypsin deficiency
  • Wilson’s disease
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22
Q

What score can be used to see the severity based on bilirubin, albumin, INR, ascites, encephalopathy?

A

Child-Pugh score

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23
Q

What score is used for estimated 3-month mortality and referral for liver transplant?

A

MELD score

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24
Q

What are the signs and symptoms of cirrhosis?

A
  • Jaundice and pruritus
  • Hepatosplenomegaly
  • Spider Naevi
  • Palmar Erythema
  • Gynaecomastia and testicular atrophy in males
  • Bruising
  • Ascites
  • Caput Medusae
  • Asterixis
  • Fatigue, malaise, weight loss
  • Oesophageal varices
  • Clubbing
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25
Q

What are the lab test investigation of cirrhosis?

A
  • ↑AST, ALT, GGT
  • ↑ Bilirubin: rises as the cirrhosis progresses
  • ↑ Alkaline phosphatase: elevated levels suggest biliary cirrhosis
  • ↑ Ammonia
  • ↑ Prothrombin time (↑ INR)
  • ↓ albumin
  • ↓ Cholinesterase
  • Macrocytic anaemia due to vitamin B12 deficiency
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26
Q

What imaging can be used to investigate cirrhosis?

A
  • USS: nodular surface, ascietes, splenomegaly, enlarged liver and portal veins
  • Fibroscan: check the elasticity and assess the degree of cirrhosis
  • CT/MRI: look for HCC, hepatosplenomegaly, abnormal blood vessel changes and ascites.
  • Liver biopsy: Confirm the diagnosis of cirrhosis.
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27
Q

What is the treatment for cirrhosis?

A
  • Avoid hepatotoxic substances
  • Vitamin B complex with thiamine (B1) and Vitamin B12 substitution
  • Nutritional diet
  • Beta blockers to lower portal hypertension
  • Spironolactone and furosemide for ascites
  • Vitamin K substitution for coagulation deficiency
  • TIPS (transjugular intrahepatic portosystemic shunt) to lower portal hypertension
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28
Q

What is decompensated cirrhosis complication?

A
  • Worsening of liver function in cirrhosis characterised by the presence of jaundice, ascites, variceal haemorrhage or hepatic encephalopathy
  • Does not respond to vitamin K
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29
Q

What is portal hypertension complication of cirrhosis?

A

Cirrhosis leads to a blockage to form in the venous return of the liver. This causes the pressure in the portal vein to increase.

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30
Q

What are the symptoms of portal hypertension?

A
  • Oesophageal varices: asymptomatic till they bleed (haematemesis)
  • Ascites: protein containing (ascitic) fluid to leak from the surface of the liver and intestine and accumulate in the abdomen.
  • Splenomegaly - ↓ WCC and platelets
  • Caput medusa: the blood tries to flow through periumbilical veins.
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31
Q
  • What is hepatic encephalopathy complication of cirrhosis?
  • What are the symptoms?
  • What are the triggers
  • What us the treatment?
A

Hepatic dysfunction results in inadequate elimination of ammonia which builds up and travel to the brain.

  • Fluctuation in mental status, cognitive function and memory loss
  • Triggers: spontaneous bacterial peritonitis,GI bleeding, Constipation, Renal failure
  • Lactulose, Abx and nutritional support
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32
Q

How can GI bleeding and constipation lead to hepatic encephalopathy?

A
  • GI bleeding: Blood from ruptured varices goes to bowel if not vomited and this has lots of protein which breaks down to ammonia ad this can cause HE.
  • Constipation – build-up of faecal material causes ammonia to build up
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33
Q
  • What is spontaneous bacterial peritonitis?

- How to treat?

A
  • Infection developing in the ascitic fluid and peritoneal lining
  • IV cephalosporin (cefotaxime)
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34
Q
  • What is hepatocellular carcinoma (HCC) complication of cirrhosis?
  • How often to screen?
  • What test is done?
A
  • Most common malignant disease associated with cirrhosis.
  • USS every six months
  • Alpha-fetoprotein test
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35
Q

What are the causes of hepatitis?

A
  • Hereditary: Wilson’s, Hemochromatosis (iron overload)
  • Drug induced: paracetamol, alcohol
  • Infection: EBV
  • Auto-immune
36
Q

What is acute hepatitis?

A
  • Inflammation that lasts less than 6 months
37
Q

What are the symptoms of hepatitis?

A
  • Abdominal pain (RUQ)
  • Fatigue
  • Pruritis (itching)
  • Muscle and joint aches
  • Nausea and vomiting
  • Jaundice
  • Fever (viral hepatitis)
38
Q

What are the investigation of hepatitis?

A
  • Raised ALT / AST (often >1,000)&raquo_space; ALP
  • High bilirubin – jaundice
  • Coagulopathy
  • Renal impairment
39
Q

What is chronic hepatitis?

A

Inflammation of the liver that lasts longer than 6 months

40
Q
  • What is fulminant hepatitis?
  • What are the features of fulminant hepatitis?
  • What are the causes?
A
  • Acute hepatitis with liver failure
  • Encephalopathy within 28 days of jaundice
  • Poor prognosis often needs transplantation
  • Paracetamol overdose, viral hepatitis
41
Q
  • What is SAAG?

- How is it calculated?

A
  • Serum Albumin Ascitic Gradient used to determine the cause of ascites.
  • > Serum albumin – albumin level of ascitic fluid.
42
Q

What are transudate causes of SAAG?

A

Transudate: SAAG >1.1 g/L

  • Liver cirrhosis with portal hypertension
  • Congestive cardiac failure
  • Nephrotic syndrome
43
Q

What are exudate causes of SAAG?

A

Exudate SAAG <1.1 g/L

  • Malignancy (liver or peritoneal metastases)
  • Peritoneal TB
44
Q

What would ascitic ta for SBP show?

A

Microscopy showing >500 WBC

45
Q

How to treat ascites?

A
  • Drain
  • Diuretics
  • Treat underling cause
46
Q

What are the 3 categories of jaundice?

A
  • Pre-hepatic
  • Hepatocellular
  • Post hepatic (obstructive)
47
Q

What are the causes of pre-hepatic jaundice?

A
  • Due to RBC breakdown (haemolysis) due to sickle cell, Incompatible blood transfusion, drug reaction
48
Q

What are the causes of hepatocellular jaundice?

A 
Common:
- Neonatal jaundice.
- Infection (viral hepatitis)
- Cirrhosis secondary to alcohol
- Cirrhosis secondary to steatohepatitis (NASH)	
- Damage by toxins or drugs.
Uncommon:
- Autoimmune liver disease
- Haemochromatosis
- Wilsons disease.
49
Q

What is the pathophysiology of hepatocellular jaundice?

A

Bilirubin is formed at a normal rate, but the compromised liver cannot excrete it due to increased hepatocyte abnormality.

50
Q

What are the 2 types of neonatal jaundice?

A
  • Unconjugated hyperbilirubinemia: can penetrate the BBB and is toxic to neural tissue and can cause bilirubin encephalopathy
    • Kernicterus is the yellow staining of the brain
  • Conjugated hyperbilirubinemia: non-toxic; always pathological.
51
Q

How to treat neonatal jaundice?

A
  • Correcting underlying abnormality
  • Fluid and caloric intake prevent deterioration
  • Unconjugated hyperbilirubinemia: phototherapy or exchange transfusion
52
Q

What is the pathophysiology obstructive jaundice?

A

Obstruction of the passage of conjugated bilirubin from hepatocyte to intestine with blockage of flow of bile through bile ducts or intrahepatic or extrahepatic duct.

53
Q

What are the causes of obstructive jaundice?

A

Common:

  • Gallstones (biliary colic, cholecystitis, cholangitis)
  • Carcinoma of head of pancreas Uncommon:
  • Sclerosing cholangitis (scarring of small ducts in liver)
  • Cholangiocarcinoma
54
Q

What are the symptoms of jaundice?

A
  • Sclera and skin: jaundice
  • Scratches from pruritus.
  • Evidence of weight loss (thenar wasting)
  • Troisier’s node (left supraclavicular node enlargement)
55
Q
  • What investigations are done in pre-Hepatic jaundice?

- What are other observation in pre-Hepatic jaundice?

A
  • Raised unconjugated bilirubin
  • Normal stool colour
  • Normal urine colour
  • No pruritus, yellow skin
56
Q
  • What investigations are done in hepatocellular jaundice?

- What are other observation in hepatocellular jaundice?

A
  • Raised conjugated bilirubin
  • Rise in ALT, AST&raquo_space; Rise in Alk Phos
  • Normal stool colour
  • Dark urine (lack of urobilin)
  • No pruritus, yellow skin
57
Q
  • What investigations are done in obstructive jaundice?

- What are other observation in obstructive jaundice?

A
  • Raised conjugated bilirubin
  • Rise in ALT, AST &laquo_space;Rise in Alk Phos
  • Pale stool (lack of stercobilin)
  • Dark urine (lack of urobilin)
  • Pruritus
58
Q

What is cholelithiasis?

What is the mechanism?

A
  • Gallstones in the gallbladder

- Bile stasis, impaired bile acid circulation → precipitation of gallstones

59
Q

What are the signs and symptoms of cholelithiasis?
What are the risk factors?
What are the lab findings?

A
  • Dull, intermittent RUQ pain especially after eating
  • 6 F’s – female, forty, fertile, fat, fair-skinned, family history
  • Normal
60
Q

What does ultrasound show for cholelithiasis?

What is the treatment?

A
  • Gallstones with posterior acoustic shadow
  • Supportive care, analgesics
  • Elective cholecystectomy for symptomatic Cholelithiasis
61
Q

What is choledocholithiasis?

A
  • Presence of gallstones in the common bile duct from gallbladder
62
Q

What are the signs and symptoms for choledocholithiasis?

A

RUQ pain > 6 h especially postprandial

63
Q

What are the lab findings for choledocholithiasis?

A
  • ↑ ALP
  • ↑ AST, ALT
  • ↑ Total bilirubin
64
Q

What investigations can be done for choledocholithiasis?

A
  • USS: dilated common bile duct, intrahepatic biliary dilatation
  • MRCP or ERCP: filling defect in the contrast-enhanced duct
65
Q

How to treat choledocholithiasis?

A
  • Supportive care, analgesics

- Endoscopic stone retrieval (ERCP)

66
Q

What is acute cholecystitis?

What can be a complication?

A
  • Inflammation of the gallbladder

- Gallstone ileus

67
Q

What are the signs and symptoms for acute cholecystitis?

A
  • Persistent RUQ pain, postprandial
  • Radiation to right scapula
  • Fever
  • Murphy sign
68
Q

What are the lab findings for acute cholecystitis?

A

↑ WBC, CRP

69
Q

What diagnostic imaging can be done for acute cholecystitis?

A

USS: gallbladder wall thickening and oedema (double wall sign)

70
Q

What is the treatment for acute cholecystitis?

A
  • Supportive care, analgesics
  • IV antibiotics
  • Cholecystectomy within 48 hours
71
Q

What is acute cholangitis?

A

Ascending bacterial infection of the biliary tract

72
Q

What are the signs and symptoms of acute cholangitis?

A
  • Charcot triad: RUQ pain, fever, jaundice

- Reynold pentad: Charcot cholangitis triad PLUS hypotension and mental status changes

73
Q

What are the lab findings for acute cholangitis?

A
  • ↑ WBC and CRP
  • ↑ ALP
  • ↑ AST, ALT
  • ↑ Total bilirubin
74
Q

What diagnostic imaging can be done for acute cholangitis?

A
  • USS: biliary dilation and/or evidence of obstruction (cholelithiasis)
  • ERCP for diagnosis and therapeutic
75
Q

What is the treatment for acute cholangitis?

A
  • Supportive care, analgesics
  • IV antibiotics
  • ERCP (Urgent biliary decompression after 24-48 hours)
76
Q

What is primary biliary cholangitis? - also known as biliary cirrohsis

A

Chronic progressive liver disease of autoimmune origin that is characterized by destruction of the intralobular bile ducts.

77
Q

What is acute pancreatitis?

A

Sudden inflammation and haemorrhaging of the pancreas due to destruction by its own digestive enzymes

78
Q

What are the causes of acute pancreatitis?

A

I GET SMASHED:

  • Idiopathic (20%)
  • Gall stones (50%)
  • Ethanol (25%)
  • Trauma
  • Steroids
  • Mumps, EBV - Infections
  • Autoimmune
  • Scorpion stings
  • Hypertriglyceridemia, hypercalcaemia and hyperparathyroidism
  • ERCP – endoscopic retrograde cholangiopancreatography
  • Drugs: sodium valproate, azathioprine, sulphonamides, furosemide
79
Q

What are the signs and symptoms of acute pancreatitis?

A
  • Upper abdominal pain that radiates into the back; it may be aggravated by eating,
  • Swollen and tender abdomen
  • Nausea and vomiting
  • Fever
  • Sweating
  • Tachycardia
  • Cullen signs: Bruising around the belly button
  • Grey turner’s sign: Bruising around the flank region
  • Fox sign: Bruising over the inguinal ligament
80
Q

What investigations are done in acute pancreatitis?

A
  • FBC
  • LFTs: hepatic impairment
  • Elevated levels of serum lipase or amylase (>3 upper limit of normal)
  • Raised CRP
  • CT scan to show pseudocysts, pancreatic necrosis, abscess or fluid collection
  • Ultrasound to look for gallstones
  • Chest X-ray to exclude perforation
81
Q

How is the diagnosis for acute pancreatitis made?

A
  • Clinical story (upper abdominal pain)
  • Elevated serum lipase or amylase (>3 upper limit of normal)
  • CT or MRI consistent with acute pancreatitis.
82
Q

How to treat acute pancreatitis?

A
  • Fluid resuscitation
  • Analgesia (morphine) + anti-emetic (Ondansetron)
  • ERCP to remove bile obstruction
  • Surgery to remove infected pancreatic necrosis
  • Antibiotics
83
Q

What are the complications of acute pancreatitis?

A
  • Pancreatic fluid collections
  • Pancreatic necrosis
  • Pseudocysts – this is collection of fluid rich in pancreatic enzymes.
  • Infection – signs of sepsis
84
Q

What is chronic pancreatitis?

A
  • Persistent chronic inflammation due to repeated bouts of acute pancreatitis.
  • Leads to fibrosis, atrophy and calcification of pancreas.
85
Q

What are the symptoms of chronic pancreatitis?

A
  • Abdominal pain
  • Jaundice
  • Steatorrhea – due to malabsorption of dietary protein (7g faecal fat/100g diet)
  • Malnutrition
  • Weight loss
  • Nausea and vomiting
86
Q

What are the complications of chronic pancreatitis?

A
  • Pancreatic digestive enzymes insufficiency
  • Deficiency in vitamin A, D, E and K which are fat soluble vitamins
  • DM: due to damage to beta cells
  • Pancreatic pseudocysts
  • Pancreatic cancer
87
Q

How to treat chronic pancreatitis?

A
  • Alcohol and cigarette cessation
  • Analgesic
  • Pancreatic enzymes plus PPI: pancreatin and omeprazole
  • Dietary modifications + enteral feeding
  • Pancreatic pseudocyst decompression

Year 3 - TCD (17 decks)

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