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Year 4 - GP > GP - Alcohol Dependency Cont (Liver, Biliary and Pancreatic Disease) > Flashcards

GP - Alcohol Dependency Cont (Liver, Biliary and Pancreatic Disease) Flashcards

1
Q

High levels of what, causes Jaundice?

A

Serum Bilirubin

  • Conjugated hyperbilirubinaemia = more common in clinical practice than unconjugated (i.e. obstrutive Jaundice is most common form of Jaundice)
    • Conjugated hyperbilirubinaemia is rarely measured in lab as signs/symptoms are used to differentiate: conjugated vs unconjugated hyperbilirubinaemia
  • Conjugated hyperbilirubinaemia –> dark urine + pale stools + pruritis (itching)
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2
Q

Jaundice caused by Conjugated Hyperbilirubinaemia can be subdivided into what catagories?

A
  1. Obstructive Jaundice - blockage of bile flow in either bile ducts or intrahepatic or extrahepatic ducts
  2. Hepatocellular Jaundice - caused by Hepatocyte damage – e.g. hepatitis, cirrhosis
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3
Q

What are some causes of Obstructive Jaundice?

A

Common:

  • CBD stones - causing Biliary Colic, Cholecystitis or ascending Colangitis
    • Note: gallstones in the gallbladder don’t cause obstructive jaundice unless they occlude the cystic duct (rare) because they don’t occlude the CBD
  • Carcinoma of head of pancreas

Uncommon:

  • Cholangiocarcinoma
  • Chronic pancreatitis
  • Bile duct stricture
  • Sclerosing Cholangitis (autoimmune)
  • Lymphnoid metastasis
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4
Q

What is the normal pathway from RBC breakdown to excretion of bilirubin derived substances?

A
  1. RBC is catabolised by macrophage –> haemoglobin is broken down to release the iron containing Heme
  2. The Fe2+ is seperated from Heme
  3. Heme converted to –> Biliverdin
  4. Biliverdin converted to –> Unconjugated Bilirubin
  5. Unconjugated Bilirubin trasported to liver by Albumin
  6. Liver forms Conjugated Bilirubin –> excretes via bile duct into duodenum
  7. Intestinal bacteria converts conjugated Bilirubin –> Urobiliogen
  8. 85-90% of Urobiliogen is converted –> Stercobiliogen –> Stercobilin (excreted in faeces, brown colour)
  9. ~10% Urobiliogen is reabsorbed into portal vein –> some of which is excreted via the Kidneys and converted to –> Urobilin
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5
Q

What are the 3 main types of Jaundice?

A
  1. Pre-Hepatic
    • Caused by excessive RBC breakdown –> ↑ unconjugated bilirubin
    • Causes:
      • Haemolytic anaemia
      • Gilbert’s syndrome (autosomal recessive mutation, reduced activity of liver enzyme that makes bilirubin water soluable)
  2. Intra-Hepatic
    • Dysfunction of the liver, can involve: loss of ability to conjugate, cirrhosis, compression of intra-hepatic sections of biliary tree (obstruction)
    • Causes ↑ unconjugated bilirubin and in some cases ↑ conjugated bilirubin in blood –> ‘mixed’ picture
    • Causes:
      • Alcoholic liver disease –> Cirrhosis
      • Hepatitis (viral or autoimmune)
      • NASH (non-alcoholic steatohepatitis) –> Cirrhosis
      • Hereditary haemochromatosis
      • Primary biliary cirrhosis/cholangitis (autoimmune)
      • Primary sclerosing cholangitis (autoimmune) - intahepatic as it affects the bile ducts inside the liver as well
      • Hepatocellular carcinoma
      • Medication
  3. Post-Hepatic
    • Obstruction of biliary drainage
    • ↑ conjugated bilirubin
    • Causes:
      • Gallstones
      • Cancer of head of pancreas
      • Changiocarcinoma
      • Biliary strictures
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6
Q

How can urine colour be used to differentiate;

conjugated or mixed hyperbilirubinaemia from unconjugated hyperbilirubinaemia?

A

Urine = Dark‘coca-cola’ in conjugated or mixed hyperbilirubinaemia (post and intra hepatic)

Urine = normal in unconjugated hyperbilirubinaemia (pre-hepatic)

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7
Q

What blood tests and their justifications might you do in a Jaundice patient? (obviously you tailor them to the patient’s history)

A
  • LFTs (AST, ALT, Alkaline phosphatase)
    • Alkaline phosphatase - ↑ in biliary obstruction (or bone injury) - if alkaline phosphate >>> than AST/ALT –> obstruction (>>> = how many folds the increase is)
    • If AST, ALT are >>> than alkaline phosphatase –> indicates hepatocellular pathology e.g. viral hepatitis
    • AST:ALT ratio is of little benefit in identifying cause of liver injury with the exception of acute alcoholic hepatitis
    • If AST:ALT ratio > 2:1 –> likely alcoholic liver disease (acute alcoholic hepatitis)
    • If AST: ALT ratio ~ 1 –> likely viral hepatitis
  • Coagulation Studies - Prothrombin time (PT) / INR can be used as a marker of liver function
  • FBC:
    • Anaemia, ↑ MCV and thrombocytopenia (low platelets) can occur in liver disease
    • WCC - determine if bacterial infection present
  • Albumin - hypoalbuminaemia (indicative of liver dysfunction)
  • U+Es - can dictate pharmacological treatment
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8
Q

What are some causes of Hepatocellular Jaundice?

A
  1. Alcoholic hepatitis or cirrohsis
  2. Viral Hepatitis
  3. Drug induced e.g. Paracetamol OD
  4. Non-alcoholic fatty liver disease
  5. Autoimmune liver disease
  6. Hereditary Haemochromatosis
  7. Wilson’s Disease
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9
Q

Patient presents with RUQ pain (which comes and goes), Jaundice and Fever - diagnosis?

A

Ascending Cholangitis (Inflammation of Bile Duct)

Charcot’s Triad:

  1. RUQ Pain
  2. Jaundice
  3. Fever

Reynold’s Pentad:

  1. Charcot’s Triad
  2. Hypotension
  3. Mental status changes
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10
Q

Patient presents with:

Severe epigastric pain (radiating to back) with guarding, nausea, vomiting and a Hx of high alcohol consumption - diagnosis?

A

Acute Pancreatitis

  • The two most common casues are gallstones and alcohol consumption
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11
Q

70 year old male presents with painless obstructive pattern Jaundice, what is the most concerning diagnosis?

A

Pancreatic or Liver Cancer

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12
Q

What are some important risk factors for Liver, Biliary and Pancreatic diseases?

A
  1. Alcohol intake (Alcoholic liver disease, pancreatitis)
  2. Drug use (including non-perscription drugs e.g. paracetamol / IV drugs - HIV)
  3. Foreign Travel
  4. Blood transfusions (Transfusional iron overload or contaminated blood)
  5. Tattoos (HIV)
  6. Unprotected sexual activity (viral hepatitis - association between Hep-B and obstructive Jaundice)
  7. Weight loss (cancers or nausea/vomiting associated ↓ appetite)
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13
Q

What is the most common cancer in the region of Liver, Biliary ducts and Pancreas?

A

Cancer of the Head of the Pancreas

  • Patients >40yrs with painless, obstructive jaundice –> exclude carcinoma of head of pancreas
  • Liver cancer is often caused by metastasis from other primaries e.g. Lung
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14
Q

A patient has Liver Cirrhosis (e.g. due to alcohol or hepatitis), what condition are they at an increased risk of?

What blood test is done as a marker of this condition?

A

Primary Hepatocellular Cancer

Serum Alpha-fetoprotein

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15
Q

What is the official recommended number of units of alcohol per week for men and women?

A

14 units per week

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16
Q

What does 14 units of alcohol look like for;

  1. Beer
  2. Wine
  3. Spirits
A
  1. 6 pints of beer (4%) - so 4/5 pints of anything stronger
  2. 7 glasses of wine (11/12% 175ml)
  3. 14 single shots of spirits (40%)
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17
Q

What is Hepatitis?

A

Liver inflammation (not necessarily infection)

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18
Q

What the cut-off duration for chronic hepatitis?

A

> 6 months

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19
Q

Describe the stages of progression / routes stemming from an episode of acute hepatitis.

A
  1. Recovery - patient recovers
  2. Chronic Hepatitis –> increasing Fibrosis –> Cirrhosis
  3. Fulminant Hepatitis (acute liver failure):
    • Death OR
    • Liver Transplant
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20
Q

What are the presenting features of Hepatitis?

A

Typically:

  1. Generally unwell
  2. Jaundice
  3. RUQ pain

Severe (when these symptoms present it is called fulminant hepatitis):

  1. Confusion (hepatic encephalopathy due to ammonia build up)
  2. Coagulopathy (↑ bruising)
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21
Q

How do patients with Chronic Hepatitis present?

A

Often they present with NO symptoms

Sometimes: fatigue, vauge RUQ pain

  • Normally discovered via routine screening of:
    • HIV +ve men as they’re at risk
    • Chronic alcoholic pts
    • Pregnant women
    • IV drug users
  • LFTs - mildly deranged
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22
Q

What is Fulminant Hepatitis?

A

Acute Hepatitis with Liver Failure

  1. Hepatic encephalopathy occuring within 28 days of onset of Jaundice
  2. Must be ‘Acute’ Hepatitis e.g. you can’t call 1st presentation of decompensated alcoholic liver disease a fulminant hepatitis - as the condition has been long-standing i.e. chronic
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23
Q

What types of problems does Liver Cirrhosis cause?

A

Loss of Function - hard to manage:

  • Jaundice - ↑ unconjugated bilirubin (due to ↓ conjugated bilirubin production i.e. function of the liver)
  • Coagulopathy - ↓ production of clotting factors = bruising/bleeds
  • ↓ Drug metabolism - drugs to watch out for; benzodiazepines and opiates
  • ↓ Hormone metabolism - ↑ oestrogen (palmar erythema, spider naevi, gynecomastia, loss of 2ndary body hair and shrinking of external genitalia)
  • ↑ Sepsis - liver has important role in managing immune system

Portal Hypertension - easier to manage:

  • Umbilical Varices (Caput Medusae)
  • Oesophageal varices –> GI bleed –> Haematemesis
  • Rectal varices i.e. Piles (Haemorrhoids)
  • Acities - fluid leaks from portal system into peritoneum
  • Encephalopathy (accumulation of nitrates)
  • Renal failure (mechanism not understood - but changes in portosystemic bloodflow –> ↑ renal vasocontriction)
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24
Q

What are some common causes of Liver Cirrhosis?

A
  1. Hazardous alcohol consumption
  2. Chronic Hepatitis B + C
  3. Autoimmune liver disease (autoimmune hepatitis, primary biliary cirrhosis)
  4. Hereditary haemochromatosis
  5. Wilson’s Disease
  6. Chronic Obstruction –> Secondary biliary cirrhosis
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25
Q

What are the physical examination signs of Liver Cirrhosis?

A
  1. Palmar erythema - ↑ oestrogen
  2. Leuconychia - ↓ albumin
  3. Spider Naevi - ↑ oestrogen
  4. Gynaecomastia - ↑ oestrogen
  5. Ascites
  6. Bruising
  7. Caput medusa - portal hypertension
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26
Q

If AST, ALT increase in many folds greater than alkaline phosphatase increase what kind of pathology is likely?

A

Hepatocellular damage/pathology

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27
Q

If Alkaline phosphatase increase is many folds greater than AST, ALT increase what kind of pathology is likely?

A

Obstructive pathology

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28
Q

What are some symptoms of Acute Alcoholic Hepatitis?

A
  1. Jaundice
  2. Tender Hepatomegaly (large tender liver)
  3. Vomiting
  4. Drinking cessation
  5. Alcohol withdrawal (shivering/shaking/tremor, sweating, nausea, visual or auditory hallucinations, tachycardia, confusion, seizures)
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29
Q

Which Liver cells are involved in the process of Fibrosis?

A

Stellate Cells

  • Stellate cells exist in the perisinusoidal space (next to the sinuoid ) - which exists between the sinusoid and hepatocytes
30
Q

Define Jaundice?

A

Jaundice is a yellowish discolouration of the skin, mucous membranes and sclera due to the accumulation within them of (either unconjugated or conjugated) bilirubin

31
Q

At what plasma bilirubin concentration (µM/L) is Jaundice clinically apparent?

A

50 µM/L​

32
Q

How much bile is produced by the liver per day?

A

500-100 ml per day

33
Q

What pH is Bile?

A

8 - 8.6 pH (alkaline)

34
Q

What is bilirubin conjugated with to make it water soluable?

A

Glucuronic Acid

  • Bilirubin is conjugated with Glucuronic acid via the action of the enzyme glucuronyl transferase
35
Q

What are some causes of pre-hepatic haemolytic Jaundice?

A

↑ RBC breakdown can be due to:

  1. RBC abnormality e.g. sickle cell anaemia
  2. Incompatible blood transfusion
  3. Drug reaction
  4. Hypersplenism (overactive spleen of any size) - can be primary (no known cause) or secondary (due to another condition e.g. malaria, TB, lupus, liver cirrohsis, lymphoma)
36
Q

Describe the stool and urine of a patient with pre-hepatic haemolytic Jaundice?

A

Stool = dark (Liver compensates to a certain extent to manage the excess unconjugated bilirubin by producing as much conjugated bilirubin as glucuronyl transferase will allow - this is excreted primarily in stool)

Urine = normal (heamolytic jaundice causes ↑ unconjugated bilirubin - which isn’t water soluable and thus can’t be excreted into the urine)

37
Q

What is Steatosis?

A

Process describing the abnormal retension of lipids within a cell or organ

When not specified further (e.g. cardiac steatosis) it refers to the Liver

38
Q

What is Steatohepatitis?

A

A type of Fatty Liver Disease

  • Characterised by inflammation of the liver + concurrent fat accumulation
  • There are 2 types of Fatty-Liver disease:
    1. Alcohol-related Fatty-Liver disease
    2. Non-alcoholic Fatty-Liver disease (NAFLD)
  • When inflammation is present in Fatty-Liver disease it is called:
    1. Alcoholic steatohepatitis
    2. Non-alcoholic steatohepatitis (NASH)
  • Steatohepatitis of any form can progress to –> cirrohsis
39
Q

What are some causes of intra-hepatic (hepatocellular) Jaundice?

A

​

  • Alcoholic liver disease –> Cirrhosis
  • Hepatitis (viral or autoimmune)
  • NASH (non-alcoholic steatohepatitis) –> Cirrhosis
  • Hereditary haemochromatosis
  • Primary biliary cirrhosis
  • Primary sclerosing cholangitis (autoimmune) - intrahepatic as it affects the bile ducts in the liver as well
  • Hepatocellular carcinoma
  • Medication
40
Q

Does Obstructive Jaundice cause unconjugated or conjugated hyperbilirubinaemia?

What are signs relating to urine + stool that indicate Obstructive Jaundice?

A

Obstructive Jaundice –> conjugated hyperbilirubinaemia

Signs of obstructive jaundice picture:

  • Urine = dark (conjugated bilirubin is water soluable thus can be excreted in the urine)
  • Stool = pale (no conjugated bilirubin entering intestine due to obstruction, thus stercobilin can’t be formed –> no dark pigment in stool)
41
Q

What is the name of the left supraclavicular lymph nodes?

What is the name of the sign when these lymph nodes are; hard and enlarged?

A
  1. Virchow’s Nodes
  2. Troisier’s Sign
42
Q

What is an ERCP?

A

Endoscopic retrograde cholangiopancreatography

  • Procedure to examine pancreatic and bile ducts
  • Endoscope is passed (orally) through the stomach into the duodenum and a cannula is passed through the endoscope, through the ampulla of Vater, to inject contract die into the pancreatic + bile ducts (viewed via X-ray)
43
Q

Summarise whether there is dark urine and or pale stools for the following:

  • prehepatic jaundice
  • hepatocellular (intrahepatic) jaundice
  • post-hepatic/obstructive jaundice
A
44
Q

In which are Liver transaminases (AST, ALT) raised:

  • prehepatic jaundice
  • intrahepatic jaundice
  • posthepatic jaundice
A

Intrahepatic (Hepatocellular)

45
Q

In which is Alkaline Phosphatase most raised:

  • prehepatic jaundice
  • hepatocellular (intrahepatic) jaundice
  • post-hepatic/obstructive jaundice
A

Post-hepatic (Obstructive)

46
Q

After an acute Hepatitis A infection, what % of people:

1) Recover
2) Develop fulminant hepatitis
3) Develop Chronic hepatitis

A
  1. Recover = 99%
  2. Fulminant hepatitis = 1-2% (more likely with underlying liver disease)
  3. Chronic hepatitis = 0%
47
Q

After an acute Hepatitis B infection, what % of people:

1) Recover
2) Develop fulminant hepatitis
3) Develop Chronic hepatitis

A

% of patients who Recover or develop Chronic Hepatitis post Hepatitis B is subject to the AGE of initial infection

  • AGE of infection:
    • < 1 yr = 90% chronic
    • 1-5 yrs = 30% chronic
    • >5 yrs = 1-5% chronic
  • 1% develop fulminant hepatitis
  • Chronic Hepatitis is associated with ↑ risk of Liver cancer
48
Q

Hepatitis A

  1. What is the typical duration of Hepatitis A infection?
  2. How does it spread between people?
  3. Can you be immunised against it?
  4. Does it require treatment?
A

Hepatitis A

  1. Typical duration of infection = 12 weeks
  2. Faeco-oral spread
  3. Yes immunisation
  4. No treatment
49
Q

Hepatitis ​B

  1. How does it spread between people?
  2. Can you be immunised against it?
  3. Does it require treatment?
A

Hepatitis B

  1. Blood (IV-drug users), Sex, Vertical (mother to child)
  2. Yes immunisation
  3. Acute = generally not needed / Chronic = antivirals, interferon (treat not cure)
50
Q

Hepatitis ​C

  1. How does it spread between people?
  2. Can you be immunised against it?
  3. Does it require treatment?
A

Hepatitis C

  1. Blood, IV-drug use, Iatrogenic (medical equipment), Vertical (mother to baby - very low rate ~1%) - often discovered on screening (no symptoms)
  2. No immunisation
  3. Yes treatment - interferon, ribavirin, protease inhibitors (expensive!!)
51
Q

After an acute Hepatitis C infection, what % of people:

1) Recover
2) Develop fulminant hepatitis
3) Develop Chronic hepatitis

A
  1. Recover = 25%
  2. Fulminant hepatitis = 0%
  3. Chronic hepatitis = 75%
52
Q

Hepatitis E is virtually identical to Hepatits A,

except one population is particularly vulnerable?

A

Pregnant women

  • High rate of maternal death due to fulminant hepatitis (unknown reasons)
53
Q

Hepatitis delta has no symptoms of its own but it worsens the prognosis of another Hepatitis virus, which?

A

Hepatitis B

54
Q

Which drugs can cause Acute Hepatitis / Liver Disease?

A
  • Paracetamol
  • Alcohol
  • Augmentin (Co-amoxiclav)
  • Flucloxacillin
  • Erythromycin
  • Methotrexate
  • Rifampicin
55
Q

What are some Hereditary causes of Liver Disease?

A
  1. Hereditary Haemochromatosis
  2. Wilson’s Disease
  3. Alpha-1-antitrypsin deficiency
56
Q

What does this CXR show?

A

Pneumoperitoneum

  • Pneumoperitoneum on a CXR implies a perforated viscus unless proven otherwise
  • E.g. perforated gastric/duodenal ulcer or small/large intestine perforation
57
Q

52 year old female present to A+E, with severe RUQ pain, cold, shivery and fever + “I have had similar pains in the past but never this bad”

What diagnoses should be considered?

A
  1. Acute Pancreatitis
  2. Perforated Ulcer
  3. Cholangitis / Biliary colic
  4. Pyenonephritis / renal colic
  5. Acute mesenter ischaemia (embolism or thrombosis)
  6. Pneumonia
  7. MI
58
Q

What is the first investigation of choice to image the Biliary Tree?

(looking for gallstones, duct dilitation and state of surround organs)

A

Ultrasound

  • To visualise stones/duct dilitation US is the preferred first choice of most radiologist
  • Then imaging can be escalated to CT or MRI if needed
59
Q

What are the features of Acute Pancreatitis?

A
  1. Acute onset Pain - epigastric / LUQ / radiates to back or L-shoulder / tender abdomen + voluntary guarding
    • Pain is severe, dull, constant, curling into ball may help
  2. Nausea + vomiting - can cause dehydration, oliguria, hypotension
  3. Hx of gallstones or binge-style alcohol consumption
  4. Can be jaundiced (severe gallstone pancreatitis)
  5. Recent ERCP
  6. Medications:
    1. Thiazide diuretics
    2. Furosemide
    3. Azathiprine (immunosuppresant used in RA, Crohn’s, UC and kidney transplant)
60
Q

Which pancreatic enzymes are ↑ in blood during Pancreatitis?

A
  1. Amylase - digests starch/carbohydrates
  2. Lipsae - digests fats
61
Q

In a pt with biliary tract obstruction, eating what type of food can cause pain to worsen/flair up?

A

Fatty food

  • Bile is secreted into the duodenum to aid fat digestion
  • If bile is secreted against a biliary obstruction the peristalsis of the biliary tract causes pain
62
Q

The presence of 3 out of 5 signs is strongly suggestive of Liver Cirrhosis,

What are the five possible signs?

A

3 out of 5 - indicates liver cirrhosis

  1. Spider Naevi
  2. Palmar Erythema
  3. Hepatomegaly
  4. Splenomegaly or Ascites
  5. Abnormal collateral veins in abdomen
63
Q

What might precipitate decompensation in previously stable liver cirrhosis?

A
  1. Infection
  2. Alcoholic Binge
  3. GI bleed
  4. Hypoglycaemia
64
Q

An Ascitic tap is performed an the serum ascitic albumin gradient (SAAG) measured - how is this calculated?

A

SAAG = (serum albumin) - (ascitic fluid albumin)

  • High SAAG ( > 1.1 g/dL) –> suggests ascitic fluid is transudate
  • Low SAAG ( g/dL) –> suggests ascitic fluid is exudate
65
Q

A ascitic tap is performed and the SAAG is > 1.1 g/dL

what does this indicate?

A

Transudate ascitic fluid due to portal hypertension

66
Q

A ascitic tap is performed and the SAAG is

what does this indicate?

A

Exudate ascitic fluid

67
Q

A ascitic tap is performed and microscopy shows

> 500 white cells per mm3, what does this indicate?

A

Spontaneous Bacterial Peritonitis (SBP)

68
Q

What are the key features of Conjugated hyperbilirubinaemia?

A

Conjugated hyperbilirubinaemia:

Features:

  1. dark urine
  2. pale stools
  3. pruritis (itching)
69
Q

What are the 2 most common causes of acute pancreatitis?

A

The two most common casues are:

  1. Gallstones
  2. Alcohol related
70
Q

What blood test can be done in suspected cases of or to screen for hepatocellular carcinoma (HCC)?

A

Serum Alpha-fetoprotein

71
Q

What are some causes of a low SAAG on an ascitic tap?

A
  • Malignancy
  • Infection
  • Pancreatitis
  • Nephrotic syndrome

Year 4 - GP (18 decks)

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