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Gastrointestinal > Jaundice > Flashcards

Jaundice Flashcards

1
Q

What is jaundice and what causes it?

generally

A

Jaundice is characterised by a yellow pigmentation of the skin and sclera, caused by high levels of bilirubin (<50uM/l).

Bilirubin is a by-product of RBC breakdown. Once formed, bilirubin is made water soluble (conjugated) by the liver and is then excreted in the urine and stools (causes stools to be pale).

A raised total bilirubin is usually due to:
• Increased breakdown of RBC’s
• Liver disease
• Blocked passage of bile to the gut (not excreted)

The causes of jaundice can therefore be divided into pre-hepatic, intra-hepatic and post-hepatic.

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2
Q

What are the causes of unconjugated hyperbilirubinaemia?

A
  • Haemolytic anaemia (Increased RBC breakdown)
  • Impaired hepatic uptake (drugs, CCF,
  • Impaired conjugations Gilbert’s syndrome, neonatal jaundice)
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3
Q

What are the causes of conjugated hyperbilirubinaemia?

A
  • Hepatocellular dysfunction (liver disease)

* Impaired hepatic secretion (cholestasis)

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4
Q

What are the Pre-hepatic causes of jaundice? (x7)

A 
Haemolytic anaemia
( Sickle cell anaemia) Hereditary spehrocytosis
Thalassaemia
Malaria
Gilbert's syndrome
Crigler-najjar syndrome
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5
Q

What causes haemolytic anaemia?

A

increased breakdown of RBC’s causes an increase in bilirubin. The liver cannot conjugate all the bilirubin so excess bilirubin is unconjugated.

There are many causes of haemolytic anaemia, including:
• Drug -induced
• Autoimmune
• Infection e.g. malaria
• Glucose-6-phosphate dehydrogenase (G6PD) deficiency
• Pyruvate kinase deficiency
• Hereditary spherocytosis:
• Haemoglobinopathies (Sickle-cell disease & Thalassaemia)

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6
Q

What is thalassaemia?

A

Thalassaemia is a hereditary condition production abnormal forms of haemoglobin. This results in an increased destruction of RBC’s and consequential rise in bilirubin.

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7
Q

What is hereditary spherocytosis?

A

Spherical shaped RBC’s that become trapped in the spleen and eventually are destroyed i.e. reduced lifespan

Therefore RBC’s breakdown more rapidly and bilirubin increases.

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8
Q

What is Gilbert’s syndrome?

A

Gilbert’s syndrome is a congenital hyperbilirubinaemia

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9
Q

What is Crigler-Najjar syndrome?

A

Crigler-Najjar syndrome is a genetic condition causing an enzyme deficiency. This enzyme moves bilirubin out of the blood into the liver.

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10
Q

What are the characteristics of pre-hepatic jaundice?

A 
Urine: Normal
Faeces: Normal
Bilirubin: increased unconjugated
ALP: normal
AST/ALT: normal
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11
Q

What are the causes of intra-hepatic jaundice?

A
  1. Viral hepatitis (A-E)
  2. Epstein Barr Virus
  3. Autoimmune hepatitis
      1. Liver disease (alcoholic/fatty)
  5. Hepatic cancer
  6. Dubin-johnson syndrome
  7. Haemochromatosis
  8. Wilson’s disease
  9. Drug misuse e.g. paracetamol
  10. Alpha-1 anti-trypsin deficiency
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12
Q

What are the characteristics of intra-hepatic jaundice?

A 
Urine: Dark (variable)
Faeces: Pale (variable)
Bilirubin: ↑ conjugated
ALP: ↑
AST/ALT: ↑↑
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13
Q

What does viral hepatitis result in?

A

Acute hepatitis has only 3 possible developments; recovery, chronic hepatitis or fulminant hepatitis.

Acute hepatitis patients present as generally unwell, jaundiced with RUQ pain.

Severe acute hepatitis patients present with confusion, coagulopathy and renal impairment

Blood tests are as follows:

  • Raised ALT/AST (often >1000)
  • Raised bilirubin

Chronic hepatitis causes an increase in fibrosis and eventually cirrhosis. It is a low-grade inflammation of the liver and is usually asymptomatic. The detection is usually based on abnormal LFT’s (mild elevation of ALT), screening or patients with cirrhosis.

Fulminant hepatitis is acute hepatitis associated with liver failure It is technically defined as the development of encephalopathy within 28days of jaundice. This has a poor prognosis which often needs transplantation.

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14
Q

Hepatitis A

  • how is it spread?
  • symptoms?
  • Immunisation?
  • Treatment?
  • Tests?
A
  • Hepatitis A is spread faeco-orally and is currently an endemic in the developing world. Hepatitis A is easily spread as the patients are asymptomatic but contagious. Due to this it is common in childhood.

Symptoms: fever, malaise, anorexia, nausea, jaundice, hepatosplenomegaly, adenopathy

Immunisation offered to travellers or those with other liver disease?

Treatment not needed. Avoid alcohol.

Tests: AST +ALT rise 20-40 days after exposure and return to normal over 5-20weeks.
IgM increases quickly in acute infection and reduced after a few weeks. IgG increases slowly
Therefore IgM positive = acute infection
IgG positive, IgM negative = Previous infection

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15
Q

Hepatitis B

  • Spread?
  • Symptoms
  • Immunisation?
  • Tests?
A

Spread: Vertical transmission (mother to child), Sexual spread, Blood (IVDU, medical)

Symptoms: Arthralgia, urticaria, fever, malaise, anorexia, nausea, jaundice, hepatosplenomegaly, adenopathy

Immunisation available

Tests:
HBsAg (surface antigen) is present 1-6 months after exposure. HbsAg >6 months defines carrier status.
HBeAg (e antigen) is present fro 1-3 months after acute illness and implies high infectivity.
IgM Anti-Hbc increases early in acute infection.

Treatment: Avoid alcohol. immunize sexual contacts. Anti-virals (pegylated interferon alpha-2a, lamivudine, entecavir, adefovir).

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16
Q

How can Hepatitis B progress and what % do?

A

Approx. 70% of acute hepatitis B will recover

1% –> Develop fulminant hepatitis (–> transplantation/death)

30% –> Chronic hepatitis, (–> increased fibrosis –>cirrhosis –> cancer).

Determinants for progression to chronic Hep B:

  • Immunosuppression
  • Age (<1 year = 90% chronic, 1-5 years = 30%)
  • Route of infection
  • Genotypes
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17
Q

Hepatitis C

  • Spread?
  • Symptoms?
  • Tests?
A

Spread: Blood, transfusions, IV drug use, sexual transmission, acupuncture.

Symptoms: early infection is often asymptomatic

Tests: LFT, anti-HCV antibodies confirm exposure, HCV-PCR confirms ongoing infection/chronicitiy.

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18
Q

How can Hepatitis C progress?

A

Approximately 25% of patients with hepatitis C will recover.

Acute hepatitis C will never cause fulminant hepatitis.

Approx. 75-85% will develop chronic hepatitis C (–> increasing fibrosis –> cirrhosis).

Approx 25% will develop cirrhosis in 20 years, and of these 4% will develop hepatocellular cancer

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19
Q

Hepatitis D:

  • Spread?
  • Tests?
  • Treatment?
A

Hepatitis D is an incomplete RNA virus (needs HBV for its assembly).

Immunisations: HBV vaccinations prevents HBD infections

Tests: Anti-HDV antibody (only asked for if HBsAG is positive)

Treatment: interferon-alpha , liver transplantation

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20
Q

Hepatitis E

A

RNA virus, similar to HAV. Associated with pics. No specific treatment. Mortality is high in pregnancy.

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21
Q

What is EBV?

A

Epstein-Barr virus is best known as the cause of infectious mononucleosis (glandular fever). It is also associated with particular forms of cancers (Hodgkin’s lymphoma, Burkitt’s lymphoma, gastric cancer and nasopharyngeal carcinoma), and autoimmune diseases (SLE, MS, rheumatoid arthritis, Sjogren’s syndrome).

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22
Q

What is Autoimmune hepatitis?

A

The disease is strongly associated with anti-smooth muscle autoantibodies and mimics viral hepatitis but without a viral infection.

Symptoms: fever, jaundice, right upper quadrant abdominal pain.

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23
Q

What is the recommended guidelines for alcohol intake?

A

Men and women should not drink more than 14 units of alcohol/week and this should be spread over more than 3 days. However, there is no safe level of alcohol consumption.

10ml of pure alcohol is equivalent to 1 unit
-1 pint of lager: 2 units
-1 measure of spirit = 1 unit
-1 small glass of wine = 1 unit
-1 medium glass of wine = 2 units
It takes an average adult around an hour to process one unit of alcohol so that there’s none left in their bloodstream

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24
Q

How does alcohol react with marijuana?

A

Alcohol can cause the body to absorb the active ingredient, tetrahydrocannabinol, faster and therefore increases the effect of cannabis.

Dizziness, nausea and vomiting, Panic, anxiety or paranoia

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25
Q

How does alcohol react with cocaine?

A

Increase the risk of heart attacks, fits and sudden death

The two drugs interact to produce a highly toxic substance called cocaethylene which increases the depressive effect of alcohol and increases the reaction to cocaine

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26
Q

How does alcohol react with ecstasy (MDMA)?

A

Alcohol can deaden the ‘high’ felt from ecstasy but worsens the ‘come down’ the next day.

Ecstasy and alcohol both dehydrate you and therefore the risk of overheating and becoming dangerously dehydrated when combining the two increases.

27
Q

How does alcohol react with amphetamines (speed)?

A

Increased respiratory rate, blood pressure and heart rate.

Speed increases the bodies temperature and causes dehydration

Alcohol and speed intensify emotions causing a loss of inhibitions.

28
Q

How does alcohol react with heroin?

A

Heroin is a depressant so decreases heart rate and respiratory rate. Alcohol is also a depressant and therefore increases the risk of overdosing.

29
Q

How does liver disease occur?

A

Exposure to alcohol or obesity will cause the liver to become fatty (steatosis). At this point, if these factors are abstained then the liver will return to normal (i.e. reduce weight, reduced alcohol intake). If the liver has continuous exposure, then it will become inflamed and fibrosis will occur – steatohepatitis. Abstinence can reverse the liver to a fatty liver  normal liver.

Acute inflammation of the liver is known as alcoholic hepatitis and can cause hospital admission. The patient will present with jaundice, a large tender liver and vomiting. Usually the patient will feel so unwell that they stop drinking alcohol and enter alcohol withdrawal – therefore, often the patient can be acutely ill from acute hepatitis with associated liver failure and alcohol withdrawal symptoms.
Note: you don’t need a fatty liver to develop alcoholic hepatitis, it can develop directly from a normal liver is the exposure is severe i.e. large quantities of alcohol. Severe liver failure can precipitate liver inflammation, failure and eventually death (even in the absence of cirrhosis).

If the patient continues the exposure after the liver becomes fatty, the liver will develop steatohepatitis (low grade inflammation associated with fatty infiltration). Alcoholic hepatitis and steatohepatitis with continued exposure will lead to the laying down of fibrous tissue, and this fibrotic development will lead to the development of cirrhosis (a complete change to the architecture of the liver).
Patients in the early stage of liver cirrhosis may remain compensated for and present late. As the cirrhosis develops, the liver functions decrease and the liver starts to decompensate. Signs of decompensation are; jaundice, ascites, encephalopathy, variceal bleeding. Once the patient starts to decompensate, their life expectancy decreases significantly – he/she may only have a 50% chance of a 2-year survival and require an immediate transplant.

30
Q

How is alcoholic liver disease treated?

A
  1. Exclude alternative causes of liver disease in people with a history of harmful or hazardous drinking who have abnormal LFT
  2. Refer to a specialist experience in the management of alcohol-related liver disease
  3. Consider liver biopsy
  4. Refer for consideration of liver transplant
  5. Offer corticosteroid treatment to people with severe alcohol-related hepatitis and a discriminant function of 32+
  6. Provide nutritional support to the patients
31
Q

What causes liver cirrhosis?

A

When cells are damaged and die off, the tissue present becomes fibrotic. This means it becomes thickened with bands of collagen and forms scar tissue. When the hepatocytes are damaged by alcohol (alcoholic liver disease), viruses (hepatitis) or other causes, the liver destruction and inflammation causes chronic scarring which is irreversible and fibrotic. This process is called cirrhosis. Because cirrhosis is irreversible, it is often referred to as “end-stage” damage.

32
Q

How does liver cirrhosis occur?

A

When the hepatocytes are damaged they come together to form regenerative nodules (colonies of living cells) and these are a classic sign of cirrhosis. Fibrotic tissue and collagen is present between the regenerative nodules as a ‘banding’ appearance.

Fibrosis is a process mediated by stellate cells which sit between the sinusoid and hepatocytes (perisinusoidal space). Stellate cells normally store vitamin A and are otherwise quiescent. When hepatocytes are damaged these release paracrine factors which activates the stellate cells. When the stellate cells are activated they lose the vitamin A, proliferate and start to secretes TGF β-1. This causes them to start producing collagen and scar tissue. As the scar tissue thickens, it compresses the portal vein and sinusoid. It is thought that in a healthy cell, the stellate cells are involved in wound healing, but when the hepatocytes are constantly injured, the stellate cells are involved in constant fibrosis.

As the stellate cells continue to compress the portal vein, the pressure within begins to increase – portal hypertension. Portal hypertension means that fluid in the vessel is more likely to be pushed into the surrounding tissue and then into large open spaces.

The fluid moves into the peritoneal cavity and causes ascites (excess peritoneal fluid). Ascites can lead to complications such as congestive splenomegaly, where the spleen becomes enlarged because the excess fluid cannot enter the liver and instead backs up into the spleen.

A port-systemic shunt occurs when the circulation diverts blood away from the liver, due to the high liver pressure (blood flow follows the path of least resistance). This causes an increase in renal vasoconstriction, which decreases blood flow through the kidneys and consequently decreased filtration, and eventually hepatorenal failure (kidney failure after liver failure).

The fibrotic tissue, pressure increase and blood diversion reduced the number of functional sinusoidal veins and the number of functional portal triads in general (bile duct, portal vein, hepatic artery). As the liver functional units decrease, the liver becomes less capable of detoxification. This allows toxins, which aren’t detoxified by the liver, to enter into the brain – hepatic encephalopathy.

33
Q

What are the consequences of liver cirrhosis?

A

Congestive splenomegaly (excess fluid cannot enter the liver, and instead backs up into the spleen)

Ascites (excess peritoneal fluid)

Portosystemic shunt –> renal vasoconstriction -> decreased kidney blood flow –> decreased filtration –> Hepatorenal failure

Reduced liver function –> reduced detoxification, –> toxins increased and enter the brain –> hepatic encephalopathy

34
Q

What is Dubin-johnson syndrome?

A

Dubin-Johnson syndrome is a rare autosomal recessive benign disorder that causes an isolated increase of conjugated bilirubin in the serum. The condition causes a black liver due to the deposition of a pigment similar to melanin. This condition is associated with a defect in the ability of hepatocytes to secrete conjugated bilirubin into the bile.

35
Q

Which drugs are associated with jaundice?

A

Haemolysis –> anti-malarial

Hepatitis

  • -> Paracetamol overdose
  • -> Isoniazid, rifampicin, pyrazinamide (TB ABX)
  • -> Sodium valproate
  • -> Statins

Cholestasis

  • -> Fllucloxacillin
  • -> Co-amoxiclav, nitrofurantoin,
  • -> Sulphonylureas
  • -> Procholperazine (anti-emetic)
36
Q

What is Haemochromatosis?

A

Haemochromatosis is an accumulation of iron in the body. Hereditary haemochromatosis and transfusional iron overload are the most important causes

37
Q

What is Wilson’s disease?

  • Signs
  • Investigations
  • Treatment
A

Wilson’s disease is a : a rare genetic disorder that causes copper poisoning in the body, due to the liver being unable to remove the excess copper build up. The extra copper then accumulates in the brain, liver and eyes.

It is an autosomal recessive disorder of a gene on chromosome 13 that codes for a copper transporting ATPase. In Wilson’s disease, intestinal copper absorption and transport into the liver are increased, but excretion of copper is impaired so accumulates in the liver and later in other organs/
Signs: Child present with liver disease (hepatitis cirrhosis fulminant liver failure). Young adults present with CNS signs; tremor, dysarthria, dysphagia dyskinesia, dystonia, purposeless stereotyped movements (e.g. hand capping), dementia parkinsonism, ataxia/clumsiness.
Investigations: Urine copper excretion, LFT’s, Serum copper, molecular genetic testing, liver biopsy, MRI
Management: Diet changes, lifelong penicillamine, liver transplant, screen siblings

38
Q

What is alpha-1 anti-trypsin deficiency?

  • Tests
  • Management
A

α-1 anti-trypsin deficiency is an autosomal recessive inherited conformational disease that can fatal. It commonly affects lungs (emphysema) and liver (cirrhosis and hepatocellular cancer). A-1AT deficiency s the main genetic cause of liver disease in children. Patients often present with dyspnoea, cirrhosis or cholestatic jaundice.
Tests: serum α-1 anti-trypsin levels, liver biopsy, phenotyping.
Management: smoking cessation, Treat emphysema, COPD and liver cirrhosis, liver transplantation

39
Q

What are the causes of post-hepatic jaundice?

A
  1. Cholelithiasis (gallstones)
  2. Tumour of the pancreas head
  3. Gallbladder cancer
  4. Cholangiocarcinoma (bile duct cancer)
  5. Pancreatitis
  6. Primary Sclerosis cholangitis
  7. Primary biliary cirrhosis
40
Q

Gallstones:

  • what are they?
  • How do they form?
A

Gallstones are small stones that form in the gallbladder. Gallstones are very common and are generally asymptomatic. They become symptomatic when they cause obstructions - usually in the cystic duct, common hepatic duct or common bile duct. Obstructions caused by jaundice cause cholecystitis (inflammation of the gallbladder). Gallstones arise when there is an imbalance in the chemical make-up of bile inside the gallbladder. They normally form when there are unusually high level of cholesterol or unusually high levels of bilirubin.

41
Q

What are the signs and symptoms of gallstones?

A

Signs and symptoms: rightupper quadrant pain, jaundice, fever

42
Q

What are the risk factors for gallstones (cholelithiasis)?

A 
Female
Forty-fifty
Fat
Fair-skinned
Fertile
43
Q

What is the treatment for gallstones?

A

o Active monitoring

o Laparoscopic or open Cholecystectomy

o ERCP (endoscopic retrograde cholangio-pancreatography) – endoscopy into the stomach and into the 2nd part of the duodenum where a wire is passed through the sphincter of oddi at the ampulla of vater to travel up the CBD and biliary system.

o Medications: Ursodeoxycholic acid tablets

o Improve diet by decreasing fat intake

44
Q

How does pancreatic cancer present?

A

Tumour of the pancreas head causes obstruction/narrowing of the common bile duct when entering into the ampulla of vater at the 2nd part of the duodenum.

Signs and symptoms:
 Painless Jaundice
 Pale stool, dark urine
 Weight loss

45
Q

What are the characterisitics of post-hepatic jaundice?

A 
Urine: Dark
Faeces: pale
Bilirubin: ↑ Conjugated
ALP: ↑↑
AST/ALT: normal
46
Q

How does gallbladder cancer and cholangiocarcinoma (bile duct cancer) cause jaundice?

A

Tumours prevent excretion of bile

47
Q

What is the role of the pancreas and what are the consequences of a poor functioning pancreas?

A

The pancreas is in the upper abdomen, directly posterior to the stomach. It is normally 10-12inches long and 2 inches wide. The pancreas is comprised of pancreatic ducts which join the common bile duct to release fluid into the ampulla of vater in the duodenum. The pancreas has 4 sections

The pancreas has 2 types of functions. The first is an endocrine function – to produce chemicals (hormones) that regulate blood sugar (e.g. glucagon, insulin, somatostatin, pancreatic polypeptide). The second is an exocrine function to produce enzymes that help digest our food e.g. pancreatic amylase (digest carbohydrates into glucose), protease (protein –> amino acids), and lipases (lipids –> glycerol and fatty acids). The digestive enzymes are release into the pancreatic duct to be released into the duodenum and there digest the food. Bile from the gallbladder reduces the size of the lipids so that it is easier for lipase to digest the lipids.

Consequences of a poor functioning pancreas include:

  • Diarrhoea, Bloating, Flatulence, Oily and foul-smelling stool
  • Weight loss, Malnutrition
  • Poor blood sugar control, Diabetes
48
Q

What are the risk factors for decreased pancreas function?

A
  • High alcohol consumption
  • High fat diet
  • Overweight/obesity
  • Use of tobacco products
  • Genetic predisposition e.g. cystic fibrosis.
49
Q

What is meant by acute pancreatitis and what causes it?

A

Acute pancreatitis means that the pancreas suddenly becomes inflamed and presents with intense pain. 5% of cases may be life threatening. In acute pancreatitis, the enzymes produced in the pancreas (amylase, protease and lipase) lose their protective coating before the leave the pancreas and therefore start to attack and digest the pancreatic tissue – auto-digestion.

The most common cause of acute pancreatitis is heavy alcohol use (40%) and gallstones (40%). Other less common causes include: 
• Abdominal trauma
• Medications
• Infections
• Tumours
• Genetic/anatomical variants
• High triglyceride levels
• High calcium levels
• Unknown (rare)

Causes can be remembered by ‘GET SMASHED’: Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion venom, Hyperlipidaemia/ Hypothermia/ Hypercalcaemia, ERCP/Emboli, Drugs

50
Q

What are the signs and symptoms of acute pancreatitis

A
  • Sudden attacks of intense pain in the central upper abdomen (epigastric region)
  • Radiation of pain to the back
  • Can have left/right pain or lower abdominal pain
  • Nausea, vomiting
  • Fever
  • Tachycardia
  • Jaundice
  • Shock
  • Rigid abdomen +/- local/general tenderness
  • Periumbilical bruising (Cullen’s sign), Flank bruising (Grey Turner’s sign) from blood vessel autodigestion and retroperitoneal haemorrhage.
51
Q

How is acute pancreatitis investigated?

A
  • Raised serum amylase (>1000u/mL). May not be raised even in severe pancreatitis.
  • Serum lipase is more specific for pancreatitis
  • ABG: monitor oxygenation and acidd-base status
  • AXR: absent psoas shadow = retroperitoneal bleeding
  • CT scan: confirm diagnosis
52
Q

How do you assess severity of acute pancreatitis?

A

3 or more positive factors detected within 48hrs of onset suggests severe pancreatitis and should prompt transfer to ICU/HDU. Mnemonic: PANCREAS
Pa02 <8 kPa

Age >55 years

Neutrophilia WBC >15 x109/L

Calcium <2 mmol/l

Renal function - Urea >16 mmol/L

Enzymes - LDH >600iu/l, AST >200iu/L

Albumin <32g/L (serum)

Sugar >10mmol/L

53
Q

How is acute pancreatitis treated?

A
  • Nil by mouth
  • 0.9% saline
  • analgesia
  • Hourly pulse, BP, Urine output
  • Daily FBC, U&E, Ca2+, glucose, amylase, ABG
  • Remove gallstone if present
54
Q

What causes chronic pancreatitis?

A

Chronic pancreatitis is caused by long-term inflammation of the pancreas, which eventually leads to irreversible destruction of pancreatic tissue.

Chronic pancreatitis develops slowly over time and is predominantly triggered by lifestyle factors – long standing heavy alcohol use or long term heavy smoking.

Other less common causes:

  • Familial
  • Cystic Fibrosis
  • Haemochromatosis
  • Pancreatic duct obstruction
  • Congenital (pancreas divisum)
  • Medications
55
Q

What are the effects and long term consequence of chronic pancreatitis?

A

During chronic pancreatitis, the patients will be less able to absorb the nutrients from their food intake as the enzymes released from the pancreas decrease. Therefore. they can have problems digesting food or absorbing sufficient nutrients.

The long term consequences of chronic pancreatitis include;
•Malnutrition leads to nutrition-related diseased (weak bones, Vision loss)
• Difficulty maintaining or gaining weight
• Persistent pain

56
Q

What are the symptoms of chronic pancreatitis?

A

The hallmark symptom of chronic hepatitis is abdominal pain which may be intermittent or chronic and is frequently very severe. Additional intense stabbing pains in the upper abdominal region are not uncommon. The pain may radiate to the back and may be triggered by eating high fat foods. As the disease progresses, the pain may become more severe and debilitating and often becomes constant.
In some cases, surgery or endoscopic treatment may be required. Other signs and symptoms include oily, foul-smelling stools with weight loss (exocrine pancreatic insufficiency) and the development of diabetes

57
Q

How is chronic pancreatitis diagnosed?

A

Diagnosis can be challenging due to the course of the disease. A CT scan is commonly used, and an MRI or endoscopic ultrasound may be used to confirm the diagnosis. In difficult to diagnose patients, a pancreatic stimulation test is used. This involves artificially stimulating the pancreas using secretin, and pancreatic fluid is extracted and analysed over 2 hours. However, this test is expensive and invasive and is therefore not frequently used.
Blood tests are not useful in diagnosing chronic pancreatitis.
Although there is no treatment for chronic pancreatitis, there are recommendations that can have an effect if detected early enough e.g. abstinence from alcohol quit smoking, avoid high-fat foods, pain management, medication (e.g. pancreatic enzyme, multivitamin and mineral supplements.

58
Q

What is primary sclerosing cholangitis?

A

A disease of the bile ducts that cause inflammation and obliterative fibrosis of bile ducts inside/outside of the liver. It impedes the flow of bile and can lead to cirrhosis of the liver, liver failure and other complications including bile duct and liver cancer.

59
Q

What are they signs and symptoms or primary sclerosis cholangitis (PSC)?

A

Pruritus + fatigue. If advanced: ascending cholangitis, cirrhosis and end-stage hepatic failure.
Bile duct, gallbladder, liver and colon cancers are more common so yearly colonoscopy +/- ultrasound are recommended.

60
Q

How is PSC diagnosed and treated?

A

Tests: Increased ALP, then increased bilirubin. AMA will be negative but ANA, SMA and ANCA may be positive.
Treatment: liver transplant, ursodeoxycholic acid may protect against colon cancer and improve LFT’s

61
Q

What is primary biliary cirrhosis and what is it caused by?

A

Interlobular bile ducts are damaged by chronic autoimmune granulomatous inflammation causing cholestasis which may lead to fibrosis, cirrhosis and portal hypertension

Cause: unknown environmental triggers + genetic predisposition

62
Q

How does primary biliary cirrhosis present?

A

often asymptomatic and diagnosed incidentally. Lethargy, sleepiness, pruritus’, jaundice, Xanthelasma, hepatosplenomegaly

63
Q

How is primary biliary cirrhosis diagnosed, complicated and treated?

A

Tests: Anti-mitochondrial antibodies (AMA) are the hallmark of PBC, increased ALP, GGT and mildly increased AST/ALT. In late disease, increased bilirubin and prothrombin time, decreased albumin.

Complications: cirrhosis, osteoporosis, malabsorption of fat-soluble vitamins (A, D, E, K) due to cholestasis and decreased bilirubin.

Treatment: liver transplantation, symptom management, vitamin supplement, regular monitoring.

Prognosis: Once jaundice develops, survival is <2years without transplantation

Gastrointestinal (17 decks)

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