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My GI > Liver,Pancreas and biliary tree clinical > Flashcards

Liver,Pancreas and biliary tree clinical Flashcards

1
Q

What are the three types of true Liver function tests?

i.e actual liver function

A
  1. Albumin
  2. Bilirubin
  3. Prothrombin time
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2
Q

what is the normal range of albumin?

A

35-50 g/L

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3
Q

What are causes of hypoalbuminemia?

A
  1. Liver disease
  2. acute phase response ( sepsis,traumatic surgery)
  3. malabsorption
  4. malnutrition
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4
Q

What is the normal state of bilirubin in the blood?

A

unconjugated

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5
Q

What is the normal level of bilirubin?

A

<17 µmol/L

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6
Q

which clotting factor is prothrombin?

A

clotting factor II

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7
Q

What does the prothrombin time measure?

A

time to taken to convert prothrombin to thrombin ( i.e how long it takes for blood to clot)

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8
Q

What is the difference between recording Prothrombin time and albumin?

A

Prothrombin has a shorter half life and therefore is more effective in detecting acute liver disease

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9
Q

What does Vitamin K deficiency cause?

A

coagulopathy.

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10
Q

How would you exclude vitamin K deficiency being a cause for a prolonged prothrombin time?

A

Give a intravenous bolus ( 10mg) of Vitamin K

If it is due to the deficiency the PT time should decrease

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11
Q

What is the normal range for prothrombin time?

A

11.5-13.5s

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12
Q

What are transaminases?

A

Hepatic enzymes that are usually intracellular but are released from hepatocytes due to liver cell damage.

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13
Q

What are the three types of liver function tests?

i.e measure extent of liver disease

A
  1. serum transaminase
  2. Alkaline phosphatase ( ALP)
  3. Gamma glutamyl transpeptidase (GGT)
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14
Q

What are the two transaminase used in LFT?

A
  1. Aspartate aminotransferase ( AST)- mitochondrial and cytosol enzyme
  2. Alanine aminotransferase ( ALT)- cytosol enzyme
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15
Q

What are the differences between ALT and AST?

A
  1. AST- is found in mitochondria and cytoplasm. ALT only Cytoplasm
  2. ALT is more sensitive.
  3. AST is found in heart,muscle,kidney and brain. While ALT only in liver
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16
Q

In viral hepatitis what is usual AST:ALT ratio?

ii. what is the exception?

A
  1. ALT is greater than AST

ii. if Cirrhosis is present AST will be greater than ALT

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17
Q

In alcoholic liver disease and steatohepatitis what is the usual AST: ALT ratio?

A

AST is greater than ALT

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18
Q

If the AST: ALT is greater than 1 in viral hepatitis what does this suggest?

A

cirrhosis

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19
Q

If AST is greater than ALT in a patient that has liver disease without cirrhosis what is the most likely cause?

A

alcohol or obesity

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20
Q

What is the role of Alkaline phophatase?

A

Catalyses the hydrolysis of organic phosphate esters.

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21
Q

Where is Alkaline phosphatase present?

A
  1. Hepatic canalicular and sinusoidal membranes
  2. Bone
  3. Placenta
  4. Intestines
  5. Kidneys
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22
Q

What causes a rise in Serum ALP?

A
  1. Both intrahepatic and extrahepatic cholestatic disease of any cause- PBC has highest levels
  2. Hepatic infiltration ( metastases)
  3. Cirrhosis- regardless of cholestatic jaundice
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23
Q

If the GGT is abnormal and the ALP is raised where is the serum ALP presumed to come from?

A

Liver

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24
Q

What is GGT?

A

enzyme involved in Glutathione metabolism and transfer of AA across cellular membranes.

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25
Q

Where is GGT found?

A

Present in cell membranes of Liver ( and pancreas and gallbladder), kidneys and bile ducts.

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26
Q

What drugs can cause a rise in GGT?

A
  1. Alcohol
  2. warfarin
  3. phenytoin
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27
Q

What happens to GGT levels in Cholestasis?

A

Rises in parallel with ALP

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28
Q

What is GGT useful in diagnosing?

A

Liver and cholestatic diseases

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29
Q

What can cause a prolongation in Prothrombin time?

A
  1. Drugs ( warfarin)
  2. Bile malabsorption- causes relative Vitamin K deficiency
  3. Consumptive coagulopathies
  4. Congenital Coagulopathy
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30
Q

What would ALT/AST > ALP suggest?

A

Hepatocellular injury

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31
Q

What would ALP> ALT/AST suggest?

A

cholestasis

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32
Q

What is the normal ratio of AST: ALT?

A

0.8

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33
Q

What does an Alpha-1 antitrypsin deficiency suggest?

A

cirrhosis and or emphysema

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34
Q

What does a reappearance of high concentration of alpha fetoprotien suggest?

A

not pregnant:
Hepatocellular carcinoma

Can also be raised with regenerative liver tissue with:

Hepatitis
chronic liver disease
teratomas

pregnant:
Most likely fetal neural defect. As Alpha fetoprotein is normally produced in fetal liver

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35
Q

What happens to urinary copper, serum copper and caeruloplasmin levels in wilson’s disease?

A

urinary copper increase

Serum copper decrease

Caeuloplasmin decrease

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36
Q

Which immunoglobulin has the most predominant rise in its serum levels due to PBC?

A

IgM

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37
Q

Which immunoglobulin has the most predominant rise in its serum levels due to Viral hepatitis?

A

IgG predominantly

and IgG4

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38
Q

Which immunoglobulin has the most predominant rise in its serum levels due to pancreatitis and cholangiopathy?

A

IgG4

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39
Q

Anti-mitochondrial antibody is found in 95% in the serum of patients which have what?

A

PBC

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40
Q

Nucleic and smooth muscle antibodies are found in patients which have what ?

A

Autoimmune hepatitis

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41
Q

Anti-nuclear cytoplasmic antibodies are found in patients with what?

A

Primary sclerosing cholangitis

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42
Q

What does a positive dipstick test for bilirubinuria suggest?

A

Presence of conjugated bilirubin- present in patients with jaundice due to hepatobiliary disease.

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43
Q

What does a negative dipstick test for bilirubinuria suggest?

A

Jaundice is mainly caused by unconjugated bilirubin

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44
Q

What are benefits of ultrasound in diagnosing a malfunctioning liver, pancreas and gall bladder?

A
  1. Detects gallstones
  2. Detects extrahepatic obstruction
  3. assessment of jaundiced patients ( to exclude obstruction)
  4. Assessment of hepatomegaly/splenomegaly
  5. identification of cirrhosis- liver edge is irregular and spleen is often enlarge in advanced cirrhosis. However normal ultrasound does not exclude cirrhosis
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45
Q

Give examples of chronic liver disease specific symptoms.

A
  1. Right hypochondrial pain- liver distention
  2. Abdominal distention due to ascites
  3. ankle swelling due to fluid retention
  4. Haematemesis and melaena - from GI haemorrhage
  5. can be asymptomatic or non- specific symptoms ( e.g. weakness,anorexia and fatigue)
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46
Q

What is pruritus due to cholestasis an early symptom of?

A

PBC

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47
Q

Give examples of acute liver disease symptoms ( won’t be specific).

A

May be asymptomatic or anicteric( without jaundice)

  1. Malaise,anorexia and fever if the symptomatic disease is viral
  2. Jaundice may appear as the illness progresses
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48
Q

What are common signs of acute liver disease?

A
  1. Jaundice ( yellow discolouration of skin)
  2. enlarged liver
  3. In cholestatic phase- pale stools and dark urine

can have spider naevi and palmar erythema in severe acute disease

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49
Q

What are the common physical signs of chronic liver disease?

A

General:

  1. Jaundice
  2. Fever
  3. Loss of body hair

Compensated:

  1. Xanthelasma
  2. parotid enlargement
  3. Spider naevi
  4. Gynaecomastia
  5. Liver ( small or large)
  6. Liver palms
  7. clubbing
  8. xanthomas
  9. spenolmegaly (rare)

Decompensated

compensated symptoms as well as

  1. Hepatic flap
  2. Oedema
  3. Ascites
  4. dilated veins on abdomen
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50
Q

What is Jaundice also known as?

A

icterus

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51
Q

What are the most common places where jaundice is observed?

A

Mucous membranes, skin and sclera(white part of eyeball)

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52
Q

What is the main cause of jaundice?

A

plasma levels of bilirubin exceed or equal to 50µmol/L

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53
Q

What are the three types of Jaundice?

A
  1. Prehepatic
  2. hepatic (hepatocellular)
  3. post hepatic (obstructive)
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54
Q

What are the two types of bilirubin?

A

Conjugated

Unconjugated

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55
Q

What are the difference between the two types of bilirubin?

A

Unconjugated is produced after the break down of RBCs

Unconjugated bilirubin then goes into liver which conjugates it.

Unconjugated is not water soluble therefore does not enter urine

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56
Q

What are the causes of prehepatic jaundice?

A
  1. Haemolysis

2. malaria

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57
Q

What is the pathophysiology of haemolytic jaundice?

A

Increased breakdown of RBCs leads to overproduction of unconjugated bilirubin.

this overwhelms the liver to conjugate the bilirubin

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58
Q

What is the stool and urine appearance of prehepatic urine?

A

Normal colour for both

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59
Q

Which type of bilirubin is responsible for prehepatic jaundice?

A

unconjugated

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60
Q

Are the LFTs abnormal or normal in prehepatic jaundice?

A

Normal

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61
Q

What makes urine dark?

A

conjugated hyperbilirubinemia

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62
Q

What are the causes of hepatic jaundice?

A

Viral hepatitis

drug induced hepatitis ( e.g. paracetamol overdose or rifampicin)

Alcoholic induced hepatitis

cirrhosis

pregnancy

some congenital disorders e.g.

  1. Gilbert’s syndrome- mild jaundice develops asymptomatically (unconjugated)
  2. Crigler- Najjar syndrome (unconjugated)
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63
Q

What does Gilbert syndrome have on the effect of hepatocellular function?

A

Decreases levels of UGT-1 . This is an enzymes that conjugates bilirubin with glucuronic acid. Therefore allows for unconjugated hyperbilirubinemia

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64
Q

What occurs in intrahepatic jaundice?

A

Hepatocellular malfunctions allowing for a rise in both forms of hyperbilirubinemia.

Either defects in secretion of bile or intrahepatic ducts

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65
Q

What are the LFT results of intrahepatic jaundice?

A

Concentration levels of both conjugated and unconjugated bilirubin rises

AST and ALT increases

ALP increases (cholestatic related)

GGT increases

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66
Q

What is the colour of the stool and urine if the patient has intrahepatic jaundice?

A

Dark urine and slightly pale stool

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67
Q

Discuss how bilirubin is produced and excreted

A
  1. RBC’s rupture and break down. During this process the haeme is broken down to eventually produce unconjugated bilirubin
  2. Unconjugated bilirubin is bound to albumin in the blood and taken to the liver
  3. Hepatocytes absorb unconjugated bilirubin and conjugates it with glucuronic acid into conjugated bilirubin
  4. conjugated bilirubin leaves the liver via the ducts and enters small intestine
  5. Conjugated bilirubin is converted either into urobilinogen by gut bacteria or reabsorbed.
  6. some urobilinogen can be reabsorbed by the kidneys. Urobilinogen is oxidized to urobilin which makes urine yellow. dark as well as conjugated bilirubin urine ( bilirubinuria).
  7. Urobilinogen is oxidised to stercobilin which makes the pool turn brown. If stercobilin is not present then stool is pale
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68
Q

What are the causes of posthepatic jaundice?

A
  1. Gallstones
  2. Primary biliary cholangitis (PBC)
  3. Primary sclerosing cholangitis (PSC)
  4. Pancreatic cancer
  5. cholangiocarcinoma
  6. Mirizzi syndrome- compression of common bile ducts by a gallstone in the cystic duct
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69
Q

what is the cholestasis?

A

failure of normal amounts of bile being secreted and reaching the intestines.

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70
Q

What are the two types of cholestasis and what are there causes?

A
  1. Intrahepatic - Hepatic jaundice i.e hepatocellular malfunction
  2. extrahepatic- obstruction jaundice i.e. obstruction in the bile ducts
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71
Q

What occurs during post hepatic jaundice?

A

Obstruction of biliary tract leads to back flow of conjugated bilirubin back into the liver and then into blood.

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72
Q

What are the LFT results of post hepatic jaundice?

A

increase in conjugated bilirubin in blood

Major increase in ALP
GGT increase
increase in AST and ALT

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73
Q

What is the stool and urine colour in post hepatic jaundice?

A

PALE stool

Dark urine

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74
Q

What is more likely to be the cause of jaundice in a young person?

A

Viral hepatitis

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75
Q

What is more likely to be the cause of jaundice in the elderly who has gross weight loss?

A

Carcinoma

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76
Q

What history should be taken into consideration when thinking about jaundice?

A
  1. Any previous episodes of Jaundice/ family history or liver problems?- Gilbert syndrome
  2. What medication are you taking?
  3. Recent surgery on biliary tract?
  4. Have they ever had carcinoma?
  5. Intravenous drug use?- Increase of Hep B or C
  6. Alcohol
  7. Men having sex with men?- increase chance of Hep B and C
  8. Traveling?- HEP E COMMON IN TRAVELERS TO SUB INDIAN CONTINENT
    HEP A COMMON IN UK
  9. Piercings/ tattoos?
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77
Q

What are the clinical examination with jaundice related patients?

ii. state what each implies

A

Exam signs for chronic liver disease:

  1. Hepatomegaly- if smooth and tender = hepatitis or extrahepatic obstruction

if irregular- metastases and cirrhosis

  1. splenomegaly - portal hypertension in chronic liver disease
    Maybe tipped due to viral hepatitis
  2. Ascites- found in cirrhosis
  3. Palpable gallbladder- carcinoma of pancreas
  4. General lymphadenopathy- lymphoma
  5. cold sores- herpes simplex virus hepatitis
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78
Q

What investigations can be carried out for Jaundice?

A

Imaging:

Ultrasound of abdomen- exclude extrahepatic obstruction

Tests:

Liver:
LFTs

Urine :
dipstick test for absence of urobilinogen and presence bilirubinuria

Haematology:
FBC

Paracetamol levels

hapatoglobins-a plasma protein that binds small amounts of hemoglobin i.e. less = anaemia

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79
Q

What is acute liver disease?

A

rapid development of hepatic dysfunction without prior liver disease

less than 6 months duration of symptoms

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80
Q

What is chronic hepatitis?

A

Hepatitis lasting longer than for 6 months

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81
Q

What are the main causes of chronic hepatitis?

A
  1. NAFLD
  2. Alcohol induced liver disease
  3. Viral hepatitis ( B,C and D)
  4. Drugs
  5. Autoimmune
  6. Hereditary: Wilson’s disease,haemochromatosis
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82
Q

What are the infective causes of viral hepatitis?

A
  1. Hepatitis A
  2. Hep B
  3. Hep C
  4. Hep D
  5. Hep E
  6. Cytomegalovirus
  7. Herpes simplex
  8. Epstein Barr virus
  9. Yellow fever
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83
Q

Which Viral hepatitis are associated with acute hepatitis?

A

A,B,C,D,E

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84
Q

Which viral hepatitis are associated with chronic hepatitis?

A

B
C
D

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85
Q

What type of virus is Hepatitis A and what is its main route of transmission?

A

RNA virus

Faecal Oral

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86
Q

What are symptoms of Hepatitis A ?

A
  1. Fever
  2. malaise
  3. Anorexia
  4. nausea
  5. Arthralgia
    most recover however if worsens then:
    This is very rare with children
  6. jaundice
  7. hepatomegaly
  8. splenomegaly
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87
Q

Where is Hep A common?

A

endemic in africa and south america- i.e travellers beware

Most infections in Childhood

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88
Q

How long is the incubation for Hep A?

A

Short (2-3 weeks)

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89
Q

What tests confirm Hepatitis A?

A

Raised AST , ALT

Raised bilirubin(in icteric stage however)

Raised Anti- HAV IgM means acute infection

IgG is detectable for life

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90
Q

What is the prognosis of Hepatitis A?

A

HAV hepatitis never leads to chronic infection

Doesn’t cause liver cancer

Very small mortality- acute hepatic necrosis

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91
Q

How do you manage Hepatitis A?

A

control by good hygiene

Vaccination prophylaxis

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92
Q

What type of virus is Hep B ?

A

DNA virus

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93
Q

What are the forms of transmission for Hep B?

A
  1. Vertical transmission- mother to child in utero. Not through breast feeding
  2. Horizontal transmission: Minor abrasions, blood to blood, sex and drug users.
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94
Q

What does getting Hep B at an older age could potentially mean?

A

Higher risk of acute infection

lower risk of chronic infection

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95
Q

What are the four phases of chronic Hep B infection?

A
  1. immunotolerant- childhood no sign of infection
  2. immunoactive- immune response starts ( adolescents) high level of HBeAg-positive infection
  3. immunosurveillance- immune control
  4. Immunoescape- reactivation of disease however negative HBeAg
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96
Q

What are the symptoms of Hep B?

A

Acute
Similar symptoms to HAV

however arthralgia and urticaria more common

Chronic

chronic liver disease symptoms

Can be asymptomatic

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97
Q

Where is Hep B common in?

A

Far east, med and africa

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98
Q

What is its incubation?

A

Long (1-5) months)

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99
Q

What are the test results for positive Hep B?

A

antigens

HBsAg- Chronic or acute infection

HBeAg- Acute infection persistence means continued infectious state and development of chronicity

Antibodies
Anti HBs- indicates immunity either from infection or vaccination

Anti HBc IgM- acute hepatitis if high titre
chronic hepatitis if low titre

Anti HBc IgG- past exposure to Hep B (HbsAg- negative)

LFT
Raised AST and ALT but can be normal

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100
Q

How do you manage Hep B?

A

Minimise exposure- safe sex and needle exchange, screening of pregnant women. avoid alcohol

vaccination prophylaxis

Acute

Entecavir or tenofovir for persistence of HbeAg

chronic

Antiviral agents:

Interferon(most common)- used for HbeAg- positive with active disease. Shouldn’t give to those with HIV or cirrhosis

Side effects: acute-influenza like illness

Oral antiviral agents
entecavir and tenofovir - excellent for both HBeAg- positive and negative patients. Few side effects

However unlike interferon most patients require very prolonged treatment even lifelong.

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101
Q

What are the potential effects of Hep B?

A

Acute

acute liver failure(adult)
or can develop into chronic hepatitis

chronic
If an active carrier:
Cirrhosis

Hepatocellular carcinoma with or without cirrhosis

Fulminant hepatic failure

Inactive carrier: unlikely to develop chronic liver disease resolution of liver can occur

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102
Q

What type of virus is Hep D?

A

incomplete RNA particle

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103
Q

Which virus activates Hep D to cause replicate?

A

Hep B

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104
Q

How do you diagnose Hep D?

A

Acute:

IgM anti-HDV in the presence of IgM anti- HBc

HDV RNA- early sign of infection

chronic :

Anti HDV with patients who are HBsAg- positive

HDV RNA

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105
Q

What are the effects of Hep D?

A

acute:

Acute hepatic failure

chronic:

cirrhosis

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106
Q

How do you manage Hep D?

A

Prevention: Hep B vaccination prevent Hep D

treatment: pegylated interferon- alfa 2a has limited effect on Hep D

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107
Q

What type of virus is Hep C?

A

RNA virus

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108
Q

How is Hep C transmitted?

A

Blood: transfusion- high with people who have haemophilia
IV drugs
sex- limited

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109
Q

Where is Hep C found?

A

UK, Africa Asia

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110
Q

Acute Hep C normally leads to chronic true or false?

A

true

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111
Q

What are the symptoms of Hep C?

A

Acute

  1. Acute infections are mainly asymptomatic
  2. Jaundice

Chronic:

Asymptomatic

malaise
fatigue
arthritis

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112
Q

How do you diagnose Hep C?

A

AST:ALT ratio less than 1 until cirrhosis

Acute

HCV RNA can be detected from 1 to 8 weeks after infection

anti HCV antibodies

Chronic

anti HCV antibodies

PCR used to detect HCV RNA in serum

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113
Q

What is the incubation for Hep C?

A

Long

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114
Q

How do you manage Hep C?

A

NO VACCINE

Antivirals
Acute:
If HCV RNA level does not decline then use peg interferon with or without ribavirin must be decided

chronic:

peg interferon alpha usually with ribavirin (and a (protease inhibitor such as telaprevir for genotype 1)

or depending on genotype can use:

Genotype 1: sofosbuvir with ( protease inhibitor) simeprevir or an NS5A inhibitor ( ledipasvir) can cure 90% of patients
more effective than interferon

genotype 2- sofosbuvir with ribavirin cure 90% of patients more effective than interferon

For genotype 3- interferon with ribavirin is prefered

side effects of telaprevir - rash and anaemia

side effects of boceprevir- anaemia

major side effects of interferon- psychosis and autoimmune (rare)

minor side effects of interferon- flu like symptoms

side effects of Ribavirin- haemolysis and pruritus(itch)- starting to be phased out at being used

HCV screening

stop drinking

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115
Q

What are the effects of Hep C?

A

Acute

Higher Majority of asymptomatic patients go on to have chronic liver disease than symptomatic ones.

Chronic:

Fibrosis than to cirrhosis

HCC - has to be with cirrhosis

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116
Q

What type of virus is Hep E?

A

RNA virus

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117
Q

How is Hep E transmitted?

A

contaminated water

found in 30% of dogs, pigs and rodents

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118
Q

What are the clinical symptoms of Hep E?

A

Very similar to Hep A

Does not cause chronic hepatitis unless patient is immunosuppressed

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119
Q

How do you diagnose Hep E?

A

IgG and IgM Anti-HEV

HEV RNA found in serum and stool via PCR

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120
Q

What are the potential effects of Hep E?

A

mortality from Fulminant hepatic failure usually very low however rises to 20% in pregnant women

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121
Q

How do you treat Hep E?

A

Vaccination in China

good sanitation

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122
Q

What are the symptoms of Epstein Barr virus causing Hepatitis?

A

Mild Jaundice

5 days of onset

causes glandular fever

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123
Q

How do you diagnose EB hepatitis?

A

Paul-bunnell test is positive and atypical lymphocytes are present in peripheral blood

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124
Q

What are the symptoms of Cytomegalovirus hepatitis?

A

Glandular fever type symptoms

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125
Q

How do you diagnose cytomegalovirus?

A

CMV DNA is positive

CMV igM is also positive( can have false positives)

liver biopsy shows intranuclear inclusions and giant cells

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126
Q

How do you treat herpes simplex?

A

aciclovir

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127
Q

What is the definition of liver failure?

A

liver injury with development of encephalopathy and coagulopathy( INR > 1.5) which occurs both acutely and late onset

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128
Q

How is acute liver failure defined?

A
  1. 7 days= hyperacute

1- 4 weeks = acute

4-26 weeks= sub acute

2.
Based on development of encephalopathy after onset of any hepatic symptom

within 8 weeks= Fulminant hepatic failure

between 8-26 weeks = subfulminant

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129
Q

What is chronic liver failure associated with?

A

cirrhosis

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130
Q

What are the causes of acute hepatic( liver ) failure?

A 
1. Viral hepatitis ( HCV is uncommon only in asia)
A
B
C
D
E
cytomegalovirus
EBV
  1. Drugs - paracetamol overdose common cause in UK

antibiotics
NSAIDs

  1. Toxins
    Amanita phalloides- mushroom toxin
  2. Hepatic failure in pregnancy- mainly acute fatty liver of pregnancy
  3. Vascular causes

ischaemic hepatitis

Budd-Chiari syndrome

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131
Q

what are the clinical features of acute hepatic failure?

A
  1. Jaundice
  2. hepatic encephalopathy
  3. Fetor Hepaticus ( smells like pear drops)
  4. fever, vomiting ,hypotension and hypoglycemia
  5. mental state varies from slight drowsiness to coma
  6. ascites and splenomegaly are rare
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132
Q

What tests should be carried out for suspected AHF?

A
  1. hyperbilirubinemia
  2. high level AST and ALT levels and INR/PT (LFT)
  3. paracetamol level
  4. FBC
  5. U&E

Imaging

abdominal ultrasound will define liver size

EEG for encephalopathy

doppler flow studies of the portal vein (and hepatic veins if Budd-chiari syndrome suspected)

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133
Q

How do you manage AHF?

A

No main treatment but treat cause if possible

  1. Important patients put in specialised unit for treatment
  2. Tilt head 20 degrees to deal with encephalopathy
  3. check FBC, U&E, LFT and INR daily

Treat complications

Cerebral oedema- 20% mannitol iV

Ascites- restrict fluid

Coagulopathy: Vitamin K IV 10mg, platelets and blood or fresh frozen plasma

prophylaxis against bacterial and fungal infection

potentially a liver transplant based on severity

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134
Q

What is the prognosis of AHF?

A
  1. cerebral oedema forms in 80% of patients however less common in subacute- 25% of deaths
  2. Bacterial and viral infections lead to death
  3. GI bleeding
  4. respiratory arrest
  5. kidney injury ( hepatorenal syndrome)
  6. Grade 1-2 encephalopathy( Altered mood- increasing drowsiness) -2/3 of patients survive
  7. grade 3-4 ( incoherent, stupor- coma) and drug induced liver failure have a worse prognosis
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135
Q

What are the causes of Autoimmune hepatitis?

A

Unknown however it is defined by abnormal of T cell function and antibodies attacking liver cell surface antigens

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136
Q

What are the symptoms of Autoimmune hepatitis?

A
  1. can be asymptomatic
  2. jaundice( fever, rash,malaise, urticaria and arthralgia). stool colour and urine change too
  3. some can have Autoimmune disease
  4. some can have acute hepatitis ( type II Autoimmune Hep)
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137
Q

How do you diagnose autoimmune hepatitis?

A

ALT and AST high levels

ALP high

IgG is very high ( double value)

PT often high

Autoantibodies

Type 1: anti nuclear (ANA) and Anti- actin (AMSA) both very high

Type 2: anti-liver/kidney also very high (anti-LKM1)

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138
Q

How do you treat autoimmune hepatitis?

A

immunosuppressant therapy: prednisolone 30 mg 2-4 weeks then lower to maintenance dose of 5-15 mg

for steroid-sparing agent then azathioprine main one used- sole long-term therapy and used for maintenance

liver transplantation if failed to respond or decompensated cirrhosis

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139
Q

what are the two types of autoimmune hepatitis?

A

Based on autoantibodies present

Type I- typical patient (80%) usually found in women younger than 40. ANA and AMSA is positive but respond well to immunosuppressants. 25% present with cirrhosis

Type II- more often older children and young adults. More common cirrhosis Anti-LKM1 positive. worse

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140
Q

what is the prognosis of autoimmune hepatitis?

A

80% of patients induce remission due to immunosuppression

HCC less frequent than viral-induced cirrhosis

can cause cirrhosis

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141
Q

What are the risk factors for Non -alcoholic fatty liver disease (NAFLD)?

A
  1. Obesity
  2. Hypertension
  3. type 2 diabetes
  4. old age ( progression)
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142
Q

What are the symptoms of NAFLD?

A
  1. Most asymptomatic
  2. Hepatomegaly may be seen
  3. inflammation of liver due to fat deposition
  4. jaundice
  5. cirrhosis
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143
Q

What are the causes of NAFLD?

A
  1. deposition of fat causing inflammation of the liver causing Non alcoholic steatohepatitis( NASH)
  2. Fibrosis of liver due to normal steatosis (fatty liver)
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144
Q

How do you diagnose NAFLD?

A

Ultrasound detects steatosis if not drinking

Liver biopsy stages of disease of steatosis

elastography can be used to detect degree of fibrosis

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145
Q

What is the staging of NAFLD?

A
  1. Steatosis (fat deposition of liver causing fatty liver)
  2. advanced fibrosis
  3. cirrhosis

Hepatitis of fatty liver ( NASH)- severe form of NAFLD

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146
Q

How do you manage NAFLD?

A

Lifestyle advice ( no alcohol, lose weight)

vitamin E - antioxidant that improves steatohepatitis. increase risk of Prostate cancer and stroke and mortality ( if above 400 IU/day)

pioglitazone also used against NASH only improves like vitamin E no cure

Bariatric surgery- not to be used if advanced cirrhosis or portal hypertension present

orlistat- causes malabsorption of dietary fat- fat soluble vitamin deficiency may occur

NASH indication for liver transplant ( 3rd highest in U.S)

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147
Q

What is the prognosis of NAFLD?

A

HCC is caused by NASH

cirrhosis

Risk factors of NAFLD are causes for many issues not just hepatic related:

obesity is cause for many malignancies

Type II diabetes

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148
Q

What is cirrhosis?

A

Scarring of liver from chronic liver disease

condition where liver responds to hepatocellular injury/necrosis and replaces damaged tissue with interlacing strands of fibrous tissue which separates regenerating nodules of functioning liver.

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149
Q

What is the shape of the liver in cirrhosis?

A

tawny coloured

small shrunken

hard

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150
Q

What are the two types of clinical cirrhosis?

A

Compensated

Decompensated

151
Q

What are differences between the two types of clinical cirrhosis?

A

compensated - clinically normal but histologically have cirrhosis. mildly abnormal blood tests can have portal hypertension.

decompensated- histologically have cirrhosis and have acute on chronic liver failure( infection causing insult- able to be treated and liver can be fixed) or end stage liver disease ( chronic liver failure)- not able to be fixed as to far down.

152
Q

What are the causes of cirrhosis?

A
  1. Alcohol
  2. Hep B(D) and C
  3. NAFLD ( particulary NASH)
  4. Wilson’s disease
  5. Budd-Chiari
  6. PBC
  7. secondary biliary cirrhosis
153
Q

What are the symptoms of cirrhosis?

A

Compensated:

  1. Xanthelasma
  2. parotid enlargement
  3. Spider naevi
  4. Gynaecomastia
  5. hepatomegaly or small liver if late disease
  6. Liver palms
  7. clubbing
  8. xanthomas
  9. spenolmegaly (rare)

Decompensated
all compensated symptoms and
1. Hepatic flap

  1. Oedema
  2. Ascites
  3. dilated veins on abdomen
154
Q

What are the potential complications of Cirrhosis?

A
  1. Coagulopathy
  2. encephalopathy
  3. oedema
  4. Portal hypertension
  5. ascites
  6. splenomegaly
  7. Variceal bleeding
  8. HCC - 2-5% third commonest death in tumours worldwide
  9. portosystemic shunt
  10. caput medusae- enlarged superficial periumbilical veins
155
Q

why in liver cirrhosis does ascites occur mainly in the abdomen?

A

because of the low albumin and very higher pressure from portal system
(large hydrostatic pressure of capillaries [Pc], low osmatic drive of capillaries [pieC])

156
Q

What tests should you carry out to diagnose cirrhosis?

ii. what are the results?

A

LFT: Increase in AST ALP and GGT- can be normal however

Albumin and PT are the best indicators. Albumin levels decrease while PT increases.

Low serum sodium - indicates severe liver disease due to a defect in free water clearance or excess diuretic therapy

Creatine- elevated concentration

Also test for suspected causes e.g. autoantibodies and alpha trypsin

Imaging:
Ultrasound and duplex- show hepatomegaly,splenomegaly,small liver, focal liver lesions and Ascites

MRI- useful in detecting tumours and caudate lobe sizes as well as presence of the right posterior hepatic notch

Liver biopsy- confirms diagnosis

157
Q

What is present in alcoholic cirrhosis rather than viral induced cirrhosis?

A

right posterior hepatic notch

158
Q

How do you manage cirrhosis?

A

Treat underlying cause and complication- overall arrest or reversal of compensated cirrhosis will occur

Good nutrition: 35-40 kcal/Kg and a protein intake of 1.2-1.5 g/Kg are recommended

small Frequent meals and snacks

Avoid alcohol- vitamin B supplementation thiamine mandatory in excess alcohol intake

Avoid NSAIDs,sedatives and opiates- may precipitate GI bleeding or renal impairment

Ultrasound screening every six months

For ascites: Aim to reduce sodium and to increase sodium excretion

Diuretics; Spironolactone first. If no response then add furosemide

check U&E regularly- especially after dose change or paranceentosos

TIPPs- if paracentesis is too regularly used

Paracentesis may be required- if too large to drain and kidneys cant take it. Give albumin regularly to avoid hypovolaemia and encephalopathy

Spontaneous bacterial peritonitis- use prophylaxis for high risk patients

encephalopathy- prophylactic lactulose and rifaximin

159
Q

What is the prognosis of cirrhosis?

A

extremely variable 5-year survival rate is 50%

Child’s grading A B C grades cirrhosis. A being best

Measures ascites, encephalopathy, bilirubin ,albumin and PT ( seconds over normal)

160
Q

What is the prognosis of acute on chronic liver failure?

A

High short term mortality

different to traditional decompensated cirrhosis

why?

based not only on the presence of organ fialure and high mortality but more likely with younger age, higher alcohol use and bacterial infection, higher level of systemic inflammation

161
Q

Portal hypertension is caused only by cirrhosis true or false?

A

false

162
Q

What are the two subgroups of cirrhosis?

A

micronodular- mainly caused by alcohol or biliary tract disease. Nodules usually less than 3 mm

macronodular- mainly chronic hepatitis nodules are of variable sizes

163
Q

What types of portal hypertension are there?

A

Prehepatic- blockage of portal vein before the liver

Intrahepatic- due to distortion of the liver architecture can be split into either presinusoidal or postsinusoidal

Post hepatic- venous blockage outside the liver (rare)

164
Q

What causes prehepatic portal hypertenstion?

A

Portal vein thrombosis or occlusion secondary to congenital portal venous abnormalities.

congenitial examples: neonatal sepsis of the umbilical vein or inherited prothrombotic conditions

165
Q

How do prehepatic patients present?

A

GI bleeding often at young age. They have normal liver function

166
Q

What does the portal vein consist of?

A
  1. Superior mesenteric vein
  2. Splenic vein
  3. Gastric vein
  4. Inferior mesenteric vein
167
Q

What happens if portal hypertension occurs?

A

The four collateral pathways of the portal system in the systemic system dilate.

This leads to them becoming engorged and dilated or varicose leading to rupture

Gastro-oesophageal junction is the main place where rupture occurs due to portal hypertension as it is superficial. It forms varices which then rupture.

other areas of the collateral pathways rarely rupture or have symptoms

168
Q

What are the causes of intrahepatic portal hypertension?

A

Presinusoidal: Schistosomiasis,sarcoidosis, PBC

post-sinusoidal: cirrhosis , alcoholic hepatitis

169
Q

What are the causes of post-hepatic portal hypertension?

A

Budd Chiari and veno occlusive disease

right heart failure is rare

170
Q

What are the symptoms of portal hypertension?

A

often asymptomatic

main clinical feature is splenomegaly and ascites

however other chronic liver disease features may be present

171
Q

why can chronic liver disease cause haematemesis?

A

ruptured oeophageal varices due to portal hypertension

172
Q

Where are normally varicies found ?

A

Gastro-oesophageal junction
and other portosystemic collateral sites

ectopic sites too

173
Q

what are the differences between rectal varices and haemorrhoids?

A

anorectal varices= dilation of portal-systemic anastomosis due to portal hypertension
haemorrhoids = prolapse of rectal venous plexus (not due to portal hypertension)

174
Q

How do you identify portal vein blockage?

A

Ultrasound with doppler imaging

175
Q

How do you manage variceal bleeding?

A
  1. Acute initial management ( i.e Variceal bleeding has occurred)

Main is rescustitation(control bleeding): Access patient, Restore blood volume, carry out ascitic tap, monitor for alcohol withdrawal( give IV thiamine) then start prophylactic antibiotics

Vasoconstrictor therapy: Restrict portal inflow by splanchnic arterial constriction

  1. Terlipressin- only vasoconstrictor proven to reduce mortality ( 2mg 6-hourly after 48 hours then 1 mg-4 hourly if still required). Don’t give to patients with ischaemic heart disease.
  2. Somatostatin - used for contraindications for terlipressin

Endoscopy- confirm diagnosis and to exclude bleeding from other site.

With endoscopy variceal banding can occur- Bands oesophageal varice which sucks varix to end of the scope.

Can’t control pulse and pressure and bleeding from endoscopic therapy then use Balloon tamponade:

Inflates balloon in stomach and pulls it so it is close to apposition to the gastro-oesophageal junction.

Complication: Aspiration pneumonia( as blood may go up oesophagus and into trachea), esophageal rupture and mucosal ulceration

Balloon tamponade is only temporary allows for preparation of TIPS or Banding

TIPS

  1. Acute Rebleed:

Transjugular intrahepatic portocaval shunt( TIPS)- used for rebleed or acute management. Creates total shunt decreasing both sinusoidal and portal vein pressures.

Far more effective at reducing rebleeding rates then endoscopic techniques

complication: Increase risk of encephalopathy
3. Primary prophylaxis ( patients with diagnosed cirrhosis and have varices that have not bled)

Endoscope to diagnose varices

Non selective beta blockers ( Propranolol and carvedilol)

If patients are tolerant or unreliable with beta blockers then use variceal band ligation.

  1. Secondary Prophaylaxis ( survived variceal bleed)

Variceal banding ligation and Non selective beta blockers are both used at the same time not like primary which is a choice between the two.

Poor liver function: Liver transplant

176
Q

What might be seen in a patient with oesophageal varices?

A

Red signs in the oesophagus

177
Q

what is ‘caput medusae’?

A

when the umbilical vein (ligamentum hepes) becomes back in use because of portal hypertension

178
Q

Patients with cirrhosis have a high risk of what?

A

bleeding as well as clotting easily

Therefore high risk of thrombosis and haemorrhage

179
Q

why should NSAIDs be avoided if possible in patients in dehydrated states (such as alcoholism/cirrhotic livers)?

A

NSAIDs inhibit vasodilator prostaglandins so will worsen kidney impairment due to vasoconstriction

(due to the high concentration of vasoconstrictors produced because of the dehydration)

180
Q

if you are prescribing a NSAID for a patient with cirrhotic liver what must be co-prescibred?

A

a proton pump inhibitor

181
Q

why can chronic liver disease cause oedema?

A

reduced albumin synthesis resulting in hypoalbuminaemia

182
Q

What is ascites?

A

Fluid within the peritoneal cavity

183
Q

What types of ascitic fluid are there?

ii. what are the main causes?

A

Straw coloured- malignancy ,cirrhosis and infection ( e.g. TB or any bacteria found in intra abdominal perforation)

Chylous(milky)- obstruction of main lymphatic duct or cirrhosis

Haemorrhagic (bloody)- Malignancy, ruptured ectopic pregnancy ,abdominal trauma or acute pancreatitis

184
Q

What factors lead to the formation of ascitic fluid?

A
  1. Sodium and water retention: Peripheral arterial vasodilation occurs which reduces effective blood volume. This in turn promotes salt and water retention
  2. Portal hypertension- increases local hydrostatic pressure
  3. Low serum albumin- reduces oncotic pressure

With patient who have ascites , urine sodium excretion rarely exceeds 5mmol in 24 hours

185
Q

What are the clinical features of asictes?

A

Abdominal swelling develops

Mild abdominal pain and discomfort are common

If worse than SBP might be present

Precipitating factors include HCC and high-sodium intake.

186
Q

How do you diagnose and investigate ascites?

A

Shifting dullness

ultrasound- darkness is the fluid surrounding nodule of liver

cell count- neutrophil count >250 cells/mm3 usually indicator of bacterial peritonitis

gram stain and culture

Protein measurement- high serum albumin= portal hypertension cause. Low= non liver related

cytology

187
Q

How do you manage ascites?

A
  1. check eGFR every two days
  2. bed rest
  3. dietary sodium restriction
  4. Avoid NSAIDS as they are sodium retaining
  5. Diuretics- main choice is spironolactone
  6. Paracentesis
  7. if too much paracentesis then use TIPS
188
Q

Discuss the differing usage of diuretics for ascites.

A

If new ascites escalates use spironolactone
chronic use causes gynaecomastia

in recurrent ascites use both spironolactone and loop diuretic(e.g. furosemide or butenamide).

Stop using diuretics temporarily if: rise in serum creatinine= over diuresis and hypovolaemia. Or if there is hyperkalemia. or if sodium falls below 128 mmol/l

189
Q

What is paracentesis?

ii what are the risks?

A

Drain in the abdomen which removes ascites

Used if there is a large volume or kidneys do react well to diuretics

ii. hypovolemia, risk of infection and encephalopathy are risks

190
Q

How do you manage risk of paracentesis?

A

Patients with normal renal function can have albumin given regularly

191
Q

When is TIPS used for ascites?

A

If ascites is regularly occurring and no spontaneous portosystemic encephalopathy

creates artificial pathway between hepatic vein in liver and portal vein in the liver via a stent.

60% have no ascites after and don’t require diuretics

192
Q

What is SBP?

A

When patients have ascites and the bacteria translocate into the peritoneum due to ascites

193
Q

How do you diagnose SBP?

A

Raised neutrophil count (250 cells /mm3)

Ascitic tap

194
Q

What is SBP exclusively associated with?

A

portal hypertension

195
Q

Which bacteria are the most common causes for SBP?

A
  1. E Coli
  2. Klebsiella
  3. enterococci
196
Q

How do you manage SBP?

A

Antibiotics with infusion of albumin

Vascular instability? then use terlipressin

Maintain renal perfusion

197
Q

What are the signs of SBP?

A

patient with ascites has quickly deteriorated

abdominal pain and pyrexia

198
Q

How does encephalopathy occur?

A
  1. Ammonia generated in the intestine by colonic flora and glutaminase bypass the liver due to portal hypertension as well as porto systemic shunts
  2. This impairs brain function by inducing several disturbances in astrocytes; these may impair mitochondrial and the glutamate-glutamine trafficking between the neurons and astrocytes.
199
Q

What are the factors leading to portosystemic encephalopathy?

A
  1. high dietary protein
  2. Gi haemorrhage
  3. constipation
  4. infection including SBP
  5. TIPS and paracentesis
200
Q

What are the symptoms of encephalopathy?

A
  1. Altered mood
  2. increased drowsiness and confusion, apraxia slow liver flap.
  3. coma if very late

signs

  1. fetor hepaticus ( sweet smell from breath)
  2. a coarse flapping tremor- when arm outstretched
  3. Loss of mental function

General: nausea,vomiting and weakness. Hyperreflexia and higher tone

201
Q

How do you test for apraxia?

A

Ask to draw a five pointed star

202
Q

How do you diagnose Encephalopathy?

A

clinical ( looking for signs)

203
Q

How do you manage encephalopathy?

A

Treat cause (look for infection, drug, liver failure)

Give lactulose-osmotic purgative reduces the colonic pH and reduce transmit time

Rifaxamin- antibiotic

Stop or reduce diuretic therapy

small frequent meal - maintain nutrition

if spontaneous consider transplantation

204
Q

Prognosis of encephalopathy?

A

Acute encephalopathy in acute hepatic failure has a very poor prognosis

in cirrhosis chronic PSE adversely affects prognosis but the course is very variable

205
Q

What is hepatorenal syndrome?

A

cirrhosis + Ascites + renal failure

Urine output is low with a low urinary sodium concentration

206
Q

what precipitating factors are the cause HRS ?

A

over vigorous diuretic therapy

NSAIDs usage

diarrhoea

paracentesis

SBP

207
Q

How do you treat HRS?

A

Terlipressin and albumin help with renal function

Liver transplantation best option

208
Q

What Is primary biliary cirrhosis/cholestasis?

A

Interlobular bile ducts are damaged by chronic autoimmune granulomatous inflammation causing cholestasis.

209
Q

Which group of people have the highest likelihood of getting PBC?

A

Middle aged women

210
Q

What are the clinical features of PBC?

A

asymptomatic mainly

usually diagnosed due to high ALP

Jaundice and itch and
hepatosplenomegaly are common
xanthelasma may be seen

211
Q

What results would you get from diagnosing PBC?

A

immunoglobulin increase ( especially IgM)

antimitochondrial antibodies (AMA) are the hallmark of PBC

High ALP and GGT and bilirubin

serum cholesterol high

imaging
ultrasound excludes extrahepatic cholestasis

Biopsy shows granulomas and cirrhosis

212
Q

What are the associate disorders of PBC?

A

Autoimmune disorders ( thyroid disease,sjogren’s syndrome and scleroderma)

dry eyes and mouth seen in 70% of patients

213
Q

How do you manage PBC?

A
  1. Ursodeoxycholic acid - improves bilirubin and aminotransferase levels. MUST be given in asymptomatic stage
  2. Vitamin A,D and K given due to malabsorption
  3. steroids- improve - do cause osteoporosis
  4. For pruritus - use cholestyramine. Rifampicin and naloxone is also useful

no response? liver transplant

214
Q

What is PSC?

A

primary sclerosing cholangitis.

Autoimmune fibrosis and stricturing of the large and medium sized bile ducts.

The fibrosis is described as onion skinning

215
Q

what is the epidemiology of PSC?

A

more common with men and those with UC

216
Q

What are the signs and symptoms of PSC?

A

Asymptomatic

Fluctuating pruritus, jaundice and cholangitis sometimes fatigue (lethargy)

hepatic failure

217
Q

How would you test for PSC?

A

High ALP and Bilirubin

Might have increase in IgM , ANA, SMA and ANCA but not AMA

Imaging

MRCP or ERCP

218
Q

What can PSC lead to?

A

cirrhosis

cancers in the Bile duct, gallbladder and colon

Hepatocellular carcinoma

219
Q

How do you manage PSC?

A

Liver transplant main way

ursodeoxycholic might help with LFT but high dosage can be harmful

if dominant lesion is sited in the extrahepatic ducts (rare) then endoscopic biliary intervention can occur

220
Q

What are the causes for secondary biliary cirrhosis?

A

bile duct strictures

Gallstones

sclerosing cholangitis

221
Q

why is hyoglycaemia a very serious clinical sign of acute liver disease?

A

because the liver usually makes glucose until the very end

222
Q

What is hereditary haemochromatosis?

A

Inherited disorder ( autosomal recessive) of iron metabolism in which increase of intestinal iron absorption leads to iron deposition in joints, liver and pancreas.

223
Q

Hereditary haemochromatosis occurs more in men than women true or false?

A

true

224
Q

What is the difference between primary and secondary haemochromatosis?

A

primary : an autosomal recessive condition which causes excess iron within the liver due increased absorption of iron from food

secondary:excess iron within the liver caused by iron overload from diet, transfusions or iron therapy

225
Q

What are the symptoms of hereditary haemochromatis?

A

early: asymptomatic or and arthralgia
late: slate grey skin, hepatomegaly and cirrhosis.

cardiac manifestations: heart failure and arrhythmias ( very common in younger patients)

Endocrinopathies: Bronze skin pigmentation ( due to melanin deposition) and diabetes - occurs late on

226
Q

how do you diagnose hereditary haemochromatosis?

A

testing:

LFT increase not always

serum iron is increased ( sometimes normal in heterozygotes)

serum ferritin is increased ( sometimes normal in heterozygotes)

Liver biopsy: Perl’s stain quantifies iron loading and shows degree of tissue damage

MRI: liver and pancreas signal intensity is dramatically reduced due to paramagnetic effect of ferritin

227
Q

How do you manage HH?

A

Venesection(phlebotomy)- will be needed for life to make sure iron does not rise again. This prolongs life and may reverse tissue damage. Doesn’t remove risk of malignancy

over the counter drugs- ensure vitamin preparations contain no iron

Screening all first degree family members

228
Q

What are the risks of HH?

A

Primary hepatocellular carcinoma

cirrhosis and fibrosis

229
Q

What is wilson’s disease?

A

rare congenital disease ( autosomal recessive) of copper deposition in various organs including the liver, basal ganglia of the brain and the cornea.

230
Q

What is copper normally bound to when carried to the liver?

ii. what is it later synthesised to?

A

albumin

ii. it is then synthesised to caeruloplasmin

rest of copper is excreted

231
Q

What are the symptoms and signs of wilsons disease?

A

More likely to be found in young adults and kids

Children: present with liver disease ( Hepatitis, cirrhosis, fulminant liver failure)

Young adults present with CNS signs ( tremor, dysarthria, dementia, parkinsonism)

cornea: kayser fleischer ring - greenish brown pigment ( use slit lamp for exam) maybe absent in young kids
mood: depression, personality change.

Cognition: memory; slow to solve problems decrease in IQ

Blue nails , arthritis and grey skin and haemolysis are common

232
Q

How do you diagnose Wilson’s disease?

A

serum copper and caeruloplasmin levels are low

urinary copper is increased

Slit lamp exam for KF rings

Genetic testing

Liver biopsy- weigh amount of copper in liver

imaging: copper deposition in CNS can be viewed with MRI

233
Q

How do you manage Wilson’s?

A

Diet: avoid food with high copper content

penciliamine- lifetime treatment is effective in chelating copper

asymptomatic screening of siblings

if acute hepatic failure or decompensated cirrhosis then transplant

234
Q

What are the risk of wilson’s?

A

fatal events include liver failure, bleeding or infection

235
Q

What is alpha antrypsin deficiency?

A

Autosomal recessive condition which causes a deficiency of alpha 1 antitrypsin enzymes leading to liver and lung problems

236
Q

What is the main role alpha 1 antryspin?

A

Inhibit the proteolytic enzyme neutrophil elastase

237
Q

What are the signs and symptoms of Alpha 1 deficiency?

A

Symptomatic patients are homozygotes with piZZ phenotype

associated diseases: emphysema, cirrhosis and HCC

symptoms: dyspnoea from emphysema,cholestatic jaundice

238
Q

How do you diagnose alpha 1 antitrypsin deficiency?

A

serum alpha 1 is usually decreased

Lung biopsy; Periodic acid Schiff ( staining method) is positive. Cirrhosis and fibrosis can be observed

239
Q

How do you manage alpha 1 deficiency?

A

Stop smoking!

Liver transplantation if decompensated cirrhosis

240
Q

What is the prognosis of alpha 1 antitrypsin deficiency?

A

Some are asymptomatic and live a healthy long term life

most die from emphysema
worse in males

241
Q

why does being a long term alcoholic increase risk of overdosing when taking too many paracetamol tablets?

A

as a long term alcoholic your body has more receptors and so the paracetamol will be metabolised much quicker and acetyl-p-benzoquinomine is formed at a much faster rate

242
Q

What are the three main liver diseases caused by alcohol?

A
  1. Fatty liver- liver cells becoming swollen with fat ( steatosis). Can sometimes progress to cirrhosis without hepatitis. improves after drink cessation
  2. alcoholic hepatitis- mallory bodies sometimes can be seen in hepatocytes along with large mitochondrias. Continue drinking leads to cirrhosis. Steatohepatitis occurs.
  3. cirrhosis- mainly micronodular type. Hepatitis may also be present sometimes
243
Q

What are the signs and symptoms of alcoholic liver disease?

A

fatty liver- often asymptomatic

symptoms: nausea, vomiting and diarrhoea hepatomegaly

alcoholic hepatitis: jaundice, chronic liver disease symptoms. Look for fever, hepatomegaly, hepatic bruit and leukocytosis mainly.

cirrhosis: chronic liver disease symptoms. alcoholic dependency. portal hypertension symptoms ( caput medusa).

244
Q

What are the general symptoms of alcoholism in the body?

A

CNS:
Acute: Violence and accidents

chronic:Neuropathies, cerebellar degeneration, dementia and wernicke-Korsakoff’s syndrome (psychosis and encephalopathy)

GI:
Acute: oesophagitis, ulceration, acute pancreatitis,

chronic: obesity, cancers, chronic pancreatitis

Cardiovascular:

Chronic: Arrhythmias, hypertension, stroke and MIs and cardiomyopathies

Resp:

Acute: overdose and aspiration

Reproduction:

chronic: testicular atrophy, decrease in testosterone and progesterone. Increase in oestrogen

Fetal alcohol syndrome

245
Q

What is fetal alcohol syndrome?

A

collection of conditions in children due to overuse of alcohol in parents

Conditions: Low IQ, growth deficiency, small eyes, behavioural problems, microcephaly, small chin, no distinct philtrum

246
Q

How do you diagnose alcoholic liver disease?

A

Fatty liver: increase Mean cell volume . Increase in GGT sign of alcoholism

Imaging: ultrasound will show fatty infiltration. Elastography will show degree of fibrosis

Alcoholic hepatitis: Increase in bilirubin, AST and ALT and ALP and prolonged PT. Low albumin may also be found.

Prolonged PT means that Liver biopsy has to be throw transjugular route

cirrhosis: see how to diagnose cirrhosis. Cba as it took me fucking ages before. I could copy and paste but nah im even to lazy for that.

247
Q

How do you manage alcoholic liver disease

A

Stop drinking alcohol!- alcohol free beers maybe?

  1. For withdrawal symptoms- diazepam
  2. for prevention of wernicke korsakoff syndrome- IV thiamine
  3. Bed rest. Limit proteins diet due to encephalopathy

Fatty liver- stop drinking should be enough

alcoholic hepatitis- see discriminant function for steroid therapy

vitamin supplementation

Liver transplant- if proven they will give it up after and continue to not drink. for cirrhosis and hepatitis

treat chronic liver disease symptoms

Hypophosphataemia is common in alcoholic withdrawal due to malnutrition

248
Q

What is delirium tremens?

A

a withdrawal symptom

249
Q

What is discriminant function?

A

Suggests which patients with alcoholic hepatitis may have a poor prognosis and benefit from steroid administration.

> 32 correlates 45% mortality at day 28

But there is a concern over accuracy

250
Q

What is the prognosis?

A

severe cases mortality can be at least 50%

encephalopathy and acute kidney failure= 90% risk

need transplant as soon as possible with acute hepatitis and cirrhosis.

risk of HCC with men in particular

251
Q

What is Budd chiari syndrome?

A

condition of the obstruction of the venous outflow of the liver owing to occlusion of the hepatic vein.

252
Q

What are the causes of budd chiari syndrome?

A

1/3 of patients it is unknown

other 2/3s

  1. Hypercoagulability states
  2. thrombophilia
  3. contraceptive pill
  4. pregnancy
  5. leukaemia
  6. abdominal wall sarcoma
  7. renal or adrenal tumours
  8. HCC.
  9. infections of the liver
253
Q

What are the symptoms of Budd chiari syndrome?

A

acute: abdominal pain, nausea, vomiting , hepatomegaly and ascites. Fulminant form of budd chiari very common in pregnant women.
chronic: Hepatosplenomegaly, jaundice, ascites, negative hepatojugular reflux and portal hypertension

254
Q

How do you diagnose Budd Chiari syndrome?

A

High protein content in ascitic fluid

LFT: High ALT

ultrasound with doppler flow show hepatic vein occlusion and abnormality of flow in the hepatic vein.

thrombophilia screening required

coagulation defects present

255
Q

How do you manage Budd chiari syndrome?

A

Thrombolytic therapy can be given

treat underlying cause

TIPS is treatment of choice

liver transplantation for chronic budd chiari

anticoagulation required after transplantation or TIPS

256
Q

what is the most common benign liver lesion?

ii. which is it more common in male or female?

A

Haemangioma

ii female

257
Q

Describe the clinical features of haemangioma?

A

usually asymptomatic.

normally small and single can be large and multiple however

Well demarcated capsule

258
Q

How do you diagnose and treat haemangioma?

A

Ultrasound: echogenic spot

CT: for venous enhancement

MRI: for high intensity area

Treatment: none required

259
Q

What is a hepatic adenoma?

ii. what are they associated with?

A

benign liver tumor composed of hepatocytes with no portal tract,central veins or bile ducts

ii. contraceptive pills and androgenic steroids

260
Q

What are the symptoms of Hepatic adenomas?

A

Asymptomatic

can present with Abdominal pain or intraperitoneal bleeding

261
Q

How do you treat hepatic adenomas?

A

Resection only required for symptomatic patients and with tumours >5cm in diameter

stop taking contraceptive pills!

262
Q

what are the 4 main benign focal nodules?

A

hemangioma
focal nodular hyperplasia
adenoma
liver cysts

263
Q

What are the clinical features of Focal nodular hyperplasia?

A
  1. benign nodule formation of normal liver tissue.
  2. classically has a central scar containing a large artery which radiates branches to the periphery
  3. form due to abnormal arterial flow
  4. SInusoids, bile ductules and kupffer cells present on histology
  5. more common in women ( young to middle aged)
  6. usually asymptomatic
264
Q

How do you diagnose and treat FNH?

A

Ultrasound and CT or MRI

FNA normal hepatocytes and kupffer cells with central core

treatment: none required

265
Q

what does hyperintense mean on MRI?

A

brighter than surrounding tissue

266
Q

what does hypointense mean on MRI?

A

darker than surrounding tissue

267
Q

what does isointense mean on MRI?

A

same colour as surrounding tissue

268
Q

what can be the complications of a hepatic adenoma?

A

rupture
haemorrhage
malignant transformation

Very rare

269
Q

Malignant transformation of hepatic adenomas are higher in men or women?

A

Men

270
Q

Which lobe is hepatic adenoma usually found in?

A

right lobe

271
Q

What is adenomatosis?

ii. what is it associated with?

A

condition with Multiple adenomas

ii. Glycogen storage disease

272
Q

How do you diagnose Hepatic adenoma?

A

Ultrasound: filling defect

CT: diffuse arterial enhancement

MRI: Hypo or hyper intense lesion

FNA: May be needed

273
Q

what are the main differences between adenomas and focal nodular hyperplasia?

A

adenoma is purely a hepatocyte tumour which FNH contains all liver ultrastructure

adenomas can bleed and become malignant while FNH can’t do either

all FNH has central scar adenomas vary

274
Q

What are the main similarities between adenomas and FNH?

A

Both hypervascular

both can cause pain

275
Q

What are the five types of cystic lesions?

A
  1. simple-liquid collection lined by an epithelium
  2. hydatid-a multilobular cyst
    (ie contains many irregular cavities)
  3. atypical
  4. polycystic lesion- embryonic ductal plate malformation of the intrahepatic biliary tree. Numerous cysts throughout liver parenchyma
  5. Pyogenic or amoebic abscess
276
Q

What are the symptoms of simple cysts?

A

Usually asymptomatic

symptoms can be :

Intracystic haemorrhage

infection

rupture

compression

277
Q

There is no biliary tree communication with simple cysts true or false?

A

true

278
Q

How do you manage simple liver cysts?

A

No follow up if in doubt image every 3-6 months

279
Q

Which bacteria causes hydatid cysts?

A

Echinococcus garanulosus

280
Q

How do patients present with Hydatid cyst?

A

usually from endemic regions of eastern europe, central america, south america, middle east or north africa

disseminated disease or erosion of cysts into IVC

281
Q

How do you diagnose Hydatid cysts?

A

anti echinococcus antibodies are present

282
Q

How do you manage Hydatid cysts?

A

Drugs: albendazole

surgery: Open cystectomy or pericystectomy ( for complete curative action)

surgery Risks: anaphylaxis and dissemination of infection

Can do percutaneous drainage-The PAIR (puncture-aspiration-injection-reaspiration; sometimes percutaneous aspiration-injection-reaspiration) procedure is a noninvasive treatment option to remove hydatid cysts. PAIR is considered an alternative treatment for cystic echinococcosis (hydatid disease) and is often indicated for patients who do not respond to surgery or benzimidazoles

283
Q

What three types of polycystic liver disease is there?

A
  1. Von meyenburg complexes ( VMC)
  2. Polycystic liver disease
  3. Autosomal dominant polycystic kidney disease (ADPKC)
284
Q

What is Von meyenburg complexes?

A

Benign cystic nodules throughout the liver.

cystic bile duct malformations originate from the peripheral biliary tree

285
Q

What is Autosomal dominant polycystic kidney disease?

A

Renal failure due to Polycystic kidneys and non renal extra hepatic features

286
Q

What are the symptoms of polycystic liver disease?

A

usually asymptomatic

Abdominal pain and distention

oesophageal varices very rare

287
Q

How do you treat PCLD?

A

pharmacological: somatostatin

Invasive procedures such as aspiration or liver transplants are very rarely used. Only used in advance PCLD

288
Q

What are liver abscesses?

A

Mass filled with pus inside the liver

289
Q

what two main types of liver abscesses are there?

A

Pyogenic

Amoebic

290
Q

What is the most common type of organism which causes pyogenic liver abcesses?

A

E.coli

Streptococcus milleri and bacteroides are also commonly seen

291
Q

What are the signs and symptoms of a pyogenic abscess?

A

acutely ill Patients:
Malaise

High Fever

rigors, anorexia, vomiting, weight loss and abdominal pain

gram negative septicaemia with shock can occur

liver is tender and enlarged with potential PE

292
Q

How do you diagnose Pyogenic abscess?

A

Bilirubin increase can occur

Raised ALP

vitamine B12 very high

ESR and CRP are often raised

Imaging;

ultrasound is useful

CT can be used if there are multiple lesions

293
Q

How do you manage pyogenic abcess?

A
  1. Aspiration with Ultrasound control
  2. Antibiotics
  3. Further drainage via a large-bore needle if resolution is slow
294
Q

What is the most common cause of the amoebic abscess?

A

Entamoeba histolytica- causes portal hypertension

295
Q

What are the signs and symptoms of Amoebic abscess?

A

Fever, anorexia weight loss and malaise

hepatomegaly

sign of PE

Jaundice unusual

296
Q

Where is pain from liver tumours most likely to be felt at?

A

RUQ

297
Q

How do you diagnose Amoebic abscess?

A

Test for amoeba - haemagglutination

diagnostic aspiration of fluid: looks like anchovy sauce

298
Q

How do you manage amoebic abscess?

A

Metronidazole

if fail to respond then aspiration especially if with multiple lesions

299
Q

what are the 6 primary liver cancer?

A 
hepatocellular carcinoma
cholangiocarcinoma
fibrolamellar carcinoma
hepatoblastoma
angiosarcoma
haemangioendothelioma
300
Q

What is the most important risk factor of HCC?

A

cirrhosis

301
Q

What are the signs and symptoms of HCC?

A
  1. Asymptomatic- if patients have cirrhosis

weight loss

Chronic liver disease signs which are pre existing

anorexia

fever

Pain in RUQ

ascites

hard enlarged mass of RUQ

liver bruit (rare)

302
Q

Where does Liver metastasise go to?

A
  1. rest of liver
  2. portal vein
  3. lymph nodes
  4. Lung
  5. Bone
  6. Brain
303
Q

Histologically what do HCC cells look like?

A

Cells resembling hepatocytes

304
Q

How do you diagnose HCC?

A

Serum alpha fetoprotein is raised. This is HCC tumour marker

ultrasound shows filling defects in 90% of cases

Tumour biopsy- less used now

305
Q

How do you manage HCC?

A

Resecting solitary tumours- as long as no jaundice or portal hypertension

liver transplant- best choice

Percutaneous ablation- temporary measure

Tumor embolization ( TACE)- inject chemotherapy selectively in to the hepatic artery then inject embolic agent. Only in patients with early cirrhosis

Sorafenib- can be used for advanced HCC but Side effects are common

306
Q

What are the causes of cholangiocarcinoma?

A

PSC

Biliary cysts

caroli’s disease

HBV HCV

307
Q

What is the main type of cholangiocarcinoma?

A

Extrahepatic

308
Q

What are the signs and symptoms of Cholangiocarcinoma?

A

Fever, abdominal pain malaise

jaundice frequent with hilar tumours

weight loss , anorexia , lethargy

cholangitis

309
Q

How do you diagnose cholangiocarcinoma?

A

Increase in bilirubin and high increase in ALP

duplex ultrasound

310
Q

How do you treat cholangiocarcinoma

A

Praying- 70% of patients when diagnosed are inoperable

Liver transplantation rarely possible

resection rarely possible

normally major hepatectomy and extrahepatic bile excision with caudate lobe resection.

loads of complication: Liver failure, bile leak and GI bleeding

311
Q

Fibro-lamellar carcinoma is related to cirrhosis true or false?

A

false

312
Q

What age group is fibro-lamellar carcinoma usually related to?

A

young age (5-35)

313
Q

What are the two main types of gallstones?

A

mainly mixed

  1. Cholesterol stones-imbalance between the ratio of cholesterol to bile salts
  2. pigment stones- predominantly composed of calcium bilirubinate or polymer-like complexes and some cholesterol. less frequent then cholesterol stones
314
Q

What three factors ensure the formation of cholesterol gallstones via crystallization from gallbladder bile?

A
  1. cholesterol supersaturation of bile
  2. Crystallization-promoting factors within bile
  3. motility of the gallbladder- gallbladder stasis leads to cholesterol crystallisation mediated by hypersecretion of mucin
315
Q

How are statins effective in treating hypercholesterolaemia?

A

competitively inhibiting HMG-CoA reductase

also reduce cholesterol secretion

316
Q

What is leptin?

A

a hormone

317
Q

What is Leptin’s effect on cholesterol?

A

increase cholesterol secretion into bile.

elevated levels of leptin during weight loss may account for increased incidence of gallstones.

318
Q

What are the two main types of bile pigment stones?

A

Black and Brown

319
Q

What are black pigment gallstones made of?

A

calcium bilirubinate and a network of mucin glycoproteins that interlace with salts

320
Q

what are black pigment gallstones associated with?

ii. why is this?

A

All major haemolytic anaemias (due to sickle cell and thalassemia)

subclinical haemolysis ( due to malaria)

Hypersplenism ( due to hepatic cirrhosis)

high prevalence in gilbert syndrome

ii. Hyperbilirubinbilia is a major risk factor for these conditions

321
Q

What are brown pigment stones composed of?

A

calcium salts of fatty acids

Calcium bilirubinate

322
Q

Where are brown stones found?

A

anywhere in the biliary tree secondary to chronic stasis and anaerobic bacterial infection

Always found in the presence of bile stasis or biliary infection

323
Q

What are the main risk factors for cholesterol gallstones?

A
  1. increasing age
  2. being a woman
  3. genetics
  4. obesity
  5. rapid weight loss
  6. diabetes
  7. ileal disease - causes loss of bile salt into the colon which promotes reabsorption of bilirubin which leads to more enterohepatic circulation causing more biliary secretion- gallstones.
324
Q

What are the signs and symptoms of gallstones?

A

usually asymptomatic

if complications arise then symptoms become recurring

325
Q

what can gallstone obstruction lead to?

A

gallstones in gallbladder- asymptomatic

gallstones in cystic duct- acute cholecystitis

gallstone in common bile duct- biliary obstruction

gallstone in pancreatic duct- pancreatitis

326
Q

What is biliary(gallstone) colic?

A

term used to describe pain associated with temporary obstruction of the cystic or common bile duct by a stone ( usually gallstone)

327
Q

What are characteristics of Biliary colic?

A

usually sudden onset

commonly felt in the mid-evening until early hours of the morning

mainly epigastrium but can be also RUQ

pain may radiate to right shoulder and right subcapsular region

nausea and vomiting accompany pain usually

associated with indigestion too

328
Q

How do you treat biliary colic?

A

can end spontaneously

or give opiate analgesia

rehydrate

Observe in 3-6 months
If the patient is getting recurrent episodes of pain consider elective cholecystectomy
If patient unfit, try to dissolve gallstones with ursodeoxycholic acid

329
Q

what does protracted pain of biliary colic with fevers and rigors imply?

A

secondary complications (cholecystitis, cholangitis or gallstone-related pancreatitis)

330
Q

what is the usual pathogenesis of acute cholecystitis?

A

gallstones obstructing outflow of bile

this becomes infected and may cause empyema (gallbladder become distended with pus) rupture and peritonitis (rare)

intense adhesions are formed

331
Q

what are the signs and symptoms of acute cholecystitis?

A

similar to biliary colic

RUQ pain is more localised and continuous

vomiting, fever,local peritonism

gallbladder mass present

murphy’s sign is present- pain on taking a deep breath when the examiners fingers are on the gallbladder

if stone moves to cystic biliary duct then obstructive jaundice and cholangitis can occur

332
Q

How do gallstones form?

A
  1. abnormal bile composition
  2. bile stasis
  3. infection
  4. excess cholesterol and bilirubin
333
Q

What is the difference between acute cholecystitis and biliary colic?

A

Inflammatory reaction occurs in cholecystitis ( local peritonism and fever) unlike in biliary colic which doesn’t

334
Q

How do you test and diagnose for Acute cholecystitis

A

increase in White cell count (leukocytosis)

raised inflammatory markers ( CRP)

Ultrasound - shows a thick-walled shrunken gallbladder

shows dilated CBD

335
Q

How do you treat acute cholecystitis?

A

Pain relief( opiate analgesia)

iv fluids and antibiotics e.g. co-amoxiclav

laparoscopic cholecystectomy is the main choice due to being incredibly safe. Needs to be urgent tho

336
Q

What are the signs and symptoms of chronic cholecystitis?

A

same as acute and flatulent dyspepsia

337
Q

What are the complications of cholecystectomy ?

A

biliary leak- from cystic duct or gallbladder bed

injury to the bile duct itself is very very rare.

338
Q

What are three main symptoms of acute cholangitis?

A

RUQ pain, jaundice and rigors

339
Q

How do you diagnose acute cholangitis?

A

elevated neutrophil count and raised inflammatory markers are common

bilirubin rise is mild

LFT rise in proportion to hyperbilirubinemia

imaging

US

CT
ERCP

340
Q

How do you manage acute cholangitis?

A

urgent bile duct drainage- via ERC

antibiotics- e.g. piperacillin

Laparoscopic cholecystectomy

341
Q

What is Gallstone ileus?

A

Stone enters through the Gallbladder into duodenum via a cholecysto-enteric fistula

Then obstructs the distal ileum.

342
Q

How do you diagnose Gallstone ileus?

A

X Ray- shows air in the cystic bile duct (pneumobilia)

Small bowel obstruction

stone found in small bowel (US)

343
Q

How do you treat Gallstone ileus?

A

Urgent laparotomy - In Small bowel enterotomy is used to remove stone

interval cholecystectomy in 3 months

344
Q

What is the most common cancer in the gall bladder?

A

adenocarcinoma- still only makes 1% of all cancers

345
Q

How do you detect adenocarcinoma?

A

MRCP

accidentally

346
Q

How do you treat adenocarcinoma of the gallbladder?

A

radical surgery with negative resection margins offers the only potential cure

if spread to lymph- curative resection

palliative chemo can be given

very few respond to radiotherapy

347
Q

what is the difference between cholangitis and cholecystitis?

A

cholangitis- inflammation and secondary infection of the bile duct due to biliary obstruction and stasis. gallstones or tumours block bile duct.

cholecystitis- inflammation of the gallbladder. mainly
due to gallstones obstructing the cystic duct

348
Q

What is acute pancreatitis

A

syndrome of inflammation of the pancreatic gland initiated by any acute injury.

349
Q

What are the causes of acute pancreatitis?

A

Remember GET SMASHED

gallstones

ethanol (alcohol)

Trauma

steroids

mumps

autoimmune

scorpion venom

hyperlipdaemia,hypothermia and hypercalcaemia

ERCP

Drugs (ace inhibitors ,antibiotics, oestrogens)

350
Q

How does gallstone pancreatitis occur?

A

gallstones cause obstruction to pancreatic drainage at the ampulla by a stone or associated oedema. intracellular calcium rises leading to extensive damage to acinar cells.

351
Q

What are the signs and symptoms of acute pancreatitis?

A

Epigastric pain is prominent accompanied with nausea and vomiting

pain can radiate to back- can be relieved if sitting forward

fever, jaundice,shock and rigid abdomen may be present

Main two signs are cullens and Grey turner’s

Cullen’s- periumbilical bruising

Grey Turner’s- flank bruising

352
Q

How do you diagnose acute pancreatitis?

A

serum amylase - dramatic increase- main test as it is very sensitive

urinary amylase- may be elevated

serum lipase levels also elevated

Chest X Ray- excludes gastro duodenal perforation- can also raise amylase

US- screening test to see if Gallstones are cause of pancreatitis

CT is the standard choice of imaging to assess severity and for complications

353
Q

what are the 6 main complications of acute pancreatitis?

A 
death
shock
pseudocyst formation
abscess formation
hypocalcaemia
hyperglycaemia
354
Q

how do you manage acute pancreatitis?

A

must assess severity of condition

  1. don’t feed by mouth - consider nasojejunal tube
  2. Give analgesia (pethidine or morphine). Note morphine may cause sphincter of oddi to contract
  3. may have to take to ITU give O2 . Give parenteral nutrition and laparotomy if pancreatic necrosis is suspected
  4. ERCP for gallstone removal may be needed if gallstone caused

GIve fluids

give antibiotics

355
Q

What are the causes of chronic pancreatitis?

A

Alcohol

chronic kidney disease

cystic fibrosis (rare)

Obstructive(rare)

trauma

Autoimmune

Recurrent acute pancreatitis

356
Q

What are the symptoms and signs of chronic pancreatitis?

A

Epigastric and often radiates through into the back

Can be episodic pain

Anorexia and weight loss can be common

Diabetes occurs late

Jaundice

357
Q

How do you diagnose chronic pancreatitis?

A

Serum Amylase and lipase may be elevated- however may not be depending on number of acinar cells still remaining

Serum IgG may be elevated for autoimmune pancreatitis

Faecal elastase- abnormal in majority of patients

US and CT - pancreatic calcification confirms diagnosis

358
Q

which is the diagnostic tool- MRCP or ERCP?

A

MRCP

359
Q

what is the function of an ERCP?

A

an interventional tool to treat common biliary duct stones causing
obstruction
(shouldnt be used for diagnostits)

360
Q

what blood gases state is usually present with acute pancreatitis?

A

metabolic acidosis

361
Q

why can pancreatitis cause a splenic pseudoaneurysm and haemorrhage?

A

the pancreatic digestive enzymes start digesting the blood vessel

362
Q

How do you manage Chronic pancreatitis?

A

give analgesia

lipase and fat soluble vitamins

No alcohol
low fat diet

Autoimmune- glucocorticoid therapy

diabetes- insulin and low fat diet

malabsorption- steatorrhoea associated with pancreatitis. pancreatic enzyme supplements and acid suppressor.

Duct drainage procedure if unremitting pain occurs

363
Q

What are the complications of chronic pancreatitis?

A

pseudocysts

diabetes

biliary obstruction

local arterial aneurysm

splenic vein thrombosis

gastric varices

pancreatic carcinoma

Ascites and PE

364
Q

what is the main type of exocrine pancreatic cancer?

A

adenocarcinoma

365
Q

What are the signs and symptoms of Adenocarcinoma of the pancreas?

A

> 70 years old

smokes

drinks alcohol

2/3s of pancreatic cancers are found in the head of the pancreas

Abdominal pain weight loss anorexia

pain radiates to back

jaundice- dark urine and pale stools and pruritus

diabetes is present in 50% of patients

unusual: polyarthritis, thromboembolic phenomena and skin nodules

Gallbladder may be palpable

hepatomegaly

splenomegaly

epigastric masses

366
Q

how do you diagnose for Pancreatic carcinoma?

A

cA19-9 increase- tumor marker but does have high false positive rate

Ultrasound ( most sensitive) or CT show pancreatic mass and dilated biliary tree

367
Q

How do you treat pancreatic carcinoma?

A

surgery:

Resection

whipple’s procedure

pain: analgesics or radiotherapy

chemotherapy after surgery

368
Q

what is the prognosis of pancreatic carcinoma?

A

pretty Shit start praying boi

unless: tumour is less than 3 cm and no nodes are involved

369
Q

what are the 3 main type of endocrine pancreatic cancers?

A

gastrinoma
insulinoma
glucagonoma

370
Q

what are the consequences of a gastrinoma?

A

produces gastrin causing increased stomach acid causing gastric/duodenal ulcers

371
Q

what are the consequences of an inulinoma?

A

produces insulin causing increased glucose uptake from the blood- hypoglycaemia

372
Q

what are the consequences of a glucagonoma?

A

produces glucagon to increase blood sugar levels- hyperglcaemia

373
Q

what is the most common cause of nodular hepatomegaly?

A

Liver metastases

374
Q

what is charcot’s triad?

ii. what is it associated with?

A

Jaundice

fever

RUQ

ii. ascending cholangitis

My GI (8 decks)

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