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SA gastro-intestine > S7) Liver and Pancreatic Pathology > Flashcards

S7) Liver and Pancreatic Pathology Flashcards

1
Q

Describe the anatomical relationship of the liver with the gallbladder and duodenum

A
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2
Q

Outline the transport and metabolism of bilirubin

A
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3
Q

Identify 3 ways in which we can measure liver dysfunction

A
  • Failure of anabolism
  • Failure of catabolism and excretion
  • Markers of hepatocyte damage/dysfunction
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4
Q

Identify 4 things produced by the liver (anabolism)

A
  • Albumin
  • Glycogen
  • Coagulation factors
  • Haematopoiesis (in foetus / adult with bone marrow failure)
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5
Q

In terms of anabolism, identify 2 indicators of poor liver function

A
  • Hypoalbuminaemia due to failure to produce albumin
  • Prolonged prothrombin time (PT/INR) due to failure to produce coagulation factors
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6
Q

Identify 5 things broken down by the liver (catabolism)

A
  • Drugs
  • Hormones
  • Haemoglobin
  • Poisons
  • Aged RBCs (after splenectomy)
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7
Q

Identify and describe 3 abnormalities of bilirubin production/excretion

A
  • Pre-hepatic jaundice: too much bilirubin in blood for lover to cope with e.g. haemolytic anemia
  • Intra-hepatic jaundice: failure of hepatocytes to conjugate (to make it water soluble) and/or secrete bilirubin e.g hepatitis, cirrhosis
  • Post-hepatic jaundice: failure of the biliary tree to convey conjugated bilirubin to duodenum e.g. biliary tree obstruction straight after the liver
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8
Q

How can excess bilirubin be measured?

A

Conjugated bilirubin is water soluble so when elevated, serum levels can be measured with a dipstick (dark yellow)

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9
Q

Identify 3 signs of pre-hepatic jaundice

A
  • Raised serum bilirubin
  • Increased urinary urobilinogen
  • No conjugated bilirubin present in urine
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10
Q

Identify 4 symptoms of pre-hepatic jaundice

A
  • Mild jaundice (lemon tinge)
  • Stools may be very dark
  • Normal urine colour
  • No pruritis
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11
Q

Identify 3 signs of intra-hepatic jaundice

A
  • Raised serum bilirubin
  • Normal urinary urobiliogen
  • Conjugated bilirubin present in urine and there will still be some healthy hepatocytes
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12
Q

Identify 4 symptoms of intra-hepatic jaundice

A
  • Moderate jaundice
  • Stools normal
  • Urine dark
  • No pruritis usually

(can see a large liver, large spleen, maybe portal hypertension if its to due with acute liver disease)

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13
Q

Identify 3 signs of post-hepatic jaundice

A
  • Raised serum bilirubin
  • Decreased urinary urobilinogen
  • Conjugated bilirubin present in urine → since the main pathway for bilirubin to leave is blocked it will travel to the kidney to be excreted
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14
Q

Identify 4 symptoms of post-hepatic jaundice

A
  • Severe jaundice (green tinge!)
  • Stools pale
  • Urine dark
  • Pruritis
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15
Q

Identify 3 enzyme markers of hepatocyte damage/dysfunction

A
  • Alanine aminotransferase (ALT) is released by inflamed/damaged hepatocytes
  • Alkaline phosphatase (Alk Phos) is present in the liver canaliculi, bile ducts and bone
  • Gamma-glutamyl transferase (Gamma GT) is present in bile duct cells
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16
Q

A raised ALT is due to hepatitis.

Identify 4 causes of hepatitis

A
  • Viral (A, B, C etc.)
  • Acute alcohol intake
  • Fatty liver disease
  • Drugs/toxins
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17
Q

Identify 2 main causes of a raised Alk Phos

A
  • Bile duct/liver disease with cholestasis
  • Bone disease
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18
Q

Identify 4 conditions which lead to bile duct/liver disease presenting with a raised Alk Phos

A
  • Biliary obstruction
  • Cirrhosis
  • Liver metastases
  • Drugs
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19
Q

Identify 4 conditions which lead to bone disease presenting with a raised Alk Phos

A
  • Bone metastases/fracture
  • Osteomalacia
  • Hyperparathyroidism
  • Paget’s disease of bone
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20
Q

Identify 5 causes of a raised Gamma GT

A
  • Biliary duct obstruction/cholestasis
  • Cirrhosis
  • Liver metastases
  • Drugs
  • Alcoholism
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21
Q

Identify 4 common liver and bile duct diseases

A
  • Hepatitis
  • Cirrhosis
  • Gallstones and biliary tract obstruction
  • Liver metastases
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22
Q

How does liver failure present?

A
  • Increased susceptibility to infections
  • Increased susceptibility to toxins and drugs
  • Increased blood ammonia (failure to clear ammonia via urea cycle)
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23
Q

Identify 6 symptoms of hepatitis

A
  • Malaise
  • Anorexia
  • Fever
  • Right upper quadrant pain
  • Dark urine
  • Jaundice
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24
Q

What are the typical blood test findings in acute hepatitis?

A
  • Normal albumin and INR
  • High serum bilirubin
  • Very high serum ALT
  • Normal/slightly raised Alk Phos
  • Normal/slightly raised Gamma GT
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25
Q

What is cirrhosis?

A

Cirrhosis is a condition caused by liver fibrosis, producing a shrunken hard nodular liver, permanent and irreversible.

can affect the function of the liver

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26
Q

Identify 3 consequences of liver fibrosis

A
  • you will see nodules appear
  • Portal hypertension due to pressure and occlusion of the liver, liver can’t expand, veins are squished, increased hydrostatic pressure → ascieties, splenomegaly, varices can burst and cause haemorrhage.
  • Reduced excretion due to pressure on the bile canaliculi

- Reduced albumin and clotting factor production due to replacement of hepatocytes by fibrous tissue

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27
Q

Identify 5 main causes of liver cirrhosis

A
  • Alcohol (drugs)
  • Consequence of viral hepatitis (B,C) (infections)
  • Fatty liver disease (deposition)
  • Idiopathic

– autoimmune

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28
Q

Identify 3 sites of portosystemic anastomoses

A
  • Anorectal junction
  • Ligamentum teres of falciform ligament
  • Oesophagogastric junction
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29
Q

In two steps, explain how oesophageal varices results from liver cirrhosis

A
  • Pressure and occlusion of the hepatic sinusoids leads to portal hypertension
  • Portal hypertension leads to portosystemic shunting, including oesophageal varices
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30
Q

Identify 5 symptoms of cirrhosis

A
  • Fatigue/weakness
  • Ascites
  • Swollen legs (hypoproteinaemia)
  • Weight loss
  • Jaundice
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31
Q

What are the typical blood test findings for cirrhosis?

A
  • May all be normal
  • May show a low albumin and/or prolonged INR
  • May show a raised bilirubin
  • May be a slight rise in ALT (if ongoing inflammation)
  • May be very mild raise in Alk Phos (if cholestasis)
  • May show a raised Gamma GT (if alcoholism)
32
Q

What is the treatment of cirrhosis?

A
  • Fibrosis is irreversible so a liver transplant is needed
  • Treatment is aimed at managing the complications
33
Q

What are the 2 main causes of gall bladder obstruction?

A
  • Gallstone migration from the gallbladder into common bile duct
  • Carcinoma of the head of pancreas
34
Q

What are the typical laboratory findings in post-hepatic/obstructive jaundice?

A
  • Normal serum albumin and INR
  • Normal/slightly raised serum ALT
  • Very high serum bilirubin
  • Conjugated bilirubin present in the urine
  • Raised Alk phos and Gamma GT
35
Q

What is cholangitis?

A

Cholangitis is an infection in the bile ducts and a life-threatening complication of common bile duct obstruction, commonly caused by E. Coli

36
Q

Why do gallstones develop?

A

Gallstones develop in the gallbladder due to chemical imbalances in the bile

high cholesterol - higher change of developing cholesterol gall stones

pregnancy

  • will feel right upper quadrant pain!!
37
Q

Biliary colic is not true colic.

What is it?

A
  • Biliary colic is pain in the right upper quadrant that radiates to the tip of the right scapula/right shouder
  • It is often precipitated by eating a fatty meal and lasts up to 6 hours
  • CCK released so gall bladder contracts and pushes gall stone up to neck of gall bladder → block duct → then over time the ball will go down
  • give pain relief and remove gall bladder
38
Q

What is acute cholecystitis?

A

Acute cholecystitis is inflammation of the gallbladder, occurring when a gallstone blocks the cystic duct and doesn’t move and commonly caused by E.coli

  • can diagnose → tell them to breathe in, feel right hand side and you can feel inflamed gall bladder and they’re in pain when you feel it
39
Q

Apart from severe gallbladder pain, how does a patient with acute cholecystitis present?

A
  • Systemically unwell
  • Pyrexia
  • Tenderness over the gallbladder
40
Q

Why is the liver a common site for metastases?

A

The liver is designed to filter the blood entering it and cancer cells can lodge in the filter

41
Q

What are the laboratory findings in liver metastases?

A
  • Raised serum bilirubin
  • Conjugated bilirubin present in the urine
  • Raised Alk Phos
  • Slightly raised ALT and Gamma GT
  • Normal serum albumin and INR
42
Q

What are the two forms of pancreatitis?

A
  • Acute
  • Chronic
43
Q

What is acute pancreatitis?

A

- Acute pancreatitis is a common condition arising from the premature activation of pancreatic proteases in the pancreas itself rather than in the duodenum

  • These proteases then autodigest the pancreas and the retroperitoneum
44
Q

Identify and describe the 2 main causes of acute pancreatitis

A
  • Alcohol alters the balance between proteolytic enzymes and protease inhibitors, thus triggering enzyme activation
  • Gallstone obstruction causes pancreatic duct hypertension and the toxic effect of bile salts contribute to enzyme activation (biliary acute pancreatitis)
45
Q

What is chronic pancreatitis?

A

- Chronic pancreatitis is rare condition caused by alcohol abuse where repeated low grade pancreatitis causes pancreatic fibrosis

  • The pancreas becomes calcified and patients suffer severe epigastric and back pain that leads to opiate addiction and not infrequently suicide
46
Q

State 2 symptoms of acute pancreatitis

A
  • Epigastric pain that goes through to the back
  • Vomiting
47
Q

How can the diagnosis of acute pancreatitis be confirmed?

A
  • Raised serum amylase / serum lipase
  • CT scan used to look for pancreatic necrosis/pseudocyst
48
Q

Describe the treatment of acute pancreatitis

A
  • Analgesia
  • Supportive treatment
  • Fluid resuscitation
49
Q

What is pancreatic cancer?

A
  • Pancreatic carcinoma is a condition resulting from the uncontrolled cell growth in the pancreas which metastasises to the rest of the body
  • Nearly all are ductal adenocarcinomas and most are in the head of the pancreas
50
Q

Describe the clinical presentation of pancreatic carcinoma

A
  • Anorexia, malaise, fatigue
  • Significant weight loss
  • Epigastric and/or back pain
  • Dark urine
  • Pale stools
  • Pruritis
51
Q

what does the liver store

A
  • glycogen
  • vitamins
  • iron
  • copper
52
Q

what metabolic processes does the liver carry out

A
  • bilirubin
  • ammonia
  • drugs
  • alcohol
  • carbs liver
53
Q

how can oedema or ascites come about

A

due to livers abnormality forming albumiun

reduced oncotic pressure harder to draw water in

54
Q

how can bleeding be caused due to a defect of the liver

A

over Time liver is damaged it can mean that it can’t produce clotting factors properly

55
Q

how can confusion come about

A

ammonia related in the liver

56
Q

what are the important symptoms of liver disease

A
  • Jaundice
  • oedema
  • bleeding
  • confusion
57
Q

which medication should be avoided to give to children

A

aspirin can cause acute liver failure

58
Q

reasons for acute liver disease

A
  • alcohol
  • paracetamol
  • viral
  • medications eg asprin
  • acute is when there has been no history of this problem before and it has just come about
59
Q

how can drugs cause liver cirrhosis (chronic liver disease)

A
  • iatrogenic → when medications become hepatotoxic and cause chronic inflammation
  • alcoholic liver disease → most common cause for chronic liver disease causes fatty changes in the liver = hepatomegaly
  • alcohol hepatitis → over the course of years when the damage is irreversible
60
Q

how can infections cause liver cirrhosis (chronic liver disease)

A

Blood borne viruses (can be transferred via IV)

  • hep B → no cure but a vaccine
  • hep C → cure but no vaccine

these use a risk for hepatocellular carcinoma

61
Q

how can deposition cause liver chirrosis (chronic liver disease)

A
  • non alcoholic fatty liver disease due to insulin resistance so built up of triglycerides
  • non alcoholic steato hepatitis → inflammation
  • hereditary haemoghromatosis → excessive deposition of iron in the liver → more feratin → so must take out blood to remove iron in circulation
  • Wilsons disease → reduced secretion of copper → copper accumulates in liver (might need a liver transplant)
62
Q

how can autoimmune conditions cause liver chirrosis (chronic liver disease)

A
  • autoimmune hepatitis → hepatocytes effected by ASMA, ANA
  • PBC
  • PSC → can be linked to ulcerative colitis
63
Q

what is the difference between the portal system and the systemic system

A
  • portal systems are veins that pass through the liver before they enter the inferior vena cava
  • systemic system are veins that don’t pass the liver to get to the inferior vena cava
64
Q

outline the portal system

A
  1. the internal mesenteric vein joins up with the splenic vein
  2. this joins to the superior mesenteric vein
  3. this then forms the portal vein
  4. the portal vein then supplies the liver with blood
  5. then hepatic veins drain into the inferior vena cava
65
Q

what are varices, which areas can be effected due to portal hypertension?

A
  • they expanded blood vessels
  • oesophagus → has anastomosis of portal and systemic veins → varices are superficial, can burst, will cause vomiting of blood
  • ano-rectal → between superior and middle and inferior rectal veins → both drain into the inferior vena cava (overlap) → can cause varices → rarely cause pain and bleed as they are tough
  • umbilicus → capa medusa, can cause distension of abdominal veins
66
Q

what us hepatorenal syndrome?

A
  • rapid deterioration of kidney due to the failing liver and portal hypertension (only due to significant failure of liver)
  • backlog of blood into arterial blood supply (splanchnic)
  • this sets of splanchnic arteriole vasodilation to relieve pressure
  • systemic circulation will see this as a drop in pressure
  • activate RAAS, to increase pressure
  • vasoconstriction of blood going to the kidney
  • reduced perfusion to kidney
  • reduced kidney function
67
Q

briefly outline the anatomy of the billary tree

A
  • right and left hepatic duct join → hepatic duct
  • hepatic duct fuses with the cystic duct (duct from gall bladder → cystic meaning bag)
  • this forms the common bile duct
  • the CBD fuses with the pancreatic duct
  • they form an ampulla of vater
  • where sphincter of oddi sits controlling release of bile
68
Q

what are the 3 direct implications of a gall stones

A
69
Q

outline some pathology that can cause post hepatic jaundice

A
  • gallstones
  • blockage in the biliary structure
  • pancreatic carcinoma
70
Q

outline some lover pathology that can present as intra hepatic jaundice

A
  • inflammation from autoimmune conditions
  • primary or metastatic malignancy inside the liver
  • cirrhosis
71
Q

what’s included in a liver function test

A
  • Albumin: can have a renal and liver cause for reduced albumin
  • ALT: Alanine Transaminase → will be revised but more raised in acute liver failure
  • AST: Aspartate Transaminase:
  • skeletal muscle ( rise in creatine kinase)
  • cardiac muscle (rise in troponin)
  • Red blood cells (FBC)
  • raised more in chronic liver failure
  • ALP: lines bile ducts (can be raised in children as their bones grow)
  • Bilirubin: unconjugated is dangerous as it can pass the blood brain barrier and can cause big problems in brain
72
Q

what will an LFT show for pre hepatic jaundice

A

everything should be normal

BUT high unconjugated bilirubin

73
Q

what does an increase in ALT and AST on an LFT show but no jaundice

A
  • hepatocellular damage
74
Q

what do high levels of unconjugated bilirubin (jaundice) and high ALP show on an LFT including epigastric and back pain show?

A
  • shows post hepatic failure
  • blockage of a bile duct
  • can be acute pancreatitis
75
Q

what test results would support having acute pancreatitis

A
  • high ALT
  • high amylase
  • high lipase
76
Q

what does ALP indicate

A

a blockage somewhere normally in the bile ducts

77
Q

what could raised:

ALT

AST

ALP

bilirubin

all suggest

A
  • mixed picture
  • ALT and AST : shows hepatocellular damage
  • ALP: could show a blockage somewhere

most likely liver metastases → direct damage to hepatocytes and can cause compression on the bile ducts

→ hepatic and post hepatic damage

SA gastro-intestine (19 decks)

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