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Gastrointestinal system > Liver and pancreas > Flashcards

Liver and pancreas Flashcards

1
Q

What hormone causes bicarbonate release and from where when chyme enters the duodenum?

A

Secretin, causes pancreas to release bicarbonate

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2
Q

What effects does CCK release have when chyme enters the duodenum?

A
  • Stimulates pancreas to release digestive enzymes - Causes gall bladder to contract and sphincter of odi to relax so bile can enter lumen
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3
Q

Other than CCK, what else stimulates enzyme and bicarbonate release form the pancreas?

A

Parasympathetic NS

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4
Q

What are the anatomical regions of the pancreas?

A

Tail, body, neck, head and uncinate (inferior to the head)

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5
Q

What components of pancreatic secretions are released by the acinar cells, and what’s released by the ductal cells?

A

Acinar= enzymes (amylases, lipases and proteases) Ductal cells= aqueous component and bicarbonate

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6
Q

What are zymogen granules?

A

These are capsules within the acinar cells which store the zymogens (enzyme precursors), until theyre ready to be released.

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7
Q

Describe the structure of the billary tree

A

Two common hepatic ducts drain into the cystic duct which drains into the gall bladder. The cystic duct is also the route of bile exit for the gall bladder, after the entry of the common hepatic duct it becomes the common bile duct. Once this joins with the pancreatic duct it becomes the hepatopancreatic duct or ampulla of vater.

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8
Q

What does bile consist of? (3)

A

bile acids, bile pigments and an alkaline solution

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9
Q

Where are bile acids, bile pigments and the alkine solution produced from?

A

Bile acids and pigments= hepatocytes

Alkaline solution= ductal cells

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10
Q

What does the gall bladder do to bile?

A
  • Stores it
  • Concentrates it

(Over concentration leads to gall stones)

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11
Q

What are bile salts?

A

Bile acids (eg cholic acid) conjugated with an amino acids (eg glycine)

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12
Q

Why are bile salts needed?

A

Because bile acids are not always soluable at duodenal pH, and if they weren’t theyd be useless.

It also gives them a hydrophillic and hydrophobic end, which enables them to emulsify fats

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13
Q

How are lipids digested and absorbed?

A
  • Bile salts break down large globules of lipids into many small gobules so increased SA for fast digestion w/ lipases.
  • Bile salts then create micelles w/ cholesterol and lipid breakdown products in
  • Micelles transport digested lipids to enterocytes where they can diffuse in
  • The lipid based molecules are built back up into TAG, phospholipids ect and packaged w/ apolipoproteins into chylomicrons which enter the lymphatics
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14
Q

Describe the recyling of bile salts

A

Bile salts not reabsorbed w/ the fats but remain in the lumen until they reach the terminal illeum where they are then reabsorbed and sent back to the liver

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15
Q

What is the functional area of a liver lobule called?

A

An acinus

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16
Q

Which area of a liver acinus is first affected by ischaemia?

A

the central zone (nearest the portal vein// zone 3) - worst blood supply as furthest from the portal triad (hepatic artery)

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17
Q

Which area of the liver acinus is first affected by toxins?

A

The peripheral zone (nr portal triad// zone 1)- this area has the best blood suppply as its nearest the hepatic artery. This does however mean its exposed to toxins first so more.

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18
Q

What is steatorrhoea and what causes it?

A

When there is fat in your poo- making it yellow, smelly and floating.

It is almost always due to pathology causing inadequate secretion of bile salts or pancreatic lipases than excess fat consumption.

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19
Q

What lies within the base falciform ligament?

A

the remenant of the fetal umbelical vein- which is also called the round ligament or ligamentum teres

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20
Q

What breaks down RBCs and where?

A

Macrophages in the spleen (and a bit in liver)

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21
Q

Describe the normal process of heame excretion after the RBC it came from is broken down

A
  1. haem is converted to bilirubin which binds to albumin in blood and goes to the liver
  2. In liver its conjugated w/ glucoronic acid by UDP glycyronyl transferase
  3. Conjugated bilirubin is water soluable so is secreted into bile canniculi
  4. Its released in bile, in the small intestine its converted into urobilinogen
  5. 10% of this is reabsorbed and travels to kidneys in blood, where its converted to urobilin and excreted (makes urine yellow)
  6. 90% is converted to stercobilin in the large bowel and is excreted in poo (makes poo dark brown)
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22
Q

What colour will urine go if there is excess conjugated bilirubin in the blood?

A

Dark yellow/ orange

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23
Q

How can excess urobilinogen be detected in the urine?

What pathology could cause increase in urobilinogen in urine?

A

No colour change but can be detected in urine?

haemolytic anaemia

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24
Q

Why do you get puritis w/ cholestasis?

A

bile not moving–> bile salts back up–> bile salts released into blood–> bile deposited in tissues–> causes itching

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25
Q

Give a cause of prehepatic jaundice?

A

haemolytic anaemia

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26
Q

What is the colour differance between prehepatic, intrahepatic and post hepatic jaundice?

A

pre= mild jaundice

Intra= moderate jaundice

Post= sevre jaundice (green tinge)

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27
Q

What will happen to the stool colour and urine colour in prehepatic jaundice?

A

Stool darker as more sterobilin excreted

Urine normal as conjugated bilirubin isnt forced into it (although there will be increased urobilin, but this can only be detected in dipstick)

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28
Q

Will there be puritis in pre, intra and/ or post hepatic jaundice?

A

In pre and intra no, as bile still able to leave

But there will be in post hepatic jaundice

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29
Q

What will happen to the serum bilirubin in prehepatic jaundice?

A

Increase

30
Q

What is intrahepatic jaundice and what causes it?

A

Failure of hepatocytes to conjugate and/ or secrete bilirubin

Eg in hepatitis or cirrhosis

31
Q

What will happen to the stool and urine colour in intrahepatic jaundice?

A

Stool normal- bile can still get out and emulsify fats, but less conjugates bilirubin released in it, so no increase in stercobilin which wouldve made it darker

Urine may be yellow/ organge/ darker if problem in conjugated bilirubin release, because it will enter blood and so urine and so make it darker.

(urine normal if problem in conjugating it)

32
Q

What will happen to the serum bilirubin levels in intrahepatic jaundice?

A

increase- liver less able to conjugate it so it will back up

33
Q

What is post hepatic jaundice?

A

failure of the billary tree to move the conjugated bilirubin into the duodenum

34
Q

What will happen to stool and urine colour in post hepatic jaundice?

A

Stool- pale yellow, smelly and floating as no bile to emulsify fats

Urine- Conjugated bilirubin not able to be excreted in bile so goes into blood, and so kidneys and so urine, making it darker

35
Q

What does low serum albumin suggest?

A

SEVERE liver dysfunction- liver normally makes it

36
Q

What does prolonged prothombin time (INR) suggest in the context of liver insult?

A

SEVERE liver dysfunction

37
Q

What may cause a raised alkaline phosphatase?

A

Bile duct disease w/ cholestasis (released from bile ducts and bile canniculi)- billary obstruction, cirhosis, liver mets, drugs

Also released from bone- Bone cancers, osteomalacia, hyperparathyroidism, pagets disease of bone

38
Q

What causes a rasied alanine aminotransferase (AST)?

A

hepatocyte inflammation or damage

39
Q

What two things can Gamma GT be raised by?

A

Bile duct obstruction

Alcoholism (its induced by alcohol)

40
Q

What can cause a high ALT? (4)

A

Hepatitis A, B and C (very high)

Acute alcohol intake

Fatty liver disease

Drugs/ toxins

41
Q

What can USS be used for in relation to the liver? (5)

A
  • See billary obstructions (stones)
  • hepatic fibrosis
  • fatty liver
  • Ascities
  • liver mets
  • detect portal hypertension
42
Q

Give 4 causes of heptatits

A
  • viral
  • drugs/ toxins
  • acute alcohol intake
  • fatty liver disease
43
Q

Describe the presentation of hepatitis

A
  • Feeling generally unwell
  • Anorexia
  • fever
  • RUQ pain
  • Dark urine
  • Jaundice (high bilirbuin)
  • NORMAL INR AND ALBUMIN (need long term insult for these to drop)
  • Very high serum ALT and AST
  • Alk P and Gamma GT generally normal
44
Q

What is cirrhosis?

A

Fibrosis of the liver due to repeated insults to the liver leading to a hard, nodular and shrunken liver.

45
Q

What can cause cirrhosis (4)?

A

Alcohol

viral hepatits (usually c)

fatty liver

Idiopathic

46
Q

How does cirrhosis lead to hamorrhoids, oesphageal varices and capus medusa?

A

Occulsion of sinusoids-> portal hypertension-> portosystemic shunting (more blood from GI tract drains into veins going directly into IVC.

Therefor increased venous pressure at anorectal junction (haemorrhoids), oesphagogastric junction (oesphageal varices) and paraumbelical veins (capus medusa)

Veins then become incompetant under such a high pressure so become varicose (dilated, twisted ect)

47
Q

How does cirrhosis lead to ascites?

A

Decreased albumin production= decreased oncotic pressure

+

Portal hypertension

48
Q

What is the presentation of somone with cirrhosis?

A
  • tiredness/ fatigue/ weakness
  • bleeding and brusing easily
  • swollen legs and abdomen
  • weight loss
  • jaundice
  • confusion, drowsiness and slurred speech due to high ammonia
  • haemorrhoids, oesphageal varices and caput medusa
49
Q

What is this?

(see photo)

A

Caput medusae

50
Q

Describe the blood results of someone with cirrhosis

A

MAY BE NORMAL

  • low albumin and maybe INR if severe
  • High albumin (may be due to compensation)
  • Slightly raised ALT and AST if ongoing inflammation
  • Alk phos normal or high if canniculi affected
  • Gamma GT induced by alcohol so high if alcohol is the cause
51
Q

How is cirrhosis treated?

A

deal with complications

only cure is transplant (ethical issues)

52
Q

What are the two leading causes of billary duct obstructions?

A

Stones

Carcinoma of head of pancreas

53
Q

What are the 2 main causes of gall stones

A

4/5 are excess cholesterol crystallisation

1/5 are due to excess bilirubin crystalisation

54
Q

What is the resulting syndrome if you get a gall stone stuck in your cystic duct?

A

billary colic

(not a true colic because pain is constant)

55
Q

What is the name for gall bladder inflammation as a result of a stone stuck in the cystic duct?

What is cholangitis?

A

cholecystitis- inflammation may be due to physcial injury/ ichaemia or due to infection

Cholangitis is inflammation of the common due to a stuck stone

56
Q

What is ascending cholangitis?

A

bacteria ascending the billary tree because bile is not flushing it out- usually E. Coli

57
Q

What will be the result of a stone stuck in the ampullar of vata?

A

cholangitis

acute pancreatitis - enzymes cannot get into dueodenal lumen, will become activated in the pancreas and auto digest it

58
Q

Describe the presentation of a billary tree obstruction?

A

rapid onset, severe right upper/ mid quadrant pain, radiating to the shoulder tip, often precipitated by eating a fatty meal, fever, post jaundice

If infection: shock, toxic, confused ect

Tenderness over gall bladder (may be palpable)

Loose, pale, floating stools

59
Q

How are billary duct obstructions diagnosed?

A

ERCP (endoscopic retrograde cholangiography)- can also remove stone with this but 5-10% mortality.

Also USS

60
Q

What is an acute pancreatic pseudocyst?

A

Pancreatic fluid accumulations, formed on the pancreas due to acute pancreatitis

They may be seen on CT and are good indications of pancreatitis

61
Q

how does alcohol lead to acute pancreatitis?

A

It alters the balance between proteolytic enzymes and protease inhibitor release, triggering enzyme activation and autodigestion

62
Q

Describe the presentation of someone with acute pancreatitis?

A

Severe, sudden onset epigastric pain through to the back.

Nausia and vomiting

Pleural effusion

Anorexia

Heptatomegaly

Other symptoms of the cause

63
Q

How can acute pancreatitis be diagnosed?

A

Raised amylase or lipase

CT scan showing pseudocyst or tissue necrosis

64
Q

How is acute pancreatitis managed?

A

No specfic treatment

Supportively- analgesia, fluid resus (can loose lots into retroperitoneal space)

65
Q

Is chronic pancreatitis common? What causes it?

A

No its rare

Its due to repeated, low grade attacks of acute pancreatitis, the commonest cause is alcohol abuse.

66
Q

Why do lots of people with chronic pancreatitis commit suicide?

A

The pancreas can calcify, and cause severe epigastric and back pain, leading to opiate abuse and often suicide.
You commonly also get T1 diabetes which reduced QoL.

67
Q

Where are the caudate and quadrate lobes in relation to eachother?

A

caudate is superior, quadrate inferior, next to gall bladder

68
Q

What is within the porta hepatis?

A

Hepatic portal vein, hepatic artery, common hepatic duct

69
Q

How is the liver suspended in the abdominal wall?

A

by the falciform, coronary and triangular ligaments and its connection to the IVC via hepatic veins

70
Q

Where is the bare area of the liver? What is it?

A

the upper portion of the right lobe.

It is an area with no peritoneal covering.

71
Q

What may cause pancreatitis?

A

GET SMASHED:

I: idiopathic

G: gallstones

E: ethanol (alcohol)

T: trauma

S: steroids

M: mumps (and other infections) / malignancy

A: autoimmune

S: scorpion stings/spider bites

H: hyperlipidaemia/hypercalcaemia/hyperparathyroidism (metabolic disorders)

E: ERCP- treatment for gall stones

D: drugs

Gastrointestinal system (9 decks)

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