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Week 1 Revision > Liver, Gall Bladder and Pancreas > Flashcards

Liver, Gall Bladder and Pancreas Flashcards

1
Q

How is the chyme secreted from the stomach corrected in the duodenum?

A
  1. Acidity is corrected by the addition of HCO3- from pancreas, liver and duodenal mucosa
  2. Hypertonicity is corrected by the osmotic movement of water across the duodenal wall
  3. Partial digestion -> completion by bile acids from the liver, and enzymes from the pancreas and duodenal mucosa.
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2
Q

Where is bile secreted from?

A

Liver

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3
Q

What are the constituents of bile? what cells are they secreted from?

A

Bile acid dependent:

  • bile acids or bile salts: cholic acid/chenodeoxycholic acid
  • cholesterol
  • bile pigment esp. bilirubin
  • secreted from cells lining canaliculi

Bile acid indepedent:

  • HCO3-
  • secreted from cells lining intra-hepatic bile ducts
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4
Q

How are bile acids secreted?

A

Stomach empties causing duodenum to release CCK.

CCK causes gall bladder contraction and release of bile acids, which together with pancreatic enzymes and HCO3- from pancreas and liver (secreted under the influence of secretin) enter the duodenum via the ampulla of Vater

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5
Q

How are bile acids recovered via the entero-hepatic circulation?

A

Either unconjugated by gut bacteria and are lost - replaced by hepatocytes

or

reabsorbed by epithelium in the terminal ileum into gut venous blood which joins the hepatic portal blood which enters the liver via the hepatic portal veins. in the liver, heaptocytes take bile acids up and resecrete them into canaliculi which flow into biliary ducts into the gall bladder for storage for secretion with the next time the stomach empties and CCK is secreted by teh duodenum.

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6
Q

How can the storage of bile salts lead to the formation of gallstones?

A

Bile salts are secreted by canaliculi inbetween meals, well before they are needed so they are stored in the gallbladder.

To reduce storage volume, they are stored in a concentrated form, which increases the risk of percipitation and formation of gall stones.

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7
Q

Gallstones are usually asymptomatic. When do they pose clinical problems? What can worsen these symtpoms?

A

When they move to the neck of gall bladder or biliary tree. here, they can cause

1) painful biliary colic
2) obstruction

both of which can cause cholecystitis (inflammation)

eating -> increase in pain (due to release of CCK -> gall bladder contraction)

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8
Q

What is biliary colic?

A

Biliary colic is the term used to describe a type of pain related to the gallbladder that occurs when a gallstone transiently obstructs the cystic duct and the gallbladder contracts. Pain is the most common presenting symptom. It is usually described as sharp right upper quadrant pain that radiates to the right shoulder, or less commonly, retrosternal. Nausea and vomiting can be associated with biliary colic. Individuals may also present with pain that is induced following a fatty meal and the symptom of indigestion. The pain often lasts longer than 30 minutes, up to a few hours.

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9
Q

What are the exocrine secretions of the pancreas?

A

HCO3-
Proteases - carboxypeptidases, trypsinogen, chymotrypsin and elastase
Amylases
Lipases

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10
Q

What are the exocrine secretions of the pancreas? From what cells are each secreted?

A

HCO3- from duct cells

proteases - chymotrypsin, trypsinogen, elastase, carboxypeptidase, amylases and lipases by acinar cells

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11
Q

What is the mechanism of HCO3- secretion from pancreatic duct cells

A

BL membrane:

  1. NA-K-ATPase sets up Na concentration gradient
  2. which is used to export H+ out of the cell via the BL membrane
  3. In the ECF, H+ combines with HCO3- to give water and CO2
  4. CO2 diffuses into duct cell via BL membrane where it recombines with water to give H+ and HCO3-

Luminal membrane - HCO3- diffuses out of cell into lumen

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12
Q

how is HCO3- secretion from pancreatic duct cells controlled?

A

Secretin.

Jejunum detects low pH -> secretes secretin -> causes pancreatic duct cells to secrete HCO3-

secretin secretion is also facilitated by CCK release from the duodenum

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13
Q

What stimulates pancreatic enzymes release?

A

gastric emptying -> duodenum -> increase in tonicity and fats -> CCK release from APUD cells -> pancreatic acinar cells -> enzyme release (+gall bladder contraction -> bile)

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14
Q

What cells is CCK released from?

A

APUD cells in duodenum

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15
Q

What is the mechanism for the digestion of fats?

A

Fats are relatively insoluble so tend to aggregate and form large globules - difficult for enzymes to effectively digest them. Acid of stomach further aggravates this.

Bile salts allow micelles to form, making fats more soluble and increase surface area on which lipases can work.

Micelles carry fats to unstirred layer next to the mucosa of the small intestine. Here, fatty acids are released and taken up by epithelial cells.

In epithelial cells, they are re-converted back into TAGs and are expelled from the cells as chylomicrons to be transported around the lymphatic system.

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16
Q

What are the two functions of bile salts?

A

1) Make fatty acids more soluble

2) Increase surface area of fatty acids on which lipases can act effectively

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17
Q

How is steatorrhoea caused?

A
  1. insufficient lipase secretion from pancreatic acinar cells
  2. insufficient bile acid secretion from liver/gall bladder

leading to presence of fat in stools -> pale, floating stools

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18
Q

What are the physical innate defences of the GI tract?

A
  1. Sight/smell
  2. memory - if you remember that it tastes bad, you wont eat it
  3. saliva - alkaline, lactoperoxidase, lysozymes, complement, polymorphs (leukocytes), IgA
  4. small intestine secretions - bile, proteolytic enzymes, nutrient deprived environment, shedding of epithelial cells
  5. small bowel and colon - anaerobic environment
  6. colonic mucous - protcts epithelium
    gut motility - 12-18 hours, segmentation and peristalsis
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19
Q

What happens if gut motility transit time increases?

A

Increased risk of infection

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20
Q

What are the cellular innate defences of the GI tract?

A
  1. neutrophils
  2. mast cells
  3. NK cells - kill viral infected cells
  4. eosinophils - parasitic infections
  5. macrophages - kupffer cells in the liver
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21
Q

How can a GI infection causing mast cell activation cause severe fluid loss?

A

mast cells activated (antigen bind IgE) -> mass mast cell degranulation -> histmaine -> increased vascular permeability and vasodilation -> fluid loss

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22
Q

What are the adaptive GI defences?

A
  1. t lymphocytes - effective against intracellular organisms
  2. b lymphocytes - IgA and IgE - effective against extracellular organisms
  3. lymphoid tissue - GALT
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23
Q

Where is GALT present? GALT infections?

A
  1. Tonsils - tonsilitis
  2. peyer’s patches - ileocecal lymphatic tissue infected by adenovirus -> mesenteric adenitis
  3. appendicitis - inflammation at base of appendix -> blockage -> stasis -> infection, purulent in cases of chickenpox, can also be caused by faecocolith or worm infeciton -> obstruction
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24
Q

What is mesenteric adenitis caused by? Where is the pain? What is it commonly mistaken for?

A

Mesenteric adenitis - infection of the ileocecal lymphatic tissue - caused by adenovirus - pain in RIF - commonly mistaken for appendicitis in children

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25
Q

what organisms are resistant to GI tract defences, mainly stomach acid?

A

Mycobacterium TB
H. pylori (produces urease -> protective ammonia cloud) - 13C urea breath test - breathe out 13C = urease present in stomach
Enteroviruses: polio, coxsackie and hep A

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26
Q

Xerostomia - complications

A

illness/dehydration -> reduced or absent saliva production - microbial overgrowth in oral and dental cavities - especially staph A -> parotitis

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27
Q

Achylordia - complications

A

Reduced or absent stomach acid production due to:

  1. pernicious anaemia
  2. drugs such as H2 antagonists and PPIs

Achlorydia increases the risk of infections with shigellosis, cholera, salmonella and C.diff in hospitals

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28
Q

What type of bug is Staph A? How can we treat it?

A

Gram positive

Treat with cephalosporins, carbapenems - meropenem and glycopeptides - vancomycin

29
Q

what can cause gut ischameia? And can result of gut ischaemia?

A

Intestinal venous thrombosis, arterial disease, and systemic hypotension can lead to gut ischaemia which leads to overwhelming sepsis and death

30
Q

Why does liver failure cause increase in hepatic encelopathy?

A

Ammonia is produced by gut bacteria and the deamination of amino acids. Liver failure results in failure of the urea cycle -> build up of ammonia causing hepatic encephalopathy

31
Q

How does cirrhosis lead to oesophageal varices, caput medusa and haemarrhoids?

A

Cirrhosis leads to portal venous hypertension which leads to portosystemic shunting. This shunting causes oesophageal varices, caput medusa and haemarrhoids.

32
Q

What chemicals does the liver deal with?

A

Bile pigments - main constituent: bilirubin from breakdown of Hb - conjugated in liver with glucoronide and sulphates - and secreted in bile -> excretion in faeces

Enzyme breakdown - insulin

Drugs

Toxins

Alcohol

33
Q

How is alcohol metabolised?

A

alcohol -> acetaldehyde by alcohol dehydrogenase

acetaldehyde -> acetate by acetaldehyde dehydrogenase

Process uses NAD+ and ATP to produce NADH and Acetyl CoA

34
Q

What are the consequences of chronic alcoholism?

A

Acetaldehyde is toxic to liver -> liver damage

low NAD+ :

  1. can’t convert lactate into pyruvate - lactic acidosis
  2. kidneys are less able to excrete uric acid -> builds up in tissues -> gout
  3. failure to activate gluconeogenesis due to decrease lactate use, low NAD+ and low glycerol (low NAD+ affects glycerol metabolism) -> fasting hyperglycaemia

low NAD+ and high Acetyl-CoA:
fatty liver - NAD+ needed for beta oxidation of FA, without, you get increased FA synthesis and ketone bodies production. FAs get converted into TAGs but lack of LDLs means that they’re not effectively transported so build up in the liver -> fatty liver.

Increase ketone bodies production also leads to keto-acidosis

35
Q

What 4 blood proteins does the liver handle?

A
  1. amino acids - synthesis via transamination
  2. thrombopoietin - regulates platelet production in bone marrow
  3. coagulation factors: fibrinogen (I), prothrombin (II), V, VII, IX, X, XI and protein S, protein C and antithrombin
  4. albumin - most abundant plasma protein that controls oncotic pressure
36
Q

When is jaundice clinically detected?

A

Bilirubin levels twice the upper limit of normal i.e. >40micromols

37
Q

How does pre-hepatic jaundice come about?

A

Increased haemolysis - too much bilirubin for liver to handle and conjugate

38
Q

What are the congenital/inherited causes of pre-hepatic jaundice

A
  1. Gilbert’s syndrome - reduced action of bilirubin conjugating enzyme: glucronyltransferase
  2. RBC membrane defects - sickle cell, hereditary spherocytosis/elliptocytosis
  3. Hb defect
  4. Metabolic defects
39
Q

What are the acquired causes of pre-hepatic jaundice?

A
  1. immune and infection
  2. mechanical - RBCs over prosthetic heart valves - lysis
  3. drugs
  4. burns
40
Q

What are the 5 lab findings of pre-hepatic jaundice?

A
  1. decreased haptoglobin - haptoglobin binds free Hb thats released from RBCs - transports to spleen for removal - too much Hb in blood means a decreased level of free haptoglobin
  2. unconjugated hyperbilirubinaemia
  3. anaemia
  4. increased LDH
  5. reticulocytosis
41
Q

What gives rise to hepatic jaundice?

A

Liver damage - liver is less able to secrete conjugated bilirubin

42
Q

Causes of hepatic jaundice?

A
  1. Congenital - wilson’s (copper overload), gilbert’s
  2. hepatitis - viral (Hep A/B/C/E, EBV), alcohol, autoimmune, haemochromatosis (iron overload), wilson’s hepatitis
  3. malignancy - hepatocellular adenocarcinoma or mets
  4. drugs - paracetamol
  5. cirrhosis - alcohol, non-alcoholic - metabolic disorders, DM and obesity
43
Q

What are the 3 lab findings of hepatic jaundice?

A
  1. elevated ASTs/ALTs
  2. unconjugated and conjugate hyperbilirubinaemia
  3. abnormal clotting
44
Q

What gives rise to post-hepatic jaundice?

A

intrahepatic causes
hepatitis, drugs, cirrhosis, primary biliary colic

extrahepatic causes

  • carcinoma of the bile duct, pancreatic duct, liver mets, porta hepatis lymph nodes, of the ampulla of Vater
  • gallstones
  • pancreatitis
  • sclerosing choleangitis
45
Q

What are the 4 lab findings of post-hepatic jaundice?

A
  1. dark urine - urobilinogen
  2. raised ALPs
  3. normal AST/ALTs
  4. conjugated bilirubinaemia
46
Q

What clinical problems can alcohol give rise to in the liver?

A
  1. alcoholic hepatitis - inflammation of hepatocytes
  2. fatty liver - reduced NAD+ -> FA synthesis occurs instead of oxidation (break down) - FA -> TAGs - low LDLs so not transported, and stored in liver
  3. cirrhosis - fibrosis and nodular formation following liver cell necrosis and regneration
47
Q

What occurs to blood flow in a cirrhotic liver?

A

Increase resistance to blood flow

48
Q

what is wernicke korsakoff’s syndrome?

A

alcohol affects thiamine absorption in GI tract, and affects thiamine storage in liver -> thiamine deficiency -> encephalopathy and fucked up brain

btw encephalopathy -> confusion and dementia

49
Q

what is palmar erythema? what condition can you get it in?

A

reddening of skin, usually over the hypothenar eminence - you get it in cirrhosis/liver disease in general due to abnormal oestradiol levels -> oestradiol causes increased vascularity

50
Q

What are the signs of liver cirrhosis?

A

Palmar erythema, anaemia, jaundice, bruising, dupuytren’s contractures

51
Q

What are dupuytren’s contractures? what condition does it occur in?

A

occurs in cirrhosis/ liver disease - flexion contracture due to thickening and scarring of fascia covering the tendons in the hand affecting hte little and ring finger most - unknown pathophysiology

52
Q

How would you investigate cirrhosis?

A
  • raised ALTs/ASTs
  • raised bilirubin
  • deranged clotting
  • raised ALPs
  • hypoalbuminaemia
53
Q

Treatment of cirrhosis

A
  1. stop drinking
  2. treat complications
  3. transplant
54
Q

Define portal hypertension

A

Portal venous pressure exceeding 20mmHg

55
Q

What is portal hypertension caused by

A

Obstruction to portal vein - compression or thrombosis

obstruction to blood flow in liver - cirrhosis, hepatoportal sclerosism schistomatosis, sarcoidis

56
Q

What are the three consequences of portal hypertension?

A
  1. ascites
  2. splenomegaly
  3. portosystemic shunting -> varices
57
Q

Why does ascites occur with portal hypertension

A

Increased pressure of the portal venous system causes blood to back up into the abdomen.

The increased hydrostatic pressure in the lumen means that less fluid is reabsorbed into blood vessels -> fluid accumulation in abdominal cavity.

Ascites can be worsened if liver damage is prominent due to resulting hypoalbuminaemia and decreased in oncotic pressure of the blood vessels.

58
Q

Why does splenomegaly occur with portal hypertension?

A

Increase BP - spleen grows in size

59
Q

Why does portosystemic shunting occur with portal hypertension?

A

portal vein makes anastomoses with systemic veins. increased pressure in portal veins causes blood to back up through the anastamoses causing a rise in blood pressure. Increased BP -> dilated veins (varices).

60
Q

What are the complications of varices?

A

They can protrude into the lumen
they can ulcerate
they can rupture -> haemorrhaging

61
Q

Where are the portosystemic anastamoses and the varices they cause?

A

Superior -> inferior rectal vein - rectal varices
Paraumbilical vein -> small epigastric vein - caput medusae
Left gastric vein -> oesophageal vein - oesophageal varcies

62
Q

What is pancreatitis?

A

inflammation of the pancreas due to pancreatic enzymes released by acini

63
Q

What are the causes of pancreatitis?

A

GET SMASHED

  • gallstones - obstruction of pancreatic duct or ampulla of vater - stasis -infection
  • ethanol - hyperstimulates pancreatic enzymes
  • trauma
  • steroids
  • mumps
  • autoimmune
  • scorpion bite
  • hyperlipidaemia
  • ECRP/iatrogenic
  • drugs
64
Q

Where can gallstones cause obstruction that would lead to pancreatitis?

A

Ampulla of vater or pancreatic duct

65
Q

How does acute pancreatitis present?

A

severe pain

oedema, haemorrhage, vomiting -> dehydration and shock

66
Q

What are the clinical findings of acute pancreatitis?

A

raised ALPs, raised bilirubin, raised amylase (pancreatic amylase released into blood), glycaemia

decreased calcium

67
Q

why do you get decreased calcium in acute pancreatitis?

A

it causes percipitation of calcium in the abdomen -> less free calcium

68
Q

How does chronic pancreatitis present?

A 
Pain
hypoalbuminaemia 
jaundice 
steatorrhoea 
malabsortiopn -> weight loss
69
Q

What is the msot common type of pancreatic carcinoma and how does it present?

A

ductal adenocarcinoma - 90% of pancreatic carcinomas
no symptoms at first, but then a lot of symptoms all at once
- vomiting
- jaundice
- malabsorption
- pain
- DIABETES - insulin from beta cells in islets of langerhans!!!!!

Week 1 Revision (14 decks)

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