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year 2 sem 1 > wk 2 GI and Liver - part 1 > Flashcards

wk 2 GI and Liver - part 1 Flashcards

1
Q

liver segments

A
  • 8
  • Each has own supply from portal vein and hepatic artery
  • Each has branch of bile duct draining it
  • Each has segment of hepatic vein draining back into IVC
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2
Q

liver microanatomy

A
  • Hepatic globules each with own supply of hepatic artery, portal vein and bile duct
  • Draining into branch of hepatic vein
  • Hexagonal shaped segments
  • Central vein draining away in the middle
  • In between portal triads in Sinusoids are where functions of liver performed
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3
Q

hepatic sinusoid

A
  • Portal triad at one side
  • Portal venous blood and oxygenated blood mix and travel along sinusoid towards central vein
  • Sinusoid lined by liver sinusoidal endothelial cells
    o These maintain blood cells in sinusoid
    o Allow passage of metabolites, plasma proteins, lipid proteins, viruses etc into space of Diss
    o Hepatocytes then maintain homeostasis, sustaining nutrients, secrete bile and detoxify drugs in space of Disse
    o As blood passes along sinusoid metabolic functions of hepatocytes change (in part due to change in oxygenation as you move down this gradient
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4
Q

liver functions

A
  • Nutrient metabolism
  • Drug Metabolism
  • Protein synthesis
  • Secretion
  • Storage
  • Immunological function
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5
Q

glucose metabolism during fasting

A
  • Dec. insulin and inc. glucagon leading to normoglycaemia

o Glycogen breakdown in periportal hepatocytes
 Major glucose store in body

o Gluconeogenesis from
 Lactate, pyruvate, amino acids, glycerol

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6
Q

glucose metabolism during feeding

A
  • Inc. insulin and dec. glucagon leading to hepatic glucose uptake
    o Glycogen deposition in hepatocytes
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7
Q

lipid metabolism

A
  • Bile digests lipids in the gut -> Chylomicrons -> liver

- Chylomicrons metabolised by lipoprotein lipase -> cholesterol, phospholipids, triglycerides and free fatty

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8
Q

protein metabolism

A
  • Amino acid is absorbed from the small intestine
    o Hepatocytes metabolise proteins via the Krebs or citric acid cycle
    o -> hormones, neurotransmitters, plasma proteins, nucleotides (purine and pyrimidine)
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9
Q

ammonia

A
  • Absorbed from the gut but also synthesised in the liver
    o Detoxified in the liver by conversion to urea by the Krebs cycle
    o By product of digestion
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10
Q

albumin

A
  • Albumin
  • 10-12g/day and 55% of circulating protein
  • Transport proteins
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11
Q

bile

A

600ml/day made up of
o Bile acids primary (made in liver) and secondary (absorbed)

Allow digestion of dietary fats through emulsification

whats in bile?
BILE ACIDS
o Phospholipids
o Cholesterol
o Conjugated drugs
o Electrolytes – Na+, Cl-, HCO3- and copper
o Bilirubin
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12
Q

bilirubin

A
  • Heme is breakdown product of red blood cells
  • In spleen heme broken down to biliverdin -> unconjugated bilirubin
  • Transported down by albumin to liver where its conjugated and made soluble
  • Then excreted in bile going into deudenum
  • Conjugated bilirubin converted to urobilinogen

o Some converted into stercobilin -> gives stools brown colour
o some reabsorbed
o Some absorbed into blood and is excreted in urine
 Kidneys convert from urobilinogen to urobilin
 And excreted in the urine (giving yellow hue)

  • When you get bile duct obstruction you get pale stools this is due to the fact bilirubin is needed to give stools brown colour
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13
Q

vitamin storage

A
  • A,D and B12 are stored in large amounts
  • Small amounts of vit K and folate are rapidly depleted with decreased liver function
  • Metabolises cholecalciferol vitamin D3 -> activated 25-(OH) vitamin D
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14
Q

mineral storage

A
  • Iron stored in ferritin and haemosiderin

- Copper (can be affected by Wilson’s disease = excess levels of copper)

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15
Q

immune functions of the liver

A
  • ‘firewall” filtering all blood from gut
  • Kupffer cells phagocytose pathogens from gut
  • Supply of important chemokines
    o Interleukins
    o Tumour necrosis factor
  • Priming t cell repsonses
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16
Q

definition of liver cirrhosis

A
  • Development of regenerative nodules surrounded by fibrous bands in response to chronic liver injury
  • > portal hypertension and end stage liver disease
  • 4000 deaths/ year due to cirrhosis
  • > 700 transplants
  • Increase in mortality overtime
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17
Q

causes of cirrhosis

A 
- Viral infection 
o	Hep N and C
- Alcohol
- Non-alcohol steato-hepatitis
- Autoimmune disorders
o	AIH
- Cholestatic liver disease
o	PBC and PSC
- Metabolic causes
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18
Q

pathology of cirrhosis

A
  • Chronic injury
  • Overtime damage
  • Loss of pancrine cells and angiogenesis
  • Depends on genetics, alcohol, obesity
  • Fibrosis in reversible as you can remove the underlying cause

o However, if underlying cause cont. u get loss of architecture, loss of function, no hepatocyte regeneration -> cirrhosis
o Outcome is liver transplantation
o Once you have cirrhosis once you remove the underlying cause it doesn’t heal
o Once have cirrhosis at risk of hepatocellular carcinoma

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19
Q

hepatocyte injury results in…

A
  • Apoptosis and necrosis of hepatocytes
  • Recruitment of macrophages
  • Activation of macrophages and hepatic stellate cells
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20
Q

fibrosis

A
  • Inflammatory response leads to secretion of pro-inflammatory and pro-fibrotic mediators
  • Trans differentiation of stellate cells into myofibroblasts
  • These lead to matrix synthesis with a-SMA and collagen 1 – matrix deposition
  • Reduction in matrix degradation
  • If remove cause of injury you get dec. prod. Of pro-inflammatory cytokines
    o Leads to matrix degradation loss of myofibroblasts too
    o Progression of fibrosis
21
Q

stellate cells

A
  • Important in gen of fibrosis and cirrhosis
  • Activation of stellate cell + portal/ perivascular fibroblasts = myofibroblast
  • Myofibroblasts lead to inc. collagen synthesis + dec. in matrix metalloproteases
  • Collagen accumulation and organ failure
22
Q

consequence of inc. sinusoidal resistance

A

-Portal hypertension
o Portosystemic collaterals
 Meaning blood can pass from portosystemic to systemic system without going through the liver

• Eg ammonia doesn’t get de-toxified by liver can go to BBB causing cephalopathy

23
Q

varices

A

 Extra blood vessels around oesophagus and stomach and spleen
 Can lead to bleeding

  • caused by portal hypertension as blood can’t flow through normal route and so creates an alternative
  • bad because blood isn’t filtered by liver
24
Q

angiogenesis

A

 Inc portosystemic collaterals

 Inc. Porto venous blood inflow more hypertension

25
Q

splanchnic vasodilation

A 
 hypotension 
 relative decreased in effective volume
 vasoconstriction
 activation. Of reno-angiotensin aldosterone system 
•	surge in water retention
•	increase fluid vol.
•	ascites
•	increased CO
•	increased venous blood flow – inc. portohypertension
26
Q

physical signs of chronic liver disease

A

Liver in cirrhosis can be small or large
- In advanced - small due to high level of scarring

Splenomegaly

  • Due to portal hypertension
  • Feeds back through splenic vein leading to hypertrophy of spleen

Loss of body hair
- Due to effects on hormones

Spider Naevi
- Due to angiogenic factors released

Neurological effects
- Due to ammonia bypass in liver

Ascites

  • Due to portal hypertension
  • Fluid retention
27
Q

how to diagnose fibrosis/ cirrhosis

A

Liver biopsy

  • Gold standard, quantative
  • Sampling error (may underscore if chose wrong place), morbidity

Serum markers

  • Widely available, non-invasive
  • Nonspecific, grey zone for intermediate fibrosis
  • Can tell if someone cirrhotic but hard to tell if fibrotic

Elastography

  • Non-invasive, fast and user-friendly, validated in chronic hepatitis
  • Cost, confounding factors
  • Hard to get reading in obese patients
28
Q

serum markers in liver cirrhosis

A

ALBUMIN

  • Decreases in end-stage liver disease due to decreased synthesis
  • T1/2 – 20 days therefore useful in cirrhosis

PROTHROMBIN TIME

  • Decreased synthesis of clotting factors (I, II, V, VII, X) -> inc. PT
  • In cirrhosis associated with more advanced disease

BILIRUBIN
- Increased in end stage cirrhosis due to decreased clearance

PLATELETS

  • Decreased in cirrhosis
  • Splenomegaly -> inc. consumption
  • Decreased thrombopoietin produced by cirrhotic liver
29
Q

fibroscans

A
  • Works because liver should be like jelly/elastic
  • As more fibrotic liver becomes more solid
  • Probe measures the stiffness of liver by sending impulses through liver
  • Diff. scores suggest different types of liver cirrhosis and idea of extent of fibrosis
30
Q

child-pugh score

A
  • Assess risk of mortality after deciding patients cirrhotic
31
Q

jaundice

A
  • Yellowish pigmentation of the skin, membranes and sclera (conjunctival membrane)
  • Jaundice (jaune) = yellow
  • Visible at bilirubin level >35umol/L
32
Q

types of jaundice

A
  • Pre-hepatic (before liver)
  • Hepatic (in liver)
  • Post hepatic (consequence of something outside the liver)
33
Q

pre-hepatic jaundice

A
  • Eg Haemolysis
  • More bilirubin into system at very beginning
  • Too much unconjugated bilirubin for liver to conjugate it all
  • As water insoluble, does not enter urine
34
Q

hepatic jaundice

A
  • Mixed type of jaundice as…
  • Liver can’t uptake unconjugated bilirubin and can’t conjugate bilirubin normally
Caused by…
Hepatocyte damage due to…
- Cirrhosis
- Viruses – hepatitis, CMV
- Drugs – paracetamol
- Alcohol
- Sepsis
- Right heart failure
35
Q

post-hepatic jaundice

A
  • Blockage type cause after liver
  • Bilirubin still conjugated and so water soluble
  • Some water-soluble bilirubin leaks out into blood stream and is excreted by kidney
  • Makes urine really dark
  • Bilirubin not getting in poo – poo really pale
  • ITCHY – due to bile salts not getting through normally and therefore in skin
Caused by…
Classifications ->
- Within the lumen eg gallstones
- Within the wall eg tumours
- External compression eg pancreas cancer (squishing bile duct)
36
Q

obstructive jaundice - malignancy

A
  • hilar cholangiocarcinoma
  • hilar lymphadenopathy
  • distal cholangiocarcinoma
  • ampullary tumours
  • pancreatic tumours
37
Q

whipples

A
  • Operation for obstructive cancers at bottom
  • Distal cholangiocarcinoma’s
  • Ampullary tumours
  • Pancreatic tumours

Take out…

  • Gallbladder
  • Distal bile duct
  • Duodenum
  • Stomach
  • Pulling up jugular lens and stitching it back together
38
Q

ERCP - endoscopic retrograde cholangiopancreatography

A
  • A camera you swallow down
  • Goes through the stomach into duodenum
  • End of it looks straight at ampulla
  • Put down wires into bottom of bile duct
  • Take samples of cancer for lab
  • Put in stents that go through the cancer and give pathway for bile to drain
  • This helps with symptoms they get from jaundice
  • Can also do this for benign disease
  • Eg gallstones
39
Q

features of obstructive jaundice

A

PALE STOOLS, DARK URINE, ITCH

40
Q

obstructive jaundice on examination

A
  • Peripheral stigmata of liver disease…
  • Finger clubbing
  • palmar erythema (red palms)
  • dupuytren’s contracture (palmar thickens, fingers bending over)
  • sclera for jaundice
  • virchow’s node (lump in neck – sign of cancer)
  • spider naevi (capillaries in skin – press them disappear and come back when release)
  • gynecomastia
  • hepatomegaly
  • splenomegaly (portal hypertension)
  • ascites
  • palpable gall bladder
41
Q

investigation for obstructive jaundice

A

haematology

  • FBC, if anaemic consider cancer
  • Abnormal clotting in liver disease
  • LFTs – raised bilirubin

Looking at patterns of liver test (not definitive)

  • If ALP> ALT/AST = obstructive picture
  • ALT/AST >ALP, liver disease

Liver screening
Ultrasound – gallstone, CBD dilatation, liver/ pancreas mass
- If blockage look for ducts in liver (if they’re blown up its post-hepatic due to high pressure)

CT abdomen with contrast, MRI/BRCP

  • Good for showing cancers
  • MRI is best test for seeing there’s stones in bile duct itself

Tissue biopsy if above unclear

42
Q

management of jaundice

A

Depends on underlying condition

  • Treat symptoms
  • Analgesia
  • IVI
  • Antibiotics if septic
  • Vit K and chlorphenamine

Treat underlying cause

  • Pre-hepatic -> stop haemolytic process
  • Hepatic -> anti-virals, prevent deterioration of cirrhosis eg alcohol, drugs
  • Obstructive – ERCP/stenting, surgery, palliative care
43
Q

gall stones basic anatomy

A
  • Gall bladder drains by cystic duct into common bile duct down the way
  • Drains upwards after cystic duct joins drains via common hepatic duct
  • Divides into left and right branches
  • Right into anterior and posterior
  • Common hepatic artery comes from the coeliac trunk
  • Cystic artery (artery to the gall bladder) comes from right hepatic artery
  • Head of pancreas down low at head of pancreas and the ampulla
  • Ligament between the liver and the duodenum
  • Bile duct
  • Hepatic artery
  • Portal vein
44
Q

incidence of gallstones

A
  • 10 to 20% of adults
  • 80% asymptomatic
  • Females 2:1 ratio to males
  • Fair, fat, fertile, forty
45
Q

types of gallstones

A

mixed gallstones -> most common

pure cholesterol gall stones

haemolysis/ haemolytic anaemia -> made of unconjugated bilirubin

46
Q

clinical presentation of gall stones

A
  • Right upper quadrant pain or epigastric pain
  • Colicky (get better then worse) or constant
  • Dyspepsia, nausea, vomiting
  • Can be mistaken for acid reflux
47
Q

gall stones symptoms

A

Biliary colic

  • Most common
  • Pain gets worse then better
  • Stones are floating around – sometimes balls get trapped = pain

Acute cholecystitis

  • Inflammation and sometimes infection
  • Pain starts as colicky but becomes more constant
  • Temperature due to inflammation
  • Treat with antibiotics
  • Sometimes emergency operation

Obstructive jaundice

  • If galls tones get out of gall bladder
  • Into the bile duct
  • Causing jaundice
  • ERCP – try to drag stone out into duodenum

Acute pancreatitis

  • Gall stone falls out of gall bladder
  • Causes pressure change in pancreatic duct as it goes down
  • Irritation and inflammation of the pancreas
48
Q

management of gall stones

A
  • Analgesia
  • Antibiotics
  • percutaneous drainage
  • ERCP
  • Surgery
49
Q

alcohol unit

A

1 unit = 10ml or 8g of pure alcohol

1 unit processed in one hour

ABV = % alcohol of total liquid volume

Units = ABV% x volume (in litres) (of drink consumed

year 2 sem 1 (13 decks)

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