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Liver and GI module > Liver > Flashcards

Liver Flashcards

1
Q

What is the function of the liver

A

Glucose and fat metabolism (gluconeogenesis and glycogenolysis, bile salts for emulsification)
Detoxifcation and Excretion (bilirubin from RBC, ammonia + urea cycle)
Protein synthesis (albumin, coagulation factors)
Storage (of iron, copper and vitamin A, D, B12)
Defence against infection (R-E system, Kupffer cells)

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2
Q

What is the normal structure of the liver? (micro+ blood supply)

A

Divided into liver lobules, sinusoids separate plates of hepatocytes in chains. kupffer cells within the sinusoids.
Blood supply via the portal vein (75%) and hepatic arteries (branch off coeliac trunk) (25%) and bile from bile ductules at the portal triad
Central vein in the centre of each lobule, where everything drains into, to head back to IVC
zones divided into 3, 1 being closest to the triad, most oxygenated, 3 being furthest away around the central vein and least oxygenated - most susceptible to damage

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3
Q

structure and function of gall bladder

A

gall bladder- to store and concentrate bile. lies under the right lobe of the liver

cystic duct from gall bladder joins hepatic duct from liver to form the common duct duct. This enters the head of the pancreas, meeting the pancreatic duct, which then opens out into the 2nd part of duodenum with the ampulla of vater- there is a sphincter (of oddi) to regulate exit

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4
Q

what are the two types of liver injury and what can they lead to?

A

acute- with either recover or go into liver failure
chronic- continuously needs to repair itself under constant damage, will repair haphardly over a long period of time. Begins to fibrose and cause cirrhosis. Can go into liver failure, can causes varicies/acities due to portal hypertension and even hepatoma

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5
Q

What can cause acute liver injury/hepatitis?

A 
Viral: Hep A, B, EBV & more 
Alcohol
Drugs
Vascular Obstruction (like heart attack to liver)
Congestion (from heart failure)
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6
Q

What can cause chronic liver injury/hepatitis

A

Viral (B, C)
Alcohol + drug use
Autoimmune (ie RA)
Metabolic- Iron overload (hemochromotosis) and copper (Wilsons disease)
NAFL + NASH (non alcoholic fatty liver-> steatohepatitis)
Alpha 1 antitrypsin deficiency

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7
Q

what are the symptoms of acute liver injury?

A

flu- like, malaise, fatigue, anorexia, nausea jaundice
rarer, if leads to failure: encephalopathy, coagulopathy, liver pain, hypoglycaemia (monitor blood glucose to prevent brain damage)

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8
Q

what are the symptoms/signs of chronic liver disease?

A 
jaundice
acities + oedema (fluid overload) 
hematemesis (vomiting blood from burst oesophageal varicies)
hepatomegaly
abnormal LFTs
easy buising
itching
confusion, 
(malaise, anorexia, nausea)
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9
Q

abdominal examination

A

light palpation
deep palpation of 9 quadrants
liver will move down on inspiration- maybe around 1cm below the rib- feel edge for knobs/tenderness- should be smooth
spleen moves down from LUQ towards RLQ- feel for this on inspiration
feel for kidneys (being able to ‘throw’ them)

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10
Q

What does the LiverFunctionTests measure?

A 
LFTs - 
bilirubin, albumin, prothrombin time (give some index of liver function)
Enzymes:
- alk phos,
- gamma - glutamyltransferase 
- AST (non specific to liver) , 
- ALT (more specific to liver)
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11
Q

what tests would you do if you suspect liver injury?

A 
LFTs
viral markers 
FBC, film, coagulation
urine
imaging
biopsy
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12
Q

what can a deficiency an alpha 1 antitrypsin cause?

A

normally helps controls inflammatory cascades
deficiency:
can cause cirrhosis of the liver (+hepatoma)
can cause emphysema

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13
Q

what is Wilsons disease and what are the signs?

A

Wilsons disease- autosomal recessive disease.
Copper accumulation in the liver (and CNS)

Urinary copper raised,
Serum copper and ceruloplasmin (copper carrying protein in the blood) will be low.

brown ring around the iris- Kayser Fleischer rings

Screen all young people with liver cirrhosis (although may present with CNS symptoms first)
Screen family if positive

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14
Q

What are the types of Jaundice and their overriding cause?

A

Raised unconjugated bilirubin
Prehepatic
(ie Gilbert’s syndrome/ hemolysis)

Raise conjugated bilirubin (also cholestatic)
Intrahepatic
(cirrhosis/ hepatitis)

Post- hepatic
(bile obstruction)

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15
Q

What is jaundice and what is its cause?

A

yellowing of the skin and sclera, due to increased serum bilirubin (either conjugated or unconjugated, depending on cause)

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16
Q

How to differentiate between pre-hepatic vs hepatic/post-hepatic jaundice, based on symptoms + why?

A

Hepatic/Post-hepatic jaundice will likely have dark urine and pale stools

This is because there is increase in conjugated bilirubin, which can’t pass into the intestines to change to urobilinogen and then urobilin and stercobilin to colour the feaces, and as there is increased conjugated bilirubin it will be excreted by kidneys in urine to make it dark

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17
Q

how does haemolytic jaundice occur?

A

increased breakdown of RBC (through any cause also causing haemolytic anaemia) means liver can’t keep up with the demand of conjugating the bilirubin. Therefore unconjugated bilirubin increases (but not soluble so cannot pass into urine)
Urinary Urobilinogen is increased though (colourless)

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18
Q

What are the causes of hepatitis/liver disease?

A 
Hepatitis (viral, alcohol, drugs autoimmune)
Neoplasm
Congestive
Ischemic
Alpha 1 antitrypsin deficiency
Sclerosing Cholangitis
Primary Billiary Cirrhosis
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19
Q

What can cause post-hepatic jaundice?

A

all obstruction by:
within lumen: gallstone/blocked stent
within wall of duct: sclerosing cholangitis
outside the duct: pancreatitis, cancer, mirizzi syndrome

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20
Q

What test would you do if obstructive gall stone is suspected?

A

ultrasound- to see dilation of the duct due to backing up from blockage by gallstone(but not all time!)

CT, MRCP, ERCP, (magnetic resonance/endoscopic retrograde cholangiopanreatography) ERCP can be used to extract also

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21
Q

4 risk factors for getting gall stones?

A

fat, female, fertile, forties

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22
Q

what are gall stones made from?

A

cholesterol mainly

also bile pigments +/- calcification

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23
Q

what can gall stones cause?

A

MOST ASYMPTOMATIC
acute cholecystitis (inflammation of gall bladder, if blocks cystic/other ducts)
bile obstruction- cholestasis (if common bile duct obstruction)
pancreatitis - if blocks sphincter of oddi/ ampulla of vater

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24
Q

what is billiary colic?

A

the term to describe the pain most commonly associated with the temporary obstruction of cystic or common bile duct

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25
Q

describe biliary colic

A

constant (unlike colic suggests)
sudden onset
severe
often felt in epigastrum (can go to RUQ) + radiate to right shoulder
nausea and vomiting poss in severe attacks

26
Q

What is cholecystitis?

A

inflammation on the gall bladder, almost always due to gall stones obstructing bile duct

27
Q

what are the symptoms+sings of cholecystitis?

A

biliary colic pain (severe, constant, sudden onset)
move to RUQ pain
becomes localised above location of gall bladder when parietal peritoneal involvement when big enough
murphy’s sign!

28
Q

what is Murphy’s sign?

A

pain when taking deep breath and examiners fingers over the location of the gall bladder- indicative of acute CHOLECYSTITIS

29
Q

what to do if cholecystitis is suspected?

A 
abdo ultrasound
laparoscopic cholecystectomy (removal of gall bladder) if found symptomatic
30
Q

What is (ascending) cholangitis?

A

bile duct infection, again often due to gall stone obstruction.

31
Q

what does ascending cholangitis present with?

A

Charcots triad: RUQ pain, fever, jaundice

Reynaud pentad: the above, plus mental confusion, and hypotension (septic shock)

32
Q

What to do if cholangitis is suspected + then if found to be correct?

A

LFT’s, blood tests, abdominal ultrasound
ERCP- to find but also remove gall stone for cause (treatment)
antibiotics!

33
Q

How do you know if its a gall bladder stone or a bile duct stone?

A

billiary pain presents in both
but pancreatitis and cholangitis will only be if bile duct stone

OR can be Mirizzi syndrome where there is a gall stone in the gall bladder but which pressed on the bile duct (so is like both)

34
Q

What is portal hypertension?

What is normal pressure?

A

increased pressure in the portal vein which goes to the liver made by the confluence of the splenic and superior mesenteric veins (blood comes from bowel and spleen)

normally at 5mmhg-10mmg + increases when eaten a meal

35
Q

What can cause portal hypertension?

A

blockage (i.e. by blood clot)

or increased resistance in the liver (as in cirrhosis/hepatitis)

36
Q

what are 2 consequences/complications of portal hypertension?

A

varices and acites

37
Q

what are varices? where are they most common + when would they be discovered?

A

when there is portal obstruction or hypertension, blood cannot pass through the portal vein as easily to the liver and is redirected and backs up into other systemic veins which also run into portal vein

oesophageal veins (most common)

vomiting blood (symptomatic)
endoscopy (asymptomatic)
38
Q

if varices are bleeding, how might one present?

A

if slow bleeding- anaemic
if massive bleed- vomiting blood
or dark stools if it bleeds into bowel

39
Q

what is ascites?

A

fluid build up in the peritoneal cavity (esp when portal pressure is above 12mmhg)

40
Q

what can cause ascites?

A 
liver disease (cirrhosis)
portal vein thrombosis
hepatoma
TB
pancreatitis
neoplasia of uterus/ovary
cardiac causes 
(anything which may cause portal hypertension)
Meigs syndrome - benign ovarian tumor which causes pleural effusion and ascites which resolves once tumor is resected
41
Q

pathogenesis of ascites

A
  • portal hypertension leads to systemic vasodilation
  • body recognises this as low blood volume
  • activates RAAS/vasopression/noradreneline
  • these cause fluid and sodium retention
  • so there is increased intravascular hydrostatic pressure (favours exit of fluid from vessels)

also hypoalbuminaemia due to liver disease
causes a lower oncotic pressure
(which also favours the exit of fluid from vessels)

both of these leads to leaking of fluid into the peritoneal cavity

42
Q

Alcoholic Liver disease

A

most common cause of liver death in the UK
excess alcohol intake decreases fatty acid oxidation and increases fatty acid synthesis leading to a fatty liver.
in genetically predisposed individuals, this will lead to liver hepatitis and cirrhosis + eventually failure

43
Q

people with liver disease are very responsive to opiates (i.e. morphine)
what would you give to someone to reverse them having taken too much?

A

IV naloxone

44
Q

why might someone who has liver disease go into a coma?

A 
hepatic encephalopathy
GI bleed
sepsis
given drug (sedatives/analgesics)
constipation (more time to absorb ammonia products)
hypokaelemia 
hyponatremia
45
Q

what other consequences might people with liver disease suffer from?

A

malnutrition (don’t feel well enough to eat, therefore may need NG tube)

coagulopathy- as cannot produce clotting factors

thrombocytopaenia (due to big spleen)

endocrine problems (as liver cannot breakdown hormones)

46
Q

why might you be able to take someone with liver disease off their antihypertensives?

A

liver disease can ‘cure’ hypertension (probably due to systemic vasodilation)
therefore can be taken off ACE inhibitor

47
Q

autoimmune hepatitis

can be easily treated with:?
who is it more common in
and what is test will often come back positive?

A

steroids

more common in women - bimodal, young then middle aged

ANA (anti nuclear antibody) and ASMA (anti smooth muscle antibody) will both often come back positive

or anti liver-kidney microsomal antibodies type 1 (LKM1) positive, other two negative

or anti soluble liver antigen antibodies (SLA) positive, ANA and ASMA negative

48
Q

what is PBC?

A

Primary Billiary Cirrhosis/Cholangitis

an auto immune condition - AMA +ve (anti mitochondrial antibodies)
a granulomatous inflammation of interlobular bile ducts- destroys them, leads to cholestasis. may leads to fibrosis of ducts and then liver tissue

once jaundice occurs, will require transplantation

49
Q

what will PBC most commonly present with?

A

fatigue and itching, may get jaundice

50
Q

What is PSC? + what other condition is it associated with?

A

Primary Sclerosing Cholangitis
idopathic condition, characterised by inflammation and then fibrosis of the bile ducts inside/outside the liver.

50% have ulcerative colitis!

51
Q

What will PSC present with?

A

itching and possibly fatigue

52
Q

What is itching a symptom of? + how would you treat it?

A

most commonly cholestasis- like in PBC and PSC
antihistamine will not help,
use colestryramine and/or rifampicin

53
Q

what is haemachromatosis? + what might blood test show?

A

autosomal recessive disorder (1 in 4 siblings)
continue to absorb iron despite iron stores being full- leads to iron deposits in the liver, pancreas, heart,

raised ferritin and saturated transferritin

54
Q

what is hepatocellular carcinoma and who does it occur in most commonly?

A

primary liver tumour
occurs in patients with cirrhosis
(most common in cirrhosis by: hep B, C, hemachromotosis)
(less common cirrhosis by: alcohol, autoimmune)

55
Q

What vaccines are there to prevent hepatitis?

A

Hep A and B have vaccines
HEP C- no vaccine!!
Hep E has vaccine in china (non licensed elsewhere,)
Don’t get Hep D without having B- therefore having hep B vaccine protects from hep D also

56
Q

what type of viruses are the hepatitis viruses?

A

all are RNA viruses, except for Hep B which is a DNA virus

57
Q

How are the hepatitis viruses spread?

A 
A- faecal oral route 
B- blood 
C- blood 
D- (only in those who have B) 
E- contaminated food/water
58
Q

What is the normal consequence of a Hep A infection?

A

always cleared acutely, never chronic infection

59
Q

Where are you likely to find hep E?

A

in England- & other DEVELOPED countries

60
Q

What is the consequence of having both Hep B and D?

A

much worse/poorer outcomes, liver transplant likely required

61
Q

What treatments are used in viral heptatitis?

A

pegylated interferon alpha 2a
ribavirin
and a direct acting antiviral (DAA)

now due to bad side effects (i.e. psychosis) of interferon, 2x DAA and ribavirin are used

Liver and GI module (1 decks)

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