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Digestive > Liver > Flashcards

Liver Flashcards

1
Q

Functions of liver

A 
detoxification
carb and glucose regulation
bile drainage
blood circulation and filtration
synthesis and storage of amino acids and proteins fats and viatmins
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2
Q

Ligamentum teres, falciform ligament, caudate lob, quadrate lobe - where

A

in middle of lobes is falciform

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3
Q

What are the ligaments of the liver

A

right traingluar ligament, coronary lig, left triangular ligamnet, venosum

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4
Q

Porta hepatitis, which way do the structures go

A

free edge of lesser omentum attaches here (carrying structures with it)
-Contains the Heaptic artery, portal vien and bile duct

BVA - anterior

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5
Q

Contributions from hepatic artery and portal vien

A

1/4 heptic artery , 3/4 portal vien

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6
Q

where does falciform ligament go to?

A

to umbilicus

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7
Q

Lymphatic drainage of liver

A

nodes at porta hepatits (coeliac nodes) (on hepatic artery)

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8
Q

ANS - visceral supply and pain to liver

A

coeliac plexus, parasympathtic - vagus
sympathetic - greater splanchnic nerves
Pain in epigastric region

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9
Q

cyctic duct

A

from neck of gall bladder joins with pancreas

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10
Q

how is bile released into duodenum

A

smooth muslce at distal end of bile duct and ampulla relax

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11
Q

is the gall bladder covered in visceral peritonium?

A

yes

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12
Q

Arterial supply to gall blader

A

cystic artery (from right hepatic artery) - passes through the triangle of calot

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13
Q

Venous supply gall bladder

A

Cystic vien (into portal vien)

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14
Q

nerve, pain of gall bladder

A

ans - via coeliac plexus (same as liver), epigastric region

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15
Q

lymph of gall bladder

A

cystic nodes - hepatic - coeliac

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16
Q

Cholelithiasis

A

Presence of gall stones

-cholesterol (green or yellow/whtite), and pigment stones (bilirubin, calcium salts usualy small and dark)

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17
Q

3 main places of porto-systemic shunting

-causes

A

-alternative vessels enlarge to try and divert blood back from portal circulation back to heart

Oesopahgeal varacies
Caput medusae (around umbilicus)
-Anus - anorectial varices
Due to portal hypertension - causes included cirrhosis
-in submucosa
-can rupture and bleed if pressure to high

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18
Q

Patterns of hepatic injury

A 
5 general responses
degeneration and intracellular accumulation 
Necrosis and apoptosis
inflammation 
regeneration
firbosis
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19
Q

What happens in hepatic failure and what are the clinical features

A

sudden and massive destruction/endpoint
loss of 80-90% capacity
increased demand - infection, gastrointestinal bleeding
High mortality
Clinical features - jaundice, hypoalbuminaemia, elevated ammonia (neurological function)

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20
Q

Cirrhosis process and what happens

A
  • fibrous septae
  • damage to hepatocytes
  • micro and macronodules - parancheal nodules (hepatocyes encircled by fibrosis)
  • change in structure - shunts, blood bypasses the liver
  • progressive fibrosis

Process - kupffer cells released cytokines, causes inflammatory response

  • results in change to hepatocytes
  • undergo apoptosis
  • inflammatory repsonse increase
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21
Q

Portal Hypertension

Pre, post and intra hepatic

A

increased resistance to portal flow

  • due to cirrosis blocking pathways of blood
  • prehepatic - obstructive thromobsis
  • posthepatic - server right sided heart failure
  • intrahepatic - cirrosis
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22
Q

Consequences of portal hypertension

A

Ascities, portal systemic shunts

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23
Q

Hep A

A

Self limiting
Does not cause chronic hepatitis
hygiene and sanitiation
asymptomatic , mild ilness, jaundice

24
Q

Hep B

A

acute hepatitis with resolution
chronic hepatitis may lead to cirrhosis or massive necrosis
blood and body fluid borne
immune repsone to viral antigens expressed on infected hepatocytes leads to liver damage

25
Q

Hep C

A

major cause of liver disease
Risk - injections and blood transfusions, medical treatments poor sanitation
acute infection usually undetected
chronic disease occurs in majority
20% develop cirrosis after 5-20 years
-most people who get acute will develop chronic hepatitis

26
Q

Autoimmune hepatitis

A

chronic progressive hepatits
genetic predisposition, presence of autoantibodies
-immunosuppression
-association with other autoimmune disease

27
Q

Drug and toxic induced liver injury

A

predictable Hepatotoxins - dose-dependent matter
-and unpredicatable
-may directly cell toxic, or act through ehpatic conversion to an active toxin activated
-cholestasis, hepatocellular necrosis, fatty liver disease, fibrosis, granulomas, vascular lesions, neoplams
-most common acute liver failure = paracetamol
most common chronic - alcohok

28
Q

Alcoholic liver disease

A

change in lipid metabolism
decreasesd export of lipoprotien and cell injury caused by reactive oxygen species and cytokines
-hepatic steatosis, alcoholic heptitis, cirrhoisos

29
Q

Non-alcoholic fatty liver disease

-what it is associated with

A
  • metabolic syndrome, obesity, type 2 diabetes, dyslipidemia, hypertension
  • initially hepatic steatosis which can progress to inflammation and then can turn to cirrosis
30
Q

Haemochromatosis

A
  • excessive accumulation of body iron
  • deposited in liver and pancreas
  • genetic defect - excesive iron abosption
  • autoskomal resessive
  • can get cirrosis, diabetes, skin pigmentation
31
Q

Cholestasis of sepsis

A

decreased bile flow, obstruction of intra or extrahepatic bile ducts

  • sepsis - infection from bacteria and toxins
  • can result as a direct effect of intrahepatic infection (bacteria cholangitis)
  • can get ischaemia related to hypotension
  • circulation microbial products (particular in context of gram negative infection)
32
Q

Autoimmune cholangiopathies

A
  • primary biliary cirrhosis (autoimmune disorder leading to destruction of bile canaliculi)
  • primarey sclerosing cholangitis (autoimmune disoer leadign to scaring of bile ducts)
33
Q

Passive congestion and centriolobular necrosis

A

Right sided cardiac decompesnation, commonly seen at autopsy, element fo preterminal circulatory failure with most deaths

34
Q

Liver tumours

A

benign neoplams - cavernous haemangiomas, hepatocellular adenoms, malignant neoplasms - hepatoceellulra carcinoma, hepatoblastoma

35
Q

Causes of jaundice - unconjugated, conjugated

A

unconjugated (indirect) - haemolysis, gilberrst syndrome
Inside liver - cholestasis - drugs, pregnancy, thyroid diesease
Obstruction inside liver - hepatitis, cirrhosis, bilary cirrhosis, large liver masses
Outside liver - obstrucion outside - galstones, bilayr pancreatic cancer, pancreatitis

36
Q

ALP

A

obstruction outside liver

increase with cancer, gall stones (anything blocking bile)

37
Q

GGT

A

obstruction outside liver

Alcohol, drugs, phenytoin, ritampicin, also fatty liver - mainly alcohol (can have fat obstructing)

38
Q

ALT and AST

A

liver specific
hepatitis , inflammation and hepatocellular injury
-ALT more liver specific
-if these are really really high than could be acute drug poisoning

39
Q

Albumin

A

liver is only source
decrease with cirrosis, illness (non-specific)
-long term ilness

40
Q

Globulins

A

Inflamation -decreases with hepatitis, cirrhosis

-decreases if synthetic function is impaired

41
Q

Prothrombin raito

A

increases with liver failyre - if syntheitic funciton is imparied

42
Q

Glucose

A

liver maintains fasting glucose, inability to maintain glucose

  • decreases
  • liver failure
43
Q

Ammonium

A

increases

44
Q

CEA

A

cancer marker-can be fore bening cirossis and hepatitis

45
Q

Gilberts syndrome

A

variant in billirubin conjugaction - so billirubin is unconjugated
other liver tests normal
jaudice
-can test - if fasting for 48 hrs and bilirubin rises 2 times

46
Q

Main causes of Liver function test abnormalities

A

Fatty liver - obesity, diabetes ect

-Viral hepatitis, alcohol

47
Q

Old treatment for Hep C

A

regiems were interferon based (made cytokines), however not very good and could get flu like symptoms
(injection)

48
Q

Current treatment

A

Antiviral agents - tablets , better cure rates

49
Q

How to treat varicies that have ruptured

A

can tie around them however need to also sort hypertension

50
Q

Causes of portal hypertension

A

Pre-hepatic - portal vien thrombosis
Intrahepatic - cirrhosis
Post hepatic - heaptic vien thrombosis, right heart failrure

51
Q

Hepatic encephalopathy

A

result of chronic liver failure
Early symptoms - mood and personality change, inverted sleep
Late - confusion, bizarre behaviour, drowsiness and coma
-advanced cirrhosis with liver failure

52
Q

Mechanisms of Hepatic encephalopathy

A

Chronic liver failure i.e functioning poorly
Liver unable to detoxify substances produce by bacteiral metbaolsim
-portosystemic collaters shunt blood back to portal ciruclaiton- does not go back to liver, so is not detoxified
-Ammonia build up in blood brain barrier
disturbs normal brain funciton

53
Q

Treatment of hepatic encephalopathy

A

lactulose - just to manage symptoms (normally a laxative)

-however will convert ammonia to a non-absobable molecule

54
Q

What is ascites

A

Fluid in peritoneum causing abdominal distention

  • can be caused by portal hypertension
  • increased pressure in protal vien, fluid shifts out inot circulation into perritoneum
  • less able to hold on to fluid in circulation
55
Q

What can be seen with portal hypertension

A

Varacies, acsites, hepatic encepahlopathy

56
Q

Budd chari syndrome

  • what it is
  • and sypmtoms
  • cause
  • management
A

acute thrombosis of hepatic vien
outflow of blood from liver obstructed
liver becomes acutely congested, hepatocellular damage
Porral hypertension occurs - ascities develop

Symptoms - acute rapdily progressive servere upper abdominal pain
jaudice, hepatomgaly, ascities, hepatic enchaplopathy

Cause - mainly no obvious cause

management - protocaval shunting often performed to divert blood flow , anticoagulants, diruertics

Digestive (15 decks)

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