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S3: Gastrointestinal > 6a.) Liver & Biliary System > Flashcards

6a.) Liver & Biliary System Flashcards

1
Q

State 3 main functions of liver and provide examples for each

A
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2
Q

State some general/”vague” symptoms of liver disease

A
  • Nausea/vomitting
  • Fatigue
  • Anorexia
  • Abdominal pain

NOTE: can also have more specific symptoms

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3
Q

What symptom does each of the following deranged functions cause:

  • Synthetic function: albumin
  • Metabolic function: ammonia
  • Metabolic function: bilirubin
  • Synthetic function: clotting factors
A
  • Albumin- oedema & ascites
  • Ammonia- confusion
  • Bilirubin- jaundice
  • Clotting factors- bleeding/easy bruising
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4
Q

What can high levels of ammonia cause?

A

Hepatic encephalopathy

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5
Q

What do we mean by acute liver failure?

State some possible causes of acute liver disease

A

Rapid onset, no previous liver disease

Causes:

  • Paracetamol overdose
  • Otehr medications e.g. tetracycline, aspirin in children
  • Acute viral infection e.g. EBV, Hep A/B
  • Acute excessive alcohol intake
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6
Q

What is cirrhosis?

State some changes to the liver tissue associated with cirrhosis

A

Scarring of liver as a result of long term liver damage; it;s end result of a lot of long term liver conditions

  • Ongoing inflammation -> fibrosis
  • Associated with hepatic necrosis
  • Nodule formation
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7
Q

Is cirrhosis reversible?

A

No- once it has devoped (over many years) it is irreversible

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8
Q

Cirrhosis develops over many years; true or false?

A

True

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9
Q

State some consequences of liver cirrhosis

A
  • Jaundice (increased bilirubin)
  • Itching (build up of other toxins)
  • Varices
  • Portal hypertension
  • Bleeding/easily bruise (lack of clotting factors)
  • Hepatic encephalopathy
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10
Q

State 5 broad categories of causes of cirrhosis

A
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11
Q

What is alcoholic liver disease?

Describe 3 main mechanisms by which alcohol damages liver

A

Damage to liver that occurs due to excesive alcohol consumption over long period of time.

  1. Fatty change/liver: after few weeks, initially reversible
  2. Alcohol hepatitis: after few years, now have fat and inflammation, initially reversible
  3. Cirrhosis: after few years
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12
Q

Alcoholic liver disease is though to be partly due to build up of what substance?

A

Acetaldehyde

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13
Q

Describe how someone with alcoholic liver disease may present

A
  • History of alcohol
  • Asymptomatic
  • General symptoms of liver disease (nausea, fatigue, anorexia, abdo pain)
  • Hepatomegaly- if have fatty liver
  • Tender hepatomegaly- if alcoholic hepatits
  • Rapid onset jaundice
  • Oedema
  • Ascites
  • Splenomegaly
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14
Q

How could you differentiate between fatty liver in alcoholic liver disease and alcoholic hepatitis in alcoholic liver disease?

A

Fatty liver

  • Hepatomegaly NON-tender

Alcoholic Hepatitis

  • TENDER hepatomegaly (RUQ pain, get to inspire, their liver will move down and touch your fingers and will hurt)
  • Rapid onset jaundice
  • Symptoms os more severe disease e.g. nausea, oedema, splenomegaly
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15
Q

Chronic viral hepatitis can cause cirrhosis; what else does it increase risk of?

A

Hepatocellular carcinoma

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16
Q

How do you treat alcoholic liver disease?

A
  • Stop consuming alcohol
  • Can have corticosteroids for inflammation if have alcoholic hepatitis
  • Liver transplant if get liver failure
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17
Q

State whether each of the following has a vaccine and/or a cure:

  • Hep B
  • Hep C
A
  • Hep B: vaccine, but no cure
  • Hep C: no vaccine but has a cure
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18
Q

Do you have symptoms if you have an acute infection with:

  • Hep B
  • Hep C
A
  • Hep B often have symptoms during acute infection
  • Hep C often asymptomatic during acute infection

**SEE INFEC MODULE TO REVISE

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19
Q

What is non-alcoholic liver disease?

Describe pathogenesis and state what it is linked to

A

Accumulation of triacylglycerides and other lipids in liver that is NOT caused by alcohol.

Though to be linked to insulin resistance

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20
Q

If someone has non-alcoholic fatty liver disease but there is also inflammation present, what is this called?

A

Non-alcoholic steatohepatitis (NASH)

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21
Q

State some risk factors for developing NAFLD

A
  • Obesity
  • Diabetes
  • Metabolic syndrome (dyslipidaemia)
  • Familial hyperlipidaemia
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22
Q

How do you manage NAFLD?

A
  • Lifestyle modifications: eat healthy, exercise, no alcohol
  • Can also give oral hypoglycaemic agents
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23
Q

State the 4 stages of NAFLD

A
  1. Steatosis (fatty liver)
  2. Non-alcoholic steatohepatitis
  3. Fibrosis
  4. Cirrhosis
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24
Q

State the most common causes of cirrhosis

A
  • Alcoholic liver disease
  • Non-alcoholic fatty liver disease
  • Hep B & Hep C chronic infection
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25
Q

Describe hereditary haemochromatosis, include:

  • What it is
  • Inheritance pattern
  • Plasma ferritin levels
  • Increased risks
  • Treatment
A
  • Abnormal iron metabolism where there is mutation in HFE gene so HFE protein which usually prevents Fe uptake into cells doesn’t owrk so excess Fe taken up into cells meaning excess Fe in tissues e.g. liver. Also get increased absorption of Fe from smal intestine
  • Autosomal recessive
  • Increased ferritin
  • Risk of developing hepatocellular carcinoma
  • Venesection
26
Q

Describe Wilson’s disease, include:

  • What it is
  • Inheritance pattern
  • Caeruloplasmin levels
  • Is it common?
A
  • Abnormal copper metabolism in which there is reduced secretion of copper from biliary system leading to an accumulation of copper in tissues
  • Autosomal recessive
  • Low caeruloplasmin
  • Rare- but if child comes in with liver disease you may query Wilson’s
27
Q

State two autoantiboides in autoimmune hepatitis

A

ASMA (anti smooth muscle antibody)

ANA (antinuclear antibodies)

28
Q

What is PBC and PSC (on image below)

Which is more commonn in men and which is more comon in women?

How can you differentiate betweent the two using antibodies?

A
  • PBC: primary biliary cirrhosis- more common women
  • PSC: primary sclerosing cholangitis- more common men
29
Q

What is Budd-Chiari syndrome?

A
30
Q
A
31
Q

What is portal hypertension?

A

Increase in blood pressure in hepatic portal system

32
Q

Describe the portal system of liver

A
33
Q

What’s the most common cause of portal hypertension?

A

Cirrhosis

34
Q

Explain how liver cirrhosis can cause portal hypertension

A
  • Fibrotic liver doesn’t expand much
  • Compresses veins entering liver from portal venous system
  • Increases hydrastaic pressure in portal venous system
35
Q

State two complications of portal hypertension

A
  • Ascites
  • Splenomegaly
36
Q

Explain how varices are formed during portal hypertension

A

During portal hypertension, blood can shunt to systemic venous circulation via porto-systemic anastomoses that are not usualy used; leads to distention of the veins at the site of anastomoses= varices

37
Q

State 3 important sites of varices; state which is most and least common

A
  • Oesophagela (most comon)
  • Anorectal
  • Umbilical (rare)
38
Q

Describe how oesophageal varices form

A
  • Portal hypertension causes blood to move into venous systemic circulation via porto-systemic anastomoses
  • Upper 2/3 oesophagus drains into oesophageal veins
  • Lower 1/3 drains into left gastric vein which drains into portal vein
  • Blood that would drain via left gastric vein will start to drain via oesophageal veins causign mucosal varices
39
Q

What can happen if oesophageal varices rupture?

A

Haematemesis

40
Q

Do anorectal varices usually cause problems?

A

No typically painless (above pectinate line) and rarely bleed

41
Q

Describe how anorectal varices can develop

A
  • Portal hypertension causes blood to move into venous systemic circulation via porto-systemic anastomoses
  • Superior rectal usually drains into portal vein
  • Blood that usually drains via SR will drain via MR and IR
  • Varices occur between superior and middle/inferior
42
Q

Describe how umbilical varices form

A
  • Ligamentum teres links liver to umbilicus
  • Usually has no blodo flow
  • Portal hypertension could cause ligamentum teres to re-open and blood flow in
  • End up with caput medusa (appearance of diliated veins on abdomen around umbilicus)
43
Q

What does the image show?

A

Caput medusa

44
Q

What is hepatorenal syndrome?

A

Development of acute kideny injury (AKI) due to cirrhosis

45
Q

How can we treat hepatorenal syndrome?

A

If we treat/reverse patients liver failure than kidney funciton dramatically improves

46
Q

Describe/draw the biliary tree

A
47
Q

How would you diangose gallstones?

A

Ultrasound. Most are radiolucent so x-ray or MRI won’t work

48
Q

Are renal calculi radiolucent?

A

No, they are radio opaque

49
Q

How are gallstones formed?

A

Formed when certian components of bile (cholesterol and bile pigments) come out of solution to form a solid in the gallbladder

50
Q

Describe biliary colic, include:

  • What it is and why it occurs
  • Symptoms
  • How you diagnose
  • Management
A
  • Temporary obstruction, by gall stone, usually in cystic duct
  • RUQ pain which is worse few hours after fatty meal (as CCK will be released)
  • Ultrasound- no inflammation
  • Analgesia, elective cholecystectomy
51
Q

State some risk factors for developing gallstones

A
  • Diet & lifestyle
  • Age (40/50)
  • Gender (more common females)
  • Pregnancy
  • Pre-existing liver disease
52
Q

Are gallstones asymptomatic?

A

Tend to be asymptomatic but cause problems when move from gallbladder into biliary tree

53
Q

Describe acute cholecystitis, include:

  • What it is
  • Symptoms
  • How diagnose
  • Treatment
A
  • Permanent impaction of a stone in cystic duct which causes inflammation of gallbladder
  • Initial presentation similar to biliary colic: RUQ, worse after fatty meal but pain persists for days
  • Ultrasound- inflammation and thick wall gallbladder. Also Murphy’s sign positive
  • Initially conservative management then cholecystectomy
54
Q

Describe Murphy’s sign positive

A
  • Patient inspires
  • You put your hand on URQ
  • Their gallbladder will hit your hand
  • Pain for patient
  • +ve sign
55
Q

Describe acute (ascending) cholangitis, include:

  • What it is
  • Symptoms
  • Treatment
A
  • Infection of biliary tree typically due to stone impactd in common bile duct or other obstructive causes
  • Present with pain, features of inflammation and jaundice (Charcot’s triad)
  • IV antibiotics, fluids, relieve obstruction
56
Q

What is Charcot’s triad?

A
  • Jaundice
  • RUQ pain
  • Fever
57
Q

Complete the diagram

A
58
Q

Describe how gallstones can cause acute pancreatitis

A

Gallstone becomes impacted in distal biliary tree and blocks secretions from pancreas/blocks pancreatic duct. Secretions can’t leave pancreas. Pro-enzymes that are usually only activated in lumen of gut become prematurely activated in ductal system of pancreras causing auto-digestion and inflammation- lead to acinar cell injury and necrosis.

59
Q

How might someone with acute pancreatitis present?

A
  • Epigastric pain that radiates to back (retroperitoneal structure)
  • Often associated with vomitting
  • Cullens & Grey Turner’s sign
60
Q

How can we diagnose acute pancreatitis?

A
  • Amylase and lipase levels
  • CT/MRI to rule out other causes and identify any necrosis
61
Q

How do we manage acute pancreatitis?

A
  • Fluids
  • Manage gallstones
  • Organ support
62
Q

Complete the following summary table

A

S3: Gastrointestinal (18 decks)

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