7. Diseases Of Liver & Biliary Tree

Question 0

What role does saliva play on defending the GIT from toxins?

Answer 0

Contains no of anti-bacterial substances: lysozymes, lactoperoxodase
Contains immune components e.g. Polymorphs, complement
Washes bacteria & toxins into stomach (acidic)

Question 1

List the common categories of toxins that the GIT is exposed to

Answer 1

Chemical
Bacterial
Viral
Protazoal
Nematodes (roundworms)
Cestodes (tapeworms)
Trematodes (flukes)

Question 2

Name 6 physical defences that protect the GIT from toxins

Answer 2

Saliva

Gastric acid

Colonic mucus

Anaerobic environments (small bowel, colon)

Gut transit

Question 3

Name one bacteria resistant to stomach acid

Answer 3

Mycobacterium Tuberculosis

Question 4

Name 3 viruses resistant to stomach acid

Answer 4

Hep A
Polio
Coxsackie

Question 5

How does the colon protect itself from the bacteria in its contents?

Answer 5

Colonic mucus layer

Question 6

What are kupfer cells?

What role do they perform?

Answer 6

Specialised macrophages in the walls of hepatic sinusoids

Promote normal liver physiology & homeostasis
Participate in liver response to toxic compounds (e.g. Ethanol):
when activated, release inflammatory mediators

Question 7

Name 3 areas where GALT is nodular

Answer 7

Peyer’s patches
Tonsils
Appendix

Question 8

What is Mesenteric Adenitis & why might it mimic appendicitis (in children)?

Answer 8

Usually a self-limiting inflammatory response, where Mesenteric lymph nodes in RLQ become inflamed.

Enlargement can mimic pain caused from later stage appendicitis

Question 9

Describe how lymphoid hyperplasia in base of appendix can lead to appendicitis

Answer 9

If lymphatic nodes at base of appendix enlarge (e.g. In response to viral stimulus), base of appendix becomes occluded.
Resulting stasis of appendix contents leads to infection & inflammation

Question 10

What are the possible causes of appendicitis?

Answer 10

Lymphoid hyperplasia at base of appendix
Faecolith
Foreign bodies
Intestinal worms

Question 11

Name 3 ways that intestinal blood supply can become compromised

Answer 11

Arterial disease
Systemic hypotension
Intestinal venous thrombosis

Question 12

In alcoholic cirrhosis of the liver, what is the basis of:
Enlarged abdomen
Splenomegaly
Hepatomegaly

Answer 12

Destruction of normal liver architecture thru cirrhosis reduces passage of blood flow thru liver.
Affects portal vein as it tries to drain liver.
Portal venous sys has no valves: raised pressure affects splanchnic vasculature draining into it.
Rise in hydrostatic pressure + drop in plasma oncotic pressure (from reduced production of Albumin) can force fluid out into peritoneal cavity.
Causes ascites (presenting as enlarged abdomen).

Spleen becomes engorged as it tried to drain portal vein.

Hepatomegaly can be caused by steatosis (abnormal collection of lipids within hepatocytes).
Occurs due to disruption in processing of lipids in liver as result of excessive alcohol consumption (reversible stage).

Question 13

What are portosystemic anastomoses?

Answer 13

In portal hypertension, resistance to portal flow through liver raises portal pressure.
When exceeds pressure in systemic veins, portal venous blood diverted via portosystemic venous anastomoses: become varicose as enlarge

Question 14

What are the 5 main locations of anastomoses?

Answer 14

Btw oesophageal tributaries of L gastric vein & veins draining rest of rest of oesophagus.
Draining into azygous sys

Btw superior rectal veins & middle/inf rectal veins.
Draining into internal iliac vein

Btw portal tributaries of retro-peritoneal organs (e.g. asc/dec colon, kidney) & lumbar veins.
Draining eventually into IVC

Btw veins in & around falciform ligament & veins of anterior abdominal wall.
Draining into epigastric veins

Btw veins of post. abdo wall & bare area of liver.
Draining into IVC

Question 15

What is portal venous system? Why is it useful?

Answer 15

when a capillary bed pools into another capillary bed through veins, without first going through the heart.
transports products of one region directly to another region in relatively high concentrations.

Question 16

Define the term cirrhosis, listing 3 characteristic features

Answer 16

Diffuse & irreversible Necrosis of the hepatocytes in the liver.
Following destruction, nodules form in liver, separated by fibrotic tissue.
Initially, liver enlarges in acute fatty liver (steatosis).

Followed by 3 stages:
Chronic hepatocyte necrosis
Chronic inflammation, leading to fibrosis
Nodule formation, following hepatocyte necrosis

Question 17

What clinical signs might you see in an examination of a patient with cirrhosis?

Answer 17

General:
Jaundice, scratch marks, confusion

hands:
Leuconychia, clubbing, palmar erythema, dupuytrens contracture, flapping tremor

eyes:
Jaundice in sclera

abdomen:
Distension (ascites), hepatosplenomegaly, caput medusa (from plrtosystemic anastomosis)

Question 18

What could be the cause of confused mental state in someone with liver disease?

Answer 18

Hepatic encephalopathy
Alcohol intoxication
Head injury
Infection, hypoxia

Question 19

If confused mental state is linked to liver disease, what possible precipitants may there be for this episode?

Answer 19

If due to hepatic encephalopathy: 
infection (chest, urinary, peritonitis)
large ingestion of protein
GI bleed (from varices)
electrolyte imbalances
constipation

Question 20

What treatment options exist for acute confusion from liver disease?

Answer 20

Antibiotics for any infection
Low protein diet
Correction of any GI bleed
Laxatives for consitpation

Question 21

Explain the process that leads to the clinical sign of shifting dullness on percussion of abdomen & flanks appearing full in someone with liver disease

Answer 21

Ascites: result of portal hypertension:
Cirrhosis can = reduced blood flow in portal vein, therefore rise in pressure.
Affects vessels draining portal vein (splanchnic vessels), causing sequestration of fluids into peritoneal space.

Portal htn also = pooling of blood in splanchnic vasculature, actovating Renin.
Resulting cascade = Na & water retention = more fluid accumulating in peritoneal cavity = ascites

Protein synthesis also reduced = reduced plasma oncotic pressure.
Easier for transduction of fluid from vasculature into peritoneal cavity

Question 22

What is the likely cause of someone with liver disease & ascites vomiting blood?

Answer 22

Portal hypertension

Oesophageal varices

Question 23

Explain how liver disease can lead to oesophageal varices

Answer 23

One of the portosystemic anastomoses.

Working back from portal vein:
Left gastric vein (portal part)
Veins in lower oesophageal mucosa (varices)
Azygous vein (systemic part)
Vena cava.

Back pressure caused by portal htn causes some vains in oesophageal mucosa (not normally engorged) to dilate.
Bleed easily (fragile) & empty blood into oesophagus & stomach

Question 24

Name 3 sites where varices can occur

Answer 24

Oesophagus Lower part of rectum Umbilical region of anterior abdominal wall

Question 25

What is jaundice?

Answer 25

Raised plasma Bilirubin (exceeding 18-24 micro mols/L) | Presents clinically as yellow pigmentation in sclera, skin, mucosal surfaces

Question 26

What are the 3 broad groups used to differentiate types of jaundice?

Answer 26

``` Pre hepatic (haemolytic): un conjugated bilirubin Hepatic (hepatocellular): mixed conjugated/un conjugated bilirubin Post hepatic (obstructive): conjugated bilirubin ```

Question 27

Name 2 disease processes that would increase breakdown of rbc's

Answer 27

Hereditary disorders (e.g. G6PD deficiency, spherocytosis, sickle cell) Acquired (e.g. Immune disorders, toxic chemicals, anti-viral drugs, physical damage from defective prosthetic heart valve, hypersplenism, infection)

Question 28

Why might an increased break down of rbc's lead to jaundice?

Answer 28

Increased rbc's = increased production of bilirubin (breakdown product of rbc's) If bilirubin production overwhelms liver's ability to conjugate it, then = un conjugated hyperbilirubinaemia (insoluble & cant pass into urine)

Question 29

Discuss the effects of deficient levels of UDP-glucuronyl transferase

Answer 29

Enzyme responsible for conjugating bilirubin in liver (making it soluble) Deficiency = un conjugated jaundice Various congenital diseases e.g. Gilberts

Question 30

Name 5 disease processes that would affect processing of bilirubin in the liver

Answer 30

``` Viral hepatitis Cirrhosis Tumours Autoimmune Haemochromatosis (iron metabolism disorder) ``` Hepatocellular jaundice = mixed conjugated/unconjugated jaundice Other liver tests will be affected

Question 31

What may cause jaundice as well as RUQ pain & fever? What classification of jaundice does this fall into?

Answer 31

Gallstones Infection in biliary tree (ascending cholangitis) If gallstones = post hepatic/obstructive

Question 32

Why might gallstones cause a fever?

Answer 32

If gallstone blocks bile duct, affects flow of bile into duodenum Combination of stasis & reduced lymphatic function allows gut bacteria to multiply in otherwise sterile env Infection can ascend (ascending cholangitis) in biliary tree, causing infection which can involve liver & then systemic blood stream, causing generalised sepsis

Question 33

Name 5 factors that can reduce/block flow of bile from liver & gall bladder

Answer 33

``` Gallstones Cancer in head of pancreas Biliary atresia (congenital blockage of biliary tree) Biliary stricture Pancreatitis ```

Question 34

Why does blocking of biliary tree outflow cause jaundice?

Answer 34

Bile consists of: bile acids, cholesterol, phospholipids, electrolytes, water, bile pigments (bilirubin & biliverdin) If bile flow blocked, bilirubin (conjugated) will not pass into gut. Instead, will be absorbed into plasma causing jaundice (hyperbilirubinaemia)

Question 35

Why would a history of pale stools & dark urine help in diagnosis of post hepatic/obstructive jaundice

Answer 35

If bile doesn't enter gut, will not be broken down into stercobilinogen (gives stool brown colour). Bilirubin at this stage soluble, so can be excreted by kidney, colouring the urine

Question 36

What tests are useful in measuring liver function & why?

Answer 36

Liver function tests: Serum albumin: Produced exclusively by liver Bilirubin: Removed from blood by normal liver. Raised plasma levels = prob with normal clearance mechanism (bust doesn't necessarily = liver damage) Glucose: Gluconeogenesis occurs in normal liver Prothrombin time: Normal Liver produces coagulation factors. Damage can increase clotting times

Question 37

What tests are useful, in measuring inflammatory changes & damage in liver?

Answer 37

Aminotransferases: Alanine aminotransferase (ALT) Aspartate amino transferase (AST) Alkaline phosphatase

Question 38

Describe the location of ALT & AST & their specificity to liver disease

Answer 38

Enzymes Present in hepatocytes Leak into plasma following damage to hepatocyte ALT specific to liver AST present in other parts of body (cardiac musc, kidneys, brain)

Question 39

What might a ratio of AST:ALT greater than 2 suggest? What might a ratio of AST:ALT less than 1 suggest?

Answer 39

Alcoholic liver disease Viral hepatitis

Question 40

What tests can be carried out to investigate viral hepatitis?

Answer 40

AST:ALT ratio: if less than 1 Other blood teats looking for surface antigens or viral immunoglobulins for different hepatitis viruses (A-E)

Question 41

Compare 2 similarities & 2 differences for Hep B & C

Answer 41

Similarities: Same route of infection (contaminated blood & body fluids vis several routes) Both can become chronic infections ``` Differences: Hep C: generally shorter incubation period (6-8weeks) more likely to become chronic in adults Cannot be vaccinated ``` Hep B: Longer incubation period (2-6m) Less likely to become chronic Can be vaccinated

Question 42

What treatment options are there for Hep B & C What are the long term outcomes of no treatment?

Answer 42

Alpha interferon Antivirals (Ribavirin & lamivudine) to reduce viral load Side effects incl fatigue & loss of appetite Chronicity of infection Poss leading to cirrhosis or hepatocellular carcinoma