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GI workbook Questions > 7. Diseases Of Liver & Biliary Tree > Flashcards

7. Diseases Of Liver & Biliary Tree Flashcards

0
Q

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

A

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

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1
Q

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

A 
Chemical
Bacterial
Viral
Protazoal
Nematodes (roundworms)
Cestodes (tapeworms)
Trematodes (flukes)
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2
Q

Name 6 physical defences that protect the GIT from toxins

A

Saliva

Gastric acid

Colonic mucus

Anaerobic environments (small bowel, colon)

Gut transit

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3
Q

Name one bacteria resistant to stomach acid

A

Mycobacterium Tuberculosis

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4
Q

Name 3 viruses resistant to stomach acid

A

Hep A
Polio
Coxsackie

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5
Q

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

A

Colonic mucus layer

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6
Q

What are kupfer cells?

What role do they perform?

A

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

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7
Q

Name 3 areas where GALT is nodular

A

Peyer’s patches
Tonsils
Appendix

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8
Q

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

A

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

Enlargement can mimic pain caused from later stage appendicitis

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9
Q

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

A

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

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10
Q

What are the possible causes of appendicitis?

A

Lymphoid hyperplasia at base of appendix
Faecolith
Foreign bodies
Intestinal worms

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11
Q

Name 3 ways that intestinal blood supply can become compromised

A

Arterial disease
Systemic hypotension
Intestinal venous thrombosis

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12
Q

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

A 
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).

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13
Q

What are portosystemic anastomoses?

A

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

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14
Q

What are the 5 main locations of anastomoses?

A

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

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15
Q

What is portal venous system? Why is it useful?

A

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.

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16
Q

Define the term cirrhosis, listing 3 characteristic features

A

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

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17
Q

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

A

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)

18
Q

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

A

Hepatic encephalopathy
Alcohol intoxication
Head injury
Infection, hypoxia

19
Q

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

A 
If due to hepatic encephalopathy: 
infection (chest, urinary, peritonitis)
large ingestion of protein
GI bleed (from varices)
electrolyte imbalances
constipation
20
Q

What treatment options exist for acute confusion from liver disease?

A

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

21
Q

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

A

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

22
Q

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

A

Portal hypertension

Oesophageal varices

23
Q

Explain how liver disease can lead to oesophageal varices

A

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
24
Q

Name 3 sites where varices can occur

A

Oesophagus
Lower part of rectum
Umbilical region of anterior abdominal wall

25
Q

What is jaundice?

A

Raised plasma Bilirubin (exceeding 18-24 micro mols/L)

Presents clinically as yellow pigmentation in sclera, skin, mucosal surfaces

26
Q

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

A 
Pre hepatic (haemolytic): un conjugated bilirubin
Hepatic (hepatocellular): mixed conjugated/un conjugated bilirubin
Post hepatic (obstructive): conjugated bilirubin
27
Q

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

A

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)

28
Q

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

A

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)

29
Q

Discuss the effects of deficient levels of UDP-glucuronyl transferase

A

Enzyme responsible for conjugating bilirubin in liver (making it soluble)

Deficiency = un conjugated jaundice

Various congenital diseases e.g. Gilberts

30
Q

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

A 
Viral hepatitis
Cirrhosis
Tumours
Autoimmune
Haemochromatosis (iron metabolism disorder)

Hepatocellular jaundice = mixed conjugated/unconjugated jaundice
Other liver tests will be affected

31
Q

What may cause jaundice as well as RUQ pain & fever?

What classification of jaundice does this fall into?

A

Gallstones
Infection in biliary tree (ascending cholangitis)

If gallstones = post hepatic/obstructive

32
Q

Why might gallstones cause a fever?

A

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

33
Q

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

A 
Gallstones
Cancer in head of pancreas
Biliary atresia (congenital blockage of biliary tree)
Biliary stricture
Pancreatitis
34
Q

Why does blocking of biliary tree outflow cause jaundice?

A

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)

35
Q

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

A

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

36
Q

What tests are useful in measuring liver function & why?

A

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

37
Q

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

A

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

Alkaline phosphatase

38
Q

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

A

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)

39
Q

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

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

A

Alcoholic liver disease

Viral hepatitis

40
Q

What tests can be carried out to investigate viral hepatitis?

A

AST:ALT ratio: if less than 1

Other blood teats looking for surface antigens or viral immunoglobulins for different hepatitis viruses (A-E)

41
Q

Compare 2 similarities & 2 differences for Hep B & C

A

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

42
Q

What treatment options are there for Hep B & C

What are the long term outcomes of no treatment?

A

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

GI workbook Questions (10 decks)

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