Session 7 - Liver, Biliary tree and pancreas 2 Flashcards Preview

ESA 3 - GI > Session 7 - Liver, Biliary tree and pancreas 2 > Flashcards

Flashcards in Session 7 - Liver, Biliary tree and pancreas 2 Deck (23)
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1
Q

What defences does the GI have against MOs?

A

1) saliva
2) Gastric acid
3) Colonic mucus
4) Enzymatic secretions
5) Anaerobic environment
6) Peristalsis - moves gut and prevents bacterial attachment

2
Q

Explain how the liver handles toxins

A

Absorption of toxins from the GI tract:

1) Toxins absorbed by villi in the GI tract
2) Taken via the hepatic portal system.
3) Kupffer cells in the liver can extract toxins form the blood and put it into the bile and secrete into the bile duct.

3
Q

What blood proteins does the liver syntehsis?

A

Albumin and clotting factors

4
Q

What components would be elevated in cholestasis? What is cholestasis?

A

Bilirubin and alkaline phosphatase

Bile cant flow from liver to duodenum

5
Q

How would you assess poor synthetic function of the liver?

A

Lack of serum album and high prothrombin time (due to clotting factors)

6
Q

How would you assess hepatic damage?

A

Aminotransferases ALT / AST.

Y-glutamyl transpeptidase, y-GT

7
Q

Name the 3 ways in which jaundice can be caused.

A
  • Prehepatic (haemolytic)
  • Hepatic (parenchymal)
  • Post hepatic (cholestatic)
8
Q

Explain how excessive haemolysis can cause jaundice. What lab findings would there be? What would cause it?

A

Excessive haemolysis results in build up of bilirubin and liver cannot cope with the all the bilirubin.

Lab findings:

o Unconjugated hyperbilirubinemia

o Increase in LDH

o Decrease in haptoglobin – binds free Hb in blood and prevents its oxidative action Indicative of anaemia due to excessive haemolysis

Causes:

o Inherited – Red cell membrane defects, haemoglobin abnormalities, metabolic defects

o Congenital hyperbilirubinaemias – Gilbert’s syndrome, Crigler-Najjar syndrome, Dublin-Johnson syndrome

o Acquired – Immune, mechanical, acquired membrane defects, infections, drugs, burns.

9
Q

What causes hepatic jaundice? What lab findings would there be?

A

Deranged hepatocyte function

Lab findings:

o Mix of conjugated and unconjugated hyperbilirubinaemia

o Increase in liver enzymes ALT and AST (reflect liver damage)

o Increase or same alkaline phosphatase (ALP) due to cholestasis o Abnormal clotting

Cause:

o Congenital – Gilbert’s syndrome

o Hepatic – Hep A, EBV, Alcohol

o Drugs – paracetamol

o Cirrhosis – Alcohol

o Hepatic tumours – Metastases

10
Q

What is cholestatic jaundice? What causes cholestatic jaundice? What lab findings would there be?

A

Obstruction of biliary system – intrahepatic or extrahepatic

Results in passage of conjugated bilirubin being blocked

Lab findings:

o Bilirubin in urine (dark)

o No urobilinogen in urine (no bilirubin enters bowel)

o Same or increase in liver enzymes (mild hepatocyte damage due to build up of pressure)

Causes:

o Intrahepatic – hepatitis, drugs, cirrhosis

o Extrahepatic – Gallstones, carcinoma, pancreatitis

11
Q

Describe the key progressions of alcoholic liver disease pathology

A
  • Fatty change
  • Alcoholic hepatitis
  • Cirrhosis – results in increased resistance to blood flow and deranged liver function. Leads to portal hypertension
12
Q

Explain the associated pathologies of portal hypertension

A

1) All blood from the gut goes through the portal vein and into the liver
2) However, in portal hypertension it cannot due to the high resistance. Therefore, the build up of the pressure results in blood from the portal system entering the systemic circulation, therefore toxins enter the blood.
3) Anastomoses also aren’t made for lots of blood to go through; e.g. oesophageal anastomoses bleed heavily, haemorrhoids from anastomoses in the rectum, opening of the ligamentum teres leading to caput medusa, opening of anastomoses in the liver bypassing it.

13
Q

What are the clinical manifestations of portal hypertension?

A
  • Splenomegaly
  • Ascites
  • Caput medusae
  • Oesophageal/rectal varices –> haemorrhage
14
Q

Describe hepatic encephalopathy and why it occurs

A
  • This is a reversible neuropsychiatric deficit
  • The liver is unable to remove ammonia from the blood due to liver damage
  • Results in build up of ammonia in blood which manifests as:

o Flapping tremor

o Personality changes

o Intellectual deterioration

15
Q

Give 3 causes of gallstones

A
  • Obstruction
  • Infection
  • Inflammation
  • Neoplasia
16
Q

What are the possible consequences of gall stones on: a) the gall bladder b) the pancreas c) the liver

A

a) Biliary colic, cholecystitis, perforation
b) acute pancreatitis
c) obstructive jaundice

17
Q

Give 4 possible causes of acute pancreatitis.

A

G - gall stones

E - ethanol

T - trauma

S - steroids

M - mumps

A - autoimmune

S - scorpion bite

H - hyperlipidaemia

E - ERCP

D - Drugs

18
Q

What are the acute and chronic consequences of pancreatitis?

A
  • Acute – oedema, haemorrhage, necrosis
  • Chronic – fibrosis, calcification
19
Q

What would lab analysis find in pancreatitis?

A
  • Increase in pancreatic amylase
  • Decrease in calcium
  • Increase in ALP
  • Increase in glycaemia
20
Q

What clinical symptoms would occur in acute pancreatitis?

A
  • Severe pain
  • Vomiting
  • Dehydration
  • Shock
21
Q

What clinical symptoms would occur in chronic pancreatitis?

A
  • Pain
  • Malabsorption – steatorrhea, decrease in albumin, weight loss
  • Jaundice
22
Q

What are the clinical features of pancreatic carcinoma?

A
  • Symptomless for a long time
  • Obstructive jaundice – palpable gallbladder
  • Pain
  • Vomiting
  • Carcinomatosis
  • Malabsorption
  • Diabetes
23
Q
A