Deck 1 - GI Flashcards

1
Q

Q. Name four functions of the liver

A

A. Glucose and fat metabolism
B. Detoxification and excretion (bilirubin, ammonia, drugs/hormones/pollutants)
C. Protein synthesis (albumin, clotting factors)
D. Defence against infection (reticuloendothelial system)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Q. Describe the macroscopic and microscropy anatomy of the liver

A

A. Lobes: R, L, caudate
B. Blood supply: portal vein (deoxygenated), hepatic artery (oxygenated)
C. Microscopic: sinusoids, hepatocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Q. What occurs to the liver during cirrhosis?

A

A. Scarring and disorganisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Q. How can chronic liver failure affect the gut?

A

A. Varices (haematemesis due to high pressure and hepatoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Q. Name two causes of acute liver injury and two causes of chronic liver injury

A

A. Acute: Viral (A, B, EBV), drugs, alcohol, vascular, obstruction, congestion
B. Chronic: alcohol, viral (b and C), auto immune, metabolic (iron, copper)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Q. Name two symptoms of acute liver injury and two symptoms of chronic liver injury

A

A. Acute: malaise, nausea, anorexia, jaundice (rarer: confusion, bleeding, liver pain, hypoglycaemia)
B. Chronic: ascites (abdo swelling), odema, haematemesis (varices), malaise, anorexia, wasting, easy bruu=ising, itching, hepatomegaly, abnormal LFTs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Q. Name 4 liver function tests

A

A. Serum bilirubin, albumin, prothrombin time
B. Serum liver enzymes
a. Cholestatic: alkaline phosphatase, gamma-GT
b. Hepatocellular: transaminases (AST, ALT) – destruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Q. Name the two classifications of jaundice and some causes

A

A. Unconjugated/Pre hepatic: Obstruction (common bile duct, pancreas –gall stone, malignancy)
B. Cholestatic/hepatic: hepatitis, drugs, immune, alcohol
C. Cholestatic/ post hepatic: (dark urine, pale stools, maybe itchy, abnormal LFTs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Q. What questions should be asked when a patient presents with jaundice?

A

A. Dark urine, pale stools, itching?
B. Changes in bowel habits? Hard to flush? Frequency?
C. Symptoms: biliary pain (upper abdo, severe, restlessness, episodic), rigors (conscious shakes – bile duct stone?), abdomen swelling, weight loss?
D. Past history:
a. Biliary disease/intervention
b. Malignancy
c. Heart failure
d. Blood products (transfusion prior to 90s – hep C)
e. Autoimmune disease
f. Drug history (drugs/herbs started recently)
g. Social history: Alcohol, potential hepatitis contact (irregular sex, IVDU, exotic travel, certain foods)
h. Family Hx/system review – rarely helpful

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Q. What investigations should be carried out when a patient presents with jaundice?

A

A. LFT: very high AST/ALT suggests liver disease
B. Ultrasound: dilated intrahepatic bile ducts = biliary obstruction
C. CT/MRI/endoscopic retrograde etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Q. Name some risk factors that increase the risk of gall stones

A

A. Female, high BMI, fertile (liver disease etc), most are asymptomatic
B. Cholecystitis (gall bladder inflammation), Cholangitis (bile duct infection/inflammation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Q. How should patients with gallstones and bile duct stones be managed?

A

A. Gallbladder stones:
a. Laporoscopic cholecystectomy, Bile acid dissolution therapy (<1/3 success
B. Bile duct stones:
a. ERCP with sphincterotomy and: removal (basket or balloon), crushing (mechanical, laser..), stent placement (90% effective – standard therapy), Surgery (large stones)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Q. What are ascites? Describe the pathogenesis and name 2 causes

A

A. Accumulation of fluid in the peritoneum
B. High BP leads to systemic vasodilation, this leads to portal HTN (causes secretion of RAAS, noradrenaline and vasopressin) leads to additional fluid retention and liver failure, low serum albumin also leads to ascites
(HF, peritonitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Q. What occurs when the liver is subject to high levels of alcohol? Which cells are associated with acute/chronic injury?

A

A. Acute alcohol related injury: hepatocyte ballooning, mediated by neutrophils, may accumulate a cytoskeletal protein (irregular and fat)
B. Fat accumulation = steatosis (macrovesicular and microvesicular droplets)
C. Chronic liver injury = lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Q. What part of the liver do toxins have the greater effect on?

A

A. The cells with the lowest blood and oxygen supply i.e. zone 3
B. Damage results in fibrosis with pericellullar fibrosis being more common in alcohol-related injury than fibrosis of portal tracts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Q. What causes portal HTH? What can this lead to?

A

A. Caused by: cirrhosis, fibrosis, portal vein thrombosis
B. Pathology: increased hepatic resistance, increase splanchnic blood flow
C. Causes: Varices (oesophageal, gastric), splenomegaly

17
Q

Q. What symptoms are associated with primary biliary cirrhosis/cholangitis?

A

A. Fatigue, itchy skin, dry eyes and mouth, pain RUQ, Spider naevi, 90% women
B. Build up of bile in liver = cirrhosis

18
Q

Q. What is haemochromatosis?

A

A. Genetic disorder (recessive) that causes uncontrolled intestinal iron absorption with deposition in liver, heart and pancreas
B. Diagnosis suggested by raised ferritin and transferrin saturation, confirmed by HFE genotyping and liver biopsy
C. When cirrhosis present, increased risk of hepatocellular carcinoma
D. Iron removal may lead to regression of fibrosis

19
Q

Q. What factors may contribute to non-alcoholic fatty liver disease?

A

A. Hypertension, hyperlipidaemia, type 2 diabetes, obesity
B. Commonest cause of mildly elevated LFTs, (usually ALT)
C. Need biopsy to distinguish from Nonalcoholic steatohepatitis
D. Treatment: weight loss!!

20
Q

Q. What is 1-antitrypsin deficiency?

A

A. Genetic (recessive), results in an inability to export 1-antitrypsin from liver
B. This can lead to liver disease (protein retention in the liver) and emphysema (protein deficiency in the blood)
C. Usually presents as a) neonatal jaundice b) chronic liver disease in adults
D. Symptoms: SOB, wheezing (e.gg. emphysema symptoms w/o smoking, chronic liver failure symps)

21
Q

Q. Name 2 causes of immune chronic liver disease

A

A. Autoimmune hepatitis, primary biliary cirrhosis, sclerosing cholangitis