Liver: case studies Flashcards

1
Q

Cholestatic enzymes

A

GGT (gamma-glutamyl transferase) and ALP (alkaline phosphatase)

This often indicate a mass or biliary obstruction

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2
Q

Inflammation enzymes

A

ALT (alkaline-transferase) and AST (aspartate-transferase)

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3
Q

What causes jaundice?

A

Elevated bilirubin. causes yellow sclera and skin.
Due to a biliary obstruction (bile release), or hepatocellular injury (lysis)

Haemolysis also causes bilirubin

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4
Q

What measure the livers synthetic function

A
Prothrombin Ratio (clotting factors)
Albumin
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5
Q

What measure the livers detox function

A

NH3 ammonia levels, if not detoxified they can build up in the brain > hepatic encephalopathy

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6
Q

If the AST and ALT are really high, what is the much common cause to look at first?

A

Viral infection, most commonly Hep A, B, C

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7
Q

Why should you be worried about blood transfusions pre 90’s

A

Because there wan’t the regulations there are now, so potentially carrier of infection. eg) hep B and C

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8
Q

Chronic Hepatitis A

A

Doesn’t exist, Hep A is benign and self-limiting

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9
Q

How do you determine if viral hepatitis is acute of chronic

A

Acute: first 6 months
Chronic: post 6 months

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10
Q

Causes of Hep B and Hep C, how are they transmitted, what do they cause and available treatment?

A
Causes of Hep B:
*** sexually transmitted
drug use
mother to child
horizontal transmission
Causes of Hep C
***Drug use
blood transfusion
low sexual transmission risk
mother to child
occupational
tattoo

Both transmittable through blood

Can lead to cirrhosis and hepatocellular carcinoma (if aqquired later some Hep B patients will resolve)

There is a vaccine for Hep B but not Hep C (incurable)

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11
Q

Interferon

A

Old drug for HCV, many adverse side -effects, low success rate (50%), a cytokine so gives flu like effect.
-given as a sub-cutaneous injection
Initially alone
the interferon + ribavirin

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12
Q

Breakthrough HCV treatment

A

Direct-acting Antiviral agents
-tablets
- Cure rates >90%
Been the cause of declining need for liver transplants

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13
Q

Oesophageal/ gastric Varices

A

Due to pressure increase due to portal hypertension (associated with cirrhosis), these are dangerous as they have potential to bleed.

Treatments: ‘Banding’, suck varices up into a cap, rubber band strangles varices and stops the bleeding

This may need to be done several times, but they can REFORM, so it’s only temporary!

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14
Q

Portal circulation consists of?

A

Portal Vein: that drains nutrient rich blood from the GI tract and spleen to the liver
venous blood passes through the
Liver > IVC > heart

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15
Q

Portal Hypertension

A

High pressure in the portal vein, more resistance making it harder for blood in the portal circulation to return to the heart.
Portosystemic shunts/collaterals form, that enlarge and try to divert blood away from the portal system to the heart > varices

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16
Q

Two most common place to get varices

A

1) Gastro-oesophageal Junction: work upwards

2) Stomach: particularly fundus

17
Q

Normal Portal BF vs Cirrhosis (Portal hypertension)

A

BP: 55mmHg
Supplies 3/4 Blood flow to liver (70% O2)
100% blood > hepatic vein > systemic circulation

BP: 12mmHg
portosystemic shunts formed > varices

18
Q

Liver intitially ______ then progressively ______

A

Liver intitially elarged then progressively shrinks

19
Q

Is fibrosis reversible?

A

Potentially if the liver is allowed time to regenerate by removing inflammatory cause. If this doesn’t occur&raquo_space; cirrhosis ‘irreversible scarring’

20
Q

What causes fibrosis

A

repeated bouts of inflammation

21
Q

Can the liver function with cirrhosis?

A

When it is mild, as the liver is good at compensating, huge reserve capacity. However as it progresses more and more function is lost (liver failure at 80-90%)

22
Q

Hepatic Encephalopathy. Early and late symptoms

A

Build up of NH3 toxins in the brain due to liver failure. THe liver is unable to detoxify substances from the bacterial metabolism. Also portosystemic shunts bypass the liver entirely (no detox at all). You get a build up of ammonia in the blood (passes blood-brain barrier)

Early Symptoms: mood and personality change. Inverted sleep pattern. (hard to diagnose)

Late Symptoms; Confusion and bizarre behaviour, drowsiness and coma.

23
Q

Treatment of HE

A

Lactulose

  • normally a laxative to treat constipation
  • decrease ammonia production by bacteria
  • makes it a non-absorbable substance > excreted

For management but not definitive treatment.

24
Q

Ascites

A

fluid accumulation in the peritoneum > abdominal distention.
Often caused by portal hypertension
-Elevated hydrostatic pressure in PV > fluid moves out of circulation
-Low oncotic pressure in PV (low serum albumin) unable to hold onto fluid

25
Q

Hypersplenism

A

1) Splenomegaly : swollen spleen

2) Low platelet count: platelets going through spleen are destroyed at a higher rate

26
Q

People can donate upto _____% of their liver

A

50%

27
Q

Definitive treatment for liver failure

A

Liver transplant

28
Q

Acute thrombosis of Hepatic veins

A

Budd-Chiari

  • outflow of blood from liver obstructed
  • liver becomes congested > hepatocellular damage
  • Results in PH with ascites forming
29
Q

Fulminant

A

very severe and sudden

30
Q

Causes of Budd-Chiari

A
75% no obvious cause
25% cause identifies
-tumor
-pregnancy
-Contraceptive pill
-clotting disorders
31
Q

Management of Budd-Chiari

A

Portocaval shunting to divert blood flow

  • TIPSS (transjugular intrahepatic portosystemic shunt): reduces resistence of BF to liver, done for PH
  • surgical

Anticoagulation : thin blood and dissolve clot

Diuretics