Liver Diseases Flashcards

(31 cards)

1
Q

Chronic Liver failure- pathology

A

↪️ occurs in those w/ chronic liver disease
Variceal bleeding
Hepatic encephalopathy
These 2 will contribute to Ascites, indicating hepatic decompensation.

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2
Q

How do u treat Ascites?

A
Paracentisis
Spironolactone (aldosterone antagonist-⬆️ excretion of Na --> H2O.
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3
Q

Hep A pathology

A

RNA

Faeco-oral route

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4
Q

Whats Acute Liver Failure? Give an example

A

Failure of liver to maintain vital functions within 6months of symptom onset, without chronic Liver disease (jaundice, hepatic encephalopathy).
E.g. Paracetamol overdose.
Sub-acute presentation
↪️ autoimmune hepatitis

⭐️high mortality- ICU due to multiorgan failure
⭐️Liver transplant

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5
Q

Hep A, what happens?

A

RNA virus
Faeco-oral route
Contaminated water –> high poverty, poor sanitation.
Can present w/ jaundice & acute hepatitis
No chronic carrier
No acute managment- tx symptoms, supportive
Active immunisation- killed virus
Passive- immunoglobulins.

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6
Q

Hep B

A
Common DNA Virus -350m in chronic state
Infection aquired in infants >90% will become chronic. 5% in adults
Effective immunisation: available
HBVsAg by recombinant DNA technology
Given at birth to infected mothers OR adults at risk
Chronic--> hepatocellular cancer
--> hepatic decompensation
Give: regulated interferon/ nucleosidete
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7
Q

Hep C

A
RNA virus --> worldwide 
Blood  contact 
West: drugs 
Developed: understerilised equipment
20 years after infx cirrhosis
NO VACCINATION 
Pegylated interferon- ribavirin
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8
Q

Hep D-what happens?

A

Incomplete RNA virus
Require Hep B to oroduce the surgace coat for a complete virus.
⬆️ incidence of heparic decompensation.

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9
Q

Hep E

A
Small RNA virus
Faeco-oral route
NO chronic carrier state
⬆️⬆️ mortality in pregnancy 
NO VACCINE-
Tx- supportive
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10
Q

What causes Jaundice?

A

Xs bilirubin in the extracellulat fluids
Either unconjucated or conjugated >1.5 mg/dl
0.5mg/dl of plasma, unconjugated.

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11
Q

Causes of jaundice?

A
  1. ⬆️⬆️ destruction of RBCs (haemolytic jaundice) –> Rapid relases of bilirubin into blood–> Liver; cannot excrete bilirubin as fast as its made.
  2. Obstruction of bile ducts
  3. Damage to ️Liver
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12
Q

What happens when there is total obstruction?

A

Bilirubin cannot be oxidised to urobilinogen –> negative urobilinogen results in urine + faeces - clay colour- lack of stercobilin. (Dark urine)

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13
Q

What can cause obstructive jaundice?

A
Gall stones
Cancer
Hepatitis
Rate of bilirubin production✔️
Conjugated bilirubin cannot pass from blood to intestines

Bile—> lymph-> most in plasma: conjugated.

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14
Q

Investigations for jaundice?

A
Diagnosis
Hemolytic- unconjugated 
Obstructive: conjugated
Severe obstructive: conjugated in urine (cz unjonjugated bound to albumin) 
Foam- intense yellow
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15
Q

Whatbare the classifications of jaundice?

A
Prehepatic- hemolytic
Hepatic
1. Congenital defect of hepatocytes
2. Hepatocellular injury or infection
Post-Hepatic
Obstruction to bile duct
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16
Q

How would u Investigate jaundice?

A

Bilirubin
ALP: proliferate in the presence of obstruction. When jaundiced: indicator of cholestasis, either intrahepatic or extra-hepatic
Aminotransferases:
AST/ALT: constituents of the hepatocyte.
Raised if hepatocellular damage

17
Q

Some other measurments of jaundice?

A

Albumin conentration: synthetic capacity of the liver+ nutritional state of the patient
Clotting factors: synthesised in the liver. Most easily assesed: prothrombin. Vit K is a cofactor of its synthesis.
AFP (alpha feroprotein) for hepatocellular carcinoma
Hepatitis virus markers

18
Q

Whats vit K?

A

Fat soluble, cannot be absorbed without bile, from intestines, due to obstruction–> reserves run out.
So!! Prothrombin time is essential before operating jaundiced patients,

19
Q

When are ALP and AST/ALT raised?

A

Hepatocellular damage : ALP ⬆️ AST/ALT ⬆️⬆️⬆️

Chopestasis: including extrahepatic biliary obstruction ALP ⬆️⬆️⬆️. AST/ALT ⬆️

20
Q

Some causes of Portal hypertension (PTHN)

A

Prehepatic: Portal vein thrombosis
Splenic vein thrombosis

Intrahepatic:
Cirrhosis (80% UK) schistosomiasis (commonest worldwide) sarcoidosis, congenital hepatic fibrosis

Post-Hepatic:
RHF, constrictive pericarditis, Budd-Chari syndrome

21
Q

What are the risks for variceal haemorrhage?

A

⬆️ portal pressure, bout 12mmHg
Variceal size
Child-Pugh score (>_8)

22
Q

What does the child-pugh score inculde + predict?

A
Risk of variceal bleeding
Bilirubin
Albumin
Ascites
Encephalopathy
Prothrombin time
23
Q

When would you suscpect varices as a cause of an upper GI bleed?

A

Alcohol abuse or cirrhosis

Look for signs: CLD–> encephalopathy, splenomegaly, ascites, hyponatraemia, coagulopathy, thrombocytopaenia.

24
Q

Variceal primary prophylaxis

A

W/o tx 30% of cirrhotic varices will bleed.
Reduce to 15% by non-selective b-blocker- propranolol)
2. Repeat endoscopic banding ligation (better for cirrhotic patients)

25
Secondary prophylaxis of bleeding varices
After initial bleed, 80% will rebleed within 2 Years. B blocker + endoscopic band ligation + transjugular intrahepatic portosystemic shunt (TIPSS) resistant to banding OR surgical shunt if TIPSS impossible
26
How do you treat acute varicceal bleeding?
ABC!! Resuscitate until haemodynamically stable (do not give 0.9% saline) Correct clotting abnormalities- Vit K + FFP IV terlipressin bolus Endoscopic banding (harder to visualise) or sclerotherapy If bleeding uncontrolled, Balloon tamponade w/ Sengstaken -Blakemore tube
27
What the Balloon tamponade w/ Sengstaken -Blakemore tube for?
If life threatening variceal bleeding, this can buy time to arrange transfer to liver clinic or surgery decompression. Uses balloons to compress gastric & oesophageal varices. Oesophageal ballon-use portable Xray for guidance.
28
How does TIPSS work?
By shunting blood away from the portal circulation through an artificial side-to-side portosystemic anastomosis created in the liver.
29
Whats non alcoholic liver disease?
Can lead to cirrhosis (1%) and Hepatocelluar cancer. Histological changes: similar to alcoholic liver disease. 1. Simple fatty change 2.'to Fat and inflammation - steatohepatitis, NASH (non alc) 3 fibrosis. Oxidative stress injury leads to lipid peroxidation in the presence of fatty infiltratiom amd inflammatiom results. 🌟 Fibrosis may then occur, which is enhanced by insulin resistance- which induces connective tissue growth factor.
30
What are some risk factors for NAFLD?
Obesity Hyperlipidaemia Hypertension T2 DM NAFLD- liver component of metabolic syndrome. Insulin resistance universal. Most pts asx. Hepatomegaly may be present. Dx: Fatty liver on USS . Liver biopsy- allows staging. Most ppl would do one if ALT persistent high x2. Elastography used to evaluate fibrosis degree.
31
Mx of NaFLD
Wt loss Strict HTN control Statin