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Abdo year 3-K > Liver Diseases > Flashcards

Liver Diseases Flashcards

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
Q

Secondary prophylaxis of bleeding varices

A

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
Q

How do you treat acute varicceal bleeding?

A

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
Q

What the Balloon tamponade w/ Sengstaken -Blakemore tube for?

A

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
Q

How does TIPSS work?

A

By shunting blood away from the portal circulation through an artificial side-to-side portosystemic anastomosis created in the liver.

29
Q

Whats non alcoholic liver disease?

A

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
Q

What are some risk factors for NAFLD?

A

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
Q

Mx of NaFLD

A

Wt loss
Strict HTN control
Statin

Abdo year 3-K (13 decks)

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