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Domain 2 > Hepatic Disease > Flashcards

Hepatic Disease Flashcards

1
Q

Define acute liver failure

A

development of hepatocellular dysfunction associated with coagulopathy and encephalopathy in patients without prior known liver disease

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2
Q

How is ALF classified?

A

According to time between jaundice and onset of encephalopathy

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3
Q

How is ALF classified according to time line of symptoms?

A

Hyperacute
Acute
Subacute

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4
Q

What are the causes of acute liver failure?

A
  1. Infective: hep B 12%
  2. Drug induced: acetaminophen 39%, phenitoin, halothane.
  3. Autoimmune disease
  4. Vascular :Budd chiari Syndrome
  5. Pregnancy : HELLP, acute fatty liver of pregnancy.
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5
Q

Define Chronic hepatic disease in

A

Chronic hepatitis is any hepatitis lasting >6months. Inflammation can lead to hepatic fibrosis, and, in some patients, there is progression to cirrhosis, characterized by nodular regeneration and disruption of the architecture of the liver, which can lead to portal hypertension.

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6
Q

What is decompansated liver cirrhosis

A

Developof portal hypertension ascites, varicella haemorrhage or liver insufficiency as marked by coagulopathy,jaundiceand encephalopathy

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7
Q

Schematic of decompensated liver dysfunction

A
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8
Q

Management strategy cirrhosis

A
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9
Q

Management

A
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10
Q
A

Management

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11
Q

Effects on cvs

A

Increased production or reduced excretion of vasodilators resulting in increased splamchnic vessels capacity which stimulated retention of na should h20, this leased to portal hypotension and further increase in capacitance e by formation of potosystemic shunts. These changes lead to hyperdynamic circulation with hypotension and tachycardia and blunted b adrenalin stimulation leading to cardiomyopathy

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12
Q

what are the ECG changes?

A

QT prolonged
BP
Coronary artery disease due to commodities

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13
Q

Pathogenesis portopulmonary hypertension

A

Not completely understood but histology also changes include midealhypertro0hy, intimate proliferation, thrombosis, and fubrosis

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14
Q

Diagnosis

A

Mean pulmonary pressure >25 /PVR > 240DYNES/s3c/m3

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15
Q

MODERATE portopulmonary hyp

A

MPP > 35-45/ PVR >250

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16
Q

Mortality rates associated with liver transplant in moderate ph

A

> 50%

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17
Q

Severe portal hypertension

A

map > 50/

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18
Q

Mortality rates associated with liver transplant in severe ph

A

100%

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19
Q

Pulmonary effect

A

Pleural effusion hydrothorax
Atelectasis diaphragm displacement ascites
aspiration pneumonia
Poto pulmonary hpt

Hepatopupmonary sx

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20
Q

Pathogenesis of hepatic pulmonary

A

Due 5o vasod8oatation 5here is increased blood flow with no matched increase in ventilation leading to vq mismatch. HPV is blunted due to blunting of vasoconstriction

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21
Q

Diagnostic criteria for hps

A
22
Q

Clinical features

A 
Exertional dyspnoea 
Fatigue 
Clubbing 
Spider angiomata 
Platypnia 
Orthodeoxia
23
Q

GIT effects; portal hypertension

A

Increased gradient between portal and hepatic vein by > 5mmhg secondary to 8ncreased vascular resistance from fibrosis and flow this inturn increase splanchnic blood flow which exacerbates pulmonary hpt

24
Q

Complications of portal hpt

A
25
Q

Ascites

A

Increase in hydrostatic pressure and translation of fluid

Reduced oncotoc pressure

26
Q

Management of ascites

A

Dietary salt restrictio
Diuretic
Paracentasis
transjugular intrahepatic potosystemic shunt

27
Q

Varicella haemorrhage incidence

A

60%

28
Q

Management

A

A- protect from aspiration
B-
C- fluid, blood, POC guided haemostatic resus, vit k
D-

Endoscopic ligation banding or sclerotheraphy
Balloon tampinade sengstaken blakemore
TIPSS

29
Q

Secondary prevention

A

Propranolol

Ocreotide

30
Q

Spontaneous bacterial peritonitis

A

Asymptomatic
Tap neutrophils cout> 200
Rx antibiotics
Prophylactic cotrimox or quinolone

31
Q

Mortality rates of sbp

A

70% at 2y

32
Q

Renal

A

Hypovolaemia
ATN
DRUG induced
Hepatorenal syndrome

33
Q

Pathophysiology of hepatic renal syndrom

A

Sympathetic and RASS activation 2nd to splachnic vasodilatation withrofound vasoconstriction

34
Q

Diagnosis of hrs

A

Cirrhosis with ascites, doubling Serum creatinine >1,5mg/dlnot reduced to < 1,5mg/dl with Albumin administration at dise 1g/kg and after min 2 day with no diuretic

35
Q

Type 1hrs

A

Acute Doubling Serum creatinine > 2,5g/dl Or 221mcmol/l in less than 2 weeks

36
Q

Type 2

A

Less aggressive course than type 1 Chara terized by asci

37
Q

Management

A

Vasoconstriction
Albumin
RRT

38
Q

Coagulation haemorrhage risk

A

Reduced vitamin dependent factor
Thrombocytopenia hyperspenism 9r uterine
Dysfibrinigenea
High tpa

39
Q

Coagulation thrombosis risk

A

Low protein c s
Low antithrombin, plaeminogen, heparin cofactor 2, alpha2 macroglobulin
Increased procogulant factor vii,vWT

40
Q

Overall coagulation

A
41
Q

Assessment of coagulation

A
42
Q

Pharmacokinetic

A

Decreased: hepatic metabolism, renal excretion, protein synthesis
Increased : total body water

43
Q

Volatile

A

Avoid enflurane and halothane
Iso reduced hepatic clearance by o,2% improves hepatic blood flow
sevoflurane 2_5 % biotransformation
Des 0.02%

44
Q

Benzos

A

Prolonged duration policy action
Worsen encephalopathy
Loran,9xaz,Texas undergoing glucoronide conjugation and less affected by liver dysfunction

45
Q

Opioids

A
46
Q

Neuromuscular blockers

A

Slow onset

Cisco independent of liver function

47
Q

Induction

A

Protocol no change

48
Q

Risk stratification child Pugh score

A
49
Q

Meld

A
50
Q

Modified king college

A
51
Q

W3at haven score

A

Domain 2 (22 decks)

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