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

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

25
Ascites
Increase in hydrostatic pressure and translation of fluid | Reduced oncotoc pressure
26
Management of ascites
Dietary salt restrictio Diuretic Paracentasis transjugular intrahepatic potosystemic shunt
27
Varicella haemorrhage incidence
60%
28
Management
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
Secondary prevention
Propranolol | Ocreotide
30
Spontaneous bacterial peritonitis
Asymptomatic Tap neutrophils cout> 200 Rx antibiotics Prophylactic cotrimox or quinolone
31
Mortality rates of sbp
70% at 2y
32
Renal
Hypovolaemia ATN DRUG induced Hepatorenal syndrome
33
Pathophysiology of hepatic renal syndrom
Sympathetic and RASS activation 2nd to splachnic vasodilatation withrofound vasoconstriction
34
Diagnosis of hrs
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
Type 1hrs
Acute Doubling Serum creatinine > 2,5g/dl Or 221mcmol/l in less than 2 weeks
36
Type 2
Less aggressive course than type 1 Chara terized by asci
37
Management
Vasoconstriction Albumin RRT
38
Coagulation haemorrhage risk
Reduced vitamin dependent factor Thrombocytopenia hyperspenism 9r uterine Dysfibrinigenea High tpa
39
Coagulation thrombosis risk
Low protein c s Low antithrombin, plaeminogen, heparin cofactor 2, alpha2 macroglobulin Increased procogulant factor vii,vWT
40
Overall coagulation
41
Assessment of coagulation
42
Pharmacokinetic
Decreased: hepatic metabolism, renal excretion, protein synthesis Increased : total body water
43
Volatile
Avoid enflurane and halothane Iso reduced hepatic clearance by o,2% improves hepatic blood flow sevoflurane 2_5 % biotransformation Des 0.02%
44
Benzos
Prolonged duration policy action Worsen encephalopathy Loran,9xaz,Texas undergoing glucoronide conjugation and less affected by liver dysfunction
45
Opioids
46
Neuromuscular blockers
Slow onset | Cisco independent of liver function
47
Induction
Protocol no change
48
Risk stratification child Pugh score
49
Meld
50
Modified king college
51
W3at haven score