Syndromes of cirrhosis Flashcards

1
Q

what does cirrhosis look like?

A

= fibrous rings separated by degenerative nodules hepatocytes

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2
Q

what makes up the portal vein?

A
  • superior mesenteric
  • splenic vein
  • gastric
  • part from inferior mesenteric
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3
Q

what does portal vein carry outflow from?

A
  • spleen
  • oesophagus
  • stomach
  • pancreas
  • small and large intestine
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4
Q

pressure in hepatic vein is usually what?

A

low

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5
Q

what are 4 collateral pathways?

A
  • Esophageal and gastric venous plexus
  • umbilical vein from the left portal vein to the epigastric venous system
  • retroperitoneal collateral vessels
  • the hemorrhoidal venous plexus
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6
Q

what could happen to anastomoses when there is portal hypertension?

A
  • engorged, dilated or varicosed = rupture
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7
Q

what is portal hypertension?

A

= portal vein pressure above normal rates of 5-8mmHg

= portal vein-hepatic vein pressure gradient greater than 5mmHg

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8
Q

what does portal hypertension represent?

A

= an increase in hydrostatic pressure within portal vein or its tributaries

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9
Q

why does portal hypertension occur?

A
  • increased resistance to portal flow

- increased portal venous inflow

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10
Q

how can you classify the causes of portal hypertension?

A

1) pre-hepatic
= blockage of portal vein before liver due to portal vein thrombosis or occlusion secondary to congenital portal venous abnormality

2) intra-hepatic
= due to distortion of liver architecture either;
- per sinusoidal
- post sinusoidal

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11
Q

what are the commonest cause of cirrhosis?

A
  • alcohol
  • hepatits C virus
  • NASH (NAFLD)
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12
Q

what are 2 types of clinical cirrhosis?

A

1) compensated

2) decompensated cirrhosis

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13
Q

describe compensated cirrhosis?

A
  • clinical normal
  • incidental finding
  • lab test or imaging abnormality
  • portal hypertension may be present
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14
Q

describe decompensated cirrshosis?

A
= liver failure
- acute or chronic 
= infection
= insult
= SIRS
  • end stage liver disease
    = insufficiency hepatocytes
    = run out of liver
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15
Q

what are clinical signs of compensated cirrhosis?

A

spider naevi

palmar erythema

clubbing

hepatomegaly

spleenomegaly

gynaecomastia

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16
Q

what are clinical signs of decompensated cirrhosis?

A

jaundice

ascites

encephalopathy

bruising

17
Q

what are 4 complications of cirrhosis?

A
  • ascites
  • encephalopathy
  • variceal bleeding
  • liver failure
18
Q

what are the general principles of treatment of decompensated cirrhosis?

A
  • remove or treat underlying cause
  • look for and treat infection
  • physiology isn normal
    = avid NaCl retention
  • switch to gluconeogensis and lipolysis and catabolism
19
Q

why is small frequent meals and snacks recommended for in cirrhosis?

A

= reduces fasting gluconeogensis and muscle catabolism

20
Q

why does ascites occur in cirrhosis?

A
  • portal hypertension
  • hepatocellular dysfunction
  • increased production fo vasodilators
  • splanchnic arteriolar vasodilation
  • activation of arterial baroreceptors
  • activation of SNS RAAS AVP ET
  • renal vasoconstriction, sodium and water retention
21
Q

how do you diagnose ascites?

A

= ultrasound

= shifting dullness

22
Q

how do you treat ascites?

A
  • improve underlying liver disease
  • look for and treat infection = SBP
  • drugs NO NSAIDS = if IV think of sodium load
  • reduce salt intake, maintain nutrition
  • diuretics = spironolactone first
  • paracentesis
  • TIPSS
  • transplantation
23
Q

what diuretic should be used for ascites?

A

= spironlactone better than amiloride

24
Q

what are 4 things that ascites paracentesis does?

A
  • rapid relief
  • risk of infection
  • encephalopathy
  • hypovolaemia
25
Q

what is spontaneous bacterial peritonitis, SBP?

A

= translocated bacterial infection fo ascites

26
Q

how do you diagnose SBP?

A

= differential
= do a tap in all ascites and cell count
- neutrophil count > 250cells/mm3

27
Q

how do you treat SBP?

A
  • Urgent
  • Antibiotics and Alba
  • Vascular instability-terlipressin
  • Maintain renal perfusion
  • HRS development very poor prognosis
28
Q

what causes encephalopathy?

A
  • microglial inflammation

- ammonia glutamate/glutamine shuttle

29
Q

how do you diagnose ecephalopathy?

A
  • flap confusion
  • any neurology
  • alcohol withdrawal
30
Q

how do you treat encephalopathy?

A
  • Look for cause-infection, metabolic, drugs, liver failure
  • Treat it
  • Lactulose to clear gut/ reduce transit time
    = Rifaxamin
  • Maintain nutritional status with small, frequent meal/snack pattern and bedtime CHO
  • If spontaneous consider transplantation
31
Q

what is primary prophylaxis of varices oesophageal?

A

Beta blockers
- propanolol
- carvideolol
= non-selective

Varicela ligation

32
Q

how do you deal with acute variceal bleeding?

A
  • resuscitation
  • pharmacological
  • timing of therapy
  • failed therapy
    = TIPSS
    = transection/shunt surgery
33
Q

describe endoscopic herpay?

A

= sclerotherapy

  • effective & long-term
  • intra-variceal
  • freehand & flexible
  • sclero-ulcers

= variceal ligation

  • banding
  • quicker eradication
  • lower morbidity
34
Q

when is balloon tamponade used?

A

= variceal bleeding

gastric balloon only

35
Q

what are risks of balloon tamponade?

A
  • complication rate
  • aspiration
  • perforation usually fatal
36
Q

what is TIPSSS?

A

trans-jugular intra-hepatic porto-systemic shunts

37
Q

when do you use TIPSSS?

A

when beta blockers and variceal ligation doesn’t work