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GI > 4- clinical syndromes of cirrhosis > Flashcards

4- clinical syndromes of cirrhosis Flashcards

1
Q

what is compensated cirrhosis?

A

what you have initially, largely asymptomatic →median survival greater than 12 years (5-7% per year move to decompensated cirrhosis)

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2
Q

what is decompensated cirrhosis?

A

worse cirrhosis than compensated - median survival is 2 years, you can go back to compensated

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3
Q

what is progression of liver to cirrhosis?

A

healthy liver→fatty liver→liver fibrosis →cirrhosis

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4
Q

what are symptoms of decompensated cirrhosis?

A
  • jaundice
  • ascites
  • hepatic encephalopathy
  • renal impairment
  • variceal bleeding
  • signs of sepsis
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5
Q

what can cause progression from compensated to decompensated cirrhosis?

A
  • systemic infection
  • alcohol
  • drugs
  • thrombus
  • dehydration
  • ischaemia
  • hepatocellular carcinoma
  • untreated cause
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6
Q

what are symptoms of compensated cirrhosis?

A

mostly asymptomatic

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7
Q

what does compensated cirrhosis have increased risk of?

A

hepatocellular carcinoma, also have asymptomatic portal hypertension

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8
Q

why does decompensated cirrhosis have high mortality?

A

due to synthetic liver dysfunction and portal hypertension

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9
Q

when should you do liver screen?

A

history of metabolic syndrome, history of alcohol, autoimmune screen, hep B&C, under 45 cellulo plasma, ferritin (haemochromatosis)

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10
Q

what is association with increased infection & cirrhosis?

A

dysbiosis = abnormal gut bacteria

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11
Q

what are components of liver screen?

A

history of metabolic syndrome, history of alcohol, autoimmune screen, hep B&C, under 45 cellulo plasma (ALT & AST), ferritin (haemochromatosis)

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12
Q

what impact on activity is important in cirrhosis?

A

sarcopenia

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13
Q

what veins make up portal vein?

A

superior mesenteric vein, inferior mesenteric vein, splenic vein & gastric vein

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14
Q

what is portal pressure usually like?

A

usually very low (5-8 mmHg) with only small gradient across liver to hepatic vein which returns blood to vena cava

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15
Q

what are causes of portal hypertension?

A
  • cirrhotic portal hypertension
  • schistosomiasis
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16
Q

what are areas to think about when common hypertension?

A
  • pre-hepatic
  • intrahepatic = presinusoidal, sinusoidal, post sinusoidal (due to distortion of liver architecture)
  • post hepatic
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17
Q

what is cause of post hepatic portal hypertension?

A

Budd-Chiari syndrome

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18
Q

what is cause of intrahepatic post sinusoidal portal hypertension?

A

veno-occlusive disease

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19
Q

what is cause of sinusoidal portal hypertension?

A
  • cirrhosis
  • alcoholic hepatitis
  • congenital hepatic fibrosis
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20
Q

what is cause of intrahepatic pre sinusoidal portal hypertension?

A
  • schistosomiasis
  • non-cirrhotic portal hypertension
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21
Q

how does cirrhosis lead to variceal bleeding?

A

cirrhosis = increased vascular resistance (blood can’t flow through liver because of structural & inflammatory changes) →pushes portal pressure up →bodies response is to cause splanchnic vasodilation (sends more blood to try and force through) →increased pressure means portosystemic collaterals & varices form →variceal bleeding

22
Q

how can ascites develop from pressure changes?

A

from increased portal hypertension = bodies response is vasodilation in splanchnic arteries = systemic hypotension = effective hypovolaemia = activation of RAAS (retention of sodium & water) = ascites

23
Q

where do varices commonly occur?

A

= predominantly at sites of naturally occuring portosystemic vascular anastomosis

  1. Oesophageal and gastric venous plexus
  2. Umbilical vein from the left portal vein to the epigastric venous system
  3. Retroperitoneal collateral vessels
  4. The hemorrhoidal venous plexus
24
Q

what screening can be done for varices?

A

oesophageal gastro duodenoscopy →repeat every 2-3 years with no varices and every 1-2 if varices

25
Q

what is primary prophylaxis for variceal bleeding (prevention of 1st incidence of variceal bleeding)?

A

Non-selective beta-blocker (propranolol) or carvedilol; band ligation

26
Q

how does someone present with acute variceal bleeding?

A

haematemesis, shock (low BP, high HR), confusion, jaundice

27
Q

what is management of acute variceal bleeding?

A
  1. ABC approach
  2. fluid restriction ( as increases BP)
  3. IV terlipressin = causes constriction of splanchnic vessels so reduce flow into portal vein
  4. IV antibiotics = infection often underlying cause of variceal bleed (even if no symptoms)
  5. stop anticoagulants
  6. consider anaesthetic support
  7. then do OGD (oesophago gastro duodenal) →suck in varices in oesophagus and band it or if gastric varices, inject thrombin or glue to coils
28
Q

what is TIPSS?

A

transjugular intrahepatic portal systemic shunt = if banding not working

29
Q

what is TIPS process?

A

→go into jugular vein and down through SVC then into hepatic vein you put hollow needle through catheter and into portal vein and put balloon down making connection between hepatic & portal vein →making stent to allow blood to bypass normal liver vasculature and decreases pressure of portal vein

30
Q

what is problem with TIPSS?

A

taking blood away from liver so making slightly hypoxic so not good for people with poor systemic function, hepatic encephalopathy (excess ammonia reaching brain) as bypassing liver so chance much higher, right sided heart failure

31
Q

what is sengstaken blakemore tube (SBT)?

A

short term to stop bleeding , gastric balloon
- self expanding metal stents →if balloons not working, if lots of varices →put in endoscopically (kept in slightly longer but still just temporarily for a couple days)

32
Q

what is secondary prophylaxis?

A

= prevent 2nd bleed

  • band ligation and keep banding any varices
  • give non-selective beta blockers (can have them alone if no OGD)
33
Q

what is pathophysiology of ascites?

A

increase hepatic vascular resistance →splanchnic vasodilation →decreased effective circulatory volume →activation of RAAS →renal sodium activity →ascites

34
Q

what are causes of ascites?

A
  • cirrhosis
  • alcoholic hepatitis
  • cardiac ac
35
Q

what is the most common cause of decompensation cirrhosis?

A

ascites

36
Q

what is transudate and exudate mean in ascites test?

A

transudate = low protein in ascites
exudate = high protein in ascites

*high albumin = exudate

37
Q

what is management of ascites?

A
  • daily weight essential →only want 0.5kg day of wieght loss, any more than kidney problems
  • low salt diet (as kidneys pulling c]back extra salt so dont want to put more in) →no salt diet not good either
  • loop diuretics
38
Q

what risk comes with draining ascites from peritoneal cavity?

A

can get post paracentesis circulatory dysfunction (drop in BP) after so give albumin

risk →pain, bleeding, perforation, infection

39
Q

what is life expectancy for recurrengt ascites?

A

6 months

40
Q

what is spontaneous bacterial peritonitis (SBP)?

A

= cause and complication of decompensated cirrhosis due to colonisation of ascites with bacteria translocated from the gut - i.e infection of ascites

41
Q

what is presentation of spontaneous bacterial peritonitis?

A
  • Classically generalised abdominal pain
  • systemically unwell/ fever
  • commonly asymptomatic
  • other features of decompensation
  • abnormal bloods (increased creatinine/ WCC/ CRP) only - need a high index of clinical suspicion)
42
Q

what LFT results can diagnose spontaneous bacterial peritonitis?

A

raised ascitic total neutrophils [TNC] on tap → >250 neutrophils/mm3 then SBP

43
Q

what is treatment of spontaneous bacterial peritonitis?

A

broad spectrum antibiotics

44
Q

what is cause of hepatic encephalopathy?

A

Due to ammonia - generated in the intestines from nitrogenous compounds from the diet, deamination of glutamine by glutaminase, and metabolism of nitrogenous substances by colonic flora

45
Q

what normally happens with ammonia in body?

A

Normally - most ammonia metabolized to urea in the liver. Skeletal muscle decreases ammonia by metabolizing ammonia to glutamine. The kidney excretes urea and generates ammonia

46
Q

what happens with ammonia in cirrhosis (that causes hepatic encephalopathy)?

A
  • In cirrhosis - portal-systemic shunts and liver failure cause a rise in blood ammonia compounded by sarcopenia and renal dysfunction
  • Increased circulating ammonia affects brain function via astrocytes; impairs mitochondria and glutamate-glutamine trafficking between neurons and astrocytes.
47
Q

what is treatment of hepatic encephalopathy?

A
  • look for cause e,g dehydration, kidney, constipation, infection
  • need to poo - 2-3 soft stools a day
  • lactulose = to clear gut and reduce transit time
  • maintain nutrition
  • rifaximin
  • look to treat portosystemic shunts
  • transplant
48
Q

what is hepatorenal syndrome?

A

complication of advanced liver disease that also causes acute kidney injury
= it’s a diagnosis of exclusion (rule out infection, dehydration, drugs)

49
Q

what should be done if acute kidney injury due to advanced liver disease?

A
  • stop diuretics - no NSAIDS or aminoglycosides (vancomycin)
  • accurate fluid balance, IV fluid
  • treat underlying cause
50
Q

what functional tests can help show acute kidney injury?

A

hyponatraemia = common & good marker
- increase in serum creatinine

51
Q

what score can be used to help determine whether liver transplant worth it?

A
  • UKELD =49 or more means higher chance of dying over next 12 months then with liver transplant

GI (56 decks)

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