4- clinical syndromes of cirrhosis

Question 1

what is compensated cirrhosis?

Answer 1

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

Question 2

what is decompensated cirrhosis?

Answer 2

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

Question 3

what is progression of liver to cirrhosis?

Answer 3

healthy liver→fatty liver→liver fibrosis →cirrhosis

Question 4

what are symptoms of decompensated cirrhosis?

Answer 4

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

Question 5

what can cause progression from compensated to decompensated cirrhosis?

Answer 5

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

Question 6

what are symptoms of compensated cirrhosis?

Answer 6

mostly asymptomatic

Question 7

what does compensated cirrhosis have increased risk of?

Answer 7

hepatocellular carcinoma, also have asymptomatic portal hypertension

Question 8

why does decompensated cirrhosis have high mortality?

Answer 8

due to synthetic liver dysfunction and portal hypertension

Question 9

when should you do liver screen?

Answer 9

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

Question 10

what is association with increased infection & cirrhosis?

Answer 10

dysbiosis = abnormal gut bacteria

Question 11

what are components of liver screen?

Answer 11

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

Question 12

what impact on activity is important in cirrhosis?

Answer 12

sarcopenia

Question 13

what veins make up portal vein?

Answer 13

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

Question 14

what is portal pressure usually like?

Answer 14

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

Question 15

what are causes of portal hypertension?

Answer 15

• cirrhotic portal hypertension
• schistosomiasis

Question 16

what are areas to think about when common hypertension?

Answer 16

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

Question 17

what is cause of post hepatic portal hypertension?

Answer 17

Budd-Chiari syndrome

Question 18

what is cause of intrahepatic post sinusoidal portal hypertension?

Answer 18

veno-occlusive disease

Question 19

what is cause of sinusoidal portal hypertension?

Answer 19

• cirrhosis
• alcoholic hepatitis
• congenital hepatic fibrosis

Question 20

what is cause of intrahepatic pre sinusoidal portal hypertension?

Answer 20

• schistosomiasis
• non-cirrhotic portal hypertension

Question 21

how does cirrhosis lead to variceal bleeding?

Answer 21

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

Question 22

how can ascites develop from pressure changes?

Answer 22

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

Question 23

where do varices commonly occur?

Answer 23

= 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

Question 24

what screening can be done for varices?

Answer 24

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

Question 25

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

Answer 25

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

Question 26

how does someone present with acute variceal bleeding?

Answer 26

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

Question 27

what is management of acute variceal bleeding?

Answer 27

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

Question 28

what is TIPSS?

Answer 28

transjugular intrahepatic portal systemic shunt = if banding not working

Question 29

what is TIPS process?

Answer 29

→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

Question 30

what is problem with TIPSS?

Answer 30

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

Question 31

what is sengstaken blakemore tube (SBT)?

Answer 31

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)

Question 32

what is secondary prophylaxis?

Answer 32

= prevent 2nd bleed - band ligation and keep banding any varices - give non-selective beta blockers (can have them alone if no OGD)

Question 33

what is pathophysiology of ascites?

Answer 33

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

Question 34

what are causes of ascites?

Answer 34

- cirrhosis - alcoholic hepatitis - cardiac ac

Question 35

what is the most common cause of decompensation cirrhosis?

Answer 35

ascites

Question 36

what is transudate and exudate mean in ascites test?

Answer 36

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

Question 37

what is management of ascites?

Answer 37

- 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

Question 38

what risk comes with draining ascites from peritoneal cavity?

Answer 38

can get post paracentesis circulatory dysfunction (drop in BP) after so give albumin risk →pain, bleeding, perforation, infection

Question 39

what is life expectancy for recurrengt ascites?

Answer 39

6 months

Question 40

what is spontaneous bacterial peritonitis (SBP)?

Answer 40

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

Question 41

what is presentation of spontaneous bacterial peritonitis?

Answer 41

- 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)

Question 42

what LFT results can diagnose spontaneous bacterial peritonitis?

Answer 42

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

Question 43

what is treatment of spontaneous bacterial peritonitis?

Answer 43

broad spectrum antibiotics

Question 44

what is cause of hepatic encephalopathy?

Answer 44

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

Question 45

what normally happens with ammonia in body?

Answer 45

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

Question 46

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

Answer 46

- 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.

Question 47

what is treatment of hepatic encephalopathy?

Answer 47

- 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

Question 48

what is hepatorenal syndrome?

Answer 48

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

Question 49

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

Answer 49

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

Question 50

what functional tests can help show acute kidney injury?

Answer 50

hyponatraemia = common & good marker - increase in serum creatinine

Question 51

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

Answer 51

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