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GI > W6 Cirrhosis > Flashcards

W6 Cirrhosis Flashcards

1
Q

What does cirrhosis look like histologically?

A

Ring of fibrosis around hepatocytes

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2
Q

What cells in the liver undergo transformation when there is chronic inflammation and where are these cells?

A

Hepatic stellate cells in the space of Disse

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3
Q

What 4 blood vessels drain into the portal vein?

A
  • gastric vein
  • splenic vein
  • superior mesenteric vein
  • part of inferior mesenteric vein
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4
Q

From what 5 structures does the portal vein carry outflow to the liver?

A
  • spleen
  • oesophagus
  • stomach
  • pancreas
  • small + large intestine
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5
Q

From what two blood vessels does blood enter the liver sinusoids and describe the blood from each (oxygenated/deozygenated)?

A
  • Hepatic artery -> oxygenated blood from celiac trunk

- hepatic portal vein -> deoxygenated nutrient rich blood

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6
Q

From what blood vessel does the blood leave the liver and where does it drain to?

A

Leaves through the hepatic vein and drains into the IVC

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7
Q

What is the approximate blood pressure of the hepatic portal vein?

A

5-8 mmHg

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8
Q

What are the four sites of anastomosis where the portal venous system joins with the systemic venous system ?

A
  • oesophageal and gastric venous plexus
  • retroperitoneal collateral vessels
  • umbilical vein from the left portal vein to the epigastric venous system
  • hemorrhoidal venous plexus (in rectum)
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9
Q

What does the lack of liver blood flow cause the liver to produce? (in addition to causing portal hypertension)

A

Causes increased production of vasodilators, enhanced sensitivity to vasodilators and resistance to vasoconstrictors

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10
Q

What does cirrhosis lead to in splanchnic blood vessels?

A

Splanchnic arteriolar vasodilation

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11
Q

What effect does splanchnic arteriolar vasodilation have on CO, SVR and MAP?

A

CO increases
SVR decreases
MAP decreases

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12
Q

What does increased CO with decreased SVR and MAP cause activation of?

A

activation of arterial baroreceptors

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13
Q

What effect does activation of arterial baroreceptors have on HR and CO?

A

HR increases

CO increases

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14
Q

Increase in HR and CO due to splanchnic arteriolar vasodilation causes activation of which vasoconstrictors?

A
  • Sympathetic Nervous System
  • RAAS
  • AVP - Arginine vasopressin
  • ET -> endothelin
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15
Q

What does activation of SNS, RAAS, AVP and ET lead to in the renal system and retention of?

A
  • renal vasoconstriction

- sodium and water retention

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16
Q

Why is portal hypertension thought to be worse in patients with cirrhosis?

A

Because there is resistance to outflow and an increase in inflow into portal circulation

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17
Q

What are 2 prehepatic causes of portal hypertension i.e. 2 causes of portal vein blockage?

A
  • portal vein thrombosis

- occlusion secondary to congenital portal venous abnormalities (e.g. premature babies with cannulised umbilical vein)

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18
Q

What can protein S, protein c or MP thrombin 3 deficiencies cause?

A

pro thrombotic conditions

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19
Q

List 2 presinusoidal intrahepatic causes of portal hypertension?

A
  • Schistosomiasis

- non-cirrhotic portal hypertension

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20
Q

What are Budd-Chiari syndrome and veno-occlussive disease examples of ?

A

Outflow obstruction problems

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21
Q

List 3 examples of postsinusoidal intrahepatic portal hypertension?

A
  • cirrhosis
  • alcoholic hepatitis
  • congenital hepatic fibrosis
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22
Q

What is difference between compensated cirrhosis and decompensated cirrhosis?

A

-Compensated -> appear normal outside
,mildly abnormal findings clinically -Decompensated -> liver failure due to acute/chronic infection/insult/SIRS or end stage liver disease

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23
Q

What 6 clinical signs might you find in patient with compensated cirrhosis?

A
  • spider naevi
  • palmar erythema
  • clubbing
  • gynaecomastia
  • hepatomegaly
  • spleenomegaly
  • OR none
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24
Q

What additional 4 clinical signs are found in patients with decompensated cirrhosis?

A
  • jaundice
  • ascites
  • encephalopathy
  • bruising
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25
Q

What is schistosomiasis?

A

acute and chronic disease caused by parasitic worms

26
Q

Why does loss of liver function lead to encephalopathy?

A

Decreased urea synthesis in liver leads to increased blood ammonia causing encephalopathy

27
Q

Decreased synthesis of what leads to ascites?

A

Albumin

28
Q

What are 5 complications of cirrhosis?

A
  • hepatocellular carcinoma
  • liver failure
  • variceal bleeding
  • encephalopathy
  • ascites
29
Q

Why is nutrition an important factor when treating patient with decompensated cirrhosis?

A

They have low threshold to switch to gluconeogenesis and lypolysis and catabolism due to limited glycogen stores

30
Q

Why are small frequent meals and snacks recommended for patients with decompensated cirrhosis?

A

As they quickly switch to gluconeogenesis and muscle catabolism especially at night

31
Q

What vitamin is mandatory for decompensated cirrhotics with excess alcohol intake and why?

A

Vitamin B1 (thiamine) cos it helps use carbs as energy

32
Q

What is target input of sodium in low sodium diet?

A

100mmol/day

33
Q

What tests can you do to check sodium levels in urine?

A

24hr urinary sodium excretion

-spot urine (if Na>K then 90% PPV that 24hr Na excretion>80mm)

34
Q

What are 7 treatment options in ascites?

A
  • low sodium diet
  • improve underlying disease
  • drugs: no NSAIDs or sodium heavy drugs
  • diuretics
  • parancentesis
  • TIPSS
  • Transplantation
35
Q

What is first line diuretic in new escalated ascites?

A

Spironolactone

36
Q

What is prescribed in addition to spironolactone in recurrent ascites?

A

Loop diuretic e.g. furosemide

37
Q

What must be carefully monitored in dose change or paracentesis in ascites?

A

-U&es

38
Q

What are risks of paracentesis?

A

Risk of infection

  • encephalopathy
  • hypovolaemia
39
Q

What is administered with paracentesis to prevent hypovolaemia?

A

albumin

40
Q

What occurs in TIPSS procedure?

A

Shunt created between hepatic portal vein and hepatic vein to prevent variceal bleeding and ascites

41
Q

What is SBP and what is prognosis?

A

Spontaneous Bacterial Pertionitis -> bacteria from gut is translocated into ascites
-prognosis usually poor

42
Q

What is treatment for SBP?

A
  • antibiotics
  • albumin
  • vascular instability treat with terlipressin
  • maintain renal perfusion
43
Q

What is investigations for SBP?

A

Do a tap in all ascites and cell count

44
Q

What can encephalopathy mimic in clinical signs?

A

Alcohol withdrawal

45
Q

3 clinical signs of encephalopathy?

A
  • flap
  • confusion
  • tremor
46
Q

Through what 3 pathways is ammonia generated in the body?

A
  • deamination of glutamine by glutaminase
  • metabolism of nitrogenous substances by colonic flora
  • in the intestines from nitrogenous compounds from the diet
47
Q

Where is ammonia metabolised to urea?

A

In the liver

48
Q

What can cause a rise in blood ammonia?

A

Portal-systemic shunts and liver failure

49
Q

What can does increased blood ammonia affect astrocytes?

A
  • can impair mitochondrial astrocytes

- can impair glutamine-glutamate trafficking between astrocytes and neurons

50
Q

What muscle can decrease blood ammonia by converting it to glutamine?

A

Skeletal muscle

51
Q

List 4 possible causes of encephalopathy.

A
  • liver failure
  • drugs e.g. sedating drugs
  • metabolic derangements e.g. electrolytes
  • infection
52
Q

Why is patient with encephalopathy given lactulose?

A

To clear gut so colonic flora has less time to produce ammonia

53
Q

Why are small frequent meals encouraged in encephalopathy?

A

To reduce fasting gluconeogenesis and muscle catabolism

54
Q

What non-absorbed antibiotic is sometimes given to patients with encephalopathy and why?

A
  • Rifaximin

- Reduces bacterial load of gut and changes pH

55
Q

What is primary prophylaxis treatment for patient with eosophageal varices?

A
  • Non selective beta blockers e.g. propranolol and carvideolol
  • variceal ligation
56
Q

What is treatment for acute variceal bleeding?

A
  • Resuscitation
  • Vasoconstrictor -> terlipressin
  • Variceal banding
  • TIPSS
57
Q

What is treatment if bleeding can’t be stopped in variceal bleeding?

A

Balloon tamponade -> Gastric balloon

58
Q

What is risk in balloon tamponade in variceal bleeding?

A

Blood aspirated into lungs and aspiration pneumonia as a result

59
Q

What is secondary prophylaxis of variceal bleeding following acute variceal bleed?

A

Both variceal band ligation and beta blockers

60
Q

Why are cirrhotic patients more prone to both excessive bleeding and blood clotting?

A

Liver makes both clotting factors and anti-clotting factors so when clotting factors low so are anti-clotting factors

61
Q

What blood test measures how long it takes the blood to clot?

A

Prothrombin time

62
Q

What scoring system is used to place patients on liver transplant list and what score does patient need to be listed?

A

UKELD score of > 49

GI (29 decks)

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