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gastrointestinal > cirrhosis > Flashcards

cirrhosis Flashcards

1
Q

what is cirrhosis

A

scarring and fibrosis of the liver

  • hepatocyte regeneration creating scar tissue
  • reversible
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2
Q

process of cirrhosis

A
  1. liver injury
  2. stellate cells in space of disse activated by cytokines produced by kupffer cells and hepatocytes
  3. stellate cells-> myofibroblast cell and produce collagen and pro-inflammatory cytokines
  4. hepatocyte damage and tissue fibrosis
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3
Q

causes of cirrhosis

A
  1. drugs, alcohol: methotrexate
  2. autoimmune hepatitis
  3. metabolic: NASH, haemachromatosis
  4. infective: hepatitis
  5. wilsons, alpha 1 antitryptin
  6. vascular: budd-chiari
  7. biliary: PBC or PSC
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4
Q

ranking of main causes of cirrhosis 6

A
  1. alcohol 50-60%
  2. viral hepatitis 10-20%
  3. PBC 5-10%
  4. cryptogenic
  5. autoimmune hepatitis
  6. haemocrhomatosis
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5
Q

cirrhosis presentation

A
  • abnormal lft
  • asymptomatic
  • systemic cutaneous signs
  • liver failure - jaundice, encepha, acites, sbp, portal hypertension
  • hepatocellular carcinoma
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6
Q

most common presentation of cirrhosis

A

ascites and jaundice

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7
Q

gold standard test for cirrhosis

A

biopsy

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8
Q

cutaneous systemic features of cirrhosis

A 
palmar erythema
clubbing
leukonychia
dupytrens contractures
hepatic flap
jaundice
spider naevi
hepatosplenomegaly 
ascites 
xanthelasma
rhinophyma
parotid swelling cheeks
bruising 
vitiligo 
gynaecomastia
caput medusae
hypoglycaemia
testicular atrophy 
paper dollar skin
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9
Q

signs of low albumin

A

ascites

leuconychia

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10
Q

signs of chronic cirrhosis >6 months

A

paper dollar skin
loss of muscle bulk
catabolic
leukonychia

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11
Q

signs of reduced aldosterone clearance in cirrhosis

A

sodium retention (contributes to ascites)

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12
Q

sign of reduced oestrogen clearance in cirrhosis

A

loss of body hair

gynaecomastia

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13
Q

4 stages of cirrhosis

A
  1. non cirrhotic: no symptoms- fibrogenesis and angiogenesis reversible
    2.compensated, no varices, scar and x-linking HVPG>6
  2. compensated cirrhosis but varices present, thick scar nodules HVPG >10
    4.decompensated cirrhosis, ascites and variceal rupture
    irreversible
    HVPG >12
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14
Q

5 signs of finger clubbing

A
  1. loss of nail bed angle
  2. fluctuation of the nail bed
  3. increased curvature
  4. drumsticking
  5. HPOA hypertrophic osteoarthropathy
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15
Q

what is HVPG

A

hepatic venous pressure gradient

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16
Q

why does HVPG increase

A 
architectual changes
fibrosis
vascular occlusion
endothelial dysfunction
increased vascular tone
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17
Q

investigations for cirrhosis

A
  • anaemia (macrocytic)
  • thrombocytopaenia
  • increased PT
  • hyponatraemia
  • low urea
  • hyperbilirubinaemia
  • increased ALT/AST
  • USS
  • endoscopy for varices or PHG
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18
Q

screening process for complications with chronic cirrhosis

A

every 6 months

  • uss for splenomegaly
  • afp
  • doppler portal vein thrombosis
  • endoscopy for varices
  • fbc: thrombocytopaenia
  • fibroscan
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19
Q

what 2 test can be done to show fibrosis

A

hyaluronic acid

fibroscan

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20
Q

what causes the thrombocytopaenia

A

splenomegaly

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21
Q

3 child-pugh score stages

A

1= prothombin 1-4 seconds, alb >35, bilirubin <34, no ascites
2=pt 5-6, 28-24, 35-50, encephalopathy 1-2, mild ascites
3= pt >6, <27, >50, 3-4 moderate-severe ascites

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22
Q

drugs to avoid with chronic cirrhosis

A
  • NSAIDS- hepatorenal failure and bleeding varices
  • ACEI: hepatorenal failure
  • codeine: constipation
  • Narcotics- constipation
  • anxiolytics- constipation
  • fibrotics-methotrexate
  • NASH-amiodarone
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23
Q

8 complications of cirrhosis

A
  1. ascites
  2. varices
  3. hepatorenal syndrome
  4. spontaneous bacterial peritonitis
  5. hyponatraemia
  6. hepatic encephalopathy
  7. hepatocellular carcinoma
  8. portal hypertension
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24
Q

4 types of varices

A

stomal
rectal
oseophageal
stomach-portal hypertensive gastropathy

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25
Q

how to determine prognosis of variceal haemorrhage

A

varices develop when HPVG is >10mmHg

varices bleed when HVPG >12mmHg

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26
Q

treatment of varices 8

A

either non-selective beta blocker carvedilol or variceal band ligation

  • cyanocrylate glue injection
  • ingection of thrombin
  • hemospray
  • sengstaken blakemore tube
  • TIPSS
  • surgical
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27
Q

prevalence of oseophageal varices in cirrhosis

A

50%

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28
Q

presentation of varices

A

hypotension
haematemesis
melaena

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29
Q

history for varices

A
  • risk factors for chronic liver disease
  • recent NSAIDS
  • abdominal sepsis/sugery
  • pancreatitis
  • umbilical vein sepsis
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30
Q

treatment of acute variceal bleeding

A 
-resuscitation 
intubation, high flow o2, iv access, 
-terlipressin 
-band ligation
-sengstaken-blakemore tube 
-davis stent
- TIPSS
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31
Q

risk of sengstaken-blakemore tube

A

aspiration
oseophageal perforation
malposition

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32
Q

what is tipss

A

transjugular intrahepatic portosystemic shunt

  • uncontrolled or recurrent variceal bleeding
  • gastric varices
  • refractory ascites
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33
Q

what is terlipressin

A

synthetic analogue of vasopressin
-used in low blood pressure
adverse ischaemic effects

34
Q

treatment of gastric variceal bleeds

A
  • carvedilol
  • or thrombin
  • cyanocrylate injection of glue
35
Q

prevalence of ascites in cirrhotics and mortality

A

50-70% develop ascites

2 yr mortality 50%

36
Q

what causes ascites in cirrhosis

A

sodium and water retention
portal hypertension
low albumin

37
Q

what is used to determine the cause of ascites

A

high serum ascites albumin gradient >11mmol/l due to portal hypertension as means low protein
-but if below cause due to pancreatitis, infection=exudative high protein

38
Q

treatment of cirrhotic ascites

A

1.sodium restritcion and diuretics
-no added salt (90mmol/l)
-spironalactone (aldosterone antagonist) and furosemide (100:40)
2.large volume paracentesis
(removal fluid >5l), fast response, high rate recurrence

39
Q

diuretic dosage for ascites and complications

A

maximum
spironalactone 400mg
furosemide 160mg

complications

  • electrolytes
  • aki
  • encephalopathy
  • painful gynaecomastia
40
Q

2 definitions of refractory ascites

A
  1. lack of response (<1.5kg weight loss/week) to high dose diurectics and low sodium diet
  2. frequent ascites recurrence after therapeutics large volume paracentesis
41
Q

treatment options for refractory ascites

A

repeated LVP (+albumin)
TIPSS
liver transplantation

42
Q

name given for patients who cannot tolerate diuretics due to the development of complications

A

diuretic intractable ascites

43
Q

2 main complications of ascites

A

AKI
-vasodilation from sepsis
-or vasoconstriction from hepatorenal syndrome
hepatorenal syndrome

44
Q

how does liver disease cause hrs

A
  • diuretics use for ascites
  • low grade renal hypoperfusion
  • spontaneous bacterial peritonitis
  • other infections
  • gi bleeding
  • circulatory dusfunction
45
Q

what is hepatorenal syndrome

A

splanchnic vasodilation causes hormonal imblanace
-VASOCONSTRICT at kidneys and impaired renal failure
due to poor arterial circulation due to liver disease
-toxins build up in the body

46
Q

type 1 vs type 2 hrs

A

type 1= rapid progressive kidney failure creatinine >221
type 2=slower onset and progression
creatinine >133= better prognosis median survival 6 months

47
Q

how does liver failure affect kidney function

A
  • fibrosis means less blood gets through
  • macula densa receives less sodium
  • constrict in efferent and relax in afferent
  • increase renin release from juxtag cells
  • overall get VASOCONSTRICTION
48
Q

HRS-AKI diagnosis criteria

A
  • dx of cirrhosis and ascties
  • dx of aki
  • no response after 2 consecutive days of diuretic withdrawal and plasma volume expansion with albumin 1g per kg
  • abscence of shock
  • no recurrent or recent use of nephrotoxic drugs (nsaids)
  • no macroscopic signs of structural kidney injury ie no proteinuria
49
Q

what level should ascites be brought down by

A

0.5kg/ weight loss a day

50
Q

prognosis of HRS 1 AND 2

A

hrs 1=2 week mortality rate 80%

hrs 2= median 6 months

51
Q

Treatment type 1 HRS

A

-terlipressin with albumin

52
Q

prevention of HRS 4

A
  • antibiotics during acute variceal haemorrhage
  • albumin during SBP
  • avoid beta blockers in therapeutic window
  • earlier detection
53
Q

treatment of AKI 1

A

remove risk factors

  • nephrotoxic durgs
  • vasodilators
  • nsaids
  • diuretics
  • treat infections
54
Q

treatment of AKI 2 and 3

A
  • stop diuretics
  • volume expansion with albumin
  • if HRS also give Terlipressin (vasoconstrict)
55
Q

diagnosis of spontaneous bacterial peritonitis

A

ascitic fluid PMN count >250 cells per mm3

often e.coli

56
Q

prevalence in ascitic patients

A

10-30%

57
Q

symptoms of sbp 4

A

abdominal pain
rebound tenderness
absent bowel sounds
fever

58
Q

mortality sbp

A

20%

59
Q

treatment of sbp

A

albumin
3rd generation cephalosporins
or
penicillins and metronidazole (vancomycin)

60
Q

long term prophylaxis for sbp

A

norfloxacin

61
Q

treatment for hypervolaemic hyponatraemia in cirrhosis

A

tolvaptan-oral v2 antagonist increases free water excretion

62
Q

pathophysiology of hyponatraemia in cirrhosis

A
  • liver disease get water and sodium retention to overcome low blood pressure systemically
  • leads to impairment of kidneys to eliminate solute free water
63
Q

path of hepatic encephalopathy

A

accumulation of gut derived neurotoxic substances eg ammonia, astrocyte damage, impaired neurotransmitters

64
Q

dx of hepatic encephalopathy

A

blood ammonia
ecg
critical flicker freq
flapping tremor

65
Q

management of hepatic encephalopathy

A
  • give lactulose
  • check constipation
  • monitoring
  • TIPSS
  • Diuretics
  • maintains fluids
  • fall precaution
  • avoid cns depressants
  • consider prophylactic intubation for grade 3/4
66
Q

how does lactulose work

A
  • laxative
  • cathartic (reduces colonic bacterial load)
  • acidifies gut lumen bacteria
  • inhibits ammoniagenic bacteria
67
Q

second line drug for hepatic encephalopathy

A

Rifaximin 400mg (gut sterilisation-antibiotic)

68
Q

grading of hepatic encephalopathy

A

1=sleep reversal so restless
2=drowsy,lethargic
3=sleepy and confused
4=coma

69
Q

hepatocellular carcinoma causes

A

nafld

viral hepatitis

70
Q

screening for HCC

A

afp and uss every 6 months

71
Q

diff dx for HCC

A 
metastasis
cholangiocarcinoma
haemangioa
adenoma
cyst 
abscess
72
Q

CT characteristics of HCC 3 stages

A

arterial phase (enhancement)
portal venous phase (washout)
portal vein thrombosis

73
Q

treatment options for HCC and size of nodules criteria

also success rate

A

-resection-possibly curative
-transplantation
single tumour <5cm or <3 nodules <3cm
-percutaneous ablation
radiofrequency ablation,ethanol
-transarterial chemotherapy TACE, delays regression often need repeating

74
Q

drug used for hcc chemotherapy

A

sorafenib

75
Q

function of albumin and why should it be used in treating decompensated cirrhosis

A
  • 70% of total plasma oncotic activity
  • high capacity molecule transport
  • free radical scavenging
  • capillary permeability effect
  • neutrophil adhesion effect
  • nitric oxide binding
  • drug binding
  • improves renal blood flow and autoregulation in cirrhosis and aki
76
Q

What is haemochromatosis

A

High iron blood due to hfe gene

77
Q

What is wilsons

A

High copper due to low carrier ceruloplasmin

78
Q

What is alpha 1 antitrypsin

A

Deficiency in alpha 1 means liver produces large amounts of abnormal alpha 1 protein which clogs up liver
Or can’t secrete normal protein properly

79
Q

What is Budd chiari

A

Thrombosis of hepatic artery usually due to mutation in clotting like jak 2

80
Q

7 drugs to avoid in cirrhosis

A 
NSAIDS
ACEI
codeine
narcotics
anxiolytics
methotrexate in fibrosis 
amiodarone in nash

gastrointestinal (26 decks)

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