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GI: liver, biliary tree and pancreas > Chronic Liver Disease/cirrhosis > Flashcards

Chronic Liver Disease/cirrhosis Flashcards

1
Q

there are ____ different types of liver disease

A

many

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2
Q

chronic liver disease is duration greater than __months with outcome of progression to _____

A

6, cirrhosis

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3
Q

stage 1 cirrhosis pathology: The activated ______

A

The activated hepatocytes, kupffer cells and inflammatory cells from inflammation release things (like cytokines) and other products of damaged cells that go on to activate the quiescent Hepatic stellate cell

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4
Q

stage 2 cirrhosis pathology : perivenular fibroblasts (stellate) undergo activation and transdifferentiation to ________. These _______ produce excessive amounts of collagens, downregulate their production of matrix ________, and show an enhanced expression of the physiological inhibitors of the MMPs (_____ and _____).

A

perivenular fibroblasts undergo activation and transdifferentiation to myofibroblasts. These myofibroblasts produce excessive amounts of collagens, downregulate their production of matrix metalloproteinases (MMPs), and show an enhanced expression of the physiological inhibitors of the MMPs (TIMP1 and TIMP2).

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5
Q

what is stage 1 - chronic liver disease?

A

causes of chronic liver disease, patient presents with signs and symptoms of the causal disease

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6
Q

what is stage 2 - chronic liver disease?

A

recurrent inflammation and the process of fibrosis - these are the stigmata of cirrhosis

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7
Q

what is stage 3 - chronic liver disease?

A

cirrhosis compensation

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8
Q

what is stage 4 - chronic liver disease?

A
  • cirrhosis decompensated
  • Get chronic liver failure
  • Acute on chronic liver failure
  • The patient presents with signs and symptoms of liver failure
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9
Q

what are the common causes of chronic liver disease?

A
  • Alcohol
  • Non-alcoholic fatty liver disease
  • Hepatitis C
  • Primary biliary cirrhosis
  • Autoimmune hepatitis
  • Hepatitis B - this is not really seen as much in the UK but in the world it is a massive cause of liver disease
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10
Q

what are the uncommon causes of chronic liver disease?

A
  • Haemochromatosis
  • Primary Sclerosing Cholangitis - this is an autoimmune disease
  • Wilsons Disease
  • alpha 1 anti-trypsin
  • Budd-Chiari
  • Methotrexate
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11
Q

NOTE: there are lots of diseases affecting the liver which are chronic such as ____ or _____ syndrome. However, they are not all chronic liver diseases - this only refers to diseases which can lead to _____ (by activation of _____ and fibrosis)

A

NOTE: there are lots of diseases affecting the liver which are chronic such as amyloid or rotor syndrome. However, they are not all chronic liver diseases - this only refers to diseases which can lead to cirrhosis (by activation of stellate and fibrosis)

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12
Q

what two main things go wrong in cirrhosis?

A
  1. loss of function of hepatocytes

2. malfunction in blood flow and generation of abnormal signalling

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13
Q

histology : the architecture of the cell is disrupted by ___ and ___. the ___ of the liver get smaller

A

fibrosis and collagen. nodules

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14
Q

which organs does the portal vein drain blood from? 6

A

the spleen, oesophagus, stomach, pancreas, small and large intestines

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15
Q

portal vein drains the spleen through the ____ ____

A

splenic vein

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16
Q

portal vein drains the oesophagus through the ____ ____

A

left gastric branch

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17
Q

portal vein drains the stomach through the ____ ____

A

left and right gastric

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18
Q

portal vein drains the pancreas through the ____ ____

A

splenic

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19
Q

portal vein drains the small and large intestines through the ____ ____

A

inferior and superior mesenteric

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20
Q

The portal vein carries __% of blood to the liver

A

75%

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21
Q

Hepatic vein flow = ____ml/min

A

1600

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22
Q

Portal vein flow = ____ ml/min

A

1200

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23
Q

Hepatic artery flow = __ ml/min

A

400

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24
Q

Hepatic vein pressure = _mmHg
Portal vein pressure = _mmHg
Hepatic artery pressure = __ mmHg

A

4,7,100

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25
Q

what are portocaval anastomosis ?

A

These are places where the portal venous system has communications (anastomosis) with the systemic venous system

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26
Q

what are the 4 collateral pathways?

A
  1. Eosophageal 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
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27
Q

In cases of ____ _____ these anastomoses may become engorged, dilated or varicosed and subsequently rupture

A

portal hypertension

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28
Q

portal hypertension is a:
- portal vein pressure above the normal range of __-__ mmHg
or
- a hepatic vein pressure gradient greater than _ mmHg

A

5-8 mmHg

a hepatic vein pressure gradient greater than 5mmHg

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29
Q

Portal hypertension represents an increase of the _____ pressure within the portal vein or its tributaries

A

hydrostatic

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30
Q

what are the two causes of portal hypertension in liver disease

A
  1. increased resistance to flow

2. increased portal venous inflow

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31
Q

Portal hypertension can be caused by things other than cirrhosis so PH can be classified according to the___ ___ ____

A

site of obstruction

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32
Q

what prehepatic causes can lead to portal hypertension? 2

A
  • portal venous thrombosis or occlusion secondary to congenital portal venous abnormalities
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33
Q

what are the tow types of intrahepatic obstruction?2

A
  1. presinusoidal

2. postsinusoidal

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34
Q

give examples of the presinusoidal causes of portal hypertension. 2

A

schistomiasis

non-cirrhotic portal hypertension

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35
Q

give examples of the postsinusoidal causes of portal hypertension. 3

A

cirrhosis, alcoholic hepatitis, congenital hepatic fibrosis

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36
Q

what posthepatic causes can lead to portal hypertension? 2

A

budd chiari syndrome and veno-occlusive disease

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37
Q

circulation changes in liver disease: what do the low albumin levels signal to the kidneys?

A

that there is low plasma volume

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38
Q

circulation changes in liver disease: the low plasma volume stimulates the kidneys to produce ___ and by the ___- system - get ____ production

A

This stimulates the kidneys to produce renin and by the RAAS system - get aldosterone production

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39
Q

the aldosterone produced by the RAAS system cannot be _____ by the liver so we get increased ___ reabsorption from the ___, ____, and the ___

A

This aldosterone cannot be metabolised by the liver so get increased sodium reabsorption from the urine, sweat, and the gut

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40
Q

which other hormones increasee in liver disease?

A

endothelin and oestrogen

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41
Q

The increase in angiotensin II, aldosterone, SNS and ADH (vasopressin) means that the kidneys are _____ as they are all _______

A

The increase in angiotensin II, aldosterone, SNS and ADH (vasopressin) means that the kidneys are squeezed as they are all vasoconstrictors

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42
Q

what is the effect of the vasoconstrictors on the kidneys?

A

leads to sodium retention, potassium loss and water retention

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43
Q

what can the loss of K do?

A

make you feel very unwell

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44
Q

what is the function of ADH?

A

stops you peeing out water and is also a vasoconstrictor

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45
Q

adh keeps more water in the body and basically____ the sodium so you get more sodium retentio

A

keeps more water in the body and basically dilutes the sodium so you get more sodium retentio

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46
Q

the vasoconstrictor hormones can all cause renal ____ but renal ________ are also produced to vasodilate the kidneys

A

failure, prostaglandins

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47
Q

what is the effect of NSAIDS on the renal prostaglandins?

A

they inhibit them and cause renal failure

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48
Q

liver disease is not associated with cancer, true/false ?

A

false - associated with hepatic carcinogenesis

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49
Q

hepatic carcinogenesis: Cirrhosis leads to recurrent hepatocyte ___ so you get cells trying to _______. This leads to cellular _____ and recurrent ___ copying. This means that mutations are more common because of the ____ of DNA being copied but also because of the _____ environment that they are copying in - lots of ____ ____ and ____

A

Cirrhosis leads to recurrent hepatocyte death so you get cells trying to regenerate. This leads to cellular hyperplasia and recurrent DNA copying. This means than mutations are more common because of the volume of DNA being copied but also because of the mitogenic environment that they are copying in - lots of oxidative stress and toxins

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50
Q

what is a mitogenic environment?

A

a toxic environment where there is lots of oxidative stress and toxins

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51
Q

hepatic carcinogenesis : why do you get inflammation

A

This is because there is deregulation in cell-cycle control and so more cells are surviving - they would normally be killed via apoptosis if this was in a non stressful environment

You get DNA damage - from ROS,RNS, and adaducts

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52
Q

what are the causes of hepatic carcinogenesis ?

A

HBV DNA integration

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53
Q

what do histological slides of hepatic carcinogenesis look like? 3

A

All the cells are really jumbled up.
The nuclei are much bigger and
the cytoplasm is smaller

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54
Q

what are the two categories of cirrhosis?

A

compensated and decompensated

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55
Q

in compensated cirrhosis They will be clinically ____ and often it is an ______ finding on ___ or ____ tests for something else

A

They will be clinically normal and often it is an incidental finding on imaging or lab tests for something else

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56
Q

what happens in decompensated cirrhosis?

A

the patient has liver failure

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57
Q

what two categories of decompensated cirrhosis is there?

A
  1. acute on chronic

2. end-stage liver disease

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58
Q

give three examples of acute on chronic decompensated liver cirrhosis?

A

insult

  • systemic inflammatory response syndrome
  • infections
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59
Q

with decompensated cirrhosis acute-on-chronic you can potnetially get the person back to _____ state

A

compensated

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60
Q

what happens in end stage liver disease?

A

you don’t have enough functioning hepatocytes so basically run out of liver

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61
Q

what are the signs of compensated liver disease ? 7

A
  • Spider naevi - more worrying if man has it
  • Palmer erythema
  • Clubbing
  • Gynaecomastia
  • Hepatomegaly
  • Splenomegaly
  • They may also have no symptoms
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62
Q

what are the signs of decompensated liver disease ? 4

A
  • Jaundice
  • Ascites
  • Encephalopathy
  • Easy bruising
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63
Q

los of liver functio which leads to decreased urea synthesis which leads to increased blood ammonia leads to ……?

A

encephalopathy

64
Q

decreased hormonal detoxification leads to increased circulatory oestrogens which leads to …..? 3

A
  • gynaecomastia
  • testicular atrophy
  • hari loss
65
Q

decreased albumin synthesis leads to ______

A

ascites

66
Q

altered liver structure:
- get decreased blood circulation leading to
- shunting leading to
- undetoxified blood anaemia which leads to
- hepatic coma which leads to
……..?

A

PORTAL HYPERTENSION

67
Q

impaired bile circulation leads to ____

A

jaundice

68
Q

pathogenesis of ascites :
1. you get ______ through portal hypertension which leads to increased production and sensitivity of ______, resistance to_______
2. This leads to _____ ______ vasodilation - this causes the activation of arterial ______s so get increased HR, ___
3. This causes activation of ___-
Causing renal vasoconstriction leading to ___ and ___ retention

A

shunting; vasodilators; vasoconstrictors; splanchnic arteriolar; baroreceptors; CO; RAAS; sodium and water

69
Q

how is ascites diagnosed clinically ?

A

through shifting dullness and ultrasound - the dark bits

70
Q

Ascites is a marker for ___ ____

A

poor prognosis

71
Q

what may develop if you get translocated infection of ascites ?

A

spontaneous bacterial peritonitis

72
Q

Do a __ in all cases of ascites and a cell count - the neutrophil will be > ___ cells/mm3

A

tap

73
Q

encephalopathy: This is a mental confusion due to failure of the liver to clear ____ waste (as ____) so it builds up in the circulation and passes to the brain, where _____ clear it (by processes involving the conversion of glutamate to _____). The excess ____ causes an osmotic imbalance and a shift of fluid ___ these cells - hence cerebral ____ which - ______ the astrocytes.

A

This is a mental confusion due to failure of the liver to clear nitrogenous waste (as ammonia) so it builds up in the circulation and passes to the brain, where astrocytes clear it (by processes involving the conversion of glutamate to glutamine). The excess glutamine causes an osmotic imbalance and a shift of fluid into these cells - hence cerebral oedema which compresses the astrocytes.

74
Q

how is a diagnosis of encephalopathy made? 3

A

Flap confusion
Any neurology
Alcohol withdrawal

75
Q

where can you get variceal bleeding?

A

Can get oesophageal, gastric, rectal and ectopic

76
Q

what are the complications of cirrhosis ?

A
  • ascites
  • encephalopathy
  • variceal bleeding
  • liver failure
  • gut oedema
77
Q

what is the variceal bleeding caused by?

A

portal hypertension

78
Q

which signs tell you about pressure in the varices 4

A
  • High HVPG (Hepatic venous pressure gradient)
  • Variceal size
  • Red colour signs - wall thickness
  • Liver failure - increased HVPG
79
Q

what is the HVPG a measure of ?

A

the difference in pressure between the portal vein and the IVC

80
Q

1/__ of varices bleed. __-___% stop and ___-___% rebleed.

A

1/3rd of varices bleed. 40-60% stop and 70-80% rebleed.

81
Q

what does gut oedema cause?

A

poor absorption

82
Q

In Cirrhosis the blood supply is effectively b_____ the liver and so drugs are not being _____

A

In Cirrhosis the blood supply is effectively bypassing the liver and so drugs are not being metabolised

83
Q

give some examples of drugs that are highly metabolised by the liver? 3 and what does this mean for these drugs in cirrhosis

A

GTN, phenytoin, calcium blockers

need to be giving lower doses

84
Q

If the IV dose of a drug in the BNF or something is much ____ than the oral dose you know that it is heavily ______ by the liver so should be weary of these in liver disease

A

If the IV dose of a drug in the BNF or something is much smaller than the oral dose you know that it is heavily metabolised by the liver so should be weary of these in liver disease

85
Q

give examples of drugs where the enzymes becomes saturated and cannnot metabolise anymore ? 2

A

alcohol and phenytoin

86
Q

why are NSAIDs a bad idea in liver disease?

A

bad idea for the kidneys because they inhibit prostaglandins which are responsible for saving the kidneys from being squeezed to death

87
Q

in liver disease there are less ___ in the plasma so you have to be careful when doing drug level tests as they may be artificially ___ because the amount of bound drug is low whereas the unbound may be really high. You need to measure the amount of ____ drug in liver disease

A

proteins, low , free

88
Q

NSAIDS mean that renal PGE synthesis is decreased and what does this lead to

A

further sodium retention and risk of hepato-renal syndrome

89
Q

Cirrhosis ___ _____are increased with nsaids

A

Cirrhosis peptic ulcers are increased with nsaids

90
Q

WHAt else do NSAIDS cause? 4

A

Asthma; hypertension; diarrhoea/colitis; CHF

91
Q

If someone is going to be on NSAIDS or a COX-2 inhibitor for a couple of weeks what should they be co-prescribed with?

A

a proton pump inhibitor

92
Q

opiates cause more ____ pretending to be neurotransmitters and disrutping normal pathways

A

amines

93
Q

what are patients with liver disease more prone to with opiates?

A

sedation

94
Q

what is the first phase of drug metabolism?

A

CYP450 biotransformation

95
Q

first phase drug metabolism : affected ___ and is useful for ___ soluble drugs

A

This is affected early and is useful for fat soluble drugs

96
Q

what is the second phase of drug metabolism?

A

conjugation

97
Q

2nd phase drug metabolism : affected ___

A

late

98
Q

in liver disease we want drugs that are metabolised ___

A

late

99
Q

give examples of drugs which have a reduced metabolism in liver disease. 6

A

opiates ; benzodiazepines; chlormethiazole; cyclosporin; metronidazole; calcium blockers

100
Q

paracetamol is converted to ____ and _____ with the byproduct ____________-

A

sulphates and glucoronides, N-acetyl- p- benzoquinoneimine

101
Q

N-acetyl-p-benzoquinoneimine which is a ____ ____ intermediate which causes hepatic _____

A

N-acetyl-p-benzoquinoneimine which is a highly reactive intermediate which causes hepatic necrosis

102
Q

in normal people why does the N-acetyl-p-benzoquinoneimine not cause problems

A

because it is inactivated by glutathione

103
Q

what happens in paracetamol toxicity

A

the glutathione stores run out and the N-acetyl-p-benzoquinoneimine can cause necrosis

104
Q

what enzymes converts paracetamol to N-acetyl-p-benzoquinoneimine?

A

P4502E1

105
Q

what are the features of liver disease which mean that paracetamol is more toxic ? 2

A
  • they have reduced glutathione stores

- increased p4502e1

106
Q

Infusion of _____(analogue) prevents paracetamol causing further problems

A

metathione

107
Q

Paracetamol is metabolised by CYP2a1 and _____ blocks the paracetamol binding to this receptor

A

alcohol

108
Q

alcohol also ___ the presence of p450 2a1 _____ meaning that you get late paracetamol ____

A

increases, receptors, toxicity

109
Q

bad _____ can also deplete your glutathione stores

A

glutathione

110
Q

for pain relief in liver disease paracetamol __g ___ ____ . do not exceed __g and avoid ____ use

A

1g twice daily , 3g, prolonged

111
Q

what is the amount of codeine that is allowed to be given to liver disease patients?

A

30 mg

112
Q

what drug should be avoided in liver disease?

A

NSAIDs

113
Q

drug induced liver disease probably has a ____ component

A

genetic

114
Q

which drugs can induce hepatitis? 2

A

amoxicillin and clavulanic acid

115
Q

Hys law is where a drug is at high risk of causing fatal liver injury
ALT/AST > __ x ULN
And bilirubin > __mg/dl

A

5, 3

116
Q

drug induced liver disease is more common in men, tru/false?

A

false

117
Q

why is frusemide not used in liver disease?

A

Reduced intra-vascular volume

Worsens hypokalaemia, hypomagnesaemia

118
Q

why is thiazide not used in liver disease?

A

hypokalaemia , hypomagnesaemia

119
Q

which diuretic is given in liver disease?

A

spironolactone

120
Q

with spironolactone aim to los __kg/ day - why

A

1

if you lose weight faster than this the kidneys will struggle so can take a long time to get rid of the fluid build up

121
Q

for sedation in liver disease patients use phase ___ metabolism ________ in __ doses. Give examples of these drugs 3

A

II, benzodiazepines, small

lorazepam; oxazepam; lormetazepam

122
Q

which antibiotics are avoided because they are nephrotoxic

A

aminoglycosides

123
Q

which antibiotics are avoided because they are epileptogenic

A

quinolones

124
Q

which antibiotic has reduced metabolism in liver disease

A

metronidazole

125
Q

what are the main areas of management in liver disease?

A
  1. remove or treat the underlying cause
  2. look for and treat infection
  3. avoid NaCl retention
  4. think about nutrition - very important
126
Q

An energy intake of ___ - ____kcal/kg and a protein intake of ___ -___g/kg are recommended.

A

An energy intake of 35-40 kcal/kg and a protein intake of 1.2-1.5g/kg are recommended.

127
Q

why is nutrition control necessary in liver disease?

A

Low threshold to switch to gluconeogenesis and lipolysis and catabolism

128
Q

what is recommended to reduce gluconeogenesis and muscle catabolism

A

small frequent meals and snacks

129
Q

when is fasting often a problem ? and what is done to solve this

A

Overnight. They are often given an NG tube

130
Q

what does vitamin B thiaminc do?

A

(cofactor in the metabolism of alcohol) mandatory in excess alcohol intake

131
Q

what are two common complications of ppoor intake and absorption of calcium, vitamin D, malnutrition and steroid use

A

Osteoporosis and osteomalacia

132
Q

Fat soluble vitamin deficiency may occur in ___ and ___. Monitor levels and supplement if necessary.

A

Fat soluble vitamin deficiency may occur in PSC and PBC.

133
Q

treatment os ____ ____ ____ in ascites is urgent

A

SBP

134
Q

which vitamins and minerals often need to be supplemented in liver disease

A
  • vitamin B thiamine
  • calcium- 2000g
    vitamine D - 20 micrograms
135
Q

in ascites ____ is given to treat vascular instability

A

terlipressin

136
Q

what other drugs are given in ascites?

A

spironolactone

137
Q

in new ascites you should escalate spironolactone whereas in recurrent ascites you should give stepwise increments of spironolactone and _____ ____

A

loop diuretic

138
Q

what needs to be measured in ascites especially after a dose change of paracentesis

A

U and E

139
Q

paracentesis gives ____ ___ but has risks of ____,____,_____

A

Rapid relief but there is risk of infection, encephalopathy and hypovolaemia

140
Q

with TIPSS for treatment of ascites

  • __% of patients who receive this will have no ascites so will be off diuretics
  • __% will have ascites but that can be controlled using diuretics
  • __% see no improvement
A

60% of patients who receive this will have no ascites so will be off diuretics
30% will have ascites but that can be controlled using diuretics
10% see no improvement

141
Q

what is a final option for ascites

A

transplant

142
Q

for treatment of encephalopathy you should loos for a cause such as ___, ____, _____, ____ ____

A

nfection, metabolic, drugs, liver failure

143
Q

what is the drug used for encephalopathy which clears the gut/reduces transit time (by pulling water from the body to the colon

A

lactulose

144
Q

what other part of treatment is important for encephalopathy

A

nutrition

145
Q

why is a carbohydrate contaning late evening snack recommended in encephalopathy treatment ?

A

this increases the carbohydrate oxidation and decreases lipid and protein oxidation rate and hence improves nitrogen balance and reduces fasting periods overnight.

146
Q

why do you regularly endoscope patients with cirrhosis ?

A

to check for varices

147
Q

what are the treatment options for varices?

A

beta blockers

  • variceal ligation
  • balloon tamponade
  • scleropathy
  • TIPSS
148
Q

B blockers for variceal treatment should be non selective true/false?

A

true

149
Q

what are the treatment steps in acute variceal bleeding? 4

A
  1. resuscitate until haemo dynamically stable -
  2. Correct clotting abnormalities with vitamin K, FFp and platelets rtansfusion
  3. Start IVI of terlipressin
  4. TIPSS or transection/shunt surgery
150
Q

what are the complications of scleropathy?

A

can get scleroulcers

151
Q

success rate of balloon tamponade is ___ -__ % what are the complications (2)

A

80-90%

  • aspiration and perforation
152
Q

what should be done for secondary prophylaxis of variceal bleeding? 3

A
  1. Variceal band ligation
  2. B blockers
  3. Also increased risk of clotting so patients will be on anticoagulation
153
Q

what is the risk with TIPSS in variceal bleeding?

A

there is a risk of encephalopathy

154
Q

transplantation can be given based on :

  1. events e.g. ___ - _____ and _____
  2. liver function e.g. ____, ___ and ___ time
  3. QoL = ____, ____ and spontaneous ______
A

Can be given based on events

  • Ascites -resistant or spontaneous bacterial peritonitis
  • Variceal bleed

Liver function based
- bilirubin , albuin, prothrombin time

QoL based
- Itchy, lethargy and spontaneous encephalopathy

155
Q

Transplant carries risks so you need to make sure the patient has a _% risk of dying from doing nothing before you transplant

A

10

156
Q

Need a UKELD score of > or = ___ to be listed for elective transplant unless what?? (2)

A

49

They have a variant syndrome

or have hepatocellular carcinoma

157
Q

what are the examples of variant syndromes ? 7

A 
Diuretic resistant ascites
Hepatopulmonary syndrome
Chronic hepatic encephalopathy
Intractable pruritus
Polycystic liver disease
Familial amyloidosis
Primary hyperlipidaemia

GI: liver, biliary tree and pancreas (20 decks)

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