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2A content- Sameera > 8. LIVER > Flashcards

8. LIVER Flashcards

1
Q

what is wernickes korsakoff syndrome and what r the 2 main associations

A

neurological disorder due lack of thiamine (vitamin B1) and alcohol abuse

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2
Q

what are the three methods that alcohol exacerbates wernicke Korsikoff syndrome (3)

A

exacerbated by alcohol intake as alcohol reduces thiamine absorption in body, increases thiamine excretion and inhibits the enzyme that activates thiamine

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3
Q

what r the two stages of WK syndrome

A

1.Wernicke’s encaphalopathy
2. Korsakoff syndrome:

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4
Q

what is wernickes encaphalopathy, why and what does this cause

A

initial inflammation of brain due to thiamine deficiency
temporary damage to thalamus and hypothalamus

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5
Q

what is korsakoff syndrome and what does this cause

A

progression of Wernicke’s (long term condition)
permanent damage to the brain- particularly to memory

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6
Q

what is thiamine needed for in the body and what does it do in the body

A

thiamine is essential for normal brain and muscle function by converting carbohydrates into energy for the CNS/ muscles

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7
Q

what is a consequence of thiamine deficiency and what can this lead to

A

build up of pyretic acid in the bloodstream which contributes to a loss of mental alertness called dry beriberi

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8
Q

causes of WK syndrome (3)

A

mainly alcohol abuse
lack of thiamine in diet (eg crohns)
anorexia

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9
Q

signs of WK syndrome (5)

A

-ataxia (lack of muscle co-ordination)
-nystagmus (lack of eye muscle co-ordination)
-ptosis
-mental confusion
-memory loss (confabulational)

miss polly needs a molly

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10
Q

3 investigations for WK syndrome and results (2, 2, 1)

A

bloods: low serum B1, high pyruvate levels
blood arterial gas: rule out hypoxia and ketoacidosis
MRI: brain imaging

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11
Q

how is WK syndrome diagnosed (2)

A

diagnosis based on history and clinical examination

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12
Q

treatment (1) for WK syndrome and when is this given (1)

A

oral or paraenteral thiamine
given on suspicion of condition

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13
Q

differentials for WK syndrome (3)

A

alcoholic ketoacidoosis
chronic hypoxia
hepatic encephalopathy

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14
Q

what is gilberts syndrome

A

body unable to process bilirubin fast enough

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15
Q

what type of inheritence is gilberts

A

autosomal recessive

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16
Q

what is gilberts syndrome the main cause of

A

hereditary jaundice

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17
Q

what can trigger gilberts syndrome episodes (4)

A

dehydration
fasting
excess alcohol
hepatitis

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18
Q

risk factors for gilberts 2

A

T1DM
male

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19
Q

explain the pathophysiology of gilberts starting with the mutation and what does it cause

A
  1. mutation in UGT1A1 gene which removes instructions to make bilirubin UGT enzyme which is essential in removal of bilirubin from body
  2. this build up levels of unconjugated bilirubin in the blood,
  3. causing mild jaundice
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20
Q

how is gilberts syndrome usually discovered

A

incidentally on tests

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21
Q

what is the proportion of asymptomatics in gilberts syndrome

A

30% of people with gilbert’s r asymptomatic

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22
Q

symptoms of gilberts (2) and what pattern do they appear in

A

slight yellowing due to mild jaundice- often see in eyes
dark urine
symptoms come in short episodes and fully resolve

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23
Q

what is crigler najjar and what symptoms does it involve (4)

A

more severe version of Gilbert’s-
involves nausea, vomiting, fatigue and abdominal pain

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24
Q

investigations for gilberts (3)

A

blood test
liver function test
sometimes a genetic test is required to confirm Gilbert’s syndrome

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25
Q

treatment for gilberts and crigler najjar 3

A

no treatment as if don’t threaten health or cause severe symptoms
can advise to avoid triggers
for crigler/ sever gilberts= phototherapy to break down excess bilirubin

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26
Q

what is a hernia

A

protrusion of an organ through a muscle/ tissue wall weakness

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27
Q

what is a reducible and irreducible hernia

A

reducible: can be manually pushed back into place
irreducible: resists manual pushing back into place

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28
Q

what r the 3 subcategories of irreducible hernias

A

obstructed, strangulated and incarcerated

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29
Q

define obstructed hernia

A

: bowel contents cannot get though the part of the bowel that has herniated

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30
Q

define strangulating hernia and what three thigns can this cause

A

reduce blood supply to bowel, causing ischaemia, gangrene and perforation of the hernia

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31
Q

define incarcerated hernia

A

contents of hernia are stuck and cannot be pushed back into place (same r irreducible)

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32
Q

what r risk factors for hernias (3)

A

things that involve abdominal muscles eg chronic cough, constipation, heavy lifting

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33
Q

what r the 2 symptoms for hernias

A

pain (particularly if obstructed/ strangulated) and a lump on location

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34
Q

treatment for hernias (1)- what type

A

usually laparoscopic surgery

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35
Q

what is the most common type of hernia

A

Inguinal Hernia

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36
Q

what happens in inguinal hernias

A

bowel passes through inguinal canal

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37
Q

additional risk factors specific to inguinal hernias (2)

A

age and male

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38
Q

what is a femoral hernia

A

bowel hernia through the femoral canal

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39
Q

risk of femoral hernia and what is required to prevent this from occuring

A

high risk of being strangulating due to rigid femoral canal borders-> treatment required immediately to save the bowel from ischaemia

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40
Q

specific risk factors for femoral hernias (2)

A

occurs in females, elderly/middle ages

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41
Q

what is umbilical hernia

A

intestine herniates through the umbilical ring

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42
Q

specific risk factors for umbilical hernias (2)

A

common in young children/ infants or women with multiple previous pregnancies

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43
Q

what is an epigastric hernia

A

intestine herniates through the lines alba above the umbilicus

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44
Q

what is an incisional hernia and what causes it

A

hernia at the site of surgical scar after surgery
due to the surgical incision which weakened the abdominal muscles

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45
Q

what is the treatment (1)for incisional hernia and what is a risk of this treatment

A

treatment: mesh repair decreases recurrence but increases infection risk

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46
Q

what is a hiatal hernia

A

stomach hernia through diaphragm aperture

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47
Q

what r the two types of hiatal hernias and what % of cases belong to each

A

sliding or rolling
20% cases r rolling
80% cases r sliding

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48
Q

what r rolling hiatal hernias

A

where the lower gastro-osophageal junction remains the the abdomen but a bulge of stomach herniates up into the chest

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49
Q

what r sliding hiatal hernias and what is a consequence of this

A

where the lower gastro-osophageal junction slides up into the chest
acid reflux

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50
Q

investigations for hernias (1, diagnostic)

A

CT: for imaging
barium swallowing for diagnosis

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51
Q

what is spontaneous bacterial peritonitis

A

acute bacterial infection of ascitic fluid in peritoneum (also known as ascites) with no obvious source

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52
Q

what r the causes of SBP (1,3)

A

bacteria that normally live in intestine and enter the abdominal cavity eg E.coli, klebsiella and strep bacteria

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53
Q

risk factors for SBP (3)

A

cirrhosis
past history of spontaneous bacterial peritonitis
ascites

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54
Q

symptoms of SBP (6)

A

often asymptomatic
fever
abdominal pain/ tenderness
altered mental state
vomiting
GI bleeding

triple A ForGiVen

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55
Q

investigations for SBP (1, diagnostic)

A

diagnosed by an absolute neutrophil count of over 250cells/mm3 in ascitic fluid (ANC test)
ascitic fluid test for cell count and culture

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56
Q

treatment for SBP (2)

A

should be given antibiotic prophylaxis
albumin (particularly for patients with renal dysfunction)

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57
Q

what r the 3 metabolic liver disease

A
  1. Haemochromatosis
  2. Wilson’s disease
  3. Alpha 1 antitrypsin
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58
Q

what does haemochromotosis cause

A

causes excess body iron

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59
Q

what type of inheritence is haemochromotosis and what is the most common cause

A

autosomal recessive disease
most common cause= hereditary haemochromatosis= autosomal recessive disease

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60
Q

what gene mutation is haemochromotosis closely linked with and what % of people have this mutation
ON WHAT CHROMOSOME

A

90% have mutation of HFE gene on chromosome 6

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61
Q

risk factors for haemochromotosis (5)

A

males (menstrual blood loss is preventative)
50 year olds
family history
T2DM
HEPATOMEGALY

starting today, here’s more Fe

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62
Q

pathophysiology for haemochromotosis starting with gene mutation

A

gene mutation causes simultaneous excess iron uptake from transferrin 1 and decrease in hepcidin synthesis (protein that regulates iron homeostasis)
this causes iron accumulation (20-30g when the normal is 3-4g)
this excess iron is deposited in the liver, heart, pancreas, kidney, heart, skin and anterior pituitary
this can lead to fibrosis or organ failure

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63
Q

symptoms of haemochromotosis (6)

A

joint pain
hypogonadism (due to anterior pituitary damage)
slate grey/ bronze skin
liver cirrhosis symptoms
osteoporosis
heart failure

Just One Look and i can Hear a bell ring- School Hall

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64
Q

investigations for haemochromotosis (4) and results

A

blood iron studies: high serum iron, high ferritin, high transferrin saturation
genetic test for HFE gene
liver biopsy: to assess for liver damage with a prussian blue stain (stains iron)
liver MRI: looks for iron overload

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65
Q

1st line treatment for haemochromotosis

A

venesection (regular removal of blood until ferritin is less than 50 micrograms) and then maintenance venesection to keep levels controlled

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66
Q

treatment for haemochromotosis if venesection is contraindicated

A

give desferrioxamine (chelating agent) which binds to free circulating iron and is excreted in the urine

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67
Q

changes in lifestyle for haemochromotosis (2)

A

reduce iron in diet and avoid fruits (contain vitamin C which can increased iron absorption)

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68
Q

what does wilsons disease cause

A

causes excess body copper

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69
Q

what type of inheritance is wilsons disease and what mutation is associated with it WHAT CHROMOSOME

A

autosomal recessive mutation of ATP78 gene on chromosome 13

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70
Q

how common is wilsons disease

A

rare

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71
Q

what age does wilsons affect patients

A

young patients (around 20 years old)

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72
Q

pathophysiology of wilsons starting with gene mutation

A

gene mutation causes mutation to transport enzyme that is involved in excess copper excretion
this causes copper to accumulate in liver cells which causes oxidative damage
excess free copper travels to the kidneys, eyes and brain and accumulate there
this causes organ specific symptoms due to the chronic accumulation of copper and can lead to organ failure

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73
Q

compare presentation of wilsons disease in children and adults

A

children tend to present with liver disease systems and adults present with CNS signs

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74
Q

symptoms of wilsons disease (split into 4 systems- 1 each)

A

hepatic symptoms= spider angiomata
neurological= Parkinsonism/ memory issues
opthalmological= Kayser Fleischer rings
renal symptoms: kidney caliculi

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75
Q

what is pathognomonic for wilsons and what is this

A

Kayser Fleischer rings: green/brown ring around cornea which r copper deposits

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76
Q

what r spider angiomata

A

small distended blood vessels, usually on chest

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77
Q

what r the 3 investigations for wilsons (6, diagnostic)

A

Blood test: low serum copper (copper in tissues), low ceruloplasmin (protein that normally transports copper)
GS: liver biopsy- high copper, hepatitis
MRI brain- cerebellar and basal ganglia degeneration
DIAGNOSTIC= serum ceruloplasmic oxidase activity is low (<200mg/L)

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78
Q

why is there low serum copper in wilsons

A

copper is deposited in the tissues and not in the bloodstream

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79
Q

what is the 1st line treatment for wilsons, what is its function and side effects (3)

A

lifelong penicillanamine (copper chelating agent)- increases removal of copper
side effects: nausea, WCC decrease, Haemoglobin decrease

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80
Q

lifestyle change needed in treatment of wilsons (1)

A

avoid copper rich food eg mushrooms, shellfish, chocolate, nuts

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81
Q

treatment for severe liver disease/ end stage liver failure

A

liver transplant

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82
Q

what is alpha 1 antitrypsin deficiency

A

deficient/ defective alpha 1 antitrypsin enzyme production (A1AT)

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83
Q

inheritance of A1AD and how does it affect heterozygous

A

autosomal recessive (but can manifest in those who r heterozygous)

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84
Q

mutation in A1AD on what chromosome

A

mutation of protease inhibitor gene (PI) on chromosome 14

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85
Q

what is the presentation of A1AD similar to

A

COPD symptoms

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86
Q

risk factors for A1AD (3)

A

young/ middle ages
male
little/no smoking history

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87
Q

symptoms of A1AD (4)

A

dyspnoea due to the emphysema
cholestatic/ obstructive jaundice (liver cannot transport bilirubin due to liver damage)
liver cirrhosis
sputum production (pink- more emphysema)= characteristic in exam

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88
Q

pathophysiology of A1AD starting with A1AD normal function and where is it made and ending with 2 organs that r affected

A

A1AT is made in liver and usually inhibits neutrophil elastase (which degrade elastic tissue)
production of defective A1AT causes high levels of neutrophil elastase which
1. degrades elastic lung tissue, causing alveolar collapse and characteristic panacinar emphysema
2. deposition of A1AT in liver causes cirrhosis

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89
Q

what is a consequence of A1AD deposition in the liver

A

increases risk of hepatocellular carcinoma

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90
Q

how is A1AD self exacerbating

A

causes A1AD deposition in the liver which causes cirrhosis which reduces A1AT production further (A1AD is produced in liver)

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91
Q

investigations (6) and results for A1AD

A

low serum AIAT (less than 20mmol/L)
barrel chest on exams
chest x-ray shows hyper inflated lungs
CT= panacinar emphysema
LFT= spirometry shoes obstruction (FEV11: FVC <0.7)
genetic test= + for PI mutation
4 to do with chest/ lungs

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92
Q

treatment for A1AD (3)

A

stop smoking
manage emphysema- inhalers (SABA/LABA)
consider HEPATIC decompensation patients for liver transplantation

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93
Q

what is primary biliary cholangitis

A

autoimmune destruction of intralobular hepatic bile ducts

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94
Q

risk factors for PBC (6)

A

female (90% cases in women)
40-50 years
smoking
family history
many previous UTIs
other autoimmune disease eg SLE

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95
Q

pathophysiology of PBC 3

A
  1. autoantibodies cause chronic granulomatous inflammation which damages intralobular bile ducts
  2. this leads to ductopenia (portal tracts are missing bile ducts)
  3. bile ducts destruction causes bile and toxins to build up in liver
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96
Q

symptoms for PBC (5)

A

initially asymptomatic
pruritus and fatigue appear earliest
then jaundice (due to blockage and build up of bile)
then hepatosplenomegaly (due to inflammation of liver)
xanthelasma (yellow growths on eyelids due to cholesterol deposits)

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97
Q

what is pruritus

A

severe itching of the skin

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98
Q

explain hepatospenomegaly

A

liver enlarges due to inflammation
liver damage causes spleen enlargement due to blood flow being blocked through the liver and backing up the portal vein to the spleen

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99
Q

why does xanthelasma occur in PBC

A

due to disruption to liver metabolism caused by cholangitis (causes deficiency of lipase which normally breaks down lipids)

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100
Q

investigations for PBC (5)

A
  1. USS: 1st line imaging to exclude extrahepatic cholestasis
  2. rule out acute hepatitis: HCVAb, HepBsAg -ve
  3. liver function test: high ALP, high conjugated billirubin, decreased albumin
  4. serology: 95% have AMA antibodies (diagnosis)
  5. liver biopsy: shows portal tract infiltrate (lymphocytes and plasma cells
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101
Q

what is the diagnosis criteria for PBC

A

diagnosis requires 2 out of the following:
1. raised ALP
2. positive AMA (antimitochondrial antibodies)
3. diagnostic liver biopsy

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102
Q

treatment for PBC (1st line, 2)

A

1st line: lifelong ursdeoxycholic acid (for symptomatic)- bile acid analogue which dampens the immune response

  1. for pruritis-> give colesyramine
  2. vitamin ADEK supplements
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103
Q

complications of PBC (4)

A

liver cirrhosis
malabsorption of fats and vitamin ADEK due to cholestasis (therefore steatoarrhea),
osteomalacia/ penia (common)
coagulopathy

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104
Q

what is steatorrhea and what causes this

A

increase in fat excretion in stool due to fat malabsorption

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105
Q

why does osteomalacia/ penia occur in PBC

A

cholangitis interferes with vitamin D metabolism which leads to decreased bone formation

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106
Q

what is coagulopathy and why does coagulopathy occur in PBC

A

bleeding condition when blood’s ability to coagulate is impaired

cirrhosis of liver impairs its ability to make clotting factors

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107
Q

what is PSC

A

autoimmune destruction of intra and extralobular hepatic duct

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108
Q

risk factors for PSC (3)

A

male (60% cases in men)
40-50 years old
strong link to IBD (esp ulcerative colitis)- 80% of PSC patients have IBD

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109
Q

compare progression rate of PBC and PSC and explain why

A

PSC progresses faster as it affects extralobular ducts as well so it progresses faster than PBC

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110
Q

what r the symptoms of PSC (5)- 4 same as PBC

A

initially asymptomatic
then pruritus and fatigue
then cholestatic jaundice
then hepatosplenomegaly
charcot triad (if common bile ducts is involved): upper abdominal pain, fever and jaundice

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111
Q

3 investigations and results for PSC (5, GS)

A
  1. liver function test: high ALP, high conjugated billirubin
  2. serology tests:
    - negative HepBsAg/ HCVAb
    - positive pANCA
  3. magnetic resonance cholangiopancreatography: distinguishes PBC and PSC based by looking at which ducts r affected (gold standard imaging)
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112
Q

treatment for PSC

A

ursdeoxycholic acid
cholestyramine for pruritus
fat soluble ADEK supplements

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113
Q

what is ursleoxycholic acid used for in PSC

A

not as effective as a treatment but decreases colon cancer risk and improves liver function tests

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114
Q

compare location of PSC and PBC

A

PBC affects small bile ducts in liver only (intrahepatic bile ducts only) , PSC affects bile ducts in and outside of the liver (intra and extra hepatic bile ducts)

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115
Q

compare smoking as a risk factor in PBC vs PSC

A

PBC usually occurs in smokers, PSC usually occurs in non-smokers

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116
Q

compare gender as a risk factor in PBC vs PSC

A

PBC usually occurs in women (90% cases r female), and PSC is male (60% cases r male)

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117
Q

is PSC or PBC a premalignant disease and what 2 cancers does it increase the risk of

A

PSC is a premalignant disease (increases risks oAf colon/ bile duct cancers)

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118
Q

compare the typical presentation course of PBC and PSC

A

PSC presents differently in different patients but PBC has a typical disease source

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119
Q

compare what PBC and PSC is associated with (1 each)

A

PBC is associated with other autoimmune conditions, unlike PSC which is associated with IBD

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120
Q

what is acute pancreatitis

A

rapid onset inflammation of pancreas

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121
Q

how many cases have mild acute pancreatitis and how many develop severe complications

A

pancreatitis is mild in 80% of cases but severe complications can develop in 20% of cases

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122
Q

causes of acute pancreatitis (mneumonic)

A

Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion venom/ spider bite
Hypercalcaemia/ hyperlipideamia (increase in intracellular calcium increases premature enzyme activation)
ERCP (endoscopic retrograde cholangiopancreatography)
Drugs eg azathioprine, NSAIDs, ACEi
GET SMASHED

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123
Q

what r the 2 main causes of pancreatitis and state the % and what type

A

Gallstones (50% of acute cases)
Ethanol (80% of chronic cases)

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124
Q

explain the pathophysiology of acute pancreatitis, starting with inflammation of pancreatic acinars 4. How to gallstones exacerbate pancreatitis 1

A
  1. inflammation of the pancreatic acinars (group of exocrine cells) causes damage
  2. leads to release of proteases, lipases and amylases into the surrounding cells
  3. proteases auto digest the cells, further increasing inflammation
  4. amylase and lipase leak into the circulation
    -> gallstones blocks the pancreatic ducts and causes accumulation of these auto digestive enzymes in the pancreas
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125
Q

presentation of acute pancreatitis (8)
2 signs, 2 non specific,

A

gradual/ sudden severe epigastric pain
pain can radiate to back in 15% of cases
jaundice
steotorrhoea
grey turner signs (purple bruising to show bleeding in flank area)
cullen sign (purple bruising to show bleeding in preumbilical area)
non specific symptoms: pyrexia, vomiting

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126
Q

investigations for acute pancreatitis (4)

A
  1. blood: high serum amylase/ lipase (gold standard)
  2. erect CXR to exclude gastroduodenal perforation (which also causes high amylase/ lipase too!)
  3. abdo US: diagnostic for gallstones
  4. CT can shows the extent of the damage
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127
Q

compare lipase and amylase as a diagnostic for acute pancreatitis

A

high lipase is more specific to pancreatitis than amylase but less routine

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128
Q

what r the 2 types of pancreatic scoring systems what do they involve

A

APACHE 2- assess severity within 24 hours (uses measurements like CRP)
Glasgow and Rowson score- production of severe attack only after 48 hours

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129
Q

what is the diagnosis criteria for acute pancreatitis

A

requires at least 2 of the following:
1. characteristic symptoms/ signs
2. increase in amylase and lipase
3. radiological evidence (eg AUSS)

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130
Q

treatment for acute emergency pancreatitis (5)

A
  1. give nil by mouth (NG tube if feeding)
  2. IV fluid via cannula
  3. analgesia eg morphine IV
  4. catheter to monitor urine
  5. antibiotic prophylaxis (prevent infection of fluid)
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131
Q

differential for acute pancreatitis

A

abdominal aortic aneurysm

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132
Q

what is a complication of acute pancreatits and why is an issue

A

systemic inflammatory response syndrome
this is life-threatening

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133
Q

state the criteria of SIRS

A

criteria= 2 of the following:
tachycardia (bpm 90+)
tachypnoea (RR of 20+)
pyrexia (38+)
increased white cell count

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134
Q

what is chronic pancreatitis and what occurs to the pancreas during this time

A

defined as at least a 3 month history of pancreatic deterioration
causes irreversible pancreatic damage due to fibrosis

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135
Q

causes of chronic pancreatitis (5)

A

alcohol (most common)
chronic kidney disease
cystic fibrosis
recurrent acute pancreatitis
pancreatic duct blockage (stones/tumor

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136
Q

symptoms of chronic pancreatitis (6)

A
  1. continuous or episodic
  2. epigastric pain
  3. radiates to back
  4. exacerbated by alcohol
  5. exocrine dysfunction eg steatorrhea
  6. endocrine dysfunction eg T2DM
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137
Q

investigations for chronic pancreatitis (2, diagnostic)

A
  1. bloods: lipase and amylase can be elevated but unlikely to be high in severe cases (such a large deficiency that there’s none left to leak out)
  2. fecal elastase is typically high (indicator of exocrine function)
  3. abdominal USS and CT= detects pancreatic calcification and dilated pancreatic duct (diagnostic)
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138
Q

treatment for chronic pancreatitis (3)

A
  1. alcohol cessation
  2. abdominal symptoms pain is treated with NSAIDs
  3. pancreatitis supplements eg enzymes, insulin for DM
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139
Q

differential for chronic pancreatitis 1

A

pancreatic cancer of head/ tail

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140
Q

what is ascites, how much is it

A

fluid collection in peritoneal cavity
defined as fluid of more than 25ml

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141
Q

what is the physiologically normal amount of ascitic fluid for men and women to have

A

men usually have no intraperitoneal fluid, women can have up to 20ml of intraperitoneal fluid depending on the stage of their menstrual cycle

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142
Q

what is the most common cause of ascites 1

A

cirrhosis

143
Q

what does ascitic fluid contain 4

A

albumin, lipids, bile acids and WBCs

144
Q

signs of ascitic fluid (50

A

flank bulging in recline position
puddle sign test
shifting dullness test
fluid thrill test
jaundice (liver symptom)

145
Q

what r the 3 investigations for ascitic fluid (2, diagnostic)

A

2 physical examinations: shifting dullness and fluid thrill (clinical signs that confirm ascites)
paracentesis (take sample of fluid) to measure SAAG and protein levels
ultrasound for visuals of peritoneal cavity (diagnostic for ascites)

146
Q

what does SAAG stand for and what does it measure
why is this useful for ascites investigations

A

serum ascites albumin gradient
test to compare albumin concentration in ascitic fluid and in patient serum (indicates the cause of the ascites)

147
Q

what is a high SAAG gradient (value, what does it indicate the cause is)

4

A

> 1.1g/dL
indicates hydrostatic pressure imbalance= portal hypertension
portal hypertension can be caused by cirrhosis, heart failure, portal vein thrombosis and Budd-Chiari syndrome

148
Q

what protein values does high SAAG have and why is this and what is it called

A

<30g/L protein (low)
due to fluid being pushed out of circulation = high albumin in serum, low in ascitic fluid
transudate

149
Q

what protein values does low SAAG have and why is this and what is it called

A

> 30g/L protein (high)
due to peritoneum being more permeable than usual so it allows albumin to pass through, resulting in the concentration of albumin in the ascitic fluid and serum being similar
exudate

150
Q

what is a low SAAG gradient (value, what does it indicate the cause is)

4

A

<1.1g/dL
indicates osmotic pressure imbalance
caused by infection (TB), peritoneal malignancy (metastasis, often from ovarian cancer), pancreatitis, kidney failure

151
Q

what is the treatment for high SAAG (3)

A
  1. salt restricted diet
  2. diuretics (spironolactone)
  3. paracentesis (removal of fluid from peritoneal cavity)
152
Q

treatment for low SAAG (1) and why (1)

A

repeat paracentesis
doesn’t respond well to diuretics or salt restriction

153
Q

complication of ascites

A

SBP

154
Q

what r the 3 types of biliary tract disease

A

Biliary Colic
Cholecystitis
Ascending Cholangitis

155
Q

what r the 5 risk factors for biliary tract diseases (5 Fs + 2)

A

fat (BMI of 30+)
female
forty (40+ years old)
fertile (previous pregnancies/ pregnancy)
fair
family history
T2DM

156
Q

what is biliary colic, when does it occur and does it involve inflammation

A

pain in abdomen due to gallstone obstructing the common bile duct/ cystic duct
often occurs after eating a large fatty meal which causes the gallbladder to contract
no inflammation occurs

157
Q

symptoms of biliary colic (2)

A

right upper quadrant pain which is episodic (constant severe episodes of pain, lasting for longer than 30 minutes)
pain is worse after a fatty meal

158
Q

investigation for biliary colic 1

A

1st line: abdominal USS for imagery of gallstones (diagnostic)

159
Q

treatment for biliary colic (4)

A

elective laparoscopic cholecystectomy if symptomatic
NSAIDs for mild pain
IM diclofenac (strong NSAID) for severe pain
lifestyles changes: decrease in size and fatty content of meals

160
Q

what is cholecystitis, what is its cause and does it involve inflammation

A

inflammation of the gallbladder
due to gallstones blocking the cystic duct which causes bile build up
yes

161
Q

symptoms of choelscystitis (5

A
  1. right upper quadrant pain
  2. pyrexia
  3. tender gallbladder
  4. pain spread to top right shoulder due to phrenic nerve involvement
  5. positive for murphy sign: press on gallbladder and ask patient to inhale (patient will wince and stop inhaling due to pain)
162
Q

investigations for cholescystitis (3)

A

FBC: leukocytosis, neutrophillia
liver function test is normal
abdominal USS shows thicken gallbladder wall (3mm)

163
Q

treatment for cholecystitis (2)

A

laparoscopic cholecystectomy surgery within a week (ideally 72 hours)
pre surgery: IV fluids, analgesia, antibiotics if required

164
Q

what is ascending cholangitis, what type of condition is it and does it involve inflammation

A

inflammation of bile duct tree due to bacteria from intestine
life-threatening infection
yes

165
Q

symptoms of ascending cholangitis (3)

A

right upper quadrant pain
fever
cholestatic/ obstructive jaundice

166
Q

investigations for ascending cholangitis (4)

A
  1. FBC: leukocytes and neutrophillia
  2. LFT: increased conjugated bilirubin
  3. abdominal USS (1st line): common bile duct dilation and gallstones
  4. MRCP (gold standard)= diagnostic and best pre-intervention management
167
Q

treatment for ascending cholangitis (2)

A

ERCP: cleans the bile duct then laparoscopic cholecystectomy once stable to prevent recurrence

168
Q

1 complication of ascending cholangitis

A

risk of sepsis

169
Q

what is acute liver failure

A

liver injury in a person with a previously normal liver

170
Q

what r the 3 characteristics of acute liver failure

A

Coagulopathy (derangement in clotting) (>1.5INR)
Hepatic encephalopathy (HE)
Jaundice

171
Q

what r the 3 types of acute liver failure

A

hyperacute, acute, subacute

172
Q

what is hyperacute liver failure

A

Hepatic Encephalopathy w/7 days of noticing jaundice

173
Q

what is acute liver failure (subtype)

A

hepatic encephalopathy w/in 8-28 days of noticing jaundice

174
Q

what is subacute liver failure

A

hepatic encephalopathy w/in 5-26 weeks of noticing jaundice

175
Q

compare the prognosis for all three types of acute liver disease

A

best prognosis= hyperacute then acute and worst= subacute

176
Q

what is fulminant hepatic failure and its onset

A

sudden onset liver failure due to massive necrosis of liver cells

177
Q

cause and histological slides for fulminant hepatic failure

A

Most common cause of it is paracetamol overdose
Histologically- multiacinar necrosis

178
Q

what is the definition of acute on chronic liver failure

A

Abrupt decline in patient w/chronic liver symptoms

179
Q

causes of acute liver failure (5)

A

Viral: Hep A,B,Ebv
Drugs- paracetamol, alcohol
Hepatocellular carcinoma
Metabolic- Wilsons, hemochromatosis, A1ATD
Budd-chairi syndrome (vascular)

180
Q

key presentation of acute liver failure (3) and other general symptoms (3)

A

KEY:
Jaundice
Coagulopathy
Hepatic encephalopathy (west haven criteria 1-4)

OTHER:
Anorexia
Nausea
Malaise (general feeling of discomfort)

181
Q

name the hepatic encaphalopathy grading system and explain each stage (remember analogy of tired angry med student coming into lectures on a monday morning)

A

West haven criteria
1. Altered mood, sleep issues
2. Lethargy, mild confusion, asterixis (inability to sustain posture-> inv movements)
3. Marked confusion
4. Coma

182
Q

pathophysiology of acute liver failure 2

A

damage and loss of hepatic cells

183
Q

4 investigations for acute liver failure

A

Bloods: high ammonia
LFT: high bilirubin and low albumin, high PT/INR, high AST and ALT
electroencephalogram: for imaging to grade hepatic encephalopathy
US to check Budd chairi

184
Q

treatment for acute liver failure (4)

A

ABCDE
fluid
analgesia
treat underlying cause

185
Q

treatment for paracetamol overdose (2)

A

activated charcoal
N acetylcysteine

186
Q

how is hepatic encephalopathy treated 1 and how does it work

A

Lactulose (increases NH3 excretion)

187
Q

how is haemorrhage treated 1

A

Vit K

188
Q

how is sepsis treated 1

A

sepsis 6 pathway

189
Q

how is increased intercranial pressure treated

A

IV Mannitol
(manny has a toll on u )

190
Q

what is budd chairi syndrome and what does it cause

A

blocked/ narrowed heptic veins by clot
causes blood to back up into the liver
causes hepatomegaly

191
Q

what is most common type of primary liver cancer

A

Hepatocellular carcinoma

192
Q

explain the pathophysiology of chronic liver failure starting with hepatitis (4)

A

hepatitis
fibrosis
then compensated cirrhosis (scars)
then decompensated cirrhosis (end stage liver failure)

193
Q

define chronic liver failure 1

A

progressive liver damage over 6 months caused by repeated insults to the liver

194
Q

what r the causes of chronic liver failure (5)

A

alcohol liver disease
non-alcoholic liver disease
viral: hep B and C
metabolic: wilsons
autoimmune: PBC, PSC

195
Q

risk factors of chronic liver disease (4)

A

Alcohol
Obesity
T2DM
Drugs

196
Q

compare compensated and decompensated cirrhosis

A

compensated- asymptomatic liver carries out normal function
decompensated- end stage liver failure

197
Q

signs of decompensated liver disease (5)

A

Jaundice
Hepatic encephalopathy
Coagulopathy
Ascites (due to Portal HTN)
GI bleeding- (due to rupture of oesophageal varices)

198
Q

name the system and explain the factors involved in assessing chronic liver failure

A

Child pugh score system
assessing prognosis and extent for chronic liver failure
ABCDE:
A-Albumin
B-bilirubin
Clotting- PT
Distension- Ascites
E- encephalopathy

199
Q

state the Child Pugh score for survival rates

A

Classes score A,B,C
A= 100% 1 year survival
B= 80% 1 year survival
C= 45% 1 year survived

200
Q

What measures the severity of ESLF (IN FULL) and what is the purpose of it

A

MELD score- model for end stage liver disease
for transplant planning

201
Q

signs of chronic liver failure (10)

A

Caput medusae
Palmar erythema
Dupuytrens contracture
Spider angioma
Gynaecomastia
Jaundice
Ascites
Hepatic encephalopathy
Portal HTN
Fetor hepaticus
APCDPFGHS

202
Q

investigations for chronic liver failure (2)

A

liver biopsy: differentiates between cirrhosis and fibrosis
LFT: high AST and ALT

203
Q

treatment for chronic liver failure (2)

A
  1. lifestyle mods: stop alcohol
  2. consider liver transplant
204
Q

what is caput medusa and cause

A

cluster of swollen veins in abdomen
Cirrhosis of liver- harder for blood to travel in portal vein- backlog of blood travels to periumbilical veins- causes caput medusae

205
Q

what is palmar erythema

A

palms turn red

206
Q

what is Dupuytrens contracture

A

fingers bend towards hand

207
Q

what is Spider angioma

A

cluster of small red blood vessel

208
Q

what is Gynaecomastia

A

man boobs

209
Q

what is fetor hepaticus

A

rotten eggs and garlic smell breath

210
Q

what 3 symptoms of chronic liver disease link with issues with oestrogen regulation

A

palmar erythema, spider angioma, gynaecomastia

211
Q

what causes hepatic encephalopathy, explain the pathophysiology and what can it lead to

A

Problems in detoxification. Accumulation of NH3 which is normally detoxified by UREA cycle. This crosses BBB and causes confusion.

212
Q

how does liver failure cause ascites

A

Low levels of albumin and portal HTN cause fluid to leak out in the abdomen into the peritoneum.

213
Q

how can liver failure lead to hypoglycaemia

A

Glucose metabolism is impaired

214
Q

why can liver failure lead to bleeding disorders?

A

Liver is responsible for the production of clotting factors (All except 3,4 and 8)

215
Q

what r the 3 stages of alcohol liver disease

A
  1. Steatosis (fatty liver, undamaged)
  2. Alcoholic hepatitis (inflammation and necrosis- Mallory bodies)
  3. Alcoholic cirrhosis
216
Q

risk factors for alcohol liver disease 4

A

Prolonged alcohol consumption
Hep C
Obesity
Female sex (susceptible at smaller units, quicker onset)

217
Q

pathophysiology of ALD and what/ how are the markers detected

A
  1. Alcohol in liver is converted into acetaldehyde whihc causes inflammation
  2. Acetylaldehyde meets NAD forms NADH
  3. High NADH tell cells to produce FA
  4. Excessive fat in the liver
    AST and ALT can leak out of cells into the blood
218
Q

signs of alcohol liver disease (early and late stages)- 2 each

A

Early stages- very little signs (N+V+ diarrhoea)
Later stages- chronic liver failure + alcohol dependency

219
Q

what r the 2 alcohol dependancy questionnaires

A

CAGE
Audit

220
Q

explain the CAGE questionaire and what does it measure

A

Should you Cut down
Are people Annoyed by your drinking
Do you feel Guilty about drinking
Do you drink in the morning (Eye opening)
alcohol dependancy
2</ dependent

221
Q

what is the AUDIT test

A

10qs used the First line

222
Q

investigations and results for chronic liver failure (3) 6,2,1

A

LFT: high bilirubin, low albumin, high PT, high GGT, high AST: ALT ratio
FBC: macrocytic non-megaloblastic anaemia
biopsy: mallory cytoplasmic inclusion bodies present

223
Q

treatment for chronic liver failure (4)

A
  1. lifestyle changes: stop alcohol, healthy diet, lower BMI
  2. diazepam for tremors/ confusion
  3. short term steroids for severe ALD
  4. B1 and folate supplements
224
Q

what condition needs to be fulfilled for liver transplant for those with ALD

A

must abstain from alcohol for 3+ months before consideration

225
Q

complications of chronic liver disease (5- into 3 categories)

A

hepatocellular carcinoma
Hepatic encephalopathy, jaundice (due to hepatocellular insufficiency)
oesophageal varices, Ascites (due to portal HPT)

226
Q

what is a mallory weiss tear and what causes it

A

oesophageal tear
(due to episodic vomiting)

227
Q

what is non alcoholic fatty liver disease

A

Fat deposition in the liver which can’t be attributed to alcohol

228
Q

4 stages of NAFLD

A

Steatosis
Steatohepatitis
Fibrosis
Cirrhosis

229
Q

risk factors for NAFLD (5)

A

Obesity
HTN
Hyperlipidaemia
T2 DM
Drugs (NSAIDs, amiodarone)

230
Q

presentation of NAFLD (1)

A

Typically, asymptomatic- any findings are incidental

231
Q

investigations and results for NAFLD (3)

A

LFT: high bilirubin, low albumin, high PT/INR
FBC: thrombocytopenia and anaemia
US: 1st line for people suspected to have NAFLD

232
Q

what happens to albumin if biliurubin is high

A

albumin will be low

233
Q

what can be done to assess risk of fibrosis in NAFLD (1)

A

non-invasive scoring system
eg Fib 4

234
Q

treatment for NAFLD (3)

A
  1. lower BMI
  2. control risk factors (eg statins, metformin , ACEi)
  3. vitamin E (helps histological appearance of fibrotic tissue
235
Q

complications of NAFLD (5)

A

Ascites
Hepatocellular carcinoma
Hepatic encephalopathy
Portal HTN
Oesophageal varices

236
Q

what is hepatitis and what causes it

A

Inflammation of the liver as a result of viral replication within hepatocytes

237
Q

what is Hep A structure (2) and method of spread (1)

A

Non-enveloped Single stranded RNA.
Picornavirus
Faeco-oral route

238
Q

risk factors for Hep A (2)

A

Travel: travelling to endemic areas
Shellfish

239
Q

Where does Hep A replicate in the body 1 and why is is self limiting 1

A

Replicates in liver
excreted in bile so self-limiting

240
Q

4 phase of a Hep A infection

A

Incubation
Prodromal
Icteric
Convalescent

241
Q

signs of Hep A infection (3 steps)

A
  1. Prodromal phase (1-2 weeks)
  2. N+V, fever, malaise (general feeling of discomfort)
  3. Then jaundice, dark urine and pale stools, hepatosplenomegaly
242
Q

investigations for Hep A (3)

A

Serology: HAV-IgM- acutely infected
LFT: high bilirubin (icteric phase) , high ALT and AST
Bloods- high ESR+ leukopenia

243
Q

treatment for Hep A and is there a vaccination available (1,1)

A

Supportive management
Travellers’ vaccine available

244
Q

complication of Hep A infection

A

Fulminant (rapid) liver failure

245
Q

what is Hep E structure (1) and method of spread (1)

A

Non-enveloped single stranded RNA
Faeco-oral route

246
Q

cause of Hep E (1)

A

Undercooked pork

247
Q

pathophysiology of Hep E (2)

A

Acute inflammation
Usually self-limiting

248
Q

symptoms of Hep E (1)

A

95% of cases are asymptomatic, as usually self-limiting

249
Q

investigations for Hep E (2)

A

Serology: HEV IgM positive
PCR: HEV RNA detected

250
Q

treatment for Hep E 1

A

supportive treatment

251
Q

complications of Hep E infection (2)

A

Chronic Hep E disease in immunosuppressed
fulminant liver disease

252
Q

Hep D structure (1) and method of spread

A

Enveloped single stranded RNA
Blood borne

253
Q

pathophysiology of Hep D (2)

A

Incomplete requires HBV for assembly
Manifests as co-infection (IgM HDV + IgG HBV)

254
Q

Hep C structure 1, type of virus 1 and method of spread (1)

A

Single stranded RNA
Flavivirus
Blood borne

255
Q

causes of Hep C infections (2)

A

Sexually transmitted
IV drug users

256
Q

symptoms of Hep C (3)

A
  1. Acutely asymptomatic
  2. few patients have flu like symptoms
  3. later presentation as chronic liver failure signs
257
Q

investigations for Hep C (2)

A

Serology: HCV antibody test
PCR- HCV RNA

258
Q

treatment for Hep C (2)

A

Direct acting Antivirals (DAA) oral ribavarin

259
Q

complication of Hep C infections (1)

A

30% cases progress to chronic liver failure

260
Q

what is the structure of Hep B 1 what type of virus is it and method of spread (1)

A

Double stranded DNA
HepaDNAvirus
Blood borne

261
Q

how is Hep B transmitted (4)

A

Needles (tattoo, IVDU)
Sexual
Vertical (mother-> child)
Horizontal (between children)

262
Q

what two bodily fluids can Hep B be found in

A

semen and saliva

263
Q

risk factors for Hep B (4)

A

IVDU
Sexually (in particular MSM)
Dialysis patients
Healthcare workers

264
Q

pathophysiology of Hep B

A

Acute infection infects hepatocyte. Cellular response usually clears it.

265
Q

what is defined as chronic Hep B infection and what can long term inflammation cause

A

Chronic HBV if HBsAg >6 months.
Inflammation can last 10 yrs. -> cirrhosis.

266
Q

symptoms of Hep B (5)

A

dark urine
pale stool
hepatosplenomegaly
urticaria (hives)
arthralgia (joint stiffness)

267
Q

Define the following
HBsAg
HBsAb
HBcAg
HBc IgM
HBc IgG
HBeAg
HBeAb

A

HBsAg- surface antigen of Hep B virus- present for 1-6 months of infection
HBsAb- antibody to Hep B surface antigen- present after 6 months of infection (denotes immunity (natural active or immunisation)
HBcAg- exposed to Hep B at some point
HBc IgM- acute infection
HBc IgG- chronic infection
HBeAg- marker of patient infectiousness
HBeAb- in all chronically infected patients or if they have cleared infection

268
Q

What is the serology of an acute Hep B infection

A

HbS Ag and anti HBC Ab IgM

269
Q

What is the serology of an chronic Hep B infection

A

HbS Ag and anti HBC Ab IgG

270
Q

What is the serology of a person vaccinated against Hep B

A

anti HbS Ag

271
Q

What is the serology of a person with natural immunity against Hep B

A

Anti HBS Ag, anti HbC Ag IgG

272
Q

treatment for Hep B infection and is there a vaccine available (1,1)

A

Pegylated interferon alpha 2A
Vaccine available given to babies- (6-in-1 at 8 weeks)

273
Q

complications of Hep B infection (2)

A
  1. 5-10% of adult cases progress to chronic liver failure + HCC risk
  2. 90% of cases in children become chronic decompensated and are associated w/poor prognosis. Transplant!!!
274
Q

what is autoimmune hepatitis and what does this cause

A

body attacks hepatocytes
chronic liver inflammation

275
Q

risk factors for autoimmune hepatatis (4)

A

-females
-other autoimmune conditions eg hashimotos
-VIRAL INFECTION
-HLA-DR3/4

276
Q

state the 2 types of autoimmune hepatatis

A

type 1 and 2

277
Q

what is T1 autoimmune hepatitis associated with (2) and what proportion of cases is this and who does this usually affect (1,1)

A

ANA (anti-nuclear antibodies)
ASMA (anti-smooth muscle antibodies)

80% of all cases
adult women

278
Q

what is T2 autoimmune hepatitis associated with (2) and what proportion of cases is this and who does this usually affect (1,1)

A

ALC-1 (anti liver cystol antibodies)
ALKM-1 (anti liver kidney microsome antibodies)

20% of cases
younger females

279
Q

signs and symptoms of autoimmune hepatitis (2)

A

25% of all cases asymptomatic
May have evidence of liver failure e.g. fever, hepatosplenomegaly, jaundice

280
Q

investigations for autoimmune hepatitis (2 tests, 2 and 4 markeres)

A

LFT: elevated ALT and AST
Serology:
ANA, ASMA +/- ALC-1 and ALKM-1

281
Q

what is the first and second line treatment for autoimmune hepatitis

A
  1. immunosuppression
    eg prednisolone and azathioprine
  2. transplant
282
Q

what is a prevention for autoimmune hepatitis (2)

A

hep a and b vaccines

283
Q

where is piecemeal nerosis seen in histology (1)

A

hepatitis

284
Q

what is cirrhosis

A

pathological process involving fibrosis and regeneration of nodules due to damage to healthy liver tissue

285
Q

causes of cirrhosis (5)

A

Alcohol abuse
Non-alcoholic fatty liver disease
Hep B and C
Autoimmune conditions (PBC, PSC, Autoimmune Hep)
Genetic metabolic (Wilsons disease, A1ATD)

286
Q

investigations for cirrhosis (GS, 1 other with 5 results)

A

GS: liver biopsy- confirms diagnosis and severity
LFT:
Low albumin
Low platelets, INR/PT high
High AST/ALT

287
Q

treatment for cirrhosis (3)

A
  1. treat underlying cause
  2. conservative approach- analgesia, fluids, good nutrition, alcohol abstinence
  3. liver transplant
288
Q

complications of cirrhosis (1) and what can this complication lead to (2)

A

Portal hypertension:
-Ascites
-Oesophageal varices

289
Q

explain the 6 steps of bilirubin metabolism from Hb to urobilinogen

A
  1. Hb- haem + Globin @ splenic macrophage
  2. Haem -> biliverdin -> unconjugated bilirubin (Biliverdin reductase)
  3. Unconjugated bilirubin transported to liver via Albumin
  4. Unconjugated bilirubin glucoronidated @ liver -> conjugated bilirubin by UDP- glucuronysyltransferase
  5. Released in bile -> duodenum @ ampulla of vatar
  6. Reduced to urobilinogen in intestines (by bacteria)
290
Q

what happens to urobilinogen at the terminal ileum (3

A
  1. 5% is reabsorbed via enterohepatic recycling and the other 5% forms urobilin and is excreted (makes urine yellow)
  2. 90% continues in colon; to stercobilin; stool
291
Q

define jaundice

A

Yellowing of skin/eye due to accumulation of conjugated/unconjugated bilirubin

292
Q

what is jaundice a sign of (1)

A

liver dysfunction

293
Q

what is prehepatic jaundice and what causes it generally 1

A

High unconjugated bilirubin- due to increased RBC breakdown

294
Q

what is intraheptic jaundice

A

High conjugated and unconjugated bilirubin

295
Q

what is post hepatic jaundice and what causes it generally 1 and what r the typical signs of this (2)

A

High conjugated bilirubin due to biliary obstruction
pale stool and dark urine

296
Q

causes of prehepatic jaundice (5)

A

Sickle cell
G6PD deficiency- Glucose-6-phophate dehydrogenase
Thalassemia
Malaria
GILBERTS syndrome

297
Q

causes of intrahepatic jaundice (4) and what is special about this

A

HCC
ALD/NAFLD
Hepatitis
PBC + PSC
causes may be mixed

298
Q

causes of posthepatic jaundice (6)

A
  1. Cholangiocarcinoma (cancer of the bile ducts)
  2. Pancreatic cancer
  3. Choledocholithiasis (gall stone in Common Bile Duct)
  4. Mirizzi syndrome- gall stone stuck in GB infundibulum- compress CBD
  5. drug-induced cholestasis
  6. autoimmune- PBC +PSC
299
Q

what are the 4 signs of jaundice (only state)

A

Courvoisier’s sign
Charcots triad
Reynolds pentad
Murphy’s sign

300
Q

what is Courvoisier’s sign (2) and what is the mostly likely cause (2) and location (1)

A

painless jaundice + palpable GB (most likely due to pancreatic cancer or cholangiocarcinoma)
60-70% occur at the head of the pancreas

301
Q

what is reynold’s pentad

A

Signs and symptoms associated w/ascending cholangitis
Fever, RUQ pain, Jaundice, confusion, hypotension
JCH, For Real thats how u feel

302
Q

what is murphys sign, what is the test and what is a + test indicative of

A

RUQ tenderness, ask patient to take breath in whilst pressing RUQ, patient experiences pain and will stop inspiring normally.
Positive test is indicative of cholecystitis

303
Q

what is the charcot triad (3)

A

biliary colic, cholecystitis, ascending cholangitis

304
Q

state whether all three conditions of the charchot triad show fever, RUQ pain and jaundice or not (1,2,3)

A

biliary colic- RUQ
cholecystitis- fever, RUQ
ascending cholangitis- fever, RUQ, jaundice

305
Q

what r the investigations for jaundice (1, 6, 2)

A

1st line: US
LFT: high bilirubin, low albumin, PT/INR, AST/ALT +, GGT and ALP +
urine: bilirubin and urobilinogen

306
Q

what is the normal urine bilirubin and urobilinogen 2

A

low bilirubin
positive urine urobilinogen

307
Q

what r the urine results for biliary obstruction 2

A

+ urine bilirubin
low urine urobilinogen

308
Q

what r the urine results for hepatic disease 2

A

+ urine bilirubin
low urine urobilinogen

309
Q

what r the urine results for haemolysis 2

A

high urine bilirubin
high urine urobilinogen

310
Q

what r the 3 types of hepatobiliary cancers

A

pancreatic cancer
Hepatocellular carcinoma
Cholangiocarcinoma

311
Q

what type of pancreatic cancer is the most common and where do these affect

A

pancreatic ductal adenocarcinomas
affect the head of the pancreas

312
Q

risk factors for pancreatic cancer (6)

A

Male
Smoking
Alcohol
DM
Chronic pancreatitis
Family history

313
Q

what proportion of pancreatic cancers affects the head, body and tail

A

60% head
25% body
15% tail

314
Q

signs of pancreatic cancer 4 and which is mosts pathognomonic

A

Courvoisier’s sign (MOST P!!)
epigastric pain radiating to the back, relived by sitting forward
trousseaus sign of malignancy

315
Q

what is Trousseau’s sign of malignancy

A

non specific episodes of vessel inflammation + clots in different parts of the body

316
Q

investigations for pancreatic cancer (1st, GS, 1)

A
  1. abdominal US (1st line)
  2. pancreatic CT (GS)
  3. CA 19-9 tumor marker positive (non diagnostic)
317
Q

treatment for pancreactic cancer

A
  1. surgery if little metastasis and post operative chemo
  2. pallitive care if metastises
318
Q

what is the prognosis for survival with pancreatic cancer

A

Very poor prognosis
5yr survival= 3%

319
Q

what is is most common type of Primary hepatocyte neoplasia and what proportion of cases does this make up

A

hepatocellular carcinoma
90% of all primary liver cancers

320
Q

risk factors for hepatocellular carcinoma (2)

A

Hep B and C
Cirrhosis from ALD/ NAFLD/hemochromatosis

321
Q

explain the pathophysiology of hepatocellular carcinoma (2) including metastasising locations

A
  1. Cancer presents as nodules throughout the liver
  2. Can metastasise via hepatic or portal veins to the lymph nodes, bones and lungs
322
Q

signs of hepatoocellular carcinoma (3)

A
  1. signs of liver failure eg jaundice, ascites, HE
  2. cancer signs eg weight loss, tired all the time
  3. irregular hepatomegaly
323
Q

investigations for Hepatocellular carcinoma (1st line, GS, 1)

A

1st line: USS
GS: CT
high serum alpha fetoprotein marker in blood

324
Q

treatment for Hepatocellular carcinoma 1

A
  1. surgical resection of tumor
325
Q

prevention for Hepatocellular carcinoma 1

A

HBV vaccine

326
Q

why r biospsys avoided in hepatocellular cancers despite the fact that they r diagnostic

A

to prevent seeding of tumour

327
Q

what r cholangiocarcinomas

A

cancer of the bile ducts

328
Q

what proportion of primary liver cancers do Cholangiocarcinoma make up and type r they usually

A

10%
adenocarcinomas

329
Q

what is the most common type of primary liver disease

A

hepatocellular carcinoma

330
Q

risk factors for Cholangiocarcinoma (4)

A

IBD
Hep B and C
Parasitic fluke worms
PSC

331
Q

signs of Cholangiocarcinoma (4) and what is important to note about the symptoms for this cancer

A

Abdominal pain
Jaundice
Weight loss
Fevers
courvoisier’s sign (but more indicative of pancreatic cancer)
late symptoms presentation as the tumour grows slowly

332
Q

investigations for Cholangiocarcinoma (4)

A

1st line: abdo US/CT
GS: ERCP
diagnostic: biopsy (taken in ERCP)
blood markers: high CEA adn CA 19-9

333
Q

why can most patients with Cholangiocarcinoma not get surgery as a treatment and what r the stats for this

A

Surgery not possible in 70% of patients as they present late

334
Q

what is defined as a paracetamol overdose

A

Paracetamol ingestion >75mg/Kg

335
Q

what does paracetamol overdose lead to mostly

A

fulminant liver failure

336
Q

symptoms of paracetomal overdose (3)

A

Acute severe RUQ
Severe n+v

337
Q

pathophysiology of paracetamol overdose

A
  1. Due to the increased paracetamol, phase 2 pathway is saturated causing a build-up of NAPQI- (by- product of phase 1 detoxification)
  2. This is toxic and is normally counteracted by glutathione but in overdose glutathione stores are depleted which means NAPQI is not metabolised and causes damage
338
Q

function of N-acetylcysteine in paracetomol overdose treatment

A

increases availability of glutathione which reduces NAPQI toxic build up

339
Q

what is portal HPT

A

High pressure in the portal vein.

340
Q

prehepatic causes of Portal HPT (1)

A

Portal vein thrombosis

341
Q

intrahepatic causes of portal HPT (2) and where are each of them most common

A

Cirrhosis (MC in UK)
Schistosomiasis (common worldwide)

342
Q

post hepatic causes of portal HPT (3)

A

Budd chairi (hepatic vein obstruction)
RHS heart failure
Constrictive pericarditis

343
Q

pathophysiology of portal HPT starting with liver cirrhosis and ending with oesophageal varices

A

Cirrhosis= high resistance to flow
Leads to splanchnic dilation and compensatory high CO
Results in fluid overload in portal vein (10> bad) ( >12 very bad)
Results in collateral blood shunting to gastroesophageal veins leads to oesophageal varices

344
Q

symptoms of portal HPT (1)

A

Mostly asymptomatic

345
Q

when is portal HPT usually present

A

Present when oesophageal varices rupture

346
Q

what is the acute treatment for oesophageal varices (2)

A
  1. Resuscitation until haemodynamically stable
  2. Consider blood transfusion (Hb <70g/L)
347
Q

how to stop bleed in the case of treating oesophageal varices (3)

A
  1. IV Terlipressin
  2. Variceal banding
  3. transjugular intrahepatic portosystemic shunt
348
Q

what does transjugular intrahepatic portosystemic shunt do (1)and what is a side effect of this (1)

A

decreases portal pressure by shunting blood to side effect: hepatic encephalopathy

349
Q

how to prevent bleed in the case of treating oesophageal varices (3)

A
  1. BB (non-selective e.g., propranolol + nitrates
  2. Repeat variceal banding
  3. Last resort liver transplant
350
Q

what is AST and ALT a marker of 1

A

hepatocellular injury

351
Q

what is GGT and ALP a marker of

A

biliary duct injury

352
Q

what is INR and what does it stand for
what does high INR/PT mean

A

international normalised ratio
measure how long it takes for blood to clot
blood takes longer to clot

353
Q

what is budd chiari

A

hepatic vein obstruction

2A content- Sameera (21 decks)

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