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
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
3
Q
what r the two stages of WK syndrome
A
1.Wernicke’s encaphalopathy
2. Korsakoff syndrome:
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
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
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
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
8
Q
causes of WK syndrome (3)
A
mainly alcohol abuse
lack of thiamine in diet (eg crohns)
anorexia
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
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
11
Q
how is WK syndrome diagnosed (2)
A
diagnosis based on history and clinical examination
12
Q
treatment (1) for WK syndrome and when is this given (1)
A
oral or paraenteral thiamine
given on suspicion of condition
13
Q
differentials for WK syndrome (3)
A
alcoholic ketoacidoosis
chronic hypoxia
hepatic encephalopathy
14
Q
what is gilberts syndrome
A
body unable to process bilirubin fast enough
15
Q
what type of inheritence is gilberts
A
autosomal recessive
16
Q
what is gilberts syndrome the main cause of
A
hereditary jaundice
17
Q
what can trigger gilberts syndrome episodes (4)
A
dehydration
fasting
excess alcohol
hepatitis
18
Q
risk factors for gilberts 2
A
T1DM
male
19
Q
explain the pathophysiology of gilberts starting with the mutation and what does it cause
A
- mutation in UGT1A1 gene which removes instructions to make bilirubin UGT enzyme which is essential in removal of bilirubin from body
- this build up levels of unconjugated bilirubin in the blood,
- causing mild jaundice
20
Q
how is gilberts syndrome usually discovered
A
incidentally on tests
21
Q
what is the proportion of asymptomatics in gilberts syndrome
A
30% of people with gilbert’s r asymptomatic
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
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
24
Q
investigations for gilberts (3)
A
blood test
liver function test
sometimes a genetic test is required to confirm Gilbert’s syndrome
25
treatment for gilberts and crigler najjar 3
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
26
what is a hernia
protrusion of an organ through a muscle/ tissue wall weakness
27
what is a reducible and irreducible hernia
reducible: can be manually pushed back into place
irreducible: resists manual pushing back into place
28
what r the 3 subcategories of irreducible hernias
obstructed, strangulated and incarcerated
29
define obstructed hernia
: bowel contents cannot get though the part of the bowel that has herniated
30
define strangulating hernia and what three thigns can this cause
reduce blood supply to bowel, causing ischaemia, gangrene and perforation of the hernia
31
define incarcerated hernia
contents of hernia are stuck and cannot be pushed back into place (same r irreducible)
32
what r risk factors for hernias (3)
things that involve abdominal muscles eg chronic cough, constipation, heavy lifting
33
what r the 2 symptoms for hernias
pain (particularly if obstructed/ strangulated) and a lump on location
34
treatment for hernias (1)- what type
usually laparoscopic surgery
35
what is the most common type of hernia
Inguinal Hernia
36
what happens in inguinal hernias
bowel passes through inguinal canal
37
additional risk factors specific to inguinal hernias (2)
age and male
38
what is a femoral hernia
bowel hernia through the femoral canal
39
risk of femoral hernia and what is required to prevent this from occuring
high risk of being strangulating due to rigid femoral canal borders-> treatment required immediately to save the bowel from ischaemia
40
specific risk factors for femoral hernias (2)
occurs in females, elderly/middle ages
41
what is umbilical hernia
intestine herniates through the umbilical ring
42
specific risk factors for umbilical hernias (2)
common in young children/ infants or women with multiple previous pregnancies
43
what is an epigastric hernia
intestine herniates through the lines alba above the umbilicus
44
what is an incisional hernia and what causes it
hernia at the site of surgical scar after surgery
due to the surgical incision which weakened the abdominal muscles
45
what is the treatment (1)for incisional hernia and what is a risk of this treatment
treatment: mesh repair decreases recurrence but increases infection risk
46
what is a hiatal hernia
stomach hernia through diaphragm aperture
47
what r the two types of hiatal hernias and what % of cases belong to each
sliding or rolling
20% cases r rolling
80% cases r sliding
48
what r rolling hiatal hernias
where the lower gastro-osophageal junction remains the the abdomen but a bulge of stomach herniates up into the chest
49
what r sliding hiatal hernias and what is a consequence of this
where the lower gastro-osophageal junction slides up into the chest
acid reflux
50
investigations for hernias (1, diagnostic)
CT: for imaging
barium swallowing for diagnosis
51
what is spontaneous bacterial peritonitis
acute bacterial infection of ascitic fluid in peritoneum (also known as ascites) with no obvious source
52
what r the causes of SBP (1,3)
bacteria that normally live in intestine and enter the abdominal cavity eg E.coli, klebsiella and strep bacteria
53
risk factors for SBP (3)
cirrhosis
past history of spontaneous bacterial peritonitis
ascites
54
symptoms of SBP (6)
often asymptomatic
fever
abdominal pain/ tenderness
altered mental state
vomiting
GI bleeding
triple A ForGiVen
55
investigations for SBP (1, diagnostic)
diagnosed by an absolute neutrophil count of over 250cells/mm3 in ascitic fluid (ANC test)
ascitic fluid test for cell count and culture
56
treatment for SBP (2)
should be given antibiotic prophylaxis
albumin (particularly for patients with renal dysfunction)
57
what r the 3 metabolic liver disease
1. Haemochromatosis
2. Wilson’s disease
3. Alpha 1 antitrypsin
58
what does haemochromotosis cause
causes excess body iron
59
what type of inheritence is haemochromotosis and what is the most common cause
autosomal recessive disease
most common cause= hereditary haemochromatosis= autosomal recessive disease
60
what gene mutation is haemochromotosis closely linked with and what % of people have this mutation
ON WHAT CHROMOSOME
90% have mutation of HFE gene on chromosome 6
61
risk factors for haemochromotosis (5)
males (menstrual blood loss is preventative)
50 year olds
family history
T2DM
HEPATOMEGALY
starting today, here's more Fe
62
pathophysiology for haemochromotosis starting with gene mutation
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
63
symptoms of haemochromotosis (6)
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
64
investigations for haemochromotosis (4) and results
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
65
1st line treatment for haemochromotosis
venesection (regular removal of blood until ferritin is less than 50 micrograms) and then maintenance venesection to keep levels controlled
66
treatment for haemochromotosis if venesection is contraindicated
give desferrioxamine (chelating agent) which binds to free circulating iron and is excreted in the urine
67
changes in lifestyle for haemochromotosis (2)
reduce iron in diet and avoid fruits (contain vitamin C which can increased iron absorption)
68
what does wilsons disease cause
causes excess body copper
69
what type of inheritance is wilsons disease and what mutation is associated with it WHAT CHROMOSOME
autosomal recessive mutation of ATP78 gene on chromosome 13
70
how common is wilsons disease
rare
71
what age does wilsons affect patients
young patients (around 20 years old)
72
pathophysiology of wilsons starting with gene mutation
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
73
compare presentation of wilsons disease in children and adults
children tend to present with liver disease systems and adults present with CNS signs
74
symptoms of wilsons disease (split into 4 systems- 1 each)
hepatic symptoms= spider angiomata
neurological= Parkinsonism/ memory issues
opthalmological= Kayser Fleischer rings
renal symptoms: kidney caliculi
75
what is pathognomonic for wilsons and what is this
Kayser Fleischer rings: green/brown ring around cornea which r copper deposits
76
what r spider angiomata
small distended blood vessels, usually on chest
77
what r the 3 investigations for wilsons (6, diagnostic)
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)
78
why is there low serum copper in wilsons
copper is deposited in the tissues and not in the bloodstream
79
what is the 1st line treatment for wilsons, what is its function and side effects (3)
lifelong penicillanamine (copper chelating agent)- increases removal of copper
side effects: nausea, WCC decrease, Haemoglobin decrease
80
lifestyle change needed in treatment of wilsons (1)
avoid copper rich food eg mushrooms, shellfish, chocolate, nuts
81
treatment for severe liver disease/ end stage liver failure
liver transplant
82
what is alpha 1 antitrypsin deficiency
deficient/ defective alpha 1 antitrypsin enzyme production (A1AT)
83
inheritance of A1AD and how does it affect heterozygous
autosomal recessive (but can manifest in those who r heterozygous)
84
mutation in A1AD on what chromosome
mutation of protease inhibitor gene (PI) on chromosome 14
85
what is the presentation of A1AD similar to
COPD symptoms
86
risk factors for A1AD (3)
young/ middle ages
male
little/no smoking history
87
symptoms of A1AD (4)
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
88
pathophysiology of A1AD starting with A1AD normal function and where is it made and ending with 2 organs that r affected
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
89
what is a consequence of A1AD deposition in the liver
increases risk of hepatocellular carcinoma
90
how is A1AD self exacerbating
causes A1AD deposition in the liver which causes cirrhosis which reduces A1AT production further (A1AD is produced in liver)
91
investigations (6) and results for A1AD
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
92
treatment for A1AD (3)
stop smoking
manage emphysema- inhalers (SABA/LABA)
consider HEPATIC decompensation patients for liver transplantation
93
what is primary biliary cholangitis
autoimmune destruction of intralobular hepatic bile ducts
94
risk factors for PBC (6)
female (90% cases in women)
40-50 years
smoking
family history
many previous UTIs
other autoimmune disease eg SLE
95
pathophysiology of PBC 3
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
96
symptoms for PBC (5)
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)
97
what is pruritus
severe itching of the skin
98
explain hepatospenomegaly
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
99
why does xanthelasma occur in PBC
due to disruption to liver metabolism caused by cholangitis (causes deficiency of lipase which normally breaks down lipids)
100
investigations for PBC (5)
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
101
what is the diagnosis criteria for PBC
diagnosis requires 2 out of the following:
1. raised ALP
2. positive AMA (antimitochondrial antibodies)
3. diagnostic liver biopsy
102
treatment for PBC (1st line, 2)
1st line: lifelong ursdeoxycholic acid (for symptomatic)- bile acid analogue which dampens the immune response
2. for pruritis-> give colesyramine
3. vitamin ADEK supplements
103
complications of PBC (4)
liver cirrhosis
malabsorption of fats and vitamin ADEK due to cholestasis (therefore steatoarrhea),
osteomalacia/ penia (common)
coagulopathy
104
what is steatorrhea and what causes this
increase in fat excretion in stool due to fat malabsorption
105
why does osteomalacia/ penia occur in PBC
cholangitis interferes with vitamin D metabolism which leads to decreased bone formation
106
what is coagulopathy and why does coagulopathy occur in PBC
bleeding condition when blood’s ability to coagulate is impaired
cirrhosis of liver impairs its ability to make clotting factors
107
what is PSC
autoimmune destruction of intra and extralobular hepatic duct
108
risk factors for PSC (3)
male (60% cases in men)
40-50 years old
strong link to IBD (esp ulcerative colitis)- 80% of PSC patients have IBD
109
compare progression rate of PBC and PSC and explain why
PSC progresses faster as it affects extralobular ducts as well so it progresses faster than PBC
110
what r the symptoms of PSC (5)- 4 same as PBC
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
111
3 investigations and results for PSC (5, GS)
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)
112
treatment for PSC
ursdeoxycholic acid
cholestyramine for pruritus
fat soluble ADEK supplements
113
what is ursleoxycholic acid used for in PSC
not as effective as a treatment but decreases colon cancer risk and improves liver function tests
114
compare location of PSC and PBC
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)
115
compare smoking as a risk factor in PBC vs PSC
PBC usually occurs in smokers, PSC usually occurs in non-smokers
116
compare gender as a risk factor in PBC vs PSC
PBC usually occurs in women (90% cases r female), and PSC is male (60% cases r male)
117
is PSC or PBC a premalignant disease and what 2 cancers does it increase the risk of
PSC is a premalignant disease (increases risks oAf colon/ bile duct cancers)
118
compare the typical presentation course of PBC and PSC
PSC presents differently in different patients but PBC has a typical disease source
119
compare what PBC and PSC is associated with (1 each)
PBC is associated with other autoimmune conditions, unlike PSC which is associated with IBD
120
what is acute pancreatitis
rapid onset inflammation of pancreas
121
how many cases have mild acute pancreatitis and how many develop severe complications
pancreatitis is mild in 80% of cases but severe complications can develop in 20% of cases
122
causes of acute pancreatitis (mneumonic)
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
123
what r the 2 main causes of pancreatitis and state the % and what type
Gallstones (50% of acute cases)
Ethanol (80% of chronic cases)
124
explain the pathophysiology of acute pancreatitis, starting with inflammation of pancreatic acinars 4. How to gallstones exacerbate pancreatitis 1
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
125
presentation of acute pancreatitis (8)
2 signs, 2 non specific,
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
126
investigations for acute pancreatitis (4)
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
127
compare lipase and amylase as a diagnostic for acute pancreatitis
high lipase is more specific to pancreatitis than amylase but less routine
128
what r the 2 types of pancreatic scoring systems what do they involve
APACHE 2- assess severity within 24 hours (uses measurements like CRP)
Glasgow and Rowson score- production of severe attack only after 48 hours
129
what is the diagnosis criteria for acute pancreatitis
requires at least 2 of the following:
1. characteristic symptoms/ signs
2. increase in amylase and lipase
3. radiological evidence (eg AUSS)
130
treatment for acute emergency pancreatitis (5)
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)
131
differential for acute pancreatitis
abdominal aortic aneurysm
132
what is a complication of acute pancreatits and why is an issue
systemic inflammatory response syndrome
this is life-threatening
133
state the criteria of SIRS
criteria= 2 of the following:
tachycardia (bpm 90+)
tachypnoea (RR of 20+)
pyrexia (38+)
increased white cell count
134
what is chronic pancreatitis and what occurs to the pancreas during this time
defined as at least a 3 month history of pancreatic deterioration
causes irreversible pancreatic damage due to fibrosis
135
causes of chronic pancreatitis (5)
alcohol (most common)
chronic kidney disease
cystic fibrosis
recurrent acute pancreatitis
pancreatic duct blockage (stones/tumor
136
symptoms of chronic pancreatitis (6)
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
137
investigations for chronic pancreatitis (2, diagnostic)
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)
138
treatment for chronic pancreatitis (3)
1. alcohol cessation
2. abdominal symptoms pain is treated with NSAIDs
3. pancreatitis supplements eg enzymes, insulin for DM
139
differential for chronic pancreatitis 1
pancreatic cancer of head/ tail
140
what is ascites, how much is it
fluid collection in peritoneal cavity
defined as fluid of more than 25ml
141
what is the physiologically normal amount of ascitic fluid for men and women to have
men usually have no intraperitoneal fluid, women can have up to 20ml of intraperitoneal fluid depending on the stage of their menstrual cycle
142
what is the most common cause of ascites 1
cirrhosis
143
what does ascitic fluid contain 4
albumin, lipids, bile acids and WBCs
144
signs of ascitic fluid (50
flank bulging in recline position
puddle sign test
shifting dullness test
fluid thrill test
jaundice (liver symptom)
145
what r the 3 investigations for ascitic fluid (2, diagnostic)
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
what does SAAG stand for and what does it measure
why is this useful for ascites investigations
serum ascites albumin gradient
test to compare albumin concentration in ascitic fluid and in patient serum (indicates the cause of the ascites)
147
what is a high SAAG gradient (value, what does it indicate the cause is)
4
>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
what protein values does high SAAG have and why is this and what is it called
<30g/L protein (low)
due to fluid being pushed out of circulation = high albumin in serum, low in ascitic fluid
transudate
149
what protein values does low SAAG have and why is this and what is it called
>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
what is a low SAAG gradient (value, what does it indicate the cause is)
4
<1.1g/dL
indicates osmotic pressure imbalance
caused by infection (TB), peritoneal malignancy (metastasis, often from ovarian cancer), pancreatitis, kidney failure
151
what is the treatment for high SAAG (3)
1. salt restricted diet
2. diuretics (spironolactone)
3. paracentesis (removal of fluid from peritoneal cavity)
152
treatment for low SAAG (1) and why (1)
repeat paracentesis
doesn’t respond well to diuretics or salt restriction
153
complication of ascites
SBP
154
what r the 3 types of biliary tract disease
Biliary Colic
Cholecystitis
Ascending Cholangitis
155
what r the 5 risk factors for biliary tract diseases (5 Fs + 2)
fat (BMI of 30+)
female
forty (40+ years old)
fertile (previous pregnancies/ pregnancy)
fair
family history
T2DM
156
what is biliary colic, when does it occur and does it involve inflammation
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
symptoms of biliary colic (2)
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
investigation for biliary colic 1
1st line: abdominal USS for imagery of gallstones (diagnostic)
159
treatment for biliary colic (4)
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
what is cholecystitis, what is its cause and does it involve inflammation
inflammation of the gallbladder
due to gallstones blocking the cystic duct which causes bile build up
yes
161
symptoms of choelscystitis (5
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
investigations for cholescystitis (3)
FBC: leukocytosis, neutrophillia
liver function test is normal
abdominal USS shows thicken gallbladder wall (3mm)
163
treatment for cholecystitis (2)
laparoscopic cholecystectomy surgery within a week (ideally 72 hours)
pre surgery: IV fluids, analgesia, antibiotics if required
164
what is ascending cholangitis, what type of condition is it and does it involve inflammation
inflammation of bile duct tree due to bacteria from intestine
life-threatening infection
yes
165
symptoms of ascending cholangitis (3)
right upper quadrant pain
fever
cholestatic/ obstructive jaundice
166
investigations for ascending cholangitis (4)
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
treatment for ascending cholangitis (2)
ERCP: cleans the bile duct then laparoscopic cholecystectomy once stable to prevent recurrence
168
1 complication of ascending cholangitis
risk of sepsis
169
what is acute liver failure
liver injury in a person with a previously normal liver
170
what r the 3 characteristics of acute liver failure
Coagulopathy (derangement in clotting) (>1.5INR)
Hepatic encephalopathy (HE)
Jaundice
171
what r the 3 types of acute liver failure
hyperacute, acute, subacute
172
what is hyperacute liver failure
Hepatic Encephalopathy w/7 days of noticing jaundice
173
what is acute liver failure (subtype)
hepatic encephalopathy w/in 8-28 days of noticing jaundice
174
what is subacute liver failure
hepatic encephalopathy w/in 5-26 weeks of noticing jaundice
175
compare the prognosis for all three types of acute liver disease
best prognosis= hyperacute then acute and worst= subacute
176
what is fulminant hepatic failure and its onset
sudden onset liver failure due to massive necrosis of liver cells
177
cause and histological slides for fulminant hepatic failure
Most common cause of it is paracetamol overdose
Histologically- multiacinar necrosis
178
what is the definition of acute on chronic liver failure
Abrupt decline in patient w/chronic liver symptoms
179
causes of acute liver failure (5)
Viral: Hep A,B,Ebv
Drugs- paracetamol, alcohol
Hepatocellular carcinoma
Metabolic- Wilsons, hemochromatosis, A1ATD
Budd-chairi syndrome (vascular)
180
key presentation of acute liver failure (3) and other general symptoms (3)
KEY:
Jaundice
Coagulopathy
Hepatic encephalopathy (west haven criteria 1-4)
OTHER:
Anorexia
Nausea
Malaise (general feeling of discomfort)
181
name the hepatic encaphalopathy grading system and explain each stage (remember analogy of tired angry med student coming into lectures on a monday morning)
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
pathophysiology of acute liver failure 2
damage and loss of hepatic cells
183
4 investigations for acute liver failure
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
treatment for acute liver failure (4)
ABCDE
fluid
analgesia
treat underlying cause
185
treatment for paracetamol overdose (2)
activated charcoal
N acetylcysteine
186
how is hepatic encephalopathy treated 1 and how does it work
Lactulose (increases NH3 excretion)
187
how is haemorrhage treated 1
Vit K
188
how is sepsis treated 1
sepsis 6 pathway
189
how is increased intercranial pressure treated
IV Mannitol
(manny has a toll on u )
190
what is budd chairi syndrome and what does it cause
blocked/ narrowed heptic veins by clot
causes blood to back up into the liver
causes hepatomegaly
191
what is most common type of primary liver cancer
Hepatocellular carcinoma
192
explain the pathophysiology of chronic liver failure starting with hepatitis (4)
hepatitis
fibrosis
then compensated cirrhosis (scars)
then decompensated cirrhosis (end stage liver failure)
193
define chronic liver failure 1
progressive liver damage over 6 months caused by repeated insults to the liver
194
what r the causes of chronic liver failure (5)
alcohol liver disease
non-alcoholic liver disease
viral: hep B and C
metabolic: wilsons
autoimmune: PBC, PSC
195
risk factors of chronic liver disease (4)
Alcohol
Obesity
T2DM
Drugs
196
compare compensated and decompensated cirrhosis
compensated- asymptomatic liver carries out normal function
decompensated- end stage liver failure
197
signs of decompensated liver disease (5)
Jaundice
Hepatic encephalopathy
Coagulopathy
Ascites (due to Portal HTN)
GI bleeding- (due to rupture of oesophageal varices)
198
name the system and explain the factors involved in assessing chronic liver failure
Child pugh score system
assessing prognosis and extent for chronic liver failure
ABCDE:
A-Albumin
B-bilirubin
Clotting- PT
Distension- Ascites
E- encephalopathy
199
state the Child Pugh score for survival rates
Classes score A,B,C
A= 100% 1 year survival
B= 80% 1 year survival
C= 45% 1 year survived
200
What measures the severity of ESLF (IN FULL) and what is the purpose of it
MELD score- model for end stage liver disease
for transplant planning
201
signs of chronic liver failure (10)
Caput medusae
Palmar erythema
Dupuytrens contracture
Spider angioma
Gynaecomastia
Jaundice
Ascites
Hepatic encephalopathy
Portal HTN
Fetor hepaticus
APCDPFGHS
202
investigations for chronic liver failure (2)
liver biopsy: differentiates between cirrhosis and fibrosis
LFT: high AST and ALT
203
treatment for chronic liver failure (2)
1. lifestyle mods: stop alcohol
2. consider liver transplant
204
what is caput medusa and cause
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
what is palmar erythema
palms turn red
206
what is Dupuytrens contracture
fingers bend towards hand
207
what is Spider angioma
cluster of small red blood vessel
208
what is Gynaecomastia
man boobs
209
what is fetor hepaticus
rotten eggs and garlic smell breath
210
what 3 symptoms of chronic liver disease link with issues with oestrogen regulation
palmar erythema, spider angioma, gynaecomastia
211
what causes hepatic encephalopathy, explain the pathophysiology and what can it lead to
Problems in detoxification. Accumulation of NH3 which is normally detoxified by UREA cycle. This crosses BBB and causes confusion.
212
how does liver failure cause ascites
Low levels of albumin and portal HTN cause fluid to leak out in the abdomen into the peritoneum.
213
how can liver failure lead to hypoglycaemia
Glucose metabolism is impaired
214
why can liver failure lead to bleeding disorders?
Liver is responsible for the production of clotting factors (All except 3,4 and 8)
215
what r the 3 stages of alcohol liver disease
1. Steatosis (fatty liver, undamaged)
2. Alcoholic hepatitis (inflammation and necrosis- Mallory bodies)
3. Alcoholic cirrhosis
216
risk factors for alcohol liver disease 4
Prolonged alcohol consumption
Hep C
Obesity
Female sex (susceptible at smaller units, quicker onset)
217
pathophysiology of ALD and what/ how are the markers detected
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
signs of alcohol liver disease (early and late stages)- 2 each
Early stages- very little signs (N+V+ diarrhoea)
Later stages- chronic liver failure + alcohol dependency
219
what r the 2 alcohol dependancy questionnaires
CAGE
Audit
220
explain the CAGE questionaire and what does it measure
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
221
what is the AUDIT test
10qs used the First line
222
investigations and results for chronic liver failure (3) 6,2,1
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
treatment for chronic liver failure (4)
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
what condition needs to be fulfilled for liver transplant for those with ALD
must abstain from alcohol for 3+ months before consideration
225
complications of chronic liver disease (5- into 3 categories)
hepatocellular carcinoma
Hepatic encephalopathy, jaundice (due to hepatocellular insufficiency)
oesophageal varices, Ascites (due to portal HPT)
226
what is a mallory weiss tear and what causes it
oesophageal tear
(due to episodic vomiting)
227
what is non alcoholic fatty liver disease
Fat deposition in the liver which can’t be attributed to alcohol
228
4 stages of NAFLD
Steatosis
Steatohepatitis
Fibrosis
Cirrhosis
229
risk factors for NAFLD (5)
Obesity
HTN
Hyperlipidaemia
T2 DM
Drugs (NSAIDs, amiodarone)
230
presentation of NAFLD (1)
Typically, asymptomatic- any findings are incidental
231
investigations and results for NAFLD (3)
LFT: high bilirubin, low albumin, high PT/INR
FBC: thrombocytopenia and anaemia
US: 1st line for people suspected to have NAFLD
232
what happens to albumin if biliurubin is high
albumin will be low
233
what can be done to assess risk of fibrosis in NAFLD (1)
non-invasive scoring system
eg Fib 4
234
treatment for NAFLD (3)
1. lower BMI
2. control risk factors (eg statins, metformin , ACEi)
3. vitamin E (helps histological appearance of fibrotic tissue
235
complications of NAFLD (5)
Ascites
Hepatocellular carcinoma
Hepatic encephalopathy
Portal HTN
Oesophageal varices
236
what is hepatitis and what causes it
Inflammation of the liver as a result of viral replication within hepatocytes
237
what is Hep A structure (2) and method of spread (1)
Non-enveloped Single stranded RNA.
Picornavirus
Faeco-oral route
238
risk factors for Hep A (2)
Travel: travelling to endemic areas
Shellfish
239
Where does Hep A replicate in the body 1 and why is is self limiting 1
Replicates in liver
excreted in bile so self-limiting
240
4 phase of a Hep A infection
Incubation
Prodromal
Icteric
Convalescent
241
signs of Hep A infection (3 steps)
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
investigations for Hep A (3)
Serology: HAV-IgM- acutely infected
LFT: high bilirubin (icteric phase) , high ALT and AST
Bloods- high ESR+ leukopenia
243
treatment for Hep A and is there a vaccination available (1,1)
Supportive management
Travellers’ vaccine available
244
complication of Hep A infection
Fulminant (rapid) liver failure
245
what is Hep E structure (1) and method of spread (1)
Non-enveloped single stranded RNA
Faeco-oral route
246
cause of Hep E (1)
Undercooked pork
247
pathophysiology of Hep E (2)
Acute inflammation
Usually self-limiting
248
symptoms of Hep E (1)
95% of cases are asymptomatic, as usually self-limiting
249
investigations for Hep E (2)
Serology: HEV IgM positive
PCR: HEV RNA detected
250
treatment for Hep E 1
supportive treatment
251
complications of Hep E infection (2)
Chronic Hep E disease in immunosuppressed
fulminant liver disease
252
Hep D structure (1) and method of spread
Enveloped single stranded RNA
Blood borne
253
pathophysiology of Hep D (2)
Incomplete requires HBV for assembly
Manifests as co-infection (IgM HDV + IgG HBV)
254
Hep C structure 1, type of virus 1 and method of spread (1)
Single stranded RNA
Flavivirus
Blood borne
255
causes of Hep C infections (2)
Sexually transmitted
IV drug users
256
symptoms of Hep C (3)
1. Acutely asymptomatic
2. few patients have flu like symptoms
3. later presentation as chronic liver failure signs
257
investigations for Hep C (2)
Serology: HCV antibody test
PCR- HCV RNA
258
treatment for Hep C (2)
Direct acting Antivirals (DAA) oral ribavarin
259
complication of Hep C infections (1)
30% cases progress to chronic liver failure
260
what is the structure of Hep B 1 what type of virus is it and method of spread (1)
Double stranded DNA
HepaDNAvirus
Blood borne
261
how is Hep B transmitted (4)
Needles (tattoo, IVDU)
Sexual
Vertical (mother-> child)
Horizontal (between children)
262
what two bodily fluids can Hep B be found in
semen and saliva
263
risk factors for Hep B (4)
IVDU
Sexually (in particular MSM)
Dialysis patients
Healthcare workers
264
pathophysiology of Hep B
Acute infection infects hepatocyte. Cellular response usually clears it.
265
what is defined as chronic Hep B infection and what can long term inflammation cause
Chronic HBV if HBsAg >6 months.
Inflammation can last 10 yrs. -> cirrhosis.
266
symptoms of Hep B (5)
dark urine
pale stool
hepatosplenomegaly
urticaria (hives)
arthralgia (joint stiffness)
267
Define the following
HBsAg
HBsAb
HBcAg
HBc IgM
HBc IgG
HBeAg
HBeAb
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
What is the serology of an acute Hep B infection
HbS Ag and anti HBC Ab IgM
269
What is the serology of an chronic Hep B infection
HbS Ag and anti HBC Ab IgG
270
What is the serology of a person vaccinated against Hep B
anti HbS Ag
271
What is the serology of a person with natural immunity against Hep B
Anti HBS Ag, anti HbC Ag IgG
272
treatment for Hep B infection and is there a vaccine available (1,1)
Pegylated interferon alpha 2A
Vaccine available given to babies- (6-in-1 at 8 weeks)
273
complications of Hep B infection (2)
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
what is autoimmune hepatitis and what does this cause
body attacks hepatocytes
chronic liver inflammation
275
risk factors for autoimmune hepatatis (4)
-females
-other autoimmune conditions eg hashimotos
-VIRAL INFECTION
-HLA-DR3/4
276
state the 2 types of autoimmune hepatatis
type 1 and 2
277
what is T1 autoimmune hepatitis associated with (2) and what proportion of cases is this and who does this usually affect (1,1)
ANA (anti-nuclear antibodies)
ASMA (anti-smooth muscle antibodies)
80% of all cases
adult women
278
what is T2 autoimmune hepatitis associated with (2) and what proportion of cases is this and who does this usually affect (1,1)
ALC-1 (anti liver cystol antibodies)
ALKM-1 (anti liver kidney microsome antibodies)
20% of cases
younger females
279
signs and symptoms of autoimmune hepatitis (2)
25% of all cases asymptomatic
May have evidence of liver failure e.g. fever, hepatosplenomegaly, jaundice
280
investigations for autoimmune hepatitis (2 tests, 2 and 4 markeres)
LFT: elevated ALT and AST
Serology:
ANA, ASMA +/- ALC-1 and ALKM-1
281
what is the first and second line treatment for autoimmune hepatitis
1. immunosuppression
eg prednisolone and azathioprine
2. transplant
282
what is a prevention for autoimmune hepatitis (2)
hep a and b vaccines
283
where is piecemeal nerosis seen in histology (1)
hepatitis
284
what is cirrhosis
pathological process involving fibrosis and regeneration of nodules due to damage to healthy liver tissue
285
causes of cirrhosis (5)
Alcohol abuse
Non-alcoholic fatty liver disease
Hep B and C
Autoimmune conditions (PBC, PSC, Autoimmune Hep)
Genetic metabolic (Wilsons disease, A1ATD)
286
investigations for cirrhosis (GS, 1 other with 5 results)
GS: liver biopsy- confirms diagnosis and severity
LFT:
Low albumin
Low platelets, INR/PT high
High AST/ALT
287
treatment for cirrhosis (3)
1. treat underlying cause
2. conservative approach- analgesia, fluids, good nutrition, alcohol abstinence
3. liver transplant
288
complications of cirrhosis (1) and what can this complication lead to (2)
Portal hypertension:
-Ascites
-Oesophageal varices
289
explain the 6 steps of bilirubin metabolism from Hb to urobilinogen
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
what happens to urobilinogen at the terminal ileum (3
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
define jaundice
Yellowing of skin/eye due to accumulation of conjugated/unconjugated bilirubin
292
what is jaundice a sign of (1)
liver dysfunction
293
what is prehepatic jaundice and what causes it generally 1
High unconjugated bilirubin- due to increased RBC breakdown
294
what is intraheptic jaundice
High conjugated and unconjugated bilirubin
295
what is post hepatic jaundice and what causes it generally 1 and what r the typical signs of this (2)
High conjugated bilirubin due to biliary obstruction
pale stool and dark urine
296
causes of prehepatic jaundice (5)
Sickle cell
G6PD deficiency- Glucose-6-phophate dehydrogenase
Thalassemia
Malaria
GILBERTS syndrome
297
causes of intrahepatic jaundice (4) and what is special about this
HCC
ALD/NAFLD
Hepatitis
PBC + PSC
causes may be mixed
298
causes of posthepatic jaundice (6)
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
what are the 4 signs of jaundice (only state)
Courvoisier’s sign
Charcots triad
Reynolds pentad
Murphy's sign
300
what is Courvoisier’s sign (2) and what is the mostly likely cause (2) and location (1)
painless jaundice + palpable GB (most likely due to pancreatic cancer or cholangiocarcinoma)
60-70% occur at the head of the pancreas
301
what is reynold's pentad
Signs and symptoms associated w/ascending cholangitis
Fever, RUQ pain, Jaundice, confusion, hypotension
JCH, For Real thats how u feel
302
what is murphys sign, what is the test and what is a + test indicative of
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
what is the charcot triad (3)
biliary colic, cholecystitis, ascending cholangitis
304
state whether all three conditions of the charchot triad show fever, RUQ pain and jaundice or not (1,2,3)
biliary colic- RUQ
cholecystitis- fever, RUQ
ascending cholangitis- fever, RUQ, jaundice
305
what r the investigations for jaundice (1, 6, 2)
1st line: US
LFT: high bilirubin, low albumin, PT/INR, AST/ALT +, GGT and ALP +
urine: bilirubin and urobilinogen
306
what is the normal urine bilirubin and urobilinogen 2
low bilirubin
positive urine urobilinogen
307
what r the urine results for biliary obstruction 2
+ urine bilirubin
low urine urobilinogen
308
what r the urine results for hepatic disease 2
+ urine bilirubin
low urine urobilinogen
309
what r the urine results for haemolysis 2
high urine bilirubin
high urine urobilinogen
310
what r the 3 types of hepatobiliary cancers
pancreatic cancer
Hepatocellular carcinoma
Cholangiocarcinoma
311
what type of pancreatic cancer is the most common and where do these affect
pancreatic ductal adenocarcinomas
affect the head of the pancreas
312
risk factors for pancreatic cancer (6)
Male
Smoking
Alcohol
DM
Chronic pancreatitis
Family history
313
what proportion of pancreatic cancers affects the head, body and tail
60% head
25% body
15% tail
314
signs of pancreatic cancer 4 and which is mosts pathognomonic
Courvoisier’s sign (MOST P!!)
epigastric pain radiating to the back, relived by sitting forward
trousseaus sign of malignancy
315
what is Trousseau’s sign of malignancy
non specific episodes of vessel inflammation + clots in different parts of the body
316
investigations for pancreatic cancer (1st, GS, 1)
1. abdominal US (1st line)
2. pancreatic CT (GS)
3. CA 19-9 tumor marker positive (non diagnostic)
317
treatment for pancreactic cancer
1. surgery if little metastasis and post operative chemo
2. pallitive care if metastises
318
what is the prognosis for survival with pancreatic cancer
Very poor prognosis
5yr survival= 3%
319
what is is most common type of Primary hepatocyte neoplasia and what proportion of cases does this make up
hepatocellular carcinoma
90% of all primary liver cancers
320
risk factors for hepatocellular carcinoma (2)
Hep B and C
Cirrhosis from ALD/ NAFLD/hemochromatosis
321
explain the pathophysiology of hepatocellular carcinoma (2) including metastasising locations
1. Cancer presents as nodules throughout the liver
2. Can metastasise via hepatic or portal veins to the lymph nodes, bones and lungs
322
signs of hepatoocellular carcinoma (3)
1. signs of liver failure eg jaundice, ascites, HE
2. cancer signs eg weight loss, tired all the time
3. irregular hepatomegaly
323
investigations for Hepatocellular carcinoma (1st line, GS, 1)
1st line: USS
GS: CT
high serum alpha fetoprotein marker in blood
324
treatment for Hepatocellular carcinoma 1
1. surgical resection of tumor
325
prevention for Hepatocellular carcinoma 1
HBV vaccine
326
why r biospsys avoided in hepatocellular cancers despite the fact that they r diagnostic
to prevent seeding of tumour
327
what r cholangiocarcinomas
cancer of the bile ducts
328
what proportion of primary liver cancers do Cholangiocarcinoma make up and type r they usually
10%
adenocarcinomas
329
what is the most common type of primary liver disease
hepatocellular carcinoma
330
risk factors for Cholangiocarcinoma (4)
IBD
Hep B and C
Parasitic fluke worms
PSC
331
signs of Cholangiocarcinoma (4) and what is important to note about the symptoms for this cancer
Abdominal pain
Jaundice
Weight loss
Fevers
courvoisier's sign (but more indicative of pancreatic cancer)
late symptoms presentation as the tumour grows slowly
332
investigations for Cholangiocarcinoma (4)
1st line: abdo US/CT
GS: ERCP
diagnostic: biopsy (taken in ERCP)
blood markers: high CEA adn CA 19-9
333
why can most patients with Cholangiocarcinoma not get surgery as a treatment and what r the stats for this
Surgery not possible in 70% of patients as they present late
334
what is defined as a paracetamol overdose
Paracetamol ingestion >75mg/Kg
335
what does paracetamol overdose lead to mostly
fulminant liver failure
336
symptoms of paracetomal overdose (3)
Acute severe RUQ
Severe n+v
337
pathophysiology of paracetamol overdose
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
function of N-acetylcysteine in paracetomol overdose treatment
increases availability of glutathione which reduces NAPQI toxic build up
339
what is portal HPT
High pressure in the portal vein.
340
prehepatic causes of Portal HPT (1)
Portal vein thrombosis
341
intrahepatic causes of portal HPT (2) and where are each of them most common
Cirrhosis (MC in UK)
Schistosomiasis (common worldwide)
342
post hepatic causes of portal HPT (3)
Budd chairi (hepatic vein obstruction)
RHS heart failure
Constrictive pericarditis
343
pathophysiology of portal HPT starting with liver cirrhosis and ending with oesophageal varices
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
symptoms of portal HPT (1)
Mostly asymptomatic
345
when is portal HPT usually present
Present when oesophageal varices rupture
346
what is the acute treatment for oesophageal varices (2)
1. Resuscitation until haemodynamically stable
2. Consider blood transfusion (Hb <70g/L)
347
how to stop bleed in the case of treating oesophageal varices (3)
1. IV Terlipressin
2. Variceal banding
3. transjugular intrahepatic portosystemic shunt
348
what does transjugular intrahepatic portosystemic shunt do (1)and what is a side effect of this (1)
decreases portal pressure by shunting blood to side effect: hepatic encephalopathy
349
how to prevent bleed in the case of treating oesophageal varices (3)
1. BB (non-selective e.g., propranolol + nitrates
2. Repeat variceal banding
3. Last resort liver transplant
350
what is AST and ALT a marker of 1
hepatocellular injury
351
what is GGT and ALP a marker of
biliary duct injury
352
what is INR and what does it stand for
what does high INR/PT mean
international normalised ratio
measure how long it takes for blood to clot
blood takes longer to clot
353
what is budd chiari
hepatic vein obstruction
