GI Flashcards

1
Q

types of liver injury

A

acute

chronic

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2
Q

acute liver injury consequences

A

recovery

liver failure

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3
Q

acute liver injury causes

A
viral (A,B, EBV)
drug
alcohol
vascular
obstruction
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4
Q

presentation of acute liver injury

A
malaise
nausea
anorexia
jaundice
(rarer=confusion, bleeding, hypoglycaemia)
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5
Q

presentation of chronic liver injury

A
ascites
oedema
varices
malaise
anorexia
easy bruising
itching
(rarer=jaundice, confusion)
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6
Q

jaundice

A

raised serum bilirubin

unconjugated or conjugated

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7
Q

unconjugated jaundice

A

pre-hepatic

e.g. gilberts, haemolysis

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8
Q

conjugated jaundice

A

hepatic/post hepatic/cholestatic
e.g. liver disease (hepatic)
bile duct obstruction (post-hepatic)

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9
Q

cholestatic (hepatic/post-hepatic) jaundice presentation

A

dark urine
pale stools
itching
abnormal liver tests

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10
Q

pre hepatic jaundice presentation

A

normal urine, stools and liver tests

no itching

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11
Q

liver disease causesand cholestatic jaundice

A

hepatitis- viral, drug, immune, alcohol
ischaemia
neoplasm
congestion

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12
Q

obstruction causes and cholestatic jaundice

A

gallstone
stricture- malignant, ischaemic, inflammatory
blocked stent

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13
Q

gallstones

A

70% cholesterol, 30% pigment, can have calcium
most form in gallbladder
1/3 of women over 60

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14
Q

gallstone risk factors

A

female
fat
fertile
liver disease, ileal disease, TPN

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15
Q

bile duct stone presentation

A

biliary pain, obstructive jaundice, cholangitis, pancreatitis
No cholecystitis

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16
Q

gallbladder stones presentation

A

biliary pain, cholecystitis
maybe obstructive jaundice
No cholangitis and pancreatitis

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17
Q

management of gallbladder stones

A

laparoscopic cholecystectomy

bile acid dissolution therapy, <1/3 success

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18
Q

management of bile duct stones

A

ERCP w/ sphincterotomy and:
removal (basket/balloon)
crushing (mechanical/laser)
stent placement

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19
Q

drug induced liver injury

A

1/10,000 patients/year
0.1-3% of hospital admissions
30% of acute hepatitis
>65% of acute liver failure

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20
Q

types of drug induced liver injury

A

hepatocellular
cholestatic
mixed

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21
Q

drugs commonly involved in liver injury

A

antibiotics- 32-45% (augmentin, ethryomycin)
CNS drugs- 15% (chlorpromazine, valproate)
immunosuppressants- 5%
analgesics-5-17% (diclofenac)
GI drugs- 10% (PPIs)
dietary supplements- 10%
multiple drugs- 20%

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22
Q

drugs not commonly involved in liver injury

A
low dose aspirin
NSAIDS (not diclofenac)
beta blockers
HRT
ace inhibitors
thiazides
calcium channel blocker
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23
Q

paracetamol induced liver failure: management

A

N acetyl cysteine

supportive treatment to correct: coagulation defects, renal failure, hypoglycaemia, fluid/electrolyte/acid-base balance

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24
Q

paracetamol induced liver failure: severity indicators

A

late presentation, NAC is less effective >24 hours
acidosis pH<7.3
prothrombin time >70 sec

consider liver transplant otherwise mortality is 80%

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25
signs of liver failure
leukonychia- white nails spider naevus ascites
26
alcoholic liver disease
main cause of liver death in UK only 10-20% of heavy drinkers get ALD 25% of sufferers stop drinking, 25% reduce poor outcome- 10 year survival= 25%
27
alcoholic liver disease: pathogenesis
hepatocytes balloon- mediated by neutrophils injured liver cells accumulate cytoskeletal protein changes in how the cells metabolise and produce fat- they accumulate fat (steatosis) fibrosis occurs
28
portal hypertension
increased hepatic resistance | increased splanchnic blood flow
29
portal hypertension causes
cirrhosis fibrosis portal vein thrombosis
30
portal hypertension: consequences
varices- oesophageal, gastric | splenomegaly
31
liver transplants and alcoholic liver disease
100/760 liver transplants/year in uk (limited by liver supply) 4000 deaths from ALD in UK/year
32
treatment for alcohol withdrawal
lorazepam
33
why are liver patients vulnerable to infection
impaired reticulo-endothelial function reduced opsonic activity leukocyte activity permeable gut wall
34
sites vulnerable to infection in those with liver disease
skin lungs (pneumonia) urinary tract septicaemia spontaneous bacterial peritonitis
35
spontaneous bacterial peritonitis and liver disease
most common infection in cirrhosis | diagnosis based on neutrophils in ascitic fluid
36
causes of renal failure in liver disease
``` infection GI bleeding myoglobinuria rental tract obstruction drugs (NSAIDS, diuretics, ace inhibitors) ```
37
coma in patients with chronic liver disease
hepatic encephalopathy- caused by ammonia hypoglycaemia intracranial event
38
cirrhosis
represents end stage liver disease residual nodules of hepatocytes constant replication of hepatocytes in this condition puts them at risk of mutations and neoplasia
39
some consequences of liver dysfunction
malnutrition coagulopathy- impaired coagulation factor synthesis, vitamin k deficiency endocrine changes hypoglycaemia
40
causes of chronic liver disease
``` alcohol non-alcoholic steatohepatitis viral hepatitis immune metabolic vascular ```
41
types of hepatitis
viral- A, B, C, CMV, EBV drug induced auto immune alcohol
42
main autoimmune diseases of the liver
autoimmune hepatitis primary biliary cholangitis primary sclerosing cholangitis
43
primary sclerosing cholangitis: raised globulins
variable
44
primary sclerosing cholangitis: autoantibodies
anti-neutrophil cytoplasmic
45
primary sclerosing cholangitis: other AI diseases
70% have one | mainly colitis
46
primary biliary cholangitis: raised globulins
IgM
47
primary biliary cholangitis: autoantibodies
antimitochondrial
48
primary biliary cholangitis: other AI diseases
33% | various
49
autoimmune hepatitis: raised globulins
IgG
50
autoimmune hepatitis: autoantibodies
antinuclear, smooth muscle, liver, kidney
51
autoimmune hepatitis and other AI diseases
40% | various
52
autoimmune hepatitis: epidemiology
1-2/10,000 in UK 70-75% women 40% present with acute hepatitis ANA, ASMA positive in 70%
53
autoimmune hepatitis: clinical variants
acute hepatitis antibody negative spontaneous remission drug/virus/transplant related
54
primary biliary cholangitis: presentation
``` itching fatigue dry eyes joint pain variceal bleeding liver failure ```
55
primary biliary cholangitis: treatment of the itch
cholestyramine helps 50% rifampicin is effective but can damage liver antihistamines dont really help
56
primary biliary cholangitis and fatigue
can be disabling | correlated with autonomic neuropathy but not disease severity
57
ursodeoxycholic acid in PBC
improves liver enzymes and bilirubin reduces inflammation but not fibrosis 70% have a good response and normal life expectancy 30% have poor response and impaired life expectancy
58
primary sclerosing cholangitis
disease of bile ducts leads to strictures and gallstones >50% have inflammatory bowel disease
59
primary sclerosing cholangitis: presentation
itching pain jaundice raised alkaline phosphatase and GGT
60
primary sclerosing cholangitis: treatment
ursodeoxycholic acid has questionable benefits | good results from liver transplant
61
hepatocellular carcinoma
adenocarcinoma mainly occurs in those with cirrhosis may present with decompensation of liver disease, weight loss, ascites
62
hepatocellular carcinoma: risks
hep B,C and haemochromatosis = highest risk | cirrhosis from alcohol or autoimmune= lower risk
63
hepatocellular carcinoma: treatment
transplant | sorafenib prolongs life
64
non-alcoholic fatty liver
``` 25% of population usually no symptoms most common cause of elevated LFTs fat, inflammation, some fibrosis no drug treatment- lose weight ```
65
non-alcoholic fatty liver: risk factors
obesity- 70% diabetes- 35-75% hyperlipidaemia- 20-80%
66
alpha 1-antitrypsin deficiency and liver disease
2% carry the allele for the gene- results in inability to export alpha 1- antitrypsin from liver to lungs leads to liver disease from protein retention and emphysema from protein deficiency
67
alpha 1-antitripsin deficiency: treatment
no treatment
68
hepatic vein occlusion
terminal or central veins become occluded by fibrous tissue | back pressure causes portal hypertension
69
hepatic vein occlusion: causes
thrombosis membrane obstruction veno-occlusive disease
70
hepatic vein occlusion: presentation
abnormal liver tests ascites acute liver failure
71
hepatic vein occlusion: treatment
anticoagulation | transjugular intrahepatic portosystemic shunt
72
hepatitis definition
inflammation of the liver
73
acute vs. chronic hepatitis
``` acute= onset up to 6 months chronic= persists after 6 months ```
74
acute hepatitis patient
``` can be asymptomatic malaise myalgia GI upset abdo pain potential jaundice raised AST, ALT ```
75
chronic hepatitis patient
``` can be asymptomatic spider naevi, clubbing etc. LFTs can be normal compensated= liver function maintained decompensated= jaundice, ascites, low albumin, coagulopathy ```
76
hepatitis A: transmission
faeco-oral person-person ingestion of contaminated food/water
77
hepatitis A: risk factors
travel household or sexual contact injecting drug use
78
hepatitis A: clinical
incubation period= 15-50 days self limiting 100% immunity after infection
79
hepatitis A: management
supportive monitor liver function manage close contacts vaccination
80
hepatitis E: presentation
95% are asymptomatic self limiting however fulminant risk increased in pregnancy extra-hepatic manifestations- neurological
81
hepatitis E: diagnosis
serology- anti HEV IgM+IgG
82
hepatitis E: managing acute infection
supportive | liaise with hepatology and consider ribavirin if it becomes acute-on-chronic liver failure
83
hepatitis E: managing chronic infection
reverse immunosuppression if possible | if REV RNA persists treat with ribavirin
84
hepatitis B: epidemiology
worldwide: 129 mill new infections/year 343 mill with chronic HBV 750,000 deaths/year
85
hepatitis B: transmission
blood-borne highly infections vertical, sexual, iatrogenic, IV drug use
86
hepatitis B: management
supportive monitor liver function consider transplant manage their contacts
87
hepatitis B: treatment
nucleoside analogues | pegylated interferon- alpha 2a
88
hepatitis B: pegylated interferon- alpha 2a
immunomodulatory- stimulates immune system weekly sub cut injections 48 week long course side effects= back pain, depression, hypothyroidism, anaemia
89
hepatitis B: nucleoside analogues
``` inhibit viral replication one tablet a day minimal side effects renal monitoring required may be needed life long ```
90
hepatitis D
defective RNA virus transmitted via blood and body fluids can be acquired simultaneously with HBV or after HBV
91
hepatitis D: test
hepatitis D antibody- if positive test HDV RNA
92
hepatitis D: treatment
pegylated interferon- alpha
93
hepatitis C: epidemiology
160,000 in England 50% undiagnosed 90% history of injecting drug use
94
hepatitis C: tests
``` HCV Ab- not detected= no recent exposure, detected= exposure) HCV RNA- not dected= no current HCV, detected= current HCV HCV genotype (1a,b,2,3,4,5,6) ```
95
hepatitis C: directly acting antivirals
combination of 2 or more of three drug classes- usually no symptoms but can have them with ribavirin (haemolytic anaemia, tiredness, dyspnoea, anxiety)
96
hepatitis C: prevention
no vaccine can be re-infected (no immunity) screening of blood products lifestyle modification
97
diarrhoea definition
3 or more loose/liquid stools within 24 hours
98
infective diarrhoea
intraluminal infection | systemic infections
99
non-infective diarrhoea
``` cancer chemical inflammatory bowel disease IBS malabsorption endocrine radiation ```
100
intraluminal infections: stool/ onset/duration
acute onset- viral/bacterial chronic- parasites and non-infectious floating stool- fat content, malabsorption
101
intraluminal infections: medication/immunocompromisation
recent antibiotics | HIV/diabetes/chemo/transplant= higher risk
102
diarrhoea: investigating stool tests
if severe, bloody, dysenteric, persistent | microscopy, culture, look for parasites and toxins (c. diff)
103
diarrhoea: investigating blood tests
blood culture inflammatory markers electrolytes and renal function
104
bloody/mucoid diarrhoea: mechanism
inflammatory invasion cytotoxin
105
bloody/mucoid diarrhoea: location
colon
106
bloody/mucoid diarrhoea: bacterial causes
shigella e. coli salmonella C. diff
107
water diarrhoea: mechanism
non-inflammatory
108
watery diarrhoea: location
proximal small bowel
109
watery diarrhoea: bacterial causes
vibrio cholerae e. coli staph. aureus
110
watery diarrhoea: viral causes
rotavirus | norovirus
111
watery diarrhoea: parasitic causes
giardia
112
diarrhoea in the UK
50-70% cases are caused by viruses e.g. rotavirus/norovirus | since the rotavirus vaccine- 70% reduction in cases
113
immunosuppressed diarrhoea
increased risk, particularly to mycobacteria, microsporidia, CMV, HSV
114
traveller's diarrhoea
occurs w/i 2 weeks of arrival
115
traveller's diarrhoea: causes
``` e. coli= 30-70% shigella=5-20% campylobacter=5-20% viral=10-20% cholera ```
116
traveller's diarrhoea: presentation
``` 2 or more unformed stool/day PLUS 1 of the following: abdo pain cramps nausea vomiting dysentery ```
117
e coli
most strains are harmless | some serotypes are pathogenic
118
enterotoxigenic e coli
non-invasive watery diarrhoea most common cause of traveller's diarrhoea leading bacterial cause in children of developing world
119
enterohaemorrhagic e coli
shiga-like toxin intensive inflammatory response can cause haemolytic uremic syndrome (bloody diarrhoea, abdo pain, no fever, haemolysis)
120
enterpathogenic e coli, | enteroaggregative e coli and diffusely adherent E coli
watery diarrhoea due to adhesion to luminal wall | non-invasive
121
cholera
contaminated food/ water cholera toxin binds to intestinal wall, cAMP production activated cystic fibrosis transmembrane conductance regulator this causes dramatic efflux of ions and water- huge volumes of diarrhoea
122
cholera symptoms
profuse water 'rice water' diarrhoea, up to 20L/day vomiting rapid dehydration
123
cholera treatment
doxycycline and fluids
124
asymptomatic c. diff
gram positive spore forming bacteria | up to 5% have it as normal flora
125
symptomatic c. diff
can be symptomatic gut flora is altered: - broad spectrum antibiotics (rule of C's) - acid reducing drugs (PPIs) - NG feeding - immunocompromised
126
c. diff symptoms
fever cramps abdominal pain bloody diarrhoea
127
c. diff treatment
metronidazole or oral vancomycin
128
diarrhoea: red flags
``` dehydration electrolyte imbalance renal failure immunocompromised severe abdo pain cancer risk factors (over 50, chronic diarrhoea, weight loss, blood in stool) ```
129
diarrhoea: key management principles
barrier nursing: side room, gloves, apron fluid and electrolytes medications: antiemetics, anti-motility
130
peptic ulcer disease: causes
helicobacter pylori: - gram negative rod - synthesises urease forming ammonia which damages gastric mucosa and neutralises acid allowing it to survive - almost 100% carriage in developing world - >50% in uk over 50s
131
peptic ulcer disease: symptoms
acquisition of H.pylori usually asymptomatic | can cause nausea, vomiting and fever
132
peptic ulcer disease: complications
``` duodenal ulcers (relieved by eating) gastric ulcers (worsened by eating) risk factor for cancer of stomach due to inflammation ```
133
peptic ulcer disease: diagnosis
stool antigen test breath test blood test for antibodies endoscopy
134
peptic ulcer disease: treatment
clarithromycin amoxicillin PPI
135
biliary sepsis/ascending cholangitis: bacterial infection
obstruction of common bile duct causes stasis of bile and so an invasion of bacteria from duodenum can be obstructed by stone, cancer, stricture or parasite
136
biliary sepsis/ascending cholangitis: gallstone risk factors
fair (northern european) female fat fertile
137
biliary sepsis/ascending cholangitis: symptoms
clinical diagnosis based on charcot's triad- jaundice, RUQ pain, fever 5-10% mortality
138
biliary sepsis/ascending cholangitis: management
IV antibiotics fluids endoscopic retrograde cholangiopancreatography
139
peritonitis causes
medical: dialysis related, TB, pelvic inflammatory disease | Surgical- perforation of GIT, trauma
140
enteric fever: causes
solmonella typhi: - typhoid fever - contaminated food/water - faeco-oral spread
141
enteric fever: signs and symptoms
``` RLQ pain high fever headache myalgia rose spots constipation ```
142
enteric fever: investigations
diagnosed through blood culture/bone marrow aspiration
143
enteric fever: complications
GI bleed perforation myocarditis abscesses
144
enteric fever: treatment
emergency surgery | antibiotics (mortality goes from 20%-1%)
145
units of alcohol
uk unit= 8 grams or 10ml pure alcohol | men and women advised not to drink over 14 units a week
146
calculating the number of units
(strength % x amount in ml)/1000
147
common drink units
wine, 13.5%, small= 1.6, large=3.3, bottle= 10 | beer- regular 4% bottle= 1.8, pint=2.3
148
excessive drinking
drinking is excessive when: it causes or elevates risk of alcohol related problems OR it complicates the management of other health problems
149
acute effects of excess alcohol intake
``` accidents/injury coma from resp depression aspiration pneumonia gastritis pancreatitis hypoglycaemia myopathy arrhythmias ```
150
chronic effects of excess alcohol intake
``` pancreatitis hypertension gastritis CHD liver damage CNS toxicity ```
151
alcohol withdrawal symptoms
tremulousness activation syndrome seizures hallucinations
152
alcohol withdrawal: delirium tremes
can be severe or even fatal | tremors, agitation, confusion, disorientation, hallucinations, seizures
153
alcohol specific and related deaths by condition
alcoholic liver disease- 82% of 5507 alcohol specific deaths (2016)
154
foetal alcohol syndrome
pre and post natal growth retardation CNS abnormalities (mental retardation, irritability, hyperactivity) craniofacial abnormalities
155
alcohol costs to the NHS
total cost in 2017 was £4.42 million | decrease in cost from previous years due to reduction of disulfiram
156
psychosocial effects of excessive alcohol consumptions
``` interpersonal- violence, rape, depression problems at work criminality poverty driving incidents ```
157
NICE guidelines recommendations for policy (preventing harmful drinking)
price- make it less affordable availability- licensing and import allowances marketing- limit exposure, especially to children
158
NICE guidelines recommendations for practice (preventing harmful drinking)
``` licensing resources for screening supporting children screening young people screening adults advice referral ```
159
primary prevention to alcoholism
know your limits campaign THINK driving campaign restriction on alcohol advertising by Ofcom minimum unit pricing
160
at risk drinking
a pattern of drinking which brings about the risk of physical or psychological harm
161
alcohol abuse
a pattern of drinking which is likely to cause physical or psychological harm
162
alcohol dependence
substance dependence is defined as a set of behavioural, cognitive and psychological responses that can develop after repeated substance use
163
alcohol dependence: pharmacological treatment
disulfiram naltrexone acamprosate calcium
164
alcohol dependence: psychosocial treatment
therapy | social support
165
key policy for alcohol intervention
models of care for alcohol misusers (MoCAM) | involves: screening and assessment, the four tier framework and care planning and co ordination
166
severity of dependence questionnaire
``` measure of dependence 20 questions: -physical withdrawal symptoms -affective withdrawal symptoms -relief drinking -frequency of alcohol consumption -speed of onset of withdrawal symptoms >30 is severe, 16-30 moderate, <16 mild ```
167
alcohol and the nervous system
alcohol potentiates gamma-amino butyric acid (major inhibitory neurotransmitter in CNS) it also inhibits major excitatory neurotransmitter- glutamate and n-methyl-d-asparate
168
tolerance
a state in which an organism no longer responds to a drug | a higher dose is required to achieve the same effect
169
alcohol withdrawal: Chlordiazepoxide absorption
``` absorbed in small intestine highly lipophilic it can be delayed in the elderly half life is 6-30 hours protein bound ```
170
alcohol withdrawal: Chlordiazepoxide distribution and metabolism
metabolised in liver crosses blood brain barrier active in CNS grey matter
171
alcohol withdrawal: Chlordiazepoxide elimination
excreted in urine in the form of its metabolites | or as conjugates
172
alcohol withdrawal: Chlordiazepoxide contraindications
``` hypersensitivity to benzodiazepines pulmonary insufficiency pregnancy chronic psychosis myasthenia gravis ```
173
alcohol withdrawal: Chlordiazepoxide dependence
short term use= low chance of dependence | risk of physical and psychological dependence increases with increased dose
174
alcohol withdrawal: Chlordiazepoxide drug interactions
alcohol- enhanced sedative effect centrally acting drugs (antipsychotics, analgesics) anti-epileptic drugs
175
alcohol withdrawal: Chlordiazepoxide side effects
``` drowsiness ataxia aggression headache resp depression impaired liver function ```
176
wernicke's encephalopathy
``` deficiency of thiamine common in dependent drinkers poor diet poor intake of vitamins poor gastro-intestinal absorption ```
177
wernicke's encephalopathy treatment
pabrinex and ongoing with vit b/thiamine
178
alcohol relapse prevention: acamprosate
mechanism of action not fully understood but believed to act on neural pathways safe no interaction with alcohol or diazepam more effective when offered as combined therapy
179
alcohol relapse prevention: disulfiram
disrupts oxidative metabolism of alcohol | results in a build up acetaldehyde
180
alcohol relapse prevention: disulfiram symptoms
``` long hangover flushing of skin tachycardia SOB nausea vomiting ```
181
alcohol relapse prevention: nalmefine
opioid receptor antagonist modifies activity at receptor sites linked to reward mechanisms effects of alcohol present but reduces feeling of reward and pleasure
182
the four tier framework
non-substance misuse specific services open access drug/alcohol services specialist community based clinics specialist in patient services
183
types of intestinal obstructions
intraluminal obstructions intramural extraluminal
184
extraluminal obstructions
outside the wall of the gut
185
intramural obstructions
within the wall of the gut
186
intraluminal obstructions
within the gut
187
intraluminal obstructions: tumours
carcinoma lymphoma tumours on the left side can obstruct more quickly than the right
188
intraluminal obstructions: diaphragm disease
caused by NSAIDS- cause submucosal fibrosis this results in diaphragm like strictures in the GI tract most common in small bowel
189
intraluminal obstructions: meconium ileus
meconium thicker and stickier
190
intraluminal obstructions: gallstone ileus
gallstones erode into the bowel causing the obstruction
191
intramural obstructions: inflammatory
crohn's | diverticulutis
192
intramural obstructions: tumours
colorectal tumours
193
intramural obstructions: neural
hirschprung's disease: | developmental where segment of bowel towards distal end hasnt got ganglion cells- no coordinated contraction
194
intramural obstructions: crohn's disease
main inflammatory cause of obstructions (granulomatous inflammation) particularly ileum deep fissuring ulcers and fibrosis
195
intramural obstructions: diverticular disease
mainly older people small outpuching of mucosae which can become inflamed (stasis of faeces) risk of rupture
196
diverticular disease pathogenesis
less fibre= more pressure in lumen of bowel to push faeces holes in muscularis for blood vessels pressure causes mucosa to be pushed through these holes causes an outpouching
197
extra luminal obstructions: adhesions
previous surgery causes fibrosis | adhesion can cause kinks in bowel resulting in obstruction
198
extra luminal obstructions: volvulus
sigmoid volvulus where sigmoid twists | can twist and untwist resulting in abdomen pain coming and going
199
extra luminal obstructions: tumours
peritoneal deposits of tumour such as ovarian cancer
200
intestinal obstruction definition
arrest/blockage of onward propulsion or intestinal contents
201
small bowel obstructions
account for 60-75% of intestinal obstructions
202
small bowel obstructions: causes
crohn's disease (25%) surgery/adhesions (60%) hernia malignancy
203
small bowel obstructions: clinical presentations
``` pain-colicky vomiting- early and follows pain tenderness constipation increased bowel sounds ```
204
small bowel obstructions: diagnosis
abdominal x-ray examination FBC CT
205
small bowel obstructions: treatment
``` aggressive fluid resuscitation bowel decompression analgesia and antiemetic antibiotics surgery ```
206
large bowel obstructions
25% of obstructions
207
large bowel obstructions: causes
90% in US/europe due to colorectal malignancy | in african countries more likely to be volvulus
208
large bowel obstructions: clinical presentations
``` abdominal pain abdominal distention bowel sounds normal, then increased lated palpable mass late vomiting constipation bloating ```
209
large bowel obstructions: diagnosis
digital rectal exam FBC abdominal x-ray CT
210
large bowel obstructions: treatment
``` aggressive fluid resuscitation bowel decompression analgesia and antiemetic antibiotics surgery ```
211
pseudo-bowel obstructions
clinical picture mimics obstruction but with no mechanical cause
212
causes of pseudo-bowel obstructions
``` intra-abdo trauma pelvic/spinal fractures postoperative states sepsis pneumonia drugs (opiates) ```
213
pseudo-bowel obstructions: clinical presentation
rapid and progressive abdominal distention and pain
214
pseudo-bowel obstructions: diagnosis
x-ray shows a gas-filled large bowel
215
pseudo-bowel obstructions: treatment
treat underlying problem | IV neostigmine
216
lower GI tumours: epidemiology
higher prevalence in elderly incidence rates higher in those with low fibre diet incidence increasing due to screening mortality decreasing
217
lower GI tumours: adenomas as a risk factor
the bigger the greater change of turning malignant | normal epithelium -> dysplastic epithelium (adenoma) -> colorectal adenocarcinoma
218
lower GI tumours: familial adenomatous polyposis as a risk factor
born with normal colons but develop lots of polyps Apc gene mutation causes beta catenin to build up resulting in increased epithelial proliferation causing more adenomas to form
219
lower GI tumours: hereditary nonpolyposis colorectal cancer as a risk factor
no DNA repair protein produced | it has a risk of further cancers in index patients and relatives
220
lower GI tumours: resection margin coding
``` R0= tumour completely excised R1= microscopic involvement of margin by tumour R2= macroscopic involvement of margin by tumour ```
221
lower GI tumours: prognosis
circumferential resection margin (CRM) +ve= 20% 5 year survival with 85% risk of local recurrence CRM -ve= 75% 5 year survival with 10% risk of local recurrence
222
lower GI tumours: staging
determine the spread of the tumour greater the spread the worse the prognosis lymph node and peritoneal involved included in staging
223
lower GI tumours: dukes' stages
A- inner lining of the bowel (95% 5 year survival) B- grown through the muscle layer of the bowel (75% 5 year survival) C- spread to at least 1 lymph node close to the bowel (35% 5 year survival) D- spread to another part of the body (25% 5 year survival)
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lower GI tumours: treatment
prevention (normal) endoscopic resection (adenomas) surgical resection chemotherapy and palliative care
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gastroduodenal ulceration and gastritis: causes
mucosal ischaemia increased acid production bile reflux helicobacter infection
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gastroduodenal ulceration and gastritis: mucosal ischaemia
reduces mucin production so no mucin barrier | this causes cell death and acid enters between cells causing ulceration
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gastroduodenal ulceration and gastritis: mucosal ischaemia treatment
reverse mucosal ischaemia | PPIs- omeprazole, lansoprazole
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gastroduodenal ulceration and gastritis: increased acid production
overwhelm defences, causing ulceration to occur
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gastroduodenal ulceration and gastritis: increased acid production causes
stress helicobacter pylori drugs such as aspirin or ibruprofen
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gastroduodenal ulceration and gastritis: increased acid production treatment
PPIs | aspirin with enteric coats
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gastroduodenal ulceration and gastritis: bile reflux
bile causes ulceration
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gastroduodenal ulceration and gastritis: bile reflux causes
alcohol in high concentrations
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peptic ulceration complications
ulcer can grow pass through the gastric wall into arteries causing a haemorrhage if it continues to grow through the muscle wall into peritoneal cavity it causes peritonitis
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malabsorption: main presentation
diarrhoea anaemia weight loss fatty stools
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malabsorption: causes
``` insufficient intake defective intraluminal digestion insufficient absorption area lack of digestive enzymes defective epithelial transport lymphatic obstruction ```
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malabsorption: defective intraluminal digestion
pancreatic insufficiency defective bile secretion bacterial overgrowth
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defective intraluminal digestion: pancreatic insufficiency
pancreatitis - no enzymes | cystic fibrosis -blocked pancreatic duct
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defective intraluminal digestion: defective bile secretion
biliary obstruction - e.g. gallstone | ileal resection - decreased bile salt uptake
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malabsorption: insufficient absorption area
gluten sensitive enteropathy crohn's disease extensive surface parasitisation small intestinal resection
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insufficient absorption area: gluten sensitive enteropathy (coeliac)
villous atrophy crypt hyperplasia increased number of lymphocytes
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insufficient absorption area: crohn's disease
inflammatory disease of the bowel reduces surface area cobblestone mucosa
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insufficient absorption area: extensive surface parasitisation
``` giardia lamblia (malabsorption and weight loss) parasites coat the surface of the vili (food cannot be absorbed) ```
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insufficient absorption area: small intestine resection
done in: morbid obesity crohn's disease infarcted small bowel
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malabsorption: lack of digestive enzymes
``` disaccharidase deficiency (lactose intolerance) bacterial overgrowth (brush border damage) ```
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malabsorption: defective epithelial transport
abetaliapoproteinaemia | primary bile acid malabsorption
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malabsorption: lymphatic obstruction
lymphoma | tuberculosis
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coeliac disease pathology
``` allergic reaction to Giliadin protein Giliadin peptide bind to antigen presenting cell APC activated cell injury Giliadin antibodies, transglutaminase Ab ```
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chronic idiopathic inflammatory bowel disease
crohn's disease | ulcerative colitis
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bowel inflammatory conditions
diverticulitis ischaemic colitis infective colitis
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crohn's disease
inflammation of bowel anywhere from mouth to anus | mainly terminal ilium
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crohn's disease: features
skip lesions passes all the way through mucosa, submucosa, muscularis propria and serosa deep fissuring ulceration fibrosis
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crohn's disease: complications of the bowel
``` malabsorption obstructions perforation fistula neoplasia anal fissures and skin tags ```
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crohn's disease: systemic complications
amyloidosis
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ulcerative colitis
inflammation with ulcer formation in the colon | starts and rectum and moves proximally, stopping at caecum
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ulcerative colitis: features
only in mucosa distinct boundary between disease and normal bowel diffuse pattern- not patchy
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ulcerative colitis: complications of the colon
blood loss toxic dilation colorectal cancer
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ulcerative colitis: complications of the joints
ankylosing spondylitis | arthritis
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ulcerative colitis: complications of the eyes
iritis uveitis episcleritis
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ulcerative colitis: complications of the skin
erythema nososum | pyoderma gangrenosum
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ulcerative colitis: complications of the liver
fatty change | chronic and/or sclerosing pericholangitis
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oesophageal adenocarcinoma: epidemiology
increases with age | more common in males
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oesophageal adenocarcinoma
barret's oesophagus | columnar lined lower oesophagus (CELLO)
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oesophageal adenocarcinoma: metaplasia
change in differentiation of a cell from one fully differentiated type to another
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oesophageal adenocarcinoma: pathogenesis
acid reflux causes metaplasia from stratified squamous to simple columnar change in cell type increases risk of adenocarcinoma
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oesophageal adenocarcinoma: pathway
normal squamous epithelium gastro-oesophageal reflux causes metaplastic oesophageal glandular epithelium reflux continues- dysplastic epithelium finally neoplastic epithelium
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oesophageal adenocarcinoma: causes
obesity is main cause of reflux
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oesophageal squamous cancer- risk factors
smoking and drinking
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oesophageal cancer: complications
difficulty swallowing early can pass into blood vessels a late presentation decreases survival rate
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gastric cancer: epidemiology
incidence is decreasing | more common in males
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gastric cancer: causes
genetic- mutation in E cadherin transport proteins environmental helicobacter infection pernicious anaemia- mucosal ischaemia
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gastric cancer: pathogenesis
``` normal mucosa intestinal metaplasia dysplasia intramucosal carcinoma invasive carcinoma ```
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gastric cancer: presentation
late presentation as tumour can grow quite large in the stomach before complications
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gastric cancer: stages
early- no spread to muscular wall (can be in lymph nodes) 90% 5 year survival late- spread to musclaris propria- 60% 5 year survival if fully resected
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coeliac disease
inflammation of mucosa of upper small bowel that occurs when gluten is introduced into the diet T cell mediated autoimmune disease where prolamin protein intolerance causes villous atrophy and malabsorption
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coeliac disease: epidemiology
1% of population affected occurs any age but peaks in infancy and 50-60 y/o affects males and females equally
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coeliac disease: risk factors
having other autoimmune disease IgA deficiency age of introduction to gluten
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coeliac disease diagnosis
should maintain gluten for at least 6 weeks before testing to get true results FBC, duodenal biopsy, serum antibody testing
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coeliac disease diagnosis: FBC
low Hb low B12 low ferritin
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coeliac disease diagnosis: duodenal biopsy
gold standard | see villous atrophy, crypt hyperplasia and increased intraepithelial white cell count
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coeliac disease diagnosis: serum antibody testing
most sensitive tests (95%) are EMA, tTG (both are IgAs and correlate with severity of mucosal damage) not sensitive if IgA deficient
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coeliac disease: treatment
live long gluten free diet correction of vitamin and mineral deficiencies DEXA scan to monitor osteoporotic risk
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coeliac disease: complications
not improving on the strict diet- non responsive coeliac disease anaemia secondary lactose intolerance T cell lymphoma
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coeliac disease: prolamins
gliadin- wheat hordeins- barley secalins- rye prolamin is a component of gluten
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coeliac disease: prolamins
gliadin- wheat hordeins- barley secalins- rye prolamin is a component of gluten
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peritonitis definition
inflammation of peritoneum
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peritonism definition
tensing of the muscles to prevent movement of peritoneum
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visceral peritoneum
on the organs autonomic innervation sensation poorly localised
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parietal peritoneum
covers abdo wall somatic innervation sensation well localised
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foregut sensation
lower oesophagus to D2, liver, spleen, gallbladder autonomic pain= epigastric region greater splanchnic T5-9
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midgut sensation
D2- 2/3 of transverse colon site of autonomic pain= umbilical region less splanchnic T10-11
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hindgut sensation
2/3 transverse colon to upper rectum autonomic pain= hypogastric region least splanchnic nerve T12/L1
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peritonitis: causes
``` inflamed organ air (ulcer, trauma) pus (bacterial) faeces/luminal contents (perforation) blood (trauma) ```
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primary peritonitis
``` inflammation on its own spontaneous bacterial peritonitis ascites diagnose with ascitic tap and blood cultures treat with broad spectum antibiotics ```
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secondary peritonitis
caused by something else e.g. chemicals or bile | treat the cause
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peritonitis: common causes of abdo pain
``` gastritis (epigastric) cholecystits (RUQ, midclavicular) pancreatitis (epigastric) appendicitis (umbilical then McBurney's point) diverticulitis (LLQ) ```
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peritonitis: epidemiology
370,000 admissions /year in uk | mortality 15%
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peritonitis: symptoms
kidney failure symptoms abdominal pain: -sudden onset= perforation -slow onset= secondary to inflammatory disease -poorly localised= irritation of visceral -localised= irritation of parietal
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peritonitis: signs
``` rebound tenderness percussion pain guarding no bowel sounds shock lying still ```
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peritonitis: complications
``` sepsis multi-organ failure kidney failure paralytic ileus abscess formation CVS events ```
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peritonitis: investigations
CT scan blood test CXR abdo XR
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peritonitis: treatment
``` treat cause fluid resuscitation antibiotics surgery after care (kidneys, phsyio, nutrition) ```
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ascites definition
abnormal accumulation of fluid within peritoneal cavity
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ascites: epidemiology
(healthy men/women= no fluid/20ml) 10-20% 5 year survival from onset signifies serious illness such as cirrhosis
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ascites causes
impaired blood flow local inflammation decreased oncotic pressure
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ascites cause by impaired blood flow
cirrhosis- portal hypertension cardiac failure constrictive pericarditis
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ascites cause by local inflammation
(leaky membrane) peritonitis abdo cancers (Esp. ovarian) infection e.g. TB
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ascites cause by decreased oncotic pressure
hypoalbuminaemia nephrotic syndrome malnutrition
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ascites: exudate fluid
high protein fluid
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ascites: exudate fluid pathology
low serum to ascites/albumin ratio outflow is fine altered oncotic pressure membrane more porous
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ascites: exudate fluid treatment
treat underlying cause
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ascites: exudate fluid causes
malignancy sepsis TB nephrotic syndrome
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ascites: transudate fluid
low protein fluid
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ascites: transudate fluid pathology
high serum to ascites/albumin ration outflow increased decreased oncotic pressure membrane okay
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ascites: transudate fluid causes
cirrhosis | cardiac failure
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ascites: transudate fluid management
treat cause diet diuretic drainage
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ascites: history
how long has swelling been there? drugs? weight loss? any obvious underlying cause?
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ascites: complications
stasis results in bacterial overgrowth- spontaneous bacterial peritonitis
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ascites: examination
presences is confirmed by demonstrating shifting dullness with percussion ultrasound/xray/ct
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ascitic tap: diagnostic aspiration
``` 10-20ml of fluid to see: raised white cell count (bacterial peritonitis) gram stain and culture cytology for malignancy amylase to exclude pancreatic ascites ```
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ascitic tap: protein measurement (transudate)
less bad | transparent due to little protein (<30g/L)
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ascitic tap: protein measurement (exudate)
``` extremely bad high protein (>30g/L) ```
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ascites: treatment
``` treat cause reduce sodium intake increase sodium excretion diuretic drain fluid ```
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ascites: risk factors
high sodium diet hepatocellular carcinoma splanchnic vein thrombosis- portal hypertension