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phase 2a clinical > GI > Flashcards

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
Q

signs of liver failure

A

leukonychia- white nails
spider naevus
ascites

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26
Q

alcoholic liver disease

A

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%

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27
Q

alcoholic liver disease: pathogenesis

A

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

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28
Q

portal hypertension

A

increased hepatic resistance

increased splanchnic blood flow

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29
Q

portal hypertension causes

A

cirrhosis
fibrosis
portal vein thrombosis

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30
Q

portal hypertension: consequences

A

varices- oesophageal, gastric

splenomegaly

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31
Q

liver transplants and alcoholic liver disease

A

100/760 liver transplants/year in uk (limited by liver supply)
4000 deaths from ALD in UK/year

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32
Q

treatment for alcohol withdrawal

A

lorazepam

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33
Q

why are liver patients vulnerable to infection

A

impaired reticulo-endothelial function
reduced opsonic activity
leukocyte activity
permeable gut wall

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34
Q

sites vulnerable to infection in those with liver disease

A

skin
lungs (pneumonia)
urinary tract

septicaemia
spontaneous bacterial peritonitis

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35
Q

spontaneous bacterial peritonitis and liver disease

A

most common infection in cirrhosis

diagnosis based on neutrophils in ascitic fluid

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36
Q

causes of renal failure in liver disease

A 
infection
GI bleeding
myoglobinuria
rental tract obstruction
drugs (NSAIDS, diuretics, ace inhibitors)
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37
Q

coma in patients with chronic liver disease

A

hepatic encephalopathy- caused by ammonia
hypoglycaemia
intracranial event

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38
Q

cirrhosis

A

represents end stage liver disease
residual nodules of hepatocytes
constant replication of hepatocytes in this condition puts them at risk of mutations and neoplasia

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39
Q

some consequences of liver dysfunction

A

malnutrition
coagulopathy- impaired coagulation factor synthesis, vitamin k deficiency
endocrine changes
hypoglycaemia

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40
Q

causes of chronic liver disease

A 
alcohol
non-alcoholic steatohepatitis 
viral hepatitis
immune
metabolic
vascular
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41
Q

types of hepatitis

A

viral- A, B, C, CMV, EBV
drug induced
auto immune
alcohol

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42
Q

main autoimmune diseases of the liver

A

autoimmune hepatitis
primary biliary cholangitis
primary sclerosing cholangitis

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43
Q

primary sclerosing cholangitis: raised globulins

A

variable

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44
Q

primary sclerosing cholangitis: autoantibodies

A

anti-neutrophil cytoplasmic

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45
Q

primary sclerosing cholangitis: other AI diseases

A

70% have one

mainly colitis

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46
Q

primary biliary cholangitis: raised globulins

A

IgM

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47
Q

primary biliary cholangitis: autoantibodies

A

antimitochondrial

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48
Q

primary biliary cholangitis: other AI diseases

A

33%

various

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49
Q

autoimmune hepatitis: raised globulins

A

IgG

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50
Q

autoimmune hepatitis: autoantibodies

A

antinuclear, smooth muscle, liver, kidney

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51
Q

autoimmune hepatitis and other AI diseases

A

40%

various

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52
Q

autoimmune hepatitis: epidemiology

A

1-2/10,000 in UK
70-75% women
40% present with acute hepatitis
ANA, ASMA positive in 70%

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53
Q

autoimmune hepatitis: clinical variants

A

acute hepatitis
antibody negative
spontaneous remission
drug/virus/transplant related

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54
Q

primary biliary cholangitis: presentation

A 
itching
fatigue
dry eyes
joint pain
variceal bleeding
liver failure
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55
Q

primary biliary cholangitis: treatment of the itch

A

cholestyramine helps 50%
rifampicin is effective but can damage liver
antihistamines dont really help

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56
Q

primary biliary cholangitis and fatigue

A

can be disabling

correlated with autonomic neuropathy but not disease severity

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57
Q

ursodeoxycholic acid in PBC

A

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

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58
Q

primary sclerosing cholangitis

A

disease of bile ducts
leads to strictures and gallstones
>50% have inflammatory bowel disease

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59
Q

primary sclerosing cholangitis: presentation

A

itching pain
jaundice
raised alkaline phosphatase and GGT

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60
Q

primary sclerosing cholangitis: treatment

A

ursodeoxycholic acid has questionable benefits

good results from liver transplant

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61
Q

hepatocellular carcinoma

A

adenocarcinoma
mainly occurs in those with cirrhosis
may present with decompensation of liver disease, weight loss, ascites

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62
Q

hepatocellular carcinoma: risks

A

hep B,C and haemochromatosis = highest risk

cirrhosis from alcohol or autoimmune= lower risk

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63
Q

hepatocellular carcinoma: treatment

A

transplant

sorafenib prolongs life

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64
Q

non-alcoholic fatty liver

A 
25% of population
usually no symptoms
most common cause of elevated LFTs
fat, inflammation, some fibrosis
no drug treatment- lose weight
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65
Q

non-alcoholic fatty liver: risk factors

A

obesity- 70%
diabetes- 35-75%
hyperlipidaemia- 20-80%

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66
Q

alpha 1-antitrypsin deficiency and liver disease

A

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

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67
Q

alpha 1-antitripsin deficiency: treatment

A

no treatment

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68
Q

hepatic vein occlusion

A

terminal or central veins become occluded by fibrous tissue

back pressure causes portal hypertension

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69
Q

hepatic vein occlusion: causes

A

thrombosis
membrane obstruction
veno-occlusive disease

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70
Q

hepatic vein occlusion: presentation

A

abnormal liver tests
ascites
acute liver failure

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71
Q

hepatic vein occlusion: treatment

A

anticoagulation

transjugular intrahepatic portosystemic shunt

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72
Q

hepatitis definition

A

inflammation of the liver

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73
Q

acute vs. chronic hepatitis

A 
acute= onset up to 6 months
chronic= persists after 6 months
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74
Q

acute hepatitis patient

A 
can be asymptomatic
malaise
myalgia
GI upset
abdo pain
potential jaundice 
raised AST, ALT
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75
Q

chronic hepatitis patient

A 
can be asymptomatic
spider naevi, clubbing etc.
LFTs can be normal
compensated= liver function maintained
decompensated= jaundice, ascites, low albumin, coagulopathy
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76
Q

hepatitis A: transmission

A

faeco-oral
person-person
ingestion of contaminated food/water

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77
Q

hepatitis A: risk factors

A

travel
household or sexual contact
injecting drug use

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78
Q

hepatitis A: clinical

A

incubation period= 15-50 days
self limiting
100% immunity after infection

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79
Q

hepatitis A: management

A

supportive
monitor liver function
manage close contacts
vaccination

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80
Q

hepatitis E: presentation

A

95% are asymptomatic
self limiting however fulminant risk increased in pregnancy
extra-hepatic manifestations- neurological

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81
Q

hepatitis E: diagnosis

A

serology- anti HEV IgM+IgG

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82
Q

hepatitis E: managing acute infection

A

supportive

liaise with hepatology and consider ribavirin if it becomes acute-on-chronic liver failure

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83
Q

hepatitis E: managing chronic infection

A

reverse immunosuppression if possible

if REV RNA persists treat with ribavirin

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84
Q

hepatitis B: epidemiology

A

worldwide:
129 mill new infections/year
343 mill with chronic HBV
750,000 deaths/year

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85
Q

hepatitis B: transmission

A

blood-borne
highly infections
vertical, sexual, iatrogenic, IV drug use

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86
Q

hepatitis B: management

A

supportive
monitor liver function
consider transplant
manage their contacts

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87
Q

hepatitis B: treatment

A

nucleoside analogues

pegylated interferon- alpha 2a

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88
Q

hepatitis B: pegylated interferon- alpha 2a

A

immunomodulatory- stimulates immune system
weekly sub cut injections
48 week long course
side effects= back pain, depression, hypothyroidism, anaemia

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89
Q

hepatitis B: nucleoside analogues

A 
inhibit viral replication
one tablet a day
minimal side effects
renal monitoring required
may be needed life long
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90
Q

hepatitis D

A

defective RNA virus
transmitted via blood and body fluids
can be acquired simultaneously with HBV or after HBV

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91
Q

hepatitis D: test

A

hepatitis D antibody- if positive test HDV RNA

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92
Q

hepatitis D: treatment

A

pegylated interferon- alpha

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93
Q

hepatitis C: epidemiology

A

160,000 in England
50% undiagnosed
90% history of injecting drug use

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94
Q

hepatitis C: tests

A 
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)
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95
Q

hepatitis C: directly acting antivirals

A

combination of 2 or more of three drug classes- usually no symptoms but can have them with ribavirin (haemolytic anaemia, tiredness, dyspnoea, anxiety)

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96
Q

hepatitis C: prevention

A

no vaccine
can be re-infected (no immunity)
screening of blood products
lifestyle modification

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97
Q

diarrhoea definition

A

3 or more loose/liquid stools within 24 hours

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98
Q

infective diarrhoea

A

intraluminal infection

systemic infections

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99
Q

non-infective diarrhoea

A 
cancer
chemical
inflammatory bowel disease
IBS
malabsorption
endocrine
radiation
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100
Q

intraluminal infections: stool/ onset/duration

A

acute onset- viral/bacterial
chronic- parasites and non-infectious
floating stool- fat content, malabsorption

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101
Q

intraluminal infections: medication/immunocompromisation

A

recent antibiotics

HIV/diabetes/chemo/transplant= higher risk

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102
Q

diarrhoea: investigating stool tests

A

if severe, bloody, dysenteric, persistent

microscopy, culture, look for parasites and toxins (c. diff)

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103
Q

diarrhoea: investigating blood tests

A

blood culture
inflammatory markers
electrolytes and renal function

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104
Q

bloody/mucoid diarrhoea: mechanism

A

inflammatory
invasion
cytotoxin

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105
Q

bloody/mucoid diarrhoea: location

A

colon

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106
Q

bloody/mucoid diarrhoea: bacterial causes

A

shigella
e. coli
salmonella
C. diff

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107
Q

water diarrhoea: mechanism

A

non-inflammatory

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108
Q

watery diarrhoea: location

A

proximal small bowel

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109
Q

watery diarrhoea: bacterial causes

A

vibrio cholerae

e. coli
staph. aureus

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110
Q

watery diarrhoea: viral causes

A

rotavirus

norovirus

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111
Q

watery diarrhoea: parasitic causes

A

giardia

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112
Q

diarrhoea in the UK

A

50-70% cases are caused by viruses e.g. rotavirus/norovirus

since the rotavirus vaccine- 70% reduction in cases

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113
Q

immunosuppressed diarrhoea

A

increased risk, particularly to mycobacteria, microsporidia, CMV, HSV

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114
Q

traveller’s diarrhoea

A

occurs w/i 2 weeks of arrival

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115
Q

traveller’s diarrhoea: causes

A 
e. coli= 30-70%
shigella=5-20%
campylobacter=5-20%
viral=10-20%
cholera
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116
Q

traveller’s diarrhoea: presentation

A 
2 or more unformed stool/day PLUS 1 of the following:
abdo pain
cramps
nausea
vomiting
dysentery
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117
Q

e coli

A

most strains are harmless

some serotypes are pathogenic

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118
Q

enterotoxigenic e coli

A

non-invasive watery diarrhoea
most common cause of traveller’s diarrhoea
leading bacterial cause in children of developing world

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119
Q

enterohaemorrhagic e coli

A

shiga-like toxin
intensive inflammatory response
can cause haemolytic uremic syndrome (bloody diarrhoea, abdo pain, no fever, haemolysis)

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120
Q

enterpathogenic e coli,

enteroaggregative e coli and diffusely adherent E coli

A

watery diarrhoea due to adhesion to luminal wall

non-invasive

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121
Q

cholera

A

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

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122
Q

cholera symptoms

A

profuse water ‘rice water’ diarrhoea, up to 20L/day
vomiting
rapid dehydration

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123
Q

cholera treatment

A

doxycycline and fluids

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124
Q

asymptomatic c. diff

A

gram positive spore forming bacteria

up to 5% have it as normal flora

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125
Q

symptomatic c. diff

A

can be symptomatic gut flora is altered:

  • broad spectrum antibiotics (rule of C’s)
  • acid reducing drugs (PPIs)
  • NG feeding
  • immunocompromised
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126
Q

c. diff symptoms

A

fever
cramps
abdominal pain
bloody diarrhoea

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127
Q

c. diff treatment

A

metronidazole or oral vancomycin

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128
Q

diarrhoea: red flags

A 
dehydration
electrolyte imbalance
renal failure
immunocompromised
severe abdo pain
cancer risk factors (over 50, chronic diarrhoea, weight loss, blood in stool)
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129
Q

diarrhoea: key management principles

A

barrier nursing: side room, gloves, apron
fluid and electrolytes
medications: antiemetics, anti-motility

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130
Q

peptic ulcer disease: causes

A

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
Q

peptic ulcer disease: symptoms

A

acquisition of H.pylori usually asymptomatic

can cause nausea, vomiting and fever

132
Q

peptic ulcer disease: complications

A 
duodenal ulcers (relieved by eating)
gastric ulcers (worsened by eating)
risk factor for cancer of stomach due to inflammation
133
Q

peptic ulcer disease: diagnosis

A

stool antigen test
breath test
blood test for antibodies
endoscopy

134
Q

peptic ulcer disease: treatment

A

clarithromycin
amoxicillin
PPI

135
Q

biliary sepsis/ascending cholangitis: bacterial infection

A

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
Q

biliary sepsis/ascending cholangitis: gallstone risk factors

A

fair (northern european)
female
fat
fertile

137
Q

biliary sepsis/ascending cholangitis: symptoms

A

clinical diagnosis based on charcot’s triad- jaundice, RUQ pain, fever
5-10% mortality

138
Q

biliary sepsis/ascending cholangitis: management

A

IV antibiotics
fluids
endoscopic retrograde cholangiopancreatography

139
Q

peritonitis causes

A

medical: dialysis related, TB, pelvic inflammatory disease

Surgical- perforation of GIT, trauma

140
Q

enteric fever: causes

A

solmonella typhi:

  • typhoid fever
  • contaminated food/water
  • faeco-oral spread
141
Q

enteric fever: signs and symptoms

A 
RLQ pain
high fever
headache
myalgia
rose spots
constipation
142
Q

enteric fever: investigations

A

diagnosed through blood culture/bone marrow aspiration

143
Q

enteric fever: complications

A

GI bleed
perforation
myocarditis
abscesses

144
Q

enteric fever: treatment

A

emergency surgery

antibiotics (mortality goes from 20%-1%)

145
Q

units of alcohol

A

uk unit= 8 grams or 10ml pure alcohol

men and women advised not to drink over 14 units a week

146
Q

calculating the number of units

A

(strength % x amount in ml)/1000

147
Q

common drink units

A

wine, 13.5%, small= 1.6, large=3.3, bottle= 10

beer- regular 4% bottle= 1.8, pint=2.3

148
Q

excessive drinking

A

drinking is excessive when:
it causes or elevates risk of alcohol related problems
OR
it complicates the management of other health problems

149
Q

acute effects of excess alcohol intake

A 
accidents/injury
coma from resp depression
aspiration pneumonia
gastritis 
pancreatitis
hypoglycaemia
myopathy
arrhythmias
150
Q

chronic effects of excess alcohol intake

A 
pancreatitis
hypertension
gastritis
CHD
liver damage
CNS toxicity
151
Q

alcohol withdrawal symptoms

A

tremulousness
activation syndrome
seizures
hallucinations

152
Q

alcohol withdrawal: delirium tremes

A

can be severe or even fatal

tremors, agitation, confusion, disorientation, hallucinations, seizures

153
Q

alcohol specific and related deaths by condition

A

alcoholic liver disease- 82% of 5507 alcohol specific deaths (2016)

154
Q

foetal alcohol syndrome

A

pre and post natal growth retardation
CNS abnormalities (mental retardation, irritability, hyperactivity)
craniofacial abnormalities

155
Q

alcohol costs to the NHS

A

total cost in 2017 was £4.42 million

decrease in cost from previous years due to reduction of disulfiram

156
Q

psychosocial effects of excessive alcohol consumptions

A 
interpersonal- violence, rape, depression
problems at work
criminality
poverty
driving incidents
157
Q

NICE guidelines recommendations for policy (preventing harmful drinking)

A

price- make it less affordable
availability- licensing and import allowances
marketing- limit exposure, especially to children

158
Q

NICE guidelines recommendations for practice (preventing harmful drinking)

A 
licensing 
resources for screening
supporting children
screening young people
screening adults
advice
referral
159
Q

primary prevention to alcoholism

A

know your limits campaign
THINK driving campaign
restriction on alcohol advertising by Ofcom
minimum unit pricing

160
Q

at risk drinking

A

a pattern of drinking which brings about the risk of physical or psychological harm

161
Q

alcohol abuse

A

a pattern of drinking which is likely to cause physical or psychological harm

162
Q

alcohol dependence

A

substance dependence is defined as a set of behavioural, cognitive and psychological responses that can develop after repeated substance use

163
Q

alcohol dependence: pharmacological treatment

A

disulfiram
naltrexone
acamprosate calcium

164
Q

alcohol dependence: psychosocial treatment

A

therapy

social support

165
Q

key policy for alcohol intervention

A

models of care for alcohol misusers (MoCAM)

involves: screening and assessment, the four tier framework and care planning and co ordination

166
Q

severity of dependence questionnaire

A 
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
Q

alcohol and the nervous system

A

alcohol potentiates gamma-amino butyric acid (major inhibitory neurotransmitter in CNS)
it also inhibits major excitatory neurotransmitter- glutamate and n-methyl-d-asparate

168
Q

tolerance

A

a state in which an organism no longer responds to a drug

a higher dose is required to achieve the same effect

169
Q

alcohol withdrawal: Chlordiazepoxide absorption

A 
absorbed in small intestine
highly lipophilic
it can be delayed in the elderly
half life is 6-30 hours
protein bound
170
Q

alcohol withdrawal: Chlordiazepoxide distribution and metabolism

A

metabolised in liver
crosses blood brain barrier
active in CNS grey matter

171
Q

alcohol withdrawal: Chlordiazepoxide elimination

A

excreted in urine in the form of its metabolites

or as conjugates

172
Q

alcohol withdrawal: Chlordiazepoxide contraindications

A 
hypersensitivity to benzodiazepines
pulmonary insufficiency
pregnancy
chronic psychosis
myasthenia gravis
173
Q

alcohol withdrawal: Chlordiazepoxide dependence

A

short term use= low chance of dependence

risk of physical and psychological dependence increases with increased dose

174
Q

alcohol withdrawal: Chlordiazepoxide drug interactions

A

alcohol- enhanced sedative effect
centrally acting drugs (antipsychotics, analgesics)
anti-epileptic drugs

175
Q

alcohol withdrawal: Chlordiazepoxide side effects

A 
drowsiness
ataxia
aggression
headache
resp depression
impaired liver function
176
Q

wernicke’s encephalopathy

A 
deficiency of thiamine
common in dependent drinkers
poor diet
poor intake of vitamins
poor gastro-intestinal absorption
177
Q

wernicke’s encephalopathy treatment

A

pabrinex and ongoing with vit b/thiamine

178
Q

alcohol relapse prevention: acamprosate

A

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
Q

alcohol relapse prevention: disulfiram

A

disrupts oxidative metabolism of alcohol

results in a build up acetaldehyde

180
Q

alcohol relapse prevention: disulfiram symptoms

A 
long hangover
flushing of skin
tachycardia
SOB
nausea
vomiting
181
Q

alcohol relapse prevention: nalmefine

A

opioid receptor antagonist
modifies activity at receptor sites linked to reward mechanisms
effects of alcohol present but reduces feeling of reward and pleasure

182
Q

the four tier framework

A

non-substance misuse specific services
open access drug/alcohol services
specialist community based clinics
specialist in patient services

183
Q

types of intestinal obstructions

A

intraluminal obstructions
intramural
extraluminal

184
Q

extraluminal obstructions

A

outside the wall of the gut

185
Q

intramural obstructions

A

within the wall of the gut

186
Q

intraluminal obstructions

A

within the gut

187
Q

intraluminal obstructions: tumours

A

carcinoma
lymphoma
tumours on the left side can obstruct more quickly than the right

188
Q

intraluminal obstructions: diaphragm disease

A

caused by NSAIDS- cause submucosal fibrosis
this results in diaphragm like strictures in the GI tract
most common in small bowel

189
Q

intraluminal obstructions: meconium ileus

A

meconium thicker and stickier

190
Q

intraluminal obstructions: gallstone ileus

A

gallstones erode into the bowel causing the obstruction

191
Q

intramural obstructions: inflammatory

A

crohn’s

diverticulutis

192
Q

intramural obstructions: tumours

A

colorectal tumours

193
Q

intramural obstructions: neural

A

hirschprung’s disease:

developmental where segment of bowel towards distal end hasnt got ganglion cells- no coordinated contraction

194
Q

intramural obstructions: crohn’s disease

A

main inflammatory cause of obstructions (granulomatous inflammation)
particularly ileum
deep fissuring ulcers and fibrosis

195
Q

intramural obstructions: diverticular disease

A

mainly older people
small outpuching of mucosae which can become inflamed (stasis of faeces)
risk of rupture

196
Q

diverticular disease pathogenesis

A

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
Q

extra luminal obstructions: adhesions

A

previous surgery causes fibrosis

adhesion can cause kinks in bowel resulting in obstruction

198
Q

extra luminal obstructions: volvulus

A

sigmoid volvulus where sigmoid twists

can twist and untwist resulting in abdomen pain coming and going

199
Q

extra luminal obstructions: tumours

A

peritoneal deposits of tumour such as ovarian cancer

200
Q

intestinal obstruction definition

A

arrest/blockage of onward propulsion or intestinal contents

201
Q

small bowel obstructions

A

account for 60-75% of intestinal obstructions

202
Q

small bowel obstructions: causes

A

crohn’s disease (25%)
surgery/adhesions (60%)
hernia
malignancy

203
Q

small bowel obstructions: clinical presentations

A 
pain-colicky 
vomiting- early and follows pain
tenderness
constipation
increased bowel sounds
204
Q

small bowel obstructions: diagnosis

A

abdominal x-ray
examination
FBC
CT

205
Q

small bowel obstructions: treatment

A 
aggressive fluid resuscitation
bowel decompression
analgesia and antiemetic
antibiotics
surgery
206
Q

large bowel obstructions

A

25% of obstructions

207
Q

large bowel obstructions: causes

A

90% in US/europe due to colorectal malignancy

in african countries more likely to be volvulus

208
Q

large bowel obstructions: clinical presentations

A 
abdominal pain
abdominal distention
bowel sounds normal, then increased lated
palpable mass
late vomiting
constipation
bloating
209
Q

large bowel obstructions: diagnosis

A

digital rectal exam
FBC
abdominal x-ray
CT

210
Q

large bowel obstructions: treatment

A 
aggressive fluid resuscitation
bowel decompression
analgesia and antiemetic
antibiotics
surgery
211
Q

pseudo-bowel obstructions

A

clinical picture mimics obstruction but with no mechanical cause

212
Q

causes of pseudo-bowel obstructions

A 
intra-abdo trauma
pelvic/spinal fractures
postoperative states
sepsis
pneumonia 
drugs (opiates)
213
Q

pseudo-bowel obstructions: clinical presentation

A

rapid and progressive abdominal distention and pain

214
Q

pseudo-bowel obstructions: diagnosis

A

x-ray shows a gas-filled large bowel

215
Q

pseudo-bowel obstructions: treatment

A

treat underlying problem

IV neostigmine

216
Q

lower GI tumours: epidemiology

A

higher prevalence in elderly
incidence rates higher in those with low fibre diet
incidence increasing due to screening
mortality decreasing

217
Q

lower GI tumours: adenomas as a risk factor

A

the bigger the greater change of turning malignant

normal epithelium -> dysplastic epithelium (adenoma) -> colorectal adenocarcinoma

218
Q

lower GI tumours: familial adenomatous polyposis as a risk factor

A

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
Q

lower GI tumours: hereditary nonpolyposis colorectal cancer as a risk factor

A

no DNA repair protein produced

it has a risk of further cancers in index patients and relatives

220
Q

lower GI tumours: resection margin coding

A 
R0= tumour completely excised
R1= microscopic involvement of margin by tumour
R2= macroscopic involvement of margin by tumour
221
Q

lower GI tumours: prognosis

A

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
Q

lower GI tumours: staging

A

determine the spread of the tumour
greater the spread the worse the prognosis
lymph node and peritoneal involved included in staging

223
Q

lower GI tumours: dukes’ stages

A

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)

224
Q

lower GI tumours: treatment

A

prevention (normal)
endoscopic resection (adenomas)
surgical resection
chemotherapy and palliative care

225
Q

gastroduodenal ulceration and gastritis: causes

A

mucosal ischaemia
increased acid production
bile reflux
helicobacter infection

226
Q

gastroduodenal ulceration and gastritis: mucosal ischaemia

A

reduces mucin production so no mucin barrier

this causes cell death and acid enters between cells causing ulceration

227
Q

gastroduodenal ulceration and gastritis: mucosal ischaemia treatment

A

reverse mucosal ischaemia

PPIs- omeprazole, lansoprazole

228
Q

gastroduodenal ulceration and gastritis: increased acid production

A

overwhelm defences, causing ulceration to occur

229
Q

gastroduodenal ulceration and gastritis: increased acid production causes

A

stress
helicobacter pylori
drugs such as aspirin or ibruprofen

230
Q

gastroduodenal ulceration and gastritis: increased acid production treatment

A

PPIs

aspirin with enteric coats

231
Q

gastroduodenal ulceration and gastritis: bile reflux

A

bile causes ulceration

232
Q

gastroduodenal ulceration and gastritis: bile reflux causes

A

alcohol in high concentrations

233
Q

peptic ulceration complications

A

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

234
Q

malabsorption: main presentation

A

diarrhoea
anaemia
weight loss
fatty stools

235
Q

malabsorption: causes

A 
insufficient intake
defective intraluminal digestion
insufficient absorption area
lack of digestive enzymes
defective epithelial transport
lymphatic obstruction
236
Q

malabsorption: defective intraluminal digestion

A

pancreatic insufficiency
defective bile secretion
bacterial overgrowth

237
Q

defective intraluminal digestion: pancreatic insufficiency

A

pancreatitis - no enzymes

cystic fibrosis -blocked pancreatic duct

238
Q

defective intraluminal digestion: defective bile secretion

A

biliary obstruction - e.g. gallstone

ileal resection - decreased bile salt uptake

239
Q

malabsorption: insufficient absorption area

A

gluten sensitive enteropathy
crohn’s disease
extensive surface parasitisation
small intestinal resection

240
Q

insufficient absorption area: gluten sensitive enteropathy (coeliac)

A

villous atrophy
crypt hyperplasia
increased number of lymphocytes

241
Q

insufficient absorption area: crohn’s disease

A

inflammatory disease of the bowel
reduces surface area
cobblestone mucosa

242
Q

insufficient absorption area: extensive surface parasitisation

A 
giardia lamblia (malabsorption and weight loss)
parasites coat the surface of the vili (food cannot be absorbed)
243
Q

insufficient absorption area: small intestine resection

A

done in:
morbid obesity
crohn’s disease
infarcted small bowel

244
Q

malabsorption: lack of digestive enzymes

A 
disaccharidase deficiency (lactose intolerance)
bacterial overgrowth (brush border damage)
245
Q

malabsorption: defective epithelial transport

A

abetaliapoproteinaemia

primary bile acid malabsorption

246
Q

malabsorption: lymphatic obstruction

A

lymphoma

tuberculosis

247
Q

coeliac disease pathology

A 
allergic reaction to Giliadin protein
Giliadin peptide bind to antigen presenting cell
APC activated 
cell injury
Giliadin antibodies, transglutaminase Ab
248
Q

chronic idiopathic inflammatory bowel disease

A

crohn’s disease

ulcerative colitis

249
Q

bowel inflammatory conditions

A

diverticulitis
ischaemic colitis
infective colitis

250
Q

crohn’s disease

A

inflammation of bowel anywhere from mouth to anus

mainly terminal ilium

251
Q

crohn’s disease: features

A

skip lesions
passes all the way through mucosa, submucosa, muscularis propria and serosa
deep fissuring ulceration
fibrosis

252
Q

crohn’s disease: complications of the bowel

A 
malabsorption
obstructions
perforation
fistula
neoplasia
anal fissures and skin tags
253
Q

crohn’s disease: systemic complications

A

amyloidosis

254
Q

ulcerative colitis

A

inflammation with ulcer formation in the colon

starts and rectum and moves proximally, stopping at caecum

255
Q

ulcerative colitis: features

A

only in mucosa
distinct boundary between disease and normal bowel
diffuse pattern- not patchy

256
Q

ulcerative colitis: complications of the colon

A

blood loss
toxic dilation
colorectal cancer

257
Q

ulcerative colitis: complications of the joints

A

ankylosing spondylitis

arthritis

258
Q

ulcerative colitis: complications of the eyes

A

iritis
uveitis
episcleritis

259
Q

ulcerative colitis: complications of the skin

A

erythema nososum

pyoderma gangrenosum

260
Q

ulcerative colitis: complications of the liver

A

fatty change

chronic and/or sclerosing pericholangitis

261
Q

oesophageal adenocarcinoma: epidemiology

A

increases with age

more common in males

262
Q

oesophageal adenocarcinoma

A

barret’s oesophagus

columnar lined lower oesophagus (CELLO)

263
Q

oesophageal adenocarcinoma: metaplasia

A

change in differentiation of a cell from one fully differentiated type to another

264
Q

oesophageal adenocarcinoma: pathogenesis

A

acid reflux causes metaplasia from stratified squamous to simple columnar
change in cell type increases risk of adenocarcinoma

265
Q

oesophageal adenocarcinoma: pathway

A

normal squamous epithelium
gastro-oesophageal reflux causes metaplastic oesophageal glandular epithelium
reflux continues- dysplastic epithelium
finally neoplastic epithelium

266
Q

oesophageal adenocarcinoma: causes

A

obesity is main cause of reflux

267
Q

oesophageal squamous cancer- risk factors

A

smoking and drinking

268
Q

oesophageal cancer: complications

A

difficulty swallowing early
can pass into blood vessels
a late presentation decreases survival rate

269
Q

gastric cancer: epidemiology

A

incidence is decreasing

more common in males

270
Q

gastric cancer: causes

A

genetic- mutation in E cadherin transport proteins
environmental
helicobacter infection
pernicious anaemia- mucosal ischaemia

271
Q

gastric cancer: pathogenesis

A 
normal mucosa
intestinal metaplasia
dysplasia
intramucosal carcinoma
invasive carcinoma
272
Q

gastric cancer: presentation

A

late presentation as tumour can grow quite large in the stomach before complications

273
Q

gastric cancer: stages

A

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

274
Q

coeliac disease

A

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

275
Q

coeliac disease: epidemiology

A

1% of population affected
occurs any age but peaks in infancy and 50-60 y/o
affects males and females equally

276
Q

coeliac disease: risk factors

A

having other autoimmune disease
IgA deficiency
age of introduction to gluten

277
Q

coeliac disease diagnosis

A

should maintain gluten for at least 6 weeks before testing to get true results
FBC, duodenal biopsy, serum antibody testing

278
Q

coeliac disease diagnosis: FBC

A

low Hb
low B12
low ferritin

279
Q

coeliac disease diagnosis: duodenal biopsy

A

gold standard

see villous atrophy, crypt hyperplasia and increased intraepithelial white cell count

280
Q

coeliac disease diagnosis: serum antibody testing

A

most sensitive tests (95%) are EMA, tTG (both are IgAs and correlate with severity of mucosal damage)
not sensitive if IgA deficient

281
Q

coeliac disease: treatment

A

live long gluten free diet
correction of vitamin and mineral deficiencies
DEXA scan to monitor osteoporotic risk

282
Q

coeliac disease: complications

A

not improving on the strict diet- non responsive coeliac disease
anaemia
secondary lactose intolerance
T cell lymphoma

283
Q

coeliac disease: prolamins

A

gliadin- wheat
hordeins- barley
secalins- rye
prolamin is a component of gluten

284
Q

coeliac disease: prolamins

A

gliadin- wheat
hordeins- barley
secalins- rye
prolamin is a component of gluten

285
Q

peritonitis definition

A

inflammation of peritoneum

286
Q

peritonism definition

A

tensing of the muscles to prevent movement of peritoneum

287
Q

visceral peritoneum

A

on the organs
autonomic innervation
sensation poorly localised

288
Q

parietal peritoneum

A

covers abdo wall
somatic innervation
sensation well localised

289
Q

foregut sensation

A

lower oesophagus to D2, liver, spleen, gallbladder
autonomic pain= epigastric region
greater splanchnic T5-9

290
Q

midgut sensation

A

D2- 2/3 of transverse colon
site of autonomic pain= umbilical region
less splanchnic T10-11

291
Q

hindgut sensation

A

2/3 transverse colon to upper rectum
autonomic pain= hypogastric region
least splanchnic nerve T12/L1

292
Q

peritonitis: causes

A 
inflamed organ
air (ulcer, trauma)
pus (bacterial)
faeces/luminal contents (perforation)
blood (trauma)
293
Q

primary peritonitis

A 
inflammation on its own
spontaneous bacterial peritonitis
ascites
diagnose with ascitic tap and blood cultures
treat with broad spectum antibiotics
294
Q

secondary peritonitis

A

caused by something else e.g. chemicals or bile

treat the cause

295
Q

peritonitis: common causes of abdo pain

A 
gastritis (epigastric)
cholecystits (RUQ, midclavicular)
pancreatitis (epigastric)
appendicitis (umbilical then McBurney's point)
diverticulitis (LLQ)
296
Q

peritonitis: epidemiology

A

370,000 admissions /year in uk

mortality 15%

297
Q

peritonitis: symptoms

A

kidney failure symptoms
abdominal pain:
-sudden onset= perforation
-slow onset= secondary to inflammatory disease
-poorly localised= irritation of visceral
-localised= irritation of parietal

298
Q

peritonitis: signs

A 
rebound tenderness
percussion pain
guarding
no bowel sounds
shock
lying still
299
Q

peritonitis: complications

A 
sepsis
multi-organ failure
kidney failure
paralytic ileus
abscess formation
CVS events
300
Q

peritonitis: investigations

A

CT scan
blood test
CXR
abdo XR

301
Q

peritonitis: treatment

A 
treat cause
fluid resuscitation
antibiotics
surgery
after care (kidneys, phsyio, nutrition)
302
Q

ascites definition

A

abnormal accumulation of fluid within peritoneal cavity

303
Q

ascites: epidemiology

A

(healthy men/women= no fluid/20ml)
10-20% 5 year survival from onset
signifies serious illness such as cirrhosis

304
Q

ascites causes

A

impaired blood flow
local inflammation
decreased oncotic pressure

305
Q

ascites cause by impaired blood flow

A

cirrhosis- portal hypertension
cardiac failure
constrictive pericarditis

306
Q

ascites cause by local inflammation

A

(leaky membrane)
peritonitis
abdo cancers (Esp. ovarian)
infection e.g. TB

307
Q

ascites cause by decreased oncotic pressure

A

hypoalbuminaemia
nephrotic syndrome
malnutrition

308
Q

ascites: exudate fluid

A

high protein fluid

309
Q

ascites: exudate fluid pathology

A

low serum to ascites/albumin ratio
outflow is fine
altered oncotic pressure
membrane more porous

310
Q

ascites: exudate fluid treatment

A

treat underlying cause

311
Q

ascites: exudate fluid causes

A

malignancy
sepsis
TB
nephrotic syndrome

312
Q

ascites: transudate fluid

A

low protein fluid

313
Q

ascites: transudate fluid pathology

A

high serum to ascites/albumin ration
outflow increased
decreased oncotic pressure
membrane okay

314
Q

ascites: transudate fluid causes

A

cirrhosis

cardiac failure

315
Q

ascites: transudate fluid management

A

treat cause
diet
diuretic
drainage

316
Q

ascites: history

A

how long has swelling been there?
drugs?
weight loss?
any obvious underlying cause?

317
Q

ascites: complications

A

stasis results in bacterial overgrowth- spontaneous bacterial peritonitis

318
Q

ascites: examination

A

presences is confirmed by demonstrating shifting dullness with percussion

ultrasound/xray/ct

319
Q

ascitic tap: diagnostic aspiration

A 
10-20ml of fluid to see:
raised white cell count (bacterial peritonitis)
gram stain and culture
cytology for malignancy
amylase to exclude pancreatic ascites
320
Q

ascitic tap: protein measurement (transudate)

A

less bad

transparent due to little protein (<30g/L)

321
Q

ascitic tap: protein measurement (exudate)

A 
extremely bad
high protein (>30g/L)
322
Q

ascites: treatment

A 
treat cause
reduce sodium intake
increase sodium excretion
diuretic
drain fluid
323
Q

ascites: risk factors

A

high sodium diet
hepatocellular carcinoma
splanchnic vein thrombosis- portal hypertension

phase 2a clinical (8 decks)

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