Gastroenterology Flashcards
1
Q
how do you classify flares of ulcerative colitis
A
2
Q
what is the triad for intestinal angina
A
colicky post-prandial abdo pain
weight loss
abdominal bruits
3
Q
what are the two types bowel ischaemia
A
- acute mesenteric ischaemia
- abdo pain severe and sudden and out of keeping with physical exam findings
- ususally caused by embolism
- classically with a history of atrial fibrillation
- management is urgent surgery
- poor prognosis
- ischaemic colitis
- acute but transient compromise of blood flow to large bowel
- can cause inflammation, haemorrhage and ulceration
- more common in watershed areas like the splenic flexure
- border of are supplied by superior and inferior mesenteric arteries
4
Q
what are the investigations for bowel ischaemia
A
- CT
- thumbprinting is seen in ischaemic colitis
5
Q
what is the management of acute mesenteric ischaemia
A
URGENT SURGERY
6
Q
what is the management of ischaemic colitis
A
usually supportive - surgery may be needed in a minority of cases if conservative measures fail
7
Q
if a patient has already eliminated gluten from their diet how long should they reintroduce it for before they can be re-investigate for coeliac
A
6 weeks
8
Q
how i coeliac diagnosed
A
- serology
- TTG IgA
- also look for endomyseal antibody to check for IgA deficiency which would give a false negative result
- endoscopic duodenal biopsy
- gold standard
- findings
- villous atropy
- crypt hyperplasia
- increase in intraepithelial lymphocytes
- lamina propria lymphocytic infiltration
9
Q
what is boerhaave syndrome
A
acute oesophageal rupture due to extreme vomiting
10
Q
what is the presentation of boerhaave syndrome
A
- triad
- prolonged violent vomiting
- sudden onset chest pain
- shock
- may also have
- surgical emphysema
11
Q
what is plummer-vinson syndrome
A
- triad of
- dysphagia (secondary to oesophageal webs)
- glossitis
- iron deficiency anaemia
- treatment is iron supplementation and dilation of the webs
12
Q
what is mallory weiss syndrome
A
- severe vomiting -> painful mucosal lacerations at the GO junction
- results in haematemesis
- common in alcoholics
13
Q
how do you calculate number of units in alcohol
A
volume in ml x (ABV/1000)
14
Q
investigation of new onset dysphagia
A
urgent endoscopy - it’s a red flag symptom
15
Q
causes of dysphagia by classification
A
16
Q
- is total iron binding capacity low or high in:
- a: iron deficiency anaemia
- b: anaemia of chronic disease
A
- a) TIBC is high in iron deficiency anaemia as the body produces more transferrin to try and carry more iron
- b) TIBC is low in anaemia of chronic disease because the body is not able to produce as much transferrin
17
Q
features of hepatic encephalopathy
A
- altered GCS
- asterixis
- constructural apraxia (inability to draw a 5 pointed star)
- triphasic slow waves on EEG
- raised ammonia level
18
Q
grading of hepatic encephalopathy
A
- Grade 1: irritability
- Grade 2: confusion, inappropriate behaviour
- Grade 3: incoherent, restless
- Grade 4: coma
19
Q
management of hepatic encephalopathy
A
- lactulose
- promotes excretion of ammonia and increases metabolism of ammonia by gut bacteria
- rifaximin
- modulates the gut flora resulting in decreased ammonia production
20
Q
what is the only investigation recommended for H.pylori post-eradication therapy
A
urea breath test
21
Q
why do patients with coeliac disease require immunisations and which immunisations do they requrie
A
- because they often have a degree of functional hyposplenism
- so they’re offered the pneumococcal vaccine
- booster every five years
- flu vaccine on an individual level
22
Q
compare adenocarcinoma and squamous cell carcinoma of the oesophagus
A
23
Q
what is the finding on PR exam in appendicitis
A
right sided tenderness
24
Q
blood results in apendicitis
A
a neutrophil-predominant leucocytosis
25
what is Zollinger-Ellison syndrome
* characterised by excessive levels of gastrin
* usually because of a gastrin secreting tumour of the duodenum or pancreas
* about 30% of cases are due to multiple endocrine neoplasia type 1 (MEN-1)
* features
* diarrhoea
* malabsorption
* multiple gastroduodenal ulcers
26
symptoms of vitamin c deficiency
* follicular hyperkeratosis
* easy bruising
* poor wound healing
* gingivitis with bleeding and receeding gums
* sjorgen's syndrome
* arthralgia
* oedema
27
diagnosis of SBP
paracentesis shows neutrophil count \>250cells/ul
28
what is the most common organism found on ascitic fluid culture in SBP
E.coli
29
what is the management of SBP
IV cefotaxime
30
what is budd-chiari syndrome
* hepatic vein thrombosis usually seen in the context of underlying haematological disease or another procoagulant condition
* it presents with a triad of:
* sudden onset abdominal pain
* ascites
* tender hepatomegaly
31
which antibodies are associated with primary biliary cirrhosis?
* anti-mitochondrial antibodies
* remember rule of M
* IgM
* anti-mitochondrial antibodies M2 subtype
* Middle aged females
32
diagnosis of PBC
* anti-mitochondrial antibodies M2 subtype highly specific and sensitive
* raised serum IgM
* imaging
* MRCP or RUQ US
* required to exclude extrahepatic biliary obstruction
33
management of PBC
* ursodeoxycholic acid
* slows disease progression and improves symptoms
* cholestyramine for pruritis
* fat soluble vitamin supplementation
* transplant
* if bilirubin \>100
* recurrence can occur in graft but not usually a problem
34
what is wilson's disease
* it is an autosomal recessive disorder characterised by excessive copper deposition in the tissues
* due ot increased copper absorption in the small intestine and decreased hepatic copper excretion
35
what is the gene affected in wilson's
ATP7B gene on chromosome 13
36
features of wilson's disease
* liver
* hepatitis
* cirrhosis
* neurological
* speech, behavioural and psychiatric problems
* dementia
* parkinsonism
* chorea
* asterixis
* eyes
* kayser-fleischer rings
* renal tubular acidosis
* haemolysis
* blue nails
37
diagnosis of wilson's disease
* slit lamp examination for kayser-fleischer rings
* reduced serum caeruloplasmin
* reduced total serum copper
* this is counterintuitive but 95% of plasma copper is carried by caeruloplasmin
* so free (non c-bound) serum copper is increased
* increased 24hr urinary copper excretion
38
management of wilson's disease
* copper chelators
* penicillamine
* trientine hydrochloride
39
describe the clostridium difficile bacterium
gram positive rod
40
how do you grade severity of clostridium difficile infection
* Mild:
* normal wcc
* Moderate
* WCC \<15x109/L
* Typically 5 loose stools per day
* Severe
* WCC \>15x109/L
* Evidence of AKI
* or temperature \>38.5C
* Life threatening
* hypotension
* partial or complete ileus
* toxic megacolon
41
diagnosis of clostridium difficile
* detection of clostridium difficile toxin in the stool
* clostridium difficile antigen positivity only shows exposure to the bacteria rather than the current infection
42
management of clostridium difficile
* mild/moderate
* oral metronidazole
* severe
* oral vancomycin
* life threatening
* combination of oral vancomycin and IV metronidazole
43
what does this sign mean
this is apple core sign of the oesophagus on barrium swallow
in the context of dysphagia this is highly suggestive of oesophageal carcinoma
44
what is the best blood test to assess severity of liver cirrhosis
albumin and coagulation
lfts are poor as they do not actually reflect liver function and are commonly low in end stage liver disease
45
differences between adenocarcinoma and squamous cell carcinoma of the oesophagus in terms of epidemiology, locaiton and risk factors
46
what happens to ferritin and TIBC in anaemia of chronic disease and why?
Ferritin (the protein that stores iron and releases it) is high, indicating that the body is storing iron outside the blood, as it wants to keep it away from bacteria that can use it to survive or a blood loss.
Total iron-binding capacity (TIBC) is low, indicating that all the iron in the body is already bound to avoid being dispersed
These are all features of anaemia of chronic disease, usually secondary to chronic infections, inflammation or neoplasias.
47
what happens to TIBC and ferritin in iron deficiency anaemia and why
high TIBC as there is no iron-bound and the ferritin is decreased as there is low iron to store
48
management of pernicious anaemia
* IM B12 replacement
* no neurological features:
* 3 injections per week for 2 weeks
* followed by 3 monthly injections
* more frequent doses if there are neurological features
49
adverse effects of PPIs
hyponatraemia
hypomagnasaemia
osteoporosis
microscopic colitis
increased risk of c.diff
50
which ulcers have pain that is made worse by eating and which ulcers have pain that gets better with eating?
duodenal ulcers: pain relieved by eating
gastric ulcers: pain worsened by eating
51
what is often used to treat acute episodes of alcoholic hepatitis
glucocorticoids such as prednisolone
52
causes of raised ferrtitin
53
how do you tell if there is iron overload
transferrin saturation
Typically, normal values of \< 45% in females and \< 50% in males exclude iron overload.
54
what is SAAG
serum abdominal albumin gradient
used to check if ascites is caused by portal hypertension or not
a raised saag indicates that portal hypertension has caused the ascites
55
what is budd chiari syndrome and how does it present
* it is hepatic vein thrombosis and it is usually seen in the context of underlying procoagulant conditions
* classical triad of:
* abdo pain - sudden and severe
* ascites
* tender hepatomegaly
56
investigations for budd chiari syndrome
US with doppler flow studies
57
what is kantor's string sign
it is seen on barium study of patients with crohns
it's a long stricture in the terminal ileym which is 'string-like'
58
treatment for severe ulcerative colitis
IV steroids given as first line
59
risks of ercp
bleeding
duodenal perforation
cholangitis
pancreatitis
60
what is the pathophys of hepatorenal syndrome
* vasoactive mediators cause splanchnic vasodilation
* this reduces systemic vascular resistance
* this results in underfilling of the kidneys
* this is sensed by the juxtaglomerular apparatus which activates raas
* this causes renal vasoconstriction
* but this isn't enough to counterbalance the effect of the splanchnic vasodilation
61
what is the management of hepatorenal syndrome
vasopressin analogues such as terlipressin
volume expansion with 20% albumin
liver transplant
62
siblings of patients with hereditary haemochromatosis have what chance of being susceptible?
25%
it is autosomal recessive
63
name two aminosalicylate drugs
sulphasalazine
mesalazine
64
side effects of aminosalicyclates
haematological adverse effects including agranulocytosis - if they get sick they need a fbc straight away
pancreatitis is 7 times more common in patients taking mesalazine than sulfasalazine
65
if someone has B12 deficiency as well as folate deficiency how should you treat
IM replacement of B12 before folate replacement
B12 replacement should occur prior to folate replacement since if folate is done first they can get subacute combined degeneration of the spinal cord
66
primary sclerosing cholangitis is associated with what autoantibody?
p-ANCA
67
anti-dsDNA antibody is primarily associated with what
SLE
68
anti-CCP antibody is highly specific for what
rheumatoid arthritis
69
anti-GBM antibody is associated with what
goodpastures syndrome
70
combination of deranged LFTs combined with secondary amenorrhoea is strongly suggestive of what
autoimmune hepatitis
71
deranged LFTs associated with ANA and anti smooth muscle antibody is what?
type 1 autoimmune hepatitis
72
what are the definitive features of acute liver failure
rapid occurance of the following:
jaundice
coagulopathy
encephalopathy
73
what is the first line antibiotic for treatment of patients with clostridium difficile
oral metronidazole
74
what would your blood gasses show in mesenteric ischaemia
metabolic acidosis so low bicarbonate
not on blood gas but they will also have elevated white blood cells
75
management of ascites
* reduce dietary sodium
* fluid restriction if sodium \<125mmol/L
* aldosterone antagonists e.g. spironolactone
* this is potassium sparing
* drainage of tense ascites by abdominal paracentesis
* oral ciprofloxacin prophylaxis if ascitic protein 15g/L or less
* transjugular intrahepatic portosystemic shunt (TIPS) may be considered in some patients
76
what is the treatment for wilson's disease
penicillamine
77
management for barretts oesophagus when dysplasia is present
endoscopic mucosal resection
endoscopic radiofrequency ablation
78
managmement of barretts oesophagus when there is metaplasia but no dysplasia
endoscopic surveillance with biopsies every 3-5 years
high dose PPIs
79
80
urea breath tests requires the person to have been off which drugs and for how long?
no abx past 4 weeks
no antisecretory drugs e.g. PPI in past 2 weeks
81
what test can you do to differentiate between IBD and IBS before you send someone for a colonoscopy
faecal calprotectin
82
what is the first line treatment for primary biliary cholangitis
ursodeoxycholic acid
83
