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Final Year Medicine Recap > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

how do you classify flares of ulcerative colitis

A
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2
Q

what is the triad for intestinal angina

A

colicky post-prandial abdo pain

weight loss

abdominal bruits

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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
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4
Q

what are the investigations for bowel ischaemia

A
  • CT
  • thumbprinting is seen in ischaemic colitis
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5
Q

what is the management of acute mesenteric ischaemia

A

URGENT SURGERY

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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

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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

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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
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9
Q

what is boerhaave syndrome

A

acute oesophageal rupture due to extreme vomiting

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10
Q

what is the presentation of boerhaave syndrome

A
  • triad
    • prolonged violent vomiting
    • sudden onset chest pain
    • shock
  • may also have
    • surgical emphysema
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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
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12
Q

what is mallory weiss syndrome

A
  • severe vomiting -> painful mucosal lacerations at the GO junction
  • results in haematemesis
  • common in alcoholics
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13
Q

how do you calculate number of units in alcohol

A

volume in ml x (ABV/1000)

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14
Q

investigation of new onset dysphagia

A

urgent endoscopy - it’s a red flag symptom

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15
Q

causes of dysphagia by classification

A
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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
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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
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18
Q

grading of hepatic encephalopathy

A
  • Grade 1: irritability
  • Grade 2: confusion, inappropriate behaviour
  • Grade 3: incoherent, restless
  • Grade 4: coma
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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
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20
Q

what is the only investigation recommended for H.pylori post-eradication therapy

A

urea breath test

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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
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22
Q

compare adenocarcinoma and squamous cell carcinoma of the oesophagus

A
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23
Q

what is the finding on PR exam in appendicitis

A

right sided tenderness

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24
Q

blood results in apendicitis

A

a neutrophil-predominant leucocytosis

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25
Q

what is Zollinger-Ellison syndrome

A
  • 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
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26
Q

symptoms of vitamin c deficiency

A
  • follicular hyperkeratosis
  • easy bruising
  • poor wound healing
  • gingivitis with bleeding and receeding gums
  • sjorgen’s syndrome
  • arthralgia
  • oedema
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27
Q

diagnosis of SBP

A

paracentesis shows neutrophil count >250cells/ul

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28
Q

what is the most common organism found on ascitic fluid culture in SBP

A

E.coli

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29
Q

what is the management of SBP

A

IV cefotaxime

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30
Q

what is budd-chiari syndrome

A
  • 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
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31
Q

which antibodies are associated with primary biliary cirrhosis?

A
  • anti-mitochondrial antibodies
  • remember rule of M
    • IgM
    • anti-mitochondrial antibodies M2 subtype
    • Middle aged females
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32
Q

diagnosis of PBC

A
  • anti-mitochondrial antibodies M2 subtype highly specific and sensitive
  • raised serum IgM
  • imaging
    • MRCP or RUQ US
    • required to exclude extrahepatic biliary obstruction
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33
Q

management of PBC

A
  • 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
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34
Q

what is wilson’s disease

A
  • 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
Q

what is the gene affected in wilson’s

A

ATP7B gene on chromosome 13

36
Q

features of wilson’s disease

A
  • liver
    • hepatitis
    • cirrhosis
  • neurological
    • speech, behavioural and psychiatric problems
    • dementia
    • parkinsonism
    • chorea
    • asterixis
  • eyes
    • kayser-fleischer rings
  • renal tubular acidosis
  • haemolysis
  • blue nails
37
Q

diagnosis of wilson’s disease

A
  • 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
Q

management of wilson’s disease

A
  • copper chelators
    • penicillamine
    • trientine hydrochloride
39
Q

describe the clostridium difficile bacterium

A

gram positive rod

40
Q

how do you grade severity of clostridium difficile infection

A
  • 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
Q

diagnosis of clostridium difficile

A
  • detection of clostridium difficile toxin in the stool
  • clostridium difficile antigen positivity only shows exposure to the bacteria rather than the current infection
42
Q

management of clostridium difficile

A
  • mild/moderate
    • oral metronidazole
  • severe
    • oral vancomycin
  • life threatening
    • combination of oral vancomycin and IV metronidazole
43
Q

what does this sign mean

A

this is apple core sign of the oesophagus on barrium swallow

in the context of dysphagia this is highly suggestive of oesophageal carcinoma

44
Q

what is the best blood test to assess severity of liver cirrhosis

A

albumin and coagulation

lfts are poor as they do not actually reflect liver function and are commonly low in end stage liver disease

45
Q

differences between adenocarcinoma and squamous cell carcinoma of the oesophagus in terms of epidemiology, locaiton and risk factors

A
46
Q

what happens to ferritin and TIBC in anaemia of chronic disease and why?

A

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
Q

what happens to TIBC and ferritin in iron deficiency anaemia and why

A

high TIBC as there is no iron-bound and the ferritin is decreased as there is low iron to store

48
Q

management of pernicious anaemia

A
  • 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
Q

adverse effects of PPIs

A

hyponatraemia

hypomagnasaemia

osteoporosis

microscopic colitis

increased risk of c.diff

50
Q

which ulcers have pain that is made worse by eating and which ulcers have pain that gets better with eating?

A

duodenal ulcers: pain relieved by eating

gastric ulcers: pain worsened by eating

51
Q

what is often used to treat acute episodes of alcoholic hepatitis

A

glucocorticoids such as prednisolone

52
Q

causes of raised ferrtitin

A
53
Q

how do you tell if there is iron overload

A

transferrin saturation

Typically, normal values of < 45% in females and < 50% in males exclude iron overload.

54
Q

what is SAAG

A

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
Q

what is budd chiari syndrome and how does it present

A
  • 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
Q

investigations for budd chiari syndrome

A

US with doppler flow studies

57
Q

what is kantor’s string sign

A

it is seen on barium study of patients with crohns

it’s a long stricture in the terminal ileym which is ‘string-like’

58
Q

treatment for severe ulcerative colitis

A

IV steroids given as first line

59
Q

risks of ercp

A

bleeding

duodenal perforation

cholangitis

pancreatitis

60
Q

what is the pathophys of hepatorenal syndrome

A
  • 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
Q

what is the management of hepatorenal syndrome

A

vasopressin analogues such as terlipressin

volume expansion with 20% albumin

liver transplant

62
Q

siblings of patients with hereditary haemochromatosis have what chance of being susceptible?

A

25%

it is autosomal recessive

63
Q

name two aminosalicylate drugs

A

sulphasalazine

mesalazine

64
Q

side effects of aminosalicyclates

A

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
Q

if someone has B12 deficiency as well as folate deficiency how should you treat

A

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
Q

primary sclerosing cholangitis is associated with what autoantibody?

A

p-ANCA

67
Q

anti-dsDNA antibody is primarily associated with what

A

SLE

68
Q

anti-CCP antibody is highly specific for what

A

rheumatoid arthritis

69
Q

anti-GBM antibody is associated with what

A

goodpastures syndrome

70
Q

combination of deranged LFTs combined with secondary amenorrhoea is strongly suggestive of what

A

autoimmune hepatitis

71
Q

deranged LFTs associated with ANA and anti smooth muscle antibody is what?

A

type 1 autoimmune hepatitis

72
Q

what are the definitive features of acute liver failure

A

rapid occurance of the following:

jaundice

coagulopathy

encephalopathy

73
Q

what is the first line antibiotic for treatment of patients with clostridium difficile

A

oral metronidazole

74
Q

what would your blood gasses show in mesenteric ischaemia

A

metabolic acidosis so low bicarbonate

not on blood gas but they will also have elevated white blood cells

75
Q

management of ascites

A
  • 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
Q

what is the treatment for wilson’s disease

A

penicillamine

77
Q

management for barretts oesophagus when dysplasia is present

A

endoscopic mucosal resection

endoscopic radiofrequency ablation

78
Q

managmement of barretts oesophagus when there is metaplasia but no dysplasia

A

endoscopic surveillance with biopsies every 3-5 years

high dose PPIs

79
Q
A
80
Q

urea breath tests requires the person to have been off which drugs and for how long?

A

no abx past 4 weeks

no antisecretory drugs e.g. PPI in past 2 weeks

81
Q

what test can you do to differentiate between IBD and IBS before you send someone for a colonoscopy

A

faecal calprotectin

82
Q

what is the first line treatment for primary biliary cholangitis

A

ursodeoxycholic acid

83
Q
A

Final Year Medicine Recap (9 decks)

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