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Year 6 > Gastro > Flashcards

Gastro Flashcards

1
Q

investigation for definitive diagnosis of Zollinger-Ellison Syndrome

A

Secretin Stimulation test

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2
Q

3 features of Zollinger-Ellison syndrome

A

multiple GI ulcers
diarrhoea
malabsorption –> weight loss

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3
Q

gold standard for diagnosis of achalasia

A

oesophageal manometry

first line: endoscopy

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4
Q

which condition shows Bird Beak sign on barium swallow

A

achalasia

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5
Q

management of chronic pancreatitis[2]

A

insulin replacement
Creon (pancreatic enzymes)

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6
Q

mode of inheritance of hereditary haemochromatosis

A

autosomal recessive

HFE gene

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7
Q

what must be checked before starting IV mannitol

A

cardiac function as it can precipitate arrhythmias

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8
Q

what does cryoprecipitate replace

A

fibrinogen therefore ideal for DIC

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9
Q

mode of inheritance of Gilbert’s syndrome

A

autosomal recessive

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10
Q

which type of ulcer is worse on eating

A

gastric

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11
Q

which type of ulcer is more likely to become malignant

A

gastric

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12
Q

most common bacteria involved in SBP [2]

A

E.coli and Klebsiella

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13
Q

first line treatment for acute constipation

A

ispaghula husk (bulk forming_

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14
Q

second line treatment for acute constipation

A

macrogol (osmotic laxative)

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15
Q

how is oesophageal metaplasia treated

A

endoscopic surveillance every 3-5 years

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16
Q

gold standard diagnostic for PSC

A

MRCP

non-invasive and fewer risks than ERCP

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17
Q

Gene involved in HNPCC

A

MSH2 (60%)
MLH1(30%)

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18
Q

Gene involved in FAP

A

APC

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19
Q

most common inheritable form of colorectal cancer

mode of inheritance

A

HNPCC

autosomal dominant

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20
Q

2nd most common inheritable form of colorectal cancer

mode of inheritance

A

FAP (rare <1%)

autosomal dominant

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21
Q

what other cancer can those with HNPCC get

A

endometrial

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22
Q

What other tumours are patients with FAP at risk of?

A

duodenal tumours

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23
Q

what are the features of Gardener’s syndrome

A

Variant of FAP with:
osteomas of the skull and mandible, retinal pigmentation, thyroid carcinoma and epidermoid cysts on the skin

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24
Q

which part of the colon does HNPCC tend to affect most

A

proximal colon

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25
Q

How much weight loss is diagnostic of malnutrition

A

Unintentional weight loss greater than 10% within the last 3-6 months

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26
Q

what BMI define malnutrition

A

<18.5

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27
Q

what combination of BMI and weight loss defines malnutrition

A

a BMI of less than 20 and unintentional weight loss greater than 5% within the last 3-6 months

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28
Q

screening tool for malnutrition

A

Malnutrition Universal Screening Tool (MUST)

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29
Q

which LFTs are raised in PSC

A

BR
GGT
ALP

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30
Q

which coagulation parameter is raised in acute liver failure

A

PT

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31
Q

what breath sign is associated with acute liver failure

A

fetor hepaticus

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32
Q

when is oral rifaximin used in treatment of hepatic encephalopathy

A

when treatment is refractory to oral lactulose

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33
Q

antihypertensive contraindicated in hiatus hernia

A

CCB

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34
Q

of the three types of jaundice, which one has ABSENT urobilinogen

A

post hepatic i.e obstructive as conjugated BR does not make it

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35
Q

ABs in PBC

A

AMA

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36
Q

diagnosis of Whipple’s disease

A

jejunal biopsy

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37
Q

management of Whipple’s disease

A

co-trimoxazole

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38
Q

how long should PPI be stopped before endoscopy

A

2 weeks

If endoscopy is negative consider 24-hr oesophageal pH monitoring (the gold standard test for diagnosis)

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39
Q

indication for liver transplant in non-paracetamol induced liver failure

A

PT >100

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40
Q

How is low-grade dysplasia on endoscopy managed

A

6 monthly surveillance and high dose PPI

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41
Q

most useful blood test for haemochromatosis

A

transferrin saturation

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42
Q

which water soluble vitamin in absorbed in the ileum

A

B12

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43
Q

What is the pathophysiology of delirium tremens?

A

unopposed glutamate activity

Acute alcohol consumption causes an increase in GABA neurotransmission. This is an inhibitory neurotransmitter. However, in those with chronically high alcohol intake, a compensatory decrease in GABA neurotransmission and increase in the excitatory neurotransmitter glutamate occurs.

This means that in cases of acute alcohol cessation, as in cases of delirium tremens, the upregulated glutamate is no longer opposed by GABA. This generates an overall excitatory state.

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44
Q

histological features of coeliac disease [3]

A

villous atrophy
crypt hyperplasia
intraepithelial lymphocytes

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45
Q

which site of the gut affected by Crohn’s contributes to gallstone formation?

A

terminal ileum

here, bile salts are reabsorbed usually

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46
Q

treatment of dermatitis herpetiformis

A

dapsone (abx)

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47
Q

surgical treatment of hiatus hernia and indication

A

Nissen’s fundoplication

when resistant to medication

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48
Q

AB in PBC

A

Positive Anti-mitochondrial antibodies (AMAs) in >90% of individuals
Raised serum IgM

anti-smooth muscle in 30%

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49
Q

main risk factor of MALT

A

H.pylori

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50
Q

main risk for EATL

A

coeliac disease

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51
Q

which fruit juice is an enzyme inhibitor

A

grapefruit

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52
Q

how is small bowel disease in Crohns best investigated

A

MRI small bowel as OGD won’t go far enough

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53
Q

what does Senna abuse cause?

A

melanosis coli

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54
Q

how many bowel movements in mild UC flare

A

<4 per day, little blood

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55
Q

how many bowel movement in moderate UC flare

A

4-6 per day, varied blood, no systemic features

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56
Q

how many bowel movements in severe UC flare

A

> 6 per day, systemic features

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57
Q

Gut layer features in UC

A

decreased goblet cells
crypt abscesses

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58
Q

Gut layer features in Crohn’s [2]

A

increased goblet cells
granulomas

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59
Q

most commonly affected part of the GIT in UC

A

rectum (LIF)

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60
Q

most commonly affected part of the GIT in Crohns

A

terminal ileum (RIF)

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61
Q

which IBD has rosethorn ulcers and cobblestoning

A

Crohns

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62
Q

which IBD has abscesses or fissures, how should they be investigated

A

Crohns; with a pelvic MRI

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63
Q

which IBD presents with non-bloody diarrhoea

A

Crohns

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64
Q

in which IBD is surgery not curative

A

Crohns

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65
Q

Extra-intestinal manifestations of IBD

A

A- Aphthous Ulcers
P- Pyoderma gangrenosum
I- iritis, anterior uveitis, episcleritis
E- Erythema nodosum
S- Sclerosing cholangitis (UC)
A- Arthritis
C- Clubbing (CD)

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66
Q

Drug for inducing remission in Crohns

A

steroids
mild: pred
severe: IV hydrocortisone
distal ileal: budesonide

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67
Q

drug for maintaining remission in Crohns

A

azathioprine or mercaptopurine

alt: aminosalicylates or biologics

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68
Q

treatment of severe fulminant UC

A

IV steroids

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69
Q

when should a colectomy done in UC flare

A

no improvement with steroids in 72 hours

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70
Q

inducing remission in UC flare

A

topical aminosalicylates e.g. mesalazine

2nd line: steroids

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71
Q

what is the emergency surgery done in UC

A

Hartman’s proctosigmoidectomy + end ileostomy

eventually Ileal Pouch Anal Anastamosis

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72
Q

how does IBS present?

A

young, female, anxious, stressed and may have depression, pain, bloating diarrhoea/constipation

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73
Q

How is IBS diagnosed as a diagnosis of exclusion

A

based on ROME III criteria:
- improvement with defaecation
- change in stool frequency, form, appearance, consistency

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74
Q

investigation of haemorrhoids

A

abdo exam with DRE

proctoscope/sigmoidscope for internal haemorrhoids

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75
Q

1st line treatment of haemorrhoids [3]

A

increased fluid and fibre intake
stool softener
topical analgesic

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76
Q

treatment of listeria monocytogenes gastroenteritis

A

amoxicillin or ampicillin

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77
Q

treatment of salmonella type, paratyphi gastroenteritis

A

ceftriaxone

cipro if sensitive

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78
Q

treatment of a campylobacter jejuni gastroenteritis

A

usually self limiting but if severe clarithromycin or ciprofloxacin

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79
Q

describe the stools in coeliac

A

watery, grey, frothy stool (increased fat)

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80
Q

which haematinics can be deficient in coeliac disease, where are they absorbed

A

iron (duodenum), folate (jejenum) and ileum (B12)

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81
Q

most sensitive AB for diagnosing coeliac

A

anti TTG (do alongside IgA)

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82
Q

management of coeliac disease

A
  • gliadin/gluten free diet
  • dietician referral with annual review
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83
Q

biochemical abnormalities in acute cholecystitis

A

ALP and amylase slightly raised

normal ALT/AST

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84
Q

what is Mirizzi syndrome

A

common hepatic duct stone impaction

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85
Q

treatment of ascending cholangitis [2]

A

IV ABx and ERCP after 24-48 hours

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86
Q

Charcot’s triad in ascending cholangitis

A

fever
jaundice
RUQ pain

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87
Q

how does cholangiocarcinoma present

A

obstructive jaundice, red flag symptoms

often asymptomatic

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88
Q

investigating of suspected gallbladder cancer

A

CT abdo

ERPC for staging

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89
Q

treatment of resectable and non-resectable gallbladder cancer

A

resectable–> cholecystectomy
non-resectable –> chemoradiotherapy +- stenting

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90
Q

what is PBC associated with

A

autoimmune diseases e.g. Sjogrens, RhA, thyroid disease

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91
Q

biochemical abnormalities in PBC

A

raised GGT/ALP
normal transaminases

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92
Q

management of PBC

A

1st line: ursodeoxycholic acid

pruritus: cholestyramine
fat-soluble vitamin supplementation
liver transplantation
e.g. if bilirubin > 100 (PBC is a major indication)

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93
Q

AB in PSC

A

pANCA

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94
Q

diagnostic investigation of PSC

A

MRCP shows beaded appearance of biliary structures

95
Q

management of PSC

A

observation, liver transplant

96
Q

complications of PSC [2]

A

cholangiocarcinoma
colorectal cancer

97
Q

AB in Type 1 autoimmune hepatitis [2]

A

ANA and ASMA

98
Q

AB in Type 2 autoimmune hepatitis

A

anti LKM

99
Q

AB in Type 2 autoimmune hepatitis

A

anti soluble liver antigen

100
Q

investigation for autoimmune hepatitis [3]

A

ANA/SMA/LKM1 antibodies
raised IgG levels
liver biopsy showing piecemeal necrosis

101
Q

management of autoimmune hepatitis [2]

A

steroids
liver transplant

102
Q

4 causes of massive splenomegaly

A

CML
myelofibrosis
malaria
lymphoma

103
Q

treatment of Wernicke’s encephalopathy

A

Thiamine (pabrinex)
magnesium
folic acid

104
Q

management of ascites [5]

A
  • restrict fluids and alcohol
  • low sodium diet
  • spironolactone
  • drainage if tense ascites
  • prophylaxis for SBP: ciprofloxacin+ propanolol
105
Q

management of refractory ascites

A

TIPSS
transplant

106
Q

initial investigation for SBP

A

abdo USS to confirm ascites

then do ascitic tap and fluid MC&S

107
Q

polymorphonuclear cell level in SBP

A

> 250

108
Q

treatment of SBP

A

tazocin (piptazobactam) or cefotaxime

109
Q

prophylaxis of SBP

A

ciprofloxacin + propanolol

110
Q

which stain is used on liver biopsy in haemochromatosis

A

Perl’s stain

111
Q

management of haemochromatosis [2 lines]

A

1st line: venesection
2nd: desferrioxamine

112
Q

4 Iines of investigation of NAFLD

A

1st: LFTs
2nd: USS
3rd: enhanced liver fibrosis panel or fibroscan
4th: liver biopsy

113
Q

management of NAFLD

A

lifestyle measures

114
Q

most specific and sensitive bloods for acute pancreatitis

A

serum lipase

115
Q

investigations for acute pancreatitis

A

serum lipase and amylase
USS and constrast CT abdo

116
Q

severity score in pancreatitis: PANCREAS

▪ P
▪ Age>55yo
▪ Neutrophils>15x109/L
▪ Ca2+ <2mmol/L
▪ Renalurea>16mmol/L
▪ Enzymes(LDH>600,AST/ALT>200)
▪ Albumin<32g/L
▪ Sugar>10mmol/L

A

▪ PaO2 <8 kPa
▪ Age>55yo
▪ Neutrophils>15x109/L
▪ Ca2+ <2mmol/L
▪ Renalurea>16mmol/L
▪ Enzymes(LDH>600,AST/ALT>200)
▪ Albumin<32g/L
▪ Sugar>10mmol/L

117
Q

severity score in pancreatitis: PANCREAS

▪ PaO2 <8 kPa
▪ A
▪ Neutrophils>15x109/L
▪ Ca2+ <2mmol/L
▪ Renalurea>16mmol/L
▪ Enzymes(LDH>600,AST/ALT>200)
▪ Albumin<32g/L
▪ Sugar>10mmol/L

A

▪ PaO2 <8 kPa
▪ Age>55yo
▪ Neutrophils>15x109/L
▪ Ca2+ <2mmol/L
▪ Renalurea>16mmol/L
▪ Enzymes(LDH>600,AST/ALT>200)
▪ Albumin<32g/L
▪ Sugar>10mmol/L

118
Q

severity score in pancreatitis: PANCREAS

▪ PaO2 <8 kPa
▪ Age>55yo
▪ N
▪ Ca2+ <2mmol/L
▪ Renalurea>16mmol/L
▪ Enzymes(LDH>600,AST/ALT>200)
▪ Albumin<32g/L
▪ Sugar>10mmol/L

A

severity score in pancreatitis: PANCREAS

▪ PaO2 <8 kPa
▪ Age>55yo
▪ Neutrophils>15x109/L
▪ Ca2+ <2mmol/L
▪ Renalurea>16mmol/L
▪ Enzymes(LDH>600,AST/ALT>200)
▪ Albumin<32g/L
▪ Sugar>10mmol/L

119
Q

severity score in pancreatitis: PANCREAS

▪ PaO2 <8 kPa
▪ Age>55yo
▪ Neutrophils>15x109/L
▪ C
▪ Renalurea>16mmol/L
▪ Enzymes(LDH>600,AST/ALT>200)
▪ Albumin<32g/L
▪ Sugar>10mmol/L

A

▪ PaO2 <8 kPa
▪ Age>55yo
▪ Neutrophils>15x109/L
▪ Ca2+ <2mmol/L
▪ Renalurea>16mmol/L
▪ Enzymes(LDH>600,AST/ALT>200)
▪ Albumin<32g/L
▪ Sugar>10mmol/L

120
Q

severity score in pancreatitis: PANCREAS

▪ PaO2 <8 kPa
▪ Age>55yo
▪ Neutrophils>15x109/L
▪ Ca2+ <2mmol/L
▪ R
▪ Enzymes(LDH>600,AST/ALT>200)
▪ Albumin<32g/L
▪ Sugar>10mmol/L

A

▪ PaO2 <8 kPa
▪ Age>55yo
▪ Neutrophils>15x109/L
▪ Ca2+ <2mmol/L
▪ Renal urea >16mmol/L
▪ Enzymes(LDH>600,AST/ALT>200)
▪ Albumin<32g/L
▪ Sugar>10mmol/L

121
Q

severity score in pancreatitis: PANCREAS

▪ PaO2 <8 kPa
▪ Age>55yo
▪ Neutrophils>15x109/L
▪ Ca2+ <2mmol/L
▪ Renal urea>16mmol/L
▪ E
▪ Albumin<32g/L
▪ Sugar>10mmol/L

A

▪ PaO2 <8 kPa
▪ Age>55yo
▪ Neutrophils>15x109/L
▪ Ca2+ <2mmol/L
▪ Renalurea>16mmol/L
▪ Enzymes(LDH>600,AST/ALT>200)
▪ Albumin<32g/L
▪ Sugar>10mmol/L

122
Q

severity score in pancreatitis: PANCREAS

▪ PaO2 <8 kPa
▪ Age>55yo
▪ Neutrophils>15x109/L
▪ Ca2+ <2mmol/L
▪ Renalurea>16mmol/L
▪ Enzymes(LDH>600,AST/ALT>200)
▪ A
▪ Sugar>10mmol/L

A

▪ PaO2 <8 kPa
▪ Age>55yo
▪ Neutrophils>15x109/L
▪ Ca2+ <2mmol/L
▪ Renalurea>16mmol/L
▪ Enzymes(LDH>600,AST/ALT>200)
▪ Albumin<32
▪ Sugar>10mmol/L

123
Q

severity score in pancreatitis: PANCREAS

▪ PaO2 <8 kPa
▪ Age>55yo
▪ Neutrophils>15x109/L
▪ Ca2+ <2mmol/L
▪ Renalurea>16mmol/L
▪ Enzymes(LDH>600,AST/ALT>200)
▪ Albumin<32g/L
▪ S

A

▪ PaO2 <8 kPa
▪ Age>55yo
▪ Neutrophils>15x109/L
▪ Ca2+ <2mmol/L
▪ Renalurea>16mmol/L
▪ Enzymes(LDH>600,AST/ALT>200)
▪ Albumin<32g/L
▪ Sugar>10mmol/L

124
Q

management of acute pancreatitis [3]

A

fluids
IV morphine
enteral feeding

125
Q

management of necrotising pancreatitis [4]

A

fluids
analgesia
IV morphine
enteral feeding

126
Q

3 early complications of acute pancreatitis

A

haemorrhage
SIRS, ARDS
hypocalcaemia and hyperglycaemia

127
Q

4 late complications of chronic pancreatitis and their management [4Ps]

A

peri-pancreatic fluid collection (admit+bowel rest)
pseudocyst (imaging, observe, -ostomy or aspirate)
pancreatic abscess (drainage)
pancreatic necrosis (conservative)

128
Q

signs and symptoms of chronic pancreatitis [3]

A
  • pain worse after a while after meal
  • steatorrhoea
  • occurs on background of long standing DM
129
Q

what measures exocrine function in the context of pancreatitis

A

faecal elastase

130
Q

imaging for chronic pancreatitis

A

USS (for gallstones)
contrast CT abdo

131
Q

most common type of pancreatic cancer

A

adenocarcinoma

132
Q

genetic risk factors for pancreatic cancer [4]

A

BRCA2
MEN
KRAS
HNPCC (Lynch syndrome)

133
Q

classic symptom of pancreatic cancer

A

painless obstructive jaundice

i.e. pale stools, dark urine, pruritus

134
Q

what is Courvoisier’s Law

A

in the presence of painless obstructive jaundice, a mass is unlikely to be gallstones

135
Q

biochemical abnormality in pancreatic cancer

A

ALP/GGT raised
BR raised

ALT/AST normal

136
Q

what is Trousseau sign in the context of pancreatic cancer

A

migratory thrombophlebitis

137
Q

main investigation of pancreatic cancer?

what sign is seen?

A

HRT-CT

double duct sign- dilatation of common bile duct and pancreatic duct

138
Q

definitive management of pancreatic cancer

A

Whipple’s resection

139
Q

treatment of symptomatic pancreatic cancer for nonsurgical candidate

A

ERCP with stenting

140
Q

what is Saint’s triad

A

Diverticular disease
Diaphragmatic hernia (hiatus)
Stones (cholelithiasis)

141
Q

investigation of acute diverticulitis

A

CT abdo

142
Q

investigation of chronic diverticular disease

A

barium enema

143
Q

treatment of acute mild diverticulitis

A

ABx

144
Q

treatment of acute severe diverticulitis [3]

A

IV abx
drip and suck
may do Hartmann’s with a primary anastomosis

145
Q

treatment of chronic diverticular disease

A

soluble, high fibre diet

146
Q

Requirement of urgent 2WW OGD in GORD [3]

A

dysphagia
upper abdo mass
age >=55 and weight loss with: dyspepsia; reflux; upper abdo pain

147
Q

requirement for non urgent OGD in GORD

A

haematemesis
age >=55 with: treatment resistant dyspepsia upper abdo pain with low Hb; N&V; raised plt

148
Q

what is done if OGD is -ve in investigation of dyspepsia

A

24 hour oesophageal pH monitoring

149
Q

1st line treatment of dyspepsia

A

review medications for causes of dyspepsia and give lifestyle advice

150
Q

2nd line treatment of dyspepsia

A

full dose PPI for 4 weeks or test and treat H.pylori

151
Q

3 methods of testing for H.pylori

A

carbon 13 urea breath test
stool antigen
serology

152
Q

how is test of cure done in dyspepsia treatment for H.pylori

A

carbon 13 urea test

153
Q

treatment of H.pylori

A

amoxicillin + clarithromycin + omeprazole

154
Q

how is OGD proven oesophagi’s treated

A

1 month PPI

followed by another month
then another month with double dose

155
Q

what medication is added to PPI in the treatment of oesophagitis proven on OGD

A

H2 RA

156
Q

how is endoscopically negative reflux treated

A

1 month PPI

2nd: 1 month H2 RA

157
Q

indications for Nissen fundoplication in dyspepsia treatment [2]

A

refractory GORD
hiatus hernia

complication: gas-bloat syndrome

158
Q

gram stain of H.pylori

A

gram -ve

159
Q

Associated diseases with H.pylori [4]

A

duodenal and gastric ulcers
gastric cancer
MALToma
atrophic gastritis

160
Q

why must albumin cover be given when doing large volume paracentesis

A

large-volume paracentesis for the treatment of ascites requires albumin ‘cover’.
Evidence suggests this reduces paracentesis-induced circulatory dysfunction and mortality

paracentesis induced circulatory dysfunction can occur due to large volume paracentesis (> 5 litres). It is associated with a high rate of ascites recurrence, development of hepatorenal syndrome, dilutional hyponatraemia, and high mortality rate

161
Q

what causes a SAAG >11

what does this indicate overall

A

Liver disorders are the most common cause
- cirrhosis/alcoholic liver disease
- acute liver failure
- liver metastases

Cardiac
- right heart failure
- constrictive pericarditis

Other causes
Budd-Chiari syndrome
portal vein thrombosis
veno-occlusive disease
myxoedema

indicates portal hypertension

162
Q

what causes a SAAG <11

A

Hypoalbuminaemia
nephrotic syndrome
severe malnutrition (e.g. Kwashiorkor)

Malignancy
peritoneal carcinomatosis

Infections
tuberculous peritonitis

Other causes
pancreatitis
bowel obstruction
biliary ascites
postoperative lymphatic leak
serositis in connective tissue diseases

163
Q

how do you calculate SAAG

A

serum albumin concentration - ascitic albumin concentration

164
Q

what may cause gallstone ileus

A

if a fistula forms between the gallbladder and duodenum

165
Q

how does gallstone ileum present

A

like bowel obstruction: Abdominal pain, distension and vomiting are seen.

166
Q

what is the Sister Mary Joseph node

A

metastatic umbilical lesion - is an important finding in advanced malignancy

167
Q

what needs to be done before starting treatment for PBC

A

MRCP or USS

exclude an extrahepatic biliary obstruction

168
Q

Squamous cell cancer in the oesophagus: location?

A

upper two thirds

169
Q

Squamous cell cancer in the oesophagus: risk factors

A

smoking
alcohol
achalasia
Plummer-Vinson syndrome
diets rich in nitrosamines

developing world

170
Q

Adenocarcinoma of the oesophagus: location

A

bottom third

171
Q

Adenocarcinoma of the oesophagus: risk factors [4]

where is it more common?

A

GORD
Barrett’s oesophagus
smoking
obesity

UK/US

172
Q

diagnosis of oesophageal cancer

A

upper GI endoscopy with biopsy

173
Q

what is transient elastography and what can it be used to measure the severity of

A

brand name ‘Fibroscan’
uses a 50-MHz wave is passed into the liver from a small transducer on the end of an ultrasound probe
measures the ‘stiffness’ of the liver which is a proxy for fibrosis which is a reflection of cirrhosis

174
Q

triad in Budd Chiari syndrome

A

sudden onset abdominal pain, ascites, and tender hepatomegaly

175
Q

key investigation in Budd Chiari syndrome

A

ultrasound with Doppler flow studies

176
Q

first line treatment of c.diff

A

oral vancomycin

177
Q

treatment of life threatening c.diff

A

oral vancomycin iv metronidazole

178
Q

2nd line treatment for C.diff

A

oral fidamoxicin

179
Q

how long ago should antibiotics and anti secretories be stopped before a urea breath test

A

antibiotics for 4 weeks
anti secretaries e.g. PPI for 2 weeks

180
Q

Screening tool that helps clinicians decide whether patient patients can be managed as outpatients or not in suspected upper GI bleed

A

Glasgow-Blatchford (pre endoscopy)

181
Q

Screening tool that provides a percentage risk of rebleeding and mortality after treatment of upper GI bleed

A

Rockall (post endoscopy)

182
Q

A recurrent episode of C. difficile within _________ of symptom resolution should be treated with oral fidaxomicin

A

A recurrent episode of C. difficile within 12 weeks of symptom resolution should be treated with oral fidaxomicin

183
Q

drugs that cause cholestasis

A

combined oral contraceptive pill
antibiotics: flucloxacillin, co-amoxiclav, erythromycin*
anabolic steroids, testosterones
phenothiazines: chlorpromazine, prochlorperazine
sulphonylureas
fibrates

184
Q

which is more common: pancreatic cancer or cholangiocarcinoma

A

pancreatic cancer

185
Q

what is offered to coeliac patients

A

pneumococcal vaccine due to functional hyposplenism

booster every 5 years

186
Q

triad of Wernicke’s encephalopathy

A

Confusion, gait ataxia, nystagmus + ophthalmoplegia

187
Q

lymphoma associated with coeliac disease

A

enteropathy associated T cell lymphoma

188
Q

adverse effects of PPI [4]

A

hyponatraemia, hypomagnasaemia
osteoporosis → increased risk of fractures
microscopic colitis
increased risk of C. difficile infections

189
Q

diagnosis and treatment of small bowel bacterial overgrowth syndrome

A

hydrogen breath test

tx: treat underlying cause, rifixamin, co-amox, metro

190
Q

risk factor for small bowel bacterial bacterial overgrowth syndrome

A

diabetes mellitus
scleroderma

191
Q

M rule of PBC [3]

A

IgM
anti-Mitochondrial antibodies, M2 subtype
Middle aged females

192
Q

electrolyte abnormality with vomiting/aspiration

A

hypokalaemia

193
Q

Triad of Plummer Vinson Syndrome

A

Triad of:
dysphagia (secondary to oesophageal webs)
glossitis
iron-deficiency anaemia

+ cheilitis

194
Q

treatment of achalasia

A

pneumatic (balloon) dilation is increasingly the preferred first-line option
less invasive and quicker recovery time than surgery
patients should be a low surgical risk as surgery may be required if complications occur
surgical intervention with a Heller cardiomyotomy should be considered if recurrent or persistent symptoms
intra-sphincteric injection of botulinum toxin is sometimes used in patients who are a high surgical risk
drug therapy (e.g. nitrates, calcium channel blockers) has a role but is limited by side-effects

195
Q

drug that may cause Heinz body anaemia

A

sulphasalazine

196
Q

how is UC normally diagnoses, but when she it be avoided

what is used instead

A

normally with colonoscopy with biopsy

avoided in severe colitis, use a flexible sigmoidoscope instead to prevent risk of perforation

197
Q

what should be given before endoscopy for variceal bleed

A

antibiotics and terlipressin

198
Q

uncontrolled haemorrhage in variceal bleed, what should be inserted

A

Sengstaken-Blakemore tube

199
Q

what is the preferred procedure done to treat variceal bleed during endoscopy

A

band ligation over sclerotherapy

200
Q

how do oesophageal varices present

A
  • large volume of fresh blood
  • melena due to swallowed blood
  • haemodynamic compromise
  • may stop spontaneously then rebleed
201
Q

how does bleeding due to oesophagitis present [5]

A
  • small volume of fresh blood
  • blood streaked vomit
  • no melena
  • stops spontaneously
  • antecedent GORD
202
Q

how does bleeding oesophageal cancer present

A
  • small volume upper GI bleed
  • erosion of major vessel
  • dysphagia and other constitutional ssx e.g. weight loss
203
Q

how does a Mallory Weiss tear present

A
  • brisk small to moderate volume bright red blood
  • following a bout of repeated vomiting
  • no melena
  • usually stops spontaneously
204
Q

how does a bleeding gastric ulcer present [3]

A
  • small low volume bleeds
  • iron def anaemia
  • erosion of significant vessel may cause haemorrhage or haematemesis
205
Q

how does bleeding gastric cancer present [3]

A
  • frank haematemesis or vomit mixed with blood
  • prodrome of dyspepsia and constitutional ssx
  • vessel erosion causing haemorrhage
206
Q

how does a Dieulafoy lesion present

A
  • AVM that produces considerable haemorrhage
  • haematemesis and melena
  • difficult to detect endoscopically
207
Q

how does diffuse erosive gastritis present

A
  • haematemesis
  • gastric discomfort
  • usually with underlying cause e.g. recent NSAIDs
  • large volume haemorrhage can occur with haem compromise
208
Q

how does a bleeding duodenal ulcer present [5]

A
  • haematemesis
  • melena
  • epigastric discomfort
  • may erode gastroduodenal artery
  • pain occurs several hours after eating
209
Q

how does an aorto-enteric fistula present

A
  • previous AAA surgery
  • major haemorrhage with high mortality
210
Q

Blatchford score 0, what should be done

A

early dischargesh

211
Q

should PPI be given before endoscopy for suspected non-variceal upper GI bleed

A

no

212
Q

treatment of alcoholic hepatitis [2]

A

glucocorticoids as determined by the Maddrey’s discriminant function (DF)
pentoxyphylline is also sometimes used

213
Q

risk factors for Budd Chiari syndrome [4]

A

polycythaemia rubra vera
thrombophilia: activated protein C resistance, antithrombin III deficiency, protein C & S deficiencies
pregnancy
combined oral contraceptive pill: accounts for around 20% of cases

214
Q

which volvulus is associated with malignancy

A

caecal

215
Q

what sign does caecal volvulus show

A

embryo sign

216
Q

treatment of sigmoid volvulus

A

rigid sigmoidoscopy with rectal tube insertion

217
Q

what sign is seen in sigmoid volvulus

A

coffee bean sign

218
Q

treatment of caecal volvulus

A

management is usually operative. Right hemicolectomy is often needed

219
Q

features of carcinoid syndrome

A

flushing (often the earliest symptom)
diarrhoea
bronchospasm
hypotension
right heart valvular stenosis (left heart can be affected in bronchial carcinoid)
other molecules such as ACTH and GHRH may also be secreted resulting in, for example, Cushing’s syndrome
pellagra can rarely develop as dietary tryptophan is diverted to serotonin by the tumour

220
Q

investigation for carcinoid syndrome [2]

A

urinary 5-HIAA
plasma chromogranin A y

221
Q

management of carcinoid syndrome

A

somatostatin analogues e.g. octreotide
diarrhoea: cyproheptadine may help

222
Q

what is carcinoid syndrome

A

usually occurs when metastases are present in the liver and release serotonin into the systemic circulation

223
Q

Mackler’s Triad of Boerhaave’s syndrome

A

Chest pain
SC emphysema
Vomiting

224
Q

which cancer is associated with apple core sign

A

oesophageal cancer

225
Q

triad of intestinal angina/chronic mesenteric ischaemia

A

severe, colicky post-prandial abdominal pain
weight loss
abdominal bruit

226
Q

features of Peutz-Jeghers syndrome

A

hamartomatous polyps in the gastronintestinal tract (mainly small bowel)
small bowel obstruction is a common presenting complaint, often due to intussusception
gastrointestinal bleeding
pigmented lesions on lips, oral mucosa, face, palms and soles

227
Q

investigation of bile-salt malabsorption

A

SeHCAT

228
Q

treatment of bile-salt malabsorption

A

bile acid sequestrants e.g. cholestyramine

229
Q

what vitamin deficiency leads to angular cheilitis

A

riboflavin (B2)

230
Q

which UC drug is more associated with pancreatitis

A

mesalazine

231
Q

which IBD has pseudo polyps

A

UC

232
Q

where is the biopsy taken in coeliac disease

A

jejunum

233
Q

most immediate measure of loss of liver synthetic function

A

PT

234
Q

why is C.diff difficult to treat

A

due to spore formation

C.difficile spores are resistant to many environmental stresses, including heat, disinfectants, and antibiotics, which makes them particularly difficult to eliminate. These spores can persist on surfaces for months, making them a significant source of transmission in healthcare settings.

Year 6 (19 decks)

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