Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

RACP Written Exam > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

Primary cause of pill oesophagitis

A

doxycycline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What causes zolliger ellison syndrome?

A

Secretion of gastrin from neuroendocrine tumours (gastrinoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Barrett;s eosphagus histo

A

metaplastic columnar epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how long is barretts when it has higher risk of malignancy?

A

> 3cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Characetistic findings of oesinophilic eosophagitis

A

stacked circular rings
strictures
linear furrows

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Microscopy which is diagnostic of eosinophilic oedeophagitis

A

> 15 eosinophils on high power field

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

eosinophilic oesophagitis mangement

A

PPI for 8 weeks, if no improvement fluticasone or budesonide slurry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

pathology of achalasia

A

progressive degeneration of ganglion cells in myenteric plexus -> failure of relaxation of lower oesophageal sphincter and loss of peristalsis in distal oesophagitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

secondary causes of achalasia

A

chagas disease
amyloidosis
sarcoidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

investigation findings in achalasia

A

barium - oesophageal dilatation, bird beak oesophageal junction
manometry - failure of relation of LOS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Achalasia management

A

pneumatic dilatation of LOS
surgical myotomy
botox (elderly)
nitrates, CCB
POEM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

risk of dilation of LOS

A

3% perforation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What pressure do varices occur and when do they bleed

A

Seen when presure gradient between portal and hepatic veins >12mmHg
Bleeding when >18
gastric varices bleed more than oesophageal varices

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What causes risk of AKI and Na and fluid retention in liver disease

A

shunting of blood flow from cardiac circulation to splanchnic leads to relative renal hypoperfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Therapies in acute variceal bleeds

A

AIm Hb >80
antibiotic prophylaxis (oral norflox or IV cipro)
somatostatin or octreotide for 3-5 days
TIPS when not controlled bleeding or recurrent
can use balloon tamponade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Prevention of varicies

A

non-selective beta blockers (propranolol, carvedilol) and maximal tolerated dose
ligation (same outcomes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Most common reason for inadequate treatment of H pylori

A

clarithromycin resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Virulence factor of H pylori

A

CagA
VacA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

H pylori resistance in australia

A

clarithromycin resistance 10%
Metronidazole 30%
amox 10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How to test for H pylori eradication

A

breath test 8 weeks after treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Which type of ulcer do you repeat endocopy after 8 weeks of PPI therapy?

A

Gastric not duodenal (higher risk of malignancy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What does forrest classification predict

A

risk of rebleeding
and which lesions need therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Why PPI 72 hours post bleeding

A

helps prevent re-bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Genetic associations with coeliac

A

HLA-DQ2 DQ8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Skin manifestations of coaelic

A

Dermatitis hepatiformis (itchy symmetrical blistering rash over scalp shoulders buttocks elbow and knees)
atrophic glossitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Associated conditions with coeliac

A

Selective IgA deficiency (false negatives of EMA and TTG)
T1DM, thyroid disease
GORD, eosinophilic eosophagitis
IBD (UC more than CD)
Glomerular IgA deposition
Autoimmune myocarditis and idiopathic dilated cardiomyopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Diagnosis of coeliac

A

TTG is preferred
endomysial (EMA)
-ve result has high negative predictive value
Both serology and small bowel bx is required
If positive serology but -ve endoscopy do HLA testing, if positive then high gluten diet for 6-12 weeks then repeat scope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Histo findings for coeliac disease

A

atrophic mucosa, loss of folds on endoscopy
complete loss of villi, crypt hyperplasia, enhanced epithelial apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Malignancy associated with coeliac disease

A

enteropathy associated T cell lymphoma (EATL) - <5% of all GI lymphomas, gluten free prevents
Small bowel adenocarcinoma HR 3.05

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Specific finding in Igg4 related disease

A

retroperitoneal fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Treatment of IGG4

A

corticosteriods
additional immunosuppressant (AZA, MMF) or biologic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Impaired synthetic function

A

INR >1.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

King’s college criteria

A

ABG pH <7.25 after fluid resus and NAC >24 hours
or all 3: PT >100/INR>6.5n Creat >300 or anuric, grade 3/4 encephalopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

LFT pattern in alcohol hepatitis

A

AST:ALT>2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

hallmark of alcoholic induced liver injury

A

neutrophil infiltration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

NAFLD progression % to cirrhosis and then to decompensation

A

25% 7-8 years then 25% to 8-10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Therapies for NASH

A

Only in those with fibrosis >2
If no DM vitamin E
If DM pioglitazone or GLP1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Type 1 vs T2 autoimmune hepatitis

A

T1: ANA, anti-smooth muscle, antiactin, antimitochondrial, anti-SLP, p-ANCA
T2: ALKM1 or ALC1 ab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

primary biliary cholangitis ab

A

antimitochondrial ab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Condition associated with primary sclerosising cholangitis

A

UC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Liver Bx for autoimmune hepatitis

A

hepatitis with lymphoplasmacytic infiltrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Autoimmune hepatitis treatment

A

Glococorticoids
- most improve in 4 weeks
Alt AZA

43
Q

Histology findings in primary biliary cirrhosis

A

non-suoourative, granulomatous, lymphocytic small bile duct cholangitis

44
Q

clinical manifestations of primary biliary cirrhosis

A

most asymptomatic
pruritis
hyperpigmentation
sjogrens 65%
scleroderma

45
Q

Diagnosis of Primary biliary cirrhosis

A

adults with cholstasis, no systemic disease, elevated ALP and AMA >1:40 is diagnostic

46
Q

Treatment of primary biliary cirrhosis

A

Ursodeoxycholic acid
2nd line obeticholic acid
Assess response with serial bx if AIH overlap

47
Q

Characteristics of Primary sclerosing cholangitis

A

chronic progressive disorder
inflammation, fibrosis and stricturing of medium and large bile ducts

48
Q

Conditions associated with primary sclerosing cholangitis

A

cholangiocarcinoma (10-20%)
70% with IBD (UC >CD)

49
Q

Diagnosis of primary sclerosising cholangitis

A

cholstatic pattern LFTs
p-ANCA
MRCP >ERCP showing abnormalities in biliary tree
liver bx only if dx uncertain

50
Q

Treatment for primary sclerosing cholangitis

A

UDCA can be beneficial
Liver tx

51
Q

Primary scleorising cholangitis survival

A

median 1 year

52
Q

Signficant fibrosis on fibroscan in cirrhosis

A

Low range has good negative predictive value
>7.5 signfiicant cirrhosis
>11 cirrhosis

53
Q

SAAG

A

SAAG > 11 suggests portal HTN

54
Q

Tap findings in SBP

A

Leuks >500
PMN >250

55
Q

Mangement of SBP

A

Ceftriaxone for 5 days
IV albumin then daily for 3 days

56
Q

Hish risk features for varicies

A

size
red wale marks
advanced liver disease

57
Q

difference between T1 and T2 hepatorenal

A

T1 more rapid, x2 increase in creatinine in < 2 weeks
T2 less severe than type 1, major clinical feature is ascities which is resistant to diuretics

58
Q

Difference between hepatopulmonary syndrome and portopulmonary syndrome

A

Hepatopulmonary -> pulmonary vascular dilatation -> hypoxia
Portopulomary -> pulmonary vasocontriction -> RHF

59
Q

What serology indicates acute HCV infection

A

HCV RNA +ve with antiHCV Ab -ve which becomes positive in 12 weeks
or
HCV RNA +ve and antiHCV positive with neagtive tests 6 motnsh prior

60
Q

Most common HCV genotype in australia

A

type 3

61
Q

Treatment duration of hep C

A

8 weeks for glecaprevir and pibrentasvir, 12 weeks for others plus if cirrhosis

62
Q

side effects of glecaprevir

A

elevation in bilirubin due to inhibition of bilirubin transporters

63
Q

Usual sustained virological response to HCV treatment

A

SVR >95%

64
Q

HCV treatment CYP and drug interactions

A

CYP3A4
PPIs
statins
OCP
amiodarone

65
Q

When are protease inhibitors contraindicated

A

in decompensated cirrhosis (B and C)

66
Q

What are the differences between genotypes of HBV

A

Genotype B - less active disease
Gene C - higher risk of HCC
Gene F - fulminant liver disease (rare)

67
Q

aminotransferase indication of higher cirrhosis risk

A

ALT (not AST)

68
Q

Extrahepatic manifestations of HBV

A

polyarteritis nodosa
membranous or MPGN

69
Q

Lynch syndrome and mutations

A

autosomal dominant
MSH2 due to deletions in EPCAM gene
MLH1 MSH2 MSH6
PMS2 most common
increased right sided colorectal Ca, endometrial and prostate

70
Q

Most common met site of HCC

A

Lungs
Then abdominal LN

71
Q

Serum marker for hcc

A

AFP

72
Q

Transplantation criteria for HCC

A

single lesion <5m or max 3 lesions <3cm
No vascular invasion
organ allocation based on MELD

73
Q

Treatment for advanced stage HCC

A

1st: Atezolizumab and bavacizumab
2nd: TKI

74
Q

Side effects of TKI

A

hand foot skin reaction
Fatal liver toxicity (rare)

75
Q

Features of HCC on CT

A

arterial enchancement
portal venous washout
LIRADS 4-5

76
Q

MRI characetistics of focal nocule hyperplasia

A

T2 hyperintense
central scar

77
Q

Mutation which causes early surgeries due to stricturing disease

A

Nod2/CARD15

78
Q

Extraintestinal manifestations associated with active GI disease in IBD

A

oral ulcers
erythema nodosa
large joint arthritis
episcleritis

79
Q

Extraintestinal manifestations independent of active GI disease in IBD

A

primary scleorising cholangitis
ank spond
uveitis
pyoderma gangrenosum
renal stones
gall stones

80
Q

What secetes faecal calprotectin

A

Neutrophils in the bowel

81
Q

Histology of UC

A

confined to mucosa and submucosa
Goblet cell depletion
crypt abscesses
crypt branching

82
Q

Endoscopy findings in crohns

A

apthous ulcers
longitudinal snail trail ulcer
cobblestoning

83
Q

Crohns histology

A

transmural ulceration
goblets preserved
granulomas
parietal metaplasia

84
Q

Treatment for mild/mod UC

A

Mesalazine
Corticosteriods
If poor prognostic features: other maintence (thiopurines and then biologics)

85
Q

Moderate/severe disease for UC

A

Iv corticosteriods, reasses day 3
if response -> steriods
no response -< surgery or 2nd line, IV cephalosporin or infliximab
if still no response -> surgery

86
Q

Treatment differences based off location in mild/mod crohns

A

if colonic use 5ASA or pred
If small bowel -> use pred

87
Q

If persistant disease in mild/mod crohns despite initial therapy?

A

MTX or thiopurine
(MTX not useful in UC)

88
Q

Management of mod/severe crohns

A

induction: systemic corticosteriods, biologics

89
Q

Treatment of stricturing crohns disease

A

if inflammatory may respond to medical therapy
if fibrotic poor response to medical therapy, usually surgical options

90
Q

Most common site of external fistula in fistulating crohns disease

A

perianal

91
Q

Fistulating crohns disease medical treatment

A

Abx: cipro and metro
minimal evidence in immunomodulators
infliximab and adalimumab

92
Q

Dose dependant thiopurine side effects

A

N+V
Leucopenia
Hepatotoxicity

93
Q

Dose independant side effects of thiopurines

A

infection
pancreatitis
hepatosplenic T cell lymphoma
non-melanoma skin cancers

94
Q

rare side effect of thiopurines

A

nodular regenerative hyperplasia

95
Q

Infliximab moa

A

Anti-TNF

96
Q

Adalimumab moa

A

anti-tNF

97
Q

Golimumab moa

A

anti-TNF

98
Q

Vedolizumab moa

A

anti-integrin

99
Q

ustekinumab moa

A

anti IL12/23

100
Q

tafacitinib moa

A

jak inihibitor

101
Q

upadacitinib moa

A

JAK inhibitor

102
Q

Ozanimod moa

A

S1p modulators

103
Q

Associations with hep C

A

insulin resistance
essential mixed cryo
lymphoma
membranoproliferative
thyroiditis
porphyria cutanea tarda
lichen planus

RACP Written Exam (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions