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RACP 2023 > GASTRO > Flashcards

GASTRO Flashcards

1
Q

SAAG results

A

> 11: cirrhosis, cardiac
- cardiac high protein normal HPVG
- cirrhosis high HPVG

< 11: malignancy, pancreatitis, TB

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2
Q

Liver failure - paracetamol
transplant criteria?

A

PLICH

pH < 7.3 after resus > 24 hours since ingestion

Lactate > 3.0

OR

3 of
- HE grade 3
- INR >6.5
- Cr > 300

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3
Q

Liver failure - non paracetamol transplant criteria?

A

BICAE

INR > 6.5

OR

3/5
- Billi > 300
- INR > 3.5
- Cause: hepatitis, DILI, indeterminate
- A: Age < 10 > 40
- Encephalopathy > 7 days

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4
Q

Polysaccharides –> oligosaccarides

Name examples

A

Galactose –> lactose and glucose

Sucrose –> fructose + glucose

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5
Q

What is absorbed in proximal intestine?

A

ADEK
CMP
Micronutrients
Thiamine
Lipids
Fe

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6
Q

IBD risk factors

A

Smoking
Gastro
Family history BIGGEST
Diet
NSAIDs small
Genes: NOD + CARD more likely to stricture and need surgery

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7
Q

Crohns vs UC macroscopic differences?

A

UC
- Erythematous
- Fine granular surface (sandpaper)
Hemorrhagic, edematous, ulcerated

Crohns
- Wall thickening
- Stenosis
- Linear serpiginous ulcers
- Mucosal cobblestoning
- Fistula tracts –> fibrotic and narrowed –> bowel obstructions
- Thickened mesentery (creeping fat) –> adhesions + fistulas
Segmental involvement; skip areas

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8
Q

Crohns vs UC microscopic differences?

A

UC
- Limited to mucosa and superficial submucosa

- Features suggestive of chronicity
	○ Distortion of crypts: bifid, reduces number, gap between bases 
	○ Mucosal vascular congestion (edema + focal haemorrhage), inflammatory cell infiltrate 
- Ileal changes Backwash ileitis --> villous atrophy, crypt regernation, increase inflammatory cells, crypt abscesses + cryptitis

Crohns
- Transmural

- Aphthoid ulcerations
	○ Can become deeper, enlarged and connect to each other --> serpiginous + linear ulcers 
	○ Can result in fistulas 
- Focal crypt abscesses + loose aggregations of macrophages --> noncaseeating granulomas in all bowel layers 
- Submucosa/subserosal lymphoid aggregates , particularly away from areas of ulceration
- Gross + microscopic skip areas
- Deep fissures Can be complicated by tracts/ abscesses
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9
Q

UC vs Crohns: complications?

A

UC
Colonic epithelial dysplasia + carcinoma

Crohns
- Cr
- NHL
- Leukaemia
- MDS

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10
Q

PSC vs PBC?

A

PBC
Intrahepatic ducts only
AI disease associated
AMA
Under 25 females
UDA alters disease progression
- Granuloma risk

PSC
Entire biliary tree
- Beading, stricturing
UC associated
P-ANCA
Men
UDA does not alter disease progression
- Cholangiocarcinoma risk

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11
Q

AI hepatitis antibodies?

A

Sm: most specific
ANA: most common
LKM1
SLA-LP

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12
Q

Genes for IBD more likely to stricture and need surgery?

A

NOD2
CARD15

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13
Q

Skin associations of IBD?

A

Pyoderma
Sweets
Erythema nodosum
Psoriasis

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14
Q

Most common extraintestinal manifestation of IBD?

A

arthritis

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15
Q

Treatment regime for UC?

A

5-ASA
Severe: add biologics/ MTX

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16
Q

Severe UC colitis treatment?

A

Steroids
Inflix/ Ciclosporin
Colectomy

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17
Q

Crohns treatment regime?

A

Steroids: induction
MTX/ Aza: maintenance
Severe: biologics
Perianal fistula: IFX (higher trough = more healing)

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18
Q

Biologic therapy options for IBD?

A

TNF-alpha
Anti-integrins
JAK inhibitors
Usteikinumab: crohns

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19
Q

H pylori treatment: first line, then alternatives

A

Amoxicillin, Clarithro, Esomep

Alternatives
Metro
doxy
levofloxacin
tetracycline
rifabutin

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20
Q

IBS Pathophys?

A

Infection –> predisposition
Genetic
Brain/gut disturbance
Altered gut flora
Abnormal serotonin
Immune activation and mucosal inflammation

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21
Q

IBS clinical manifestations

A

Pain
Bloating
Change in stool consistency
Alt diarrhoea/constipation
UGI symptoms

SHOULD BE NO BLEEDING, ANEMIA, FEVER, WEIGHT LOSS

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22
Q

IBS diagnostic criteria

A

Recurrent abdominal pain, on average, at least 1 day per week in the last 3 months, associated with ≥2 of the following criteria:

Related to defecation
Associated with a change in frequency of stool
Associated with a change in form (appearance) of stool

23
Q

IBS treatment options

A

Low FODMAP
No Abs: rip only if refractory diarrhea
High fibre/osmotics for constipation
Anticholinergics for pain

Probiotics: little evidence but can help

24
Q

Haemachromatosis genes + Pathophysiology?

A

HFE gene, C282Y mutatoion

Lack of hpeicidin: deposition of excess iron

25
Q

Clinical manifestations Haemachromatosis

A

Bronze/tanned skin
Arthralgia
Lethargy + weakness = MOST COMMON

Involvement of organs
- CM
- CCF
- Hepatomegaly
- Arrhythmias

26
Q

Haemachromatosis investigations

A

High transferrin: changes first
High ferritin
> 1000 + elevated transaminases high chance of having cirrhosis
< 1000 : accurate predictor of absence of cirrhosis

Low TIBC

27
Q

Haemchromatosis Management

A

Phlebotomy
- Improves life expectancy + fibrosis regression; however cirrhosis irreversible

Fe chelating agents: desferroxiamine

28
Q

Wilsons gene

A

ATP7B

29
Q

Wilsons diagnostic testing:

A

High ceruloplasmin
High Ur Copper
Low uric acid
LFTs: AST:ALT >1, high bill:ALP ratio

GOLD STANDARD: biopsy

30
Q

Refeeding syndrome electrolyte disturbances?

A

Low Ph, Mg, K
Low thiamine –> Wernickes

31
Q

PPI SE’s

A
  • GI
    • C diff + enteris infections
    • Microscopic colitis
  • Impaired nutrient absorption
    • Hypomagnesemia
    • B12 malabsorption
    • Ca carbonate
    • Fe
  • Risk of fracture
  • Kidney
    • Increased risk of CKD
    • Interstitial nephritis
32
Q

H pylori testing

A

Urea breath testing: Urea with a labeled carbon isotope (non-radioactive 13C or radioactive 14C) is given by mouth; H. pylori cleaves urea – ammonia  CO2 that can be detected in breath samples.

Stool antigen testing
§ Indicates ongoing H pylori
§ Most cost effective

Serology
§ (+) : current or past infection
Limited use –> concerns re accuracy

33
Q

· Crigler-Najjar syndrome:

A

Characterised by complete absence (Type 1) or marked reduction (Type 2) in bilirubin conjugation

Autosomal recessive

34
Q

Bilirubin metabolism

A

Check notes

35
Q

Pathophys of Coeliacs?

A

HLA DQ2 / DQ8: 99% of individuals with celiac disease

CD4+ T cells have crucial role in responding to gluten
○ Gluten is modified by enzyme transglutaminase –> becomes more immunogenic
○ B cells help amplify response
CD8+ intraepithelial lymphocytes important cellular component of villous damage

36
Q

Coeliac diagnosis: antibodies

A

tranglutaminase IgA
endomysial IgA
Antireticulin IgA
antigliadin IgA

37
Q

Complications of Coeliacs

A

Refractory disease
Small bowel lypmhoma / adenocarcinoma

38
Q

NASH: what do you see on biopsy?

A

Inflammation
Hepatic ballooning
Fibrosis

39
Q

Imaging for NASH diagnosis:

A

US UNRELIABLE AT DETECTING STEATOSIS
NON CON CT < CT WITH CONTRAST < US < MRI
Biopsy

40
Q

Prognostic factors for NALFD?

A

Cirrhosis/fibrosis biggest prognostic factor

Ferritin
○ Higher = assoc with fibrosis and increased all cause mortality
Death
○ CVD BIGGEST CAUSE

41
Q

Management of alcoholic liver disease?

A

Moderate alcoholic hepatitis (Low MELD score)
- Dietitian
○ Supplementation micronutrients, esp thiamine
- Ensure enough energy and protein take
- NG feeding if PO intake inadequate
- IV albumin for volume expansions

Severe (High MELD score)
- Steroids
○ Controversial
○ Assess response with decr in billirubin concentration
- NAC
- Transplant
○ Need to be abstinent > 6 months
- Social support

42
Q

Pharyngeal pouch featuers

A

It is more common in older patients and is 5 times more common in men
* neck swelling which gurgles on palpation
* Halitosis

43
Q

Stricture features?

A
  • Difficulty with solid food
    • ASSOC WITH GERD
44
Q

Oesophageal ring features

A

○ Dysphagia to hard solids
○ Modify way they eat
○ Episodes of difficulty swallowing hard solids
§ NO GERD
NOT PROGRESSIVE

45
Q

Achalasia features

A

Failure of relaxation of LOS + non propagation of peristaltic wave

- Loss of ganglion cells within esophageal myenteric plexus ? AI cause due to latent HSV1

Normally
○ Inhibitory neurons mediate LES relaxation (NO)
○ Absence –> impaired relaxation and absent peristalsis

46
Q

Achalasia management

A

First line in young/healthy: POEMS then LES Haller
First line in older/comorbid: Balloon dilatation
Not suitable for quick endoscopy: pharmacotherapy, botox

47
Q

Barrett’s treatment

A

Nondysplastic + ALL patients
- PPI daily
○ Lower rate of dysplasia
- Discuss risks and benefits re: surveillance every 3-5 years
○ Patient decision

Indefinite grade
- BD PPI first
- Then repeat endoscopy
○ If still indefinite, confirm with pathologist

Low grade
- Confirm with pathologisy
- CAN repeat endoscopic in 6 months
○ If persistent low grade dysplasia
§ Endoscopic ablative therapy (RECENT CHANGE –> RECOMMENDED) of any visible micosal irregularities + RFA
- Antisecretory therapy

High grade
- Assessment of surgical risk
- OPTIONS
○ Ivor Lewis Oesophagectomy
§ assoc with significant risk
○ Endoscopic mucosal resection
§ Involves removal of tissue
○ Endoscopic submucosal dissection
○ Radiofrequency ablation

48
Q

Eosinophilic oesophagi’s tx?

A
  • PPI (1)
    ○ High response rate
    • Topical steroid (2)
      ○ Inhaler –> swallow budesonide
      ○ Dispersible capsule available now (PO budesonide)
    • Dilatation
      ○ I: isolated stricture
    • PO steroids
      • Dupilimumab
49
Q

Eosinohpilic oesophagitis features on scope

A

○ Concentric rings ‘corrugated iron’ and longitudinal furrows
○ White plaques
Histology: eosinophil infiltration

50
Q

Investigations for pancreatitis

A

Endoscopy – if elevated LFTs/ gallstone pancreatitis
o I: gallstone pancreatitis and cholangitis, common bile duct obstruction (visible stone on imaging), dilated common bile duct, or increasing liver tests without cholangitis.
o Within 72 hrs of pain onset
o In the absence of common bile duct obstruction, ERCP is not indicated for (mild or severe) gallstone pancreatitis without cholangitis.
§ When in doubt about bile duct obstruction in the absence of cholangitis, liver tests can be rechecked in 24 to 48 hours to determine if they improve or a magnetic resonance cholangiopancreatography (MRCP) or endoscopic ultrasound (EUS) could be performed to determine if there are stones in the common bile duct.

EUS/MRCP
●Indications for EUS/MRCP prior to ERCP –
EUS or MRCP should be performed to determine the need for ERCP in the following patients:
*Persistent elevation of liver tests and/or dilation of common bile duct without overt cholangitis
*Pregnant patients
*Altered anatomy that would make an ERCP technically challenging

51
Q

C diff treatment

A

(1) PO vanc PREFERRED/ metro
(2) Bezlotoxumab if ep in last 6 months/ vanc/ Fidoxamicin
(3) FMT

52
Q

EIM of IBD that are associated with ACTIVE GI disease?

A

Episcleritis
Arthritis
Erythema Nodosum
Oral ulcers

53
Q

EIM of IBD that are INDEPENDENT of GI disease?

A

Uveitis
AS
PSC
Pyoderma
Kidney Stones

54
Q

Ab markers of UC vs Crohns

A

UC: pANCA
Crohns: ASCA

RACP 2023 (17 decks)

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