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
Clinical manifestations Haemachromatosis
Bronze/tanned skin Arthralgia Lethargy + weakness = MOST COMMON Involvement of organs - CM - CCF - Hepatomegaly - Arrhythmias
26
Haemachromatosis investigations
High transferrin: changes first High ferritin > 1000 + elevated transaminases high chance of having cirrhosis < 1000 : accurate predictor of absence of cirrhosis Low TIBC
27
Haemchromatosis Management
Phlebotomy - Improves life expectancy + fibrosis regression; however cirrhosis irreversible Fe chelating agents: desferroxiamine
28
Wilsons gene
ATP7B
29
Wilsons diagnostic testing:
High ceruloplasmin High Ur Copper Low uric acid LFTs: AST:ALT >1, high bill:ALP ratio GOLD STANDARD: biopsy
30
Refeeding syndrome electrolyte disturbances?
Low Ph, Mg, K Low thiamine --> Wernickes
31
PPI SE's
- 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
H pylori testing
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
· Crigler-Najjar syndrome:
Characterised by complete absence (Type 1) or marked reduction (Type 2) in bilirubin conjugation Autosomal recessive
34
Bilirubin metabolism
Check notes
35
Pathophys of Coeliacs?
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
Coeliac diagnosis: antibodies
tranglutaminase IgA endomysial IgA Antireticulin IgA antigliadin IgA
37
Complications of Coeliacs
Refractory disease Small bowel lypmhoma / adenocarcinoma
38
NASH: what do you see on biopsy?
Inflammation Hepatic ballooning Fibrosis
39
Imaging for NASH diagnosis:
US UNRELIABLE AT DETECTING STEATOSIS NON CON CT < CT WITH CONTRAST < US < MRI Biopsy
40
Prognostic factors for NALFD?
Cirrhosis/fibrosis biggest prognostic factor Ferritin ○ Higher = assoc with fibrosis and increased all cause mortality Death ○ CVD BIGGEST CAUSE
41
Management of alcoholic liver disease?
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
Pharyngeal pouch featuers
It is more common in older patients and is 5 times more common in men * neck swelling which gurgles on palpation * Halitosis
43
Stricture features?
- Difficulty with solid food - ASSOC WITH GERD
44
Oesophageal ring features
○ Dysphagia to hard solids ○ Modify way they eat ○ Episodes of difficulty swallowing hard solids § NO GERD NOT PROGRESSIVE
45
Achalasia features
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
Achalasia management
First line in young/healthy: POEMS then LES Haller First line in older/comorbid: Balloon dilatation Not suitable for quick endoscopy: pharmacotherapy, botox
47
Barrett's treatment
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
Eosinophilic oesophagi's tx?
- 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
Eosinohpilic oesophagitis features on scope
○ Concentric rings 'corrugated iron' and longitudinal furrows ○ White plaques Histology: eosinophil infiltration
50
Investigations for pancreatitis
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
C diff treatment
(1) PO vanc PREFERRED/ metro (2) Bezlotoxumab if ep in last 6 months/ vanc/ Fidoxamicin (3) FMT
52
EIM of IBD that are associated with ACTIVE GI disease?
Episcleritis Arthritis Erythema Nodosum Oral ulcers
53
EIM of IBD that are INDEPENDENT of GI disease?
Uveitis AS PSC Pyoderma Kidney Stones
54
Ab markers of UC vs Crohns
UC: pANCA Crohns: ASCA