Dunedin-Gastro Flashcards
Which high resolution manometry shows features consistent with achalasia?
A
What is achalasia?
Impaired lower oesophageal sphincter relaxation and peristalsis in distal oesophagus.
Due to myenteric plexus inflammation
Experience dysphasia for solids and liquids
Barium swallow- birds beak
What is the proposed model for the development of achalasia?
1) Viral trigger/ HLA Class II/ Mutations and SNPs
2) extracellular matrix turnover and wound repair, inflammatory infiltrate, humeral response (myenteric antibodies)
3) myenteric plexitis, ganglion cell loss, fibrosis, impaired LES
What is the treatment options for achalasia?
Surgical: Pneumatic dilation (recommended initial therapy) , Peroral endoscopic myotomy (POEM), Heller myotomy (HM) with Dor fundoplication. Complication: GERD. Esophagectomy
Medical: botulinic toxin injection, CCB, isosorbide dinitrate
Botulinum injection causes sub-mucosal fibrosis which can interfere with future surgical therapies
What is the clinical presentation of eosinophilic oesophagitis?
younger patient M>F
food bolus obstruction
chronić dysphagia solids >liquids
refractory GORD
chronic immune mediated condition related to food
infiltration of eosinophils into oesophageal mucosa >15/hpf
chronic inflammation leads to deposition of sub epithelial fibrous tissue
What is the management of eosinophilic oeseophagitis?
Double dose PPI for 8 weeks.
if not resolved:
*topical steroids 6-12 weeks (swallowed fluticasone propionate, swallowed viscous budesonide)
*dietary therapy: targeted diet, six-food elimination diet, elemental diet
Alternative therapies: endoscopic dilation in case of stenosis, prednisone, some role of immunomodulators (dupulimab) or antiallergic agents
What is included in the 6-food elimination diet?
Milk, soy, wheat, egg, nut and fish/seafood
What is the histology of Barrett’s oesophagus?
Stratified squamous epithelium replaced by cardiac type mucus secreting columnar epithelium +/- intestinal metaplasia
What is the rate of Barrett’s oesophagus progression to oesophageal adenocarcioma? and is there anything to slow/slow progression?
No dysplasia –> 0.12%
Low grade dysplasia –> 1.8%
high grade dysplasia –> 10%
if have GORD symptoms at least once a week, the risk of oesophageal adenocarcinoma is markedly increased 7.7 vs 1
Stop/slow progression:
- PPI, PPI + aspirin (less evidence)
- surgical therapy not more effective than PPI
- low grade dysplasia confirmed on 2 occasional 6 months apart by two pathologist- can trial endoscopic radiofrequency ablation.
- high grade dysplasia: oesophagectomy vs endoscopic resection
Describe the pattern of development of oesophageal adenocarcinoma compared to CRC?
oesophageal adenocarcinoma: develops in non-linear pattern over 4 years
CRC: develops in linear pattern over 10 years
Discuss screening programs for Barrett oesophagus
1) Not recommended in general population
2) consider in those with chronic reflux and multiple risk factors (Age >50 years, male sex, white race, central obesity, smoking use, first-degree relative with BE or oesophageal adenocarcinoma and presence of hiatal hernia)
3) not usually in men/women <50 with chronic GORD
Evidence for Barrett’s surveillance is weak However post-ablation should do annual gastroscopy for 5 years
What is the role of PPI initiation prior to endoscopic diagnosis in upper GI bleeding?
And post-procedure?
Pre-procedure PPI does NOT reduce mortality, the need for surgery, or the proportion of patients with high risk stigmata. DOES reduce need for endoscopic intervention
Post procedure: IV bolus + 72 hour infusion
What is the relationship between H.Pylori and ITP?
H.Pylori can cause ITP as anti-cage antibodies cross-react with platelet antigens
Is there a good use of tranxemic acid in GI bleeding?
not really
Describe the classification of peptic ulcers
Forest 1 and 2A, collective risk of bleeding is 50%
What is the management of Peptic Ulcers?
epinephrine injection + endoscopic intervention
What was the older triple therapy treatment for H.Pylori? What is the newer Quadruple therapy.
Older therapy (CAP): Clarithromycin + amoxicillin/metronidazole + PPI (omeprazole)
High levels of treatment failure owing to clarithromycin +/- metronidazole resistance
NOW- triple therapy should NOT be prescribed unless H.Pylori clarithromicin resistance rates are known to be <15%
If Resistance >15%, use Quadruple therapy for 14 days
- clarithromycin + metronidazole + amoxicillin + PPI OR
- Bismuth + metronidazole + tetracycline + PPI
Can also use sequential therapy
- PPI + amoxicillin for 5 days, then PPI + clarithromycin + metronidazole for 5 days
Describe post-eradication testing for H.Pylori
Should be done for everyone after 4 weeks of treatment
- urea breath test, faecal antigen testing, or endoscopy
- before the breath test, W/H bismuth/antibiotics for >28 days, W/H PPI >7-14 days
- before pre-faecal antigen, W/H PPI for 14 days
What to manage antiplatelet therapy in an UGI bleed.
IF aspirin used for PRIMARY prophylaxis –> W/H
If used for SECONDARY prophylaxis –> continue aspirin, but can W/H second antiplatelet (unless low risk ulcer in which case continue both)
When to scope a patient with a GP bleed on warfarin?
when INR <2.5
Describe the rates of major GI bleed in non-valvular AF on DOAC
Dabigatran and rivaroxoban highest bleeding risk
then warfarin
then apixaban
Describe reversal agents for NOACS
Dabigatran –> idarucizumab
Xa inhibitors –> Andexanet alpha, combination of clotting factors
Describe the histological features of coeliac disease
Increased intra-epithelial lymphocytes
Crypt hyperplasia
Villous atrophy
Describe testing for Coeliac disease
Anti-TTG IgA (main test)
Anti-endomysial IgA (very specific test but test is difficult)
In IgA deficiency, use IgG test- TTG-IgG, anti-DGP IgG, anti-endomysial IgG
Which haplotypes are associated with Coeliac disease?
HLADQ2/DQ8
more common in DOWN syndrome, Turners, William’s syndrome
What are the fat soluble vitamins?
ADEK
What deficiencies should you test for in Coeliac disease?
Iron deficiency anaemia
Fat soluble vitamins (ADEK)
B12 deficiency
Folate deficiency
Copper deficiency
Bone disease
Describe refractory Coeliac disease
Type 1 (85%)- lymphocyte infiltrate is the same as that in untreated CD. manage with steroids +/- steroid sparing agents e.g. azathioprine
Type 2 (15%)- CD3+ve intra-epithelial T cells with abnormal surface markers +/- oligoclonal T-cell expansion. Mx consider cladribine. High risk of transformation to enteropathy associated T-cell lymphoma (EATL)
Describe bilirubin metabolism
What are some cutaneous and extremity manifestations of cirrhosis
*spider angiomas
*gynaecomastia
*feminization- inversion of male pubic hair pattern, loss of axillary or chest hair
*palmar erythema
*testicular atrophy
*Jaundice
*nail changes- Terry nails, Muehrchke nails, clubbing
*hypertrophic osteoarthropathy
*dupuytren’s contracture
Clinical signs of cirrhosis
parotid gland enlargement (alcohol)
fetor hepaticus
ascites
caput medusae
splenomegaly
Cruveilhier-Baumgarten murmur
asterixes
Describe the stages of hepatic encephalopathy
Minimal- required neurophysiological testing- stroop test, animal naming
Grade 1- sleep/wake reversal, change in behaviour, mild confusion
Grade 2- lethargy, moderate confusion
Grade 3- Stupor, arousable, incoherent
Grade 4- unresponsive to pain. intubate
What is the role of measuring ammonia in hepatic encephalopathy?
*Gaseous ammonia (pNH3) may be more important (pH dependent).
*gaseous ammonia can pass blood brain barrier
*venous ammonia less valuable
What is the MOA of lactulose and lactitol in the treatment of hepatic encephalopathy?
1) laxative- decreases gut transit time
2) Decrease the pH of the gut lumen- lactic acid and acetic acid production thus trapping NH4
What is the treatment of hepatic encephalopathy?
1) lactulose and lactitol
2) Rifaximim (works by decontaminating the gut)
*can consider vegetable *proteins, branched-chain Amino acids
What is SAAG?
serum ascitic albumin gradient (SAAG)
ie serum albumin minus ascites albumin
if >11g/L then high, suggest portal HTN. (alcoholic hepatitis, heart failure, massive hepatic metastasis, bud-chiari syndrome, portal vein thrombosis, portal fibrosis, schistosomiasis)
If low –> leaky capillaries/tumour
*peritoneal carcinomatosis, peritoneal tuberculosis, pancreatitis, serositis, nephrotic syndrome
Ascites fluid analysis
total protein, if <10g/L –> high risk for SBP
Glucose –> similar to serum unless being consumed
LDH - increase in infection.
consider perforation if 2 out of 3 are present:
total protein >10
glucose <2.8 mmol/L
LDH greater than the upper limit of normal
What are the most common pathogens in spontaneous bacterial peritonitis?
Gut bacteria: e.coli and klebsiella
What is the treatment for spontaneous bacterial peritonitis?
cefotaxime 2gm, fluoroquinolone
IV terlipressin and IV albumin (on day 1 and day 3)
some people suggest to stop the non-selective b-blocker but this is debatable
Who do we do Spontaneous bacterial peritonitis prophylaxis for?
1) history of SBP, prolonged/indefinite use of TMP/SMX or daily fluoroquinolone
2) fluid protein <10, or total albumin <15
3) cirrhosis with gastrointestinal bleeding –> ceftriaxone 1g daily followed by TMP/SMX twice a day or ciprofloxacin 500mg twice a day for 7 days
What is the normal portal pressure? when do we worry about portal HTN?
<5mmHg
> 10mmHg worried about portal HTN
> 12mmHg worries about portal-hepatic pressure
What are causes of portal HTN?
Prehepatic –> portal and splenic vein thrombosis, splenomegaly
Intrahepatic –>
*pre sinusoidal (schistosomiasis, PBC, sarcoid)
*sinusoidal (arsenic, drugs eg amiodaroine, MTX), ALD, NAFLD
*post-sinusoidal: sinusoidal obstruction syndrome, budd-chiari, AL
Post-hepatic –> cardiac disease (CHF), constrictive pericarditis, IVC obstruction (budd-chiari)
What is the treatment of gastroesophageal varices?
pre-primary prophylaxis –> treat the underlying liver disease
Primary prophylaxis (varices present, never bled) –> screening endoscopy 1-3 years, non-selective B-blocker eg propranolol or carvedilol, endoscopic vatical ligation
Secondary prophylaxis (bled in past) –> endoscopic vatical ligation AND NSBB
Bleeding –> resus, abx, lower portal pressure (octreotide/terlipressin/sandostatin), TIPSS (transjugular intrahepatic port-systemic shunt), surgical shunt, occlude the varix (balloon tamponade, vatical ligation, sclerotherapy/cyanoacrylate glue, oesophageal stent)
How to assess haemostatic abnormalities in Liver disease?
INR useless
consider thromboelastography (TEG) or rotational thromboelastography (ROTEM)
How to treat haemostat abnormalities in liver disease with bleeding
VIt K
consider DIC
cryoprecipitate
avoid prothrombin complex, FFP, platelets
What is the mechanism behind hepatorenal syndrome?
portal HTN –> splanchic arterial vasodilation –> increased cardiac output initially –> decreased systemic vascular resistance –> decrease in cardiac output
Describe the hepatitis’s
Hepatitis A
- faecal-oral route
- 28 day average incubation, no chronic disease.
- Vaccinate high risk groups, vaccinate up to the time of departure in the young, two weeks prior in older, immunocompromised, or those with liver disease.
-post-exposure prophylaxis with single dose of vaccine within 2 weeks in healthy persons 1-40 years.
- no treatment
Hep B
- incubation period 1-4 months
- chronicity determined by age of infection
- antiviral therapy not indicated for acute infection unless FHF, severe, or protracted illness.
- Mx: entecavir, or tenofovir, interferon (cant use is decompensated cirrhosis), lamivudine (safe in pregnancy)
Describe the phases of hepatitis B chronic infection
- Immune tolerant (replicative)- large amount of HBV DNA and e-
antigen, normal transaminases. May last 10-30 years.
*Replicative (Immune clearance) – Possible clearance of e-
antigen, may be HBc IgM Ab positive and alpha-fetoprotein may increase. Elevated transaminases. May recur (abortive immune clearance)
- Low or nonreplication phase/ Inactive carrier state- HBeAg negative and anti-HBeAb positive. DNA may be undetectable. Has to have normal ALT and low/no DNA over a one year period. HBsAg levels low.
- HBeAg-negative chronic hepatitis- Moderate HBV replication, HBeAg negative. Either residual virus or precore mutant
What is a common extra hepatic manifestation of HCV?
*Lichen Planus (v common)
*essential mixed cryoglobulinaemia (leukocytolastic vasculitis, arthralgia, membranoproliferative glomerulonephritis, neurological disease, peripheral neuropathy)
*Porpyria cutanea tardia (due to decreased activity of uroporphyrinogen decarboxylase)
Describe the azathioprine metabolism
people can intermittently shunt. some people develop it in pregnancy
some people are shunters, you jsut cant get 6TGN levels higher despite giving more 6-MP or azathioprine
What is the MOA of vedoluzimab?
Humanised IgG1 monoclonal antibody to alpha4beta7 integral
Prevents lymphocyte migration from bloodstream to gut.
Gut specific
Describe predictors of colectomy in IBD
deep ulcers
extensive loss of surface
well-like ulcers
large mucosal abrasions
Indications:
- dysplasia
- fulminant colitis/toxic megacolon
- failure of medical therapy
Describe Bristol stool chart
Describe different hamartomatous polyposis syndrome
Peutz-Jeghers Syndrome –>
*perioral pigmentations, pigmentations of fingers, upper and lower gastrointestinal hamartomatous lesions, small bowel and pancreatic cancer, colorectal cancer and sex-cord tumours
*LKB1 mutation (STK11)
Familial juvenile polyposis
* gastrointestinal hamartomatous polyps, increased risk of gastrointestinal cancer
* Smad4, BMPRIA, PTEN
Cowden’s disease
* colonic hamartomatous polyps, benign and malignant neoplasms of thyroid, breast, uterus and skin
Bannayan-Ruvalcaba-Riley Syndrome
*microcephaly, fibromatous, hamartomatous polyposis, hemangiomas, speckled penis
*PTEN mutation
Describe screening/surveillance of FAP and HNPCC
Summaries colorectal cancer genes and inheritance pattern
