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Dunedin-Gastro Flashcards

1
Q

Which high resolution manometry shows features consistent with achalasia?

A

A

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2
Q

What is achalasia?

A

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

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3
Q

What is the proposed model for the development of achalasia?

A

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

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4
Q

What is the treatment options for achalasia?

A

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

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5
Q

What is the clinical presentation of eosinophilic oesophagitis?

A

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

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5
Q

What is the management of eosinophilic oeseophagitis?

A

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

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6
Q

What is included in the 6-food elimination diet?

A

Milk, soy, wheat, egg, nut and fish/seafood

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7
Q

What is the histology of Barrett’s oesophagus?

A

Stratified squamous epithelium replaced by cardiac type mucus secreting columnar epithelium +/- intestinal metaplasia

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8
Q

What is the rate of Barrett’s oesophagus progression to oesophageal adenocarcioma? and is there anything to slow/slow progression?

A

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

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9
Q

Describe the pattern of development of oesophageal adenocarcinoma compared to CRC?

A

oesophageal adenocarcinoma: develops in non-linear pattern over 4 years

CRC: develops in linear pattern over 10 years

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10
Q

Discuss screening programs for Barrett oesophagus

A

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

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11
Q

What is the role of PPI initiation prior to endoscopic diagnosis in upper GI bleeding?

And post-procedure?

A

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

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12
Q

What is the relationship between H.Pylori and ITP?

A

H.Pylori can cause ITP as anti-cage antibodies cross-react with platelet antigens

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13
Q

Is there a good use of tranxemic acid in GI bleeding?

A

not really

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14
Q

Describe the classification of peptic ulcers

A

Forest 1 and 2A, collective risk of bleeding is 50%

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15
Q

What is the management of Peptic Ulcers?

A

epinephrine injection + endoscopic intervention

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16
Q

What was the older triple therapy treatment for H.Pylori? What is the newer Quadruple therapy.

A

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

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17
Q

Describe post-eradication testing for H.Pylori

A

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

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18
Q

What to manage antiplatelet therapy in an UGI bleed.

A

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)

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19
Q

When to scope a patient with a GP bleed on warfarin?

A

when INR <2.5

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20
Q

Describe the rates of major GI bleed in non-valvular AF on DOAC

A

Dabigatran and rivaroxoban highest bleeding risk
then warfarin
then apixaban

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21
Q

Describe reversal agents for NOACS

A

Dabigatran –> idarucizumab
Xa inhibitors –> Andexanet alpha, combination of clotting factors

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22
Q

Describe the histological features of coeliac disease

A

Increased intra-epithelial lymphocytes
Crypt hyperplasia
Villous atrophy

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23
Q

Describe testing for Coeliac disease

A

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

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24
Which haplotypes are associated with Coeliac disease?
HLADQ2/DQ8 more common in DOWN syndrome, Turners, William's syndrome
25
What are the fat soluble vitamins?
ADEK
26
What deficiencies should you test for in Coeliac disease?
Iron deficiency anaemia Fat soluble vitamins (ADEK) B12 deficiency Folate deficiency Copper deficiency Bone disease
27
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)
28
Describe bilirubin metabolism
29
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
30
Clinical signs of cirrhosis
parotid gland enlargement (alcohol) fetor hepaticus ascites caput medusae splenomegaly Cruveilhier-Baumgarten murmur asterixes
31
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
32
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
33
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
34
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
35
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
36
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
37
What are the most common pathogens in spontaneous bacterial peritonitis?
Gut bacteria: e.coli and klebsiella
38
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
39
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
40
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
41
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)
42
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)
43
How to assess haemostatic abnormalities in Liver disease?
INR useless consider thromboelastography (TEG) or rotational thromboelastography (ROTEM)
44
How to treat haemostat abnormalities in liver disease with bleeding
VIt K consider DIC cryoprecipitate avoid prothrombin complex, FFP, platelets
45
What is the mechanism behind hepatorenal syndrome?
portal HTN --> splanchic arterial vasodilation --> increased cardiac output initially --> decreased systemic vascular resistance --> decrease in cardiac output
46
What is the management of hepatorenal syndrome-AKI?
1) fix volume with albumin 2) terlipressin (S/E arrhythmias, cyanotic digits, splanchnic ischaemia) 3) norepinephrine and albumin 4) midodrine/octreotide/albumin
47
What is a cause of isolated bilirubin elevation?
Gilbert syndrome- uridine diphosphoglucuronate- glucuronosyltransferase 1A1 Crigler-Najjar syndrome (unconjugated) Rotor and dubin-johnson syndromes (conjugated) Haemaolysis (unconjugated)
48
What is a cause of isolated alkaline phosphate? (non-hepatic)
Bone disease (fracture, Paget's, hyperparathyroidism, osteomalacia, hyperthyroidism, tumour) pregnancy
49
What immune cell does primary biliary cholangitis involve?
T-lymphocytes
50
When are antimitochondrial antibodies positive?
in primary biliary cirrhosis specificity of 98%
51
What is the treatment of primary biliary cholangitis?
ursodeoxycholic acid obeticholic acid
52
What is the median survival of primary sclerosing cholangitis without a liver transplant?
12 years
53
What are investigation findings for primary sclerosing cholangitis?
atypical P-ANCA 30-80%, hypergammaglobulinaemia in 30% +/- ANA, ASMA, RF Cholangiographic diagnostic- beading, structuring NOTE- IgG4 associated cholangitis is very hard to distinguish from primary sclerosing cholangitis
54
What are complications of primary sclerosing cholangitis?
*Cholangiocarcinoma: 10-15% *Gallbladder cancer: 3-14% *cirrhosis/portal HTN *fat soluble vitamin deficiency/steatorrhea *colon cancer *metabolic bone disease *Cholangitis
55
Treatment for primary sclerosing cholangitis
*ursodeoxycholic acid will provide symptom control *endoscopic treatment of dominant biliary strictures *Liver transplant
56
What Is the timing of fulminant hepatic failure?
Need to involve liver transplant people develop acute liver injury, hepatic encephalopathy, elevated PT/INR hyper acute <7 days acute 7-21 days subacute >21 days and <26 weeks monitor with PT/INR- up to 4 times a day
57
What is the criteria for liver transplant in fulminant hepatic failure?
1) acetaminophen induced liver failure: arterial pH <7.30 OR grade 3 or 4 encephalopathy with PT >100seconds and Cr >340 mg/L 2) Non-acetaminophen induced liver failure - PT >100 seconds OR any three of the: - Age <10 or >40 years - non-A and non-B viral hepatitis, idiosyncratic drug reaction, Wilson, Jaundice >7 days prior to encephalopathy, PT >50 seconds, bilirubin >180mg/L
58
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)
59
Describe the extra-hepatic manifestations of hepatitis B
- polyarteritis nodosa - glomerular disease (membranous nephropathy, MPGN, nephrotic syndrome) - serum sickness (arthritis, rash)
60
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
61
Describe indications for HBV treatment
*anyone with cirrhosis *Immune active chronic HBV *if HBeAg positive, HBV DNA >20,000, HBeAg pos with ALP 2x ULN *if HBeAG negative, HBV DNA >2000 IU/ml, with ALT 2xULN
62
What is the management of hepatitis B?
- Mx: entecavir, or tenofovir, interferon (cant use is decompensated cirrhosis), lamivudine (safe in pregnancy)
63
Describe the natural history of HCV
1) acute infection leads to chronic infection in 60-85% 2) 20-30% with chronic HCV will develop cirrhosis over 20-30 years 3) many will develop hepatocellular carcinoma note, congitive impairment independent of liver disease stage
64
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)
65
Describe the drugs for Hep C
Generally very good, 90% recover 1) Glecaprevir/pibrentasvir contraindicated in hypersensitivity, severe liver
66
Describe Hep E
*RNA virus transmitted in water/feces *highest incidence in Asia, Africa, middle eat, and central america *animal reservoir (rodents, deer, boar) *acute disease in non-immunocompromised patients *chronic disease in those with transplants *fulminant hepatic failure in 15-25% in women who are pregnancy *Diagnosis with PCR detection of HEV or IgM ab to HEV
67
What are specific therapies for drug-induced liver disease?
NAC for paracetamol L-carnitine for valproic acid overdose
68
What is the minimum threshold to cause alcoholic liver disease?
40-80gm/day for men 20-40gm/day for women
69
What causes the AST/ALT >2 in alcoholic liver disease?
Due to hepatic deficiency of pyridoxal 5'-phosphate.
70
How to treat alcoholic hepatitis?
- Prednisone 40mg daily for 28 days OR - pentoxifylline 400mg TDS
71
What are the types of autoimmune hepatitis?
Type 1 - SMA and ANA, anti-actin Ab Type 2 - Anti-LKM1
72
What is the treatment of autoimmune hepatitis?
Treatment not required in asymptomatic patients with normal or minimally elevated transaminases and gamma globulin levels and minimal necroinflammatory activity on biopsy. Pred +/- azathioprine Normalisation of labs and histology usually takes over 12 months
73
What are the genes involved in haemochromatosis?
HFE gene mutations --> C282Y or H63D note, HFE is similar to MHC Class 1 proteins and must bind beta 2-microglobulin
74
What is the mechanism of hepcidin?
1) reduces iron transfer across the basolateral membrane of enterocytes by binding ferroportin 2) Induces macrophages to store iron 3) IL-6 upregulates Hepcidin --> anaemia of chronic disease
75
What are the blood tests in haemochromatosis?
Transferrin sat >45% Ferritin >200ng/ml in men or >150ng/ml in women
76
What are extrahepatic manifestations of haemochromatosis?
Improvement with phlebotomy: - cardiomyopathy - hypogonadism No improvement with phlebotomy - diabetes in 50% - arthropathy (pseudo gout, chonedrocalcinosis) second and third MCP
77
What is the pathogenesis of Wilson disease? and Clinical manifestations?
Accumulation of copper in the liver and brain Clinical manigestation: 1) Liver disease (steatosis, fulminant hepatic failure with Coombs-negative haemolytic anaemia, cirrhosis, acute liver failure) 2) neurological disease (MRI may show basal ganglia hyperintensity on T2-weighted images), elevated copper in CSF 3) Psychiatric
78
What is unique about LFT in Acute liver failure Wilsons disease ?
ALP is typically normal
79
How to diagnose Wilsons disease?
Serum copper is LOW (decreased ceruloplasmin Urine copper 2-3x normal 24 hour urine after 500mg D-penicillamne >1600 mcg Cu diagnostic More are compound heterozogytes
80
What is the treatment for Wilsons disease?
1) Copper removal via chelators --> D-penicillamine (can worsen Neuro symptoms), trientine, tetrathiomolybdate 2) low copper diet 3) oral zinc (interferes with Cu absorption
81
What is the leading cause for mortality after a liver transplant?
Infection- highest risk in the first 3 months CMV- arthralgias, leukopenia, recent treatment for rejection Complications post liver transplant: - biliary obstruction or hepatic arter thrombus - HTN - Diabetes - dyslipidaemia - metabolic bone disease - malignancy (should do an annual full exam with full body dermatologic exam), annual PSA or PAP
82
What are causes of chronic pancreatitis including genetic causes?
-Genetic- CFTR, SPINK1, PRSS-1 -Alcohol abude - ductal obstruction (trauma, stone, pseudocyst) - tropical pancreatitis - autoimmune pancreatitis - systemic disease - SLE, hyperparathyroidism, idiopathic
83
What is the pathogenesis in chronic pancreatitis?
Poorly understood a) increase in protein secretion without increase in bicarbonate b) patchy inflammatory change
84
What is the best imaging modality for chronic pancreatitis?
*MRI Brain *fecal elastase is the most sensitive and specific lab test
85
How to manage pancreatic insufficiency (conservatively)?
*Low fat diet (20gm/day) *pancreatic enzyme supplements *Medium chain triglycerides
86
What is the most common type of pancreatic cancer?
ductal adenocarcinoma
87
What germline mutations are associated with pancreatic cancer?
BRCA1, BRCA2, and PALB2
88
What is the treatment of IBD?
Chrohns disease - induction: steroids - Maintenance: azathioprine/6-MP, TGN/MTX or biologic - surgery Ulcerative colitis - if distal colitis can give 5-ASA rectally, if pancolitis give it oral - steroids - Maintenance: oral 5-ADA< azathioprine, IV cyclophosphamide, surgery Biologics - infliximab, adalimumab - anti-integrin: vedoluzimab - anti-IL12/23: ustekunimab
89
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
90
Are thiopruines safe in pregnancy?
Yes. no evidence of teratogenicity. no effect on male fertility.
91
What are treatment targets in IBD?
1) symptom control 2) normalisation of CRP 3) decrease in calprotectin 4) endoscopic healing, normalised QoL and absence of disability in Crohns, we look for transmural healing in UC, we look for histological healing
92
What is the MOA of ustekunimab? S/E
Monoclonal antibody that target the p40 subunit of IL-12 and IL-23 herpes zoster! resp infection
93
What is the MOA of vedoluzimab?
Humanised IgG1 monoclonal antibody to alpha4beta7 integral Prevents lymphocyte migration from bloodstream to gut. Gut specific
94
Fertility and IBD
* No evidence that UC or CD affect fertility * in males. sulphasalazine causes reversible oligospermia * cesarean section in indicated in active peri-anal disease or active rectal involvement *if conception occurs at a time of quiescent disease, the risk of relapse is the same as in non-pregnant women. pregnancy influence the course of inflammatory bowel disease.
95
IBD drugs and pregnancy
methotrexate and thalidomide are contraindicated metronidazole and cipro should be avoided first trimester Anti-TNF drugs can cross the placenta in the 3rd trimester
96
Vaccinations and immunomodulator therapy such as in IBD
- Can give live-vaccines after 3-6 months after stopping immunomodulator therapy - wait at least 3 weeks after immunisation with a live vaccine before starting immunomodulator treatment
97
Describe symptoms of fulminant colitis
1) bloody stool frequency >6/d 2) tachycardia 3) hyperthermia 4) anaemia <105 5) high ESR
98
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
99
Managing acute fulminant ulcerative colitis
IV steroids azathioprine cyclosporine+ infliximab may need surgery
100
How soon after UC do we monitor for colon cancer?
Colonoscopy after 8-10 years after pan colitis if low risk --> 5 years intermediate risk (extensive UC/CD with mild active inflammation, post-inflammatory polyps) --> 3 ears high risk (extensive UC/CD with mod-severe active inflammation), PSC --> every year
101
What is the criteria for IBS?
Recurrent abdominal pain on at least one day/week for the last 3 months (with symptom onset at least 6 months ago*): * PLUS 2 or more of: – Association with defaecation – Change in stool frequency – Change in stool consistency
102
Describe Bristol stool chart
103
What is the treatment of IBS?
Diet --> peppermint oil Psychological treatment --> reassurance Hypnotherapy Analgesia --> anti-spasmodics (mebeverine, hyoscine butylbromide/buscopan) TCA--> amitriptylline/nortriptyline SSRIs Avoid NSAIDS and opiates/opiods Laxatives - avoid lactulose, trial fibre, polyethylene glycol, stimulants, anti-diarrheas (loperamide) Bile acid sequestrates - cholestid/cholesitpol Antibiotics- limited evidence
104
What is a FODMAP diet?
Fermentable Oligo-saccharides Di saccharides Monosaccharides and Polyols
105
What is the genetics of Familial adenomatous polyposis? What clinical syndromes does it form?
APC gene chromosome 5 Clinical syndromes: 1) Gardner's syndrome --> osteomas, odontomas, epidermoid cysts, dermoid tumours 2) Turcot's syndrome --> CNS malignancies 3) Attenuated FAP
106
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
107
108
Describe screening/surveillance of FAP and HNPCC
109
Summaries colorectal cancer genes and inheritance pattern
110
Describe when to do bowel cancer screening
FIT 2yearly ages 45-74
111
Approach to polyps in screening colonoscopy
1) Hyperplastic polyps --> small and in left colon, no risk of malignancy 2) tubular adenomas --> all have low grade dysplasia, more concerning if high grade dysplasia, villous component is of relevance 3) sessile serrated lesions/ adenomas - any dysplasia is concerning, easily missed
112
Describe follow up screening of colonoscopy
1-2 adenomas --> 10 year 3-4 adenomas --> 5 years 5-9 adenomas --> 3 years >10 adenomas- 1 year
113
What is the most common cause of acute diarrhoea illness?
(1) norovirus (2) non-STEC e.coli (3) campylobacter

Aisha (45 decks)

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