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RACP exam > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

What are autoimmune disorders associated with coeliacs disease

A

Autoimmune thyroiditis, type 1 DM, Addisons, Sjogrens, AI hepatitis, Primary biliary cirrhosis

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2
Q

Coeliacs is associated with what clinical signs

A

Splenic atrophy, IgA deficiency, Atrophic gastritis, Dermatitis herpetiformis

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3
Q

What HLA is coeliacs disease associated with

A

HLA D23 or DQ8

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4
Q

Antibodies to test in coeliacs disease

A

Anti TTG (can to IgA or IgG if IgA deficient) , Anti endomysial anti gliadin, if serology negative consider IgA deficiency producing false negative

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5
Q

Small bowl biopsy findings for coeliacs

A

duodenal flattening / scalloping, lymphocytic lamina propria infiltration *CD4+ T cells, histological improvement needs 6 months, symptoms improve in 2 weeks

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6
Q

causes of villous atrophy

A

coeliacs, Autoimmune enteropathy, CVID, collagenous or tropical sprue, giardia, Crohns, GI lymphoma, eosinophilic gastroenteritis, TB, Whipples disease, Zollinger Ellison sx, other food intolerance

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7
Q

Symptoms / signs of malabsorption

A

Anaemia (Fe, B12, folate deficiency), weakness ( K+), Bruising (vit K), Glossitis / angular stomatitis (vitamin B group deficiencies), Peripheral neuropathies (B1,B2), oedema (protein deficiency), Bone pain (osteomalacia),

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8
Q

Faecal fat estimation in malnutrition

A

more than 7 g per day abnormal. Steatorrhea is one of the clinical features of fat malabsorption and noted in many conditions such as exocrine pancreatic insufficiency (EPI), celiac disease, and tropical sprue.

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8
Q

B12 deficiency cause

A

Pernicious anemia is a relatively rare autoimmune disorder that causes diminishment in dietary vitamin B12 (cobalamin) absorption, resulting in B12 deficiency and subsequent megaloblastic anemia. It affects people of all ages worldwide, particularly those over 60.8. Antibodies to intrinsic factor in GI.

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8
Q

Causes of acute NON BLOODY diarrhoea

A

viral, bacterial (shigella, salmonella, campylobacter - mild), E coli, Cholera, clostridia, protozoan -> guardia, crytpsporidia, Cylospora, strongyloides, food toxins, Malaria

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8
Q

Test for small bowel overgrowth

A

C14 glycocholate breath test - abnormal in bacteria overgrowth and ileal disease

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8
Q

Slightly above average risk for colon ca screening regime

A

98% population, FOBT every 2 years life age > 50, consider sigmoidoscopy every 5 years from 50

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8
Q

causes of acute BLOODY diarrhoea

A

Shigellosis (bacillary dysentery), Enterohaemorrhagic E coli, Campylobacter, Yersinia, Salmonella, Amoebic dysentery, Antibiotic associated colitis, rarely schistosoma, tricuris

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8
Q

Risk factors for risk stratification for colon ca

A

Age, symptoms, personal hx of bowel disease, family history of bowel cancer (1st degree v second degree) and age of onset, diet, lifestyle and smoking

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8
Q

Cat 2 - moderately increased risk colon ca screening regime

A

1-2% population - Colonoscopy every 5 years from 50 OR every 5 years from 10 years younger than the earliest family member diagnosed. Consider FOBT in intervening years.

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8
Q

Cat 3 - colon cancer risk screening regime

A

<1% population.
FAP - flex sig yearly/ second yearly starting from age 12-15; then prophylactic surgery. I no po;yposis by age 35 then changed 3 yearly, then 5 yearly after age 50
HNPCC - colonoscopy every 1-2 years from age 25 or 5 years earlier than youngest family member

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9
Q

Scope regime after polyps

A

adenomatous = villous or tubulovillous generally scope every 3 years if have hx of large >1cm non malignant polyps

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9
Q

Treatment for stage II CRC

A

Surgical resection - Consider chemotherapy - 5FU, oxaliplatin

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10
Q

Treatment for stage III CRC

A

Adjuvant chemo (FOLFOX -FU + oxaliplatin, capecitabine)

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11
Q

Treatment for stage IV CRC

A

palliative surgery +/- palliative chemotherapy +/- adjuvant RT on case by case basis

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12
Q

Cetuximab / Panitumamab

A

EGFR - left sided CRC with RAS wildtype, SEs acne form rash but thought to be good sign of efficacy

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13
Q

Capecitabine (Xeloda) side effects

A

Diarrhoea, hand and foot syndrome (erythematous and desquamating feet and hands)

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14
Q

Oxaliplatin side effects

A

Peripheral neuropathy , liver toxicity, diarrhoea/ constipation, pulmonary fibrosis, rhabdomyolysis

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15
Q

Extracolonic manifestations of UC

A

Ankylosing spondylitis, arthritis, pCS/ cirrhosis, Ca bile duct, Amyloidosis, Anaemia, VTE, ulcers, Erythema nodosum, pyoderma gangrenosum, Uveitis, conjunctivitis, episcleritis

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16
Q

Antibody for Crohns and UC

A

ASCA (anti saccharomyces Cerevisiae - common yeast found in the bowel)

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17
Q

Disease severity of UC

A

Mild < 4 motions per day, normal HR/ temp, minimal bleeding (sulfasalazine /mesalazine - can use Azathioprine/6MP)
Severe - > 6 motions per day, febrile, HR > 90, Abdo pain, bleeding ++ (cyclosporine salvage therapy, can use infliximab
Fulminant - >10 motions per day, continuous bleeding, fever, tachycardia, Abdo pain and distension - IV/PO steroids, topical steroids (foam enema) 20% flare steroid resistant - surgery proctocolectomy + ileoanal reservoir

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18
Q

Causes of hepatosplenomegaly

A

Chronic liver disease with portal HTN, leukaemia, lymphoma, MPD, CMV, infiltration - sarcoid/ amyloid, Connective tissue disease (SLE), Acromegaly, thryotoxicosis

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19
Q

Ascites

A

Exudate > 25g/L protein

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20
Q

Causes of ascites

A

liver failure, portal HTN, abdominal malignancy, CCF, CRF/ASRF, infection - consider peritoneal TB

21
Q

SAAG

A

Ascitic fluid albumin - serum albumin = if gradient > 11g/L the HAVE portal HTN, if gradient <11 then no portal HTN

22
Q

Crohn’s disease extracolonic manifestations

A

similar to UC except - more gallstones (PSC less common), renal disease (urate and oxalate stones) obstruction, infections from fistulae to the bladder, malabsorption, osteomalacia

23
Q

Crohns disease treatment

A

Pred 15-40mg induction >60% effective at inducing remission, budesonide for mild ileo-caecal disease.
AZA or 6MP slow onset 12 weeks strong evidence for remission induction and maintenance, use of over 2 steroid courses per year. Cease after 4 years if no attacks (20% relapse)
MTX - IM if failed aza
Infiximab / adamilumab (anti TNF)
75% require surgical intervention

24
Q

5-ASA

A

Mesalazine (for L ileocolitis), Osalazine and basalazide (for L colitis), topical preparations available, antibacterial, anti inflammatory (via COX) and immunomodulatory effects

25
Q

6-MP & AZA (MOA)

A

AZA rapidly absorbed metabolised to 6-MP -> purine analogues with no purine ribonucleotide synthesis and decreased cell proliferation -> immunomodulatory activity

26
Q

Infliximab (MOA)

A

Monoclonal IgG.-IGg4 against TNFa, TNFa key inflammatory cytokine and mediator of intestinal inflammation -> increased expression in IBD, infliximab blocks TNFa in serum and at cell surface + lyses producing Macrophages and T cells via complement fixation and antibody dependent cytotoxicity

27
Q

Hep B DNA / RNA ?

A

DNA

28
Q

Outcomes of Hep B infection

A

75% transient and subclinical disease
30% Sx
1% fulminant hepatic failure
5% chronic HBV in adults
note: 90% chronicity in neonates

29
Q

HCC risk in HBV

A

risk 0.5% per year
- high HBV DNA, male, older age, ETOH, smoking, high ALT, HBeAg positive, cirrhosis

30
Q

Entecavir / Tenofovir

A

entecavir (nucleoside analogue), tenofovir (nucleotide analogue)
advantages: ease of administration (once-daily oral dosing)
well tolerated
entecavir and tenofovir are highly potent and have a high genetic barrier to resistance
disadvantages
prolonged (potentially lifelong) therapy required
risk of hepatitis flare when therapy is stopped
adverse effects
generally well tolerated
tenofovir: minor reduction in bone mineral density; kidney impairment reported rarely, including Fanconi syndrome

31
Q

peginterferon alfa-2a (an interferon)

A

Chronic Hep B
advantages
defined treatment duration (48 weeks)
no risk of resistance
also active against hepatitis D infection in patients with co-infection
disadvantages
weekly subcutaneous injection
much more likely to cause significant adverse effects than oral antiviral drugs
poor response rates
can trigger an acute hepatitis flare
not recommended in patients with cirrhosis or in pregnancy
adverse effects
influenza-like symptoms, anorexia, psychiatric disorders (eg depression, suicidal ideation), fatigue and weight loss are common
can cause thyroid dysfunction and bone marrow suppression, and trigger autoimmune disease

32
Q

Treatment of chronic Hep B

A

Treatment regimens
For adults with chronic hepatitis B who require treatment, use:

1 entecavir 0.5 mg orally, daily

OR

1 tenofovir disoproxil fumarate 300 mg orally, daily

OR

1 tenofovir disoproxil maleate 300 mg orally, daily

OR

1 tenofovir disoproxil phosphate 291 mg orally, daily.

Peginterferon may be used instead of entecavir or tenofovir in selected adults with chronic hepatitis B who are not cirrhotic. Peginterferon is used more commonly in patients in the immune clearance (HBeAg positive chronic hepatitis) phase than those in the immune escape (HBeAg negative chronic hepatitis) phase. Peginterferon should only be used when recommended by a specialist with expertise in the management of viral hepatitis. The recommended dose is:

peginterferon alfa-2a 180 micrograms subcutaneously, once weekly for 48 weeks [Note 5].

33
Q

Child Pugh classifications

A

Ascites - absent / mod / tense
Encephalopathy - None, grade I-II, grade III-IV
Serum albumin - >35, 30-35, <30
Serum bilirubin - <34.2, 34 - 51, > 51
INR - < 1.7, 1.7 - 2.3, >2.3

34
Q

HEP C natural progression

A

Exposure -> 75% Asx 25% Sx -> 80-95% persistance -> 5-20% clearance.
IVDU, Blood Tx < 1992
Cirrhosis 20% is at 20 years
Risk factors for progression to cirrhosis : ETOH, Steatosis, DMT2, Iron overload, mal > 40, HBV, immunosuppression, Genotype, viral load, response to Rx

35
Q
A
35
Q

Extrahepatic manifestations Hep C

A

2% - essential mixed cryglobulinaemia, Menbranoprliferatiuve GN, Porphyria cutanea tarda, Leukocytoclastic vascultitis.

36
Q

Hep C treatment

A

Peg INFalpha and ribavirin
Measure at 12 weeks >2 log decrease
SEs - Peg INF a: malaise, fatigue, depression, neutropenia, thrombycytopaenia, thyroid disease, insomnia, diarrhoea, Ribavirin: Anaemia, rash , pruritic, highly teratogenic
Contraindications: Severe depression, CCF, renal failure, pregnancy/inadequant contraceptions, ongoing drug use, Cirrhosis in HBV patients (risk severe flare)

37
Q

HCC + HBV/ HCV and cirrhosis

A

HCC in HBV can develop in the absence of cirrhosis, HCC in HCV develops after cirrhosis

38
Q

HCC diagnosis

A

histology 2% risk tract seeding OR 2cm arterial enhancing on 2 different modalities OR > 2cm arterial enhancing on single modality + AFP > 400

39
Q

Treatment of HCC

A

Partial hepatectomy : Single lesion < 5cm, single lobe, no vascular invasion, no portal hypertension, good hepatic function (child Pugh A) 90% 5yr survival good pt selection
Liver transplantation - unresectable due to poor liver reserve AND solitary lesion < 5cm Or multiple tumours < 3cm largest < 4,.5cm and total < 8.5 cm AND no vase invasion, regional nodes / mets, 75% 5 yr surv.
ETOH Ablation, RF ablation, trans arterial chemoembolisation (doesnt inc survival), stereotactic radiotherapy for mets, sorafenib increases survival.

40
Q

Portal hypertension def and mortality

A

> 12mmHg (normal < 6), >20 mmHg is a predictor of complications, ~50% cirrhotics develop varies.
Child Pugh determines mortality; A 1%, B 25-30%, C 50% mortality.

41
Q

portal hypertension treatment

A

Antibiotics (timentin) 72 hours, octreotide (dec rebleed risk, no inmrpoved mortality) terlipressin / banding - improves mortality. TIPPS if all else fails, Hypertensive gastropathy -> argon plasma coagulation

42
Q

Portal hypertension prophylaxis

A

Propranolol - dec bleed risk by 50%, no clear mortality benefit
Risk of bleeding- vary size large 30%and annual risk ,c child Pugh class - best predictor of mortality, red spot - best predictor of bleeds, Hepatic venous pressure of > 18 best predictor of complications, continued ETOH abuse

43
Q

Hep B disease progress

A
44
Q

Autoimmune pancreatitis

A

swollen sausage shaped pancreas + low attenuation at head Ddx Is pancreatic cancer - associations with UC, Sjogrens and RA - Test ANA, Anti smooth muscle Abx, increased IgG4

45
Q

Hereditary pancreatitis

A

AD inheritance, needs yearly US and highs risk of chronic pancreatitis and pancreatic cancer, ANA and IgG4 +ve

46
Q

Autoimmune hepatitis

A

HLA DR3 & 4, jaundice anorexia fatigue, ALT / AST elevated, hypergammaglobulinaemia, Extrahep manifestation in 10-50% autoimmune thyroid disease, synovitis /arthoropathy, ITP, DMT1, haemolytic anaemia, vitiligo, alopecia, CREST, RA< Celiac, UC, PSC
Treatment: Prednisolone +/- azathioprine
Type 1”classic”: ANA, anti smooth muscle, anti actin, anti soluble liver / pancreas antigen
Type 2 - Anti LMK-1, anti liver cytosol 1

47
Q

Primary biliary cirrhosis onset and symptoms

A

onset > 30 T lymphocyte mediated attack on bile ducts, 50% asymptomatic
Symptoms: Prurutis, fatigue, hyperpigmentation, PBC arthropathyDiagnosis: inc ALP, inc GGT, AST/ALT normal, antimitochondrial ABs - AMA in 05%, ANA esp ant centromere - in creased risk of progression to liver failure, hyperlipidaemia.

48
Q

PBC diagnosis

A

Diagnosis: inc ALP, inc GGT, AST/ALT normal, antimitochondrial ABs - AMA in 95%, ANA esp ant centromere - in creased risk of progression to liver failure, hyperlipidaemia.

49
Q

PBC treatment

A

Ursodeoxycholic acid (improves survival, dec progressions in early stage disease, improves biochem, dec varies, dece liver transplantation)

50
Q

PBC associations

A

Sjogrens / Sick Sx, Scleroderma / CREST, RA, thyroid dysfunction, IBD

51
Q

PSC features

A

70% associated with IBD, Chronic cholestatic liver disease characterised by liver inflammation and fibrosis in intra and extra hepatic bile ducts. Smoking. Prognosis 85% 5 year survival; Cholangiocarcinoma in 10-20%the, HCC in 2%

52
Q

PSC diagnosis

A

ANCA in 65-95%
ANA esp anti centromere - increased risk of progression to liver failure
Hyperlipideamia

53
Q

PSC treatment

A

nothing proven to alter progression of disease
Ursodeoxycholic acid improves LFTs but does not have survival benefit or delay need for liver transplant
PSC recurrence 8-20%
decreased varicose, decreased liver transplantation

54
Q

Define acute liver failure

A
55
Q

What are the clinical features of acute liver failure

A
56
Q

Kings college criteria for paracetamol overdose

A
57
Q

Kings college criteria for non paracetamol overdose

A
58
Q

Child Pugh scoring

A
59
Q

What would you expect to show on the results of an acetic tap in the event of cardiac ascites?

A

High SAAG >11
High ascetic protein >2.5

60
Q

Explain management of spontaneous bacterial peritonitis

A

Ceftriaxone 2g/ cefotaxime (cipro for penicillin allergy)

61
Q

Contraindications to terlipressin

A

IHD, cardiac arrhythmias, cardiomyopathies, obliterative arterial disease of the lower limbs, asthma, COPD, CVD, age >70

RACP exam (4 decks)

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