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MEDICINE NEW > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

What are the side effects of Proton Pump Inhibitors (Omeprazole)?

A

Lack of acid = gastroenteritis (diarrhoea) + lack of B12

Can’t go in the sun (photosensitivity) as they have no hair (alopecia) so they get thin bones (osteoporosis)
and LFTs get higher…

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2
Q

What preparation should the patient undergo before a colonoscopy?

A

Few days before- low fibre diet, no seeds, nuts, raw fruit + veg
Day before- bowel prep meds, clear liquids (black tea and coffee)
On day- don’t eat or drink 2 hours beforehand

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3
Q

Who is eligible for the occult blood test screening?

A

60-69 year olds

Every 2 years

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4
Q

Commonest types of renal calculi?

A

Calcium oxalate 45%
Mixed calcium oxalate/phosphate 25%
Calcium phosphate 10%
Triple phosphate 10%

Urate 10%
Cystine 1%
Xanthine <1%

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5
Q

Staghorn calculi of ammonium magnesium phosphate or triple phosphate and are predisposed to form in the presence of which two bacteria

A

Ureaplasma urealyticum and Proteus infections

Urinary tract will be alkaline

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6
Q

What are the 3 common sites for berry aneurysms?

A
  1. Posterior communicating artery with the internal carotid (CN 3 affected)
  2. Anterior communicating artery with the anterior cerebral
  3. Bifurcation of middle cerebral a
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7
Q

3 medical conditions associated with berry aneurysms?

A
  1. Polycystic kidneys
  2. Coarctation of the aorta
  3. Ehlers Danlos
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8
Q

Patient has a thunderclap headache, what test should you do.
If negative what is the next test to perform?

A
  1. CT
  2. Lumbar puncture 12 hours after onset (if no CI)CSF is xanthochromic from Hb breakdown
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9
Q

What medication can you give to patients with SAH to reduce vasospasm?

A

Nimodipine IV- calcium antagonist = less ischaemia

Ultimately need to refer for neurosurgery- endovascular coiling or surgical clipping

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10
Q

Name of the radiology sign where bowel is trapped between the liver and diaphragm (mimics bowel obstruction)

A

Chilaiditi sign

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11
Q

How is hyperacute, acute and subacute fulminant liver failure defined?

A 
Hyperacute= encephalopathy within 7 days of jaundice
Acute= within 8 to 28 days
Subacute= within 5 to 26 weeks
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12
Q

Which viruses can cause liver failure?

A

Hep B, Hep C + CMV

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13
Q

Signs of acute (fulminant) liver failure:

A
  1. Jaundice
  2. Hepatic encephalopathy
  3. Asterixis
  4. Constructional apraxia (can’t copy a 5 pointed star)
  5. Fetor hepaticus
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14
Q

Blood tests for a patient with fulminant liver failure:

Encephalopathy + jaundice + asterixis

A

FBC- neutrophilia may be EtoH or infection, GI bleed?
U+Es- may be giving laxatives as Rx so need baseline
LFTs- liver failure
Clotting- high PT and INR
Glucose- hypoglycaemic
Pregnancy test- HELLP
Paracetamol level, serology (hepatitis, EBV, CMV),
Ferritin, a1-antitrypsin, caeruloplasmin (low), autoantibodies

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15
Q

Rx of encephalopathy:

A

Excess ammonia

Lactulose TDS
Enemas (reduce numbers of nitrogen forming-bacteria)
Abx to reduce bacteria- metronidazole, rifaximin

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16
Q

Drug causes of jaundice split by pre-hepatic, hepatic and obstructive causes:

A

Pre-hepatic: anti-malarials can cause haemolysis (+ dapsone given for dermatitis herpetiformis)

Hepatic: TB drugs- isoniazid, pyrazinamide, rifampicin; paracetamol

Obstructive- PPPCOS:
Penicillin, Prochlorperazine (anti-D2 R), Pill
CO-amoxiclav,
Sulfonylureas (gliclazide)

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17
Q

What level of bilirubin produces visible jaundice?

A

> 60umol/L

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18
Q

What form of bilirubin is insoluble?

A

Unconjugated bilirubin, when it has been broken down from globin of haemaglobin.

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19
Q

Causes of unconjugated bilirubinaemia

A

Overproduction- haemolysis, ineffective erythropoeitin
Impaired hepatic uptake- drugs (rifampicin), right heart failure
Impaired conjugation- Gilbert’s, Creigler Najjar (neonates, total lack)
Neonatal jaundice

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20
Q

Causes of conjugated hyperbilirubinaemia

A

Hepatocellular dysfunction: hepatocyte damage ± cholestasis

Impaired hepatic excretion

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21
Q

Causes of jaundice in a previously stable patient with cirrhosis:

A 
Sepsis, constipation
Malignancy- HCC
Drugs, Alcohol
GI bleeding
Interventions
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22
Q

King’s criteria for paracetamol induced overdose:

A

PParaCE

pH < 7.3 when it’s 24 hours after ingestion

Or all 3 of:
PT >100s
Creatinine >300umol/L
Encephalopathy- grade 3 (asterixis, incoherent) or grade 4 (coma)

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23
Q

King’s non-paracetamol liver failure:

A

PT > 100s

Or 3 of:
Age <10 years or >40 years
Bilirubin >300
Clotting- PT >50
Drug induced liver failure (not paracetamol)
Encephalopathy onsetting 1 week after onset of jaundice

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24
Q

What drugs caused your chronic liver failure MAM?

A

Methotrexate (lung fibrosis, bone marrow suppression)
Amiodarone (slate grey skin, thyroid, lung fibrosis, peripheral neuropathy)
Methyldopa

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25
Q

What do routine bloods can tell you in a patient who has chronic liver disease?

A

FBC- macrocytic anaemia (EToH), normocytic (variceal bleed)
Clotting, albumin, PT+INR- synthetic function
Ammonia level- in suspected encephalopathy
U+Es- hepatorenal syndrome (urea produced by liver so caution in interpretation)

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26
Q

Child Pugh Score for grading of cirrhosis and risk of variceal bleeding?

A

ABCDE

Values for max score shown 
Albumin <28
Bilirubin >51
Clotting >6
Distension ascites moderate
Encephalopathy 3-4
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27
Q

Common organisms causing spontaneous bacterial peritonitis + Rx:

A

E Coli, Klebsiella (G -ve), Streps

Broad sprectrum: Tazocin + cephalosporin

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28
Q

Drug induced lupus:

A

Hydralazine
Isoniazid
Procainamine/ Penicillinamine / Phenytoin

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29
Q

Why is Cregler Najjer syndrome so much more severe than Gilbert’s?
(Cregler causes neonatal jaundice with kernicterus)

A

Unlike Gilbert’s, where there is low activity of the enzymes conjugating bilirubin, in Crigler-Najjer’s there is virtually absent enzyme activity
(In uridine diphosphate glucuronosyltransferase enzyme)

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30
Q

What is Mirrizi’s syndrome?

A

Obstructive jaundice caused by compression of the common bile duct due to gallstone impaction in the cystic duct- associated with cholangitis)

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31
Q

Teenager with repeated jaundice, diagnosed with Dubin Johnson syndrome- what is this?

A

Like many of the inherited liver diseases it has autosomal recessive inheritance (as it’s due to abnormal protein activity so other gene can compensate)

Defective hepatocyte excretion of conjugated bilirubin into bile canaliculi.
Liver biopsy diagnoses, no Rx needed

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32
Q

Bloods to do in a patient with pre-hepatic jaundice:

A 
FBC- haemolytic anaemia
Clotting
Blood film- schistocytes (fragmented RBCs), parasites
Reticulocyte count
Coombs- autoimmune
Haptoglobulins- bind free Hb
Monospot tes- EBV IgM

U+E, LFTs, Albumin, Paracetamol levels
Blood cultures, serology

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33
Q

What width of bile dile implies dilation?

What IHx is warranted if seen on USS?

A

> 6mm suggests obstruction

ERCP if dilated and LFTs not improving

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34
Q

Imaging recommended in a jaundiced patient where obstructive jaundice is suspected?

What is next line if bile ducts look normal?

A

USS- look for dilated bile ducts or stones
ERCP- if dilated + LFTs not improving

MRCP- if no stone is found but can see stones in gallbladder
Liver biopsy- if bile ducts are normal

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35
Q

Name some features of the different stages of encephalopathy:

A

Stage 1: sleep-wake reversal, constructional apraxia (5pt star)
Stage 2: confused, behaviour change ± liver flap
Stage 3: incoherent, restless
Stage 4: coma

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36
Q

What are the 3 features of hepatorenal syndrome?

A

Cirrhosis
Ascites
Renal failure

(This car is driving nowhere good)

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37
Q

Pathophysiology of hepato-renal syndrome?

A
  1. Portal hypertension initially (may lead to circulating vasodilator increase + NO release +bacterial migration + angiogenesis)
  2. Arteries in the splanchnic and systemical system dilate.
  3. As vascular resistance drops, baroreceptors activate angiotensin system, ADH (vasopressin activation) and sympathetic activation.
  4. Sympathetic output causes vasoconstriction of kidney
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38
Q

Rx of different types of hepatorenal syndrome?

A

Cirrhosis + ascites + renal failure (if other causes of renal failure like vasculitis and glomerulonephritis have been excluded)

Type 1- worse, rapidly progressing > Terlipressin reduces hypovolaemia (counters all the ADH around)
Median survival 2 weeks

Type 2- steady deterioration, transjugular intrahepatic portosystemic stent shunting (TIPS) to reduce pressure and portal hypertension

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39
Q

Difference between King’s criteria and Child-Pugh grading of cirrhosis:

A

King’s predicts outcomes of acute liver failure, so included variables are: age, bilirubin, clotting (PT), drug-induced, encephalopathy >1 week post-jaundice

Child-Pugh is for chronic liver failure, variables relate to long-term prognosis:
Albumin, Bilirubin, Clotting (PT), Distension- acites, encephalopathy

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40
Q

How is spontaneous bacterial peritonitis confirmed?

A

> 250/mm3 neutrophils in ascitic tap

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41
Q

What screening tests can be used for patients with cirrhosis to look out for hepatocellular carcinoma?

A

3 monthly USS ± AFP

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42
Q

Rx for pruritis in cirrhosis?

A

Cholestyramine (binds bile acids in the gut to reduce recycling of them and uptake)

Once in the gut 3 things happen to conjugated bilirubin

  1. Uptaken into the circulation (recycled)
  2. Converted to urobilinogen, reabsorbed and excreted in urine
  3. As urobilinogen, converted to stercobilinogen and remains in gut
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43
Q

Management of ascites in cirrhosis?

A

Similar to heart failure:
Fluid restrict 1.5L
Low salt diet
Spironolactone (acts on angiotensin axis) ± furosemide
Daily weights
Parencentis with concomitant albumin infusion

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44
Q

Aside from hepatorenal syndrome what other causes of deteriorating renal function may be linked to the patient’s cirrhosis?

A

Reduce clearance of immune complexes by the liver may lead to more lodging in the kidney > IgA nephropathy or glomerulosclerosis

Hep C- membranoproliferative GN (mesangiocapillary GN)
Hep B-membranous nephropathy (baby in membrane, mum is so shocked she gets goosebumps which are nodular hence polyarteritis nodosum associated)
a1-antitrypsin- membranoproliferative GN

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45
Q

Which ethnicity is at risk of hereditary haemochromatosis?

A

Celtic- northern europe ancestry

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46
Q

Genetic inheritance of haemochromotosis:

A

Autosomal recessive (like most liver pathologies)
Chromosome 6- HFE gene
Increased iron reabsorption in the gut

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47
Q

Features of haemochromatosis:

A

Relate to where iron is deposited
DM (pancreas), hypogonadism (pituitary)
Hepatomegaly/cirrhosis, dilated cardiomyopathy, slate-grey skin, osteoporosis
Arthralgia (joints)

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48
Q

Tests in a patient with bronze diabetes:

A

Bloods: high ferritin (iron stores) + transferrin saturation (carrier)
Raised LFTs, HbA1c (DM)

Liver MRI: iron overload
Liver biopsy: Perl’s stain quantifies iron loading and severity
Echo: check for cardiomyopathy

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49
Q

Rx for haemochromatosis:

A

1st. Venesection: a unit a week until ferritin <50ug/L, then 2 monthly
2nd. Desferrioxamine: binds free iron in blood and increases excretion

Check for diabetes
Relative screening

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50
Q

What is the pathophysiology of a1-antitrypsin deficiency?

A

A1-antitrypsin is a serine protease inhibitor that dampens down inflammatory cascades
In lung it prevents tissue damage from neutrophilic elastase enzymes.

Without it patients are at risk of emphysema, cirrhosis and hepatocellular carcinoma 
Chromosome 14 (autosomal recessive)
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51
Q

How are the different types of a1-antitrypsin distinguished genetically?

A

Can’t measure a1 enzyme levels as it is an acute phase protein

Mobility electrophoresis:
If medium (PiMM) then enzyme is normal
If slow (s) or very slow (z), patient is heterozygotic (PiMZ or PiSZ) then unlikely to be affected

Only if two very slow forms (zz aka PiZZ) is the patient affected

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52
Q

Patient has been getting breathless and jaundiced, with xray showing emphysematous pattern. How is a1-antitrypsin investigated?

A

Electrophoresis of a1-antitrypsin (PiZZ forms, very slow)
Serum a1-antitrypsin levels (but is an acute phase reactant)

Liver biopsy: Periodic acid Schiff +ve

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53
Q

How does y-glutamyltransferase (y-GT) help distinguish the cause of raised alk phos?

A

Y-GT produced by liver, pancreas, kidney + intestine but not bone
So if Alk Phos is raised but y-GT is not it is more likely to be bone turnover

However alk phos is produced by kidney and intestine too so if both raised, it could be most of the abdominal organs

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54
Q

If AST: ALT ratio is more than 2, what cause of hepatocellular injury is likely?

A

Alcoholic liver disease

May also have a high y-GT, macrocytosis and normal alk phos

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55
Q

Gold standard to identify cause of chronic liver disease?

A

Liver biopsy- tells definitively

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56
Q

Biopsy shows liver granulomas, what could be differential for this finding?

A 
Primary biliary cirrhosis
Sarcoid, PAN, SLE, Wegener's
TB, syphilis, HIV + toxoplasmosis/CMV/mycobacteria
Isoniazid, carbemazepine, allopurinol
Lymphoma
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57
Q

How is Primary Biliary Cirrhosis typically found?

A

Incidental finding of raised alk phos on routine LFTs in 50s

  • asymptomatic
  • progresses to cirrhosis
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58
Q

How is PBC diagnosed?

A

Often find raised alk phos in asymptomatic patient

Anti-mitochondrial Abs
(Anti-Mi2 is most specific)

Raised IgM
USS: shows no extrahepatic cholestasis cause
Generally biopsy not required

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59
Q

Rx of primary biliary cirrhosis:

A

Fat-soluble vitamins (ADEK- as absorption is low with cholestasis)
Ursodeoxycholic acid- protects hepatocytes from bile-acid apoptosis

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60
Q

How does primary sclerosing cholangitis differ from primary biliary cirrhosis in the part of the liver affected?

A

PBC- granulomatous inflammation of interlobular bile ducts, more benign, anti-mitochondrial Ab
PSC- extrahepatic ducts which may cause PBC secondarily, UC associated, more aggressive + likely to get cancer of colon/gallbladder/liver, ANCA or Smooth muscle Ab

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61
Q

What imaging will distinguish PBC from PSC typically?

A

ERCP demonstrates extrahepatic bile duct involvement/fibrosis as well as intrahepatic (strictures + beading of bile duct), whereas in PBC intralobular small bile ducts are affected.
PSC can cause PBC

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62
Q

Patient has epigastric pain, jaundice fever and an itchy rash of raised red wheals.
On examination you note swollen tender finger joints. Can’t find any evidence of alcoholic, fatty or hepatic cause. What may be the cause?

A

Autoimmune hepatitis, associated with other autoimmune conditions:
Type 1 DM, thyroiditis, coeliac disease, RA

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63
Q

What autoantibodies are associated with different types of autoimmune hepatitis?

A

Type 1: responds to immunosupression, 80% smooth-muscle Abs, 10% anti-nuclear Ab, raised IgG

Type 2: presents in children, less treatable, anti-liver kidney microsomal type 1 abs (LKM1 +ve), smooth muscle -ve

Type 3: soluble liver antigen Abs, or liver-pancreas antigen Abs

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64
Q

Rx of autoimmune hepatitis

A

Immunosupression: prednisolone, azathioprine

Like all cirrhosis: liver transplant

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65
Q

What is the difference between steatosis and steatohepatitis?

A

Both may occur in NASH
Steatosis- increased fat in hepatocytes (may occur in alcoholism Wilson’s)
Steatohepatitis- inflammation also

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66
Q

Name the chromosomes involved in:

  1. Haemochromatosis
  2. A1-antitrypsin
  3. Wilson’s
A
  1. 6- HFE
  2. 14
  3. 13
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67
Q

Pathophysiology of Wilson’s disease?

A

Absorption of copper is normal but conjugation with caeruloplasmin for transport and excretion into bile is impaired- defective copper transporting ATPase is cause.
Therefore low caeruloplasmin
24 hour copper excretion is high (overflows but not enough)

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68
Q

Neuropsych symptoms of Wilson’s disease:

A

Medulla deposition- dysarthria, dysphagia
Basal ganglia- dyskinesias, dystonias, tremor, parkinsonism, micrographia, calculations
Cerebellar- ataxia, clumsiness
Frontal- dementia, reduced memory + IQ, irritable
Psych- depression, mania, labile emotions, libido change, delusions

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69
Q

Tests to check in a 20 year old patient with arthralgia, raised LFTs, tremor, dysarthria, who you suspect Wilson’s:

A

Urine- 24 hr copper (raised as it overflows)
Bloods- serum caeruloplasmin (low), serum copper (low), LFTs
Gene testing- chromosome 13
Liver biopsy
Slit lamp- Kayser Fleischer rings
MRI head- degeneration of basal ganglia, fronto-temporal, cerebellar, brainstem

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70
Q

Rx of Wilson’s disease:

A

Low copper diet (liver, chocolate, nuts, mushrooms)

  1. Penicillamine (SE- lupus, leucopenia, thrombocytopenia, haematuria)
  2. Trientine dihydrochloride
  3. Liver transplant
71
Q

Causes of severe oral ulcers:

A

Inflammatory: Crohn’s, coeliac,
Behçet’s, lichen planus, pemphigus, pemphigoid
Infections: herpes simplex (±erythema multiforme), syphilis

72
Q

Rx of minor ulcers and major ulcers

A

Minor- tetracycline mouth wash may be used

Major- corticosteroids or thalidomide (anti- IL6, 10, 12 etc)

73
Q

Vitamin deficiencies causing cheilitis:

A

Vitamin B2 or iron

74
Q

What’s the risk of transmission of blood bourne viruses in needle stick injuries?

A

Rule of 3:
0.3% HIV
3% Hep C
30% Hep B

75
Q

Which of hepatitises are DNA and which are RNA virus?

A

Hep B- DNA
All rest are RNA

Notifiable disease

76
Q

Which Hep B antibody is negative in chronic infection?

A

Anti-HBs

77
Q

What symptoms are associated with a viral cause of acute hepatitis?

A

Flu-like prodrome 6 weeks before (myalgia, fever, coryzal symptoms)

Incubation time is 6-8 weeks

78
Q

What is dyspepsia?

A 
A non-specific group of symptoms which include:
Bloating
Epigastric pain
Early satiety
Nausea
79
Q

Rx of H Pylori

A

PAC:
PPI
Amoxicillin
Clarythromycin

80
Q

Rx of candidiasis of the throat?

A 
Nystatin suspension (you CAN in NY)
Amphoteracin lozenges

Fluconazole if oropharyngeal thrush

81
Q

Causes of gingivitis (gum inflammation ± hypertrophy):

A

(AM NowFED up of CYCLIn in the PHEN)

Acute Myeloid Leukaemia
Nifedipine, cyclosporin, phenytoin
Penned in by:
Pregnancy, a ship (scurvy)

82
Q

Perioral brown freckles (on lips) indicate what diseases?

The A’s

A

AD Peutz Jeghers- germ line mutations of tumour supressor genes leading to GI polyps (obstruction + cancer risk)

Addison’s brown spots in mouth (increased ACTH)
Antimalarials
Angry melanoma

83
Q

A patient has red pigmented spots on their lip and similar on their tongue, what inherited cause may be responsible?

A

Osler-Weber-Rendu
Hereditary Telangiectasia

The telangiectasia may cause epistaxis and GI bleeds, associated with AV malformations in the cerebral, pulmonary and hepatic circulations

84
Q

What vitamin deficiencies cause glossitis?

A

Vitamin B12, folate (subacute combined degen of the cord, neuropathy)
Iron (angular stomatitis, conjunctival pallor, koilonychia)

85
Q

What is the lymphatic drainage of the tongue?

A

Anterior 1/3- submental
Middle 1/3- submandibular
Posterior 1/3- deep cervical

86
Q

Causes of xerostomia? (Dry tongue)

A

Autoimmune- Crohns, Srögrens,
Anticholinergics- tricyclics
Radiation, dehydration

87
Q

Differential of white intra-oral lesion:

A

Idiopathic keratosis, smoking (leukoplakia)
Infection: candidiasis, syphilis, HIV related oral hairy laukoplakia
Tumour: squamous papilloma, carcinoma
Autoimmune: lupus, lichen planus

88
Q

Differential for odynophagia (pain on swallowing, different from dysphagia):

A

Cancer
Oesophageal ulcer
Candida
Spasm

(Malignant, trauma, infection, mechanical)

89
Q

What might a CXR show you in a patient with dysphagia?

A

Signs of aspiration pneumonia (bulbar palsy may cause difficulty swallowing)
Mediastinal fluid level
No gastric bubble (achalasia)

90
Q

When would barium swallow be first line investigation for dysphagia rather than upper endoscopy ± biopsy?

A

It’s controversial but:
Previous proximal esophageal cancer surgery
Caustic injury or radiotherapy damage (may be tortuous stricture, risky to go in blind with endoscope)

May be done after endoscopy if mechanical obstruction suspected (ie if extrinsic source of compression)

91
Q

Match the following barium swallow findings:

  1. Corkscrew oesophagus
  2. Dilated tapering oesophagus
A
  1. Diffuse oesophageal spasm (abnormal non-peristaltic contractions)
  2. Achalasia
92
Q

IHx for dysphagia:

A

CXR + FBC/U+Es

1st: Upper GI endscopy
Barium swallow

2nd: if suspected motility disorder (ie dysphagia to solids and liquids) then 
Oesophageal manometry (measures pressures at lower oesophageal sphincter)
93
Q

Describe achalasia and it’s symptoms:

A

Failure of lower oesophageal sphincter to relax due to myenteric plexus degeneration

PC: dysphagia, regurgitation, substernal cramps, weight loss

94
Q

Rx of achalasia:

A

Medical: Ca chanel blockers + nitrates
Non-invasive: Botox injections
Invasive: Endoscopic balloon dilatation
or Heller’s cardiomyotomy (cut in the lower oesophageal sphincter)
+ then PPIs

95
Q

Risk factors of oesophageal cancer:

A

PMH:
Dyphasia- Achalasia, Plummer Vincent syndrome (web)
Dypepsia- GORD + Barratt’s
Palmar hyperkeratosis- Tylosis

SHx:
Tabacco, smoking

96
Q

What findings on ABG suggest severe vomiting:

A

Metabolic hypochloraemic alkalosis

Raised bicarbonate- parietal cells produce bicarb as they produce H+

97
Q

Differential of vomiting and features associated with each type:

A

Vomit in AM- raised ICP, pregnancy
Vomit post food- gastroparesis, gastric stasis (DM)
Vomit relieving pain- peptic ulcer
Iatrogenic- post surgery/drugs

98
Q

Causes of dysphasia:

A

Broadly 3 categories: Obstructive, Motility or Functional disorders

Obstructive: intrinsic or extrinsic
Intrinsic malignant- cancer
Intrinsic benign- oesophageal web/ stricture, oesophagitis
Extrinsic- compression by lymph nodes, goitre, lung cancer, L atrial enlargement

Motility:
Focal- Achalasia, diffuse oesophageal spasm, systemic sclerosis
Central- pseudobulbar palsy, Srögren’s, myaesthenia gravis

99
Q

How does the cause of nausea impact your choice of anti-emetic?

A

Vestibular or during pregnancy: antihistamine
Drug induced or post-surgery: 5-HT antagonist (ondesetron)
Partial obstruction: 5-HT antagonist
Due to gastric stasis: DA- antagonist (pro-kinetic)

100
Q

What symptoms define dyspepsia:

A

A vague group of symptoms which include:
Epigastric pain related to hunger or specific foods
± bloating, early satiety, heartburn (retrosternal pain + reflux), tender epigastrium

101
Q

ALARMS symptoms for dyspepsia:

A 
Anorexia
Loss of weight
Anaemia
Recent onset/progressive
Malaena/haematemesis
Swallowing difficulty

Or over 55, not on NSAIDs, lasting >4 weeks

102
Q

How does the management of dyspepsis differ depending on the age of the patient?

A

Over 55 or ALARMS: upper GI endoscopy
Under 55: lifestyle modifications* + test for H Pylori (urea breath test)

*stop NSAIDs, over the counter antacids, review in 1 month

103
Q

How would you procede in a patient under 55 who has dypepsia and has tested negative for H Pylori?

A

No ALARM symptoms- PPI trial for 4 weeks
Then upper GI endoscopy

If ALARM symptoms- Upper GI endoscopy before H Pylori test

104
Q

Drugs putting a patient at risk of duodenal ulcer?

A

NSAIDs
SSRIs- (think antidepressants)
Steroids

105
Q

How long do you need to stop PPI’s for before an endoscopy?

A

2 weeks

106
Q

SEs of PPIs:

A

Lack of gastric acid:
Vit 12 deficiency, gastroenteritis
Alopecia, osteoporosis, LFTs raised

107
Q

Differential of dyspepsia:

A 
Functional
Ulcer- gastric/duodenal
Oesophagitis/GORD
Inflammation- gastritis/duodenitis
Gastric malignancy
108
Q

What aspects of reflux are required to diagnose GORD?

A

2 episodes of heartburn a week

Or complications- oesophagitis, ulcers, strictures, iron-deficiency

109
Q

Symptoms of GORD that indicate it’s occurrence or complications of it:

A

Heartburn, belching, acid regurgitation, odynophagia (suggests ulcer or oesophagitis)

Nocturnal asthma, cough, voice hoarseness
Dysphagia- malignancy

110
Q

What is Barrett’s oesophagus?

A

Distal oesophageal epithelium undergoes metaplasia from squamous to columnar cells, predisposing the patient to oesophageal cancer

111
Q

How do they indications for an endoscopy in a patient with GORD differ from those with dyspepsia?

A

Dyspepsia- ALARMS or over 55
GORD- ALMS still applies (anaemia, loss of weight, malaena/haematemesis, swallow difficulty) or over 55

Also for GORD- persistent vomiting, palpable mass, symptoms despite Rx

112
Q

IHx for a patient with new onset GORD over 55

A

1st: Upper GI endoscopy
2nd: if normal endoscopy, 24hr oesophageal pH or manometry (pressure testing)

113
Q

Rx of GORD

A

Conservative: stop NSAIDs, bisphosphonates, Anti-Ca2+, nitrates
Small meals, avoid hot drinks, alcohol, spice, citrus

Medical: antacids or alginates (foamy barrier), lanzoprazole if oesophagitis

Surgical: Nissen fundoplication, radiofrequency ablation of dysplasia

114
Q

How is severity of GORD stratified:

A

Los Angeles classification:
Between 2 mucosal fold tops
1- mucosal breaks <5mm
2- mucosal break >5mm
Extending beyond 2 mucosal fold tops
3- mucosal break affecting <75% of oesophageal circumference
4- mucosal break affecting >75% of oesophageal circumference

115
Q

Patient is found to have peptic ulcers on endoscopy, for options for further treatment are there?

A

Medical: eradication of H Pylori (PPI, amoxicillin, Clarithromycin
PPIs

Surgical: if intolerant of medical Rx  
Selective vagotomy (avoiding nerve to pylorus enabling gastric emptying)
Gastrectomy (Zollinger Ellison)

Different options if complications arise (pyloric stenosis, haemorrhage)

116
Q

Surgical Rx of peptic ulcer complications

  1. Haemorrhage
  2. Perforation
  3. Pyloric stenosis
A

Haemorrhage:
Endoscopic- adrenaline injections, diathermy, laser coagulation
Surgical- sewing up ulcer

Perforation:
Conservative approach can be tried if not peritonitic (drip + suck, Abx)
Laparoscopic approach preferred

Pyloric stenosis:
(Occurs from scarring with duodenal ulcers)
Endoscopic balloon dilatation, highly selective vagotomy

117
Q

Which type of hiatus hernia in adults warrant prophylactic surgical repair?

A

Diagnosed with barium swallow
Rolling (gastro-oesophageal junction remains below the diaphragm) as risk of strangulation

Sliding can be managed conservatively- weight loss and PPIs

118
Q

Name three causes of steatorrhoea and typical features that distinguish it:

A

Features: floating, offensive smell, hard to flush, gas

  1. Pancreatic exocrine insufficiency (chronic pancreatitis, CF)
  2. Coeliac disease
  3. Giardia (protozoa)
119
Q

What are the 3 main groups of infective diarrhoea in the UK, name some causes within these categories:

A
  1. Bacterial- E Coli, Salmonella, Shigella, Campylobacter
  2. Viral- rotavirus (commonest), norovirus
  3. Protozoal- Amoebic dysentery, giardiasis
120
Q

Which antibiotic causes a diarrhoeal side effect by having a pro-kinetic effect on the gut?

A

Erythromycin

121
Q

Medications causing diarrhoea?

A 
Antibiotics
B block- propranolol
Cytotoxics
Digoxin
Emeprazole + Ebruprofen (NSAIDs)
122
Q

What test can be done to determine whether a patient complaining of non-flushing loose stools does in fact have steatorrhoea?

A

Faecal fat excretion test
C13-hiolein breath test (a specific pancreatic enzyme digests it resulting in radiolabelled CO2 production)

Used to diagnose pancreatic exocrine insufficiency (like chronic pancreatitis) or malabsorption (coeliac disease, giardia)

123
Q

Tests to consider for a patient with acute diarrhoea:

A

Stool sample: MC+S; C Diff toxin; Ova, Cysts + Parasites
Blood: FBC, U+E, CRP, LFTs, TFT, transglutaminase Abs
C13-hiolein breath test: if suspecting pancreatic exocrine insufficiency

Flexible sigmoidoscopy

124
Q

What Rx can be given for diarrhoea.

When should it be avoided?

A

Loperamide
Codiene phosphate

CI: overflow diarrhoea (do a DRE)
obstruction (obvs)
colitis (ie bloody diarrhoea- can precipitate toxic megacolon)

125
Q

What causes diarrhoea, which on endoscopy may cause yellow plaques on inflamed non-ulcerated plaques

A

Clostridium Difficile (G +ve)- pseudomembranous colitis

126
Q

Tests for suspected C Diff pseudomembranous colitis:

A

Stool sample- glutamate dehydrogenase test
Toxin ELISA
PCR for toxin

AXR- thumb printing

127
Q

Rx of pesudomembranous colitis:

A

C Diff- strains may be non-pathogenic (no toxin produced) or pathogenic (type A or B toxin)

  1. Metronidazole PO
  2. Vancomycin PO (if complications, or severe disease)
  3. Stool transplant
  4. Colectomy- if toxic megacolon
128
Q

What should you suspect in a patient with constipation and menorrhagia?

A

Hypothyroidism

129
Q

Which features in patients would make you consider investigation of constipation for?

A

Over 40
HPC: Weight loss, tenesmus
EHx: PR mucus or blood

130
Q

4 types of laxative?

A
  1. Bulk forming- more faecal mass (Bran, Fybogel, Ispagula)
  2. Stimulant (bisacodyl, senna, glycerol, sodium picosulfate)
  3. Stool softeners (arachis oil, paraffin)
  4. Osmotic laxatives (lactulose, macrogel, phosphate enemas)
131
Q

CI for different types of laxative

A

Bulk forming: avoid in obstruction
Stimulant: avoid in obstruction and acute colitis, may drop K+
Stool softeners: paraffin causes fat vitamin malabsorption
Osmotic: good for encephalopathy

132
Q

What is the Rome Criteria, what’s it used for?

A 
For diagnosing constipation (2 of):
In 25% of bowel movements there's
     Straining
     Digital evacuation
     Tenesmus
     Lumpy/hard stools
     Sensation of blockage
Less than 3 poos a week
133
Q

Anorectal causes of constipation:

A

Structural: fissure, stricture, rectal prolapse (rectocele)
Malignant: anal/colorectal cancer
Infection: herpes

134
Q

Name 6 categories that describe the causes of constipation:

A

Lifestyle: poor diet/fluids/exercise, old age, lack of privacy, depression
Anorectal disease: cancer, strictures, fissures, rectal prolapse
Intestinal disease: obstruction from cancer, diverticulosis, strictures, IBS, post-op pain
Metabolic/endocrine: high Ca, low K+, hypothyroidism
Drugs: opiates, iron, diuretics, Ca blockers
Neuromuscular: nerve injury, sclerosis, neuropathy

135
Q

What medication can you give to a patient who waiting for urgent endoscopy following GI bleed?

A

High dose PPI- 80mg Omeprazole

Acidity of the stomach prevents clotting

136
Q

What features are involved in the Glasgow Blatchford score and what are in the Rockall score?

(What’s it used for?)

A

Assessing severity + risk of upper GI bleed
Rockall post-endoscopy = risk of re-bleed

Glasgow Blatchford Score:
urea, Hb, BP, presence of malaena/ syncope/ liver or heart disease

Rockall Pre-endoscopy: age, BP + pulse, comorbidity
Rockall Post-endoscopy: diagnosis, signs of recurrent haemorrhage

137
Q

What features on endoscopy suggest intervention is required in upper GI bleeding?

A 
High risk of rebleeding if there is:
Active bleeding (80%)
A visible vessel (50%)
Adherent clot (30%)
- use an endoclip

*NB: visible findings form part of the Rockall score for predicting risk

138
Q

The veins forming the 5 sites of portal systemic anastomoses:

A
  1. P = oesophageal, S = azygos
  2. P = paraumbilical, S = superficial abdominal wall v’s
  3. P = superior rectal, S = inferior rectal
  4. P = colic veins, S = posterior abdominal wall
  5. P = hepatic veins, S = phrenic v

All systemic veins ultimately drain into the IVC, all portal veins drain into the hepatic portal vein

139
Q

What primary or secondary prophylaxis can be offered to cirrhotic patients to reduce the risk of variceal bleed?

A
  1. Non-selective b blockers (Propranolol)
  2. Repeat endoscopic banding ligation

Secondary
1. + 2. + TIPS (transjugular intra-hepatic porto-systemic shunt
Surgical shunt if TIPS not possible

140
Q

Patient with oesophageal varicies has been resuscitated, what can you use to stem blood loss until transfer to a specialist centre?

A

Sengstaken Blakemore tube

Check position with xray before inflating

141
Q

Management features of a variceal bleed:

A

Crystalloids (avoid saline)
Blood
Consider FFP, platelets, vitamin K
IV Terlipressin (somatostatin)

Endoscopic banding or sclerotherapy
Sengstaken-Blakemore tube > transfer for TIPS

142
Q

Gold standard for diagnosing coeliac disease?

A

Duodenal biopsy using Upper GI Endoscopy

143
Q

How does the bowel prep differ for sigmoidoscopies compared to colonoscopies?

A

Sigmoidoscopy- needs a phosphate enema

Colonoscopy- needs sodium picosulfate BD day before, low residue diet

144
Q

What are the CI’s to colonoscopy:

A

Ischaemic colitis
Diverticulitis (risk of perforation)
MI in last month (big fluid shifts for preparation)

145
Q

Patient has fever, abdominal pain and jaundice.

How do you investigate a suspected cholangiocarcinoma?

A

ERCP + biopsy

Associated with liver flukes (from eating raw fish), PSC, Hep B+C, DM

146
Q

Which parts of the bowel does UC affect?

A

Rectum- proctitis
Left colon- colitis
Whole colon- pancolitis
Bit of the ileum- backwash ileitis

147
Q

Which form of IBD is better if smoking?

A

UC

Think Crohns affects the mouth which will be irritated by cigarette smoke

148
Q

Extra-intestinal signs of UC:

A

Hands: clubbing
Face: episcleritis, uveitis, conjunctivitis, oral ulcers, amyloidosis (big tongue)
Abdo: fatty liver, PSC, cholangiocarcinoma
Back: sacroilitis, ank spond
Legs: large joint arthritis, pyoderma gangrenosum, erythema nodosum

149
Q

What is Truelove + Witts criteria used for?

A

Assessing severity of UC

Features include:
Motions, degree of rectal bleeding
Temp at 6am, HR
Hb, ESR

150
Q

Management of UC:

A

Induce remission:
1. 5-ASA, steroids PR + PO
2. ciclosporin + infliximab
3. surgery- protocolectomy with terminal ileostomy
Colectomy with ileo-anal pouch

Maintenance: 5-ASA (mesalazine, sulfasalazine)

151
Q

Which IBD is granulomatous?

A

Crohns

IHx: colonoscopy + biopsy (microscopic granulomas may be present within normal looking mucosa)

Capsule endoscopy for small bowel, or occasionally barium enema

152
Q

Management of Crohns

A

Induce remission:
Steroids
Biologics- infliximab (anti-TNFa) or adalimumab

153
Q

Diagnostic features for IBS:

A

Pain relieved by defecation
OR
Pain with change in bowel habit or frequency with 2 of:
Urgency, incomplete evacuation, bloating, mucus PR

154
Q

What features in a history would make you be likely to diagnose IBS?

A

Age: over 40
PC: anorexia, weight loss or waking at night to poo
EHx: mouth ulcers
IHx: raised CRP, ESR, Hb

155
Q

Rx options for IBS?

A

Low FODMAP diet

Constipation: stimulant laxatives
Diarrhoea: loperamide
Colic: mebeverine (anticholinergic)
Psych: cognitive behavioural therapy, tricyclics, hypnosis

156
Q

Describe the type and distribution of pancreatic carcinoma?

A

Ductal adenocarcinoma
60% head
25% body
15% tail

KRAS2 gene mutation

157
Q

What is the tumour marker for pancreatic cancer?

A

CA19.9

Non-specific

158
Q

Best imaging for staging and diagnosing suspected pancreatic carcinoma?

A

Endoscopic sonography

Is superior to MRI and CT

159
Q

What is a Whipple’s procedure?

A

Pancreato-duodenectomy
Used for removing masses from the head of the pancreas or rarely a carcinoid tumour.

Small bowel connects the bile duct, stomach and rest of small bowel (= Roux loop)
The tail of the pancreas is attached to the Roux loop

160
Q

What are the conditions caused by a lack of vitamin B1?

A

Thiamine deficiency:
Wet beriberi- high output heart failure
Dry beriberi- peripheral neuropathy
Wernicke’s encephalopathy- 1 confusion 2 ataxia 3 opthalmoplegia
Korsakoff’s- retrograde amnesia, apathy, confabulation

161
Q

3 features of Wernicke’s encephalopy:

A

Confusion, ataxia and opthalmoplegia (lateral gaze palsy, nystagmus etc)

Pabrinex (PRIOR TO GLUCOSE)

162
Q

What results from a deficiency of vitamin B3 (nicotinic acid)?

A 
Pellagra- losing 3 aspects of sociability
Diarrhoea
Dementia
Dermatitis
Depression

Rx: nicotinamide

163
Q

What is the origin of carcinoid tumours?

A

Neural crest cells (enterochromaffin cells) capable of producing 5-HT

164
Q

Symptoms of a carcinoid tumour?

A 
Occurs in liver dysfunction- failing to breakdown the 5-HT
All associated with toilets:
Wheezing
Flushing
Diarrhoea

CCF- alot of fluid

165
Q

IHx for a patient with flushing, wheezing and diarrhoea who has a mass on their appendix, and you suspect a carcinoid tumour?

A

24 hr 5HIAA (5-hydroxyindoleaceatic acid = 5-HT metabolite)

Plasma chromogranin A: reflects tumour mass- precursor to neuroendocrine peptides

Indium octreotide scintigraphy

166
Q

Rx of carcinoid tumours and carcinoid syndrome?

A

Carcinoid syndrome occurs when liver dysfunction means an accumulation of 5-HT
Octreotide-somatostatin analogue blocks release of tumour mediators

Tumours: surgery (tumour is bright yellow)

167
Q

Which HLA are associated with:

  1. Coeliac disease
  2. Ank spond
  3. SLE
A
  1. HLA DQ2/DQ8, in Camden market, Queue 2 8 gluten free
  2. HLA B27, Boys Backs, aged 27
  3. HLA DR2, Dark Rash on 2 cheeks
  4. HLA DR3, (3 Little Pigs + Straw Shack =
    Liver- autoimmune hepatitise, Pancreas- T1DM, Srögrens, SLE)
168
Q

IHx for coeliac disease

A

> 5% probability:

  1. duodenal biopsy, tissue transglutaminase IgA
  2. HLA genotyping (DQ2/DQ8), IgA level ± a-gliadin IgG

<5% probability
1. Tissue transglutaminase IgA ± IgA level

169
Q

What suggests ceoliac disease if found on duodenal biopsy?

A

Subtotal villous atrophy
Crypt hyperplasia
More WBCs in the epithelium

170
Q

Causes of pancreatitis:

A

Alcohol
Familial, cystic fibrosis, haemachromatosis
Pancreatic duct obstruction

171
Q

Why are USS’s preferable to ERCP/MRCP in suspected chronic pancreatitis?

A

Injection of chemical risks acute attack

C13-hiolein breath test can confirm lack of pancreatic exocrine enzymes (broken down to C13- CO2)
Glucose
AXR- calcium

172
Q

Indication for surgery in patients with chronic pancreatitis?

A

Unremitting pain- can put in a stoma to drain duct or remove pancreas

173
Q

Features of the CAGE screening test?

A

Cutting down?
Annoyed by other people suggesting?
Guilty?
Eye opener

2+ = dependency

174
Q

A known alcoholic is in shock and has surgical emphysema felt in the neck, what is the likely diagnosis?

A

Boerhaave’s syndrome- vomiting against a closed glottis leads to oesophageal rupture

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