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Alex's MRCP Cards > Gastro > Flashcards

Gastro Flashcards

1
Q

Brush border enzymes? And enzyme in saliva?

A
  • Maltase: cleaves disaccharide maltose to glucose + glucose
  • Sucrase: cleaves sucrose to fructose and glucose
  • Lactase: cleaves disaccharide lactose to glucose + galactose

Amylase found in saliva and breaks starch down into sugar

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2
Q

GI Hormones?

A
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3
Q

GI Acid - mediators, factors increasing and decreasing?

A

Mediators

  • Gastrin
  • Vagal stimulation
  • HIstamine

Increasing

  • Gastrinoma
  • Small bowel resection
  • Systemic mastocytosis (increased histamine levels)
  • Basophilia

Decreasing

  • Drugs - H2 antagonists, PPIs
  • Hormones - secretin, VIP, GIP, CCK
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4
Q

Where does a pharyngeal pouch arise?

A

Killian’s dehiscence (triangular area in wall of pharynx between thyropharyngeus and cricopharyngeus muscles)

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5
Q

Stereotypical histories for causes of gastroenteritis?

A
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6
Q

Incubation periods of causes of gastroenteritis?

A
  • 1-6 hrs: Staphylococcus aureus, Bacillus cereus
  • 12-48 hrs: Salmonella, Escherichia coli
  • 48-72 hrs: Shigella, Campylobacter
  • > 7 days: Giardiasis, Amoebiasis
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7
Q

Leading causes of C.diff?

A

Previously clindamycin

Now 2nd/3rd gen cephs (Ciprofloxacin)

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8
Q

Exotoxins?

A

Released by gram +ve bacteria

  • Diphtheria - diphtheric membrane on tonsils caused by necrotic mucosal cells –> necrosis of myocardial, nerual and renal tissue
  • S.aureus –> acute gastroenteritis, toxic shock syndrome, staphylococcal scalded skin syndrome
  • Clostridium tetani - lockjay
  • Choleras –> activation adenylate cyclase –> rasied cAMP, increased chloride secretion
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9
Q

Acute management of varices?

A
  • Resuscitation
  • Correct clotting - FFP, vitamin K, beriplex
  • Terlipressin (constriction of splanchnic vessels, contraindicated in IHD –> Octreotide as alternative)
  • Prophylactic abx
  • Endoscopy –> band ligation
  • Sengstaken-blakemore tube (if endoscopy not ready and uncontrolled haemorrhage)
  • Transjugular intrahepatic portosytemic shunt (TIPSS) if above fails
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10
Q

Prophylaxis of variceal haemorrhage?

A
  • Propranolol: Reduced rebleeding and mortality compared to placebo
  • Endoscopic variceal band ligation (EVL) is superior to endoscopic sclerotherapy. Performed at two-weekly intervals until all varices have been eradicated. PPI cover is given to prevent EVL-induced ulceration
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11
Q

Management of Barrett’s oesophagus?

A
  • Endoscopic surveillance with biopsies
  • Low grade dysplasia: high-dose proton pump inhibitor for 8-12 weeks
  • High grade dysplasia: surgery or cryotherapy.
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12
Q

Typical histories of causes of dysphagia?

A
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13
Q

What is achalasia? What is the gold standard test? What is seen on the test?

A

Failure of oesophageal peristalsis

LOS contracted, esophagus above dilated.

Test = oesophageal manometry

  • In achalasia - loss of peristalsis of distal oesophagus, failure of LOS to relax during swallowing (increased residual relaxing pressure)
  • In scleroderma - loss of peristalsis in distal oesophagus but lower resting LOS pressure
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14
Q
A
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15
Q

Management of achalasia?

A
  • Intra-sphincteric injection of botulinum toxin
  • Heller cardiomyotomy
  • Balloon dilation
  • Drug therapy has a role but is limited by side-effects
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16
Q

Boerhaave’s syndrome?

A
  • Full thickness laceration/perforation of oesophagus
  • Left side of lower oesophagus
  • Odynophagia and surgical emphysema in the neck
  • CXR - pneumomediastinum, gas effusion, pneumothorax
  • Oesophagram to confirm leak - water soluble contrast then barium if no leak demonstrated
  • Causes - vomiting (against closed glottis - bulimia), foreful coughing (obstruction by food)
  • Early operation is management
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17
Q

H.pylori associations?

A
  • Peptic ulcer disease (95% of duodenal ulcers, 75% of gastric ulcers)
  • Gastric cancer
  • B cell lymphoma of MALT tissue (eradication of H pylori 80% causes regression)
  • Atrophic gastritis
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18
Q

Sensitivity/Specificity of H.pylori tests?

A
  1. Urea breath test - sensitivity 95-98%, specificity 97-98%
  2. Rapid urease (CLO) test - sensitivity 90-95%, specificity 95-98%
  3. Serum antibody - sensitivity 85%, specificity 80%
  4. Culture gastric biopsy - sensitivity 70%, specificity 100%
  5. Gastric biospy (histology) - sensitivity 95-99%, specificity 95-99%
  6. Stool antigen test - sensitivity 90%, specificity 95%
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19
Q

Peutz-Jegers sydnrome?

A
  • Autosomal dominant
  • Numerous harmatomatous polyps in the GI tract
  • Pigmented freckles on lips, face, palms and soles
  • 50% die by age 60 from GI cancer
  • Histological appearance = arborisation
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20
Q

Most common oesophageal cancer? RIsk factors for both? Most common location?

A
  • Adenocarcinoma is most common
  • Squamous cell carcinoma is the other
  • Middle 1/3 is most common
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21
Q

Gastric cancer associations?

A
  • H. pylori infection (although it is protective against esophageal cancer)
  • Blood group A: gAstric cAncer
  • Gastric adenomatous polyps
  • Pernicious anemia
  • Smoking
  • Diet: salty, spicy, nitrates
  • May be negatively associated with duodenal ulcer
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22
Q

Dukes Staging?

A
  • Duke A (Stage I) - tumour confined to the bowel wall (i.e. mucosa and submucosa).
  • Duke B (Stage II) - invades through the muscle wall.
  • Duke C (Stage III) - involves lymph nodes
  • Stage IV - distant metastases
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23
Q

Prognostic indicators post-complete bowel ca resection?

A
  • Poorly differentiated histological type.
  • Tumour adherence to adjacent organs.
  • Bowel perforation.
  • Colonic obstruction at the time of diagnosis.
  • Venous invasion by the tumour
24
Q

Bowel ca - adjuvant chemo and radio?

A
  • Adjuvant chemotherapy in high risk stage II and all stage III
  • Adjuvant radiotherapy in rectal carcinomas - combined with chemo in stage II/III to reduce risk of local/metastatic relapse
25
Q

Three types of colon cancer?

A
  • Sporadic (95%)
  • Hereditary non-polyposis colorectal carcinoma (HNPCC, 5%)
  • Familial adenomatous polyposis (FAP, <1%)
26
Q

Common mutation in sporadic bowel ca?

A
  • >50% colon cancers show allelic loss of the adenomatous polyposis coli (APC) gene
  • activation of the K-ras oncogene, deletion of p53 and DCC tumour suppressor genes lead to invasive carcinoma
27
Q

HNPCC - what is it? Criteria? Screening?

A
  • Autosomal dominant condition - most common inherited colon cancer
  • 90% develop cancers - poorly differentiated and highly aggressive

Amsterdam Criteria

  • At least 3 family members with colon cancer
  • Span at least two generations
  • At least one case diagnosed before 50 years

Screening

  • Colonoscopy every 2 years from 20 to 40 years age then annually
  • Check mutation in DNA or mismatched repair gene.
28
Q

FAP?

A
  • Rare autosomal dominant condition
  • Leads to formation of hundreds of polyps by age 30-40
  • Inevitably develop cancer
  • Due to mutation in APC (ch 5)
  • Management - total colectomy with ileo-anal pouch formation in 20s
  • FAP families also at risk from duodenal tumours
29
Q

Zollinger-Ellison syndrome?

A

Excessive levels of gastrin, usually from a gastrin secreting tumour usually of the duodenum or pancreas. Leads to multiple gastroduodenal ulcers.

  • Presentation = abdominal pain, diarrhea and malabsorption.
  • Diagnosis = Fasting gastrin levels OR secretin stimulation test (secretin normally suppresses gastrin - in ZE it is not suppressesd as gastrin source is not the stomach)
30
Q

Gastric MALT Lymphoma? VIPoma?

(VIP = vasoactive intestinal peptide - in SI, pancreas; stimulates secretion by pancreas and intenstines; inhibites acid and pepsinogen secretion)

A

Gastric MALT Lymphoma

  • Associated with H.pylori (95%)
  • Good prognosis - if low grade 80% respond to H.pylori eradatication
  • Paraproteinaemia may be present

VIPoma

  • 90% arise from pancreas
    • Large volume diarrhoea, weight loss, dehydration, hypokalaemia, hypochloraemia (gastric acid production low)
31
Q

What is angiodysplasia associated with?

A
  • Aortic stenosis
    • vWF proteolysed in turbulent blood flow around aortic valve. vWF is most active in vascular beds with high shear stress (such as angiodysplasia) - deficiency increases bleeding risk from such lesions
32
Q

Drug causes of pancreatitis?

A

Azathioprine, mesalazine, didanosine, bendroflumethiazide, furosemide, pentamidine, steroids, sodium valproate

33
Q

Features of acute pancreatitis?

A
  • Pain is typically worse 15 to 30 minutes following a meal
  • Steatorrhoea: symptoms of pancreatic insufficiency usually develop between 5 and 25 years after the onset of pain
  • Diabetes mellitus develops in the majority of patients.
34
Q

Pancreatic pseudocyst?

A
  • Complication of acute pancreatitis and are localised collections of pancreatic fluid and debris in the lesser sac
  • Contained within a fragile wall of granulation tissue which eventually forms a fibrous capsule

Cannot be diagnosed until more than 6 weeks after acute attack

  • Abdominal pain/mass
  • Fever
  • Persistently raised lipase/LFTs

Small pseudocysts resolve spontaneously - >6cm (can cause haemorrhage/infection) need endoscopic/percutaneous drainage or surgical management

35
Q

Pancreatic cysts?

A
  • Serous cystadenoma - benign
  • Mucinous cystadenoma - benign but potentially malignant
36
Q

Malabsorption?

A
37
Q

UC vs Crohn’s?

A
38
Q

Management of UC?

A

Inducing Remission

  • Oral/rectal aminosalicylates or steroids

Maintaining Remission

  • Oral aminosalicylates
  • Cancer screening

Acute Flare

  • IV steroids
  • LMWH
  • Elemental diet
  • Monitoring - daily examination, bloods, AXR, stool chart
39
Q

Factors increasing risk of cancer in UC?

A
  • Disease duration > 10 years
  • Patients with pancolitis
  • Onset before 15 years old
  • Unremitting disease
  • Poor compliance to treatment
40
Q

Mangement of Crohn’s?

A

General

  • Stop smoking
  • Some evidence suggests avoid NSAIDs/COCP

Inducing Remission

  1. Steroid/Budesonide - elemental diet can be used if concerned RE steroid side effects
  2. ​5-ASA (Mesalazine) second line
  3. Azathioprine/Methotrexate/Mercaptopurine can be used as add on to steroid (not monotheraphy)
  4. Infliximab in refractory/fistulating disease

Maintaining Remission

  1. Azathioprine/Mercaptopurine
  2. Methotrexate
  3. 5-ASA (Mesalazine) should be considered if previous surgery

Surgery

  • 80% eventually have surgery
41
Q

Whipple’s disease?

A
  • Rare multi-system disorder caused by Tropheryma whippelii infection
  • HLA-B27 association - middle aged men
    • Malabsorption: diarrhea, weight loss
    • Large-joint arthralgia (seronegative arthropathy)
    • Lymphadenopathy
    • Skin: hyperpigmentation and photosensitivity
    • Pleurisy, pericarditis
    • Neurological symptoms (rare): ophthalmoplegia, dementia, seizures, ataxia, myoclonus
42
Q

Whipple’s disease Ix and Mx?

A

Ix

  • Jejunal biopsy shows deposition of macrophages containing Periodic acid-Schiff (PAS)
    granules
  • CRP and ESR
  • Hypoalbuminemia

Mx

  • IV penicillin then oral co-trimoxazole for a year
43
Q

Microscopic colitis triad?

A
  1. Watery diarrhoea
  2. Normal colonoscopy
  3. Increased inflammation of lamina propria of the colon

Associated with NSAIDs, PPIs, Ticlopidine, Cimetidine

Treatment is stopping the offending medication

44
Q

Coeliac HLA associations? Associated conditions?

A
  • HLA-DQ2, HLA-B8, HLA-DR3, HLA-DR7
  • Dermatitis herpetiformis, T1DM, Autoimmune hepatitis
45
Q

Complications of coeliac?

A
  • Anemia: iron, folate and vitamin B12 deficiency (folate deficiency is more common than vitamin B12 deficiency in coeliac disease)
  • Hyposplenism
  • Osteoporosis
  • Lactose intolerance
  • Enteropathy-associated T-cell lymphoma of small intestine
  • Subfertility, unfavourable pregnancy outcomes
  • Rare: esophageal cancer, other malignancies
46
Q

Coeliac investigations?

A

Immunology

  • Tissue transglutaminase (TTG) antibodies (IgA) first line
  • Endomyseal antibody (IgA)

Jejunal Biopsy

  • Reintroduce gluten for at least 6 weeks prior to testing
  • Villous atrophy, crypt hyperplasia, increase in intraepithelial lymphocytes, lamina propria infiltration with lymphocytes
47
Q

Causes of jejunal villous atrophy other than Coeliac?

A
  • Tropical sprue
  • Hypogammaglobulinemia
  • Gastrointestinal lymphoma
  • Whipple’s disease
  • Cow’s milk intolerance
48
Q

What is Tropical Sprue? Diagnosis? Treatment?

A

Most common in Cairbbean/Far East. SI malabsorption, thought to be infectious in origin.

Diagnosis

  • Jejunal biopsy
    • Villous atropgy, villous crypts, mononuclear cellular infiltrates, enlarged epithelial cells, large nuclei secondary to folate and/or B12 deficiency

Treatment

  • Tetracyclines up to 6 months
  • Folate and B12 correction
49
Q

Short bowel syndrome management?

A
  • >100cm jejunum - can have oral intake
  • <100cm then TPN
50
Q

Diagnosis and management of SBP?

A
  • Ascitic tap - neutrophils >250 cells/ul
  • Management = IV cefotaxime
  • Prophylactic abx
    • patients who have had an episode of SBP
    • patients with fluid protein <15 g/l and either Child-Pugh score of at least 9 or hepatorenal syndrome
      • Give ciprofloxacin or norfloxacin
51
Q

Ascities Classification?

A
  • Serum-ascites albumin gradient (SAAG)
    • Classifies ascites into portal hypertensive (<1.1 g/dL) and non-portal hypertensive (>1.1 g/dL)
52
Q

LFTs?

A
  1. Bilirubin
    • Breakdown of heme –> binds albumin and taken up by liver –> conjugated which makes it water soluble –> excreted in urine
    • If mentions no bili in urine then it is unconjugated
  2. Albumin
    • Sensitive marker of hepatic function (not in acute phase, long half life - 20 days)
  3. Transferases (ALT/AST)
    • Rise indicates hepatocellular damage - >1000 suggests drug induced hepatitis, acute viral hepatitis, ischaemic/autoimmune hepatitis
  4. GGT
    • Related to bile ducts. Raised in cholestasis (raised ALP), but if ALP normal suggests induction of hepatic metabolic enzymes (alcohol or enzyme inducing drugs)
  5. ALP
    • Bile ducts and bone
    • Physiologiclaly increased in bone turnover (adolesence) and 3rd trimester (produced by placenta)
53
Q

AST/ALT ratio?

A
  • Chronic Liver disease - ALT > AST
  • Established cirrhosis - AST > ALT

Ratio > 2 suggests alcoholic liver disease, <1.0 suggests non-alcoholic liver disease

54
Q

Causes of hepatomegaly?

A

Common

  • Cirrhosis - in early, later decreases in size. Non-tender, firm.
  • Malignancy - metastatic or primary. Hard, irregular liver edge.
  • RHF - firm, smooth tender liver edge. May be pulsatile.

Other

  • Abscess: pyogenic, amoebic
  • Glandular fever
  • Hematological malignancies
  • Hemochromatosis
  • Hydatid disease
  • Malaria
  • Primary biliary cirrhosis
  • Sarcoidosis, amyloidosis
  • Viral hepatitis
55
Q

Hep B antibody/antigen summary?

A

HBsAg => + Infected

HBeAg => + Infectivity marker high

AntiHBs => + Cured / Vaccinated

AntiHBc =>if IgM + => acute infection if IgG + => chronic infection

In window period everything is negative but AntiHBc (IgM) => +

56
Q
A
57
Q

Mnemonic for drugs causing hepatocellular picture?

A
  • • Statins
  • • Paracetamol
  • • Anti-tuberculosis: isoniazid, rifampicin, pyrazinamide
  • • Nitrofurantoin
  • • Sodium valproate
  • • Halothane
  • • MAOIs/Methyldopa
  • • Alcohol/Amiodarone
  • • Phenytoin

Alex's MRCP Cards (13 decks)

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