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Gastroenterology Flashcards

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1
Q

Describe the pathology of ulcerative colitis:

A
  • red raw mucus that bleeds easily
  • from rectum up to ileocaecal valve, continuous
  • can present with toxic megacolon or lead drain pipe colon
  • loss of haustrations and pseudo polyps on barium enema
  • inflammatory cells infiltrate lamina propria
  • neutrophils migrate to gland walls and create crypt abscesses
  • depletion of goblet cells and mucin from epithelium
  • no inflammation beyond submucosa (unless fulminant disease)
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2
Q

What are the extra-intestinal manifestations for UC and Crohn’s:

A 
related to disease activity:
-episcleritis (more common in Crohn's)
-pauciarticular, asymmetrical arthritis
-osteoporosis
-erythema nodosum
not related to disease activity:
-uveitis (more common UC)
-primary sclerosis cholangitis (more common UC)
-polyarticular, symmetrical arthritis
-clubbing
-pyoderma gangrenosum
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3
Q

What classifies are mild, moderate and severe UC flares?

A
  • mild: <4 stools/day, no systemic disturbance
  • moderate: 4-6 stools/day, minimal systemic disturbance
  • severe: >6 stools/day, systemic disturbance
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4
Q

How do you treat mild-moderate flare ups and severe flare ups of UC?

A

mild-moderate:

  • proctitis: topical ASA
  • procto-sigmoiditis: topical ASA or oral ASA or oral ASA with topical corticosteroid or oral ASA with oral corticosteroid
  • extensive disease: hospital, IV ciclosporin, IV corticosteroids
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5
Q

Maintaining remission following mild to moderate UC flare-up and following severe lapse or >=2 exacerbations/year:

A

mild to moderate:
-proctitis and proctosigmoiditis: topical ASA or oral ASA with rectal ASA or oral ASA
-left sided and extensive: low maintenance dose oral ASA
after severe lapse:
-oral azathioprine
-oral mercaptopurine

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6
Q

Explain the pathology of Crohn’s including histology and what is seen on a small bowel enema:

A
  • anywhere from mouth to anus
  • inflammation to serosa - prone to strictures, fistulas, adhesions
  • deep ulcers and skip lesions
  • goblet cells and granulomas
  • Kantor’s string sign
  • proximal bowel dilation
  • rose-thorn ulcers
  • fistulae
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7
Q

Inducing remission in Crohn’s:

A
  • glucocorticoids for 5 days followed by infliximab
  • azathioprine or mercaptopurine as add ons with TMPT check
  • metronidazole for peri-anal disease
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8
Q

Maintaining remission in Crohn’s:

A
  • azathioprine or mercaptopurine

- methotrexate

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9
Q

What is coeliac disease and what are the typical signs and symptoms:

A
  • autoimune sensitivity to gluten
  • villous atrophy leads to malabsorpiton
  • HLA DQ8 and DQ2
  • diarrhoea
  • failure to thrive
  • persistent GI symptoms
  • fatigue
  • weight loss
  • anaemia
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10
Q

What are the conditions associated with Coeliac?

A
  • autoimmune thyroid
  • dermatitis herpetiformis
  • IBS
  • type I diabetes
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11
Q

What are the complications of Coeliac?

A
  • anaemia
  • hyposplenism
  • osteoporosis
  • lactose intolerance
  • enteropathy associated T cell lymphoma of small intestine
  • subfertility
  • rarely oesophageal cancer
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12
Q

How do you investigate Coeliac?

A
  • re-introduce gluten 6 weeks before testing
  • tissue transglutaminase antibodies
  • endomyseal IgA antibodies
  • anti-casein
  • duodenal biospy: villous atrophy, crypt hyperplasia, increased intraepithelial lymphocytes, lamina propria infiltration with lymphocytes
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13
Q

What is peutz-jeghers and what does it cause?

A
  • autosomal dominant
  • LKB1, STK11
  • polyps not malignant but manny die from GI cancer
  • GI bleeding
  • obstruction e.g. intussusception
  • hamarmatous polyps
  • pigmented lesion on lips, palms, soles and face
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14
Q

What is a pharyngeal pouch and how does it present?

A
  • posteromedial diverticulum through Kilian’s dehiscence
  • more common in males and elderly
  • causes halitosis, neck swelling which gurgles, dysphagia, regurgitation, aspiration
  • manage surgically
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15
Q

What is the main risk factor for oesophageal candidiasis?

A

steroid inhaler use

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16
Q

How does systemic sclerosis present?

A 
dysphagia
CREST
-calcinosis
-Raynaud's
-oeophageal dysmotility
-sclerodactlyly
-telangiectasia 
LES pressure is decreased instead of increase (e.g. in achalasia)
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17
Q

How does myasthenia gravis present?

A
  • dysphagia with liquids and solids

- intraocular muscle weakness, ptosis

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18
Q

How does globus hystericus present?

A
  • may have history of anxiety
  • symptoms intermittent and relieved by swallowing
  • usually painless
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19
Q

What is carcinoid syndrome and how does it present?

A
  • metastases in liver release serotonin
  • may also be with lung
  • causes flushing, diarrhoea, bronchospasm, hypotension, right heart valve stenosis
  • other mol e.g. ECTH and GnRH
  • pellagra rare as dietary tryptophan diverted to serotonin by tumour
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20
Q

Presentation of gallstones/cholelithiasis:

A
  • colicky RUQ pain postprandially
  • worse after fatty meal - increased CCK contracts bladder
  • abnormal LFTs
  • n&v
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21
Q

How can you distinguish biliary colic, acute cholecystitis, gallbladder abscess and cholangitis?

A
  • biliary colic: colicky abdominal pain, no jaundice or fever
  • acute cholecystitis: Murphy’s sign, sometimes deranged LFTs, vomiting, no jaundice
  • gallbladder abscess: swinging pyrexia
  • cholangitis: bile duct inflammation secondary to stones, Charcot’s triad, jaundice, severely septic and unwell
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22
Q

What size gallstones can be safely left?

A

<5mm

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23
Q

Where is diverticulosis most common?

A

sigmoid colon

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24
Q

Presentation of diverticulitis:

A
  • change in bowel habit
  • intermittent LLQ abdo pain
  • n&v, bloating
  • urinary frequency, urgency, dysuria,
  • PR bleeding
  • pneumaturia, faecaluria (fistula)
  • low grade pyrexia
  • reduced bowel sounds
  • guarding, rigidity - perforation
  • lack of improvement with Tx - abscess
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25
Signs seen in pancreatitis:
- Cullen's - periumbilical discolouration - Grey-Turner's - flank discolouration - ischaemic Purtscher retinopathy
26
Factors seen in pancreatitis:
- >55yo - hypocalcaemia - hyperglycaemia - hypoxia - neurtophilia - increased LDH and AST
27
What are some causes of hyperamylasaemia other than pancreatitis?
- pancreatic pseudocyst - mesenteric infarct - perforated viscus - acute cholecystitis - DKA
28
Causes of pancreatitis:
- Gallstones - Ethanol - Trauma - Steroids - Mumps - Autoimmune + ascaris infection - Scorpion venom - Hypertriglyceridaemia, hyperchylomicronaemia, hypercalcaemia, hypothermia - ERCP - Drugs
29
Complications of pancreatitis:
- peripancreatic fluid collections which may resolve or develop into pseudocysts or abscesses - pseudocysts - 4 or more weeks after - pancreatic necrosis - pancreatic abscess - infected psuedocyst - haemorrhage - ARDS
30
Common features of GI ischaemia:
- abdominal pain - rectal bleeding - diarrhoea - fever - blood: increased WCC, lactic acidosis
31
Predisposing factors of GI ischaemia:
- age - AF - emboli causes: endocarditis, malignancy - CVD risk factors: smoking, HTN, diabetes - cocaine
32
Most common place for ischaemic colitis and signs on x-ray:
- watershed area e.g. splenic flexure - territory supplied by superior and inferior mesenteric - thumbprinting on x-ray - mucosal oedema/haemorrhage
33
Causes of AAA:
- standard arterial disease: HTN, diabetes, smokers | - connected tissue disease
34
What is the protocol for managing AAA:
<3cm - no further action 3-4.4cm - small, rescan every year 4.5-5.4cm - medium, rescan every 3 months >=5.5cm - large, refer within 2 weeks for vascular surgery
35
Mallory Weiss tear:
- history of antecedent vomiting - painful mucosal lacerations at GO junction - small amount of blood - common in alcoholics - resolves spontaneously
36
Hiatus hernia of gastric cardia:
- longstanding history of dyspepsia - overweight - no dysphagia or haematemesis
37
Oesophageal rupture investigation:
CXR: infiltrate or effusion
38
Peptic stricture:
- longer history dysphagia (not progressive) - GORD symptoms - no systematic features
39
Dysmotility disorders:
- episodic, non progressive dysphagia | - retrosternal pain
40
Plummer-Vinson syndrome:
- dysphagia (oesophageal web) - glossitis - iron deficiency anaemia
41
Boerhaave syndrome:
severe vomiting leads to rupture
42
Oesophageal adenocarcinoma vs squamous cell:
Adenocarcinoma: -lower third near junction -GORD, Barrett's, smoking, achalasia, obesity Squamous cell: -upper two thirds -smoking, alcohol, achalasia, Plummer Vinson, diet rich in nitrosamines
43
Causes of peptic ulcers:
- H Pylori: 95% duodenal ulcers, 75% gastric ulcers - drugs: NSAIDs, SSRIs, corticosteroids, bisphosphonates - Zollinger Ellison
44
Duodenal vs gastric ulcers:
- duodenal pain relived by eating, more common | - gastric worse after eating
45
What scoring system is used for acute GI bleeding?
Blatchford score
46
Resuscitation for acute GI bleeding:
- ABC, wide bore venous access - platelet transfusion if needed - FFP if decreased fibrinogen , PTT - prothrombin complex concentrate if on warfarin and active bleeding
47
Management of Varices:
- ABCDE and correct clotting - vasoactive agents: terlipressin, octreotide - band ligation - sclerotherapy - Sengstaken-Blakemore tube - TIPSS (connects hepatic to portal vein)
48
Varices prophylaxis:
- propranolol | - endoscopic vatical band ligation
49
H. Pylori, management and investigations:
- gram negative - associated with peptic ulcers, gastric cancer, B cell lymphoma of MALT tissue, atrophic gastritis - no association with GORD - PPI + amoxicillin + clarithromycin - PPI + metronidazole + clarithromycin - urea breath test (good post eradication) - serum antibody (positive after eradication) - gastric biopsy - stool antigen - rapid urease
50
C diff
- gram positive rod - pseudomembranous colitis - loss of bowel architecture and thumb-printing - caused by clindamycin, ceftriaxone, cefaclor, PPI - diagnosis by CDT in stool, antigen shows exposure not current infection - can develop severe toxic megacolon - first line metronidazole 10-14 days - oral vancomycin - fidaxomicin - life threatening: oral vancomycin and IV metronidazole - also bezlotoxumab - stop opioid medications
51
How do you treat GORD?
- endoscopically proven: full dose PPI 1-2mo, no response double dose 1 mo - not proven: full dose PPI 1 mo, no response H2RA or pro kinetic 1 mo
52
Complications of GORD:
- oesophagitis - ulcers - anaemia - benign strictures - Barret's - oesophageal carcinoma
53
Angiodysplasia, diagnosis and management:
- vascular deformity of GI tract predisposing to iron def anaemia and bleeding - assoc with aortic stenosis - diagnose with colonoscopy and mesenteric angiography if acute bleeding - use endoscopic cautery or argon plasma coat - antifibrinolytics e.g. tranexamic acid
54
Achalasia, features, investigations and treatment:
- degenerative loss of ganglia from Averbach's plexus - contracted sphincter and dilated oesophagus - dysphagia of both liquid and solids, regurgitation of food, heartburn - oesphageal manometry, bird's beak on barium swallow, (tertiary contractions give rise to corkscrew appearance), wide mediastinum on CXR - treat with intra-sphincteric injection of botulinum toxin - Heller cardiomyotomy - pneumatic balloon dilation
55
Alcohol Ketotacidosis:
- malnourishment breaks down fat - ketones - metabolic acidosis - elevated anion gap - elevated serum ketone gap - normal or low glucose - treat with saline and thiamine
56
Diagnosis and management of SBP: (+most common bacteria)
- paracentesis: neutrophil count >250cells/uL - most commonly e-coli - IV cefotaxime
57
When would you give someone antibiotic prophylaxis for SBP?
- previous episode - fluid protein <15g/L and either Child Pugh score of 9 or hepatorenal syndrome - oral ciprofloxacin or norfloxacin if cirrhosis and ascites
58
SAAG >11g/L
indicates portal hypertension -cirrhosis, alcoholic hepatitis, cardiac ascites, mixed ascites, massive liver metastases, fulminant hepatic failure, Budd-Chiari, portal vein thrombosis, veno-occlusive disease, myxoedema, fatty liver of pregnancy
59
SAAG <11g/L
- peritoneal carcinomatosis - tuberculous peritonitis - pancreatic ascites - bowel obstruction - biliary ascites - postoperative lymphatic leak - serositis in CTD
60
Management of ascites:
- reduce dietary sodium - fluid restriction if sodium <125mmol/L - aldosterone antagonist e.g. spironolactone - drainage if tense ascites (albumin cover to reduce paracentesis induced circulatory dysfunction) - prophylactic Abx to reduce risk SBP (ciprofloxacin or norfloxacin) - TIPS
61
Features of refeeding syndrome:
- metabolic abnormalities after starvation - catabolism switches abruptly to carb metabolism - hypophosphataemia, hypokalaemia, hypomagnasaemia (Torsades), abnormal fluid balance, organ failure
62
Risk factors of refeeding syndrome:
- BMI <16kg/m2 - unintentional weight loss >15% in 3-6 months - little nutritional intake >10 days - reduced ions prior to feeding - history of alcohol abuse, drug therapy, chemo, diuretics, antacids
63
What is Whipple' disease and what are the features?
- multi system disorder by infection of Tropheryma Whippelii - more common in HLA B27 and middle aged men - malabsorption: diarrhoea and weight loss - large joint arthralgia - lymphadenopathy - hyperpigmentation and photosensitivity - pleurisy and pericarditis - neuro symptoms
64
Investigation and management of Whipple's disease:
- jejunal biopsy - macrophages containing periodic acid Shiff granules (PAS) - oral co-trimoxazole and IV penicillin
65
What is the most common inheritable CRC?
HNPCC
66
Symptoms with villous adenoma:
- non-specific lower GI - secretory diarrhoea - microcytic anaemia - hypokalaemia
67
Zollinger Ellison syndrome (features and diagnosis)
- excessive gastrin, usually duodenum or pancreas - 30% as part of MEN I - multiple gastroduodenal ulcers, diarrhoea, malabsorption - diagnose with fasting gastrin level, secretin simulation test
68
What happens in Barret's oesophagus, risk factors and management:
- metaplasia of lower oesophageal mucosa - squamous becomes columnar - increased risk of adenocarcinoma - short: <3cm - RF: GORD, male, smoking, central obesity - Manage: endoscopic surveillance biopsy every 3-5 years, high dose PPI, endoscopic mucosal resection, radio frequency ablation
69
Histology of gastric cancer:
- signet ring cells - contain mucin vacuoles which displace nucleus to side - increased number = poorer prognosis
70
Associations of gastric cancer:
- H Pylori - blood group A - gastric adenomatous polyps - pernicious anaemia - smoking - diet: salty, spicy, nitrates - negatively associated with duodenal ulcers
71
Tumour types of GO junction:
- Type I: true oesophageal cancers associated with Barrett's - Type II: carcinoma of cardia, arising from cardiac type epithelium or short segments intestinal metaplasia at OG junction - Type III: sub cardial, spread across junction
72
Treatment of gastric cancer:
- >5-10cm from OG junction - sub-total gastrectomy - total if <5cm - type II - oesophagogastrectomy - confined to muscosa (early) - endoscopic sub-mucosal resection - lymphadenectomy - chemotherapy
73
Most common location for CRC:
- rectal | - sigmoid
74
Types of CRC:
- 95% sporadic - 5% HNPCC - <1% FAP
75
FAP
- more than 100 adenomatous polyps in colon and rectum - APC gene (over 80% of CRC) - autosomal dominant - 100% incidence if untreated
76
What is Gardner's syndrome in FAP:
- osteomas of skull and mandible - retinal pigmentation - thyroid cancer - epidermoid cysts on skin
77
Turcots syndrome:
- polyposis - colonic tumours - CNS tumours - APC, MLH1 and PMS2
78
HNPCC
- most common inheritable (Lynch syndrome) - CRC without extensive polyposis - more right sided, histologically more mutinous and dense lymphocytic infiltrates - associated with endometrial cancer, pancreatic, renal and CNS - MSH2, MLH1 and PMS2 - Amsterdam criteria
79
What is the Amsterdam criteria?
- must have 3 in 2 successive generations showing HNPCC tumours with 1 >50yo - exclude FAP
80
Cowden disease
- multiple hamartomas - many mucocutaneous lesions, trichilemmomas, oral papillomas and aural keratosis - breast cancer and thyroid disease - PTEN
81
MYH associated polyposis
- autosomal recessive, multiple adenomatous polyps in GI tract - in colon - KRAS mutations (oncogenes)
82
CRC screening:
``` Faecal Immunochemical Test -screening every 2 years men and women 60-70yo -type of faecal occult blood test -abnormal results - colonoscopy Flexible sigmoidoscopy ```
83
Referral in CRC:
Urgent (within 2 weeks) ->=40yo with unexplained weight loss AND abdominal pain ->=50 yo with unexplained rectal bleeding ->=60 yo with iron deficiency anaemia or change in bowel habit -occult blood in faeces Consider -rectal/abdominal mass -unexplained anal mass or ulceration -<50yo with rectal bleeding and pain, change in weight or anaemia
84
Management of SIBO:
rifaximin

Gastroenterology (4 decks)

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