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Gastroenterology > Gastroenterology > Flashcards

Gastroenterology Flashcards

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
Q

Signs seen in pancreatitis:

A
  • Cullen’s - periumbilical discolouration
  • Grey-Turner’s - flank discolouration
  • ischaemic Purtscher retinopathy
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26
Q

Factors seen in pancreatitis:

A
  • > 55yo
  • hypocalcaemia
  • hyperglycaemia
  • hypoxia
  • neurtophilia
  • increased LDH and AST
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27
Q

What are some causes of hyperamylasaemia other than pancreatitis?

A
  • pancreatic pseudocyst
  • mesenteric infarct
  • perforated viscus
  • acute cholecystitis
  • DKA
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28
Q

Causes of pancreatitis:

A
  • Gallstones
  • Ethanol
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune + ascaris infection
  • Scorpion venom
  • Hypertriglyceridaemia, hyperchylomicronaemia, hypercalcaemia, hypothermia
  • ERCP
  • Drugs
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29
Q

Complications of pancreatitis:

A
  • 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
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30
Q

Common features of GI ischaemia:

A
  • abdominal pain
  • rectal bleeding
  • diarrhoea
  • fever
  • blood: increased WCC, lactic acidosis
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31
Q

Predisposing factors of GI ischaemia:

A
  • age
  • AF
  • emboli causes: endocarditis, malignancy
  • CVD risk factors: smoking, HTN, diabetes
  • cocaine
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32
Q

Most common place for ischaemic colitis and signs on x-ray:

A
  • watershed area e.g. splenic flexure - territory supplied by superior and inferior mesenteric
  • thumbprinting on x-ray - mucosal oedema/haemorrhage
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33
Q

Causes of AAA:

A
  • standard arterial disease: HTN, diabetes, smokers

- connected tissue disease

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34
Q

What is the protocol for managing AAA:

A

<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
Q

Mallory Weiss tear:

A
  • history of antecedent vomiting
  • painful mucosal lacerations at GO junction
  • small amount of blood
  • common in alcoholics
  • resolves spontaneously
36
Q

Hiatus hernia of gastric cardia:

A
  • longstanding history of dyspepsia
  • overweight
  • no dysphagia or haematemesis
37
Q

Oesophageal rupture investigation:

A

CXR: infiltrate or effusion

38
Q

Peptic stricture:

A
  • longer history dysphagia (not progressive)
  • GORD symptoms
  • no systematic features
39
Q

Dysmotility disorders:

A
  • episodic, non progressive dysphagia

- retrosternal pain

40
Q

Plummer-Vinson syndrome:

A
  • dysphagia (oesophageal web)
  • glossitis
  • iron deficiency anaemia
41
Q

Boerhaave syndrome:

A

severe vomiting leads to rupture

42
Q

Oesophageal adenocarcinoma vs squamous cell:

A

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
Q

Causes of peptic ulcers:

A
  • H Pylori: 95% duodenal ulcers, 75% gastric ulcers
  • drugs: NSAIDs, SSRIs, corticosteroids, bisphosphonates
  • Zollinger Ellison
44
Q

Duodenal vs gastric ulcers:

A
  • duodenal pain relived by eating, more common

- gastric worse after eating

45
Q

What scoring system is used for acute GI bleeding?

A

Blatchford score

46
Q

Resuscitation for acute GI bleeding:

A
  • ABC, wide bore venous access
  • platelet transfusion if needed
  • FFP if decreased fibrinogen , PTT
  • prothrombin complex concentrate if on warfarin and active bleeding
47
Q

Management of Varices:

A
  • ABCDE and correct clotting
  • vasoactive agents: terlipressin, octreotide
  • band ligation
  • sclerotherapy
  • Sengstaken-Blakemore tube
  • TIPSS (connects hepatic to portal vein)
48
Q

Varices prophylaxis:

A
  • propranolol

- endoscopic vatical band ligation

49
Q

H. Pylori, management and investigations:

A
  • 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
Q

C diff

A
  • 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
Q

How do you treat GORD?

A
  • 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
Q

Complications of GORD:

A
  • oesophagitis
  • ulcers
  • anaemia
  • benign strictures
  • Barret’s
  • oesophageal carcinoma
53
Q

Angiodysplasia, diagnosis and management:

A
  • 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
Q

Achalasia, features, investigations and treatment:

A
  • 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
Q

Alcohol Ketotacidosis:

A
  • malnourishment breaks down fat - ketones
  • metabolic acidosis
  • elevated anion gap
  • elevated serum ketone gap
  • normal or low glucose
  • treat with saline and thiamine
56
Q

Diagnosis and management of SBP: (+most common bacteria)

A
  • paracentesis: neutrophil count >250cells/uL
  • most commonly e-coli
  • IV cefotaxime
57
Q

When would you give someone antibiotic prophylaxis for SBP?

A
  • 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
Q

SAAG >11g/L

A

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
Q

SAAG <11g/L

A
  • peritoneal carcinomatosis
  • tuberculous peritonitis
  • pancreatic ascites
  • bowel obstruction
  • biliary ascites
  • postoperative lymphatic leak
  • serositis in CTD
60
Q

Management of ascites:

A
  • 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
Q

Features of refeeding syndrome:

A
  • metabolic abnormalities after starvation
  • catabolism switches abruptly to carb metabolism
  • hypophosphataemia, hypokalaemia, hypomagnasaemia (Torsades), abnormal fluid balance, organ failure
62
Q

Risk factors of refeeding syndrome:

A
  • 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
Q

What is Whipple’ disease and what are the features?

A
  • 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
Q

Investigation and management of Whipple’s disease:

A
  • jejunal biopsy - macrophages containing periodic acid Shiff granules (PAS)
  • oral co-trimoxazole and IV penicillin
65
Q

What is the most common inheritable CRC?

A

HNPCC

66
Q

Symptoms with villous adenoma:

A
  • non-specific lower GI
  • secretory diarrhoea
  • microcytic anaemia
  • hypokalaemia
67
Q

Zollinger Ellison syndrome (features and diagnosis)

A
  • 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
Q

What happens in Barret’s oesophagus, risk factors and management:

A
  • 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
Q

Histology of gastric cancer:

A
  • signet ring cells
  • contain mucin vacuoles which displace nucleus to side
  • increased number = poorer prognosis
70
Q

Associations of gastric cancer:

A
  • H Pylori
  • blood group A
  • gastric adenomatous polyps
  • pernicious anaemia
  • smoking
  • diet: salty, spicy, nitrates
  • negatively associated with duodenal ulcers
71
Q

Tumour types of GO junction:

A
  • 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
Q

Treatment of gastric cancer:

A
  • > 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
Q

Most common location for CRC:

A
  • rectal

- sigmoid

74
Q

Types of CRC:

A
  • 95% sporadic
  • 5% HNPCC
  • <1% FAP
75
Q

FAP

A
  • more than 100 adenomatous polyps in colon and rectum
  • APC gene (over 80% of CRC)
  • autosomal dominant
  • 100% incidence if untreated
76
Q

What is Gardner’s syndrome in FAP:

A
  • osteomas of skull and mandible
  • retinal pigmentation
  • thyroid cancer
  • epidermoid cysts on skin
77
Q

Turcots syndrome:

A
  • polyposis
  • colonic tumours
  • CNS tumours
  • APC, MLH1 and PMS2
78
Q

HNPCC

A
  • 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
Q

What is the Amsterdam criteria?

A
  • must have 3 in 2 successive generations showing HNPCC tumours with 1 >50yo
  • exclude FAP
80
Q

Cowden disease

A
  • multiple hamartomas
  • many mucocutaneous lesions, trichilemmomas, oral papillomas and aural keratosis
  • breast cancer and thyroid disease
  • PTEN
81
Q

MYH associated polyposis

A
  • autosomal recessive, multiple adenomatous polyps in GI tract
  • in colon - KRAS mutations (oncogenes)
82
Q

CRC screening:

A 
Faecal Immunochemical Test
-screening every 2 years men and women 60-70yo
-type of faecal occult blood test
-abnormal results - colonoscopy 
Flexible sigmoidoscopy
83
Q

Referral in CRC:

A

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
Q

Management of SIBO:

A

rifaximin

Gastroenterology (4 decks)

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