g a s t r o Flashcards

1
Q

what are the key sx seen in patients with gastro/hepatology disease

A
abdominal pain
jaundice
haematemesis 
malaena
diarrhoea
nausea and vomiting
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2
Q

what are differentials for abdominal pain

A

https://litfl.com/abdominal-pain-ddx/

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3
Q

what are differentials for haematemesis

A

VINTAGE

  1. Varices
  2. Inflammation
     Oesophago-gastro-duodenitis  PUD: DU is commonest cause
  3. Neoplasia
     Oesophageal or gastric Ca
  4. Trauma
     Mallory-Weiss Tear = Mucosal tear due to vomiting
     Boerhaave’s Syndrome  Full-thickness tear, 2cm proximal to LOS
  5. Angiodyspepsia and vascular abnormalities
     Angiodysplasia
     HHT
     Dieulafoy lesion: rupture of large arteriole in stomach or
    other bowel
  6. Generalised bleeding diathesis
     Warfarin, thrombolytics  CRF
  7. Epistaxis
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4
Q

what are the differentials for dysphagia

A
1. Inflammatory
 Tonsillitis, pharyngitis
 Oesophagitis: GORD, candida
 Oral candidiasis
 Aphthous ulcers
2. Mechanical Block 
Luminal
 FB
 Large food bolus 
Mural
 Benign stricture
 Web (e.g. Plummer-Vinson)
 Oesophagitis
 Trauma (e.g. OGD)
 Malignant stricture
 Pharynx, oesophagus, gastric
 Pharyngeal pouch 
 Extra-mural
 Lung Ca
 Rolling hiatus hernia
 Mediastinal LNs (e.g. lymphoma) 
 Retrosternal goitre
 Thoracic aortic aneurysm
3. Motility Disorders
  Local
 Achalasia
 Diffuse oesophageal spasm
 Nutcracker oesophagus
 Bulbar / pseudobulbar palsy (CVA, MND)
4. Systemic
 Systemic sclerosis / CREST  MG
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5
Q

what are the differentials for diarrhoea

A
  1. Acute
    Suspect gastroenteritis Travel, diet, contacts?
  2. Chronic
     Diarrhoea alternating ̄c constipation: IBS
     Anorexia, ↓wt., nocturnal diarrhoea: organic cause
  3. Bloody
     Vascular: ischaemic colitis
     Infective: campylobacter, shigella, salmonella, E. coli,
    amoeba, pseudomembranous colitis
     Inflammatory: UC, Crohn’s
     Neoplastic: CRC, polyps
  4. Mucus
     IBS, CRC, polyps
  5. Pus
     IBD, diverticulitis, abscess
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6
Q

what are the ddx for jaundice

A

pre hepatic = excess BRR production = haemolytic anaemia, ineffective erythropoiesis (thalassaemia)

hepatic unconjugated = reduced BR uptake: drugs - contrast, RMP, CCF

hepatic unconjugated = reduced BR conjugation: hypothyroidism, Gilbert’s, Crigler-Najjar

hepatic uncojugated = neonatal jaundice = both increase production and reduced conjugation

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7
Q

what are the features to ask about in history of suspected upper GI bleed

A
Previous bleeds
 Dyspepsia, known ulcers
 Liver disease or oesophageal varices
 Dysphagia, wt. loss
Drugs and EtOH
 Co-morbidities
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8
Q

what are signs to look out for O/E in upper GI bleed

A
signs of CLD
PR:melaena
Shock?
 Cool, clammy, CRT>2s
 ↓BP (<100) or postural hypotension (>20 drop)  ↓ urine output (<30ml/h)
 Tachycardia
 ↓GCS
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9
Q

what are the common causes of upper GI bleeding

A
PUD: 40% (DU commonly)
 Acute erosions / gastritis:20%
Mallory-Weiss tear: 10%
 Varices: 5%
Oesophagitis: 5%
Ca Stomach / oesophagus:<3%
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10
Q

what score is used to determine severity of bleed/ mortality

A

Rockall score
can be done pre and post endoscopy

Initial score pre-endoscopy

 Age
 Shock: BP, pulse
 Comorbidities

Final score post-endoscopy
Final Dx + evidence of recent haemorrhage:

 Active bleeding
 Visible vessel
 Adherent clot

Initial score ≥3 or final >6 are indications for surgery

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11
Q

what are oesophageal varices and what is the pathophysiology. which veins are affected

A

Portal HTN → dilated veins sites of porto-systemic anastomosis: L. gastric and inferior oesophageal veins

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12
Q

what are the causes of portal HTN

A

Pre-hepatic: portal vein thrombosis

Hepatic: cirrhosis (80% in UK), schisto (commonest
worldwide), sarcoidosis.

Post-hepatic: Budd-Chiari, RHF, constrict pericarditi

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13
Q

what is the first line and second line bleed prevention for oesophageal varices

A

1O: β-B, repeat endoscopic banding

2O: β-B, repeat banding, TIPSS

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14
Q

how does TIPPS work

A

interventional radiology creates articifical channel between hepatic vein and portal vein = reduce portal pressure

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15
Q

describe the acute management of upper GI bleed

A

 100% O2, protect airway
 2 x 14G cannulae + IV crystalloid infusion up to 1L.
 Bloods: FBC, U+E (↑ urea), LFTs, clotting, x-match
6u, ABG, glucose
Blood if remains shocked
 Group specific or O- until X-matched
Variceal Bleed
 Terlipressin IV (splanchnic vasopressor)
 Prophylactic Abx: e.g. ciprofloxacin 1g/24h
Maintenance
 Crystalloid IVI, transfuse if necessary (keep Hb≥10)
 Catheter + consider CVP (aim for >5cm H2O)
 Correct coagulopathy: vit K, FFP , platelets
 Thiamine if EtOH
 Notify surgeons of severe bleeds
Urgent Endoscopy Haemostasis of vessel or ulcer:
 Adrenaline injection
 Thermal / laser coagulation
 Fibrin glue
 Endoclips
Variceal bleeding:
 2 of: banding, sclerotherapy, adrenaline,
coagulation
 Balloon tamponade ̄c Sengstaken-Blakemore tube
 Only used if exsanguinating haemorrhage or failure of endoscopic therapy
 TIPSS if bleeding can’t be stopped endoscopically
After endoscopy
 Omeprazole IV + continuation PO (↓s re-bleeding)
 Keep NBM for 24h → clear fluids → light diet @ 48h
 Daily bloods: FBC, U+E, LFT, clotting
 H. pylori testing and eradication
 Stop NSAIDs, steroids et.c.
Indications for Surgery
 Re-bleeding
 Bleeding despite transfusing 6u
 Uncontrollable bleeding at endoscopy
 Initial Rockall score ≥3, or final >6.
Open stomach, find bleeder and underrun vessel.

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16
Q

describe the macroscopic similarities and differences between UC and Crohn’s

A

UC = rectum and colon + backwash ileus. continuous distribution, no strictures.

Crohn’s = mouth to anus esp terminal ileum. skip lesions. strictures.

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17
Q

describe the microscopic similarities and differences between UC and Crohn’s

A

UC = mucosal, crypt abscesses, shallow borad ulceration, pseudopolyps, drainpipe colon due to loss of haustral markings, string sign of Kantour - narrowing of lumen

Crohn’s = transmural, cobblestone mucosa, fibrosis, non caseous granuloma, fistulae, rose thorn ulcers

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18
Q

describe the aetiology of UC and Crohn’s

A
UC = smoking protective, TH-2 mediated 
`Crohn's = smoking increases risk, TH1/TH17 mediated
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19
Q

describe the presentation, sx in IBD and differences in UC vs Crohn’s

A

systemic = fever, malaise, anorexia, wt loss in active disease

abdominal = diarrhoea (bloody in UC), abdominal discomfort, tenesmus, faecal urgency

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20
Q

what are the clinical signs seen in IBD

A

tender, distended abdomen
aphthous ulcers, glossitis
abdominal tenderness

Crohn’s;

RIF mass
perianal abscess, fistulae
tags
anal/ rectal strictures

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21
Q

what are extra abdominal manifestations of IBD

A
1. Joints
Arthritis (non-deforming, asymm) Sacroiliitis
Ank spond
2. HB
PSC + cholangiocarcinoma (esp. UC) Gallstones (esp. Crohn’s)
Fatty liver
3. Other
Amyloidosis
Oxalate renal stones (esp. Crohns)
4. Skin
Clubbing
Erythema nodosum
Pyoderma gang (esp. UC)
5. Eyes
Iritis
 Episcleritis
Conjunctivitis
22
Q

what are the complications seen in IBD

A
  1. toxic megacolon = diameter greater than 6cm, risk of perforation
  2. malignancy = CRC, cholangiocarcinoma
  3. strictures = obstruction
  4. venous thrombosis

Crohns

  1. fistulae
  2. strictures = obstruction
  3. abscesses = abdominal, anorectal
  4. malabsorption = fat = gallstones, steatorrhoea, b12 megaloblastic anaemia, vit d osteomalacia, protein oedema
23
Q

what investigations are required in ulcerative IBD

A

Bloods:
 FBC: ↓Hb, ↑WCC  LFT: ↓albumin
 ↑CRP/ESR
 Blood cultures
Stool
 MCS: exclude Campy, Shigella, Salmonella…  CDT: C. diff may complicate or mimic
Imaging
 AXR: megacolon (>6cm), wall thickening  CXR: perforation
 CT
 Ba / gastrograffin enema
 Lead-pipe: no haustra
 Thumbprinting: mucosal thickening
 Pseudopolyps: regenerating mucosal island
Ileocolonoscopy + regional biopsy: Baron Score

24
Q

how is the severity of UC determined

A

Truelove and Witts criteria

motions, PR bleed, temp, HR, Hb, ESR

mild, moderate and severe

25
Q

How is acute severe UC managed

A
Resus: Admit, IV hydration, NBM
 Hydrocortisone: IV 100mg QDS + PR
 Transfuse if required
 Thromboprophylaxis: LMWH
 Monitoring
 Bloods: FBC, ESR, CRP, U+E  Vitals + stool chart
 Twice daily examination
 ± AXR
26
Q

describe the acute complications of severe UC

A
  1. Perforation
     Bleeding
     Toxic megacolon (>6cm)
     VTE
27
Q

in severe acute UC if no improvement vs improvement

A

Improvement → oral therapy
 Switch to oral pred + a 5-ASA
 Taper pred after full remission

No Improvement → rescue therapy
 On day 3: stool freq >8 or CRP >45
 Predicts 85% chance of needing a colectomy during
the admission
 Discussion between pt, physician and surgeon
 Medical: ciclosporin, infliximab or visilizumab (anti-T cell)
 Surgical

28
Q

what drugs are used to induce UC remission

A

Oral Therapy
 1st line: 5-ASAs
 2nd line: prednisolone

Topical Therapy: mainly left-sided disease
 Proctitis: suppositories
 More proximal disease: enemas or foams
 5-ASAs ± steroids (prednisolone or budesonide)

29
Q

what drugs are used to maintain remission in UC

A

1st line: 5-ASAs PO – sulfasalazine or mesalazine
 Topical Rx may be used in proctitis

 2nd line: Azathioprine or 6-mercaptopurine
 Relapsed on ASA or are steroid-dependent
 Use 6-mercaptopurine if azathioprine intolerant

 3rd line: Infliximab / adalimumab

30
Q

what are the indications for surgery in UC

A

Toxic megacolon
 Perforation
 Massive haemorrhage
 Failure to respond to medical Rx

31
Q

what investigations are required for IBD Crohn’s, what results are expected

A

Bloods: (top 3 are severity markers)  FBC: ↓Hb, ↑WCC
 LFT: ↓albumin
 ↑CRP/ESR
 Haematinics: Fe, B12, Folate
 Blood cultures Stool
 MCS: exclude Campy, Shigella, Salmonella…
 CDT: C. diff may complicate or mimic Imaging
 AXR: obstruction, sacroileitis  CXR: perforation
 MRI
 Assess pelvic disease and fistula
 Assess disease severity
 Small bowel follow-through or enteroclysis
 Skip lesions
 Rose-thorn ulcers
 Cobblestoning: ulceration + mural oedema
 String sign of Kantor: narrow terminal ileum
Endoscopy
 Ileocolonoscopy + regional biopsy: Ix of choice  Wireless capsule endoscopy
 Small bowel enteroscopy

32
Q

how is severity of Crohn’s determined

A

temp, albumin reduces, ESR, CRP, WCC, HR increases

33
Q

describe how acute severe Crohn’s is managed

A
Resus: Admit, NBM, IV hydration
 Hydrocortisone: IV + PR if rectal disease
 Abx: metronidazole PO or IV
 Thromboprophylaxis: LMWH
 Dietician Review
Elemental diet
 Liquid prep of amino acids, glucose and fatty
acids
 Consider parenteral nutrition
 Monitoring
 Vitals + stool chart
 Daily examination
34
Q

what action is taken when no improvement or improvement in acute sever crohn’s

A
Improvement → oral therapy
 Switch to oral pred (40mg/d)
No Improvement → rescue therapy
 Discussion between pt, physician and surgeon
 Medical: methotrexate ± infliximab
 Surgical
35
Q

what drugs are used to induce remission in Crohn’s

A
Supportive
 High fibre diet
 Vitamin supplements
Oral Therapy
 1st line
 Ileocaecal: budesonide
 Colitis: sulfasalazine
 2nd line: prednisolone (tapering)
 3rd line: methotrexate
 4th line: infliximab or adalimumab
36
Q

what investigations and management is given in Crohns peri anal disease

A

MRI + EUA Rx
 Oral Abx: metronidazole
 Immunosuppression ± infliximab  Local surgery ± seton insertion

37
Q

what drugs are used to maintain remission in Crohn’s

A

1st line: azathioprine or mercaptopurine  2nd line: methotrexate
 3rd line: Infliximab / adalimumab

38
Q

before using azathioprine what levels should be checked

A

+TPMT activity should be assessed before starting

39
Q

what are the indications for surgery in crohns

A

Emergency
 Failure to respond to medical Rx
 Intestinal obstruction or perforation  Massive haemorrhage
 Elective
 Abscess or fistula
 Perianal disease  Chronic ill health  Carcinoma

40
Q

what is the pathophysiology behind coeliac disease

A

HLA-DQ2 (95%) and DQ8

CD8+ mediated response to gliadin in gluten

41
Q

how does coeliac present

A

GLIAD

gi malabsoption = carbs, fat, protein, vitamins

lymphoma and carcinoma = enteropathy associated T cell lymphoma, adenocarcinoma of small bowel

immune associations = PBC, T1DM, IgA deficiency

anaemia = MCV increased or decreased

dermatological = dermatitis herpetiformis, aphthous ulcers

42
Q

what investigations are required in coeliac disease

A

Bloods: FBC, LFTs (↓alb), INR, Vit D and bone, red cell
folate, serum B12
 Abs
 Anti-endomysial IgA (95% specificity)
 Anti-TTG IgA
 Both above ↓ ̄c exclusion diet
 Anti-gliadin IgG persist ̄c exclusion diet)
 IgA ↑ in most but may have IgA deficiency
 Stools
 Stool cysts and antibody: exclude Giardia
 OGD and duodenal biopsy
 Subtotal villous atrophy
 Crypt hyperplasia
 Intra-epithelial lymphocytes

43
Q

how is coeliac managed

A
Lifelong gluten-free diet
 Avoid: barley, rye, oats, wheat
 OK: Maize, soya, rice
 Verify diet by endomysial Ab tests
 Pneumovax as hyposplenic
 Dermatitis herpetiformis: dapsone
44
Q

what is refeeding syndrome

A

emtabolic abnormalities which occur on feeding a person following a period of starvation.

It occurs when an extended period of catabolism ends abruptly with switching to carbohydrate metabolism

45
Q

what are the metabolic consequences of referring syndrome

A

hypophosphataemia
hypokalaemia
hypomagnesaemia: may predispose to torsades de pointes
abnormal fluid balance

these abnormalities can lead to organ failure

46
Q

which patients are at high risk of re feeding syndrome

A

low BMI
unintentional weight loss of 1-=15 percent over a few months
little nutritional intake
hx pf alcohol abuse, drug therapy inc insulin chemo

47
Q

if a patient hasn’t eaten for > 5 days, aim to re-feed at

A

no more than 50% of requirements for the first 2 days

48
Q

histology in crohns vs UC

A

CROHNS = inflammation in all layers from mucosa to serosa
increase goblet cells, granulomas

UC = no inflammation beyond submucosa, inflammatory cell infiltrate in lamina propria, crypt abscess, depletion of goblet cells, no granulomas

49
Q

radiology in crohns vs UC

A

Crohns = small bowel enema = kantor string sign - structuring

proximal bowel dilation

rose thorn ulcers

fistulae

UC = loss of haustrations, pseudopolys, drainpipe colon

50
Q

pain on swallowing is known as

A

odynophagia