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Y3 SOFIA > Key Conditions: Gastro > Flashcards

Key Conditions: Gastro Flashcards

1
Q

PEPTIC ULCER DISEASE: Definition

A

Ulceration of the areas of the GI tract caused by exposure to gastric acid.

Gastric and duodenal most common

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2
Q

PEPTIC ULCER DISEASE: Explain the risk factors and aetiology

A

Imbalance between damaging acid, pepsin and mucosal protective mechanisms

Correlation with H. pylori and NSAID use

Rarely it is due to Zollinger-Ellison syndrome

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3
Q

PEPTIC ULCER DISEASE: Summarise the epidemiology

A

V Common. Annual incidence is about 1–4/1000.

More common in males.

Duodenal ulcers = 30s

Gastric ulcers = 50s

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4
Q

PEPTIC ULCER DISEASE: Recognise the presenting symptoms

A

Epigastric abdominal pain: relieved by antacids

May present with complications (e.g. haematemesis, melaena).

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5
Q

PEPTIC ULCER DISEASE: Recognise the signs on examination

A

Epigastric tenderness

Signs of complications (e.g. anaemia, succession splash on auscultation in pyloric stenosis)

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6
Q

PEPTIC ULCER DISEASE: Identify appropriate investigations

A

Bloods:

  • FBC: looking for anaemia
  • Amylase: exclude pancreatitis

H pylori tests:

  • 3C-Urea breath test
  • Stool antigen test

Imaging:
- Upper GI Endoscopy: Biopsy to rule out malignancy >60 and presenting with dyspepsia

OR >55 + weight loss

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7
Q

PEPTIC ULCER DISEASE: Create a management plan

A

Acute: resuscitation if perforated or bleeding. IV PPI, bleeding stops –> oral

Endoscopy/ surgery for acute

Triple therapy 1-2 weeks if H. Pylori +ve
= Clarithromycin-based triple therapy (a PPI plus clarithromycin plus either amoxicillin or metronidazole)

If H. pylori -ve :
=Treat with PPIs or H2-antagonists (Ranitidine). Stop NSAID use (especially diclofenac), use misoprostol (prostaglandin E1 analogue), if NSAID use is necessary.

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8
Q

PEPTIC ULCER DISEASE: Identify complications

A

Haemorrhage (haematemesis, melaena), perforation, penetration, scarring –> gastric outlet obstruction, malignancy (recurrent –> adenocarcinoma for the stomach)
Only about 1% per year get a major complication

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9
Q

PEPTIC ULCER DISEASE: Summarise the prognosis

A

Overall lifetime risk is about 10%.

Generally good as peptic ulcers associated with H. pylori can be cured by eradication

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10
Q

GORD: Definition

A
  • Inflammation of the oesophagus

- caused by reflux of gastric acid and/or bile

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11
Q

GORD: Explain the aetiology/ risk factors

A
  • Disruption of mechanisms that prevent reflux (physiological LOS)
  • Prolonged oeso- phageal clearance contributes to 50% of cases
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12
Q

GORD: Summarise the epidemiology

A

COMMON

5-10% prevalence in adults

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13
Q

GORD: Recognise the presenting symptoms

A
  • Substernal burning discomfort or ‘heartburn’ aggravated by lying supine, bending or large meals and drinking alcohol- relieved by antacids
  • Waterbrash. Regurgitation of gastric contents.
  • Aspiration may result in voice hoarseness, laryngitis, nocturnal cough and wheeze
  • Dysphagia (caused by formation of peptic stricture after long-standing reflux)
  • Pneumonia (rare)
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14
Q

GORD: Recognise the signs on physical examination

A
  • Usually normal
  • Epigastric tenderness
  • Wheeze on chest auscultation
  • Dysphonia (difficulty speaking)
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15
Q

GORD: Identify appropriate investigations

A
  • PPI trial (further tests if symptoms don’t improve after 8 weeks)
  • OGD (For oesophagitits, brushings to exclude malignancy. Barrett’s?)
  • Ambulatory pH monitoring ( pH <4 more than 4% of the time is abnormal)
  • Barium swallow (hiatus hernia or peptic stricture)
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16
Q

GORD: Generate a management plan

A
  • Lifestyle; wt loss, smoking cessation, avoiding large meals in the evening, elevating head of bed
  • Antacids and alginates, H2 antagonists (e.g. ranitidine) or PPIs (e.g. lansoprazole)
  • Annual OGDs to monitor for Barrett’s
  • Anti-reflux surgery
  • Nissen fundoplication (fundus of the stomach is wrapped around the lower oesophagus –> reduces any hiatus hernia and reflux
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17
Q

GORD: Identify the possible complications

A
  • Oesophageal ulceration, peptic stricture, anaemia,
  • Barrett’s oesophagus and oesophageal adenocarcinoma
  • Associated with asthma and chronic laryngitis
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18
Q

GORD: Summarise the prognosis

A
  • 50% respond to lifestyle changes alone
  • withdraw from drug therapy usually associated with relapse
  • 20% of patients undergoing endoscopy for GORD have Barrett’s oesophagus
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19
Q

HIATUS HERNIA: Definition

A

Protrusion of the stomach from the abdominal cavity into the thorax through diaphragmatic hiatus

2 types:

  • Sliding
  • Paraoesophageal/ rolling (oesophagus + stomach stay in normal place but part of the stomach squeezes up next to the oesophagus –> bubble of stomach next to the thorax)
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20
Q

HIATUS HERNIA: Summarise the aetiology/ risk factors

A

AGE: Decline of diaphragm tone and inc intra-abdominal pressures e.g. repetitive coughing

Pregnancy, obesity, ascites

21
Q

HIATUS HERNIA: Summarise the epidemiology

A

Obesity
Pregnancy
M>F
Previous gastrooesophagal surgery

22
Q

HIATUS HERNIA: Recognise the presenting symptoms

A
  • Heartburn
  • Regurgitation

Uncommon:

  • Haematemasis
  • Chest pain
  • Cough
  • Dysphagia
23
Q

HIATUS HERNIA: Recognise signs on physical examination

A
  • Heartburn
  • Regurgitation
  • Obesity

Uncommon:

  • Haematemasis
  • Chest pain
  • Cough
  • Dysphagia
24
Q

HIATUS HERNIA: Identify appropriate investigations

A

CXR: Enlarged gastric bubble?

Upper GI series: radiograph with barium suspension

Endoscopy: if severe symptoms to check for oesophagitis/ dysplasia

25
Q

HIATUS HERNIA: Generate a management plan

A

Lifestyle changes: same as GORD + avoidance of substances inhibiting the lower oesophageal sphincter; nicotine, chocolate, caffeine, fatty foods, and medications (CCBs, nitrates, beta blockers)

Avoid alcohol and acidic food, smaller meals, elevate head, avoid eating before bed

Medical: PPIs

Surgery to repair a rolling hiatus hernia

26
Q

HIATUS HERNIA: Identify the possible complications

A

Oesophageal dysplasia –> adenocarinoma

Bloating after surgery

Uncommon: Gastric volvolus (emergency) –> ischaemia/ obstruction

27
Q

HIATUS HERNIA: Summarise the prognosis

A

Most patients with sliding have adequate relief with medical therapy

28
Q

CHRON’S DISEASE: Definition

A

Chronic GRANULOMATOUS inflammatory disease that can affect any part of the GI tract.

+ UC = IBD

29
Q

CHRON’S DISEASE: Explain the aetiology/ risk factors

A

Cause thought to be interplay between genetic and environmental factors.

Inflammation can occur anywhere along GI tract (40% involving the terminal ileum) with ‘skip’ lesions. Transmural inflammation. Crampy abdominal pain w risk of fistulas, abscess and obstruction.

RFs:

  • caucasians/ Ashkenazi Jews
  • Age: 15-40 and 60-80
30
Q

CHRON’S DISEASE: Recognise the presenting symptoms

A
  • diarrhoea
  • crampy abdominal pain
  • fever, malaise and weight loss
  • GI bleeding

N.B must exclude TB

31
Q

CHRON’S DISEASE: Recognise the signs on physical examination

A
  • RLQ abdominal tenderness
  • palpable abdo mass
  • oral ulcers
  • perianal: skin tags, fistulae, abscesses, and sinus tracts (DRE for occult blood)
  • erythema nodosum and pyoderma gangrenosum
  • clubbing

Signs of complications (eye disease, joint disease, skin disease)

32
Q

CHRON’S DISEASE: Identify appropriate investigations

A

FBC:

  • Anaemia: chronic blood loss/ inflammation, iron malabsorption +/ B12/ folate deficiency (terminal ileum effected)
  • Leukocytosis: chronic inflammation and corticosteroid use
  • Thrombocytosis: active inflammation

U&Es
LFTs (dec albumin)
inc ESR (sometimes CRP)
Serum Ferritin, B12, Folate

Stool microscopy: C difficile

IMAGING:
AXR: toxic megacolon
Abdo CT: thickened terminal ileum?
Endoscopy and biopsy (OGD/ colonoscopy) –> granulomas

33
Q

CHRON’S DISEASE: Generate a management plan

A

ACUTE

  • Fluid resuscitation, IV or oral corticosteroids, 5-ASA analogues (e.g. mesalazine, sulfasalazine)
  • Analgesia
  • PNR may be necessary
  • Monitor markers of activity (fluid balance, ESR, CRP, platelets, stool frequency, Hb and albumin)

Long term:
. Steroids: For treating acute exacerbations.
. 5-ASA analogues (e.g. sulfasalazine, mesalazine): dec relapses. mild-to-moderate disease.
. Immunosuppression:
steroid-sparing agents (e.g. azathioprine, 6-mercaptopurine,
methotrexate) to dec relapses.
. Anti-TNF agents (e.g. infliximab, adalimumab): Very effective agents for remission. Usually reserved for refractory cases.

Advice: Stop smoking, dietician referral. Education and advice (e.g. from inflammatory bowel disease nurse specialists)

Surgery: failure to thrive for children/ failure of medical treatment (resection + stoma implantation)

34
Q

CHRON’S DISEASE: Identify possible complications and their management

A

GI: Haemorrhage, bowel strictures, perforation, fistulae (between bowel, bladder, vagina), perianal fistulae and abscess, GI carcinoma (5% risk in 10 years), malabsorption

Extraintestinal features: Uveitis, episcleritis, gallstones, kidney stones, arthropathy, sacroiliitis, ankylosing spondylitis, erythema nodosum and pyoderma gangrenosum, amyloidosis

35
Q

CHRON’S DISEASE: Summarise prognosis

A

Chronic relapsing condition.

Two-thirds will require surgery at some stage and two-thirds of these >1 surgical procedure

36
Q

ULCERATIVE COLITIS: Definition

A

Chronic relapsing and remitting inflammatory disease affecting the large bowel.

(starts distally, rectal sparing, mainly effecting mucosa and submucosa, continuous lesions)

37
Q

ULCERATIVE COLITIS: Aetiology and risk factors

A

Unknown.

Suggested hypotheses include genetic susceptibility HLA-B27, immune response to bacterial or self-antigens, environmental factors, altered neutrophil function, abnormality in epithelial cell integrity

Positive family history of IBD (15%). Associated with serum pANCA

NSAIDs

38
Q

ULCERATIVE COLITIS: Summarise the epidemiology

A
  • 1/1500 in developed world
  • inc prevalence in caucasians and Ashkenazi Jews
  • Peak onset between 20-40 yrs.
  • > 40yrs more common in M
39
Q

ULCERATIVE COLITIS: Recognise presenting symptoms

A
  • Bloody or mucous diarrhoea (stool frequency = severity
  • Tenesmus and urgency.
  • Crampy abdominal pain before passing stool
  • weight loss, fever

Symptoms of extra GI manifestations

40
Q

ULCERATIVE COLITIS: Recognise signs on physical examination

A
  • Symptoms of iron deficiency
  • Dehydration
  • Clubbing
  • Abdominal tenderness, tachycardia
  • Blood, mucus and tenderness on PR examination
41
Q

ULCERATIVE COLITIS: Identify appropriate examinations

A

Bloods:

  • FBC ( dec Hb, inc WCC)
  • inc ESR or CRP, dec
  • albumin
  • cross-match if blood loss
  • LFT

Stool: Culture as infectious colitis is a differential Faecal calprotectin – marker for
disease severity

AXR: To rule out toxic megacolon

Flexible sigmoidoscopy or colonoscopy (and biopsy): Determines severity and dysplasia

Barium enema: Mucosal ulceration with granular appearance and filling defects (pseudo-
polyps), featureless narrowed colon, loss of haustral pattern

42
Q

ULCERATIVE COLITIS: Generate a management plan

A

Markers of activity: bloods, diarrhoea frequency (< 4 = mild, 4–6 = moderate, >6 =severe), bleeding, fever

Acute exacerbation:
- IV rehydration, IV corticosteroids, ABX, bowel rest, PRN may be necessary, DVT prophylaxis, monitor fluid balance and vital signs closely

Mild Disease:
- Oral or rectal 5-ASA analogues e.g. sulphasalazine and/or rectal steroids

Mod/ Sev Disease:
- Oral steroids and oral 5-ASA. - Immunosuppression with azathioprine, cyclosporine, 6-mercaptopurine, infliximab

Advice: Patient education and support. Treatment of complications. Regular colonoscopic surveillance.

Surgical: Failure of medical treatment, presence of complications or prevention of colonic carcinoma. Proctocolectomy with ileostomy or an ileo-anal pouch formation

43
Q

ULCERATIVE COLITIS: Identify possible complications and their management

A

GI: Haemorrhage, toxic megacolon, perforation, colonic carcinoma, gallstones and PSC.

Extra-GI manifestations (10–20%): Uveitis,ankylosing spondylitis, erythema nodosum, pyoderma gangrenosum, osteoporosis (from steroids), amyloidosis.

44
Q

ULCERATIVE COLITIS: Summarise prognosis

A

A relapsing and remitting condition, with normal life expectancy

Poor prognostic factors (ABCDEF): Albumin (< 30 g/L), blood PR, CRP raised, dilated loops of bowel, eight or more bowel movements per day, fever (>38)

45
Q

HERNIA: Definition

A

The protrusion of a viscus through an abnormal opening

Irreducable: cant be pushed back into the right place
Incarceration: the contents of the hernial sac are stuck inside by adhesions Obstructed: if bowel contents cannot pass through them
Strangulated: if ischaemia occurs

46
Q

HERNIA- Inguinal: Definition

A

Indirect (80%)
Pass through the internal inguinal ring, along inguinal canal and through the abdominal wall, laterally to inferior epigastric vessels
If large they can also pass through external inguinal ring
- Common in children (4% male babies: failure of the inguinal canal to close properly after passage of the testes in utero)

Direct (20%)
Push directly forward through the posterior wall of the inguinal canal into a defect in the abdominal wall (Hesselbach’s triangle) Medial to inferior epigastric vessels

47
Q

HERNIA- Femoral: Definition

A

Bowel enters the femoral canal, below the inguinal ligament.
Points down the leg
Inferior and lateral to pubic tubercle
Likely to be irreducible and strangulate due to rigidity of the femoral canal

48
Q

HERNIA: Explain the aetiology/ risk factors

A

Inguinal:

  • Most common time of hernia
  • M > F
  • Infants: M
  • Adults: chronic cough, constipation, urinary obstruction, heavy lifting, ascites, past abdo surgery

Femoral:

  • W> M
  • Middle aged + elderly
49
Q

HERNIA: Explain epidemiology

A

Inguinal:

  • M> F
  • Direct = elderly
  • Indirect= children

Y3 SOFIA (2 decks)

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