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Belle Phase 2a > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

Coeliac disease

A

Inflammation of the mucosa of the upper small bowel in response to GLUTEN

AUTOIMMUNE (T cell mediated)

Intolerance to PROLAMIN (in wheat, barley, rye, oats) which is a component of gluten protein

Causes VILLOUS ATROPHY

Leads to MALABSORPTION

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2
Q

Coeliac disease epidemiology

A

1% of population in the UK

Peaks in infancy + 40-60 years

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3
Q

Familial link and risk in coeliac disease

A

10% risk in 1st degree relatives

HLA associated: HLA DQ2 (90%)

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4
Q

Coeliac disease risk factors

A

Other autoimmune diseases: T1DM, autoimmune thyroid, Addisons

Test all new cases of T1DM for coeliac

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5
Q

Pathophysiology coeliac disease

A

SMALL BOWEL (particularly the jejunum)

Gliadin = breakdown product of gluten
Tissue transglutaminase (tTG) Ab
Ab-gliadin complex is presented to a transferrin receptor
Endocytosed accross the gastric mucosa into lamina propria
Deamidation
Deamidated gliadin phagocytosed by HALDQ8 cells
Macrophages signal an immune response (pro-inflammatory cytokines > cascade)

Results in:
VILLOUS ATROPHY > malabsorption
CRYPT HYPERPLASIA
Raised intraepithelial lymphocytes

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6
Q

Clinical presentation of coeliac disease

A 
Often asymptomatic 
Failure to thrive in young children
Malabsorption (due to villous atrophy)
- STEAORRHOEA (can’t absorb fat)
- ANAEMIA (can’t absorb B12, folate, iron)
- Osteomalacia (can’t absorb vitamin D)
UNINTENTIONAL WEIGHT LOSS
Fatigue
DIARRHOEA
Aphthous ulcers 
Angular stomatitis 
Dermatitis herpetiformis
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7
Q

Complications of untreated coeliac disease

A

Vitamin deficiency
Anaemia
Osteoporosis

Increased risk of malignancy:
Enteropathy-associated T-cell lymphoma

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8
Q

Investigations for coeliac disease

A

1st line: raised anti-tTG antibodies

  • very high sensitivity and specificity
  • false negatives may occur in people with IgA deficiency as anti-tTG is IgA

Gold standard: endoscopy + duodenal biopsy

  • villous atrophy
  • crypt hypertrophy
  • raised intracellular WBCs

Can also test for IgA endomysial antibody (anti-EMA) but less sensitive

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9
Q

Treatment of coeliac

A

Lifelong gluten-free diet

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10
Q

Inflammatory Bowel Disease (IBD)

A

Chronic
Autoimmune

Umbrella term for two main diseases that cause inflammation of the GI tract:
Crohn’s disease
Ulcerative colitis

Relapsing & remitting

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11
Q

Key features of Crohns: NESTS

A

Not usually blood or mucus (but can occur)
Entire GI tract (mouth to anus)
Skip lesions on endoscopy (non-continuous inflammation)
Terminal ileum and Transmural
Smoking is a risk factor

Cobblestone appearance (ulcers and fissures in mucosa)
Non-caseating granuloma inflammatory lesions
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12
Q

Key features of Ulcerative colitis: UC CLOSE UP

A 
Continuous and circumferential inflammation; crypt abscesses 
Limited to colon and rectum
ONLY superficial mucosa affected 
Smoking is protective
Excrete blood and mucus

Use aminosalicylates and Uveitis
Primary sclerosis cholangitis and pseudo-polyps

DEPLETED goblet cells (mucosal barrier destruction)

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13
Q

Risk factors for ulcerative colitis

A

Family history

NSAIDs (can trigger onset and flares)
Chronic stress (can trigger flares)
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14
Q

Ulcerative colitis epidemiology

A

Presentation at 20-40 years old
Higher incidence than Crohns
Incidence is 3x higher in non-smokers

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15
Q

Symptoms of UC

A

Diarrhoea
Abdominal pain
Passing blood and mucus
Weight loss

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16
Q

Signs of UC

A

Acute: fever, tachycardia, tender abdomen

Extraintestinal: clubbing, nutritional deficits

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17
Q

Complications of UC

A

Colon:

  • Blood loss
  • Colorectal cancer

Skin:

  • Erythema nodosum
  • Pyoderma gangrenosum

Joints:

  • Ankylosing spondylitis
  • Arthritis

Eyes:
- Uveitis

Liver:
- sclerosing cholangitis

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18
Q

Investigations of UC

A

Blood tests:

  • raised CRP & ESR in active inflammation
  • raised WCC
  • raised platelets
  • anaemia (normocytic of chronic disease)
  • pANCA may be +ve (-ve in Crohn’s)

Gold standard:

  • DIAGNOSIS: sigmoidoscopy + biopsy
  • further: full colonoscopy + biopsy

Further testing:
Abdominal X-Ray
Ultrasound, CT and MRI

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19
Q

Treatment of UC

A 
MILD TO MODERATE DISEASE
1st line: aminosalicylate
- 5-aminosalicyclic acid (5-ASA) 
- sulfasALAZINE, mesALAZINE, olsALAZINE
- oral or rectal route 
2nd line: oral corticosteroids e.g. prednisolone

SEVERE DISEASE
1st line: IV corticosteroids e.g. hydrocortisone
2nd line: IV ciclosporin

SEVERE W/ NO RESPONSE: colectomy
- surgery is possible as it only affects the colon and rectum

MAINTAINING REMISSION: Aminosalicylate, AZATHIOPRINE

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20
Q

Crohn’s disease risk factors

A 
Stronger genetic association than UC
Family history
Smoking 
NSAIDs (exacerbate) 
Chronic stress (trigger flares)
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21
Q

Crohn’s epidemiology

A

Northern Europe and North America
Females > males
Presentation mostly at 20-40 years

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22
Q

Crohn’s disease symptoms

A

Small bowel: Abdo pain, weight loss

Colon: Bloody diarrhoea, pain on defecation

Systemic: Fever, fatigue, anorexia

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23
Q

Crohn’s disease signs

A

Bowel ulceration
Abdo tenderness
Abdo mass

Extraintestinal:
oral aphthous ulcers (more common in Crohn’s than UC)
skin, joint and eye problems

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24
Q

Crohn’s disease complications

A 
Malabsorption 
Small bowel obstruction 
Colorectal cancer
Anaemia 
Perianal disease e.g. fissures
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25
Q

Crohn’s disease investigations

A

Blood tests:

  • raised CRP & ESR
  • raised WCC
  • raised platelets
  • anaemia (normocytic of chronic disease)
  • pANCA negative

Gold standard: colonoscopy + biopsy
- granulomatous transmural inflammation

Small bowel imaging: to detect proximal disease

Abdominal X-ray
MRI
Ultrasonography

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26
Q

Crohn’s disease treatment

A

MILD/MODERATE DISEASE
1st line: Oral prednisolone

SEVERE DISEASE
1st line: IV hydrocortisone

If NOT RESPONSIVE to steroids: Anti-TNF antibodies (Infliximab)

MAINTAINING REMISSION: AZATHIOPRINE (Methotrexate if intolerant to Azathioprine)

OTHER
Smoking cessation
Correct iron/B12 deficiencies
Antibiotics for perianal disease

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27
Q

IBD: upper RIGHT quadrant pain

A

Crohn’s disease

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28
Q

IBD: LEFT quadrant pain

A

Ulcerative colitis

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29
Q

Screening test for IBD

A

Faecal calprotectin

  • release by the intestines when inflamed
  • > 90% specific and sensitive to IBD in adults
  • doesn’t differentiate UC and Crohn’s
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30
Q

Surgery in Crohn’s disease

A

Resection of worst affected areas of bowel
Never fully cures

Indications:
Failure of medical therapy
Obstruction from strictures
Fistulae, abscesses, perianal disease

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31
Q

Irritable bowel syndrome (IBS)

A

Functional bowel disorder = mixed group of abdominal symptoms with no organic cause

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32
Q

IBS epidemiology

A

More common in females

1 in 5 in western world

Age of onset = under 40 years

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33
Q

IBS risk factors

A

GI infections
Anxiety and depression
Eating disorders
Previous severe long term diarrhoea

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34
Q

IBS symptoms

A

Chronic: 6+ months
Exacerbated by stress, food, menstruation

3 types:
IBS-C: with constipation
IBS-D: with diarrhoea
IBS-M: mixed

Consider IBS if a patient reports ANY:
Abdominal pain
Bloating
Change in bowel habit

Multi-system disorder:

  • painful periods
  • bladder symptoms e.g. frequency
  • joint hyper mobility
  • fatigue
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35
Q

NICE diagnostic criteria for IBS

A

ABDOMINAL PAIN which is either related to
- DEFECATION
and/or
- associated with altered stool FREQUENCY (increased or decreased)
and/or
- associated with altered STOOL FORM or appearance (hard, lumpy, loose, or watery)

And there are at least two of the following:

Alternative conditions with similar symptoms have been excluded
Passage of rectal mucus
Symptoms worsened by eating
Abdominal bloating (more common in women than men), distension, or hardness
Altered stool passage (straining, urgency, or incomplete evacuation)

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36
Q

Differential diagnoses for IBS

A

IBD
Coeliac
Lactose intolerance
Colorectal cancer

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37
Q

Investigations for IBS

A

Rule out differentials:

  • tTG for coeliac
  • faecal calprotectin for IBD
  • FBC for anaemia
  • colonoscopy for IBD + colorectal cancer
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38
Q

IBS treatment

A

1st line: General healthy DIET + exercise ADVICE

  • small frequent non-processed meals
  • IBS-C: soluble fibre

1st line medication:
IBS-D: Loperamide (Imodium)
IBS-C: Laxatives e.g. docusate, linaclotide
Pain/bloating: antispasmodics e.g. buscopan

2nd line medication: 
Tricyclic antidepressants (amitriptyline)

3rd line medication
SSRI antidepressants

Can be used in conjunction with psychological therapies e.g. cognitive behaviour therapy (CBT)

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39
Q

Acute appendicitis

A

Sudden inflammation of the appendix

Most commonly caused by an obstruction of the appendix which results in the invasion of gut organisms into the appendix wall leading to INFLAMMATION, necrosis and rupture

Most common surgical emergency

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40
Q

Causes of obstruction to the appendix

A

Faecoliths (stony mass of compacted faeces)
Bezoars (partially digested material collected in the stomach)
Trauma
Intestinal worms
Lymphoid hyperplasia

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41
Q

Key clinical presentation of appendicitis

A

ABDOMINAL PAIN
- starts central (umbilicus) and migrates to the right iliac fossa within the first 24 hours

Inflammation irritates overlying peritoneum (peritonitis) causing tenderness at McBurney’s point (1/3 from anterior superior iliac spine to umbilicus)

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42
Q

Other classic features of appendicitis

A 
Guarding on abdominal palpating
Pyrexia
Nausea and vomiting 
Rosvings sign (palpation of LIF causes pain in RIF)
Coughing causes pain
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43
Q

Key differential diagnoses of appendicitis

A 
Ectopic pregnancy: serum hCG
Meckel’s diverticulum 
UTI 
Constipation 
Food poisoning
Crohn’s (acute terminal ileitis)
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44
Q

Investigations acute appendicitis

A

Diagnosis:

  • Clinical presentation
  • Blood tests: raised WCC (neutrophils), raised CRP & ESR (inflammation)

GOLD STANDARD: CT scan (highly specific and sensitive)

Ultrasound: inflamed appendix and appendix mass
Pregnancy test: exclude ectopic pregnancy
Urinalysis: exclude UTI

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45
Q

Management of appendicitis

A

GOLD STANDARD = laparoscopic appendicectomy

IV antibiotics (metronidazole) and IV fluids

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46
Q

Complications of appendicitis

A

Perforation

Appendix mass: the omentum sticks to the inflamed appendix forming a mass in the RIF

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47
Q

Three types of bowel obstruction

A

Small bowel obstruction (60-75%)
Large bowel obstruction
Psuedo-obstruction

All can be serious and potentially fatal

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48
Q

Causes of small bowel obstruction

A

INTRA-ABDOMINAL ADHESIONS (60%) - usually due to previous abdo surgery or infections e.g. peritonitis

Hernias
Malignancy
Crohn’s disease

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49
Q

Pathophysiology of small bowel obstruction

A

Distension above the blockage > increased pressure pushes blood vessels within bowel wall > compressed vessels results in ischaemia, necrosis, perforation

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50
Q

Clinical presentation of SBO

A

PAIN: initially COLICKY but then diffuse, higher in the abdomen than LBO, INTERMITTENT

Profuse VOMITING following pain (occurs earlier in SBO than LBO) - think SB IS CLOSER TO MOUTH

Increased bowel sounds (tinkling)

Abdominal distention

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51
Q

Small bowel obstruction Ix

A

1st line: abdominal X-ray

  • distended loops of bowel proximal to obstruction
  • no gas distal to obstruction (i.e. large bowel)

GOLD STANDARD: non-contrast CT - localises the obstruction

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52
Q

Causes of large bowel obstruction

A

MALIGNANCY (90%) - more common in West

Volvulus (twisting of the bowel on its mesenteric axis, sigmoid colon most common place)
Diverticulitis
Crohn’s disease

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53
Q

Clinical presentation of LBO

A

Abdominal pain

  • more CONSTANT & DIFFUSE than SBO
  • usually occurs lower in the abdomen (LIF)

Much more ABDOMINAL DISTENTION than SBO

Palpable mass e.g. hernia

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54
Q

Investigations for LBO

A

Digital rectal exam (DRE)

  • empty rectum
  • hard compacted stools

1st line: Abdo X-Ray
- peripheral gas shadows proximal to blockage

Gold standard: CT

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55
Q

Management of an obstructed bowel (SBO, LBO)

A

Aggressive fluid resuscitation

Decompression of the bowel “drip and suck”

  • IV fluids to hydrate
  • NG tube

Analgesia, anti-emetics

Antibiotics

Surgery to remove obstruction

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56
Q

Pseudo bowel obstructions

A

Present identically to SBO/LBO but underlying cause should be treated first

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57
Q

Bacterial causes of diarrhoea

A

Campylobacter jejuni
E. Coli
Salmonella
Shigella

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58
Q

Viral causes of diarrhoea

A

Majority of diarrhoea cases are VIRAL

Children = rotavirus
Adults = norovirus
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59
Q

Management of diarrhoea

A

Oral rehydration therapy (IV fluids given if very severe)

Treat the underlying causes (bacterial normally treated with metronidazole)

Anti-emetics e.g. metoclopramide

Anti-motility agents e.g. loperamide

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60
Q

Ischaemic bowel diseases

A

Acute mesenteric ischaemia
Chronic mesenteric ischaemia (intestinal angina)
Ischaemia colitis

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61
Q

Causes of acute mesenteric ischaemia

A

Superior mesenteric artery (SMA) THROMBOSIS

SMA EMBOLISM (due to AF)

Mesenteric venous thrombosis

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62
Q

Presentation of acute mesenteric ischaemia

A

Classic triad:
Acute, severe abdo pain (constant and central)
No abdo signs on examination
Rapid hypovolaemia > shock

AF + severe abdo pain = AMI

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63
Q

Acute mesenteric ischaemia investigations

A

Diagnostic: CT angiography
- visualise blockages (difficult to perform)

Bloods:

  • increased Hb concentration due to blood loss
  • metabolic acidosis + raised lactate
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64
Q

Management of AMI

A

Fluid resuscitation
IV heparin
Antibiotics (metronidazole)
Surgery to remove necrotic bowel

Mortality: >50%

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65
Q

Causes of ischaemic colitis

A

Thrombosis
Emboli
Low flow states (low CO/arrhythmias)
Surgery

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66
Q

Presentation of ischaemic colitis

A

Sudden onset LIF pain
Passage of bright red blood
Signs of hypovolaemic shock (tachycardia, fatigue)

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67
Q

Ischaemic colitis investigations

A

1st line: CT to rule out rupture

Gold standard: colonoscopy + biopsy

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68
Q

Mallory Weiss tear

A

Haematemesis from tear in oesophageal mucosa

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69
Q

Causes and risk factors for Mallory Weiss tear

A 
ALCOHOLISM
Hyperemesis gravidarum (severe nausea and vomiting during pregnancy) 
Gastroenteritis 
Bulimia 
Chronic cough
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70
Q

Tar like, black, greasy and offensive stools caused by digested blood

71
Q

Presentation of Mallory Weiss tear

A

Haematemesis
Melaena
Sx of hypovolaemic shock

72
Q

Investigations Mallory Weiss tear

A
  1. Rockall score (risk of bleeding: <3 = low risk)
  2. Haemoglobin (FBC), Urea (U&Es), coagulation (INR, FBC for platelets), Liver disease (LFTs), Crossmatch blood
  3. ECG and cardiac enzymes
73
Q

Management Mallory Weiss tear

A 
ABCDE
Terlipressin (oesophageal varices)
Urgent endoscopy (oesophagogastroduodenoscopy/OGD)
74
Q

Oesophageal varices

A

Dilated veins at sites of portosystemic anastomosis (left gastric & inferior oesophageal veins)

75
Q

Causes of oesophageal varices

A

Pre-hepatic: portal vein thrombosis
Hepatic: CIRRHOSIS > PORTAL HYPERTENSION
Post hepatic: Budd Chiari syndrome, RHF

76
Q

Oesophageal varices clinical presentation

A

Haematemesis
MELAENA
Sudden collapse (Sx of haemodynamic instability)

77
Q

Investigations oesophageal varices

A
  1. Urgent endoscopy
  2. FBC, U&Es, clotting (INR), LFTs
  3. CXR, Ix PHT
78
Q

Treatment for oesophageal varices

A

ABCDE
Rockall score
TERLIPRESSIN + prophylactic broad spectrum AB (ciprofloxacin)

79
Q

Barrett’s Oesophagus

A

Metaplasia of the lower oesophageal mucosa (STRATIFIED SQUAMOUS to COLUMNAR epithelium with goblet cells)

Pre-malignant: RF for adenocarcinoma of the oesophagus

80
Q

Causes and RF for Barrett’s oesophagus

A 
GORD
Male (7:1) 
Caucasian 
FHx
Hiatus hernia 
Obesity
Smoking
Alcohol
NSAIDs
81
Q

Classic patient Px of Barrett’s oesophagus

A

Middle aged Caucasian male with long history GORD and dysphasia

82
Q

Investigations Barrett’s oesophagus

A

Endoscopy + Biopsy

83
Q

Management of Barrett’s oesophagus

A

Lifestyle advise: weight loss, reduce caffeine, avoid smoking
Acid neutralising medication: Gaviscon
Proton pump inhibitors: OmePRAZOLE, LansoPRAZOLE
Endoscopic surveillance with biopsies

84
Q

Risk factors for progression to adenocarcinoma in Barrett’s oesophagus

A 
Male
Older age 
>8cm segment 
Intestinal metaplasia 
GORD duration
Alcohol, smoking, obesity 
Achalasia
85
Q

Adenocarcinoma oesophageal cancer

A

Most common type in the DEVELOPED world e.g. UK

RF: GORD, Barrett’s, Smoking, Obesity

Location: Lower 1/3 (near GO junction)

86
Q

Squamous oesophageal cancer

A

Most common type in the DEVELOPING world

RF: SMOKING, Alcohol, Low fruit/veg/fibre, Hot drinks

Location: Upper 2/3

87
Q

Presentation of oesophageal cancer

A

THROAT LUMP
LONG HISTORY OF DYSPEPSIA

ALARMS:
Anaemia 
Loss of weight 
Anorexia 
Recent onset progressive symptoms 
Regurgitation 
Swallowing difficulties: PROGRESSIVE DYSPHAGIA
88
Q

Oesophageal cancer investigations

A

1st line: Upper GI endoscopy + biopsy
(REFER WITHIN 2 WEEKS)

Staging: CT scan or endoscopic ultrasound

89
Q

Oesophageal cancer management

A

OPERABLE: surgical resection + adjuvant chemotherapy

Palliation (relief of symptoms without cure)

90
Q

Gastrooesophageal reflux disease

A

Lower oesophageal sphincter (LOS) dysfunction

Leads to reflux of gastric contents leading to symptoms of OESOPHAGITIS

91
Q

RF GORD

A 
Hiatus hernia 
Smoking
Alcoholism
Obesity 
Pregnancy
92
Q

Oesophageal presentation of GORD

A

Heartburn/retrosternal pain: related to meals, worse when lying down, relieved by antacids

Acid regurgitation

Odynophagia: painful sensation in the oesophageal regions that occurs in relation to swallowing

93
Q

Dyspepsia

A

Non specific term to describe indigestion symptoms e.g. heartburn

94
Q

Extra oesophageal symptoms of GORD

A

Nocturnal asthma
Chronic cough
Laryngitis, Sinusitis

95
Q

GORD Red Flags

A 
Dysphagia 
>55 years
Weight loss
EPIGASTRIC PAIN
Treatment resistant DYSPEPSIA 
Anaemia
Raised platelets

= ENDOSCOPY (Refer for Upper GI endoscopy within 2 weeks)

96
Q

Management of GORD

A

Non-pharmacological: smoking cessation, stop drinking alcohol, lose weight, sleeping position

Pharmacological: PPIs e.g. lansoprazole, H2 receptor antagonists (antihistamines) e.g. ranitidine, Alginates (form a gel raft at top of stomach)

Surgical: laparoscopic/Nissen fundoplication (tying fungus around the LO to narrow the LOS)

97
Q

Peptic ulcers

A

Break in the lining of the GASTRIC or DUODENAL MUCOSA

98
Q

RF peptic ulcers

A

H. pylori
NSAIDs e.g. ibuprofen
ZE syndrome
Increased acid: stress, alcohol, caffeine

99
Q

Investigations Peptic Ulcer

A

Diagnosis: Endoscopy

- Rapid Urease Test (H. pylori test)

100
Q

Peptic ulcer management

A

Lifestyle modifications
Treat underlying cause:
- stop NSAIDs
- eradicate H. pylori (PPI, clarithromycin, amoxicillin)

101
Q

Helicobacter pylori

A

Gram negative aerobic bacteria

Damages the epithelial lining of the stomach resulting in gastritis, ulcers and increased risk of stomach cancer

Damages epithelial cells:
Avoids the acidic environment by forcing its way into the gastric mucosa
Produces ammonia to neutralise the stomach acid

102
Q

Gastric ulcer

A

Location: lesser curvature of gastric antrum

RF: H. pylori, Smoking, Drugs, Stress, NSAIDs, mucosal ischaemia

Presentation: Epigastric pain WORSE ON EATING and RELIEVED BY ANTACIDS, Haematemesis, Melaena (DARK blood in stools due to degradation by intestinal enzymes)

103
Q

Duodenal ulcer

A

MORE COMMON

Location: 1st part of duodenum

RF: H. Pylori, Smoking, Drugs, Alcohol

Presentation: Epigastric pain BEFORE MEALS and AT NIGHT and RELIEVED BY EATING
Haematemesis, Melaena (DARK blood in stools due to degradation by intestinal enzymes)

104
Q

Complications of peptic ulcers

A

Haemorrhage
Perforation
Gastric outflow obstruction
Malignancy

105
Q

Drugs that cause peptic ulcer

A

NSAIDs
SSRI
Corticosteroids
Bisphosphonates

106
Q

Gastritis

A

Inflammation of the stomachs mucosal lining

107
Q

RF Gastritis

A 
Autoimmunity 
H. Pylori
Bile reflux 
NSAIDs
Stress
Alcohol
108
Q

Gastritis clinical presentation

A

Epigastric pain
Nausea and vomiting
Dyspepsia

109
Q

Gastritis investigations

A

H. pylori (Urease test)

Endoscopy + biopsy

110
Q

Management of gastritis

A

Addressing cause
H. pylori eradication (PPI, Clarithro, Amox)
Correction of vitamin deficiency

111
Q

Diverticulum

A

Outpouching of the gut mucosa with penetrating arteries

112
Q

Diverticulosis

A

Presence of multiple diverticula
“Wear and tear of the bowel”
Very common >50 years

113
Q

Diverticulitis

A

Inflammation in the diverticula

RF: low fibre diets, obesity, NSAIDs

114
Q

Diverticula disease

A

Diverticula are symptomatic

115
Q

Meckel’s diverticulum

A

Common congenital abnormality of the GI tract
2-3% of population
Usually asymptomatic

116
Q

True diverticula

A

Contain all the layers of the GI wall (mucosa, muscularis propria, adventitia) e.g. Meckel’s

117
Q

False diverticula

A

Only involve the submucosa and mucosa

118
Q

Where in the colon are diverticula most likely to form

A

SIGMOID COLON

  • Smallest luminal diameter
  • Highest pressure
  • presents in LIF

DESCENDING COLON

119
Q

Presentation of diverticulitis

A 
Left iliac fossa pain with tenderness 
Palpable LIF mass
Constipation
Tachycardia 
Fever
120
Q

Diverticulitis investigations

A

Bloods: raised WCC, ESR & CRP

Imaging: Erect CXR, AXR and CT

121
Q

Treatment of diverticulitis

A

Oral co-amoxiclav
Oral/IV ciprofloxacin
Analgesia + clear liquid diet
Severe: surgical resection

122
Q

Presentation of diverticular disease

A

Altered bowel habit
Abdominal pain
Bleeding PR

123
Q

Investigations for diverticular disease

A

CT (acute)

Colonoscopy

124
Q

Management for diverticular disease

A

High fibre diet and fluids +/- laxatives

Surgery

125
Q

Gastric cancer types

A

Type 1: intestinal/differentiated (70-80%)

Type 2: diffuse/undifferentiated (20%)

126
Q

Gastric cancer risk factors

A

Male
H. Pylori
Chronic gastritis
Older age

127
Q

Signet ring cell carcinoma

A

Type of adenocarcinoma (mucus producing)

Most often found in gastric cancer

128
Q

Criteria for 2 week wait endoscopy in gastric cancer

A 
Upper abdominal mass +
- Dysphagia (any age)
Or
- Aged >55 + weight loss and:
- Upper abdominal pain
- Reflux
- Dyspepsia
129
Q

Clinical presentation of gastric cancer

A

Often late presentation
Anorexia, nausea, weight loss, anaemia, dysphagia, vomiting
Epigastric pain (better with antacids)
Paraneoplastic syndromes

130
Q

Gastric cancer investigations

A

Gastroscopy: 8-10 biopsies
Endoscopic USS: depth of invasion
CT/MRI/PET

131
Q

Management of gastric cancer

A

Nutritional support (fruit, veg, fibre = protective)
Surgical resection
Chemo

Prognosis: 60% 5 year survival

132
Q

Risk factors for colon cancer

A 
Family Hx - younger presentation
IBD
Diet (red meat, low fibre)
Obesity
Colorectal polyps 
Smoking
133
Q

Diagnosis of colon cancer

A
  1. Faecal occult blood test
    a) >50 + bowel habit change or IRON DEFICIENT ANAEMIA
    b) >60 + anaemia
  2. Colonoscopy + biopsy
  3. Flexible sigmoidoscopy / Barium enema / CT colonoscopy
134
Q

Management of colon cancer

A

Surgical resection depending on area

E.g. descending colon = left hemicolectomy

135
Q

Example of hereditary causes of colon cancer

A

Familial adenomatous polyposis (FAP) - AUTOSOMAL DOMINANT

136
Q

Staging of colon cancer

A

Dukes staging system
A) confined to submucosa
B) invasion through muscularis without lymph node involvement
C) invasion through muscularis with lymph node involvement
D) presence of distant metastases

137
Q

Types of diarrhoea

A 
Inflammatory
Dysentery 
Secretory
Osmotic
Exudative
138
Q

Clinical tool to classify faeces

A

Bristol stool chart

139
Q

Red flags for abdominal cancer

A 
PR bleeding
Abdominal mass
Weight loss
FHx
Anaemia
Age >60
Bowel habit
140
Q

Complications of bowel obstruction that would lead to emergency surgery

A

Bowel ischaemia

Strangulation

141
Q

Non-invasive tests for H. pylori

A

C-Urea breath test

Faecal antigen test

142
Q

Gastritis differentials

A

GORD
Gastric carcinoma
Peptic ulcer

143
Q

Clinical features of haemorrhoids

A

Bright red bleeding
Discomfort/pain
Pruritis ani
Pain on passing stools

144
Q

Pathophysiology of haemorrhoids

A

Swelling and inflammation of veins in the rectum and anus

145
Q

Two types of haemorrhoids

A

Internal: painless covered in mucus, prolapse

External: painful, covered with skin

146
Q

Treatment of haemorrhoids

A 
Stool softeners 
High fibre diet
Adequate fluid intake 
Band ligation
Haemorrhoidectomy
147
Q

Causes of acute diarrhoea

A

Bacterial: salmonella from food poisoning
Viral: norovirus (associated with cruise ships)
IBS/IBD
Anxiety
Drugs e.g. NSAIDs, PPIs

148
Q

Potential complications of diverticulitis

A 
Large bowel perforation
Fistula formation
Large bowel obstruction
Bleeding
Mucosal inflammation
149
Q

If Terlipressin is contraindicated in oesophageal varices, what drug should be used?

A

Somatostatin

150
Q

MOA of terlipressin in oesophageal varices

A

Increase in ARTERIAL vascular resistance = decrease in arterial blood supply = reduction of pressure in portal circulation

151
Q

Abdominal pain
Mucousy stools
Painful diarrhoea

A

Suspect IBD

152
Q

Mouth ulcers

Which IBD?

A

Crohn’s - from mouth to anus

153
Q

Young child: underweight, tired all the time, intermittent stomach pain, nausea, diarrhoea

FH: autoimmune conditions

A

Coeliac disease

FIRST LINE: serology for TTG (IgA)

GOLD STANDARD investigation: endoscopic intestinal biopsy
- duodenal/jejunal biopsy: villous atrophy + crypt hyperplasia

OTHER: FBC (anaemia), CRP & ESR (inflammation)

154
Q

Treatment in acute variceal haemorrhages

A

Endoscopic variceal band ligation

155
Q

Achalasia

A

Lower oesophageal spinchter fails to relax causing failure of oesophageal peristalsis

156
Q

HNPCC

A

hereditary nonpolyposis colorectal cancer gene

increases the risk of cancers including COLORECTAL and ENDOMETRIAL CANCER

157
Q

Why does a Mallory Weiss tear occur following SEVERE VOMITING

A

Sudden rise in intragastric pressure causes the oesophageal mucosa to tear

158
Q

Virchows node

A 
Left supraclavicular lymph node
Gastric cancer (Trosiers sign)
159
Q

Gastroenteritis

A

Bacterial or viral causes
Diarrhoea and vomiting (dehydration)
(Unlikely to be associated with bleeding)

160
Q

Absorption location: bile salts

A

Terminal ileum

161
Q

Absorption location: iron

162
Q

Absorption location: Vitamin B12

A

terminal ileum

163
Q

Absorption location: folate

A

Duodenum and jejunum

164
Q

Why do NSAIDs cause stomach irritation

A

Mucus secretion is stimulated by prostaglandins
COX-1 is needs for prostaglandin synthesis
NSAIDs inhibit COX-1 = no mucus for protection

165
Q

Causes of diarrhoea

A 
Viral: rotavirus (children), norovirus
Bacterial: E. coli, Salmonella, C.diff
Parasitic
Antibiotics: rule of Cs (cephalosporins)
Other: anxiety, food allergy
Chronic: IBS, IBD, coeliac, bowel cancer
166
Q

Risk factors for infective diarrhoea

A

Foreign travel
Crowded area
Poor hygiene

167
Q

Commonest dermatological manifestation of IBD

A

Erythema nodosum

168
Q

Most likely part of bowel affected in UC

A

Rectum (starts here)

169
Q

Large bowel blood supply

170
Q

Explain this diagram

171
Q

AF + severe abdo pain

A

Acute mesenteric ischaemia

172
Q

Parietal cells secretions

A 
Gastric acid (HCl) - H+/K+ ATPase (action of PPIs)
Intrinsic factor
173
Q

Location of action of ranitidine

A

Enterochromaffin cells secrete histamine which works on parietal cells via H2 receptors
Ranitidine is a H2 antagonist = reduce gastric acid secretion from parietal cells

174
Q

Skin turgor and dry mucus membranes

A

Dehydration

Belle Phase 2a (14 decks)

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