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GASTRO Flashcards

1
Q

Causes of acute UGIB

A

• Peptic ulcer disease (PUD) 35–50%.
• Gastroduodenal erosions 8–15%.
• Oesophagitis 5–15%.
• Mallory–Weiss tear 15%.
• Varices 5–10%.
• Other: upper GI malignancy, vascular malformations. Consider also facial trauma,
nose bleed, or haemoptysis as causes of swallowed blood.

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2
Q

Symptoms of upper GI bleed

A

Haematemesis, or melaena, dizziness (especially postural), fainting, abdominal pain, dysphagia?

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3
Q

Sx of upper GI bleed

A

Hypotension (in young may be pos- tural only), tachycardia (not if on beta-blocker), reduced JVP, reduced urine output, cool and clammy, signs of chronic liver disease (p260), eg telangiectasia, purpura, jaundice (biliary colic + jaundice + melaena suggests haemobilia). NB: ask about previous GI problems, drug use, alcohol.

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4
Q

UGIB: what do you need to ascertain first in management?

A

ABCDE
Is the patient shocked?
• Cool and clammy to touch (especially nose, toes, fingers) reduced capillary refill.
• Pulse >100bpm, JVP not visible
• Systolic BP <100mmHg or postural drop (>20mmHg on standing).
• Urine output <30mL/h.

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5
Q

UGIB: if patient is in shock what is the immediate management?

A

Protect airway and keep NBM Insert two large-bore cannulae (14–16G)
Urgent bloods: FBC, U&E, LFT, glucose, clotting screen, crossmatch 6 units
Rapid IV crystalloid infusion up to 1L
If signs of grade III or IV shock (p805) give blood Group specific or O Rh–ve until crossmatch done
Otherwise slow crystalloid infusion1 to keep lines open
Transfuse as dictated by haemodynamics
Correct clotting abnormalities Vitamin K, FFP, platelet concentrate
Consider referral to ICU or HDU, and consider CVP line to guide fluid replacement. Aim for >5cmH2O CVP may mislead if there is ascites or CCF
Catheterize and monitor urine output. Aim for >30mL/h
Monitor vital signs every 15min until stable, then hourly
Notify surgeons of all severe bleeds
Urgent endoscopy for diagnosis ± control of bleeding
• Within 4 hours if variceal bleeding
• Within 12–24 hours if patient unstable on admission

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6
Q

Why should you avoid saline in decompensated patients?

A

Avoid saline in patients with decompensated liver disease (ascites, peripheral oedema) as it worsens ascites and, despite a low serum sodium, patients have a high body sodium. Use whole blood or salt-poor albumin for resuscitation, and 5% dextrose for maintenance.

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7
Q

Symptoms of upper GI bleed

A

Haematemesis, or melaena, dizziness (especially postural), fainting, abdominal pain, dysphagia?

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8
Q

Sx of upper GI bleed

A

Hypotension (in young may be pos- tural only), tachycardia (not if on beta-blocker), reduced JVP, reduced urine output, cool and clammy, signs of chronic liver disease (p260), eg telangiectasia, purpura, jaundice (biliary colic + jaundice + melaena suggests haemobilia). NB: ask about previous GI problems, drug use, alcohol.

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9
Q

UGIB: what do you need to ascertain first in management?

A

ABCDE
Is the patient shocked?
• Cool and clammy to touch (especially nose, toes, fingers) reduced capillary refill.
• Pulse >100bpm, JVP not visible
• Systolic BP <100mmHg or postural drop (>20mmHg on standing).
• Urine output <30mL/h.

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10
Q

UGIB: if patient is in shock what is the immediate management?

A

Protect airway and keep NBM Insert two large-bore cannulae (14–16G)
Urgent bloods: FBC, U&E, LFT, glucose, clotting screen, crossmatch 6 units
Rapid IV crystalloid infusion up to 1L
If signs of grade III or IV shock (p805) give blood Group specific or O Rh–ve until crossmatch done
Otherwise slow crystalloid infusion1 to keep lines open
Transfuse as dictated by haemodynamics
Correct clotting abnormalities Vitamin K, FFP, platelet concentrate
Consider referral to ICU or HDU, and consider CVP line to guide fluid replacement. Aim for >5cmH2O CVP may mislead if there is ascites or CCF
Catheterize and monitor urine output. Aim for >30mL/h
Monitor vital signs every 15min until stable, then hourly
Notify surgeons of all severe bleeds
Urgent endoscopy for diagnosis ± control of bleeding
• Within 4 hours if variceal bleeding
• Within 12–24 hours if patient unstable on admission

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11
Q

Why should you avoid saline in decompensated patients?

A

Avoid saline in patients with decompensated liver disease (ascites, peripheral oedema) as it worsens ascites and, despite a low serum sodium, patients have a high body sodium. Use whole blood or salt-poor albumin for resuscitation, and 5% dextrose for maintenance.

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12
Q

Causes of dysphagia

A

Mechanical block
Malignant stricture
Oesophageal cancer Gastric cancer Pharyngeal cancer
Benign strictures
Oesophageal web or ring
Peptic stricture
Extrinsic compression
Lung cancer
Mediastinal lymph nodes Retrosternal goitre Aortic aneurysm
Left atrial enlargement Pharyngeal pouch
Motility disorders
Achalasia (see opposite) Diffuse oesophageal spasm Systemic sclerosis (p554)
Neurological
bulbar palsy Pseudobulbar palsy Wilson’s or Parkinson’s disease Syringobulbia
Bulbar poliomyelitis Chagas’ disease Myasthenia gravis
Others
Oesophagitis (reflux or Candida/HSV) Globus (=“I’ve got a lump in my throat”: try to distinguish from true dysphagia)

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13
Q

Rx Candidiasis

A

Nystatin suspension 100,000U (1mL swill and swallow/6h) or amphotericin lozenges. Fluconazole for oropharyngeal thrush.

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14
Q

What is leukoplakia

A

an oral mucosal white patch that will not rub off and is not attributable to any other known disease. It is a premalignant lesion, with a transformation rate, which ranges from 0.6% to 18%. Oral hairy leucoplakia is a shaggy white patch on the side of the tongue seen in HIV, caused by EBV.

When in doubt, refer all intra-oral white lesions

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15
Q

What must you ask patients presenting with dysphagia?

A

1 Was there difficulty swallowing solids and liquids from the start?
Yes: motility disorder (esp if non-progressive, eg achalasia, CNS, or pharyngeal causes). No: Solids then liquids: suspect a stricture (benign or malignant).
2 Is it difficult to make the swallowing movement?
Yes: Suspect bulbar palsy, especially if patient coughs on swallowing.
3 Is swallowing painful (odynophagia)?
Yes: Suspect cancer, oesophageal ulcer (benign or malignant), Candida (eg immu- nocompromised or poor steroid inhaler technique) or spasm.
4 Is the dysphagia intermittent or is it constant and getting worse? Intermittent: Suspect oesophageal spasm.
Constant and worsening: Suspect malignant stricture.
5 Does the neck bulge or gurgle on drinking?
Yes: Suspect a pharyngeal pouch

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16
Q

Signs of dysphagia

A

Is the patient cachectic or anaemic? Examine the mouth; feel for supraclavicular nodes (left supraclavicular node = Virchow’s node—suggests intra-abdominal malignancy); look for signs of systemic disease, eg systemic sclerosis (p554), CNS disease.

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17
Q

Dysphagia Ix

A

Bloods:
FBC (anaemia); U&E (dehydration);

Imaging
CXR (mediastinal fluid level, no gastric bubble, aspiration).

Upper GI endoscopy ± biopsy—in high dysphagia, precede by barium swallow for pharyngeal pouch (± ENT opinion).
2nd-line: video fluoroscopy to identify dysmotility, eg achalasia.
Oesophageal manometry if barium swallow is normal.

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18
Q

Causes of dysphagia

A 
Oesophagitis 
Diffuse oesophageal spasm
Achalasia
Benign oesophageal stricture
Oesophageal cancer
CNS causes
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19
Q

Describe referred pain, citing appendicitis as an example

A

May share pathways/routes of travel with other sensory nerves

CNS confuses location/origin of signal

‘Assumes’ pain is of dermatomal (skin) origin

For example, with the appendicitis:

Visceral afferent nerves travel with T10-11 nerves

Brain misinterprets origin of signal

Pain perceived to originate from T10-11 dermatome (umbilicus)

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20
Q

What are alarm symptoms associated with dyspepsia?

A
  • dysphagia
  • weight loss
  • vomiting
  • anorexia
  • haematemesis or melaena.

Patients aged ≥55 years who demonstrate these features have a higher possibility of significant gastrointestinal pathology and should be investigated on an urgent basis.

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21
Q

Ulcers: causes

A

infections, e.g. herpes simplex, erythema multiforme (Steven–Johnson syndrome), etc.; other ulcerations of the gastrointestinal tract, e.g. coeliac disease, regional ileitis (Crohn disease), ulcerative colitis, disseminated (or systemic) lupus erythematosus, Behçet disease, etc.; squamous cell carcinoma and other less common tumours; and trauma including ill-fitting dentures.

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22
Q

Causes of vomiting

A

•Gastrointestinal disease

  • Small bowel obstruction
  • gastric outflow tract obstruction
  • gastroenteritides

•Sepsis

  • Gastroenteritis (Campylobacter)
  • urinary tract infection (E. coli), biliary sepsis (E. coli)

•Drugs

  • Opiates
  • antibiotics e.g. clarithromycin
  • chemotherapy
  • levodopa

•Poisoning

  • Paracetamol
  • alcohol excess
  • digoxin and aminophylline toxicity

•Metabolic

  • Uraemia
  • hypercalcaemia
  • diabetic ketoacidosis

•CNS disease

  • Raised intracranial pressure
  • vestibular disorders e.g. motion sickness
  • migraine

•Reflex – severe pain

  • Myocardial infarction
  • biliary colic

•Pregnancy
-Hyperemesis gravidarum

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23
Q

Define the cluster of symptoms used to describe the cause of dyspepsia

A

reflux-like dyspepsia (heartburn-predominant dyspepsia)

ulcer-like dyspepsia (epigastric pain relieved by food or antacids)

dysmotility-like dyspepsia (nausea, belching, bloating and premature satiety).

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24
Q

How does the site of pain change between paired and unpaired structures?

A

Pain from an unpaired structure, such as the pancreas, is midline and radiates through to the back. Pain from paired structures is felt on and radiates to the affected side, e.g. renal colic.

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25
Q

How will your differentials change in males compared to females?

A

Boys with abdominal pain may have torsion of the testis. In women, consider gynaecological causes, e.g. ruptured ovarian cyst, pelvic inflammatory disease, endometriosis or an ectopic pregnancy.

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26
Q

How does the character of inflammation and colicky pain differ?

A

Inflammation usually produces constant pain exacerbated by movement or coughing. Colicky pain arises from hollow structures, e.g. small or large bowel obstruction, or the uterus during labour. It lasts for a short period of time (seconds or minutes), eases off and then returns.

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27
Q

What are the common patterns of radiation?

A
  • Pain radiating from the right hypochondrium to the shoulder or interscapular region may reflect diaphragmatic irritation, e.g. in acute cholecystitis.
  • Pain radiating from the loin to the groin and genitalia is typical of renal colic.
  • Central upper abdominal pain radiating through to the back, partially relieved by sitting forward, is common in pancreatitis.
  • Central abdominal pain, which later shifts into the right iliac fossa, occurs in acute appendicitis.
  • The combination of severe back and abdominal pain may indicate a ruptured or dissecting abdominal aortic aneurysm.
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28
Q

Faeculent vomiting is a sign of what?

A

late feature of distal small-bowel or colonic obstruction

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29
Q

What is ascites?

A

Ascites is an accumulation of fluid in the peritoneal cavity.

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30
Q

What is an exudate and what does it signify?

A

Exudates from the peritoneal membrane have a higher protein content than transudates and indicate inflammatory or malignant disease

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31
Q

Causes of mouth ulcers

A
  • Idiopathic aphthous ulceration (most common)
  • Gastrointestinal disease:

–Inflammatory bowel disease
–Coeliac disease

•Infection:

–Viral – herpes simplex virus (HSV), human immunodeficiency virus (HIV), Coxsackie
–Fungal – candidiasis
–Bacterial – syphilis, tuberculosis

•Systemic disease:

–Reactive arthritis (see p. 686)

–Behçet syndrome

–Systemic lupus erythematosus

•Trauma:

–e.g. Dentures

•Neoplasia:
–e.g. Squamous cell carcinoma

•Drugs:
–In erythema multiforme major, toxic epidermal necrolysis
–Chemotherapy, antimalarials

•Skin disease:
–Pemphigoid
–Pemphigus
–Lichen planus

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32
Q

Which virus causes oral cancers?

A

Human papillomavirus 16

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33
Q

Pre malignant lesions in the mouth

A

leucoplakia (single adherent white patch), lichen planus, submucous fibrosis and erythroplakia (a red patch)

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34
Q

Management of squamous cell carcinoma in the mouth

A

Treatment is by surgical excision, which may require extensive neck dissection to remove involved lymph nodes and/or radiotherapy. Ablative treatment with photodynamic therapy is being pioneered for early lesions.

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35
Q

What is the origin of the malignant tumours of the mouth?

A

Malignant tumours of the mouth account for 1% of all malignant tumours in the UK. The majority develop on the floor of the mouth or lateral borders of the tongue.

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36
Q

What is leucoplakia associated with?

A

Persistent white patches can be due to leucoplakia, which is associated with alcohol and (particularly) smoking; it is pre-malignant. A biopsy should always be taken;

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37
Q

histology of leucoplakia will show what?

A

histology shows alteration in the keratinization and dysplasia of the epithelium

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38
Q

What is glossitis and what is it associated with?

A

Glossitis is a red, smooth, sore tongue associated with vitamin B12, folate, iron, riboflavin and nicotinic acid deficiency. It is also seen in infections due to Candida.

39
Q

What are some diseases of the salivery glands?

A

•Dry mouth (xerostomia):
–Sjögren syndrome
–Drugs (e.g. antimuscarinic, anti-parkinsonian, lithium, tricyclics, monoamine oxidase inhibitors (MAOIs))
–Radiotherapy
–Psychogenic
–Dehydration
•Acute sialadenitis:
–Viral (e.g. mumps)
–Bacterial (e.g. Staphylococcus, Streptococcus)
•Salivary duct obstruction:
–Calculus
•Sarcoidosis (see pp. 1118–1120)
•Neoplasms (3% of all tumours worldwide):
–Pleomorphic adenoma (15% become malignant and can cause VII lower motor neurone signs)

40
Q

Cells lining the oeseophagus? How does the change in the stomach-how is this recognised?

A

The oesophagus is lined by stratified squamous epithelium, which extends distally to the squamocolumnar junction where the oesophagus joins the stomach, recognized endoscopically by a zigzag (‘Z’) line, just above the most proximal gastric folds.

41
Q

What is the most common cause of vitamin B12 deficiency?

A

Vitamin B12 deficiency is caused by the malabsorption of vitamin B12. The commonest cause is pernicious anaemia. There is atrophic gastritis leading to a failure in the production of intrinsic factor. This is an autoimmune condition and is associated with other autoimmune diseases, such as thyroid disease and vitiligo.

42
Q

What is pernicious anaemia often linked to?

A

gastric carcinoma

43
Q

What can cause a reduction in iron absorption?

A

High dietary content of phosphates and phytate (in chapatti flour) can inhibit iron absorption by forming insoluble complexes.

44
Q

What causes an increase in iron absorption?

A

pregnancy and iron-deficiency anaemia

45
Q

What are the two main plexi of nerves in the alimentary system?

A
  • The submucosal plexus or Meissner plexus on the outer edge of the submucosa adjacent to the circular muscle layer
  • The myenteric plexus or Auerbach plexus lying between the circular and the longitudinal muscle layers.
46
Q

What does Cholecystokinin do?

A

↑ Enzyme secretion

↑ Contraction

47
Q

Where is Gastrin produced? What does it do?

A

G cells, antrum of stomach

Parietal cells in the body of the stomach ↑ Acid secretion
Enterochromaffin-like cells ↑ Histamine secretion
Gastrointestinal mucosa ↑ Growth

48
Q

What is xerostomia?

A

Dry mouth

Disease of the salivary glands may lead to impaired secretion of saliva, giving rise to xerostomia (dry mouth).

49
Q

What is Sjögren syndrome?

A

Sjögren syndrome is an autoimmune condition in which saliva-secreting cells are destroyed. There may be associated parotid gland enlargement, with ensuing dry mouth. Dry eyes, skin and vagina are also clinical features. This condition can occur in association with other systemic autoimmune diseases (e.g. rheumatoid arthritis, thyroid disease, etc.). Difficulty with swallowing because of the lack of lubrication and mouth ulcers and oral infections may be a manifestation of systemic disease.

50
Q

What is water brash?

A

‘Water brash’ is a symptom in which there is a sudden inflow of saliva into the mouth, but without the stimulation of food. This is sometimes associated with peptic ulceration and inflammatory bowel disease.

51
Q

Anti-emetics H1 receptor antagonist

A

Cyclizine-50mg/8h PO/IV/IM-GI causes

Cinnarizine 30mg/8h PO Vestibular disorders

52
Q

Anti-emetics d2 receptor antagonist

A

Metoclopramide 10mg/8h PO/IV/IM GI causes; also prokinetic

Domperidone
60mg/12h PR; 20mg/6h PO
Also prokinetic

Prochlorperazine
12.5mg IM; 5mg/8h PO
Vestibular/GI causes

Haloperidol 1.5mg/12h PO Chemical causes, eg opioids

53
Q

Anti-emetics 5HT3 receptor antagnoist

A

Ondansetron 4mg/8h IV slowly

Doses can be much higher for, eg, emetogenic chemotherapy

54
Q

ALARMS

A

Alarm symptoms: Anaemia (iron deficiency); Loss of weight; Anorexia; Recent onset/progressive symptoms; Melaena/haematemesis; Swallowing difficulty.

55
Q

symptoms of oesophageal symptoms

A
  • Dysphagia: discomfort experienced as obstruction when swallowing solids or fluids
  • Odynophagia: pain when swallowing
  • Heartburn: retrosternal pain experienced as a burning sensation that may spread to the neck and across the chest, often worse in the supine position or when bending over
  • Reflux: when food or liquid regurgitates into the mouth without any rise in intra-abdominal pressure (as in vomiting).
56
Q

Major risk factors for duodenal ulcer

A

H. pylori (90%); drugs (NSAIDS; steroids; SSRI)

57
Q

Minor risk factors for duodenal ulcer

A

increased Gastric acid secretion; increased gastric emptying (decreased duodenal pH); blood group O; smoking. The role of stress is debated.

58
Q

Sx and symptoms of duodenal ulcer

A

Epigastric pain typically before meals or at night, relieved by eating or drinking milk. 50% are asymptomatic; others experience recurrent episodes.

Sx: epigastric tenderness

59
Q

Diagnosis of duodenal ulcer: Ix

A

Upper GI endoscopy (stop PPI 2wks before). Test for H. pylori. Measure gastrin concentrations when off PPIS if Zollinger–Ellison syndrome (p730) is suspected.

60
Q

Duodenal ulcer ddx

A

Non-ulcer dyspepsia; duodenal Crohn’s; TB; lym- phoma; pancreatic cancer

61
Q

Where do gastric ulcers commonly occur and in which population?

A

occur mainly in the elderly, on the lesser curve. Ulcers else- where are more often malignant.

62
Q

Gastric ulcers: risk factors

A

H.pylori (~80%); smoking; NSAIDS; reflux of duodenal contents; delayed gastric emptying; stress, eg neurosurgery or burns (Cushing’s or Curling’s ulcers).

63
Q

Gastric ulcer: symptoms

A

Asymptomatic or epigastric pain (related to meals ± relieved by antacids) ± weight loss

64
Q

Gastric ulcer: Ix

A

Upper endoscopy to ex- clude malignancy (stop PPI >2wks before, see FLOWCHART); multiple biopsies from ulcer rim and base (histology, H. pylori ) and brushings (cytology). Repeat endoscopy (eg if perforation or bleeding) to check healing (biopsy if suspicious of gastric ca).

65
Q

Management of gastric ulcers

A

Lifestyle: Purge stress by creating opportunities for people to move from disease into health through dialogue and reflection on their lives—eg would he/she see benefit in reduction in alcohol and tobacco use? Both will help. Avoid any aggravating foods.

H. pylori eradication: Triple therapy is 80–85% effective at eradication.

Drugs to reduce acid

If symptoms persist, re-endoscope, recheck for H. pylori, and reconsider differential diagnoses (eg gallstones).

Surgery: p626.

66
Q

Pharmacological management of gastric ulcers

A

PPIS are effective,
eg lansoprazole 30mg/24h PO for 4 (DU) or 8 (GU) wks. H2 blockers have a place
(ranitidine 300mg each night PO for 8wks).

Drug-induced ulcers: Stop drug if possible. PPIS may be best for treating and preventing GI ulcers and bleeding in patients on NSAID or antiplatelet drugs.

Misoprostol is an alternative with different SE

67
Q

Complications of gastric ulcers

A

Bleeding, perforation, malignancy, gastric outflow reduced .

68
Q

Hiatus hernia: outline the difference between rolling and sliding hiatus hernia

A

Sliding hiatus hernia (80%) is where the gastro-oesophageal junction slides up into the chest. Acid reflux often happens as the lower oesophageal sphincter becomes less competent in many cases.

Rolling hiatus hernia (20%) is where the gastro-oesophageal junction remains in the abdomen but a bulge of stomach herniates up into the chest alongside the oesophagus. As the gastro-oesophageal junction remains intact, gross acid reflux is uncommon.

69
Q

Clinical features of hiatus hernia

A

Common: 30% of patients >50yrs, especially obese women. 50% have symptomatic gastro-oesophageal reflux.

70
Q

How does excessive vomiting cause an imbalance in acid-base status?

A

leads to large losses of secreted acids from the body.

may result in metabolic alkalosis.

71
Q

How does diarrhoea cause an imbalance in acid-base status?

A

excessive loss of fluid (and hence NaHCO3) in faeces.

may result in metabolic acidosis.

72
Q

Pathophysiology of diarrhoea

A

1). Secretory diarrhoea
Increased active secretion, or an inhibition of absorption. No structural damage, e.g. cholera.

2). Osmotic diarrhoea
Loss of water due to a heavy osmotic load, e.g. in maldigestion (e.g. Coeliac disease), where the nutrients remain in lumen, in turn pulling water into the lumen.

3).Motility-related diarrhoea
Abnormally high GI motility, decreasing time available for absorption of nutrients and water. Can occur in diabetic neuropathy.

4). Inflammatory diarrhoea
Damage to the mucosal lining or brush border leads to a passive loss of protein-rich fluids, and a decreased ability to absorb these lost fluids. Caused by bacterial infections, viral infections, parasitic infections or autoimmune problems e.g. inflammatory bowel disease.

73
Q

What is the general approach in treating diarrhoea?

A

Maintenance of fluid/electrolyte balance (especially Na+ and K+).
Anti-infective agents.
Anti-diarrhoeal agents.

74
Q

What questions should you ask in the history, for a patient presenting with diarrhoea?

A

Work (is he a chef?—don’t work until an infective cause is ruled out)

Acute or chronic? If acute (<2wks) suspect gastroenteritis—any risk factors? HIV; achlorhydria, eg PA, p328, or on acid suppressants, eg PPI?
Travel?
Diet change?
Contact with D&V?
Any fever/pain?
Chronic diarrhoea alternating with constipation suggests irritable bowel (p276). Weight loss, nocturnal diarrhoea and anaemia mandate close follow-up (UC/Crohn’setc?).

75
Q

What does bloody diarrhoea indicate?

A 
Campylobacter, 
Shigella/Salmonella (p426), 
E. coli, 
amoebiasis (p436), 
UC, Crohn’s, colorectal cancer (p618), 
colonic polyps, pseudomembranous colitis, 
ischaemic colitis (p622). 
Fresh PR bleeding!
76
Q

Diarrhoea w mucus

A

occurs in IBS(p276), colorectal cancer, and polyps

77
Q

Diarrhoea w frank pus

A

suggests IBD, diverticulitis, or a fistula/abscess. White cells are microscopically absent in amoebiasis, cholera, E. coli and viruses.

78
Q

Common causes of diarrhoea

A
  • Gastroenteritis
  • Parasites/protozoa
  • IBS (p276)
  • Colorectal cancer
  • Crohn’s; UC; coeliac
79
Q

Less common causes of diarrhoea

A
  • Microscopic colitis
  • Chronic pancreatitis
  • Bile salt malabsorption • Laxative abuse
  • Lactose intolerance
  • Ileal/gastric resection
  • Overflow diarrhoea
  • Diverticular disease
  • Bacterial overgrowth
  • C. difficile (BOX)
80
Q

Non GI/rare causes of diarrhoea

A
  • Thyrotoxicosis
  • Autonomic neuropathy • Addison’s disease
  • Ischaemic colitis
  • Tropical sprue •Pellagra • Gastrinoma
  • VIPoma • Carcinoid•Amyloid
81
Q

Drugs that cause diarrhoea

A

• Antibiotics3 • PPI
• Propranolol • NSAIDS
• Cytotoxics • Digoxin • Laxatives
Alcohol

82
Q

O/E px presenting with diarrhoea, what are you looking for?

A

Dehydration—dry mucous membranes, reduced skin turgor
capillary refill >2s; shock (!think of cholera)
Any fever, weight loss, clubbing, anaemia, oral ulcers , rashes or abdominal mass or scars?
Any goitre/hyperthyroid signs? Do rectal exam for masses (eg rectal cancer) or impacted faeces (if you don’t put your finger in, you’ll put your foot in it by missing this diagnosis that never responds to codeine!)

83
Q

Initial Ix for diarrhoea

A

• Blood
FBC: reduced MCV/Fe deficiency, eg coeliac or colon ca;
MCV increased if alcohol abuse or reduced B12 absorption, eg in coeliac or Crohn’s; eosinophilia if parasites.

Raised ESR/CRP: Infection, Crohn’s/UC, cancer.

U&E: Low K+≈severeD&V.
Raised TSH:Thyrotoxicosis.

Coeliac serology.

• Stool MC&S: Bacterial pathogens, ova cysts, parasites C. diff toxin. Faecal fat excretion or 13C-hiolein (highly labelled triolein) breath test (nicer and reliable) if symptoms of chronic pancreatitis, malabsorption, or steatorrhoea

84
Q

Diarrhoea: special tests/imaging

A
  • Rigid sigmoidoscopy With biopsy of normal and abnormal looking mucosa: ~15% of patients with Crohn’s disease have macroscopically normal mucosa.
  • Colonoscopy/barium enema (malignancy? colitis?) !Avoid in acute episode. If normal, consider small bowel radiology (eg Crohn’s) ± ERCP (chronic pancreatitis).
85
Q

Hx constipation

A

Ask about frequency, nature, and consistency of stools. Is there blood or mucus in/on the stools? Is there diarrhoea alternating with constipation (eg IBS, p276)? Has there been recent change in bowel habit? Any pain?Ask about diet and drugs.

86
Q

What is barrett’s oesophagus

A

It is more common in middle-aged men and is premalignant for adenocarcinoma of the oesophagus, requiring careful surveillance with repeated endoscopy and intensive medical therapy. High-grade cases may need mucosal ablation or surgery

87
Q

What is the danger with prolonged vomiting?

A

Prolonged vomiting or aspiration of gastric juice can lead to hypo(check this) chloraemic, hypokalaemic, metabolic alkalosis. Excessive loss of alkaline intestinal fluid leads to metabolic acidosis. Death may result unless intravenous infusions of NaCl, dextrose and K+ are given. This is particularly important in hyperemesis gravidarum – prolonged vomiting in pregnancy.

88
Q

Differentiate between pain caused by reflux and cardiac ischemia pain

A

Reflux pain: burning, worse on bending, stooping or lying down
•Seldom radiates to the arms
•Worse with hot drinks or alcohol
•Relieved by antacids

Cardiac ischaemic pain
•Gripping or crushing
•Radiates to neck or left arm
•Worse with exercise
•Accompanied by dyspnoea
89
Q

Ix constipation

A

(?None in young, mildly affected patients.)

Indications for investigation: age >40yrs; change in bowel habit; associated symptoms (weight loss, PR mucus or blood, tenesmus).

Blood: FBC, ESR, U&E, Ca2+, TFT.

Sigmoidoscopy and biopsy of abnormal mucosa.
Barium enema/colonoscopy if suspected colorectal malignancy. Transit studies; anorectal physiology; biopsy for Hirschprung’s etc are occasionally needed.

90
Q

Conservative management of constipation

A

Often reassurance, drinking more, and diet/exercise advice is all that is needed. Treat causes . A high-fibre diet is often advised, but may cause bloating without helping constipation

91
Q

Bulking agents MOA

A

INCREASE faecal mass, so stimulating peristalsis. They must be taken with plenty of fluid and may take a few days to act.

92
Q

Bulking agents CI

A

difficulty in swallowing; GI obstruction; colonic atony; faecal impaction

93
Q

Bulking agents -examples

A

Bran powder 3.5g 2–3 times/d with food (may hinder absorption of dietary trace elements if taken with every meal).

Ispaghula husk, eg 1 Fybogel® 3.5g sachet after a meal, mixed in water and swal- lowed promptly (or else it becomes an unpleasant sludge).

Methylcellulose, eg Celevac® 3–6 500mg tablets/12h with ≥300mL water. S

terculia, eg Normacol® granules, 10mL sprinkled on food daily.

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