SPR L20 Pathophysiology of GI Tract Flashcards Preview

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Flashcards in SPR L20 Pathophysiology of GI Tract Deck (31):
1

Learning Outcomes

(for general perusal)

See picture

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Summary of gastrointestinal function

List the main GI functions

  • Gut motility propels and mixes food

  • Digestion: exocrine secretion

  • Absorption

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Summary of gastrointestinal function

Give the details of the following GI functions

  1. Gut motility propels and mixes food

  2. Digestion: exocrine secretion

  3. Absorption

  1. Circular and longitudinal smooth muscle, Sphincters

  2. Breaks down complex molecules

    Organic molecules (eg enzymes, bile salts, mucus)

    HCl (stomach)/HCO3- (all other areas)

    7-8 l secreted/re-absorbed each 24hrs

  3. Large surface area: Mucosal folds, Villi, Microvilli

    Specific absorption mechanisms: 2˚ active transport (Glucose, Galactose, Amino acids)

    Facilitated diffusion (Fructose)

    Diffusion/chylomicron formation/exocytosis: Lipids

5

Symptoms/signs: gastrointestinal motility

 

  • Swallowing difficulties: dysphagia and choking
  • GORD: heartburn (indigestion/dyspepsia), regurgitation
  • Vomiting: nausea, haematemesis
  • Obstruction: pain, nausea and vomiting, constipation
  • Diarrhoea
  • Constipation
  • Faecal incontinence

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Pathophysiology of Swallowing

(Tongue/soft palate/pharynx/larynx)

Outline the Neurological conditions affecting pharynx

  • IX (sensory)
  • X +XII (motor: somatic)
  • bulbar palsy; (LMN defects IX, X+XII):
    • sensory loss and lower motoneurone defects (or muscle weakness)
    • reduced palatal sensation
    • reduced gag reflex
    • choking
    • dysphonia (recurrent laryngeal n.)
    • flaccid/wasted tongue
  • pseudobulbar palsy; (UMN defects X + XII). As for bulbar palsy except:
    • normal palatal sensation
    • normal/increased gag reflex
    • spastic tongue
    • (maybe increased jaw jerk: motor Vth n.)

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Pathophysiology of Swallowing

  1. What does Lower oesophageal obstruction lead to? 
  2. List the possible causes?

  1. dysphagia ± pain
  2.  
  • benign stricture
    • peptic (GORD), corrosives
  • oesophageal carcinoma
  • achalasia

    • failure of peristalsis

    • poor relaxation of lower oesophageal   sphincter

      • loss of inhibitory postganglionic nitrergic nerves (parasympathetic)

 

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How can Achalasia be diagnosed?

With a barium swallow

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Pathophysiology of gastro-oesophageal reflux disease (GORD)

  1. ​Outline the pathophysiology of GORD

  1. Failure of normal anti-reflux mechanisms:
  • Transient relaxation of lower oesophageal sphincter between meals
  • Loss of the flap valve effect of the intra-abdominal   oesophagus/diaphragmatic constriction
    • sliding hiatus hernia
  • Failure of mucosal defence mechanisms
    • mucus/HCO3-
    • epithelial junctional complexes

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Pathophysiology of gastro-oesophageal reflux disease (GORD)

  1. ​What are the consequences of GORD?
  2. What is it aggravated by?
  3. What does long term-scarring lead to?

  1. Acid reflux leads to oesophagitis and heartburn, Regurgitation
  2. Aggravated by increases in intra-abdominal pressure
  3. Long term scarring leads to stricture/dysphagia

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Pathophysiology of gastro-oesophageal reflux disease (GORD)

What are the principles of treatment of GORD?

  • Weight loss
  • Increase mucosal protection
    • Alginates
  • Antacids to neutralise pH
  • Reduce gastric acid
    • H2 receptor blockers
    • Proton pump inhibitors
  • Accelerate gastric emptying:
    • Dopamine antagonists (metaclopramide)

13

Pathophysiology of vomiting

  1. Where is the vomiting centre?
  2. What are the stimuli for vomiting?
  3. What are the physiological changes that take place on vomiting?
  4. What does fluid loss lead to/cause?
  5. What does HCL loss cause?

  1. Medulla oblongata
  2. Emotion, motion, circulating chemicals, Pharyngeal stimulation, gastric/duodenal irritation/distention 

  3. Oesophageal sphincters relax, glottis closes, stomach relaxes, abdominal mm./diaphragm contracts, duodenum contracts

  4. dehydration

  5. hypochloraemic alkalosis

14

Pathophysiology of bowel obstruction

Outline the symptoms arising from the small or large intestine?

 

What are the causes?

  • Paralytic ileus or mechanical obstruction
  • Colicky pain
  • Nausea/vomiting/constipation
  • Dehydration
  • Abdominal distension
  • Increased bowel sounds
  • X-ray: dilated bowel loops and fluid levels

Causes:

  • Lumen (eg foreign object)
  • Wall (eg tumour)
  • Outside wall (eg adhesions)
  • Ileus (no bowel sounds ± pain)

15

Pathophysiology of diarrhoea

  1. Define
  2. What can cause increased motility?
  3. What can malabsorption be caused by?
  4. When can there be inflammation (blood diarrhoea)?
  5. What can increased secretions be brought about?

  1. Organic causes, stool weight >250 g/day

  2. Viral gastroenteritis

    Hyperthyroidism

    Diabetic autonomic neuropathy

  3. Osmotic diarrhoea

  4. Infective, eg shigella, Inflammatory bowel disease

  5. Enterotoxins - Vibrio cholerae, E.coli, C.difficile

         Bile salts and fatty acids (ileal   resection)

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Pathophysiology of constipation

  1. Define constipation?

  2. What is Normal transit time?

  3. What is Slow transit time?

  1. 2 or more of following for >12 weeks:
  • <3 stools/week
  • straining > 25%
  • hard stools
  • incomplete evacuation
  • anorectal blockage by stools

2. <6 days: 60% cases, perception of constipation from straining and hard stools

3. >6 days: 15% - mainly young women, onset after puberty, often <1 stool/week

 

 

17

Pathophysiology of constipation

  1. What are defactory disorders?
  2. What is megacolon?
    1. What are the causes?

  1. Defecatory disorders: 25% - Contraction external anal sphincter during straining, Anterior rectocele, Rectal mucosal prolapse during straining

  2. Dilated colon

    1. Hirschprung’s disease - aganglionic segment rectum, failure of relaxation of internal sphincter

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Pathophysiology of constipation

How is constipation managed?

  • Refer defecatory disorders
  • Increase dietary fibre and fluid
  • Laxatives in severe cases or for acute relief
    • Bulk-forming
    • Stimulant
    • Osmotic
    • Suppositories
    • Enemas

19

Physiology of defecation

  1. Outline the Int. Anal Sphincter
  2. Outline the Ext. Anal Sphincter

  1. Smooth m., parasympathetic innervation 
  2. Striated muscle, somatic innervation

See picture

20

Pathophysiology of faecal incontinence

Give examples of the following causes of faecal incontinence

  1. Neurological/Psychological 
  2. Anal sphincter dysfunction
  3. Other causes

  1. spinal trauma (S2-S4)

    stroke

    pudendal nerve damage

    spina bifida

    MS

    dementia

  2. sphincter damage, eg during childbirth

    pudendal nerve damage

    perineal descent

  3. rectal prolapse

    impaction with overflow

    severe diarrhoea

21

Pathophysiology of salivary glands

How can a dry mouth be caused?

 

 

 

  • Sjögren’s syndrome
  • drugs
    • antimuscarinic
    • antihistamines
    • antiparkisonian
    • tricyclics
  • dehydration, shock
  • Salivary duct obstruction
    • Calculus

22

Physiology of gastric acid secretion

​Outline the following

  1. Control of acid secretion
  2. mechanisms involved in acid secretion

See picture

23

Pathophysiology of peptic ulcer disease

  1. What is the main clinical feature?
  2. What are the complications?

  1. Break in the epithelial surface of the stomach or duodenum down to muscularis mucosae. Epigastric pain and nausea
  2. bleeding: haematemesis/melaena                  perforation

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Pathophysiology of peptic ulcer disease

Outline the pathogenesis of the following...

  1. Duodenal ulcer
  2. Gastric Ulcer

3. Outline the treatment of PUD

  1. H. pylori plus increased acid, reduced bicarbonate, genetic susceptibility
  2. pan gastritis, decreased acid, reduced mucosal resistance

  3. H. pylori eradication

    antacids/alginates

    reduce acid secretion

     - PPI

     - H2 receptor blocker

25

Pathophysiology of malabsorption

How can failure of DIGESTION come about?

  • deficiency of digestive enzymes
    • pancreatic failure (lipase, amylase, protease, etc)
      • cystic fibrosis
      • chronic pancreatitis
    • specific deficiencies
      • lactose intolerance
  • bile salt deficiency
    • failure of lipid digestion/absorption
      • bile duct obstruction
      • bacterial overgrowth
      • ileal resection

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Pathophysiology of malabsorption

How can failure of ABSORPTION come about?

  • reduced surface area small intestine
    • coeliac disease (gluten enteropathy)
      • sub-total villous atrophy
  • intestinal resection
    • jejunal resection (limited effect)

    • ileal resection

      • reduced enterohepatic recirculation of bile salt

        • bile salt deficiency

        • bile salt diarrhoea

        • gallstones

      • reduced B12 absorption

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Pathophysiology of malabsorption

What are the consequences of malabsorption?

  • diarrhoea/steatorrhea
  • weight loss/failure to thrive
  • abdominal pain
  • micronutrient deficiencies:
    • Fe2+-deficiency (microcytic anaemia)
    • B12 deficiency (macrocytic anaemia)
    • Fat soluble vitamin deficiency with fat malabsorption:
      • Vit A: night blindness
      • Vit D: osteomalacia
      • Vit E: haemolysis, neurological deficit
      • Vit K: clotting deficiency

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Pathophysiology of malabsorption

Consequences of malabsorption

  • diarrhoea/steatorrhea
  • weight loss/failure to thrive
  • abdominal pain
  • micronutrient deficiencies​​

Outline the micronutrient deficiencies that can occur...

In particular, what do the following fat soluble vitamine deficiency with fat malabsorption cause?

  1. Vit A
  2. Vit D
  3. Vit E
  4. Vit K

  • Fe2+-deficiency (microcytic anaemia)
  • B12 deficiency (macrocytic anaemia)
  • Fat soluble vitamin deficiency with fat malabsorption
  1. clotting deficiency
  2. haemolysis, neurological deficit
  3. osteomalacia
  4. night blindness

29

Pathophysiology of malabsorption

What are the principles of management of malabsorption?

  • treat underlying disorder
    • gluten exclusion
    • treat bacterial overgrowth
  • supplement deficient enzymes
    • pancreatic deficiency
  • limit fat intake with steatorrhoea
  • treat micronutrient deficiencies
    • B12, Fe2+, etc
  • bypass digestion (elemental diet)
  • bypass absorption (parenteral nutrition) 

30

Pathophysiology of GIT bleeding

  1. What are the causes of upper GIT bleeding?
  2. What are the consequences of an acute upper GI bleed?

  1. Reflux oesophageus, Mallory - weiss syndrome, varices, gastric varices, Gastric and Duodenal Ulcer, Gastric carcinoma (uncommon), Haemorrhagic gastropathy and erosions, hereditary telangiectasia (uncommon)
  2. haemetemesis (shock, CV collapse) and melaena (black, tarry stools)

31

Pathophysiology of GIT bleeding

  1. What are the causes of lower GIT bleeding?
  2. What are the consequences of an acute lower GI bleed?
  3. What are the consequences of chronic GI bleedin?

  1. Carcinoma of caecum, Meckel's Diverticulum, Diverticula, Angiodysplasia (occult), ischaemic colitis (less common), Carcinoma, polyps (small bleeds bu frequent), Colitis, Crohn's Ulcerative Colitis, solitary ulcer of rectum, Haemorrhoids (common with smaller recurrent bleeds), Anal fissue (common) -  see picture
  2. fresh or altered blood clots

  3. microcytic anaemia (Fe2+ deficiency)

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