Session 7 Flashcards

1
Q

What constitutes Diarrhoea

A

Loose or watery stools
More than 3 times a day
Acute = less than 2 weeks

Is a symptom

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2
Q

Pathophysiology of diarrhoea

A

Unwanted substance in gut stimulates secretion and motility to get rid of it

Primarily down to epithelial function (secretion) rather than increased gut motility

Colon is overwhelmed and cannot absorb the quantity of water it receives from ileum

There is normally 99% absorption of water from the gut

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3
Q

How much water is usually in stool per day

A

Less than 100 mls

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4
Q

How does fluid move down the GI tract under normal conditions

A

Follows osmotic forces generated by the movement of electrolytes/nutrients (paracellular/transcellular)

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5
Q

2 broad categories of diarrhoea

A
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6
Q

Concept behind osmotic diarrhoea

A

Substance in gut that cannot be broken down easily

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7
Q

Concept behind secretory diarrhoea

A

Toxin or bacterial infection: epithelial cells trying to flush out

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8
Q

Details of secretory diarrhoea

A

Secretory- electrolyte transport is messed up

too much secretion of ions (net secretion of chloride or bicarbonate)

Cause of diarrhoea will affect the messenger systems that control ion transport

Infectious toxins

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9
Q

Details of osmotic diarrhoea

A

Gut lumen contains too much osmotic material (malabsorption)

Ingesting material that is poorly absorbed (antacids-magnesium sulphate)

Inability to absorb nutrients (eg lactose in lactase deficiency)

Will settle if you stop consuming offending substance

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10
Q

Other causes of diarrhoea

A

Too little absorption of sodium- water and sodium stay in gut :
- Reduced surface area for absorption
- Mucosal disease/bowel resection (coeliac or inflammatory bowel disease such as Crohns)
- Reduced contact time/intestinal rush- increased peristalsis (diabetes/IBS)

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11
Q

Constipation definition

A

Suggestive if hard stools, difficulty passing stools or inability to pass stools

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12
Q

What amounts to constipation

A

In in over 25% of defacations you are having:
- straining
- lumpy or hard stools
- feeling of incomplete evacuation
- feeling of obstruction or blockage

Or if having fewer than 3 unassisted bowel movements a week

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13
Q

Risk factors for constipation

A

Female vs male 3:1
Certain mediations such as opioids or anti diarrhoea
Low level of physical activity
Increasing age (but also common in children under 4)

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14
Q

Pathophysiology of constipation

A

Normal transit constipation (often related to other psychological stressors)
Slow colonic transport
Defacation problems

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15
Q

Features of slow colonic transport causing constipation

A
  • Large colon: megacolon
  • Fewer peristaltic movements and shorter ones
  • Fewer intestinal pacemaker cells present (interstitial cells of Cajal)
  • Systemic disorders (hypothyroidism, diabetes)
  • Nervous system diseases (Parkinson’s, MS)
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16
Q

Features of defecation problems causing constipation

A

Cannot coordinate the muscles of defecation
Disorders of the pelvic floor
Disorders of anorectum

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17
Q

How does normal poo pass

A
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18
Q

Treatments for constipation

A
  • Psychological support
  • Increased fluid intake
  • Increased activity
  • Increased dietary fibre (only useful for mild constipation)
  • Fibre medication
  • Laxatives
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19
Q

Types of laxatives

A

Osmotic- magnesium sulphate, disaccharides
Stimulatory (chloride channel activators)
Stool softeners

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20
Q

Features of appendix

A

Diverticulum off caecum at L1
Complete longitudinal layer of muscle
Separate blood supply coming up through mesoappendix mesentery from the ileocolic branch of SMA

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21
Q

Difference between muscle layers of appendix and colon

A

Muscle has complete longitudinal layer

Colon has incomplete bands called teniae coli

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22
Q

Why is location of appendix important

A

Changes presentation of acute appendicitis

Retro-caecal, pelvic, sub-caecal, para-ileal

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23
Q

Broad categories of appendicitis

A

Acute (mucosal oedema)
gangrenous (transmural inflammation and necrosis)
Perforated

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24
Q

Classic explanation for appendicitis

A
  • Blockage of appendices lumen creates a higher pressure in the appendix (faecolinth, lymphoid hyperplasia, foreign body)
  • Causes venous pressure to rise (oedema in walls of appendix)
  • Harder for arterial blood to supply appendix
  • Ischeamia in walls
  • Bacterial invasion follows
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25
Q

Alternative explanation for appendicitis

A

A viral or bacterial infection causes mucosal changes that allow bacterial invasion of appendiceal walls

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26
Q

Classic presentation of appendicitis

A

<60% of cases

  • Poorly localised umbilical pain
  • Anorexia
  • Nausea/vomiting
  • Low grade fever
  • 12-24 hrs = pain moves to right iliac fossa and gets more intense
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27
Q

When may one not get right iliac fossa pain in appendicitis

A

When it is retro-caecal or pelvic, parietal peritoneum in right iliac fossa does not come into contact with inflamed appendix

Supra-pubic pain, right sided rectal or vaginal pain

Pregnancy

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28
Q

Appendicitis signs

A

Patients appear slightly ill
Slight fever/tachycardia
Generally lie quite still as peritoneum inflamed
Localised right quadrant tenderness
Rebound tenderness in right iliac fossa appears to be relatively specific

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29
Q

Where is appendix usually found anatomically

A

McBurney’s point

2/3 of the way from umbilicus to ASIS

30
Q

Appendicitis diagnosis and treatment

A

Blood tests- raised WBC very non specific
history/physical examination
Rebound tenderness in RIF
Pregnancy test/urine dip to rule out pregnancy or UTI
(Ct scan shows distended appendix that doesn’t fill with contrast)

Treatment: open appendicectomy or laparoscopic appendicectomy

31
Q

Features of Diverticulosis

A

Asymptomatic
Colon (85% in sigmoid)
Outpouchings of mucosa and submucosa herniate through the muscularis layers
Occurs along where nutrient vessels (vasa recta) penetrate the bowel wall
Thought to be caused by increased intra-luminal pressure (low fibre diet)

32
Q

What is acute diverticulitis

A

Diverticula become inflamed or perforate (+/- bleeding and abscess formation)
25% of people with diverticulitis

33
Q

What is diverticulitis disease

A

Pain but no inflammation or infection

34
Q

Pathophysiology of acute diverticulitis

A

Entrance to diverticula is blocked by faeces
Inflammation eventually allows bacterial invasion of the wall
Can lead to perforation

35
Q

Difference between complicated and uncomplicated diverticulitis

A

Uncomplicated: inflammation and small abscesses confined to colonic wall
Complicated: larger abscesses, fistula, perforation

36
Q

Symptoms of acute diverticulitis

A

Abdominal pain at site of inflammation (usually left lower quadrant)
Fever
Bloating
Constipation
Haematochezia (occasionally large amounts of blood loss)- passage of fresh blood through anus

37
Q

Signs of acute diverticulitis

A

Localised abdominal tenderness
Distension
Reduced bowel sounds
Signs of peritonitis (following perforation)

38
Q

Diagnosis of acute diverticulitis

A

Raised WBC (need pregnancy test to exclude ectopic)
Ultra sound scan
CT scan
Colonoscopy if large haematochezia
Elective colonoscopy after symptoms have settles to determine cause if unclear

39
Q

Treatment of acute diverticulitis

A

Antibiotics, fluid resuscitation, analgesia (if uncomplicated, maybe no fluids needed )

Surgery if perforation or large abscesses need to be drained (occasionally partial colectomy)

40
Q

Features of the rectum

A

12-15cm long, passes through pelvic floor
Has continuous band of outer longitudinal muscles (unlike teniae coli)
Curved shape anterior to sacrum
Parts of it covered in peritoneum, parts extra-peritoneal
Temporary storage of faces prior to defecation

41
Q

What stimulates urge to defecate

A

Stretching of rectum

42
Q

Blood supply to rectum

A

Several arteries that form a plexus

Superior rectal artery- from IMA
Middle rectal artery- from internal iliac
Inferior rectal artery- from pudendal

43
Q

venous drainage to rectum

A

Portal drainage through superior rectal vein

Systemic drainage through internal iliac vein - potential for Porto-systemic anastomosis

prone to varices

44
Q

Where is the start of the anal canal

A

Proximal border of the anal sphincter complex

45
Q

Rectum and Anal canal anatomy

A

Rectum points anteriorly
Pubo-rectalis sling changes the direction of the anatomy
Anal canal points posteriorly

46
Q

Factors required for anal continence

A
  • Distensible rectum
  • Firm bulky faeces
  • Normal anorectal angle
  • Anal cushions
  • Normal anal sphincters
47
Q

What makes up anal sphincter complex

A

Internal involuntary sphincter

External anal sphincter

48
Q

Features of internal sphincter

A

Involuntary- autonomic control
80% of resting anal pressure
Thickening of circular smooth muscle

49
Q

Features of external anal sphincter

A
  • Striated muscle
  • Deep section- upper anal canal, mixes with fibres from levator ani, joins with pubo-rectalis to form sling
  • Superficial and subcutaneous sections
  • Nerve supply from pudendal nerve
  • 20% of resting pressure
50
Q

Features of defecation reflex

A
51
Q

Features of delay

A
52
Q

Features of Defacation

A
53
Q

Features of important line in anal canal

A

Dentate line

Junction of hindgut and proctodaeum (ectoderm)

54
Q

Features of above dentate line

A

Visceral pain receptors
Columnar epithelium
Hindgut

55
Q

Features of below dentate line

A

Somatic pain receptors
Stratified squamous epithelium
Proctodaeum

56
Q

Features of anal cushions

A

Complex Venous plexuses
3+ areas of tissue
Anal continence
Connection between veins and some arteries

57
Q

What are haemorrhoids

A

Symptomatic anal cushions

58
Q

2 classifications of haemorrhoids

A

Internal or external

59
Q

Features of internal haemorrhoids

A

Most common
- Loss of CT support
- Above dentate line
- Relatively painless
- Enlarge and prolapse through anal canal
- Bleed bright red blood/pruritis

60
Q

Treatment for internal haemorrhoids

A

Increased hydration
High fibre diet
Avoid straining
Rubber band ligation
Surgery

61
Q

Grades of haemorrhoids internal

A
62
Q

Features of external haemorrhoids

A

Below dentate line

Swelling of anal cushions which may then thrombose
Very painful
Surgery has good outcome- thrombosed external haemorrhoids

63
Q

What are anal fissures

A

Linear tears in the anoderm (usually posterior midline)
Passing of hard stool (can follow diarrhoea too)
Pain on defecation (passing razor blades)
Haematochezia

64
Q

What is anoderm

A

Ectodermal derived, stratified squamous

65
Q

Underlying causation of anal fissure

A

High internal anal sphincter tone
Reduced blood flow to anal mucosa

66
Q

Treatment for anal fissures

A

Hydration
Dietary fibre
analgesia
Warm baths
Medication to relax the internal anal sphincter

67
Q

Common causes of haematochezia in order of most common to least

A
  • Diverticulitis
  • Angiodysplasia
  • Colitis (IBD, infective)
  • Colorectal cancer
  • Anorectal disease (haemorrhoids, anal fissure)
  • Upper GI bleeding (large bleed with fast transit)
68
Q

What is angiodysplasia

A

Small vascular malformation in bowel wall

69
Q

Features of malaena

A

Black tarry stools
Offensive smelling
Due to Hb being altered by digestive enzymes and gut bacteria

70
Q

Common causes of Malaena

A

Upper GI bleeding:
- peptic ulcer disease
- Variceal bleeds
- Upper GI malignancy
- Oesophageal/gastric cancer

71
Q

Uncommon causes of malaena

A

Gastritis
Meckel’s diverticulum
Iron supplements