Session 7 Flashcards

(71 cards)

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
Alternative explanation for appendicitis
A viral or bacterial infection causes mucosal changes that allow bacterial invasion of appendiceal walls
26
Classic presentation of appendicitis
<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
27
When may one not get right iliac fossa pain in appendicitis
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
28
Appendicitis signs
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
29
Where is appendix usually found anatomically
McBurney’s point 2/3 of the way from umbilicus to ASIS
30
Appendicitis diagnosis and treatment
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
Features of Diverticulosis
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
What is acute diverticulitis
Diverticula become inflamed or perforate (+/- bleeding and abscess formation) 25% of people with diverticulitis
33
What is diverticulitis disease
Pain but no inflammation or infection
34
Pathophysiology of acute diverticulitis
Entrance to diverticula is blocked by faeces Inflammation eventually allows bacterial invasion of the wall Can lead to perforation
35
Difference between complicated and uncomplicated diverticulitis
Uncomplicated: inflammation and small abscesses confined to colonic wall Complicated: larger abscesses, fistula, perforation
36
Symptoms of acute diverticulitis
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
Signs of acute diverticulitis
Localised abdominal tenderness Distension Reduced bowel sounds Signs of peritonitis (following perforation)
38
Diagnosis of acute diverticulitis
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
Treatment of acute diverticulitis
Antibiotics, fluid resuscitation, analgesia (if uncomplicated, maybe no fluids needed ) Surgery if perforation or large abscesses need to be drained (occasionally partial colectomy)
40
Features of the rectum
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
What stimulates urge to defecate
Stretching of rectum
42
Blood supply to rectum
Several arteries that form a plexus Superior rectal artery- from IMA Middle rectal artery- from internal iliac Inferior rectal artery- from pudendal
43
venous drainage to rectum
Portal drainage through superior rectal vein Systemic drainage through internal iliac vein - potential for Porto-systemic anastomosis prone to varices
44
Where is the start of the anal canal
Proximal border of the anal sphincter complex
45
Rectum and Anal canal anatomy
Rectum points anteriorly Pubo-rectalis sling changes the direction of the anatomy Anal canal points posteriorly
46
Factors required for anal continence
- Distensible rectum - Firm bulky faeces - Normal anorectal angle - Anal cushions - Normal anal sphincters
47
What makes up anal sphincter complex
Internal involuntary sphincter External anal sphincter
48
Features of internal sphincter
Involuntary- autonomic control 80% of resting anal pressure Thickening of circular smooth muscle
49
Features of external anal sphincter
- 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
Features of defecation reflex
51
Features of delay
52
Features of Defacation
53
Features of important line in anal canal
Dentate line Junction of hindgut and proctodaeum (ectoderm)
54
Features of above dentate line
Visceral pain receptors Columnar epithelium Hindgut
55
Features of below dentate line
Somatic pain receptors Stratified squamous epithelium Proctodaeum
56
Features of anal cushions
Complex Venous plexuses 3+ areas of tissue Anal continence Connection between veins and some arteries
57
What are haemorrhoids
Symptomatic anal cushions
58
2 classifications of haemorrhoids
Internal or external
59
Features of internal haemorrhoids
Most common - Loss of CT support - Above dentate line - Relatively painless - Enlarge and prolapse through anal canal - Bleed bright red blood/pruritis
60
Treatment for internal haemorrhoids
Increased hydration High fibre diet Avoid straining Rubber band ligation Surgery
61
Grades of haemorrhoids internal
62
Features of external haemorrhoids
Below dentate line Swelling of anal cushions which may then thrombose Very painful Surgery has good outcome- thrombosed external haemorrhoids
63
What are anal fissures
Linear tears in the anoderm (usually posterior midline) Passing of hard stool (can follow diarrhoea too) Pain on defecation (passing razor blades) Haematochezia
64
What is anoderm
Ectodermal derived, stratified squamous
65
Underlying causation of anal fissure
High internal anal sphincter tone Reduced blood flow to anal mucosa
66
Treatment for anal fissures
Hydration Dietary fibre analgesia Warm baths Medication to relax the internal anal sphincter
67
Common causes of haematochezia in order of most common to least
- Diverticulitis - Angiodysplasia - Colitis (IBD, infective) - Colorectal cancer - Anorectal disease (haemorrhoids, anal fissure) - Upper GI bleeding (large bleed with fast transit)
68
What is angiodysplasia
Small vascular malformation in bowel wall
69
Features of malaena
Black tarry stools Offensive smelling Due to Hb being altered by digestive enzymes and gut bacteria
70
Common causes of Malaena
Upper GI bleeding: - peptic ulcer disease - Variceal bleeds - Upper GI malignancy - Oesophageal/gastric cancer
71
Uncommon causes of malaena
Gastritis Meckel’s diverticulum Iron supplements