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S3: Gastrointestinal > 7b.) Distal GI Tract Pathology > Flashcards

7b.) Distal GI Tract Pathology Flashcards

1
Q

What is diarrhoea?

A

Stools are loose and or/regular

  • Loose or watery
  • More than 3 times a day
  • Acute diarrhoea (< 2 weeks)
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2
Q

What percentage of water is reabsorbed by small intestine and colon?

A

99%

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3
Q

Describe the generic pathophysilogy of diarrhoea

A

Unwanted substance in gut stimulates secretion and motility to get rid of it; diarrhoea is primary down to the secretion rather than increased gut motility. Colon is overwhelmed and cannot absorb the quntity of water it receives from the ileum.

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4
Q

State the two broad categories of diarrhoea

A
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5
Q

State roughly how much water is reabsorbed in each part of small and large intestine

A
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6
Q

Describe 2 main mechanisms of secretory diarrhoea

A

Excessive secretion of anions

  • Whatever is causing diarrhoea (e.g. infectious toxins) affects messenger control system that controls ion transport
  • Excessive secretion of Cl- and HCO3- into lumen
  • Water follows

Reduced/inhibition of reabsorption of Na+

  • Less Na+ absorbed, less water follows
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7
Q

Secretory diarrhoea can be due to excessive secretion of anions (Cl- and HCO3-) or reduced reabsorption of Na+; state some likely causes of each

A
  • Excessive secretion of anions:
    • Infection
  • Reduced reabsorption of Na+:
    • Reduced surface area due to mucosal disease e.g. coeliac or bowel resection e.g.crohn’s disease
    • Reduced contact time (intestinal rush) e.g. due to diabetes, IBS
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8
Q
A
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9
Q

Describe why osmotic diarrhoea occurs

How can you stop it?

A
  • Gut lumen contains too much osmotic material due to malabsorption; malabsorption may occur because:
    • Person has ingested material that’s poorly absorbed e.g. antacids like magnesium sulfate
    • Inability to absorb nutrients e.g. lactose intolerance

Stop it by not ingesting the offending substance

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10
Q

What is constipation?

A

You have hard stools, difficulty passing stools or an inability to pass stools

*Having fewer than 3 unassited bowel movements per week

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11
Q

State some risk factors for constipation

A
  • Female vs male (3:1)
  • Certain medications
  • Low level physical activity
  • Increasing age (but also common in children under 4)
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12
Q

Constipation can be classed as primary or secondary; state some primay and secondary causes

A

Primary (defects in colonic function)

  • Normal transit constipation
  • Slow transit constipation
  • Evacuation disorder

Secondary (drug or underlying medical condition)

  • Medications
  • Physical obstrction
  • Metabolic & endocrine disorders
  • Neurological & myopathic disorders
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13
Q

Primary constipation can be divided into:

  • Normal transit constipation
  • Slow colonic transport
  • Defaecation problems

… state some causes of each

A

Normal transit constipation

  • Related to psycholgoical stressors

Slow colonic transport

  • Megacolon
  • Fewer and shorter peristaltic movements
  • Fewer intestinal pacemaker cells present (interstitial cells of Cajal)
  • Systemic disorders (e.g. hypothyroidsim, DM)
  • Nervous system disease (e.g. parkinsons, MS)

Defaecation problems

  • Cannot coordinate muscles of defaecation often due to disorders of pelvic floor or anorectum
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14
Q

State 6 possible treatments for diarrhoea

A
  • Psychological support
  • Increased fluid intake
  • Increased activity
  • Increased dietary fibre (only useful for mild constipation)
  • Fibre medication
  • Laxatives
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15
Q

State, and describe, 5 types of laxatives

A
  • Stool bulking agents: increase stool bulk by drawing water around their fibres (need adequete fluid intake)
  • Osmotic laxatives: increase osmotic pressure in lumen and draw water into lumen
  • Stool softners: these liquids are retained in stool and help with ease of passage of stool
  • Stimulants: stimulate mucosal enteroendocrine cells which in turn stimulate motility and fluid secretion
  • Specific receptor agonists & antagonists: stimulate motility
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16
Q

Give an example of each of the types of laxatives

A
  • Stool bulking agents: fibres supplements
  • Osmotic laxatives: magnesium sulphate, dissaccharides
  • Stool softners: liquid paraffin, arachis oil
  • Stimulants: sena
  • Specific agonists and antagonists: 5HT4 agonists
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17
Q

What does this x-ray show?

A
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18
Q

Describe the longitudinal muscle layer around the appendix

A

Has a complete longitudinal layer of muscle (unlike caecum which has teniae coli)

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19
Q

Describe the blood supply of the appendix

A

Appendicular artery which is a branch of the ileocolic branch of SMA- gets to appendix via mesoappendix (mesentery of appendix)

*Important to note it has a separate blood supply to caecum

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20
Q

The appendix isn’t always in one position; state some possible positions it can be in

A
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21
Q

What is appendicitis?

A

Inflammation of the appendix

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22
Q

Describe the 3 broad classifications/categories of appendicitis

A
  • Acute (mucosal oedema)
  • Gangrenous (transmural inflammation and necrosis)
  • Perforated
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23
Q

There are 2 explanations for the cause of appendicitis (classical and alternative); explain the classical explanation for the cause of appendicitis

A
  • Appendix lumen blocked by faecolith, lymphoid hyperplasia or foreign body
  • Increases intraluminal pressure in appendix
  • This causes venous pressure in appendix to rise leading to mucosal oedema
  • Mucosal oedema makes it harder for arterial blood supply to supply appendix
  • Ischaemia of walls of appendix
  • Ischaemia allows bacterial invasion of appendix wall
  • Necrosis and/or perforation occurs
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24
Q

There are 2 explanations for the cause of appendicitis (classical and alternative); explain the alternative explanation for the cause of appendicitis

A

A viral or bacterial infection causes mucosasl changes that allow bacterial invaseion of appendiceal walls

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25
Q

What % of appendicitis cases follow a classical presentation?

A

<60%

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26
Q

Describe the classical presentation of appendicitis; include symptoms and signs

A

Symptoms

  • Poorly localised peri-umbilical pain (irritate visceral peritoneum)
  • Anorexia
  • Nausea/vomitting
  • After 12-24 hours pain felt more intensely in right iliac foss (irritate parietal peritoneum)

Signs

  • Low grade fever
  • Tachycardia
  • Slightly ill
  • Localised right quadrant tenderness
  • Rebound tenderness in right iliac fossa
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27
Q

State and explain a potential cause of an atypical presentation of appendicitis

A

Appendix in different position e.g. retro-caecal or pelvic position as this means it won’t come into contact with the parietal peritoneum overlyng the right iliac fossa. May get supra-pubic, right sided rectal or vaginal pain

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28
Q

Why is appendicitis often difficult to diagnose in children and pregnancy?

A
  • Children: symptoms are much more non-specific
  • Pregnancy: anatomy altered
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29
Q

Describe how you can diagnose appendicitis

A
  • Blood tests: raised WBC
  • History/physical examination: may be classic presentation & rebound tenderness
  • Pregnancy test: rule out pregnancy
  • Urine dip: rule out UTI
  • CT scan: appendix doesn’t fill with contrast
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30
Q

Describe the treatment for appendicitis

A

Appendicectomy (either open or laparoscopic)

31
Q

What is diverticulosis?

Where does it often occur in GI tract?

A

Mucosa and submucosa herniate through muscularis propria (called pseudo-diverticula)

Occurs where nutrient vessels (vasa recta) penetrate bowel wall as these are areas of weakeness. 85% in sigmoid colon.

32
Q

Diverticula are thought to be casued by….?

A

Increased intraluminal pressure (a low fibre diet could cause this)

33
Q

What is average size of diverticula?

A

3-10mm

34
Q

Describe difference between:

  • Diverticulosis
  • Diverticular diseae
  • Acute diverticulitis
A
  • Diverticulosis: diverticula are present but patient asymptomatic
  • Diverticular disease: diverticula cause symptoms such as pain
  • Acute diverticulitis: diverticula inflamed or infected
35
Q

What is acute diverticulutis?

Describe the pathophysiology of acute diverticultiis

A

Inflammation and/or infection of a diverticulum

Similar pathophysiology to appendicitis:

  • Entrance to diverticula is blocked by faeces
  • Increases pressure in diverticula
  • Venous pressure increases causing oedema in walls
  • If blocks arterial supply can lead to ischaemia
  • Inflammation allows bacterial invasionof wall of diverticula
  • This can lead to perforatoin
36
Q

Describe:

  • Uncomplicated diverticulitis
  • Complicated diverticulitis
A
  • Uncomplicated: inflammation & small abcesses confined within colonic wall
  • Complicated: larger abcesses, fistula, perforations
37
Q

State symptoms and signs of diverticulitis

A

Symptoms

  • Abdo pain (usually left lower quadrant as usually in sigmoid colon)
  • Fever
  • Bloating
  • Constipation (inflammation can block colonic lumen)
  • Haematochezia (fresh blood often mixed with stool)

Signs

  • Localised abdomen tenderness
  • Distension
  • Reduced bowel sounds
  • Signs of peritonitis (if perforated)
38
Q

How would you diagnose diverticulitis?

A
  • Blood tests: increased WBC
  • Pregnancy test: rule out pregnancy
  • Ultrasound
  • CT scan
  • Colonoscpy if large haematochezia
  • Elective colonoscopy (after symptoms have settled to reduce risk of perforation during procedure)
39
Q

How do you treat acute diverticulitis- include treatment for uncomplicated and complicated?

A

Uncomplicated:

  • Antibiotics
  • Fluid resucitation
  • Analgesia

Complicated:

  • Large abcess need to be drained
  • Surgery for perforation- may consider partial colectomy
40
Q

How long is the rectum?

Describe the structure of the rectum

A

12-15cm

  • Continous band of longitudinal muscle
  • Curved shape anterior to sacrum
  • Some parts intra- and some parts extraperitoneal
41
Q

State the role of rectum in defaecation

A

Acts as temporary storage; stretching of rectum then stimulates urge to defaecate

42
Q

Describe the arterial blood supply to the rectum

A

Blood supply is from several arteries that form a plexus:

  • Superior rectal artery (continuation of IMA)
  • Middle rectal artery (branch of internal iliac)
  • Inferior rectal artery (branch of pudenal artery)
43
Q

Describe the venous drainage of the rectum

A
  • Upper 1/3 drain into superior rectal vein which drains into portal vein
  • Middle & lower 1/3 drain into systemic venous system via inferior rectal vein draining to interal iliac
44
Q

Describe the structure/anatomy of the anal canal, include:

  • Where anal canal extends from and to
  • Which direction anal canal points (and relate this to direction of rectum)
  • What muscle causes direction change
A
  • Starts at proximal border of anal sphincter complex and extends to anus
  • Anal canal points posteriorly, rectum points anteriorlu
  • Puborectalis sling changes direction
45
Q

The anal canal is involved in continence; state 4 features of anal canal required for continence

A
  • Distensible rectum: otherwise pressure would increase and exceed pressure anal sphincter can withstand
  • Normal anorectal angle
  • Anal cushions
  • Normal anal sphincters
46
Q

Describe the anal sphincter complex (what sphincters is it made of)

A

Includes an internal involuntary sphincter (80% of resing anal pressure) and an external voluntary sphincter (20% of resting anal pressure)

47
Q

Describe the structure of the internal anal sphincter, include the type of muscle and it’s neuronal control

A
  • Thickening of circular smooth muscle
  • Autonomic control
48
Q

Describe the structure of the external anal sphincter, include:

  • Different sections
  • Nerve supply
A

Has 3 sections all made of striated muscle:

  • Deep
    • Upper anal canal
    • Mixes with fibres from levator ani
    • Joins with puborectalis to form sling
  • Superficial
  • Subcutaneous

Nerve supply from pudendal nerve

49
Q

Describe the process of defaecation

A
50
Q

Describe the gastrocolic reflex

A

Stomach activity, in response to food and drink, leads to ileocaecal relaxation and increased musuclar activity in gut to cause mass movement

51
Q

Where is the dentate line?

Describe how both epithelium and pain receptors changes either side of the dentate line

A

Dentate lin is junction of hindgut and proctodaeum (ectoderm)

  • Above dentate line:
    • Visceral pain receptors
    • Columnar epithelium
  • Below dentate line:
    • Somatic pain receptors
    • Stratified squamous epithelium
52
Q

Describe what anal cushions are

A

Three cushions of loose connective tissue arranged circumferentially above dentate line; they contain a venous plexus (haemorrhoidal plexus)- but there are some connections to some arteries also. Venous plexus can dilate to help aid with continence.

53
Q

State, and briefly describe, the two classes of haemorrhoids

A
  • Internal: above dentate line and are covered in columnar or transitional mucosa
  • External: below dentate line and are covered in stratified squamous epithelium
54
Q

Which is most common, internal or external haemorrhoids?

A

Internal

55
Q

Describe how internal haemorrhoids form

A
  • Loss of connective tissue support in anal cushions above dentate line
  • Veins in venous plexus enlarge and prolapse through anal canal due to lack of support
56
Q

Describe presentation of someone with internal haemorrhoids

A
  • Bright red blood after you poo
  • Pruritis of anus
  • Relatively painless
57
Q

Describe treatment for internal haemorrhoids

A
  • Increased hydration/fibre in diet (to try and soften stools to reduce trauma to haemorrhoids as this can cause bleeding)
  • Avoid straining
  • Rubber band ligation
  • Surgery to remove or put them back inside
58
Q

Describe the 4 grades of internal haemorrhoids

A
59
Q

Describe how external haemorrhoids form

A
  • Swelling of anal cushions extending below the dentate line
  • Represent residual redundant skin from previous episodes of haemorrhoid inflammation
  • Visible at anal verge
  • Very painful if thrombose
60
Q

Describe the presentation of someone with external haemorrhoids that are NOT thrombosed

A
  • Lump around anus
  • Usually asymptomatic: no pain or bleeding
  • Pruritis
  • Hygience difficulty due to redundant folds of skin
61
Q

Describe the typical presentation of someone with thrombosed external haemorrhoids

A
  • Visible lump
  • Very painful
62
Q

How would you treat external haemorrhoids?

A

Surgery to remove

63
Q

What is an anal fissure?

When do they typically occur?

What causes them?

A

Linear tear in andoderm (usually the posterior midline)

Typically occur following passage of large, hard bowel movement.

Underlying causes which can increase risk of anal fisure are high interal anal sphincter tone and reduced blood flow to anal mucosa

64
Q

Describe symptoms of anal fissure

A
  • (severe) pain of defaecation
  • Haematochezia
65
Q

Describe the management of anal fissures

A
  • Increased fibre & water (soften, increase ease of passing stools)
  • Warm baths
  • Medication to relax anal sphincter
66
Q

Most anal fissures resolve on their own; true or false

A

True

67
Q

State some causes of haematochezia, starting with most common firsst

A
  • Diverticulitis
  • Angiodysplasia (small vascular malformation in bowel wall)
  • Colitis e.g. UC, infections
  • Colorectal cancer
  • Anorectal disease e.g. haemorrhoids, anal fissure
  • Upper GI bleeding e.g. large bleed with fast transit
68
Q

What % of upper GI bleeding is caused by peptic ulcers?

A

40%

69
Q

What is melaena?

Why does it have it’s characteristic appearance?

A
  • Black, tarry, offensive smelling stools associated with upper GI bleeding
  • Hb has been modified by gut bacteria
70
Q

State some common causes of upper GI bleeding

A
  • Peptic ucler disease
  • Variceal bleeds
  • Upper GI maligancy
  • Oesophageal/gastric cancer
71
Q

State some uncommon causes of melaena

A
  • Gastritis
  • Meckel’s diverticulum
72
Q

State one non-pathological cause of melaena

A

Fe supplements

73
Q

Why are internal haemorrhoids painless?

A

Because they originate above pectinate line and there is only somatic innervation below the pectinate line

S3: Gastrointestinal (18 decks)

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