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BRS 2 > gastroenterology > Flashcards

gastroenterology Flashcards

1
Q

what is the range of the cervical oesophagus?

A

upper oesophageal sphincter to sternal notch (between 15-20cm on the whole tract)

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2
Q

what kind of muscle is present in the cervical oesophagus?

A

skeletal

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3
Q

what is the range of the upper thoracic oesophagus?

A

20-25cm

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4
Q

what is the range of the middle thoracic oesophagus?

A

25-30cm

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5
Q

what kind of muscle is present in the upper and middle thoracic oesophagus?

A

skeletal and smooth

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6
Q

what is the range of the lower thoracic oesophagus (oesophageogastric junction)?

A

30-40cm

until lower oesophageal sphincter

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7
Q

what is the range of the abdominal oesophagus?

A

40-45cm

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8
Q

which levels does the oesophagus run between?

A

C5 - T10

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9
Q

what are the 4 anatomical contributions to the lower oesophageal sphincter?

A

3-4 cm distal oesophagus within abdomen

diaphragm surrounds LOS (left and right crus)

intact phrenicoesophageal ligament

angle of His

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10
Q

what is the benefit of having 3-4 cm of the distal oesophagus within the abdomen?

A

increased abdominal pressure extrinsically compresses lower oesophageal sphincter to maintain seal

lower oesophageal sphincter pressure increases in proportion to increase intra-abdominal pressure

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11
Q

what is the advantage of the diaphragm surrounding the lower oesophageal sphincter?

A

left and right diaphragm wrap around oesophagus (crus), meet phrenicoesophageal

action like a pair of scissors - contraction of diaphragm compresses distal oesophageal sphincter

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12
Q

what is the phrenoesophageal ligament?

A

ligament attaching oesophagus to diaphragm

extension of inferior diaphragmatic fascia

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13
Q

what is the function of the phrenicoesophageal ligament?

A

allows independent movement of diaphragm and oesophagus during respiration and swallowing

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14
Q

how can the structure of the phrenicoesophageal be described?

A

two limbs - upper and lower

upper limb - attaches oesophagus to superior surface of diaphragm

lower limb - attaches cardia region of stomach to inferior surface of diaphragm at cardiac notch of stomach

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15
Q

what is the angle of His?

A

(normally) acute angle between abdominal oesophagus and fundus of stomach at oesophagogastric junction

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16
Q

how does the angle of His help prevent GORD?

A

fundus of the stomach expanded by air

due to normal anatomy and relations of the oesophageal hiatus oesophagogastric junction structures are pushed from left to right

this pushes closed thegastroesophageal flap valve (or “rosette”)

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17
Q

what happens during stage 0 of swallowing (oral phase)?

A

chewing and saliva prepare bolus

both oesophageal sphincters constricted

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18
Q

what happens during stage 1 of swallowing (pharyngeal phase)?

A

pharyngeal musculature guides food bolus towards oesophagus

upper oesophageal sphincter opens reflexively

lower oesophageal sphincter opens by vasovagal reflex (receptive relaxation reflex)

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19
Q

what happens during stage 2 of swallowing (upper oesophageal phase)?

A

upper sphincter closes

superior circular muscle rings contract

inferior circular muscle rings dilate

sequential contractions of longitudinal muscle

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20
Q

what happens during stage 3 of swallowing (lower oesophageal phase)?

A

lower oesophageal sphincter closes as food passes through

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21
Q

how is motility of the oesophagus determined?

A

pressure measurements (manometry)

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22
Q

what is the pressure of the oesophagus during peristalsis?

A

40 mmHg

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23
Q

what is the resting pressure of the lower oesophageal sphincter?

A

20 mmHg

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24
Q

when does the lower oesophageal sphincter reach its lowest pressure?

A

decreases to <5 mmHg

during receptive relaxation

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25
Q

what effect does lowering pressure in the lower oesophageal sphincter have?

A

allows food to pass into stomach

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26
Q

what mediates the decrease in pressure in the lower oesophageal sphincter?

A

secretion by postganglionic inhibitory noncholinergic nonadrenergic neurons (NCNA, NANC, Neurocrine) in enteric nervous system

vasoactive intestinal peptide (VIP), gastrin release peptide (GRP), enkephalins

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27
Q

what are the 3 types of abnormal oesophageal contraction that can cause absence of a stricture?

A

hypermotility

hypomotility

disordered co ordination

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28
Q

what is dysphagia?

A

difficulty swallowing

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29
Q

what must be ascertained when investigating dysphagia?

A

localisation - cricopharyngeal sphincter, distal

for solid or fluid (indicates severity)

intermittent or progressive

precise or vague in appreciation

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30
Q

what is odynophagia?

A

pain on swallowing

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31
Q

what is regurgitation?

A

return of oesophageal contents from above an obstruction

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32
Q

what is reflux?

A

passive return of gastroduodenal contents to mouth

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33
Q

what is achalasia an example of?

A

condition causing hypermotility

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34
Q

what causes achalasia?

A

loss of ganglion cells in Aurebach’s myenteric plexus (lower oesophageal sphincter wall)

causes decreased activity of inhibitory NCNA neurones, cannot relax lower oesophageal sphincter

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35
Q

what are some secondary diseases that cause oesophageal motor abnormalities similar to primary achalasia?

A

Chagas’ disease (South American chronic infection with parasite Trypanosoma Cruzi)

protozoa infection

amyloid/sarcoma/eosinophilic oesophagitis

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36
Q

what is the proposed model of achalasia pathophysiology?

A

environmental trigger (chronic infection - varicella zoster, HSV-1 etc.)

maybe genetic predisposition or genetic factors including mutations

non autoimmune inflammatory infiltrates increase

promotes extracellular turnover, wound repair, fibrosis

loss of immunological tolerance

apoptosis of neurons

causes humoral response

leads to myenteric neuron abnormalities, autoimmune myenteric plexitis, vasculitis, absence of peristalsis and impaired relaxation of lower oesophageal sphincter

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37
Q

what are some symptoms of achalasia?

A

dysphagia

regurgitation of food

retrosternal pain

weight loss

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38
Q

what are some serious complications of achalasia?

A

oesophagitis, pneumonia

x28 risk of oesophageal cancer

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39
Q

how can achalasia cause oesophagitis or pneumonia?

A

aspiration of oesophageal contents containing bacteria

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40
Q

how does impaired relaxation of the lower oesophageal sphincter in achalasia have negative effects?

A

increased resting pressure of lower oesophageal sphincter

receptive relaxation sets in late and is too weak (during reflex, pressure in sphincter is higher than the stomach)

swallowed food collects in oesophagus - increased pressure throughout

oesophagus dilates, propagation of peristaltic waves ceases

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41
Q

how can the course of achalasia be described?

A

insidious onset, symptoms for many years before seeking help

progressive dilation of oesophagus

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42
Q

how is achalasia treated?

A

pneumatic dilation

weakens sphincter by circumferential stretching (sometime tearing) of its muscle fibres

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43
Q

how effective is pneumatic dilation in the treatment of achalasia?

A

70-90% initially respond

many later relapse

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44
Q

what is the surgical follow-up after failed pneumatic dilation in treatment of achalasia?

A

Heller’s myotomy - continuous myotomy, 6cm on oesophagus and 3cm onto stomach (cuts muscle to get rid of stricture)

usually followed up with Dor fundoplication for protection - anterior fundus wrapped around oesophageal exposed mucosa and sutured to right side of myotomy

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45
Q

what are the risks of surgical intervention in achalasia?

A

oesophageal and gastric perforation (difficult to cut through muscle without damaging mucosa) - 10-16%

division of vagus nerve - rare

splenic injury - 1-5% (fundus linked to spleen)

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46
Q

how could achalasia be treated endoscopically?

A

peroral endoscopic myotomy (POEM)

not as effective as surgical intervention

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47
Q

how is a peroral endoscopic myotomy carried out?

A

endoscope enders dilated oesophagus, mucosal incision

creation of submucosal tunnel

myotomy - cuts through muscle as much as necessary

closure of mucosal incision

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48
Q

what is scleroderma an example of?

A

condition causing hypomotility

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49
Q

what is scleroderma?

A

autoimmune disease

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50
Q

how does scleroderma cause hypomotility?

A

hypomotility in early stages due to neuronal defects, causes atrophy of oesophageal smooth muscle

distal peristalsis eventually stops

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51
Q

how does scleroderma cause GORD?

A

distal peristalsis eventually stops

lower resting pressure of lower oesophageal sphincter

nothing to prevent reflux into distal oesophagus

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52
Q

what is GORD due to scleroderma often associated with?

A

CREST disease

calcinosis, Raynaud’s phenomena, esophageal, sclerodactyly, telangiectasia

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53
Q

how is scleroderma treated?

A

exclude organic obstruction

improve force of peristalsis with prokinetics (cisapride)

dilatation if all else fails

(once peristaltic failure occurs, condition is irreversible)

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54
Q

what is corkscrew oesophagus an example of?

A

disordered coordination

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55
Q

what are the features associated with corkscrew oesophagus?

A

diffuse oesophageal spasm

incoordinate contractions cause dysphagia and chest pain

pressures 400-500 mmHg

severe hypertrophy of circular muscle

barium swallow shows corkscrew shape

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56
Q

how is corkscrew oesophagus treated?

A

may respond to forceful pneumatic dilation of cardia

results not as predictable as achalasia

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57
Q

what are some vascular anomalies that cause dysphagia?

A

dysphagia lusoria

double aortic arch

58
Q

how does dysphagia lusioria cause dysphagia?

A

right subclavian artery branches off aorta and goes behind oesophagus (rather than just to the right)

constricts oesophagus against trachea

59
Q

how can dysphagia lusoria be fixed?

A

reconnect subclavian artery to where it should be (branch off right common carotid)

60
Q

how does a double aortic arch cause dysphagia?

A

another arch forms a loop around the oesophagus and trachea, constriction

61
Q

how can the anatomy of oesophageal perforations be described?

A

3 areas of anatomical constriction

  • cricopharyngeal
  • aortic and bronchial (aorta and bronchus cross oesophagus)
  • diaphragmatic and sphincter (oesophagus goes through diaphragm)

pathological narrowing (cancer, foreign body, physiological dysfunction)

62
Q

what are the possible aetiologies for oesophageal perforation?

A

iatrogenic - most from endoscopies (OGD) (over half)

spontaneous rupture (Boerhaave’s) - 15%

foreign body - 12%

trauma - 9%

intraoperative - 2%

malignant - 1%

63
Q

when are OGD related oesophageal perforations more common?

A

in presence of diverticula or cancer

64
Q

what are the main iatrogenic causes of oesophageal perforations?

A

OGD - 0.03%

stricture dilatation - 0.1-2%

sclerotherapy - 1-5%

achalasia dilatation - 2-6%

65
Q

what is the commonest location for an OGD to cause oesophageal perforation?

A

cricopharyngeal muscle

66
Q

what causes spontaneous oesophageal perforation (Boerhaave’s)?

A

sudden increase in intra-oesophageal pressure with negative intra-thoracic pressure

essentially vomiting against closed glottis

67
Q

what is the commonest location for spontaneous oesophageal perforation (Boerhaave’s)?

A

left posterolateral aspect of distal oesophagus

68
Q

why can swallowing disk batteries be a problem?

A

foreign body causing oesophageal perforation

causes electric burns if stuck in mucosa

69
Q

what are some foreign bodies that may cause oesophageal perforation?

A

disk batteries

magnets

sharp objects

dishwasher tablets

acid/alkali

70
Q

what is the most likely form of trauma to cause oesophageal perforation in the neck?

A

penetrating

71
Q

what is the most likely form of trauma to cause oesophageal perforation in the thorax?

A

blunt force

72
Q

what are some signs of oesophageal perforation caused by trauma?

A

(difficult to diagnose)

dysphagia

blood in saliva

haematemesis

surgical emphysema (leakage of air causes crepitations)

73
Q

what surgeries may cause intraoperative oesophageal perforation?

A

hiatus hernia repair

Heller’s cardiomyotomy

pulmonary surgery

thyroid surgery

74
Q

what are some malignant causes of oesophageal perforation?

A

(poor prognosis)

advanced cancers

radiotherapy

dilatation

stenting

75
Q

how does oesophageal perforation present?

A

pain 95%

fever 80%

dysphagia 70%

emphysema 35%

76
Q

what investigations are done in a case of oesophageal perforation?

A

chest x-ray (chest full of fluids, gastric juices etc. - air near mediastinum if emphysema )

CT (contrast outside oesophagus)

swallow (gastrograffin)

OGD

77
Q

how is oesophageal perforation managed intitially?

A

NBM

IV fluids

broad spectrum antibiotic and antifungals

intensive care/ high dependency level care

bloods (including G&S)

tertiary referral centre

78
Q

what questions should be considered in a surgical emergency for oesophageal perforation?

A

(2x mortality if 24h delay in diagnosis)

is the perforation transmural or intramural?

where is it and on which side?

how big?

is leak well defined or diffuse?

79
Q

when should operative management not be used in oesophageal perforation treatment?

A

minimal contamination

contained

unfit

80
Q

how can oesophageal perforation be managed conservatively?

A

covered metal stent

81
Q

what are the steps for surgical management of oesophageal perforation?

A

chest drains required

primary repair optimal

  • debride tissue
  • cut through muscle to determine extent of mucosal tear
  • stich mucosa and muscle closed

may add vascularised pedicle flap (some intercostal muscle attached to artery, vein and nerve - attach over repair)

may add gastric fundus buttressing (e.g. Dor) for added strength

82
Q

what happens during an oesophagectomy?

A

only if damage is too severe for anything else - definitive solution

remove damaged parts, attach viable oesophagus to stomach

either reconstruction or oesophagostomy and delayed reconstruction

83
Q

what increases lower oesophageal sphincter pressure and inhibits reflux?

A

acetylcholine

histamine

prostaglandins (PGF2 alpha)

alpha adrenergic agonists

protein rich foods

84
Q

what decreases lower oesophageal sphincter pressure and promotes reflux?

A

beta adrenergic agonists

dopamine

prostaglandins (PGI2, PGE2)

chocolate

fat

smoking

85
Q

what causes sporadic reflux?

A

unexpected pressure on full stomach

swallowing

transient sphincter opening

86
Q

what are 3 mechanisms that protect following reflux?

A

volume clearance - oesophageal peristalsis reflex returns reflux volume

pH clearance - saliva increases pH (buffers acidity)

epithelium - barrier properties

87
Q

what factors can diminish pressure in the lower oesophageal sphincter?

A

increased frequency of transient sphincter opening (swallowing air, drinks containing CO2)

decreased volume clearance (abnormal distal oesophageal peristalsis)

slowed pH clearance (e.g. decreases salivary flow - sleep, chronic deficiency or decreased buffering capacity of saliva - smoking)

hiatus hernia (abdominal oesophagus displaced into thorax - not as much intra-abdominal pressure for sphincter closure)

direct irritation/damage to oesophageal mucosa (citrus, spice, alcohol, NSAIDs)

88
Q

how is a sliding hiatus hernia associated with GORD?

A

variable association with GORD

most patients with severe stages of GORD have a hernia

however, many with GORD do not have a hernia and many with a hernia do not have GORD

89
Q

why is an OGD carried out in a case of GORD?

A

exclude cancer

check for oesophagitis, peptic stricture, Barrett’s oesophagus

90
Q

what investigations are carried out in a case of GORD?

A

OGD

oesophageal manometry

24hr oesophageal pH recording

91
Q

what medical interventions are used in treating GORD?

A

lifestyle changes (weight loss, stop smoking, alcohol)

PPIs

92
Q

what surgical interventions are used in treating GORD?

A

dilatation peptic strictures

laparoscopic Nissen’s fundoplication (stitches tighten left and right crux around oesophagus, fundus of stomach wrapped around oesophagus - dividing blood supply from spleen)

93
Q

what are the functions of the stomach?

A

breaks food into smaller particles (acid and pepsin)

holds food, releasing it in controlled steady rate into duodenum

kills parasites and certain bacteria

94
Q

what is secreted by the stomach in the cardia and pyloric region?

95
Q

what is secreted in the body and fundus of the stomach?

A

mucus

HCl

pepsinogen

96
Q

what is secreted in the antrum of the stomach?

97
Q

where are the tubular glands of the stomach found?

A

invaginate into mucosa

98
Q

what are the 4 types of gastritis?

A

erosive and haemorrhagic

nonerosive, chronic active

atrophic (fundal gland)

reactive

99
Q

what are some causes of erosive and haemorrhagic gastritis?

A

NSAIDs (damages mucosa)

ischaemia (e.g. vasculitis, marathon running - blood diverted elsewhere)

stress (multi-organ failure, burns, surgery, CNS trauma)

alcohol abuse, corrosives

trauma (gastroscopy, foreign body, retching/vomiting)

radiation trauma

100
Q

what is the main risk of erosive and haemorrhagic gastritis?

A

acute ulcers - gastric bleeding, perforation of stomach wall

101
Q

which part of the stomach does nonerosive, chronic active gastritis usually affect?

102
Q

what causes nonerosive, chronic active gastritis?

A

Helicobacter pylori colonisation of antrum

103
Q

how does Helicobacter pylori cause gastritis?

A

diminishes mucosal protection

can stimulate antral gastrin liberation and consequently fundal gastric juice secretion, allowing development of chronic ulcers

104
Q

how can Helicobacter pylori colonisation be addressed?

A

antibiotics

amoxicillin, clarithromycin, pantoprazole - 7-14 days

105
Q

which part of the stomach does atrophic (fundal gland) gastritis usually affect?

106
Q

what causes atrophic (fundal gland) gastritis ?

A

gastric juice and plasma contain autoantibodies - (IgG, plasma cells infiltrates, B lymphocytes)
against parts and products of parietal cells (microsomal lipoproteins, gastrin receptors, carboanhydrase, H+/K+-ATPase, intrinsic factor)

causes parietal cell atrophy

causes acid and IF secretion to fall (achlorhydria)

IF antibodies block the binding of cobalamines to IF or the uptake of IF–cobalamine complexes by cells in the ileum, ultimately resulting in cobalamine deficiency with pernicious anaemia

107
Q

who can atrophic (fundal gland) gastritis cause cancer?

A

more gastrin liberated in response to cobalamine deficiency - gastrin-forming cells hypertrophy

hyperplasia of enterochromaffin-like (ECL) cells occurs, probably as a consequence of the high level of gastrin (ECL cells carry gastrin receptors, responsible for producing histamine in gastric wall)

hyperplasia can progress to a carcinoid

main danger - extensive metaplasia of the mucosa (precancerous condition) may lead to carcinoma of the stomach

108
Q

where does reactive gastritis occur?

A

surrounding of erosive gastritis, ulcers or operative wounds

109
Q

how can operative wounds cause reactive gastritis?

A

operations on antrum or pylorus may lead to enterogastric reflux

causes bile salts, pancreatic and intestinal enzymes to attack gastric mucosa

110
Q

what are the 4 mechanisms regulating gastric secretion?

A

neural

endocrine

paracrine

autocrine

111
Q

how is gastric secretion stimulated via neural mechanisms?

A

ACh

postganglionic transmitter of vagal parasympathetic fibres

muscarinic M1 receptors and via neurons stimulating gastrin release by gastrin-releasing peptide (GRP)

112
Q

how is gastric secretion stimulated via endocrine mechanisms?

A

gastrin (originates from G cells in antrum)

113
Q

how is gastric secretion stimulated via paracrine mechanisms?

A

histamine

secreted by ECL cells and mast cells in gastric wall

114
Q

how is gastric secretion inhibited via endocrine mechanisms?

A

secretin (small intestine)

115
Q

how is gastric secretion inhibited via paracrine mechanisms?

A

somatostatin

116
Q

how is gastric secretion inhibited via paracrine and autocrine mechanisms?

A

prostaglandins (PGE2, PGI2)

TGF-alpha

adenosine

117
Q

what does gastric secretion result in?

A

parietal cells produce H+ ions in gastric juice (contain H+/K+-ATPase in luminal membrane)

chief cells enrich glandular secretion with pepsinogen

118
Q

how does mucus protect the stomach?

A

mucus film (0.1-0.5mm) protects gastric epithelium (secreted by epithelial cells, depolymerized by pepsins so it can be dissolved)

prostaglandins stimulate epithelium to secrete HCO3- (enriched in liquid layer directly over epithelium, also diffuses into the mucus film, to buffer H+ penetrating from gastric lumen)

epithelium itself (apical cell membrane, tight junctions) has barrier properties to largely prevent the penetration of H+/remove H+ that has penetrated (Na+/H+ exchange carrier only basolateral) - regulated by epidermal growth factor (EGF) contained in saliva and bound to receptors of the apical epithelial membrane. glutathione-dependent, antioxidative mechanisms are also part of this cytoprotection

good mucosal blood flow is last line of defence - quickly removes H+, supplies HCO – and substrates of energy metabolism

119
Q

what are the 3 mechanisms of epithelial repair in the stomach?

A

migration

gap closed by cell growth

acute wound healing

120
Q

how does migration repair epithelial damage in the stomach?

A

adjacent epithelial cells flatten

close gap through sideways migration along basal membrane

takes ~30mins

121
Q

what stimulates cell growth to repair epithelial damage in the stomach?

A

ECF

TGF-alpha

IGF-1

GRP

gastrin

122
Q

when are acute wound healing processes initiated to repair epithelial damage in the stomach?

A

basement membrane destroyed

123
Q

what happens during acute wound healing processes to repair epithelial damage in the stomach?

A

attraction of leukocytes and macrophages

phagocytosis of necrotic cell residua

revascularization (angiogenesis)

regeneration of extracellular matrix

epithelial closure by restitution and cell division after repair of basement membrane

124
Q

how do NSAIDs (e.g. indomethacin, diclofenac, aspirin) cause ulcers?

A

anti-inflammatory and analgesic action is based on cyclo-oxygenase inhibition further blocking prostaglandin synthesis (from arachidonic acid) - in this case, in gastric and duodenal epithelia

this causes decreased HCO – secretion (weakened mucosal protection), stops inhibition of acid secretion

also damage mucosa locally by non-ionic diffusion into mucosal cells (pH of gastric juice &laquo_space;pK’ of NSAIDs)

danger of bleeding increased

125
Q

what are some things that cause acute ulcers?

A

stress

  • major surgery
  • extensive burns
  • multi-organ failure

impaired blood flow through mucosa correlate with high cortisol concentration in plasma

126
Q

what are some psychogenic factors that favour ulcer development?

A

strong emotional stress without outward “safety valve”/disturbed ability to cope with normal stress (high cortisol)

psychogenically raised gastric acid and pepsinogen secretion

stress related bad habits (smoking, alcohol, aspirin intake)

127
Q

what are some rare causes of ulcers?

A

tumours autonomically secreting gastrin (gastrinoma, Zollinger-Ellison syndrome)

systemic mastocytosis

basophilia with high plasma histamine

128
Q

how does Helicobacter pylori cause ulcers?

A

has urease to survive acidity - produces CO2 & NH3 and HCO3 & NH4 to buffer H+

causes inflammation of gastric mucosa

ulcer formation due to infection

129
Q

how does Helicobacter pylori affect the epithelium?

A

increased chemical attack by: oxygen radicals formed by bacteria themselves, leukocytes and macrophages from immune response, pepsins (H. pylori stimulates pepsinogen secretion)

gastric antrum infection frequently leads to duodenal ulcer (probably related to increased gastrin secretion due to infection) - acid and pepsinogen liberation raised, duodenal epithelium exposed to increased chemical attack

causes metaplasia of the epithelium, which favours H. pylori embedding, leading to duodenitis and increased metaplasia, etc.

130
Q

what are the clinical outcomes of Helicobacter pylori infection?

A

asymptomatic or chronic gastritis >80%

chronic atrophic gastritis, intestinal metaplasia
gastric or duodenal ulcer 15-20%

gastric cancer, MALT lymphoma <1%

131
Q

what are some surgical indications of emergency in ulcer treatment?

A

intractability after medical therapy

haemorrhage

obstruction

perforation

132
Q

what steps should be taken if ulcers don’t heal within 12 weeks?

A

change medication - observe another 12 weeks

check serum gastrin (antral G-cell hyperplasia or gastrinoma [Zollinger-Ellison syndrome])

OGD - biopsy all 4 quadrants of ulcer to rule out malignancy if refractory

133
Q

how is an ulcer treated medically?

A

PPIs, H2 blockers

antibiotics - amoxicillin, clarithromycin, pantoprazole 7-14 days

134
Q

how can the wall structure of the colon be described?

A

innermost layer - mucosa, contains mucin producing glands

  • epithelium
  • lamina propria
  • muscularis mucosae

submucosa

muscularis

  • circular muscle
  • longitudinal muscle

outermost - serosa, main vessels and nerve supply

  • areolar connective tissue
  • epithelium
135
Q

what nerves are present in the serosa of the colon?

A

submucosal plexus (Meissner’s plexus)

myenteric plexus (Auerbach’s plexus) - ganglia concentrated below taenia coli

pacemakers for the bowel

136
Q

how can the parasympathetic innervation of the lower GI tract be described?

A

vagus innervates ascending colon and most of transverse colon

pelvic nerves innervate more distally

137
Q

how can the sympathetic innervation of the lower GI tract be described?

A

lower thoracic and upper lumbar spinal cord

138
Q

which nerves control the external anal sphincter?

A

somatic motor fibres in pudendal nerves

139
Q

what is Hirschsprung’s disease?

A

no enteric intramural ganglia

140
Q

what do afferent sensory neurons in the lower GI tract detect?

141
Q

what are the 6 types of lower GI tract disorders?

A

inflammatory

  • IBD
  • microscopic colitis

infective

  • C. diff
  • E. coli (etc.)

structural

  • diverticular disease
  • haemorrhoids
  • fissures

functional
- IBS

neoplastic
- colonic polyps, colon cancer

other
- neurological, metabolic, vascular

BRS 2 (10 decks)

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