Smooth Muscle Flashcards
Where in the GI tract is there skeletal muscle?
pharynx, top third of oesophagus, external anal sphincter
What are the two types of smooth muscle in the GI tract? Where is each type found?
phasic = rapid contraction and relaxation, body of oesophagus, antrum, small and large intestines tonic = sustained contractions, sphincters (LOS, IC, IAS), upper stomach
What are the interstitial cells of CAJAL?
What is the characteristic of their resting membrane potential?
What are they coupled to and how?
Pace-making cells - an intrinsic property of the ICC based on their ionic conductances.
They are electrically coupled to the smooth muscle cells through low resistance gap junctions, allowing the spread of the slow wave
Spontaneous oscillating membrane potential is key to the cells of CAJAL
ELECTRICAL ACTIVITY OF THE SMOOTH MUSCLE FIBRES
What stimulates depolarisation of the smooth muscle fibres? What does this initiate?
What stimulates hyperpolarsastion of the smooth muscle? What is the purpose of this?
Stretch, ACh, parasympathetics
- Elicits a depolarising event, spans a theoretical threshold, generation of AP’s
Noradreanaline, sympathetics
- Lower membrane potential further away from the threshold.
What is the difference in appearance of tonic and phasic activity on an electrical activity monitor?
tonic goes up and plateaus, sustained contraction
phasic up and down
Consider the role of Ca2+ on smooth muscle contraction
Ca2+ influx
Binds to calmodulin protein
Activates myosin light chain kinase
Requires ATP to phosphorylate myosin –> interacts with actin to mediate a contractile event
How is relaxation initiated in smooth muscle?
How is relaxation maintained?
Need to dephosphorylate myosin
Do this by myosin light chain phosphatase
Suppress contractile events.
Also sequester Ca2+ in SR to prevent stimulation of contraction.
VIP mediates PKA pathway to phosphorylate myosin light chain kinase, cannot bind to calmodulin, cannot initiate contraction.
Describe how the contraction controlled through Ca2+.
The cell may extrude Ca2+ via the Na-Ca exchange of a Ca2+ pump but this would deplete intracellular calcium.
Instead Ca2+ is sequestered in the SR (mediated by SERCA-type Ca2+ pump) is the most important mechanism by which the cell returns Ca2+ to its resting levels
What are the major excitatory and inhibitory neurotransmitters?
What are some other forms of control?
Excitatory = ACh
Inhibitory = VIP and NO
Hormones released from endocrine cells into blood can also act via circulation
Regulation also by the enteric nervous system
What are the types of movement in the GIT:
- Propulsive movements –>
- Non-propulsive movements –>
- Interdigestive –>
peristalsis
segmentation
migrating motor complex (MMC)
What are the 3 pathologies of GIT motility?
- Hirchsprungs disease = congenital lack of neuronal ganglionic cells in the ENS plexi
- Chagas disease = infectious disease of a parasitic nature, resulting in the signification reduction in the number of ganglionic cells in the ENS
- Achalasia = dramatic reduction in the number of neuronal cells in the lower oesophageal segment, failure to relax
- What is the embryology of Hirschsprung disease?
- What is the consequence of Hirschsrungs?
- What are the symptoms?
- arrest of cranio caudal migration of vagal neural crest cells in the hindgut.
EAS always involved, classified by aganglionic distance up colon - Prevents propulsion of the faecal stream –> megacolon and hypertrophy of normal proximal colon
- vominting, consitpation, abdominal distention, intestinal obtruction, failure to pass meconium in newborns, male predominance, more common in disorders such as Down’s syndrome and Waardenburg syndrome
How to you evaluate a patients in Hirschsprungs?
What is the treatment?
plain abdominal radiography - contrast enema
rectal manometry - pressure changes in anal canal
biopsy - absence of ganglion cells, hypertrophy, hyperplasia of nerve fibres
Treatment = removal of aganglionic segment and subsequent anastomosis
- What is the parasite that lead to Chaga’s disease?
- What 2 systems does it primarily affect?
- What areas of GIT are affected?
- What are the 3 pathological features of the colon?
- Trypanosoma cruzi
- Cardiologic and gastrointestinal manifestations
- Primarily affects oesophagus and colon but can be entire GIT
- Degeneration and decreased number of intrinsic myenteric neurones, defecting of interstitial cells of CAJAL, ganglion cell damage by T lymphocytes
- What is the clinical presentation of achalasia?
- How is it diagnosed?
- What is the treatment?
1. solid dysphagia postprandial regurgitation chest pain weight loss 2. plain film radiography, barium swallow, birds beak endoscopy to rule out tumours oesophageal manometry 3. gold standard is surgical myotomy pneumatic dilation botulinum toxin nitrates and calcium channel blockers
