Motility of the GI System Flashcards

1
Q

Tonic vs phasic contractions

A

Tonic- maintain constant level of contraction without regular periods of relaxation - Stomach, lower esophagus, ileocecal and internal anal sphinctors
Phasic- periodic contractions followed by relaxation- esophagus, stomach, small intestine and tissues involved in mixing and propulsion

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2
Q

Slow waves

A

They are not APs
Bring membrane potential closer to threshold, number of APs on top of slow wave determine strength of contraction
Increases probability Ca channels will open in smooth muscle

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3
Q

Factors increasing amplitude of slow waves and number of APs

A

Stretch
Ach
Parasympathetics

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4
Q

Factors decreasing amplitude of slow waves and number of APs

A

NE

Sympathetics

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5
Q

Submucosal plexus

A

Controls GI secretions and local blood flow

Generate spontaneous slow wave activity

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6
Q

Myenteric plexus

A

B/w longitudinal and circular layers
Controls GI movements
Generate spontaneous slow wave activity

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7
Q

Interstitial cells of cajal

A

Pacemaker cells for GI smooth muscle
Generate and propagate slow waves
Slow waves spread rapidly to smooth muscle via gap junctions
Located in myenteric plexus (and submucosal plexus?)

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8
Q

3 phases of swallowing

A

Oral phase- voluntary
Pharyngeal phase- involuntary
Esophageal phase- involuntary- control by the swallowing reflex and enteric nervous system

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9
Q

Pharyngeal phase of swallowing

A

Soft palate is pulled upward–>epiglottis moves–>UES relaxes–>peristaltic wave of Cxs initiated in pharynx–>food propelled through open UES

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10
Q

Esophageal phase of swallowing

A

Primary/Secondary peristaltic wave
Food in pharynx–>afferent sensory input via vagus/glossopharyngeal nerve–>swallowing center in medulla–>brainstem nuclei–> efferent input to pharynx

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11
Q

Primary peristaltic wave

A

Continuation of pharyngeal peristalsis
Controlled by the medulla
Cannot occur after vagotomy

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12
Q

Secondary peristaltic phase

A

Occurs if primary wave fails to empty the esophagus or if gastric contents reflux into the esophagus
Medulla and ENS are involved
Can occur in absence of oral and pharyngeal phases
Occurs even after vagotomy

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13
Q

Achalasia- what happens

A

Difficulty getting food into stomach from esophagus
Impaired peristalsis
Incomplete relaxation of LES during swallowing, food backs up
Elevation of LES resting pressure

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14
Q

What causes those problems to happen in achalasia

A

Decreased numbers of ganglion cells in myenteric plexus
Degeneration preferentially involves inhibitory neurons involving NO/VIP
Damage to nerve sin the esophagus, preventing it from squeezing food into stomach

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15
Q

GERD - what causes

A

Changes in the barrier b/w the esophagus and stomach (e.g. LES relaxes abnormally or weakens)
Motor abnormalities that result in abnormally low pressures in LES; if intragastric pressure increases such as following a large meal, during heavy lifting or pregnancy

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16
Q

Receptive relaxation

A

Decrease pressure and increased volume of the orad region of stomach
Vagovagal reflex
CCK decrease contractions and increased gastric distensibility

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17
Q

Retropulsion

A

Peristaltic waves move food from mid stomach to antrum (caudad portion of stomach)
Wave of contraction closes the pylorus
Retropulsion is contraction in reverse direction sending gastric contents back up into stomach for further mixing and reduction of size

18
Q

Secretin and GIP effect on gastric contractions

A

Decrease AP and force of contractions

19
Q

Factors increasing rate of gastric empty time

A

Decreased distensibility of the orad stomach
Increased force of peristaltic contractions of caudad stomach
Decreased tone of pylorus
Increased diameter and inhibition of the segmenting contractions of the proximal duodenum

20
Q

Factors inhibiting gastric emptying

A

Relaxation of orad (increase in distensibility)
Decreased force of peristaltic contractions
Increased tone of pyloric sphincter
Segmentation contractions in intesine

21
Q

Entero-gastric reflex- fats vs acids vs hypertonicity in duodenum

A

Negative feedback from duodenum will slow down the rate of gastric emptying
Acid in duodenum–>stimulate secretin release–>inhibit stomach motility via gastrin inhibition
Fats in duodenum–>stimulate CCK and GIP–> inhibit stomach motility
Hypertonicity in duodenum–> unknown hormone–>inhibit gastric emptying

22
Q

Gastroparesis description and cause

A

Slow emptying of stomach/paralysis of stomach in absence of mechanical obstruction
Diabetes mellitus is common cause
Injury to vagus nerve can cause

23
Q

Migrating myoelectric complex MMC

A

Large particles of undigested residue remaining in the stomach are emptied by this complex
Periodic, bursting peristaltic contractions occurring at 90min intervals during fasting
Motilin plays significant role in mediating the complex
Inhibited during feeding

24
Q

MMC and bacterial overgrowth

A

Small intestinal bacterial overgrowth SIBO is condition of colonic bacteria overabundance in small intestine
MMC is importing for cleansing mechanisms in the small intestine and preventing SIBO

25
Q

Segmentation contractions

A

Generates back and forth movements
Produces no forward, propulsive movement along the small intestine
My guess is helps with mixing/absorption

26
Q

Slow waves in the intestine

A

Always present whether contractions are occurring or not
Unlike in stomach, slow waves do not initiate contractions in small intestine
Spike potentials (APs) are necessary for muscle contraction to occur
Slow wave frequency sets the maximum frequency of contractions

27
Q

Myenteric plexus vs submucosal (Meissner) plexus regulation

A

Myenteric plexus mainly regulates the relaxation and contraction of the intestinal wall
Submucosal plexus senses the lumen environment

28
Q

Serotonin role in regulation of peristaltic contractions

A

Serotonin is released by enterochromaffin cells and binds to receptors in the IPANs, initiating the peristaltic reflex

29
Q

Gastrin, CCK and motilin effect on contractions

A

Stimulate (as well as insulin)

30
Q

Secretin effect on contractions

A

Inhibit (as well as glucagon)

31
Q

Vomiting reflex

A

Coordinated by medulla
Nerve impulses transmitted by vagus and sympathetic afferents to brain stem nuclei
Reverse peristalsis in small intestine–>stomach and pylorus relaxation–>forced inspiration to increase abdominal pressure–>movement of the larynx–>LES relaxation–>glottis closes–>forceful expulsion of gastric contents

32
Q

Regulation of flow of contents into large intestine at ileocecal junction

A

Distention of ileum causes relaxation of the sphincter
-allows flow of contents from ileum into colon
Distention of colon causes contraction of sphincter
-prevents passage of contents from colon to ileum

33
Q

ENS innervation of large intestine

A

Concentrated beneath teneae

Innervate muscle layers

34
Q

Parasympathetic innervation of large intestine

A

Vagus- Cecum, ascending and transverse colon

Pelvic nerves: sacral portion of spinal cord S2-4: descending and sigmoid colon, rectum

35
Q

Sympathetic innervation of large intestine

A

Superior mesenteric ganglion- proximal regions
Inferior mesenteric ganglion- distal regions
Hypogastric plexus- distal rectum and anal canal

36
Q

Innervation of external anal sphincter

A

Somatic pudendal nerves

37
Q

Motility of rectum and anal canal and rectosphincteric reflex

A

If passive distention of rectum is sufficiently large, it triggers active contraction of rectal smooth muscles
Passive rectal distention also triggers relaxation of the smooth muscle of the internal anal sphincter (rectosphincteric reflex)
If defecation is not desired, the skeletal muscle of the external anal sphincter contracts by an involuntary reflex

38
Q

Rectosphincteric reflex neural control

A

Controlled partially by ENS
Reflex is reinforced by activity of neurons within the spinal cord
Sensation of rectal distention and voluntary control of the external anal sphincter are mediated by pathways within the spinal cord that lead to cerebral cortex
-Destruction of these pathways causes a loss of voluntary control of defecation

39
Q

Hirschsprung disease

A

Caused by absence of ganglion cells from segment of colon
Results in low VIP levels–>smooth muscle constriction/loss of coordinated movement–>colon contents accumulate
Present at birth, causes constipation
Newborn may present with poor feeding, jaundice, vomiting

40
Q

Vicro-vagal reflex

A

Generally stimulatory- increase motility, secretomotor, vasodilatory activities
Vagus carries both afferents and efferents

41
Q

Intestino-intestinal reflex

A

Depends on extrinsic neural connections; inhibitory

If an area of the bowel is grossly distended, contractile activity in the rest of the bowel is inhibited