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B3 > Physiology Week 1 > Flashcards

Physiology Week 1 Flashcards

1
Q

What are the three parts of the pharynx?

A

nasopharynx, oropharynx, and laryngopharynx

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2
Q

Describe how the nasopharynx blocks passage of food into the lungs

A

At the base of the nasopharynx there is a soft palate and penduluous uvula that block passage of food into the lungs

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3
Q

Describe how the oropharynx prevents large particles from entering the lung

A

The mucous layer of the oropharynx traps any large particles in the air that we breathe - instead of entering the lung, pass with the mucous into the stomach

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4
Q

What is the pharynx?

A

Wiki says: The pharynx (plural: pharynges) is the part of the throat that is behind the mouth and nasal cavity and above the esophagus and the larynx, or the tubes going down to the stomach and the lungs.

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5
Q

The laryngopharynx is a common pathway that allows both air as well as food to pass through the lungs and stomach. What happens when the air goes to the stomach? What about when food goes to the lungs?

A

air in stomach - burp

food in lungs - cough

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6
Q

Describe swallowing AKA deglutination

A

1) In buccal phase, the tongue presses against the hard palate, and the food bolus is forced into the oropharynx
2) In the pharyngeal-esophageal phase, the uvula and larynx rise to prevent food from entering the nasal cavity/trachea. The tongue blocks off the mouth.
- The upper esophageal sphincter relaxes and food enters the esophagus.
- during this phase, respiration is inhibited via reflex
3) The constrictor muscles of the pharynx contract, and food is forced down esophagus. The upper esophageal sphincter contracts after food enters.
4) Persistalsis moves food to the stomach.
5) The gastroesophageal sphincter surrounding the cardial oriface opens and food enters the stomach,

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7
Q

Which muscle is a major contributor to the upper esophageal sphincter high pressure zone?

A

cricopharyngeal muscle (skeletal)

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8
Q

Pharyngeal muscles contract to push food bolus into esophagus. What are the two muscular layers of the pharynx?

A

outer circular

inner longitudinal

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9
Q

Describe the three outer circle muscles of the pharynx and their function

A

Inferior, middle, superior constrictors

During swallowing, these muscles constrict to push food downwards.

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10
Q

Describe the three inner longitudinal muscles of the pharynx and their function

A

stylopharyngeus, salpingopharyngeus, palatopharyngeus

during swallowing, these shorten and widen the pharynx

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11
Q

True/False: All of the pharyngeal muscles are innervated by CNX.

A

False - all but the stylopharyngeus which is innervated by CNIX (glossopharyngeal)

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12
Q

True/False: The swallowing center is located in the medulla and each half controls the ipsilateral side

A

True

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13
Q

The major peripheral sensory inputs to the swallowing center are carried by which three nerves?

A

1) maxillary branch of TRIGEMINAL (V)
2) GLOSSOPHARYNGEAL (IX) on posterior 1/3 of tongue, tonsil, pharynx, middle ear
3) VAGUS (X) superior laryngeal branch

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14
Q

The motor output of the swallowing center is via the motor branches of which 5 nerves?

A

1) trigerminal (V)
2) facial (VII0
3) glyossopharyngeal (IX)
4) vagus (X)
5) hypoglossal (XII)

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15
Q

What is oropharyngeal dysphasia and what causes it (2 factors)?

A

Oropharyngeal dysphasia is the failure of the normal propulsion of the bolus from the mouth to the esophagus.

Caused by failure of the driving fore (propulsion) or an obstruction to flow

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16
Q

What occurs in oropharyngeal dysphasia when:

a) the muscles that move larynx are weakened
b) the muscles around the soft palate or the superior pharyngeal constrictors are weakened

A

a) aspiration [food enters larynx]

b) regurgitation into the nose

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17
Q

Describe four sources of failure of propulsion (driving force) that would lead to oropharyngeal dysphasia

A

brain, cranial nerve, myoneural junction, muscle

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18
Q

Describe two sources of obstructions that would lead to oropharyngeal dysphasia

A

mass effect, incomplete UES sphincter relaxation

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19
Q

Describe four diseases that cause muscle weakness leading to oropharyngeal dysplasia

A

CVA, poliomyelitis, myasthenia gravis, dermatomyositis

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20
Q

Describe two diseases that would lead to obstructions to flow

A

tumor or abscess

cricopharyngeal achalasia [failure of relaxation of muscle around UES]

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21
Q

Describe the cause and symptoms of dermatomyositis

A

dermatomyositis is a acquired muscle dz/inflamm myopathy.
Cause is UNK, thought to be viral
Sx: difficulty swallowing, muscle weakness, stiffness or soreness; purple or violet upper eyelids; purple-red skin rash, SOB

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22
Q

Describe the types of muscle found in the esophagus and the related diseases.

A

Cervical esophagus and top of thoracic includes the upper esophageal sphincter, skeletal muscle
dz: polymyositis, myasthenia gravis

Lower 2/3 includes thoracic and abdominal parts and contains the lower esophageal sphincter, smooth muscle
dz; scleroderma and achalasia

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23
Q

Describe primary peristalsis in the esophagus.

When do the sphincters open?

A

Primary peristalsis is triggered by swallowing.
The lower esophageal sphincter relaxes before the propagating contraction.
When a person swallows, tension receptors stimulation contraction in the pharynx which coincides with relaxation of UES and LES. They remain relaxed until the wave reaches them.

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24
Q

Describe the latency of esophageal contractions.

A

In normal persistalsis, there is an increasing latency period for each subsequent contraction.
The contractions are thought to be controlled by excitatory motor neurons, whereas the latency is thought to be controlled by activation of inhibitory motor neuron.

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25
Q

Describe what happens to esophageal contractions when an NO Blocker or an NO Blocker plus Atropine is added.

A

When an NO blocker is given, the latency gradient disappears, suggesting that inhibitory motor neurons release NO prior to contractile wave.

When NO blocker and atropine [antimuscarinic agent] given, this results in simultaneous and low-amplitude contractions suggesting that excitatory cholingeric motor neurons release Ach to activate muscarinic receptors and produce contraction.

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26
Q

Describe the intrinsic and extrinsic sphincters located in the lower esophagus.

A

intrinsic - smooth muscle LES
extrinsic - crural diaphragm (skel muscle)

anatomically superimposed on each other and anchored by the phrenoesophageal ligament

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27
Q

Describe neural control of esophageal peristalsis in the proximal portion (upper 1/3) of the esophagus

A

skeletal muscle
Innervated by somatic lower motor neurons whose cell bodies are located in the brain stem’s nucleus ambiguous (NA)
vagus nerves from the NA release Ach where they activate nicotinic receptors to produce relaxation followed by contraction

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28
Q

Describe neural control of esophageal peristalsis in the more distal portion (lower 2/3) of the esophagus

A

smooth muscle
innervated by vagal pregang fibers whose cells bodies are found in the dorsal motor nucleus (DMN)
- synapse with neurons whose cells body are located in the MYENTERIC PLEXUS
vagus nerves from the DMN release Ach that activates nicotinic receptors

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29
Q

Describe the action of atropine/NO synthase inhibitors in the proximal esophagus vs the distal esophagus

A

In the proximal esophagus, increases the latency of contraction
In the distal esophagus, decreases the latency of contraction

Overall increases the speed of contraction

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30
Q

Briefly describe the difference between primary and secondary peristalsis

A

primary - initiated by swallowing, medulla
secondary - initiated by esophageal distension, local enteric reflexes

[THIS IS VERY SIMPLE VERSION]

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31
Q

Describe the contractions secondary peristalsis

A

Triggered by distention in smooth muscle portion of the esophagus
Contraction nearer to the mouth is followed by a descending pressure wave that coordinates LES opening.

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32
Q

Describe the enteric nervous system’s role in secondary peristalsis

A

Upon distension, intrinsic sensory neurons in the myenteric plexus activate both ascending excitatory nerve pathways and descending inhibitory nerve pathways within the myenteric plexus.
Ascending interneurons activate excitatory motor neurons that release Ach to smooth muscle leading to contraction above the bolus.
Descending interneurons activate inhibitory motor neurons that release NO and VIP to cause relaxation of smooth muscle below the bolus

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33
Q

Describe the evidence that shows LES relaxation is strictly neurogenic. [2 drugs]

A

Tetrodotoxin (TTX) blocks LES relaxation - TTX acts strictly on neurally-mediated responses but has no effect on smooth muscle.

Hexamethonium also blocks LES relaxation. This is a nicotinic receptor antagonist.

Overall, vagal stimulation is what relaxes LES.

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34
Q

What is the major inhibitory neurotransmitter in LES relaxation?

A

nitric oxide

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35
Q

What occurs to peristalsis when NO is blocked?

A

latency prior to esophageal contraction shortens
basal LES pressure inc
LES relaxation abolished

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36
Q

Describe three symptoms of esophageal/LES dysfunction

A

1) gastroesophageal reflux symptoms
2) dysphagia [failure of propulsive force, obstruction to flow, in coordination of contraction and relaxation]
3) esophageal pain (non-cardiac)

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37
Q

Describe GERD, its causes, and risk factors

A

LES does not close all the way allowing reflux of food, liquid, and stomach acid which causes symptoms and may damage the esophagus.

Risk factors - EtOH, hiatal hernia, obesity, pregnancy, scleroderma, smoking

Certain medications can bring it on or make it worse, examps are TCAs, anticholinergics, beta blockers, bronchodilators

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38
Q

Describe a hiatal hernia including its symptoms

A

A hiatal hernia occurs when part of your stomach pushes upward through your diaphragm

Many have no symptoms, but some have GERD

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39
Q

Describe Barrett’s esophagus

A

Change in the normal lining of the esophagus to a lining similar to the lining of the stomach
Basically, squamous –> columnar mucosa
GERD damages squamous lining and then through metaplasia, squamous cells are replaced by columnar cells.
Goblet cells are needed to dx

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40
Q

Why is Barrett’s esophagus a cause for concern?

A

Can lead to esophageal cancer, which only has a 5% recovery rate

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41
Q

What causes erythema seen in Barrett’s esophagus?

A

hyperemia (inc in blood flow) of capillaries under and in the mucosa

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42
Q

Esophageal causes are the second most common causes of chest pain after cardiac. Describe the three basic steps in diagnosing non-cardiac chest pain.

A

1) rule out cardiac cause
2) trial of proton pump inhibitors
3) if no improvement, send for pH monitoring vs manometry vs upper endoscopy

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43
Q

Describe the autoimmune component of myasthenia gravis and how this disease is treated

A

The immune system destroys neuromuscular junctions [motor end plates, and therefore the Ach receptors located there]
Leads to failure of pharyngeal propulsion
Therapy involves stopping this immune rxn and prolonging Ach activity [immunosuppressants and Achesterase inhibitors]

fun fact- myasthenia commonly involves bulbar innervated muscles

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44
Q

Describe esophageal achalasia

A

Rare disease where the LES fails to relax. Leads to difficulty swallowing food.

Characterized by incomplete LES relaxation, inc LES tone, and lack of peristalsis of the esophagus.

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45
Q

Describe nutcracker esophagus

A

disorder of the movement of the esophagus

super strong contractions that are very painful

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46
Q

Describe parasympathetic innervation of the GI tract

A

cranial and sacral regions of spinal cord innervate via vagal and pelvic nerves

vagus innervates most of tract and gut via nicotinic and muscarinic receptors

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47
Q

True/False: The biggest parasympathetic innervation to GI tract is from muscarinic receptors

A

FALSE - nicotinic

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48
Q

Describe sympathetic innervation of the GI tract

A

innervates through thoracic and lumbar regions of spinal cord via celiac, superior, mesenteric and inferior mesenteric ganglia

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49
Q

Describe the preganglionics of the GI tract

A

cholinergic forming nicotinic synapses post ganglionic noradrenergic nerves

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50
Q

Describe ENS innervation to the GI tract

A

innervates through neurons that lie within the wall of the GI tract and is as an independent integrative system

innervate all regions of GI tract

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51
Q

Describe the effector control mechanisms regulated by the enteric nervous system (4)

A

1) contraction of muscle coats
2) secretion
3) absorption across the mucosal lining
4) blood flow inside the walls of the GI tract

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52
Q

True/False: The gut has the highest concentration of serotonin in the body

A

True

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53
Q

Name the three types of cells involved in the enteric nervous system

A

1) motor neurons (excitatory, inhibitory)
2) afferent/sensory neurons
3) interneurons (ascending, descending)

54
Q

Describe the four functions of the enteric nervous system (reflexes and motor patterns)

A

1) peristaltic reflex= coordinating activity, ascending contraction and descending relaxn
2) accommodation= relaxing to fit food
3) segmentation = allows for adeq abs of nutrients
4) migrating motor complex = clearing of non-digestible materials to colon

55
Q

True/False: There are more neurons in your GI tract than in your spinal cord

A

True

56
Q

Where is the myenteric plexus located in the GI tract?

A

between the outer longitudinal and inner circular layers (ICOL)

There is a second ganglia in the submucosa called the submucosal plexus also

57
Q

What are the gut’s equivalent to Schwann cells?

A

enteric glial cells

58
Q

True/False: There are only myelinated nerves within enteric ganglia

A

FALSE - both myelinated and unmyelinated.

Most are unmyelinated though.

59
Q

What is the main role of the myenteric plexus?

A

control activity of longitudinal and circular muscle layer

60
Q

What is the main role of the submucous plexus? How many layers are found in humans?

A

The submucous plexus (closer to the mucosa} modulates blood flow and secretion from cells in the mucosa. Three layers in humans.

61
Q

True/False: There are neurons that inerconnect the myenteric and submucosal plexus

A

True

62
Q

True/False: The musculature of the GI tract is inner circular outer longitudinal

A

TRUE

63
Q

The inferior muscularis mucosae in the GI tract acts to regulate ______ activity

A

villi

64
Q

What two GI motility behaviors does the stomach exhibit?

A

accommodation, antral peristalsis

65
Q

What three GI motility behaviors does the small intestine exhibit?

A

peristalsis, mixing, segmentation

66
Q

What two motility behaviors does the colon exhibit?

A

haustral movements, propulsion

67
Q

What are the three types of receptors located in the GI tract?

A

1) mechanoreceptors - muscle, mucosal
2) chemoreceptors - acid, osmotic, AA, lipid, glucose
3) thermoreceptors

68
Q

Muscular distortion of the GI tract will impart force (pressure on gut contents). Describe the changes with storage/accommodation and flow/propulsion

A

1) storage/acommodation=reduced force, dec intraluminal P

2) flow/propulsion=inc force, inc intraluminal P

69
Q

Many GI motor patterns generate ______ movement of contents. This mixes food thoroughly with secretions and exposes the mucosa to food located t/o the diameter of the GI tract

A

turbulent

70
Q

True/False: Sphincters exhibit stationary contraction/relaxation

A

True

71
Q

Describe three types of propagating contraction/relaxation

A

peristalasis
propulsion
migrating motor complex

72
Q

True/False: Segmentation is a mixed form of contraction/relaxation

A

True

73
Q

Propagating contractions exhibit descending ______ during peristalsis

A

inhibition

74
Q

The gastric _____ allows for accommodation to occur

A

fundus [relaxes]

75
Q 
what happens to the
a) gastric volume
b) compliance
c) gastric tone
during gastric accommodation
A

gastric volume and compliance inc

gastric tone dec

76
Q

Gastric accommodation is _____ mediated by the substance ____

A

vagally, NO

77
Q

The contractile activity of the stomach propagates from _______ to _____, which allows for digestion and break of material to occur

A

corpus, antrum

78
Q

What are the three mechanisms that regulate gastric reservoir function?

A

1) feedback relaxation
2) receptive relaxation
3) adaptive relaxation

79
Q

What are the two neurotransmitters involved in inhibiting gastric motility and increasing fundic storage capacity?

A

VIP and NO

80
Q

What is segmentation’s function?

A

allows for adequate mixing of luminal contents to ensure adequate absorption

81
Q

Describe Dogiel type I neurons

A

single long axon

interneurons and motor neurons

82
Q

Describe Dogiel type II neurons

A

rounded cell bodies
numerous projections
sensory neurons in gut wall
large

83
Q

Name three inhibiting neurotransmitters in the descending projection of the enteric nervous system

A

NO, VIP, purines

84
Q

Name two excitatory neurotransmitters in the ascending projection of the enteric nervous system

A

Ach, tachykinins (such as substance P)

85
Q

True/False: Orally projecting neurons in the muscle layers are inhibitory motor neurons, whereas aborally projecting dogiel type I neurons in the muscle layers are excitatory motor neurons

A

FALSE VICE VERSA

86
Q

True/False: ENS uses at least 20 neurotransmitters and innervates all regions of the GI tract

A

True

87
Q

Special cells such as enterchromaffin cells release _______ in an early step in transduction of sensory information, activating intrinsic and extrinsic afferents that go through ENS pathways

A

serotonin

88
Q

______ controls peristaltic propulsion of luminal contents and requires ______ to determine distance and direction of propagation

A

neural regulation, gating mechanisms

89
Q

WIthin the enteric nervous system, _________ exist which are much simpler than neuromuscular junctions of skeletal muscles. Most motor axons release transmitters from ________ (swellings in the axon) that can then diffuse over relatively large distances to effector cells.

A

neuroeffector junctions; varicosities

90
Q

Describe the two types of muscle contractions that are stimulated by excitatory motor neurons

A

1) stimulated by membrane depolarization (excitatory junction potentials)
2) stimulated by direct release of calcium from intracellular stores (pharmaco-mechanical coupling)

91
Q

Inhibitory motor neurons produce inhibitory junction potentials that suppress contractile activity how?

A

K+ channels open

move membrane in a negative direction away from threshold and thus reduce intracellular calcium

92
Q

Excitatory junction potentials are mediated by ____ and _____

A

Ach, substance P

93
Q

Inhibitory junction potentials are mediated by _____ or _____

A

nitric oxide, vasoactive intestinal peptide

94
Q

Interstitial cells of cajal (intramuscular) intercept transmitter release from both excitatory and inhibitory enteric motor nerve endings. Which cells are mainly targeted by inhib motor nerve endings?

How do voltage changes in these cells spread to smooth muscle cells?

A

PDGFR-alpha cells

voltage changes spread to smooth muscle cells via gap junctions

95
Q

True/False: The insterstial cells of cajal (intramuscular) are pacemaker cells

A

FALSE - Myenteric (MY) is the pacemaker type not IM

96
Q

If there is failure of interstitial cells of cajal (intramuscular) to develop in the gastric fundus, what happens?

A

neural responses in smooth muscle to nerve stimulation are eliminated

THIS MEANS THAT MOTOR NERVE ENDINGS DO NOT
DIRECTLY INNERVATE SMOOTH MUSCLE CELLS BUT INNERVATE ICC-IM THAT ACT AS INTERMEDIARIES.

97
Q

All regions of the gut are under control of (3 types)

A

endocrine cells, hormone regulation, immuno cells

98
Q

What is Hirschsprung’s DZ?

A

during development of ENS, the vagal nerve does not fully develop throughout gut and an aganglionic section. Typically occurs in distal colon regions.
Affects males more than females.
If nerves don’t develop, newborn have constriction downstream and huge distended region upstream.
Only cure is removal of aganglionic section via surgery
WIll have issues t/o life
Major pathway affected is RET signaling pathway

99
Q

What is gastroparesis?

A

Gastroparesis is a GI motility disorder of the stomach

It is characterized by delayed emptying of food from stomach into small bowel in absence of mechanical obstruction

100
Q

True/False: Gastroparesis affects about 5% of the population and is more commonly found in men than women

A

FALSE - more common in women

101
Q

Approx ____ of patients with insulin-dependent diabetes have diabetic gastroparesis. There is a slightly higher incidence in patients with type II

A

55%

102
Q

Describe the A1C test.

A

Measures what percentage of RBC’s is glycated (coated with sugar); and tells you blood sugar levels for last 2-3 months.

103
Q

Describe symptoms of gastroparesis

A

esophagitis, Mallory-Weiss tears, severe PUD, N/V, epigastric fullness despite eating a few bites, bloating, heartburn

104
Q

What are Mallory-Weiss tears?

A

Severe and prolonged vomiting can result in tears in the lining of the esophagus. The esophagus is the tube that connects your throat to your stomach. Mallory-Weiss syndrome (MWS) is a condition marked by a tear in the mucous membrane, or inner lining, where the esophagus meets the stomach

105
Q

What three types of foods aggravate gastroparesis symptoms?

A
  • foods high in fibers such as raw fruits and veggies
  • eating greasy or rich foods
  • drinking beverages high in fat or carbonation
106
Q

Which of the following is not an agent associated with gastroparesis?

a) alcohol
b) nicotine
c) proton pump inhibitors
d) histamine (H2) receptor antagonists
e) none of the above

A

none of the above

all are associated

107
Q

Describe the differences between Grades 1, 2, and 3 Gastroparesis severity according to the Abell Scoring System

A

Grade 1=mild intermittent sx, controlled by diet mods
Grade 2=moderately severe sx, no weight loss, prokinetic drugs + antiemetic agents req
Grade 3=pts are refractory to meds, unable to maintain nutrition orally, require ER visits, may req surgery

108
Q

What is a bezoar?

A

solid collection of food, mucus, vegetable fiber, hair or other material that cannot be digested in the stomach.
they may be softened, dissolved or broken up during an upper GI endoscopy.

109
Q

Upper GI endoscopy is a method used to dx gastroparesis. What type of anesthetic is used?

A

liquid anesthetic that is gargled or sprayed on the back of the throat

general anesthesia may also be given

110
Q

What are the benefits of using ultrasonography over upper GI endoscopy to dx gastroparesis?

A

anesthesia is not required

US can be distinguished btwn gallbladder dz and pancreatitis vs gastroparesis

111
Q

Describe the scintigraphy method of dxing gastroparesis

A

looks at gastric emptying using solids labeled with a y-emitting radioscope

if more than 10% of meal is in stomach after 4 hours, the person has gastroparesis

meal normally used is egg

112
Q

Describe the wireless motility capsule or “Smart Pill” method of dxing gastroparesis

A

temperature, pH and pressure measurements are plotted on motility graph

there are limitations - not administered to pts with gastric bezoars, swallowing d/os, GI obstruction, Crohn’s, diverticulitis, etc

113
Q

Desribe the paracetamol/APAP testing method of diagnosing gastroparesis

A

After intake of paracetamol/APAP, serial blood samples are taken.
usefulness limited to evaluation of emptying of liquids, generally not diagnostic tool

114
Q

Describe the use of radio opaque markers to diagnose gastric emptying

A

Have pt swallow multiple radio opaque markers

Take XRs periodically to track emptying of stomach

115
Q

Describe the breath test used to diagnose gastroparesis

A

1) octanoic acid - pt eats meal with small amount of radioactive material; breath samples taken over several hours to measure amount exhaled; results determine how fast the stomach is emptying

116
Q

Describe the two other breath tests used to diagnose other things [not gastroparesis]

A

hydrogen breath test - lactose intolerance

urea breath test - H. pylori

117
Q

What are five problems associated with gastroparesiss?

A

1) severe dehydration due to persistent vomiting
2) GERD [can lead to esophagitis]
3) bezoars
4) malnutrition
5) dec quality of life [work absences]

118
Q

What four issues can bezoars cause in those with gastroparesis

A

N/V, obstruction and inferfere with medication absorption, difficulty managing blood glucose levels in those with DM

119
Q

What are five diseases that can lead to gastroparesis?

A

DM, autonomic neuropathy, diabetic autonomic neuropathy, myopathy, viral infections

120
Q

What are two possible causes of gastroparesis?

A

neuropathies [extrinsic and intrinsic], abnormalities of interstitial cells of cajal

121
Q

How is gastroparesis treated?

A

first level - restoration of fluids an electrolytes, dietary modifications, glucose control
second level - prokinetic therapy at each meal, anti emetics at night
third level - non pharmacological interventions such as gastric pacing and surgery

122
Q

How is the diet modified to treat those with gastroparesis?

A

six small meals a day instead of 3 large ones;
chew food well;
drink noncarbonated fluids with each meal;
walking after a meal;
avoiding high fat and fibrous foods

In those with severe gastroparesis, liquid or puree diet may be prescribed

123
Q

What are the three steps of the gastroparesis diet?

What is the overall goal?

A

The overall goal is to reduce sx and maintain adequate fluids and nutrition

Step 1=liquids
Step2=add’l calories via small amount of dietary fat [pts at this level are usually able to tolerate this amount]
Step3= long-term maintenance, fat is limited to 50gm per day; fibrous foods restricted

124
Q

What foods should be avoided by those with gastroparesis?

What foods are recommended?

A

recommended=plain saltine crackers; gatorade and soft drinks; fat-free consomme and buillon all others

avoid=milk, fruits and veggies, all other breads and grains; meat; fats and oils

125
Q

What are two prokinetic drugs used to treat gastroparesis?

Which was used previously and withdrawn? Why?

A

metoclopramide (reglan) and erythromycin

Cisapride was withdrawn due to cardiac arrhythmias. Stimulated sterotinin receptor-4.

126
Q

Metoclopramide (Reglan) is the only drug approved by the FDA to treat gastroparesis. What is it’s action?
What are its side effects?

A

dopamine antagonist
inc tone and amplitude of gastric contractions and relaxes the pyloric sphincter and duodenal bulb
also rescues N/V
side effects - fatigue and depression

127
Q

Describe erythromycin’s action and its side effects

A

Erythromycin acts as a motilin receptor agonist stimulating the migrating motor complex (interdigestive period) and smooth muscle contraction.

Side effects are cramps, nausea, altered cardiac conduction

128
Q

Gastric electrical stimulation is a non-pharmacological treatment of gastroparesis. How does it work?

A

Laparascopic placement of electrodes in the stomach
Connected to neurostimulator in a pocket of abd wall

GES may reduce symptoms (especially dyspepsia and vomiting) as well as need for nutritional supplementation

129
Q

Parenteral nutrition is another form of treatment for gastroparesis. What is it and what are the five different tubes used?

A

Parenteral nutrition (PN) is the feeding of a person intravenously, bypassing the usual process of eating and digestion

nasogastric tube, gastrostomy tube, nasoduodenal tube, nasojejunal tube, jejunostomy tube

130
Q

Hemin is another potential non-pharmacological treatment for gastroparesis. Describe

A

HO1 is expressed by M2 macrophages who have cytoprotective effect on ICC pacemaker cells; appears related to prodn of small amounts of CO.

HO-1 expression low in pts with diabetic gastroparesis and can be supplemented via IV injection of hemin.

However, fails to sustain levels beyond a week and did not improve sx, need more research.

131
Q

True/False: 1 in 2 diabetic will end up with gastroparesis

A

TRUE

132
Q

True/False: Idiopathic gastroparesis is the most common form

A

FALSE most rate

B3 (7 decks)

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