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Unit 5: LGS > Week 1 > Flashcards

Week 1 Flashcards

1
Q

Path of food

A

Mouth –> Pharynx –> Esophagus –> Stomach –> Small Intestine –> Colon –> Rectum –> Toilet

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2
Q

What is preventing the food from going backwards

-name the sphincters and where they reside in pathway of food

A
  • Sphincters
  • Mouth–> Pharynx–> Upper Esophageal Sphincter–> esophagus–> Lower Esophageal Sphincter–> Stomach–> Pylorus–> Small intestine–> Ileocecal Valve–> Colon–> Rectum–> Internal Anal Sphincter–> External Anal Sphincter–> Toilet
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3
Q

Sphincters

-anatomy

A

-Involuntary smooth muscles (there are a few voluntary ones in particular regions such as the external anal sphincter

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4
Q

characteristics when depicting the structure of the GI tract

A
  • Continuous, open tube
  • Microvilli and crypts (function to increase surface area)
  • Primarily made of smooth muscle containing calmodulin, Ca++, Myosin light chain kinase (MLCK), etc.
  • Lined with epithelium
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5
Q

main categories of function of the GI tract

A
  • Digestion: Include Chemical and Mechanical components
  • Absorption: Gets nutrients into the body
  • Secretion: Secrete substances to help break the food down
  • Motility: Need the food to move through the whole system
  • Excretion: Get rid of waste
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6
Q

Digestion Overview

  • broken into
  • regulated by
A

-Cephalic- what happens prior to eating (Smell food–> salivate and stomach growls in anticipation)
Gastric- digestion in the stomach
Intestinal- digestion in the intestines
- different hormones: Paracrine- signaling neighboring cells/ cells in close proximity
Autocrine- signaling self
Endocrine- Signaling a distant organ/tissue (usually has to enter the blood stream)

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7
Q

GI and autonomic nervous system

-what is it innervated by?

A
  • Parasympathetic:

- Sympathetic

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8
Q

Where does the Vagus nerve enter the abdomen

A

through the esophageal plexus at the level of T10.

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9
Q

Parasympathetic

-where are the pre and post ganglionis cell bodies? What neurotransmitters are included?

A
  • Preganglionic cell bodies: are located in the dorsal nucleus of CNX (Vagus nerve), Neurotransmitters include Acetylcholine acting on nicotinic receptors
  • Postganglionic cell bodies: are located in the organ wall, Neurotransmitters include Acetylcholine acting on muscarinic receptors
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10
Q

Sympathetic

-where are the pre and post ganglionis cell bodies? What neurotransmitters are included?

A
  • Preganglionic cell bodies: located in the lateral horn of the spinal cord at levels T5-L3; Neurotransmitters include Acetylcholine acting on nicotinic receptors; Postganglionic cell bodies: In celiac, Aorticorenal, Superior Mesenteric, and Inferior Mesenteric ganglia;
    Neurotransmitters include norepinephrine acting on adrenergic receptors
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11
Q

Where do fibers from preganglionic cell bodies of thoracic sympathetic innervation converge? what about lumbar?

A
  • Fibers in the thoracic region converge to form the Greater, Lesser, and Least Splanchnic nerves.
  • The fibers in the lumbar region form the Lumbar Splanchnic nerve.
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12
Q

Sensory information of GI

A
  • (afferent fibers) send signals from the GI system to the brain
  • Reach the brain by traveling with the sympathetic fiber pathways
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13
Q

Enteric Nervous System

-types of plexus

A
  • Myenteric

- Submucosal

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14
Q

Myenteric

  • what does it act on?
  • function?
  • neurotransmitters?
A
  • acts on the smooth muscle
  • Functions to regulate smooth muscle contraction and relaxation
  • Neurotransmitters involved:
    Excitatory/Contraction: Acetylcholine
    Inhibitory/Relaxation: Nitric Oxide
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15
Q

Submucosal

  • what does it act on?
  • function?
  • neurotransmitters?
A
  • directed to the epithelium
  • regulate epithelial secretory functions (enzymes for digestion as well as lubrication)
  • Neurotransmitters involved:
    Secretion Response: caused by Acetylcholine
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16
Q

mediators that regulate the afferent signal from inside the intestinal lumen
-function

A
  • Chemoreceptors and mechanoreceptors sensing changes in macromolecules, hormones, pH, and distention/stretch of the smooth muscle
  • environmental changes send sensory neurons back to engage the enteric nervous system to get an immediate response from the parasympathetic reflex
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17
Q

Process of mastication

A
  • involves muscles of mastication and salivary glands
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18
Q

Muscles of mastication

-innervation?

A
  • Temporalis, masseter, medial and lateral pterygoids

- Innervated by V3 (mandibular branch of trigeminal n.)

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19
Q

Salivary Glands

A
  • Sublingual, submandibular, and Parotid gland
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20
Q

Sublingual, submandibular

  • innervation
  • Preganglionic nerve body
  • Postganglionic nerve body
A
  • Innervated by parasympathetics
  • Preganglionic nerve body: superior salavatory nucleus; Fibers exit the brainstem through the corda tympani (branch of the facial nerve)- hitches a ride to the oral cavity along the lingual n which is going to the tongue.
  • Postganglionic nerve body: in the submandibular ganglion and will continue to finally synapse at the glandular tissue.
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21
Q

Parotid gland

  • innervation
  • Preganglionic nerve body
  • Postganglionic nerve body
A
  • Innervated by parasympathetics
  • Preganglionic cell bodies: inferior salavatory nucleus; Exits the brainstem via the glossopharyngeal n
  • Postganglionic cell bodies: otic ganglion; Travels via the auriculotemporal n (which is a branch of V3/mandibular n. of the trigeminal n.) to finally synapse at parotid glandular tissue.
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22
Q

Deglutition

A
  • complex process that transfers food blous from mouth to pharynx and esophagus into stomach
  • Stage 1: voluntary; bolus is compressed against hard palate and pushed from mouth into oropharynx
  • Stage 2: Involuntary and rapid; soft palate is elevated by Levator palatini and uvula (musculus uvulae) sealing off nasopharynx; suprahyoid and logitudinal pharyngeal muscles contract to elevate larynx and close it off using the epiglottis; pharynx widens and shortens to recieve food bolus
  • Stage 3: Involuntary, sequential contraction of all three pharyngeal constrictor muscles creating a peristaltic ridge that forces the food bolus inferiorly into the esophagus
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23
Q

How is epiglottis activated?

A
  • by the pharyngeal lifters (stylopharyngeus, salpingopharyngeus, and palatopharyngeus) to close off the larynx/airway
  • All of these are innervated by the Vagus n. except stylopharyngeus, which is innervated by the glossopharyngeal n.
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24
Q

How is the larynx elevated?

A
  • Suprahyoid muscles also activate to pull superiorly on the hyoid bone to elevate the larynx; Ant Digastric, mylohyoid
  • Both innervated by branch of V3 (nerve to mylohyoid)
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25
Q

Peristalsis

A
  • type of contraction occuring in the esophagus during stage 3 of deglutition
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26
Q

Peristaltic contraction function

A
  • Creates a pressure gradient that helps push the bolus down towards the stomach
  • Superior 1/3 contraction occurs within 1-2 seconds of swallowing; Middle 1/3 within 3-5 seconds; Inferior 1/3 within 5-8 seconds and finally ends at the lower esophageal sphincter
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27
Q

Muscle in esophagus

-innervation

A
  • Striated muscle: Innervated by somatic neurons (Acetylcholine acting on nicotinic receptors)
  • Smooth muscle (contraction and dilation needs to happen in a coordinated, rhythmic fashion… Muscle upstream contracts while muscle downstream relaxes/dilates to accept the incoming bolus.)
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28
Q

Smooth muscle contraction and dilation

A
  • Contraction: Acetylcholine acting on muscarinic receptors; Gαq–> IP3 and DAG–> Release Ca++ from Sarcoplasmic Reticulum–> Contraction
  • Dilation: NO (nitric oxide); GC–>cGMP–> MLLP (myosin light chain phosphatase)–> relaxation
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29
Q

Primary vs. Secondary Peristalsis

A
  • Primary: first time a bolus is swallowed
  • Secondary: A second contraction that follows the first one to clear whatever is left behind
  • Example: If you eat a second bolus within a 5 second window of the first bolus, the first peristalsis will stop to let the second one will catch up. Then the two will go down together.
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30
Q

problems swallowing and it feels like the food is getting stuck…. What could be going on

A
  • Structural problem–> fibrosis or anatomical variation
  • Functional problem–> neural control or the actual muscle that isn’t functioning correctly (our patient has uncontrolled diabetes so this(neuropathy) is a possibility)
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31
Q

How do we get the bolus into the stomach?

A
  • Has to go through the lower esophageal sphincter
  • As the bolus comes down, muscle stretches, and pressure increases–> causes relaxation of the lower esophageal sphincter–> can enter stomach.
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32
Q

lower esophageal sphincter

  • resting state
  • importance of relaxing and closing
  • what are we trying to prevent
A
  • resting state, it is tonically contracted/closed
  • We want the lower esophageal sphincter to close back to prevent acid reflux.
  • If there is a failure to relax–> cant swallow all the way and food can’t get into the stomach
  • If there is a failure to contract–> acid reflux/ food can come back up
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33
Q

If there is an x-ray that shows food is getting stuck in esophagus and unable to get into stomach what is most likely the problem?

A
  • Ganglion cells in the myenteric plexus
  • myenteric plexus is coordinating the smooth muscle contraction and relaxation, and these events are not being regulated correctly in this patient
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34
Q

gastrointestinal agents used in motility disorders

A
  • Antiemetics
  • Laxatives
  • Prokinetics
  • Antidiarrheals
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35
Q

scintigraphy test

  • what is it?
  • what is it testing?
  • normal?
A
  • look at gastric emptying
  • looking at the amnt of food that’s in the stomach after a period of time.
  • After about 2.5 hours or so, you should have most of the food passing thru the stomach into the duodenum, b/c it has to get into the intestinal phase of digestion.
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36
Q

diabetes effects on gastric motility

A

-causes neurodisruption so that nerves innervating stomach do not work correctly and stomach is unable to perform functions normally

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37
Q

receptive relaxation

  • what is it?
  • when does it start?
A
  • The ability of the stomach to relax as the volume
    increases.
  • start in early stages of digestion
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38
Q

stomach tone

A
  • stomach has an increased tone which means it is stiff

-

39
Q

Cephalic stage of digestion

  • what is it?
  • caused by?
  • what initiates it?
A
  • you see, you smell, you are about to taste food and your body initiates this response
  • caused by Vagovagal response: vagal afferents to activate vagal efferents
  • You smell something, and it’s going to initiate it.
40
Q

3 parts of stomach

A
  • Fundus: The reservoir
  • Body
  • Antrum
41
Q

Stomach stretch

  • what happens?
  • what type of neuro response is this?
A
  • stretch in the wall signals mechanoreceptors (a neuron) which will release ACh (acetylcholine) from pre-ganglionic neuron which activates post-ganglionic neuron and since we want relaxation to occur post-ganglionic would release NO and VIP (vasoactive intestinal/inhibitory peptide)
  • intrinsic
42
Q

Intrinsic vs extrinsic nerve innervation to stomach

A
  • Myenteric plexus is intrinsic response

- CNS, vagal response is extrinsic

43
Q

How is extrinsic nerve innervation activated?

A
  • Sensory can go back to the dorsal vagal complex to initiate vagal response, to then come back again through ACh-help to initiate more of these enteric plexus, so the myenteric plexus is now having further and further inhibitory response, and you have more and more NO and VIP being released to release it.
44
Q

Mechanical digestion

  • what is it?
  • what activates it?
A
  • mixing and grinding; breaks it into small pieces

- vagal response

45
Q

End product of mechanical digestion

A
  • small pieces after a certain period of time will exit thru the pylorus, this causes stretch of duodenum which will further relax out the stomach through exact same mediators of Ach and NO/VIP
46
Q

Importance of chemical digestion in regulation of gastric digestion

A
  • chemical mediators breaking down fats, lipids, carbohydrates and stretch of duodenum will then send chemical signals. The I cells in the duodenum will be activated by fat and protein and release CCK (Cholecystokinin
47
Q

Increase of CCK

A
  • sends sensory responses back to initiate more of a vagal response so that you get a further decrease in tone, meaning you get more receptive relaxation to occur.
48
Q

How does stomach relax out?

A
  • NO is released into smooth muscle,
  • NO activates GC to cGMP and cGMP stimulates myosin light chain phosphatase–> dephosphorylates the myosin light chain and relax the smooth muscle
49
Q

Why can duodenum cause receptive relaxation?

A
  • Stretch of the duodenum and release of CCK slows down gastric emptying. Slowing down gastric emptying leaves more time to the duodenum so that nutritional content can catch up
  • CCK reduces the tone of the stomach and the reduction of tone means that the stomach can hold more food. Also since the stomach volume is increased there is less pressure in the stomach and since the food can only pass from the stomach to the intestine with an increase in pressure it allows the food the stay in the stomach for a while so the intestine can start to absorb nutrients as it is pushed through
50
Q

Mixing and grinding

A
  • mechanical digestion of the stomach
51
Q

Pacemaker cells

  • also known as
  • found?
  • function
  • regulates
  • what occurs during fasting
  • importance during fasting
  • what occurs during fed state?
A
  • interstitial cells of Cajal (ICC)
  • found in the body of the stomach
  • set basal electrical rhythm: max rate of contraction that can occur
  • both fasting and fed states
  • It’s just a rhythm and by itself is not enough to induce an AP and actually get smooth muscle contraction.
  • need natural rhythm to occur at all times in the gut so you can establish a flow of constant movement
  • Combination of nerve invnervation + ICC cells + Basal electrical rhythm will now set multiple contractions, the ones that you actually see to allow for segmentation, peristalsis, and mixing and grinding
52
Q

Gastro smooth muscle contraction

A
  • while you’re getting NO and VIP released at fundus of the stomach, you’re having strong contractions in the body and the antrum through Ach from vagus
  • you will have multiple contractions occurring
  • contractions will cause food to go in both direction
  • ## anterograde food will be pushed up against closed pylorus and retrograde food will be pushed towards to retrograde contraction that has begun
53
Q

Gastric emptying

  • How does food get into duodenum
  • pylorus during fed state
  • regulators
A
  • The pylorus stays relatively closed for long periods of time and acts as a wall for the food to be pushed up against to help break it down
  • The pylorus will transiently open and only allow for food particles less than 1mm in size to pass through, anything bigger has to be broken down more
  • Ach causes contraction for food to be pushed into duodenum, CCK helps to slow gastric wmptying to make sure duodenum can handle the amount of food coming in and begin absorption, serotonin also helps
54
Q

Early satiety and diabetes

  • tone
  • contractions
  • emptying
A
  • diabetes is causing a disruption in the neural functioning.
  • gastric tone will probably remain increased because receptive relaxation not working as efficiently so he can’t relax out to allow more food to come in so he feels full faster.
  • Also, contractions occurring during mixing and grinding will probably be lessened because intrinsic and extrinsic responses are lessened
  • Also, the responses that mediate gastric emptying into the duodenum may also be dulled as well.
55
Q

Bloating and diabetes

A
  • since food is staying in stomach it is causing bloating

- could also be caused by specific food being eaten that create a lot of gas

56
Q

Treatment for patient with diabetes who has prolonged gastric emptying

A
  • serotonin antagonists
  • Serotonin endogenously slows down gastric emptying by binding to inhibitory nerves so by blocking serotonin we allow for gastric emptying to continue and hurry up
57
Q

Serotonin in gastric

  • what does it do?
  • drug receptors
  • example
A
  • inhibits cholinergic activation and smooth muscle stimulation
  • drugs have most selectivity for are the serotonin Type 3 receptors; also drugs that are target against the serotonin Type 4 receptors, however these are not in use in the US
  • Alosetron is a serotonin antagonist
58
Q

Dopamine

  • what does it bind?
  • what does it do?
  • medication
A
  • binds D2 receptors in the ENS and is inhibitory
  • As a neurotransmitter, dopamine is excitatory in the CNS, whereas it is inhibitory in the ENS; inhibits smooth muscle motility
  • antagonist; Domperidone
59
Q

Motilin

A
  • located in the cholinergic neurons
  • activated by macrolides
  • stimulatory to smooth muscle contractions
60
Q

μ-opioid receptors

A
  • Inhibits cholinergic activation/stimulation of the gut
61
Q

Macro nutrients and how they’re consumed

A
  • Glucose solution exits out first, followed by protein solution, and then fat. Solids take longer than liquid because you’re dealing with bigger size and more density
62
Q

retrograde repulsion

A
  • continued mixing and grinding of food that is not small enough to get into duodenum
63
Q

Fat and digestion

A
  • slower than protein b/c it floats in the food. Any fat placed at body temp turns into liquid. Because the fat floats on top of the stomach content, it takes longer to empty out. In addition to this, lipids activate CCK that slows down the gastric emptying.
  • So the fats stay in the stomach longer
64
Q

Diabetes and diet to treat slow gastric emptying

A

○ Low-fat diet
○ Small meals
○ If gastric emptying is dependent on both size and caloric density, telling him to have more liquid based or smaller meals could help him out. He also needs to refrain from a high-fat diet.

65
Q

Vommiting

  • trigger
  • what is activated?
  • flow
A
  • disruption/distension in the gastric mucosa
  • activate the chemoreceptor triggering zone which is going to stimulate a programmed vomiting response.
  • something activates the chemoreceptor triggering zone to do the programmed vomiting response. Patient will take a deep breath which closes the glottis and raises up the soft palate so nothing gets into the lungs or nasal passage. At the same time, there is contraction of the thoracic cavity, diaphragm, and abdominal cavity to cause the intra-abdominal pressure to increase. The pylorus is closed, so the only way the food content can go is backwards and LES relaxes so the high abdominal pressure squeezes the stomach and push content up into the esophagus.
    The brain switches the reversal pressure in the thoracic cavity and so it creates this high pressure cavity in the thoracic area. By doing so, then the stuff that’s in the esophagus gets pushed out into the mouth.
66
Q

why mouth waters before we vomit

A

Nausea stimulates the salivary glands to produce more saliva because saliva is mucus and bicarb which will protect your esophagus and teeth.

67
Q

pharmacological tx for out pt who has gastroparesi

A
  • Prokinetics to stimulate gut activity
  • Dopamine antagonists
  • Metoclopramide: a prokinetic AND antiemetic
  • Macrolides: act on motilin receptors but the tolerance happens relatively quickly, so usually done acutely
68
Q

Anti-emetics

A 
• D2 antagonists
• 5-HT3 antagonists
• Corticosteroids
• NK1 antagonists
• Antihistamines
• Anticholinergics
- Cannabinoids
69
Q

Segmentation

  • what is it?
  • where?
  • how? what muscle?
A
  • series of contractions
  • in the small intestines to the more that fluid is moving around, the smaller and smaller those particles are becoming, the more they’re getting to those enzymes, and the better absorption that you’re going to have.
  • ACh but it’s contraction of the circular muscles
70
Q

Peristalsis

  • what?
  • how? what muscle?
  • relaxation
A
  • forward movement to bring it more aborally.
  • Ach; getting contraction of the circular muscles, and shortening of the longitudinal muscles
  • caused by NO or VIP. NO is released straight from neurotransmitter and is a gas that goes directly into cell
71
Q

Movement of colon

A
  • s retrograde and forward flow. This is to mix it up and form the waste material that’s going to get out of there.
  • In ascending and the transverse colon is where you have a lot of that back and forward movement, because this is going to be where a lot of your electrolytes and your water are going to be reabsorbed or excreted out depending on what your body needs.
  • In descending colon, it’s the high amplitude propagations pushing everything in that forward direction toward the rectum.
72
Q

Defecation

- what happens

A

As the feces is entering into the rectum, you’ll get relaxation of the internal anal sphincter and so it’s then ready for defecation.

73
Q

Laxative agents

A
  • bulk forming laxatives
  • stool surfactant agent
  • osmotic laxatives
  • stimulant laxatives
  • Chloride secretion activators
  • Opioid receptor agonist
  • Serotnin 5-HT4-receptor agonists
74
Q

Bulk-forming laxatives

A

indigestible, hydrophilic colloids that absorb water, forming a bulky, emollient gel that distends the colon and promotes peristalsis

75
Q

Stool Surfactant agents

A
  • soften stool material, permitting water and lipids to penetrate. They may be administered orally or rectally.
76
Q

Osmotic Laxatives

A

soluble but nonabsorbable compounds that result in increased stool liquidity due to an obligate increase in fecal fluid.

77
Q

Stimulant Laxatives

A

induce bowel movements through a number of poorly understood mechanisms. These include direct stimulation of the enteric nervous system and colonic electrolyte and fluid secretion.

78
Q

Chloride secretions activators

A
  • increase secretion of chloride into the intestine which stimulates intestinal motility and shortens intestinal transit
  • examples: Lubiprostone and Linaclotide
79
Q

Lubiprostone

A

stimulating the type 2 chloride channel (ClC-2) in the small intestine which increases chloride-rich fluid secretion into the intestine, which stimulates intestinal motility and shortens intestinal transit time

80
Q

Linaclotide

A

minimally absorbed, short amino acid peptides that stimulate intestinal chloride secretion by binding to and activating guanylate cyclase-C on the luminal surface. leads to increased intracellular and extracellular cyclic guanosine monophosphate (cGMP) with activation of the cystic fibrosis transmembrane conductance regulator (CFTR), followed by chloride-rich secretion and acceleration of intestinal transit

81
Q

Opioid receptor antagonists

A

opioids have significant constipating effects so blocking them will stop constipation

82
Q

Serotonin 5-HT4-receptor agonists

A

5-HT4receptors on the presynaptic terminal of submucosal intrinsic primary afferent nerves are activated which stimulates calcitonin gene-related peptide, which stimulates second-order enteric neurons to promote the peristaltic reflex

83
Q

antidiarrheal agents

A
  • Opioid Agonists
  • Bismuth compounds
  • Bile salt-binding resins
  • Octerotide
84
Q

Bismuth compounds

A

salicylate inhibits the Cl- secretions and also the prostaglandins that are causing the secretion

85
Q

Migrating Motility Complexes

A
  • Start by initiation in the stomach by the ICC cells
  • There are no neurotransmitters or true stimulates that initiate this. It is simply what the GI tract uses to get rid of any residual content after a meal, and completely clear it out.
86
Q

Migrating Motility Complexes

A
87
Q

3 phases of MMCs

A
  • I- Period of quiescence: Nothing is going on and is silent
  • II- Start to get an increase in action potential frequency: There is still no propulsion because this phase is only functioning to prepare for phase III
  • III- Burst of intense contractions that allow for propagation to occur: Motilin is produced which helps make the action potentials needed to clear out the residual gastrointestinal content
88
Q

Pylorus in fasting state

A

pylorus will be open

89
Q

Pylorus in fasting state

A
  • pylorus will be open
  • since the pylorus is open the propogations from the ICC cells are able to push anything ft over in the stomach, small intestines, and colon to be moved out.
90
Q

What do you tell pt who has swallowed a ring?

A

have the kid fast, allowing for opening of the pylorus, which will allow for any residual content (including the ring) get cleared out

91
Q

What could interfere with migrating Motility Complexes

A

Anything that can disrupt the normal neural reflexes

92
Q

external anal sphincter

A
  • only relax voluntarily
  • Contraction of the rectus abdominus will allow for an increase in pressure of the abdominal cavity–> changes the angle of the rectosigmoid junction–> material can exit
93
Q

Difference between flatulence and defecation

A

In flatulence contraction of the abdominal muscles and change in the rectosigmoid angle is not needed

94
Q

Valsalva maneuver

A
  • moderately foreceful attempted exhalation against closed airway (closing mouth and pinching nose)
  • increases pressure in the chest which as well as causes changes in heart rate and blood pressure

Unit 5: LGS (5 decks)

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