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Block 3; Week 3 Michelle > Smith > Flashcards

Smith Flashcards

1
Q

What is dysbiosis?

A

microbial imbalances on or inside the body

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2
Q

Is there dysbiosis in a healthy status? What is there?

A

Healthy Status
Normal behavior, emotion, nociception
Normal levels of inflammatory cells & mediators
Normal gut microbiota

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3
Q

Is there dysbiosis in a stressed state?

A

Stress/Disease
Changes in behavior, cognition, emotion, nociception
Altered levels of inflammatory cells & mediators
Intestinal dysbiosis

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4
Q

What is the effect of sympathetic stimulation on the gut?

A

decrease in secretions & peristalsis
blood redirected away from the gut & to other places like the brain
NE released

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5
Q

What is the effect of parasympathetic stimulation on the gut?

A

increase in secretions & peristalsis

ACh released

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6
Q

What are some of the things that can affect the gut?

A 
bacteria
toxins/chemicals
parasites
hormones
nutrients
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7
Q

What percentage of the vagus nerve is sensory?

A

80-90%

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8
Q

Self-contained inside the gut are what neurons?

A

IPANs: intrinsic primary afferent neuron

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9
Q

What portions of the GI does the vagus innervate?

A

stomach
SI
1/3 of colon

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10
Q

What are some afferent nerves that supply the GI that go thru the paravertebral/prevertebral ganglia to get there? Where are their cell bodies located?

A

Greater splanchnic nerve
Lumbar colonic nerve
Hypogastric nerve
DRG

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11
Q

Where are the cell bodies of the afferent vagal fibers?

A

nodose ganglia

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12
Q

Where are the cell bodies of the pelvic nerves found?

A

in the DRG of the sacral region of the spinal cord

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13
Q

What are the 3 pathways that connect the gut to the CNS?

A
  1. Vagal afferents–>upper GI
  2. Pelvic afferents–>colorectal (colon, rectum, internal anal sphincter)
  3. splanchnic afferents–>throughout GI tract, nociceptive
    * *pudendal nerves
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14
Q

What percentage of the splanchnic nerve fibers are afferent? Where are their cell bodies found?

A

7%

Cell bodies in the DRG

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15
Q

Some of the extrinsic afferent nerves are chemosensitive & some are not. What are these chemical agents that some are sensitive to?

A 
ATP
bradykinin
capsaicin
5-HT
histamine
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16
Q

What are the differences b/w a generator potential & an action potential?

A 
Generator Potential: 
graded; larger stimulus-->larger potential-->large frequency of AP firing; but if doesn't meet threshold-->no AP
**dependent on coupled transmitters
doesn't propagate-->local phenomenon
no refractory period
AP: 
all or none
refractory period
propagation
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17
Q

What is the process of a spinal reflex?

A 
Visceral Afferent Neuron
Interneuron (in spinal cord)
Pregang efferent
Postgang efferent
Effector
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18
Q

What counts as mechanical stimuli in the gut?

A

stretch
pressure
distortion
shearing forces

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19
Q

What counts as signaling molecules released from Peyer’s patches in the gut?

A

Proteases
histamine
serotonin
cytokines

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20
Q

What types of luminal contents would signal enteroendocrine cells to release gut peptides?

A

nutrients
toxins
antigens

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21
Q

What types of gut peptides would enteroendocrine cells release?

A

hormones

neuropeptides

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22
Q

What areas of the brain are activated by the gut peptides released by enteroendocrine cells?

A

area prostrema
dostral vagal complex
hypothalamus

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23
Q

What is the function of endocrine cells in the GI tract?

A

They are detectors that analyze luminal contents, survey mucosal status, & activate afferent neurons.

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24
Q

What are 5 examples of endocrine cells in the GI tract?

A 
I cells in duodenum
S cells in stomach & intestine
EE cells in gut
EC cells
lymphoid tissue
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25
Q

What do the I cells in the duodenum release? When do they release it? What happens next?

A

CCK
released in response to fat & protein digestion
CCK causes satiation; increases gastric blood flow & mucous protection
CCK inhibits gastric motility & emptying

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26
Q

What do the S cells in the stomach & intestine release? When does it release it? What is the response?

A

Release Secretin
in response to duodenal acidification
It enhances pancreatic exocrine secretion & bile flow.

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27
Q

What do the enteroendocrine cells in the gut do?

A

Release up to 20 different kinds of neuropeptides that can stimulate the vagal afferents in a paracrine fashion or the brain in an endocrine fashion

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28
Q

Where is most of the serotonin in the body stored?

A

90% of 5-HT stored in EC cells

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29
Q

What stimulates EC cells to release their stores? What do they store? What is the effect?

A

mechanical & chemical stimulation
5-HT/serotonin
Activates peristalsis (intrinsic)
Activates relaxation of the stomach (extrinsic afferent neurons)

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30
Q

Where is the lymphoid tissue found in the gut? What cell types are found here?

A 
Peyer's patches
antigen-sampling M cells
macrophages
eosinophils
neutrophils
mast cells
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31
Q

Of the gut nerves we have been talking about…which are sympathetic? Parasympathetic?

A

Sympathetic: Splanchnic nerves, Hypogastric nerves
Parasympathetic: Vagus, Pelvic nerves

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32
Q

What percentage of sympathetic nerves are afferent fibers?
What percentage of the vagus nerve?
Pelvic nerves?

A

Sympathetic: 20% afferent
Vagus: 80% afferent
Pelvic: 50% afferent

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33
Q

What do the vagal neurons sense?

A

pH & distention of the stomach

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34
Q

What do the pelvic neurons sense?

A

distention of the rectum & colon

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35
Q

Which set of visceral afferent nerve fibers senses pain in the gut?

A

Sympathetic nerves–splanchnic nerves

nociception

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36
Q

What does splanchnic stimulation elicit? Vagal stimulation?

A

Splanchnic: pain!!
Vagal: nothing.

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37
Q

Which set of afferent nerve fibers regulate visceral tone, distention, motility & secretion?

A

Parasympathetic: vagal & pelvic

38
Q

What conditions include chronic visceral pain? How is this treated?

A

cancer
severe peripheral vascular disease
Surgically sectioning sympathetic nerve trunks, but not parasympathetic nerve trunks

39
Q

What are there more of:
visceral sensory neurons
mechanosensory neurons?
What is the result of this?

A

10X as many mechanosensory neurons

Result: visceral sensations are diffuse & difficult to localize

40
Q

Describe the neuron type of vagal & spinal afferents.

A

pseudounipolar

41
Q

Describe the neuron type of IPANs.

A

multipolar

42
Q

Where are IPANs found? What do they sense?

A

found only in the intestine & gut

sense mucosal stimulation & stretch

43
Q

The vagus returns info to the brainstem via what? What type of info?

A

nucleus tractus solitarius
BP
CO2
Gut distention

44
Q

What is another name for tonic mechanoreceptors? What’s the deal with them?

A 
Wide Dynamic Range
tonic activity @ rest
responds to contraction/distention
**it signals filling of: stomach, colon, rectum
**discomfort/pain in: organ inflammation
45
Q

What is another name for high threshold mechanoreceptors? What’s the deal with them?

A

Phasic
low activity @ rest
responds to high levels of organ distention
**chemosensitive to inflammatory mediators
**receptive fields in serosa & mesentery

46
Q

What are some inflammatory mediators?

A

BK, eicanosoids, free radicals

47
Q

What are silent nociceptors sometimes considered? What’s the deal with them?

A

sometimes considered chemonociceptors
silent @ rest
mechanosensitive during inflammation via inflammatory mediators
In colon mucosa: sensitive to luminal chemicals & fine tactile stimulation

48
Q

What are IMAs?

A

Intramuscular arrays
individual branch of a vagal afferent fiber
vagal mechanoreceptors that innervate GI smooth muscle

49
Q

What are IGLEs?

A

intraganglionic laminar endings
vagal afferent fiber terminating in several intraganglionic laminar endings
mechanotransduction sites of vagal tension receptors in stomach

50
Q

What are IVAs?

A

mucosa intravillous arbors

chemical receptors in mucosal units

51
Q

How can the 5-HT released by enterochromaffin cells in the gut end up in general circulation?

A

if it is taken up into portal blood & taken up into platelets via SERT. Then it won’t be degraded by MAO. It can go into the liver & then into general circulation.

52
Q

What type of a reflex is emesis?

A

a somato-autonomic reflex

integrated in the medulla oblongata

53
Q

What 2 drugs target 5-HT3 receptors to stop emesis? Which part of the pathway is this? What is one situation that they don’t work particularly well in?

A

Ondansetron
Granisetron
**this is where the serotonin released by EC cells in the SI activates the vagal afferent neurons
**palliative care

54
Q

What is often taken in Parkinson’s disease treatment that increases vomiting?

A

dopamine agonist

55
Q

At which points in the pathway of emesis is dopamine involved?

A

There are dopamine receptors in the CTZ, NTS, & stomach vagus neurons.

56
Q

How do the drugs metoclopramide & domperidone inhibit emesis?

A

They are both dopamine receptor antagonists. They work on dopamine receptors in the stomach & upper SI.

57
Q

What is haloperidol & where does it work?

A

It is a dopamine antagonist & it works in the CTZ.

58
Q

What is cyclizine & where does it work to stop emesis?

A

antihistamine & antimuscarinic drug.

works in the brainstem.

59
Q

What are 2 kinda broad drugs that inhibit emesis?

A

levomepromazine & prochlorperazine

60
Q

What are the 2 diseases under the umbrella of inflammatory bowel disorders?

A

Crohn’s disease

Ulcerative Colitis

61
Q

What portion of the GI tract is affected in Crohn’s disease? What are the common symptoms?

A 
SI & LI
abdominal pain
vomiting
diarrhea
blood in stool
fatigue
weight loss
growth problems
62
Q

What does the bowel of a Crohn’s patient look like when it is affected? What are the extreme things that can happen to the bowel?

A

cobblestone appearance of the mucosa (from linear ulcerations)
patchy inflammation that extends into all the tissue layers
Extreme Results: fistulas, absecesses, strictures

63
Q

WIth IBD what’s the deal?

A

the immune system is overreacting to normal bacteria and causing a ton of inflammation

64
Q

What portion of the GI tract is mainly affected w/ ulcerative colitis? What are the symptoms?

A

LI
bloody diarrhea
abdominal cramping
urgent need for bowel movement

65
Q

What are 2 common types of ulcers?

A

gastric ulcers–stomach

duodenal ulcers–SI

66
Q

What causes gastric ulcers?

A

H. Pylori that is usu fine in the stomach sometimes causes inflammation. When this happens tissue is damaged & ulcers form & pain results.

67
Q

Irritable Bowel Syndrome is considered a functional gastrointestinal disorder. What happens w/ this? What is thought to cause it?

A

strong contractile activity of the gut

visceral afferent nerve hypersensitivity is thought to be the cause…

68
Q

Aside from visceral afferent hypersensitivity what are other possible causes?

A

Neurotransmitter imbalance
infection
psychosocial factors
altered bowel motility

69
Q

What are the symptoms of IBS?

A

abdominal pain with changes in frequency of bowel movements.
Diarrhea or constipation or both
whitish mucus in stool
bloated abdomen

70
Q

T/F Inflammation is involved in IBS as well as IBD.

A

FALSE. only IBD.

NOT IBS. Thus, IBS is less serious in terms of long term consequences.

71
Q

Gastric ulcers & gastritis both cause inflammation in the stomach. What does this do to visceral sensitivity?

A

This causes visceral hypersensitivity to gastric distention.

72
Q

Describes what happens in an injury to cause an increased sensitization of nociceptive fibers.

A

injury
inflammatory soup (from injured cells & other cells)
Sensitization of nociceptive fibers

73
Q

What types of substances, present in the inflammatory soup, cause pain?

A 
K+
H+
ATP
Bradykinin
Histamine
Prostaglandins
74
Q

If after an injury the firing gets really intense…what 2 substances might be released from afferent neurons?

A

Calcitonin Gene Related Peptide (CGRP)

Substance P

75
Q

What are TRP receptors?

A

they are transient receptive potential receptors

  • *found on afferent neurons
  • *responsive to temp
  • *responsive to certain substances, like capsaicin
  • *when these things activate the TRP there is a transient depolarization of the terminal membrane
76
Q

What is hyperalgesia?

A

exaggerated pain in response to a painful stimulus

77
Q

What is allodynia?

A

pain in response to an innocuous stimulus

78
Q

What is secondary hyperalgesia?

A

a receptive field expansion that enables input from non-injured tissue to cause pain

79
Q

What causes all these things: hyperalgesia, allodynia?

A

Central sensitization
an increase in synaptic efficacy & a decrease in inhibition; central amplification
Basically, you’re injured & now you have a low threshold for sensory inputs to effect a pain circuit.

80
Q

What is the convergence theory of referred pain?

A

This theory recognized that somatic sensory fibers & visceral sensory fibers both have cell bodies in the same DRG in the spinal cord & synapse w/ the same interneurons.
Sometimes the brain just can’t discriminate.

81
Q

Explain the basic idea behind visceral organ cross-sensitization.

A

2 inputs converge on the same second order spinal neuron in the spinal cord…one is insulted & the other is also amplified
This often happens b/w the colon & bladder…people w/ IBS also have bladder hypersensitivity b/c of cross-sensitization.

82
Q

What is congenital analgesia?

A

rare genetic disorder in which you can’t feel pain

life-threatening b/c you have no warning mechanism!!

83
Q

Describe the Gate Control Theory of Pain.

A

It involves a gating mechanism located in the dorsal horn of the spinal cord.
Inhibitory neuron in spinal cord acts as the gate.
projection cells go to the brain & signal pain.
Large nerve fibers stimulate both inhibitory & projection & therefore no pain is felt. This means that there was a normal stimulus.
Small nerve fibers (nociceptive) inactivates the inhibitor & activates the projection. Gate open.
Descending pathways from the brain can stop some of this pain.

84
Q

Describe when opiods can & cannot be good options for treatment of gut pain.

A

Opiods suppress pain.
Good: if you have painful diarrhea b/c a side effect is constipation.
Bad: if elderly or have other complications b/c constipation is a major side effect along with a number of others.

85
Q

What are the 3 opiod-derivatives that are approved by the FDA?

A

loperamide
diphenoxylate
difenoxin

86
Q

What are 3 sources of cannabinoids? What is the ligand that makes it up?

A

Endogenous
Synthetic
Plant-derived
*anandamide

87
Q

What are the 2 beneficial receptors that anandamide activates? What are the effects?

A

CB1: antiulcer, reduction in gastric & intestinal motility, reduction in intestinal secretions
CB2: reduction in cytokines, visceral pain & contractility

**can be useful to treat the inflammation of IBD

88
Q

What receptor that is bad can be activated if you smoke too much marijuana? What are the results?

A

TRPV 1
This increases inflammation, contractility, & hypersecretion.
Can cause vomiting, polydipsia, desire to take repeated hot showers.

89
Q

What is SSRI? Lidocaine?

A

SSRI: selective serotonin reuptake inhibitor
Lidocaine: local anesthetic

90
Q

What is dysbiosis?

A

a condition w/ microbial imbalances inside or on the body; prominent in GI & on skin

91
Q

T/F Sensitization of sensory pathways during acute episodes of gastroenteritis contributes to the development of postinfectious functional GI disorders.

A

True.

Block 3; Week 3 Michelle (9 decks)

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