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M1 Block 5 > Week 1 > Flashcards

Week 1 Flashcards

1
Q

What causes slow waves in the GI tract?

A

Interstitial cells of Cajal induce slow waves that do not induce action potential

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2
Q

What is the neural control of the GI tract?

A
  • 2 plexuses
  • Myenteric plexus
  • Submucosal plexus
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3
Q

Describe the layers of the myenteric plexus & Submucosal plexus

A

Outermost to Innermost
- Longitudinal smooth muscle
- Myenteric Plexus
- Circular Smooth muscle
- Submucosal smooth muscle
- Epithelium

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4
Q

What innervates the GI plexuses from the colon to anus?

A

Pelvic N coming off the SNS from S2-S4

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5
Q

What are excitatory NT in the enteric NS?

A

Acetylcholilne
Substance P
Serotonin

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6
Q

What are the inhibitory NT of the enteric NS?

A

VIP & NO

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7
Q

What cells secrete Gastrin?
What stimulates its release?
What inhibits it?

A
  • Gastrin is secreted from G cells
  • Stimulated by: Ingestion of food, nervousness, physical distension, decaf & regular coffee, wine
  • Inhibited by: Acidifcation of antrum
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8
Q

What are some effects of gastric secretion?

A
  • Stimulatory effect
  • Growth of mucosa cells
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9
Q

What cells secrete CCK?
What stimulates CCK?

A
  • CCK released by I cells
  • Stimulated by: Fat, Peptide, A.A. in chyme
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10
Q

What are the downstream effects of CCK?

A
  • Relax sphincter of Oddi allowing flow of bile and pancreatic enzymes into duodenum
  • Contract gallbladder to release bile
  • Increase pancreatic enzyme secretion
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11
Q

________________ induces Zollinger-Ellison syndrome. Which is:

A
  • Gastrinoma is a non B-cell tumor of the pancreas or G-cells tumor in duodenum
  • Causing increase of epithelial cell layer
  • Secretion of Gastrin which induces increase of mucosa cells
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12
Q

_____________-___________ syndrome induced by gastrinoma causes the following symptoms: Duodenal ulcers, diarrhea, steatorrhea, hypokalemia, peptic ulcer. What causes the hypokalemia & steatorrhea?

A
  • Steatorrhea: because there is increased gastrin released resulting in more HCl release = lower pH. The lower pH inactivates pancreatic lipase and bile salt precipitation. Thus fats are not broken down and are excreted
  • Hypokalemia: because there is loss of gastric juices which have lots of K+
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13
Q

What test is used for Gastrinoma/Zollinger-Ellison syndrome?

A
  • Chirhostim test
  • Use synthetic secretin to see if this inhibits the Gastrin
  • Gastrin inhibition = normal function b/c secretion blocks gastrin
  • If cont. secretion of Gastrin = tumor b/c tumor will not respond to negative feedback
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14
Q

What cells secrete Secretin?
What stimulates its release?

A
  • Secretin comes from S-cells
  • Secretin inhibits Gastrin release which inhibits HCl = increased pH
  • Stimulates liver & pancreas to release bicarb
  • Tropic effect of pancreas
  • Simulate pepsin release from stomach
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15
Q

What cells release GIP/GLIP AKA Glucose dependent insulinotropic peptide?

A
  • Released by K cells of duodenum & proximal jujenum
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16
Q

What stimulates release of GIP & GLIP?
What are the downstream effects?

A
  • Stimulated by ingestion of foods including oral glucose (not released if administered IV glucose)
  • Effect: insulin release via feedforward control & inhibits gastric acid secretion
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17
Q

GILP/GIP is a hormone classified as an enterogastrone. What is an enterogastrone?

A

Hormones released from intestine that acts on stomach to inhibit acid secretion

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18
Q

What cells secrete Motilin?

A
  • Released by M-cells of duodenum & proximal jujenum
19
Q

What stimulates the release of Motilin?
What are the downstream effects?

A
  • Stimuli: Fasting
  • Effects: upper GI motility & contributing to slow wave contractions
20
Q

Somatostatin and Histamine are both paracrine hormones meaning:

A

They are hormones that acts locally and do not enter blood stream

21
Q

What stimulates the release of Somatostain?
What are the effects?

A
  • Stimuli: Acid & Acetylcholine
  • Effects: Inhibit release of gut hormones, inhibit parietal acid secretion
22
Q

What stimulates the release of histamine in the GI?
What are the downstream effects?

A
  • Stimuli: Gastrin & ACh
  • Effects: Acid secretion
23
Q

Differentiate Intrinsic control of the GI tract vs Extrinsic control:

A
  • Intrinsic: Enteric NS further specified as myenteric & submucosal plexus
  • Extrinsic: ANS
24
Q

What is the location of the myenteric plexus & what is its purpose?

A
  • Most outer plexus b/t longitudinal (outermost) & circular SM layers (innermost)
  • Increase tonic contraction, increase frequency & intensity
  • Inhibitory Influence: decrease sphincter tone
25
Q

Where is the submucosal plexus found?
What is its function?

A
  • Located b/t circular smooth muscle (outermost) and epithelium (innermost)
  • Functioning in: secretion, absorption, and contraction of muscularis mucosa
26
Q

Describe Parasympathetic innervation of the GI

A
  • Upper half-Colon: Vagus N
  • Colon to Anus: Pelvic N through sacral inn. S2-S4
  • Post-ganglions synapse with ENS neurons
27
Q

Describe the sympathetic innervation of GI

A
  • Pre-ganglions emerge from T5-L2 to form to synapse in prevertebral ganglia
  • Post-Ganglions originate from ganglia and innervate the entire gut. Terminate in the ENS
  • Tend to inhibit/decrease activity in ENS
28
Q

Describe sensory afferent neurons in the GI

A
  • Dendrites at the epithelium receiving input
  • Info can be sent to submucosal plexus or myenteric plexus or to brain/higher level
29
Q

Describe Vasovagal reflex:

A
  • Controls gastric motor and secretory activity w/afferent & efferent activity via vagus
30
Q

The _______________________ do not induce action potential in GI, what does?

A
  • Interstitial cells of Cajal don’t induce AP
  • Induced by Voltage dependent Ca+2 channels
31
Q

What induces peristalsis? What blocks it?

A
  • Peristalsis can be induced by distention, PNS, or irritation of gut epithelium
  • Can be blocked by atropine
  • Atropine is a ACh blocker
32
Q

What is Hirshsprung disease?

A

Missing myenteric plexus so no peristalsis can occur

33
Q

What cells secrete α amylase & lipases?
Describe the saliva composition here

A
  • Acinar cells at the distal end of salivary glands
  • When secereted, this saliva is isotonic with the body.
  • But as saliva moves towards release, it is modified
34
Q

Describe the modification of saliva through the duct

A
  • Distal to acinar cells and proximal to secretion, there is no movement of water
    -Na+ & Cl- are reabsorbed in exchange for H+ and HCO-3 respectively
  • K+ is secreted in exchange for H+ reabsorption
  • With no water reabsorption, Saliva is now hypotonic
35
Q

Describe how Acinar cells modify saliva

A
  • Acinar cells have CFTR channels where in cAMP causes efflux of Cl- into saliva
  • Na+ follows Cl- to balance charge
  • H20 follows solute gradient
36
Q

Aside from initiating digestion of starches and lipids, what are some other functions of saliva?

A
  • Allowing tase molecules to dissolve
  • Activate tase receptors
  • Destroy bacteria, has IgA
37
Q

Why is it important to brush your teeth in the morning?

A
  • Saliva flow decreases during sleeping
  • Since saliva kills bacteria, at night it can build up
38
Q

What normally induces saliva secretion?
What else can induce saliva secretion?

A
  1. PNS normally induces via M3 receptors and secretes watery alkaline saliva
  2. When SNS induces saliva secretion b/c the person is stressed, the β1 & β2 receptors secrete a protein rich saliva making it feel drier
39
Q

Cystic fibrosis is a mutation of: __________ channel. Inducing what changes to saliva?

A
  • Mutation of CFTR channels which causes saliva have higher content of Ca+, Na+, and proteins
40
Q

Describe receptive relaxation of stomach:

A

Swallowing center initiates relaxation of stomach smooth muscle

41
Q

What is achalasia?

A
  • Motility disorder of lower 2/3 esophagus due to dysfunction of myenteric plexus
  • Inability of lower esophageal sphincter to relax & pressure is high
  • Causes megaesophagus
42
Q

What induces primary peristalsis?

A

Vagus N

43
Q

What induces secondary peristalsis?

A

Enteric NS

44
Q

Is contraction or relaxation occurring in the UES during swallowing? What about LES?

A
  • Relax

M1 Block 5 (1 decks)

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