47-48 Cephalic Oral Esophagus Flashcards

1
Q

Generally, what is the cephalic phase?

What are its stimuli?

A
  • Activation of the GI tract in readiness for the meal

- Idea of food, smell, auditory, visual

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2
Q

What is the pw of the cephalic phase, and what is the GI response?

A
  • Thought/sense -> cortex/hypothalamus -> lower pons/upper medulla–dorsal motor nucleus (DMN, somas of vagus) -> parasymp (vagus) stimulation
  • Increased salivary secretion (CN IX); increased gastric, pancreatic, and GB secretions; relaxation of Sphincter of Oddi
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3
Q

What is the oral phase?

A

Generally the same as cephalic phase except food is in the mouth (input from tongue, mouth, pharynx)
- Chewing also occurs

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4
Q

What is mixed in w/food during chewing?

A

Salivary amylases, lingual lipases, salivary mucin (lube)

–> enhanced activation of GI system

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5
Q

What is absorbed in the mouth?

A

Only some drugs (e.g. alcohol)

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6
Q

What is Xerostomia? What problems can it lead to?

A

AKA dry mouth

  • Impaired salivary secretion
  • The decrease in secretion reduces pH in the oral cavity: tooth decay, esophageal erosions, difficulty swallowing
  • Congenital or autoimmune.
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7
Q

Name the mm. involved in chewing. Which is most important?

What n. innervates them?

A
  • Temporalis (Most Important)
  • Masseters
  • Lateral + Medial Pterygoids

Distinct branches of trigeminal (CN V)

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8
Q

What are the 3 general places GI secretions can come from?

A
  • Glands associated w/the tract (e.g. pancreas)
  • Glands of the gut wall (e.g. Bruner’s)
  • Intestinal mucosa itself
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9
Q

What are the 3 general receptor types that can initiate GI glandular secretion?

A

Chemical, mechanical, osmotic

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10
Q

What’s a secretagogue?

A

Any substance that stimulates secretion

- Act on secretory cells, work as endocrine, paracrine or neurocrine modulators

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11
Q

Describe the 3 main types of salivary secretions.

A
Serous: water, electrolytes, enzymes
 - parotid (mostly)
Mucous: mucin glycoprotein
 - sublingual (mostly)
Mixed
 - submandibular
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12
Q

What 2 main anatomical structures make up a salivary gland?

A
  1. Acinus (secretary portion)

2. Duct system (intercalated duct -> striated duct)

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13
Q

In 1 word, what is the general structure of GI glands?

A

“Tubuloalveolar”

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14
Q

What is an acinus/what are acini?

What do they produce?

A

“Basic secratory unit”: The blind end of the branching duct system, lined with acinar cells
- Produce initial saliva composed of water, ions, enzymes, mucus.

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15
Q

After the initial mucus is produced in the secretary acini, what then do the ductal cells do?

A

As the saliva passes thru, they modify the electrolyte concentration to produce the final saliva.

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16
Q

How is saliva stimulated to leave the ducts?

What types of cells are stimulated to perform this?

A
  • Exclusively neural (it’s an exception; other GI ducts are both neural and hormonal)
  • Myoepithelial cells (lining the ducts) contract, pushing the saliva out
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17
Q

Define: adenoma.

A

A benign tumor formed from glandular structures in epithelial tissue

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18
Q

How much saliva is produced per day?

A

1L/day

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19
Q

What are the 3 functions of saliva?

A
  • Lubrication
  • Protection
  • Digestion (initial)
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20
Q

How, specifically, does saliva provide protection (4 points)?

A
  • Dilutes and buffers ingested food
  • Neutralizes gastric acids and pepsin that come up to mouth
  • Washes away bacteria
  • Contains lysozyme, which lyses bacterial cell walls
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21
Q

Saliva composition varies based on what factor?

A

Salivary flow

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22
Q

What are the major salt components of saliva?

A
  • Na+, K+, Ca2+, Mg2+, Cl-, F-
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23
Q

Major organic constituents of saliva and their functions?

A
  • Salivary alpha amylase (initial starch digestion)
  • Lingual lipase (lipid digestion)
  • Glycoprotein (mucin forms mucus when hydrated)
  • Lysozyme (attacks bacterial cell wall)
  • Kallikrein (converts plasma protein into bradykinin- a potent vasodilator)
24
Q

Is saliva hyper, iso, or hypotonic, usually?

Therefore, is there net absorption or secretion of solute?

A

Hypotonic (decreased osmolarity)

- Net absorption

25
Q

Explain the 2-step process by which saliva is formed.

A
  1. Formation of an isotonic plasma-like solution by the acinar cells – known as the primary secretion/initial saliva.
  2. Modification of this plasma-like soln by the ductal cells to produce hypotonic final saliva.
26
Q

During step 2 of the saliva formation process, what transporters are present on the luminal and basolateral membranes?

A
LUMINAL:
Na+/H+ exchange
Cl-/HCO3- exchange
H+/K+ exchange
BASOLATERAL:
NKP
Cl- channels
27
Q

What 2 ions is the final saliva sln high in? Low in?

A

High in K+ and HCO3-; low in Na+ and Cl-

28
Q

Would saliva be more similar to plasma if it is produced w/a high flow rate or a low flow rate?

A

High flow rate, because there is less time for modification by ducts.
- Exception: HCO3- secretion is selectively stimulated when saliva production is stimulated (e.g. parasymp stim)

29
Q

What nervous system stimulates saliva secretion?

A

Stimulated by both sympathetic and parasympathetic, although parasymp stim is dominant (applies to acinar and ductal cells)

30
Q
What parasympathetic nerve branches provide input to the 3 salivary glands?
What postganglionic NT is released?
What receptor class does this NT bind?
What intracellular cascade occurs?
A
  • Branches of Facial (CN VII) and Glossopharyngeal (CN IX)
  • Post-ganglionic neurons release ACh
  • > Interacts with muscarinic receptors
  • > production of IP3 and increased intracellular Ca++
31
Q
What sc segment do sympathetic nerves branches from to provide input to the 3 salivary glands?
Where do the preganglionic nn. synapse?
What postganglionic NT is released?
What receptor class does this NT bind?
What intracellular cascade occurs?
A
  • T1-T3
  • Superior cervical ganglia
  • NE
  • > Interacts w/beta-adrenergic receptors
  • > cAMP - increased saliva secretion
32
Q

What is inhibited during swallowing?

A

Respiration (via interactions between respiratory & swallowing centers)

33
Q

Where is the neural swallowing center located?

A

Medulla + lower pons

34
Q

How does the afferent limb of the swallowing reflex begin?

A

Touch/stretch receptors near opening of the pharynx are stimulated (after the voluntary beginning phase)
- Sensory impulses travel to the swallowing center

35
Q

What efferent impulses leave the swallowing center during the reflex? (and what general types of neurons go to each?)

A

Motor impulses from swallowing center travel to the pharynx and upper esophagus (via cranial nerves) and to the remaining esophagus (via vagal motor neurons).

36
Q

Name the 3 phases of swallowing.

A
  1. Oral
  2. Pharyngeal
  3. Esophageal
37
Q

Is the oral phase of swallowing voluntary or involuntary?
How is the oral phase of swallowing initiated?
What receptors are activated?

A
  • Voluntary
  • Initiated when tongue forces a bolus of food back towards pharynx
  • activates stretch receptors -> initiates involuntary swallowing reflex
38
Q

*Describe what is occurring during the (involuntary, less than 1 sec) pharyngeal phase.

A

1) The soft palate moves up and palatopharyngeal fold moves inward (prevents reflux into nasopharynx), food moves into pharynx
2) Epiglottis moves down, covers opening to larynx as larynx moves upward (prevents food entry to trachea)
3) UES relaxes to receive bolus
4) Pharynx contracts (initiates peristaltic wave of contractions), bolus reaches esophagus
5) UES closes (part of same reflex)

39
Q

Is the esophageal phase controlled by the ENS, the swallowing reflex, or both?

A

Both (first ENS involvement)

40
Q

What n. controls the UES? LES?

A

UES: glossopharyngeal (IX)
LES: vagus (X)

41
Q

*Describe what is occurring during the (involuntary) esophageal phase of swallowing.

A
  1. UES closes after bolus is in (via reflex)
  2. Primary peristaltic contraction: waves coordinated by the reflex push bolus thru
  3. Secondary peristalsis: distension from the primary contractions stimulate ENS to repeat more waves
  4. Peptidergic fibers in the vagus nerve release VIP, causes LES to open
  5. Receptive relaxation: during step 4, orad stomach simultaneously relaxes (decreases pressure)
  6. Bolus enters stomach, LES closes tightly
42
Q

What pressure is lower, esophageal or abdominal?

What issues does this create that are solved by the UES and LES?

A

Esophageal

  • UES: keeps are out
  • LES: blocks gastric reflux
43
Q

In terms of epithelia, describe the transition from esophagus to stomach.

A

Esophagus: stratified squamous epithelium
Stomach: simple columnar epithelium

44
Q

What do esophageal cardiac glands release?

A

Mucus

45
Q

What layer is damaged in GERD?

A

The esophageal epithelium (stratified –> simple)

46
Q

Increase in intra-abdominal pressure can lead to what dz?

A

GERD–LES fails to keep out gastric contents

47
Q

What are some e.g.’s of conditions that can cause GERD?

How is chronic GERD treated? (give 2 major meds and their basic actions)

A
  • Pregnancy, morbid obesity

- H2 receptor antagonists- e.g. ranitidine to reduce gastric acid secretion. Or proton pump inhibitors- e.g. omeprazole.

48
Q

What is hiatal hernia?
What are the major sx?
What are some common causes?

A

A reflux dz: Upper stomach protrudes into chest cavity thru esophageal hiatus

  • Sx: pain, acid reflux
  • Causes: genetic predisposition, obesity, weight lifting, constipation

(estimated that 60% of the population over 60 years of age has some degree of hiatal hernia)

49
Q

What is achalasia?
What are the sx?
What is the tx?

A

The smooth m. layer of esophagus does not have normal peristalsis and the LES does not relax normally in response to swallowing.

  • Sx: dysphagia, regurgitation, chest pain
  • Tx: surgical (myotomy along esophagus). Meanwhile, pts must be treated with Ca2+ channel blockers, botox injection in the LES, and other muscle relaxants.
50
Q
Define vomiting (simply).
What is it preceded by?
A

Mouth ejection of gastric or gastroduodenal contents

- Preceded by nausea, irregular heartbeat, dizziness, sweating, retching, etc.

51
Q

Try to name 7 causes of vomiting.

A
  • Tactile: stimulation of back of throat
  • Irritation/distension of stomach and duodenum
  • Elevated intracranial pressure (e.g. cerebral hemorrhage)
  • Rotation/acceleration of the head (e.g. motion sickness)
  • Intense pain
  • Chemical agents (e.g. emetics): act on upper portions of the GI tract or on specialized chemoreceptors in the brain
  • Emotional factors
52
Q

Where is the vomiting center?

A

Reticular formation of pons

53
Q

*What occurs during the vomiting reflex?

A
  • Reverse peristalsis of the small intestine
  • Relaxation of the pyloric sphincter and stomach (receives contents)
  • Forced expiration against closed glottis + forceful contraction of abd muscles (v T-pressure, ^ A-pressure)
  • Relaxation of LES, UES, and esophagus + contraction of pylorus and antrum
  • -> contents expelled
54
Q

What occurs during “retching”?

A

UES remains closed, gastric content is forced into esophagus but does not enter pharynx (often precedes vomiting)

55
Q

*What are the sx of autonomic d/c that can also occur during vomiting?

A

Salivation, dilation of pupils, sweating, pallor, rapid and irregular heart beat.