GI Physiology 3 Flashcards

(66 cards)

1
Q

Mucosal surface of the stomach - antrum

A

Just before the pyloric sphincter
Important endocrine organ
Important in regulating GI function

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2
Q

Mucosal surface of the stomach - describe

A

It has pits and is highly invaginated

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3
Q

Gastric cells and secretions - Cells include

A

Surface mucous and neck cells
Parietal cells
Chief cells

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4
Q

Gastric cells and secretions - Surface mucous cells and neck cells - secrete what
What is their function

A

Secrete mucus bicarbonate

Function in gastroprotection

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5
Q

Gastric cells and secretions - Parietal cells - secrete what

What are their functions?

A

HCl - protein digestion sterilization, nutrient absorption

Intrinsic factor - Vit B12 absorption

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6
Q

Gastric cells and secretions - Chief cells - secrete what

What is their function

A

Secrete pepsinogen

Function in protein synthesis

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7
Q

Important regulatory cells include

A

ECL cells
Neurons
G cells
D cells

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8
Q

Important regulatory cells - ECL cells secrete what?

What is their function

A

Secrete histamine
Function in promoting HCl secretion
Histamine is an important paracrine regulator

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9
Q

Important regulatory cells - Neurons - secrete what? Function how?

A

Secrete ACh

Function to promote mucus secretion, promote HCO3 secretion, and promote HCl secretion

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10
Q

Important regulatory cells - G cells - secrete what? Function?

A

Secrete gastrin

Functions to promote HCl secretion

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11
Q

Important regulatory cells - D cells - secrete what? Function?

A

Secrete somatostatin
Functions in suppressing HCl secretion
It is a negative regulator - works in both paracrine and endocrine function

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12
Q

Direct regulation of the parietal cell - acid secretion is regulated directly through

A
Paracrine pathways (histamine)
Endocrine pathways (gastrin)
Neurocrine pathways (Ach)
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13
Q

Direct regulation of the parietal cell - how is acid secretion regulated directly through paracrine pathway?

A

Histamine!
Binds to H2 receptors
H2 promotes acid secretion
If taking drug that blocks H2 receptor - acid suppression

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14
Q

Direct regulation of the parietal cell - how is acid secretion regulated directly through endocrine pathways?

A

Gastrin!
Gastrin is a hormone that binds to CCK2
Gastrin is released from the antrum
Gastrin stimulates the parietal cell to secrete acid

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15
Q

Direct regulation of the parietal cell - how is acid secretion regulated directly through neurocrine pathways?

A

Ach!

Muscarinic receptors respond to Ach

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16
Q

Intrinsic factor is released by what cells

A

Parietal!

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17
Q

Parietal cell secretions - IF

A

Vit B12 is released during gastric disruption
Once released, vit B12 binds to haptocorrin
IF will bind to Vit B12 to form a complex
Complex will remain bound throughout intestine and will be absorbed in the ileum
Our body cannot see vit B12 unless it is in complex with IF

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18
Q

Diseases that impact parietal cells will cause changes in

A

IF secretion which will then change vit B12 absorption which can then lead to anemia
Stomach atrophy can also lead to vit B12 deficiency

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19
Q

Deficiency in IF and/or vit B12 can lead to

A

Inc risk of infection

Changes in nutrient absorption

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20
Q

Key gastric secretions

A

Acid (HCl)
Pepsinogen
Mucus
Intrinsic Factor

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21
Q

Components of gastric secretions - Pepsinogen

A

Pepsinogen is released and as moves through mucosal gel layer is inactive (pH is not right)
Lower pH will activate pepsinogen - we don’t want this to happen until it is in the lumen
Once activated, pepsin can help convert pepsinogen to pepsin

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22
Q

Components of gastric secretions - Pepsinogen - what is required for the activation of pepsinogen to pepsin

A

HCl!

Optimal activity for pepsin activation is pH of 1.8 to 3.5

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23
Q

Components of gastric secretions - Mucus - Protective factors - the mucus layer is made up of

A
Mucin
Phospholipids
Electrolytes
Water
Bicarbonate
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24
Q

Components of gastric secretions - Mucus - Within the gel layer we have mucin which is

A

a glycosylated protein

Important for coding and protecting throughout the GI tract

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25
Components of gastric secretions - Mucus - Protective factors - The mucus layer protects by
Creating a physical barrier Inc pH at mucosal surface Preventing activation of pepsinogen
26
Components of gastric secretions - Mucus - Mucus secretion is stimulated by
``` Neurocrine = Ach Paracrine = Prostaglandins ```
27
Components of gastric secretions - Mucus - Mucus secretion stimulated by Ach and Prostaglandins - Prostaglandins key roles include
Mucus and HCO3 secretion Suppression of HCl secretion (negative regulator) Inc gastric blood flow
28
Components of gastric secretions - Mucus - If disruption of mucosal layer
Pepsinogen can become activated at the stomach surface (rather than waiting until lumen) and it will attack the tissue and eventually lead to ulcer development
29
Things that increase acid secretion? | Things that decrease acid secretion?
``` Increase = Ach, Histamine, Gastrin Decrease = Prostaglandins ```
30
Components of gastric secretions - Mucus - Acid secretion is regulated directly through
Protaglandins (specifically PGE2) which decreases or inhibits signaling through the histamine pathway Targets the same pathway that histamine does - so prostaglandins turn off the histamine response
31
Acid-Peptic Disease includes
Gastritis | Ulcers
32
Acid-Peptic Disease - Gastritis
Infiltration of inflammatory cells without a break in the mucosal barrier
33
Acid-Peptic Disease - Ulcer
Breakthrough in mucosal lining
34
Acid-Peptic Disease - Primary causes of acid peptic disease
H pylori infection | NSAIDs and Aspirin
35
Acid-Peptic Disease - Other causes
``` Inc number of parietal cells High serum gastrin levels Loss of acid mediated neg feedback on gastrin secretion (loss of somatostatin) Rapid gastric emptying Cigarette smoking Alcohol use Dec mucosal HCO2 secretion GERD ```
36
Acid-Peptic Disease - H pylori are key inducers of gastritis and gastric ulcers - H pylori description
It expresses urease which will help to buffer HCl by generating NH3 and CO2 NH3 is also toxic to gastric epithelium So H pylori can set up its own domain that is more neutral than that of the stomach (pH of 1 or 2)
37
Acid-Peptic Disease - H pylori are key inducers of gastritis and gastric ulcers - H pylori expresses virulence factors that will what
Allow for adhesion to the epithelium Will induce immune response Breakdown mucus layer that protects the epithelium
38
Acid-Peptic Disease - Caused by NSAIDs - NSAIDs do what
Inhibit the enzyme COX1 and COX 2 and dec prostaglandin synthesis (COX normally produces PGE2) So in presence of chronic NSAID use, you get gastric irritation and inhibit healing
39
Acid-Peptic Disease - Caused by NSAIDs - Decrease in prostaglandins leads to (opp of func of prostaglandins)
Dec in gastric blood flow Dec in mucus/HCO3 secretion Inc in acid secretion Therefore NSAIDs will cause damage to the mucosa when prostaglandin synthesis is inhibited
40
Gastric motor activity
Storing Churning Emptying
41
Gastric motor activity - Storing
Reservoir function in which the stomach fills and stores contents 2 steps = Receptive relaxation and Gastric accommodation
42
Gastric motor activity - Churning
Mixing and initiation of digestion After food enters the stomach a propulsive movement (peristalsis) will begin Pyloric sphincter stays closed though so moving contents of stomach towards a wall Contents move back and forth (Retropulsive movement) The rhythmic phase of these contractile forces is called antral systole
43
Gastric motor activity - Churning - end result
Products smaller than 2 mm will eventually pass through the pylorus Particles larger than that will pass into the duodenum during interdigestive period (approx 2 hours later)
44
Gastric motor activity - Storing - steps
Receptive Relaxation - Mediated by vagus - Initiated by swallowing - Relaxation in anticipation of food Gastric accommodation - Relaxation in response to gastric and duodenal filling or stretch - Mediated by ENS
45
Gastric motor activity - Emptying
Delivery of food to duodenum
46
Gastric motor activity - Rate of emptying
``` Depends on the content of the ingested material Liquid will move through first Glucose moves through quickly Protein slower Fat is even slower ```
47
Gastric motor activity - Emptying - Control of emptying rate
Controlled through neuronal and hormonal regulation Hormones = secretin, CCK, gastrin Neurons = ACh, NO, 5HT, VIP
48
Gastric motor activity - Emptying - Stimulus/Mediator/Result Stimulus = HCl in duodenum
Mediator = secretin Result = humeral regulators from the duodenum and stomach decrease emptying (they dec relaxation of pyloric sphincter so it stays closed) DELAYS GASTRIC EMPTYING
49
Gastric motor activity - Emptying - Stimulus/Mediator/Result Stimulus = Fat n duodenum
Mediator = CCK Result = humeral regulators from the duodenum and stomach decrease emptying (they dec relaxation of pyloric sphincter so it stays closed) DELAYS GASTRIC EMPTYING
50
Gastric motor activity - Emptying - Stimulus/Mediator/Result Stimulus = protein in the stomach
Mediator = gastrin Result = humeral regulators from the duodenum and stomach decrease emptying (they dec relaxation of pyloric sphincter so it stays closed) DELAYS GASTRIC EMPTYING! This is a big one!
51
Gastric motor activity - Emptying - Stimulus/Mediator/Result Stimulus = duodenal distention and osmolarity
``` Mediator = Ach and 5HT Result = Feedback reflexes from the duodenum cause pyloric contraction ```
52
Gastric motor activity - Emptying - Stimulus/Mediator/Result Stimulus = Vagal efferents (the one he said to know)
Mediator = NO Relaxation of the pyloric region and therefore promotes gastric emptying PROMOTES GASTRIC EMPTYING
53
Multiple roles of CCK - what stimulates its release (relating to its function in the stomach)
Fat stimulates CCK release | Functions to reduce emptying
54
Emesis - definition
Expulsion of gastric and duodenal contents from the GI tract via the mouth
55
Emesis - preceded by
Nausea, Tachycardia, Dizziness, Sweating, Mydriasis, Retching, Inc saliva production
56
Emesis - key motility events
Wave of reverse peristalsis | Contraction of abdominal mm and resp mm
57
Emesis - sign of
Pathophysiological condition that may or may not be GI related
58
Emesis - purpose of inc saliva
Protection of the oral cavity from the acid that is about to come up (inc mucin and bicarb with inc in saliva)
59
Emesis - reverse peristalsis of what
The duodenum and the stomach (NOT THE esophagus)
60
Emesis - Key NTs
5HT Ach Dopamine Histamine Key NT for the gut is 5HT (relays signal from gut to CNS)
61
Emesis - causes can be (general)
``` Medications GI disorders CNS causes Endocrine Infections ```
62
Emesis - causes - Medications
Chemo Analgesics Antibiotics Narcotics *
63
Emesis - causes - GI disorders
5HT will be involved! ``` Mechanical obstruction Gastroparesis Radiation injury Functional bowel disorders Intraperitoneal inflammation ```
64
Emesis - causes - CNS
Inc ICP Emotional responses Psychiatric conditions Tumors
65
Emesis - causes - Endocrine
Pregnancy Uremia Diabetic ketoacidosis
66
Emesis - causes - Infections
VIral/Bacterial gastroenteritis