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Practice Topics Exam 5 > GI Physiology 3 > Flashcards

GI Physiology 3 Flashcards

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
Q

Components of gastric secretions - Mucus - Protective factors - The mucus layer protects by

A

Creating a physical barrier
Inc pH at mucosal surface
Preventing activation of pepsinogen

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26
Q

Components of gastric secretions - Mucus - Mucus secretion is stimulated by

A 
Neurocrine = Ach
Paracrine = Prostaglandins
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27
Q

Components of gastric secretions - Mucus - Mucus secretion stimulated by Ach and Prostaglandins - Prostaglandins key roles include

A

Mucus and HCO3 secretion
Suppression of HCl secretion (negative regulator)
Inc gastric blood flow

28
Q

Components of gastric secretions - Mucus - If disruption of mucosal layer

A

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
Q

Things that increase acid secretion?

Things that decrease acid secretion?

A 
Increase = Ach, Histamine, Gastrin
Decrease = Prostaglandins
30
Q

Components of gastric secretions - Mucus - Acid secretion is regulated directly through

A

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
Q

Acid-Peptic Disease includes

A

Gastritis

Ulcers

32
Q

Acid-Peptic Disease - Gastritis

A

Infiltration of inflammatory cells without a break in the mucosal barrier

33
Q

Acid-Peptic Disease - Ulcer

A

Breakthrough in mucosal lining

34
Q

Acid-Peptic Disease - Primary causes of acid peptic disease

A

H pylori infection

NSAIDs and Aspirin

35
Q

Acid-Peptic Disease - Other causes

A 
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
Q

Acid-Peptic Disease - H pylori are key inducers of gastritis and gastric ulcers - H pylori description

A

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
Q

Acid-Peptic Disease - H pylori are key inducers of gastritis and gastric ulcers - H pylori expresses virulence factors that will what

A

Allow for adhesion to the epithelium
Will induce immune response
Breakdown mucus layer that protects the epithelium

38
Q

Acid-Peptic Disease - Caused by NSAIDs - NSAIDs do what

A

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
Q

Acid-Peptic Disease - Caused by NSAIDs - Decrease in prostaglandins leads to (opp of func of prostaglandins)

A

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
Q

Gastric motor activity

A

Storing
Churning
Emptying

41
Q

Gastric motor activity - Storing

A

Reservoir function in which the stomach fills and stores contents
2 steps = Receptive relaxation and Gastric accommodation

42
Q

Gastric motor activity - Churning

A

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
Q

Gastric motor activity - Churning - end result

A

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
Q

Gastric motor activity - Storing - steps

A

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
Q

Gastric motor activity - Emptying

A

Delivery of food to duodenum

46
Q

Gastric motor activity - Rate of emptying

A 
Depends on the content of the ingested material
Liquid will move through first
Glucose moves through quickly
Protein slower
Fat is even slower
47
Q

Gastric motor activity - Emptying - Control of emptying rate

A

Controlled through neuronal and hormonal regulation
Hormones = secretin, CCK, gastrin
Neurons = ACh, NO, 5HT, VIP

48
Q

Gastric motor activity - Emptying - Stimulus/Mediator/Result

Stimulus = HCl in duodenum

A

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
Q

Gastric motor activity - Emptying - Stimulus/Mediator/Result

Stimulus = Fat n duodenum

A

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
Q

Gastric motor activity - Emptying - Stimulus/Mediator/Result

Stimulus = protein in the stomach

A

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
Q

Gastric motor activity - Emptying - Stimulus/Mediator/Result

Stimulus = duodenal distention and osmolarity

A 
Mediator = Ach and 5HT
Result = Feedback reflexes from the duodenum cause pyloric contraction
52
Q

Gastric motor activity - Emptying - Stimulus/Mediator/Result

Stimulus = Vagal efferents (the one he said to know)

A

Mediator = NO
Relaxation of the pyloric region and therefore promotes gastric emptying
PROMOTES GASTRIC EMPTYING

53
Q

Multiple roles of CCK - what stimulates its release (relating to its function in the stomach)

A

Fat stimulates CCK release

Functions to reduce emptying

54
Q

Emesis - definition

A

Expulsion of gastric and duodenal contents from the GI tract via the mouth

55
Q

Emesis - preceded by

A

Nausea, Tachycardia, Dizziness, Sweating, Mydriasis, Retching, Inc saliva production

56
Q

Emesis - key motility events

A

Wave of reverse peristalsis

Contraction of abdominal mm and resp mm

57
Q

Emesis - sign of

A

Pathophysiological condition that may or may not be GI related

58
Q

Emesis - purpose of inc saliva

A

Protection of the oral cavity from the acid that is about to come up (inc mucin and bicarb with inc in saliva)

59
Q

Emesis - reverse peristalsis of what

A

The duodenum and the stomach (NOT THE esophagus)

60
Q

Emesis - Key NTs

A

5HT
Ach
Dopamine
Histamine

Key NT for the gut is 5HT (relays signal from gut to CNS)

61
Q

Emesis - causes can be (general)

A 
Medications
GI disorders
CNS causes
Endocrine
Infections
62
Q

Emesis - causes - Medications

A

Chemo
Analgesics
Antibiotics
Narcotics *

63
Q

Emesis - causes - GI disorders

A

5HT will be involved!

Mechanical obstruction
Gastroparesis
Radiation injury
Functional bowel disorders
Intraperitoneal inflammation
64
Q

Emesis - causes - CNS

A

Inc ICP
Emotional responses
Psychiatric conditions
Tumors

65
Q

Emesis - causes - Endocrine

A

Pregnancy
Uremia
Diabetic ketoacidosis

66
Q

Emesis - causes - Infections

A

VIral/Bacterial gastroenteritis

Practice Topics Exam 5 (13 decks)

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