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Physio Exam 3 > Wold 3 > Flashcards

Wold 3 Flashcards

1
Q

But, there are only 2

stomach**

A

2 glandular regions in the stomach.

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2
Q

There are 3 sections of the

A

stomach.

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3
Q

Pepsinogen is a

A

zymogen (i.e., it is a proenzyme that needs to be cleaved to become active)

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4
Q

Parietal cells produce

A

intrinsic factor

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5
Q

pancreas is an

A

exocrine gland

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6
Q

pancreas

Exocrine

A 
bicarbonate ions
  digestive enzymes (many, many, many digestive enzymes)
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7
Q

CCK Secretion is potentiated by

*Pancreas

A

secretin

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8
Q

Pancreatic Bicarbonate secretion is essentially the same

A

as HCl secretion in reverse.

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9
Q

Regulation of Pancreatic Bicarbonate Secretion:

Hormone regulation by

A

secretin

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10
Q

Regulation of Pancreatic Bicarbonate Secretion

Feedback regulation by

A

acidity

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11
Q

CCK strongly potentiates the effects of

A

secretin

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12
Q

Liver:

Secretes bile into small ducts called

A

bile canaliculi

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13
Q

Liver

Canaliculi converge and drain into

A

larger bile ducts.

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14
Q

Small Intestine types of muscle contractions:

Peristalsis: progressive contractions of successive sections of

A

circular smooth muscle

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15
Q

Small Intestine types of muscle contractions

Segmentation: closely spaced contractions of

A

circular muscle layer. When this is rhythmic (i.e., sites of the circular contractions alternate between contraction and relaxation), chyme/bolus is mixed and slowly moved downward.

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16
Q

Bacteria can ferment some of these undigested substances, which will then be absorbed in the

A

large intestine, but this comes at a price…

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17
Q

motility in large intestine occurs as slow

A

“segmentation” contracts

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18
Q

large intestine; peristaltic-like contractions occur

A

3 – 4 times per day

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19
Q

How do we digest a meal?

Mouth

A

Chewing, salivation, amylase, lipase

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20
Q

How do we digest a meal?

Stomach

A

HCl, pepsinogen, lipase, gastrin

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21
Q

How do we digest a meal?

Small Intestine

A

Hormones—Secretin, Cholecystokinin

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22
Q

How do we digest a meal?

Accessory Organs

A

Pancreas—proteases, lipase, amylase, HCO3-

Liver—bile

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23
Q

How do we digest a meal?

Small Intestine

A

Absorption—carbohydrates, proteins, fats, vitamins, minerals

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24
Q

How do we digest a meal?

Large Intestine

A

Absorption—Na+, Cl-, water

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25
Q

Chyme has to ——- in order for us to digest a meal

A

keep moving

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26
Q

Stomach churning

Rate is determined by

A

pacemaker cells,

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27
Q

Stomach churning

magnitude determined by

A

excitatory stimuli

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28
Q

Stomach

Peristalsis from

A

body to pyloric sphincter

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29
Q

Small Intestine

Segmentation and Peristaltic contractions
Peristalsis controlled by

A

migrating myoelectric complex (initiated by motilin)

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30
Q

Primary purpose of the large intestine is to actively transport

A

Na+ from lumen to blood.

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31
Q

Large intestine

Also, bicarbonate secretion is coupled to

A

Cl- ion absorption.

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32
Q

Bacterial fermentation of some of the food bolus contents maximizes the absorption of nutrients from food in the

A

large intestine

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33
Q

Small Intestine Motility

During absorption ——- occur.

A

segmentation contractions

34
Q

Small Intestine Motility

After most absorption has occurred,

A

peristaltic contractions occur.

35
Q

Small Intestine Motility

Peristalsis is driven by a

A

migrating myoelectric complex.

36
Q

peristalsis in small intestine

Starts in

A

lower stomach and travels about 2 feet prior to dying out

37
Q

peristalsis in small intestine

Initiated by the intestinal hormone

38
Q

Absorption is maximized when the

A

chyme/bolus is continuously brought into contact with the intestinal tissue (constant movement)

39
Q

The liver synthesizes, about

A

20-60 mg of bile salts a day

40
Q

——– of bile salts are secreted a day.

A

1,200-3,600 mg

41
Q

Bile salts are recycled through the

A

enterohepatic circulation

42
Q

Bile

A

Bile salts (and other salts)
Lecithin
Cholesterol
Bile pigments (like bilirubin) and other metabolic end products
Trace metals
Bicarbonate ions (secreted by epithelial cells of ducts, stimulated by secretin)

43
Q

In general, the same factors that affect HCl secretion also affect

A

gastric motility/emptying.

44
Q

Enterogastrone is a hormone produced by

A

intestinal cells

45
Q

Enterogastrone

inhibit the secretion or motility in the

46
Q

Secretin, and CCK are

A

enterogastrones.

47
Q

Regulation of HCl Secretion

Intestinal phase—initially enhances

A

HCl secretion. But, later in digestion, the intestinal phase is inhibitory.

48
Q

Regulation of HCl Secretion

when pH of chyme < 3, =

A

secretin produced

49
Q

Regulation of HCl Secretion

High H+, amino acids, and fatty acids stimulate

A

CCK, which ↓HCl production

50
Q

Regulation of HCl secretion

Gastric phase—

A

distension, proteins, peptides and amino acids. Increase in gastrin secretion.

51
Q

Somatostatin is a potent inhibitor of

A

HCl secretion via 2 mechanisms
Effects on G Cell
Effects on Parietal Cell

52
Q

Inputs to Parietal Cells Regulate

A

Acid Secretion

53
Q

Histamine is the strongest

A

HCl stimulant.

54
Q

Histamine release can be triggered by

A

gastrin or Ach

55
Q

Gastrin and Ach can have direct effects on

A

parietal cells.

56
Q

Parietal cells: In all cases, activation of receptors results in second messenger activation that increases the ability of

A

parietal cell to release H+ and Cl-

57
Q

Mucous—Mucous Neck Cells

A

Throughout all sections of stomach

58
Q

HCO3-—Epithelial Cells

A

Throughout all sections of stomach

59
Q

Gastrin—G Cells

A

Antrum (Pyloric Gland Area)

60
Q

Somatostatin—D cells

A

Throughout the stomach at the base of the gastric glands

61
Q

Histamine—

A

Enterochromaffin-like cells

62
Q

HCl—Parietal Cells

A

Fundus and Body (Oxyntic Gland Area)

63
Q

Intrinsic Factor—Parietal Cells

A

Fundus and Body (Oxyntic Gland Area)

64
Q

Pepsinogen—Chief Cells

A

Body and Antrum (Oxyntic and Pyloric Gland Area)

65
Q

stomach

Delivers the chyme to the duodenum at a rate compatible with

A

The secretion rate of bile salts, bicarbonate ions, and digestive enzymes
Rate of enzymatic breakdown of proteins, lipids, and carbohydrates
Small intestine transit

66
Q

Phases of GI Control

A

cephalic, gastric, intestinal

67
Q

Cephalic Phase

A

(parasympathetic nerve fibers affecting ENS)

68
Q

Cephalic phase Initiated when

A

receptors in head are stimulated

69
Q

Gastric Phase

A 
(short and long neural reflexes and gastrin)
Distension
Acidity
Amino acids
Peptides
70
Q

Intestinal

A 
(short and long neural reflexes, secretin, CCK, and GIP)
Distension
Acidity
Osmolarity
Various digestive products
71
Q

Each GI hormone participates in a

A

feedback control system to regulate some aspect of the GI lumen
e.g., CCK stimulated by fatty acids, stimulates enzyme production by pancreas, which will reduce CCK and reduce pancreas activation

72
Q

Each GI hormone affects more than

A

one type of target cell

e.g., CCK can stimulate pancreas, liver, gallbladder, and inhibit stomach emptying

73
Q

GI Hormones can have

A 
synergistic effects (one can potentiate the other)
e.g., secretin enhances the effects of CCK
74
Q

Four hormones play a large role in regulating digestion

Gastrin

A

Cholecystokinin (CCK)
Secretin
Glucose-dependent insulinotropic peptide (GIP)

75
Q

Receptors GI

A

Mechanoreceptors
Osmoreceptors
Chemoreceptors

76
Q

GI: changes Initiated by

A

Distension of the wall
Chyme osmolarity
Chyme acidity
Chyme concentrations

77
Q

ENS Motor Neurons

A

Muscle Contractions

Gland Function

78
Q

ENS: Interneurons

Regulate

A

interactions between different layers of the GI tissue

79
Q

GI Neurons

A

Autonomic nervous system

Enteric nervous system

80
Q

Paracrine mediators

Produced by

A

local cells

Reach target cells via diffusion

81
Q

Hormones

Produced by

A

endocrine cells

Reach gut via the blood

Physio Exam 3 (19 decks)

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