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GastroIntestinal > Introduction to Gastrointestinal Physiology Lecture (TEST 2) > Flashcards

Introduction to Gastrointestinal Physiology Lecture (TEST 2) Flashcards

1
Q

Gastrointestinal Tract: Main Functions

A

A) Digestion and Absorption of Nutrients

B) Main properties of the GI that are responsible for its role in digestion and Absorption:

1) Motility
2) Secretions

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2
Q

Organization of the GI Tract

A
  • Sphincters RESTRICT the passage of Intestinal Content to OPTIMIZE Digestion and Absorption

a) Upper Esophageal Sphincter
b) Lower Esophageal Sphincter
c) Pylorus
d) Sphincter of Oddi
e) Oleocecal Valve
f) Internal Anal Sphincter
g) External Anal Sphincter

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3
Q

Small Intestine Wall Structure

A

Functional Layers:
1) Mucosal Layer

2) Submucosa

3) Muscle Layers:
a) Circular Muscle
b) Longitudinal Muscle

4) Serosa

  • ENTERIC Nervous System (ENS) or “Nervous System of the GI Tract”:
    a) SUBMUCOSAL Plexus
    b) MYENTERIC Plexus
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4
Q

GI Function is Regulated by the interplay between Central, Autonomic, and Enteric Nervous System

A
  • The GI Tract is innervate by the Autonomic Nervous System (ANS) and the Enteric Nervous System
    a) Extrinsic Nervous System
    b) Intrinsic Nervous System
  • The EXTRINSIC Nervous System has Cell Bodies located OUTSIDE the Gut Wall
  • The INTRINSIC Nervous System has Cell Bodies located WITHIN the Wall of the Gut
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5
Q

Parasympathetic Innervation of the GI Tract

A
  • Via the VAGUS and PELVIC Nerves
  • Preganglionic Nerve Cell Bodies are located in the BRAINSTEM or the SACRAL Spinal Cord
  • POSTGANGLIONIC Neurons lie in the WALL OF THE ORGAN (Enteric Neuron in the Gut Wall)
  • Synapse between the PRE and POST Ganglionic Cell is NICOTINIC (nAChRs)
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6
Q

Sympathetic Innervation of the GI Tract

A
  • Via Nerves that run between the Spinal Cord and the PREVERTEBRAL Ganglia, and between these Ganglia and the Organs of the Gut
  • PREGANGLIONIC EFFERENT FIBERS arises within the Spinal Cord and end in the PREVERTEBRAL Ganglia
  • POSTGANGLIONIC Fibers from the PREVERTEBRAL Ganglia Innervates MYENTERIC and SUBMUCOSAL PLEXUSES and other elements of the ENS
  • Mostly, PREGANGLIONIC EFFERENT Fibers release ACh, while POSTGANGLIONIC EFFERENT Nerves release NE!!!!!
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7
Q

ENS: “The Second Brain or Little Brain in the Gut”

A
  • Contain 200 to 600 Million Neurons
  • Comprises the Myenteric and Submucosal Plexuses
  • Innervated by EXTRINSIC Nervous System
  • Acts as an Integrating Center
    a) AFFERENT Neurons (Ex: Sensory Neurons)
    b) INTERNEURONS
    c) EFFERENT Neurons (Ex: Motor Neurons)
  • Can exert its function WITHOUT CNS Input
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8
Q

CNS has important roles in the Regulation of GI Function

A
  • VAGO-VAGAL REFLEX!!!!!
    (Ex: Gastric Receptive Relaxation Reflex)
  • Modulate ENS Responses
  • Centers that CONTROL Food Intake are located in the Brain
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9
Q

Cellular Communication is key in Regulation of the GI Function

(Paracrine Regulation)

A

Paracrine Regulation:
- Action of peptides (Ex: Somatostatin) or other Messenger Molecules (Ex: Histamine)

  • Released by ENTEROENDOCRINE Cells (EECs) or other Sensing Cells
  • Paracrine act LOCALLY
  • Paracrine signals reach their target cells by DIFFUSION over SHORT DISTANCES
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10
Q

Somatostatin

A
  • Secreted by D CELLS of the GI Mucosa
  • STIMULI: DECREASE in Luminal pH
  • ACTIONS:
    a) INHIBIT Gastic H+ Secretion
    b) INHIBIT Secretion of other GI Hormones
  • Is also Secreted OUTSIDE the GI Tract:
    a) Hypothalamus
    b) Delta Cells of the EXOCRINE Pancreas
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11
Q

Histamine

A
  • In the Stomach, it is STORED and SECRETED by ENTEROCHROMAFFIN-Like Cells (ECL) in Gastric Glands
  • TARGET: Parietal Cells!!!!
  • ACTION: Stimulate ACID PRODUCTION
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12
Q

Cellular Communication is key in Regulation of the GI Function

(Endocrine Regualtion)

A
  • Action of Hormones
  • EECs contain Secretary Granules filled with Hormone peptides that are released upon STIMULATION
  • Hormones are secreted into the PORTAL Circulation, Pass THROUGH the Liver, Reach the SYSTEMIC Circulation, and finally bind to Specific Receptors on TARGET CELL!!!!!!
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13
Q

Gastrin

A

Hormone Family:
- Gastrin/ CCK

Site of Secretion:
- G Cells of Stomach

Stimuli of Secretion:

  • Small peptides and Amino Acids
  • Distention of the Stomach
  • Vagal Stimulation (GRP)
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14
Q

Cholecystokinin (CCK)

A

Hormone Family:
- Gastrin/ CCK

Site of Secretion:
- I Cells of the DUODENUM and JEJUNUM

Stimuli of Secretion:

  • Small peptides and Amino Acids
  • Fatty Acids
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15
Q

Secretin

A

Hormone Family:
- Secretin/ Glucagon

Site of Secretion:
- S Cells of the Duodenum

Stimuli of Secretion:

  • H+ in the Duodenum
  • Fatty Acids in the Duodenum
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16
Q

Glucose Dependent Insulinotropic Peptide (GIP)

A

Hormone Family:
- Secretin/ Glucagon

Site of Secretion:
- Duodenum and Jejunum

Stimuli of Secretion:

  • Fatty Acids
  • Amino Acids
  • Oral Glucose
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17
Q

Gastrin Actions

A
  • INCREASE GASTRIC H+ Secretion
  • Stimulates Growth of Gastric Mucosa
  • ZOLLINGER-ELLISON Syndrome: Gastrin Secreting Tumors
    a) INCREASE Circulating levels of Gastrin
    b) INCREASE Acid Secretion by Parietal Cells
    c) HYPERTROPHY of the Gastric Mucosa
    d) Duodenal Ulcers
    e) Steatorrhea (Inappropriate digestion of Fat)
18
Q

CCK Actions

A
  • INCREASE Pancreatic Enzyme Secretion
  • INCREASE Pancreatic HCO3- Secretion (Not a Direct Effect; it potentiates the Effects of Secretin)
  • Stimualtes CONTRACTION of the GALLBLADDER and Relaxation of the Sphincter of ODDI
  • Stimulates Growth of the EXOCRINE Pancreas and GALLBLADDER (Trophic Effect)
  • Inhibits Gastric Emptying
  • Can also act as a Paracrine Signal
19
Q

Secretin Actions

A
  • INCREASE Pancreatic HCO3- Secretion
  • INCREASE Biliary HCO3- Secretion
  • DECRREASE Gastric H+ Secretion
  • Inhibits Trophic effect of Gastrin on Gastric Mucosa
  • Can also act as a Paracrine Signal
20
Q

GIP Actions

A
  • INCREASE Insulin Secretion from Pancreatin BETA CELLS!!!!!!!
  • DECREASE Gastric H+ Secretion
21
Q

Cellular Communication is key in the Regulation of the GI Function

(Neural Regulation)

A
  • Action of Neurotransmitters
  • AP are needed for Neurotransmitter release from NERVE TERMINALS in the GI Tract
  • Neurotransmitter molecules DIFFUSE ACROSS the Synapse and bind to their SPECIFIC Receptors in the POSTSYNAPTIC Cell
22
Q

Acetylcholine (ACh)

A

SOURCE:
- Cholinergic Neurons

ACTIONS:
- CONTRACTION of Smooth Muscle

  • RELAXATION of Sphincters
  • INCREASE Salivary Secretion
  • INCREASE Gastric Secretion
  • INCREASE Pancreatic Secretion
23
Q

Norepinephrine (NE)

A

SOURCE:
- Adrenergic Neurons

ACTIONS:
- RELAXATION of Smooth Muscle

  • CONTRACTION of Sphincters
  • INCREASE Salivary Secretion
24
Q

Vasoactive Intestinal Peptide (VIP)

A

SOURCE:
- Neurons of the Mucosa and Smooth Muscle

ACTIONS:
- RELAXATION of Smooth Muscle

  • INCREASE Intestinal Secretion
  • INCREASE Pancreatic Secretion
25
Q

Gastrin- Releasing Peptide (GRP)

A

SOURCE:
- Neurons from Gastric Mucosa

ACTIONS:
- INCREASE Gastrin Secretion

26
Q

Enkephalins

A

SOURCE:
- Neurons of the Mucosa and Smooth Muscle

ACTIONS:
- CONTRACTION of Smooth Muscle

  • DECREASES intestinal Secretion
27
Q

Neuropeptide Y

A

SOURCE:
- Neurons of the Mucosa and Smooth Muscle

ACTIONS:
- RELAXATION of Smooth Muscle

  • DECREASES Intestinal Secretion
28
Q

Substance P

A

SOURCE:
- Co-release with ACH

ACTIONS:
- CONTRACTION of Smooth Muscle

  • INCREASE Salivary Secretion
29
Q

Neuronal Centers that Control feeding and satiety are located within the Hypothalamus

A

Neuronal centers of the HYPOTHALAMUS that participate on the Regulation of Foot Intake:

a) LATERAL NUCLEI (LH)—-> Feeding Center
b) VENTROMEDIAL NUCLEI (VM) —> Satiety Center
c) PARAVENTRICULAR NUCLEI (PV)
d) DORSOMEDIAL NUCLEI (DM)
e) ARCUATE NUCLEI (Arc)

Most of the Integration Signaling Regulating Food Intake and Energy Expenditure happens in the ARCUATE NUCLEUS!!!!!!!!!**

30
Q

Crosstalk between Neural and Hormonal Regulations is KEY to Maintain Energy Balance

A
  • Neural and Hormonal Control systems not only regulates food intake but also energy storage and expenditure
  • Hypothalamus receives many types of signals:
    a) Neural Signals from the GI Tract

b) Chemical signals from Nutrients in the Blood
c) Signals from GI Hormones
d) Signals from Adipose Tissue
e) Signals from Cerebral Cortex (Sight, Smell, and Taste)

31
Q

Two Pathways: Part I

Alpha Melanocortin (Alpha- MSH) Pathway

A
  • Alpha-MSH released by PROOPIOMELANOCORTIN (POMC) Neurons
  • Alpha-MSH binds to MCR-4 present in Second order Neurons

***INHIBITS FOOD INTAKE and INCREASES METABOLISM!!!!!!!!!!!!!!!!!!!

32
Q

Two Pathways: Part II

Neuropeptide Y (NPY) Pathway

A
  • Hunger signals stimulate the Release of NPY
  • NPY Binds to Y1R
  • Neurons that release NPY also release AGOUTI-RELATED PEPTIDE (ABRP)
  • AGRP is an Antagonist of MCR-4

***INCREASE FEEDING BEHAVIOR and STORAGE of CALORIES!!!!!!!!!!!!!

33
Q

Both Pathways Antagonize Eachother

A
  • Peptides that stimulate the Alpha-MSH Pathway INHIBIT the NPY System
  • ACRP released from the NPY pathway is an ANTAGONIST of MCR-4

** Some cases of OBESITY have been related to MUTATIONS in the POMC and MCR-4 Genes!!!!!!!**

34
Q

The Vagus Nerve a “Super Highway”

A
  • Several peptides that stimulate Satiety and Decrease Feeding Activate Receptors on VAGAL AFFERENTS
  • The Vagal —> NTS —> Hypothalamus Circuit produces responses related to Feeding Behavior and Metabolism
35
Q

Hormones released form the GI Tract, Pancreas, and Adipose Tissue Regulate Feeding Behavior

A

1) Ghrelin
2) Insulin
3) CCK
4) PYY
5) Leptin
6) Appetitive-Suppressing Hormone

36
Q

Ghrelin

A
  • Secreted mainly by Endocrine Cells in the Stomach
  • Binds to Growth Hormone SECRETAGOGUE Receptors
  • In the Hypothalamus it stimulates Neurons that release NPY
  • Appears in INITIATE the Feeding Response

Other Actions:

  • INCREASE Appetite
  • INCREASE Gastric Motility
  • INCREASE Gastric Acid Secretion
  • INCREASE Adipogenesis
  • INCREASE Insulin Secretion
37
Q

Insulin

A
  • Transported across BBB
  • Binds to Receptors in Satiety and Hunger Centers within the Hypothalamus (POMC and NPY Systems)
  • In patient with TYPE I DIABETES MELLITUS there is an INCREASE in FOOD INTAKE associated with DECREASE in INSULIN

Actions:

  • DECREASE Appetite
  • INCREASE Metabolism
38
Q

CCK

A
  • released by I CELLS in the DUODENUM
  • ELICITS SATIETY
    a) Acts on Vagal —> NTS —> Hypothalamus Circuit
    (Result: DECREASE Ghrelin)

b) DECREASE Gastric Emptying
(Result: INCREASE Gastric Distention)

39
Q

PYY

A
  • Released by EECs (L CELLS) of the ILEUM and COLON
  • Binds to Y2 Receptors of the Hypothalamus
    a) INHIBITS NPY Neurons
    b) Releases INHIBITION of POMC Neurons
  • Potential as APPETITE SUPPRESSOR
40
Q

Leptin

A
  • Secreted by Cells in ADIPOSE TISSUE and by ENDOCRINE Cells in the Stomach
  • Binds to Receptors in SATIETY and HUNGER Centers within the Hypothalamus (POMC and NPY Systems)
    a) INHIBITS NPY Pathway
    b) Stimulates POMC Pathway
41
Q

Appetite- Suppressing Hormone

A
  • DECREASE Appetite
  • INCREASE Metabolism
  • DECREASE Ghrelin Release
  • Appears to be part of NEGATIVE FEEDBACK SYSTEM for the Regulation of Food Intake

GastroIntestinal (21 decks)

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