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29 Cards in this Set
- Front
- Back
1. What is the function of the GI tract?
How is the GI tract organized? Why is this organization advantageous? |
Provide the appropriate environment for the physical and chemical breakdown of food and the absorption of the products of digestion
Organized into concentric layers of muscle, nerves, blood vessels & CT Provides functional advantages for long term processing of food |
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2. What four separate but interdependent systems control and coordinate the GI tract?
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1. Neural
2. Endocrine 3. Paracrine 4. Smooth muscle |
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3. What provides the neural control?
What does this network form? What are intrinsic nerves? What is the ENS influenced by? |
Have Auerbach's & Meissner's plexi
Forms the enteric nervous system (ENS) or "little brain" Intrinsic nerves are nerves of the controlling circuits w/in the bowel ENS is influenced by nerves from the CNS |
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4. What are the characteristics of the ENS?
How are axon terminal from the ENS to the effector organs of the GI tract? |
1. Planarian like nerve network
**capable of complex reflex activity 2. Mesh-like structure **allows ENS to adapt to large changes in volume w/o putting harmful physical stress onto the nerves Generally in the synapse en passant or bouton en passant arrangement |
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5. What are the advantages to having ENS or "little brain" neural control?
Three things |
1. Fewer nerves required in the medulla up to the cortex
2. Fewer large and vulnerable pathways 3. Ability to adapt to normal volume changes in the tract w/o stretching and depolarizing nerve fibers |
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6. How do CNS nerves affect end organs?
What processes long and short reflexes? What do long arc reflex pathways involve? What do short arc reflex pathways involve? |
CNS nerves generally do not directly affect the end organs
Long and short arc reflexes are processes by the ENS Long arc pathways involve extrinsic and ENS (intrinsic) nerves Short arc reflex pathways involve intrinsic nerves |
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7. Where does the stimulus for the short arc reflexes originate from?
What do nerves from the receptor interact with? What does this stimulate? What does these nerves do? What else is sent to the CNS? |
Stimulus originates from the visceral sensory receptors
Interact w/ the plexi Stimulate efferent nerves Efferent nerves stimulate/inhibit the viscera Afferent data is also sent to the CNS |
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8. Where does the stimulus for the long arc reflexes originate from?
What will the response from the CNS do? What do parasympathetics generally do? What do sympathetics generally do? What does this stimulate? What does these nerves do? What else is sent to the CNS? |
Stimuli from the viscera stimulate the CNS
Responses from the CNS will either enhance or reduce visceral activity Parasympathetics enhance activity Sympathetics decrease activity |
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9. What do most long arc reflexes act through?
What are the exceptions? How are endocrines secreted? How are paracrines secreted? |
Act through the myenteric plexi
Exceptions occur in sympathetic efferents Endocrines are secreted into the blood and flow to their respective target cells Paracrines are secreted by a paracrine cell and diffuse through the ISF to their respective targets |
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10 .What is the primer mover for the GI tract?
What does this influence? What are the two types based upon innervation? |
Smooth muscle
Exerts a controlling influence upon how rapidly food will be processes 1. Single Unit 2. Multi Unit |
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11. How many cells in a bundle are innervated in a single unit smooth muscle?
How is the innervation? What do single unit smooth muscles include? What is the acronym? |
One cell in a bundle is innervated
Innervation by the synapse en passant or the bouton en passant type of arrangement Includes GI, uterine & urinary bladder SUVSM (single unit visceral smooth muscle) |
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12. How many cells are innervated in a multi unit smooth muscle?
What do multi unit smooth muscles include? What are two characteristics of muscle cells (aka muscle fibers)? |
Many cells in a bundle are innervated
Includes ciliary, erector pili, arterial & venous smooth muscle Muscle cells are thin and long |
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13. What do SUVSM cells contain?
What does the rudimentary SR of SUVSM's do? What is special about the membrane of SUVSM? How are SUVSM cells joined physically? How are they joined electrically? |
Contain actin (thin filaments) and mysoin (thick filaments)
SR sequesters Ca Membrane has invaginations (caveolae) to increase surface area and may cat as points where Ca may enter the cells into the SR Physically by intermediate junctions Electrically by gap junctions |
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14. What is the key to triggering contraction of smooth muscle?
How must the concentration of this ion be to effect a contraction? What are three pathways that can increase [Ca] in the cell cytoplasm? |
[Ca] in the cytosol
**normally is 10^-9 M range Must increase to 10^-6M range to elicit a contraction 1. Voltage regulated channels 2. Receptor activated channels 3. Receptor activated release of SR Ca **2 &3 many not generate AP |
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15. What two pathways can lower [Ca] in the cell cytosol?
How the resting potential of SUVSM? What is this rhythmic fluctuation of the resting potential termed? What does this function to do? |
1. Ca pump to extracellular space
2. SR re-sequestration of Ca Not at a steady voltage **fluctuates in rhythmic manner between -45 to -55 mV Basic Electrical Rhythm (BER) BER functions as a metronome or timer setting the rate (frequency) of contractions |
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16. What is the BER a response to?
What does an absence of ICC's result in? What stimulates ICC's? What is BER depolarization due to? What is BER repolarization due to? |
Response to depolarization caused by nearby interstitial cells of cajal (ICC)
Results in areas w/ no BER ICC's stimulated by neuropeptides (Steele factor) from ENS Depolarization - small increases in Ca and Na plus decreased K Repolarization - decreased Ca and Na plus increased K |
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17. What happens when SUVSM potential exceeds threshold?
(four things) What does increased inward Ca conductance occur? |
1. Ca spike
**large increase in inward Ca conductance 2. Inward Na currents are small 3. K outward current contributes to repolarization of cell 4. Metabolic steps involving contractile elements are triggered by increase [Ca] Occurs w/ ligand stimulated SR and ligand Ca channels |
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18. What does Ca bind with when increased intracellular Ca triggers a cascade of metabolic steps?
What does CAM activate? What happens to myosin? What does the myosin now do? |
Binds w/ calmodulin to form CAM complex
CAM activated myosin light chain kinase (MLCK) an ATPase Myosin is phosphorylated Phosphorylated myosin now forms a cross-bridge w/ actin |
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19. What alterations of shape does the phosphorylated myosin-actin cross bridge undergo?
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1. Phosphate ADP comes off
2. Swiveling of head occurs **swiveling creates tension and shortening |
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20. What does additional ATP do to the myosin-actin cross bridge?
What occurs? (three things) |
Additional ATP breaks the actin-myosin cross bridge
1. Myosin head is re-phosphorylated (CAM is still active) 2. Head resets back to original position 3. Formation of a new cross bridge on actin **cycles is repeated and this resetting is relatively fast |
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21. How many bonds need to be phosphorylated for the sequence in SUVSM?
How does SUVSM contraction compare to that of skeletal muscle? What happens to the cross bridge as intracellular Ca is lowered by Ca re-sequestering or externally directed pumps? What is this called? |
Only 40% of bonds need to be phosphorylated for a nearly 100% maximal tension contraction
20 times slower A slow breaking of the cross bridge may take place This is a latch bridge |
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22. What does a latch bridge formation create?
How does it affect contraction? |
Formation creates a sustained level of muscular contraction (tonus)
**very prominent in vascular smooth muscle less so in visceral smooth muscle Results in an even higher efficiency of contraction **less energy spent for prolonged contraction |
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23. What two events occurs during the relaxation of SUVSM?
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1. Lowered intracellular Ca
*consequent to cessation of stimulus *[Ca]i lowering mechanisms are always on 2. Myosin light chain dephosphorylation *stop the recycling process |
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24. When intracellular Ca is reduced what happens to CAM?
As a result what happens to MLCK? What dephosphorylates the myosin light chain? |
Ca separates from CAM
MLCK is no longer activated Myosin light chain phosphatase which is always activated **if the actin-myosin attachment persists, the bridge is now termed a latch bridge |
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25. What are some regulatory proteins in SUVSM?
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1. Calponin (mainly)
2. Caldesmin **both increase rate of relaxation 3. Protein kinase C **increase tension and slows relaxation |
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26. What happens to smooth muscle when it is stretched?
What happens time though and why? What is decreased tension? What is increased length? |
When rapidly stretched, SM reflexively generates tension
In time, tension falls off although muscle remains stretched Mechanism is attributable to internal rearrangement of microfibrils Decreased tension = accommodation Increased length = creep |
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In the absence of external tension, how much can SM reduced it length to?
What is reduction in length due to? What does this prevent? |
Reduce its length to only 0.3 times its original optimal length
Reduction in length is due to intrinsic activity of the ICC This prevents an empty viscus from taking up excess room |
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28. What are four interdependent control systems necessary?
(three reasons) |
1. Backup in case one system malfunctions
2. Multi-controlled response to changing external as well as internal conditions is more effective 3. Reduces changes of over or under response to changes |
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29. If only one control system were present, a monopoly would exist.
What is so bad about monopolies? |
Monopolies concentrate too much power into too few resources
In a physiologic paradigm, monopolistic control systems will not respond w/ precision to altered conditions **significant overshoots and undershoots of targeted values will occur regularly |