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Undergraduate 4

Additional Physiology Flashcards




gastrointestinal mobility
Mouth -> esophagus -> stomach -> small intestine -> large intestine
Accessory Glands/organs: salivary glands, pancreas (enzymes & bicarb.), liver (bile)
Gastrointestinal system works to deliver nutrients and water to the body by breaking down food (digestion) and absorbing these smaller solutes that are moved (motility) through the different sections of the GI tract
GI tract anatomy
GI tract varies along its length but has a common structure organization:
Mucosa: epithelial layer, lamina propria (capillaries, enteric neurons & immune cells), and a smooth muscle layer (lamina muscularis mucosae)
Submucosa: loose connective tissue & larger blood vessels and glands
Muscle Layer: Muscularis externa has 2 layers of smooth muscle (SM)
Inner layer of circular SM (changes diameter) and an outer layer of longitudinal SM (changes intestinal length)
Serosa: Layer of connective tissue covered by epithelial cells that surround the tract
gastrointestinal motility
Segmentation: Segments along the small intestine contract for mixing
Moves the intestinal content back and forth to provide mixing and increases the time for nutrient absorption
Peristalsis: Propels the bolus forward
Involves the contraction and shortening of the circular muscle and relaxation of the longitudinal muscle before the bolus and the shortening of the longitudinal muscle and relaxation of the circular muscle after the bolus
smooth muscle
Spindle shaped cells with a single nucleus
Contain thick myosin filaments, thin actin filaments (contain tropomyosin, but no troponin) and intermediate filaments that help support the structure of the cell
Actin and myosin in SM are not regularly arranged so there is no striated pattern (No sarcomeres or myofibrils)
Actin filaments are anchored to dense bodies (same protein as in z-bands) that are found throughout the SM cell
SM does not have T-tubules or lateral sacs and they have a poorly developed SR
Innervation of the SM
Sympathetic and Parasympathetic)
 SM cells can be innervated by more than one neuron and each neuron can make multiple contacts with each cell

SM cells do not have a specialized motor end plate.  Neurons synapse at varacosities which contain the presynaptic machinery to release neurotransmitters that bind to receptors that are spread across the SM cell to regulate contraction
SM action potentials
SM can have different types of action potentials: spike, spike followed by a plateau, spikes on slow waves
In the small intestine the
interstitial cells of Cajalhave pacemaker activity and create slow wave Aps (BER)- normal is 12 cycles per minute
Neural stimulation can modify contraction rate and strength but is not necessary to initiate contraction
sources of calcium
Voltage Gated Ca Channels: influx of extracellular calcium
Ca release from the SR: Ca induced Ca release (Ryanodine receptors open when bound with Ca) or 2nd messenger (IP3) from activation of a GPCR 
SM contraction
Depolarization causes an increase in intracellular [Ca] -> 4 Ca ions bind to Calmodulin (CaM) -> Ca-CaM complex work in 2 ways to initiate contraction
(1) Caldesmon and Calponin are proteins that are bound to actin and tropomyosin and inhibit actin-myosin binding -> Ca-CaM bind to caldesmon- or calponin-tropomyosin complex -> causes a conformational change to unmask the myosin binding site on actin

(2) Ca-CaM bind to Myosin Light Chain Kinase (MLCK) and activates it -> MLCK uses ATP to phosphorylate Myosin Light Chain (MLC) -> P-MLC undergoes a conformational change that increases the ATPase activity of the Myosin head -> allows Myosin to bind actin -> initiates cross bridge cycling -> increase tension
relaxation of SM
Decrease intracellular Ca by pumping Ca out of the cytosol (SERCA, PMCA, Na/Ca exchanger)
Myosin Light Chain Phosphotase (MLCP) : dephosphorylates MLC -> inhibits MLC’s ability to bind actin -> stops cross bridge cycling
MLCP is always active so:
When intracellular [Ca] is high, MLCK activity is higher than MLCP
When intracellular [Ca] is low, MLCK activity is lower than MLCP
enteric nervous system
Primary neural mechanism that controls GI function
Neurons mostly found in: Submucosal (Meisner’s) plexus and Myenteric (Auerbach’s) plexus
parasympathetic innervation
Parasympathetic neurons travel along the vagus nerve and synapse with the ENS or directly to the GI tract
Release Methacholine  as the neurtransmitter on effector cells
ACh release will result in an increase in baseline tension and an increase in frequency

acts on muscarnic receptors and causes a decreases in adenylyl cyclase whcihc will then decreases the formation of cAMP from ATP> whits will decreaes cAMP and reduce the phosphoraltation activity of PKA> results in decreases phos. of MLCK > so there then is a higher afinity for calcium calmodulin interaction for MLCK , increasing the ability to phosphoralte MLC so there is increase in contraction and frequecny due to methacholine affects on ICC


sympathetic innervation

what is the mechanisms for epinephrine

Sympathetic neurons travel through the splanchnic nerve and can synapse to the ENS or directly to effector cells
Release Norepinephrine as neurotransmitter on effector cells
Results in a decrease in tension and a decrease in contraction frequency

stimulates beta receptor> increase adneyle cylase> increases formation of cAMP from ATP> increase in cAMP activates PKA> phosphraltes MLCK and then the affinity of calcium/ calcmodulin for MLCK and decreases ability of MLCK to phosphoralate MLC> decrease in contraction and tensiton
what are the effects of epinephrine
the hormone mimics sympathetic activity to the enteric plexus through a g-protien coupled receptor
ADP what does ADP mimic
ATp released from the sympathetic neurons
what was the expected results for epi, Mch, ADP and calcium free

epi-decrease amp, normal baseline, decrease frequency

Mch- increase amp, normal baselin, decrease frequency

Adp- DECREASE AMP normal res

calcium free- decrease amp and baseline, normal frequency

what pathway does epinephrine, MCH and ADP take?

epi- B2 adrenergic receptors . Gs protien pathway

MCH- M2 receptors> Gi/Gs pathway

ADP activates P2Y purginergic receptors> Gq pathway


effect of calcium free ringers solution


two sources of calcium




- causes a decreases in tension

extracellular calcium is important for slow waves and contraction of the ICC


- voltage gate ca channels; influx of extracellular calcium

- calcium release from the SR; calcium induced calcium release


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