Term
| Describe all the events of ECC |
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Definition
| Ach diffuses across the synaptic cleft and bind to and opens CG Na+ channels on the motor end plate, allowing Na+ to influx into the cell via simple diffusion. this influx increases the MP my 20 mv (MEPP) reaching thresholdand opening adjacent VG Na+ channels further increasing the MP to 30 mv producing an AP. |
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Term
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Definition
| cell charge= ATP/(ADP+AMP) ^cell charge v metabolism ^ATP v ADP+AMP intrinsic regulation negative feedback |
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Term
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Definition
1. stored glucose+ATP--(hexalate kinase)--> G-6-PO4+ATP
2. G-6-PO4--> F-6-PO4
3. F-6-PO4+ATP--(PFK)-->F-1, 6-PO4+ADP
4. F-1, 6-PO4----> DHAP
---->GAP
5. GAP+Pi+NAD+---->1,3PG+NADH2
6. 1,3DPG+ADP----> 3PG+ATP
7.3PG---->2PG
8.2PG---->PEP
9. PEP+ADP--(pyruvate kinase)--> pyruvate+ATP
***reactions 5-9 occur twice!*** |
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Term
| Where does the energy produced in ETS come from? |
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Definition
| ETS is a series of redox reactions involving membrane proteins called cytochromes, several reactions liberate enough energy for cytochromes to pump a protein across the membrane.This active transport across the membrance creates a charge gradient&concentration on the side that drives the H+ proton into the matric via facilitated diffusio. The carrier protein is ATPase Syhtentase. The H+ diffusion liberates enough energy allowing ATPase Synthentase to phosphorylate ADP |
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Term
| Increase skeletal muscle activity will alter a host of metabolic variables. List them |
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Definition
^H+- drop in cell charge ^anaerobic metabolism turning on glycolysis (2pyruvates and a lactate)
^CO2-Krebs cycle is stimulated (6pyruvate->6CO2)
^K+- ^muscle contraction-> ^CGK+ channels oepn -> ^rate of repolarization-> ^K+ efflux -> ^extracellular K+ levels
^Adenosine- ATP fuels ECC: ATP->ADP+Pi, ADP->AMP+PI, AMP->Adenosine+Pi
^osmolarity- because of increase in H+, CO2, K+ and Adenosine
vO2- O2 is the final e- acceptor in ETS so ECC->vO2
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Term
| How will these variables change Blood flow? |
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Definition
increased variable-> stimulate endothelium of arterioles->secreting nitric oxide-> relaxing smooth muscle of the tunica media-> vasodilation |
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Term
| 3 ways body indirectly increases blood flow |
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Definition
increase HR
increase SV
Increase Venoconstriction |
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Term
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Definition
| aortic barroreceptor: measures systemic BP Carotid barrorecptor:measures cerebral BP |
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Term
| What do these short term sensors do? |
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Definition
| ^blood flow-> ^stretch -> ^AP frequency to the CCC |
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Term
| Short Term BP is regulated by what structure? |
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Definition
| mediated by the ANS- cardiovascular control center (medulla) this is extrinsic regulation |
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Term
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Definition
| it takes the frequency (feedback) from the barroreceptors and compares it to set point, if there is a difference this is called an error signal which will be sent to the appropriate effectos (heart, arterioles, veins) |
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Term
| How does the cardiac center extrinsically restore BP? |
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Definition
| CC- affected by B1 receptor • (decreased BP) -> Decreased para stim -> decreased Ach-> decreased CGK+ channels-> decreased k+ efflux -> decreased repolarization of membrane-> increases HR-> increases CO-> increases BP • (Decreased BP) -> increased sym Stim. -> increased NE released -> increased CGCa+2 channels open-> increased Ca+2 influx-> increased troponin -> increase crossbridge formation -> force production -> increased SV-> increased CO -> increased BP • (Decreased BP) -> increased sym stim -> increased NE released -> increased CGCa+2 channels open -> increased membrane potential -> increased spontaneous depolarization of SA node -> Increased HR -> increased CO -> increased BP |
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Term
| explain fully how venous return alters blood flow to active skeletal muscle? |
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Definition
| ^VR->^EDV->^Ventricular stretch->^myofilament overlap->^x-bridge->^force of contraction->^SV->^CO; allowing blood to be pumped more forcefully to active skeletal muscle. |
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Term
| If NBF increases how will this change BP? |
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Definition
| ^NBF->more water moves out of capillaries and into tissues causing swelling->vPV->vVenous Return-> v EDV-> vSV because (SV=EDV-ESV)->vCO (CO=HRxSV)-> vMABP (MABP=COxTPR) |
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Term
| If NBF decreases how will this change BP? |
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Definition
| ^NBF->less water moves out of capillaries and into tissues causing shrinking->^PV->^Venous Return-> ^EDV-> ^SV because (SV=EDV-ESV)->^CO (CO=HRxSV)-> ^MABP (MABP=COxTPR) |
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Term
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Definition
| 02 is carried by our red blood cells, specifically hemoglobin contained in our RBC |
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Term
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Definition
| 4 polypeptides (protein) with iron atoms in the center- a heme configuration (like cyotchromes) Hb+02 HbO2 The change in concentration of any variable in the equation, alters the concentration of the other variables. |
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Term
| Why in fight or flight will ventilation and O2 increase? |
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Definition
| anaerobic metabolism causes metabolic acidosis which drives ventilation. In short hyperventilation helps buffer metabolic acidosis-this process is called compensatory repirstory akalosis Central chemoreceptors (medulla) will increase temp decrease 02- lowering ventilation centrally |
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Term
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Definition
| This AP travels down the sarcolemma and into the T-tubules depolarizing them. This causes the S.R. and terminal cisternae to also depolarize. This change in MP opens VG Ca+2 channels allowing Ca+2 to influx into the sarcoplasm where it binds to TNC (a subunit of troponin) causing a conformational change pulling tropomyosin off of actin's myosin binding site allowing a cross-bridge to form. This liberates ADP+Pi (energy) brining the myosin heads to low energy state. this causes another CC opening the ATP binding sites allowing ATP to bind an break the cross bridge formation causing another CC. Thi causes ATPase to split ATP liberating energy and returning myosin heads to high energy state. |
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