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44 Cards in this Set
- Front
- Back
Eye metabolism
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The eye is comprised of living tissue that have energy and material needs. These needs are met through conventional metabolic pathways
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Tears
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bathe exterior of cornea
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Aqueous humor
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bathes interior of cornea
Composed of salts, albumin, globulin, glucose, others.. Brings nutrients to lens and removes metabolic waste |
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Vitreous Humor
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Gelatinous
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Cornea
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Part of the CNS!!
High activity of glutathione reductase Permeable to oxygen -ROS! -Correction by glutathione |
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Metabolic fuel of Cornea
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Glucose
30% ATP form glycolysis 65% ATP from PPS -Interconversion to provide glycolysis intermediates |
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Lens
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ALIVE!!
No blood supply Metabolically active Nutrients and waste: aqueous humor |
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Crystallins
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Proteins that make the lens
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Epithelia surrounding lens
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Makes enzymes, albuminoids, and membrane proteins
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Lens Protection
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Na+/K+ pumps, glutathione, proteins synthesis, and other metabolic events
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Lens Sensitivity
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Sensitive to:
-Redox rxns -Osmolarity -High lvls of metabolites -UV radiation |
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Energy for Lens
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Seems to come from peripheral cells
85% glycolysis 10% PPS 3% TCA/ETC |
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Lens Growth
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From the periphery throughout life
From birth to 80 increases 3x in size and 1.5x thickness |
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Presbyopia
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Loss of near vision
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Cataract Causes
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Only known disease of Lens
Senile cataracts: Age related Rearrangement of proteins in lens Breakdown of protein molecules Diabetic Cataracts: Increased osmolarity due to activity of aldose reductase and polyol (aldose) dehydrogenase from elevated glucose Results in increased sorbitol (unused and accumulates) Changes osmolarity |
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Cataract Symptoms
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Light scattering properties develop
No known cures Side effect of cataract and surgical treatments is glaucoma |
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Energy for Retina
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Anaerobic glycolysis, like the lens
Vascular tissue Lactate dehydrogenase -Can use NADH OR NADPH |
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Macula
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Center of retina
Contains Fovea centralis - center of macula |
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Fovea Centralis
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Avascular
Spot of greatest visual activity |
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Mitochondria and Rods and Cones
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Mitochondria located in rods and cones not in outer segments where visual pigments are located
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Light enters eye through
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Lens
Reaches the outer segment of rods and cones Signal transduction begins |
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Pigmented Epithelial Layer
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Absorbs excess light and prevents reflection
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Processes of Light
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Photochemical
Kinetic Biochemical Electrical |
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Photon
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A discrete particle of light
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Rods and Cones
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Photoreceptor cells
Proteins contain the prosthetic group 11-cis-retinal |
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Pigment in Rods
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Rhodopsin
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Pigment in Cones
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Red, green, or blue
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When Photon Strikes a Rod
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11-cis-retinal is ISOMERIZED by the energy to all-trans-retinal
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Isomerization of 11-cis-retinal
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Happens in picoseconds
Results in a string of stepwise events Creation of metarhodopsin Disassociation of opsin and all-trans-retinal restoration of 11-cis-retinal ALL KINETIC OR MECHANICAL EVENTS |
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Metarhodopsin
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Active molecule with half-life of 60 seconds
Complexes with TRANSDUCIN |
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Transducin
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G PROTEIN
alpha subunit activates a phosphodiesterase PDE changes cGMP to 5' GMP -closes Na+ channels -Change in membrane potential -Electrical event |
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Termination and reset
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Metarhodopsin is acted on by rhodopsin kinase
-Product has high affinity for arrestin -Now cannot bind to transducin -Allows ONE (ONLY ONE) cycle to happen -Hydrolysis of the Pi restores the arrestin and then soon the rhodopsin |
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Rod Cells
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can detect a signal as LOW as 5 photons
The signal, different form many neurons, is not an all or nothing event Graded intensity from deviation from the -30mV steady state to -35mB and number of rods that fire |
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Differences between Rods and Cones
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Cones are domain of color
Uses 11-cis-retinal but different pigments, rods use rhodopsin pigment Each cone has one pigment Rods are FAR MORE SENSITIVE Cones respond FAR FASTER -Rods for low light -Cones for rapidly changing |
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Pases of Blood Coagulation
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Procoagulation - Clot formation
Anticoagulation - Stopping clot formation Fibrinolysis - Clot dissolution |
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Zymogens in Coagulation
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FX to FXa
Key in phase one is to active FX to FXa |
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FXa
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Responsible for prothrombin activation
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Thrombin
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A key enzyme in making the clot
Responsible for fibrin formation and a host of other factors |
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Tissue Factor
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Activated during injury and acts as a receptor for FVII
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Fibrinogen
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Thrombin activates fibrinogen and a platelet receptor
Fibrinogen is cut by thrombin creating a molecule capable of aggregation |
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Sites of Fibrin aggregation activate platelets
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Aided by a thrombin receptor (activated by thrombin)
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Why Not anywhere else (Sites of fibrin aggregation that activate platelets)
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No exposed receptors
Activators are not at a high enough concentration Endothelium secrets postacyclin which inhibits platelet aggregation |
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Anticoagulation Phase
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Beings IMMEDIATELY with coagulation phase
Inhibitors bind with active proteins and enzymes Inhibitor activity increases and zymogens are activated Anticoagulation phase increases as coagulation phase increases Coagulation stops and complexes are removed by the liver |
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Fibrinolysis
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Plasminogen has a high affinity for active fibrin
Tissue plasminogen activator activates plasminogen to plasmin -TP-A also binds to fibrin Plasmin hydrolyzes the clot to soluble proteins In both clot formation and removal, proteins are used up, not recycled |