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Physiology - Block 1 - Part 1

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davidwurbel7's version from 2015-06-06 18:09

Section

Question Answer
Chemical specificity, competition and saturation are the characteristics ofCarrier-Mediated Transport
The binding sites for solute on the transport proteins are stereospecificChemical Specificity
Glucose transport in the lumen of the intestine can also transport which closely related sugar moleculeGalactose
Renal Threshold of blood glucose at which glucose will be present in the urine200 mg/dL
Normal pO2 in the alveoli100 mmHg
Extracellular Na+ concentration135 - 145 meq/L
Extracellular K+ contraction3.5 - 5 meq/L
Normal Osmolality in ECF280 - 295 mOsm/L
Increase of force of contraction by the accumulation of Ca+2Contractility
The osmotic pressure at capillaryColloid Oncotic Pressure
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Types of Transportation

Question Answer
Type of transport of glucose on the intestinal lumen sideSecondary Active Transport
Type of transport of galactose on the intestinal lumen sideSecondary Active Transport
Type of transport of fructose on the intestinal lumen sideFacilitated Diffusion
Type of transport of glucose on blood lumen sideFacilitated Diffusion
Type of transport of galactose on blood lumen sideFacilitated Diffusion
Type of transport of fructose on blood lumen sideFacilitated Diffusion
Substances that are lipid soluble, such as the blood gases or steroids, can diffuse directly through the lipid bilayerSimple Diffusion
Transport of a substance along the gradient with the help of a carrier protein in membrane without the use of ATPFacilitated Diffusion
Transport of solutes from lower to higher concentration (against/uphill gradient)Primary Active Transport
Type of transport in which solutes coupled with sodium gets transported against the gradientSecondary Active Transport
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Concentration

Question Answer
An index of concentration of particle per liter of solutionmOsm (miliosmolar) or mOsm/L
An index of concentration of molecules dissolved per liter of solutionMm (millimolar) or mM/L
Isotonic solutions300 mOsm
Isotonic solutions150 mM Nacl
Two solutions having the same calculated osmolarityIsosmotic solution
The solution having higher osmolarity than that of other solution comparedHyperosmotic solution
The solution having lower osmolarity than that of other solution comparedHyposmotic solution
Equation for the calculation of osmolarityConcentration (mmol) x g (number of particles of solute in solution)
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Body Fluids

Question Answer
60% of the body weightWater
A man weighing 70 Kg will have how much water42 Liters of water
ICF makes up how much of the TBW2/3
ECF makes up how much of the TBW1/3
Plasma makes up how much of the ECF1/4
Interstitial fluid makes up how much of the ECF3/4
Substances(lipid soluble) are distributed wherever water is found. Eg: Isotopic water (D20) or Titrated water, and antipyrineMarkers for TBW
Substances that distribute throughout the ECF but do not cross the cell membranes. Eg:Mannitol and InulinMarkers for ECF
Substances that distribute in the plasma but not in ISF. Eg: Radioactive albumin and evans blueMarkers for Plasma
Calculated by TBW – ECFICF
Calculated by ECF – Plasma volumeISF
Means that the solution does not change the volume of the body cellsIsotonic Solution
Means that the solution causes body cells to shrinkHypertonic Solution
Means that the solution causes body cells to swellHypotonic Solution
Osmolarity of all body fluids is the same in a steady state and close to300 mOsm/L
Approximation estimation of plasma osmolarity2([Na+])
Accurate estimation of plasma osmolarity (POsm)2([Na+]) + ([glucose] / 18) + ([BUN] / 2.8)
Causes the change to ECF osmolarity, water will shift across cell membranes to make the ICF osmolarity equal to the new ECF osmolarityDisturbance
The change in volume of ICF occurs only by changes inECF Osmolarity
An addition of isosmotic fluid into ECF; Increase in ECF volume without any change in the volume of ICF; There is no change in osmolarity of ECF & ICF; At new steady state - Increase in volume of ECF with no change in volume of ICF; No change in osmolarity of both (Example administration of NS IV)Isosmotic Volume Expansion
A rise in ECF osmolarity initiated the disturbance; Increase in ECF osmolarity causes shift of water from ICF to ECF; At new steady state - There is decrease in volume of ICF and an increase of volume of ECF; Increase in osmolarity of both (Example Hyperaldonsteronism - more NaCl is absorbed in the distal tubule and collection duct with water follow)Hyperosmotic Volume Expansion
A fall in ECF osmolarity initiated the disturbance; Decrease in ECF osmolarity causes shift of water from ECF to ICF; At new steady state - There is increase in volumes of both ECF & ICF; Decrease in osmolarity of both (Examples - polydipsia, Lung cancer (small cell carcinoma)Hyposmotic Volume Expansion
There is loss of isosmotic fluid from ECF; There is decrease in ECF volume without any change in the volume of ICF; There is no change in osmolarity of ECF & ICF; No shift of water between ECF and ICF; At new steady state - Decrease in volume of ECF with no change in volume of ICF; No change in osmolarity of both (Examples: Diarrhea, Burns, hemorrhage, severe vomiting (Loss of isotonic fluid)Isosmotic Volume Contraction
A rise in ECF osmolarity initiated the disturbance; Increase in ECF osmolarity causes shift of water from ICF to ECF; At new steady state - There is decrease in volumes of both ECF & ICF; Increase in osmolarity of both (Examples: Water deprivation, Excessive sweating, Fever, Diabetes insipidus, Drinking alcohol, Loss of hypotonic fluid)Hyperosmotic Volume Contraction
A fall in ECF osmolarity initiated the disturbance; Loss of hypertonic fluid; Decrease in ECF osmolarity causes shift of water from ECF to ICF; At new steady state - There is increase in volume of ICF and a decrease in vol of ECF; Decrease in osmolarity of both (Examples: Diuretics (MCC) Addison’s disease, Aldosterone deficiency)Hyposmotic Volume Contraction
Hormone that regulates concentration of sodium in the extracellular compartmentADH
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Membrane Potential

Question Answer
No net moment of ions through the membraneEquilibrium Potential
Membrane potential when the cell is not actively in a depolarized stateResting Membrane Potential
The gates open and /or close in response to a membrane voltage changeVoltage-Gated Channel
Channels includes a receptor to a specific substrate or Ligand (Hormones, Neurotranmitters); Channels open and close when a ligand binds to themLigand-Gated Channel
Depolarization that occurs on the end plateEnd Plate Potential
Refers to the number channels that are open in a membrane for a given ionMembrane Conductance
Sum of the concentration force and the electrical forceNet Force
Membrane only permeable to Cl- ionsDiffusion Potential
Determined by the concentration difference across the membraneConcentration Force
Determined by the electrical difference across the membrane (usually measured in mV)Electrical Force
Equilibrium potential for Na++65 mV
Equilibrium potential for K+-85 mV
Equilibrium potential for Ca+2+120 mV
Equilibrium potential for Cl--90 mV
Resting membrane potential (RMP)-70 mV
The potential difference that exists across the cell membrane at restResting Membrane Potential (RMP)
High permeability for potassium ions at rest; Concentration difference of potassium between ECF and ICF; Sodium-potassium pump maintains concentration gradient for K+ across the cell membrane are the reason forResting Membrane Potential (RMP)
Chemical gradient decreases; Magnitude of RMP also decreases; RMP becomes less negative or more positive; The cell becomes depolarizedHyperkalemia
The chemical gradient increases; Magnitude of RMP also increases, RMP becomes more negative or less positive; The cell becomes hyperpolarizedHypokalemia
The phenomenon of rapid depolarization followed by repolarization of membrane potentialAction Potential
To generate an AP, the membrane potential must reach theThreshold Potential
Threshold potential of neurons and skeletal muscle -50 mV
Depolarized peak of neurons and skeletal muscle +35 mv
Hyperpolarized limit of neurons and skeletal muscle-85 mV
At threshold potential (-50 mV), these channels openVoltage-Gated Na+ Channels
At depolarized peak (+35 mV), these channels closeVoltage-Gated Na+ Channels
At depolarized peak (+35 mV), these channels openVoltage-Gated K+ Channels
The hyperpolarization of neurons is due to the slow closure ofVoltage-Gated K+ Channels
Activation gate and inactivation gate are the two components of aVoltage-Gated Na+ Channels
At which potential is the activation gate closed and the inactivation gate is openResting Membrane Potential
At which potential is the activation gate open and the inactivation gate is openDepolarization (Action Potential)
At which potential is the activation gate open and the inactivation gate is closedAction Potential Peak
At which potential is the activation gate closed and the inactivation gate is closedHyperpolarization (Repolarization)
The maximal number of voltage-gated Na+ channels are open is at which point of an AP curveThreshold Potential
The maximal number of voltage-gated K+ channels are open (Max conductance of K+) is at which point of an AP curveMid-point of Repolarization
Voltage-gated K+ begin to open at which point of an AP curveMid-point of Depolarization
A period during which a second AP cannot be elicited with a threshold stimulusRefractory Period
Period during which another action potential cannot be elicited, no matter how strong the stimulus isAbsolute Refractory Period (ARP)
The period during which a second AP can be elicited by a stimulus stronger than the thresholdRelative Refractory Period (RRP)
Action potential jumps from one node of Ranvier to anotherSaltatory Conduction
The speed of propagation of an action potentialConduction velocity (CV)
The diameter of nerve fiber and Myelination of nerve fiber are the two factors that contribute toConduction velocity (CV)
Due to loss of Myelin sheath around nerve fibers of central nervous system; Clinical features include severe muscle weakness, blurring of vision, diplopia, nystagmus, optic neuritisMultiple Sclerosis
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Chemical Synaptic Transmission

Question Answer
Specialized junctions through which neurons signal to each other and to non-neuronal cells such as those in muscles or glandsChemical Synapses
This ion causes the release of neurotransmitters into the synaptic cleftCa+2
Influx of sodium through Na+ ion channels in postsynaptic membrane. Membrane potential is driven to positive potential (depolarization). If it is able to reach threshold, an action potential is produced in postsynaptic neuronExcitatory Synapses
Acetylcholine, Norepinephrine, Aspartate, and Glutamate are which type of neurotransmittersExcitatory Neurotransmitters
An Influx of chloride through Cl- ion channels in postsynaptic membrane. Membrane potential is driven to more negative than at resting potential (hyperpolarization). Membrane potential goes away from threshold and postsynaptic neuron is not able to produce an action potentialInhibitory Synapses
Glycine and GABA are which type of neurotransmittersInhibitory Neurotransmitters
Alzheimer’s disease (Senile dementia) is caused by loss of which neurotransmitterAcetylcholine
Parkinson’s disease is a loss of which neurotransmitterDopamine
Schizophrenia is the overproduction of which neurotransmitterDopamine
The synapse between the axon terminal of a motor neuron and a skeletal muscle fiberNeuromuscular Junction
Comprised of a single motor neuron & the muscle fibers it innervatesMotor Unit
Paralysis stemming from damage to the brain or spinal cordUpper Motor Unit Lesion
Paralysis stemming from damage to the peripheral motor neuronsLower Motor Unit Lesion
ACh is degraded to choline and acetate byAcetylcholinesterase
The choline within the synaptic cleft remaining after the cleaving for ACh by acetylcholinesterase is taken back into the presynaptic terminal byNa+-Choline Cotransporter
Toxin which blocks the release of ACh from the presynaptic neuronBotulinum
Drug used that competes with ACh for nicotinic receptors on the motor end plateCurare
Toxin which binds irreversibly to Ach receptors found in krait’s venomα- Bungarotoxin
History of ptosis (drooping of eyelids), easy fatigability even for simple day to day tasks, progressive muscle weakness; Drooping eye lids (Ptosis); Double vision (Diplopia); Decreased facial expressions; Dysphagia (difficulty in swallowing); Dysarthria (difficulty in speech); Daily routines are tiring; antibodies to Ach receptors; Treatment using anticholinesterase agents such as Neostigmine and PyridostigmineMyasthenia Gravis
Treatment for Myasthenia Gravis uses which medicationNeostigmine and Pyridostigmine (Acetylcholinesterase Inhibiters)
Characterized by skeletal muscle weakness; May be associated with small cell carcinoma of lungs or any other autoimmune disorder; Antibodies destroy voltage gated calcium channels in presynaptic nerve terminalLambert-Eaton Syndrome
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