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132 Cards in this Set
- Front
- Back
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asthma
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abnormally high amounts of IgE antibodies
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thick mucus production
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mucin
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albuterol bronchodilator
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beta 2 adrenergic agonist
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mag sulfate
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bronchodilation in acute asthma
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What are the risk factors of PE
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venous inj, smoking, clotting
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peripheral diabetes
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failure of glucose transporter
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Prereceptor diabetes
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abnormal insulin receptor
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What inhibits insulin release from the beta cells
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smoking
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What increases GLUT 4 transporters
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exercise
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What is a halmark of Diabetes insipidius
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low urine specific gravity 1.001-1.01
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Urine osmolality in Di
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200mOsm/kg of water or less
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What drugs can you use for DI?
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vasopressing or DDAVP...acts on V2 receptors 10 mcg
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What is Hemoglobin S
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deoxygenated form, the hemoglobin binds to one another....leads to ischemia, pain and organ disfunction
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What are treatments of Sickle cell?
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bone marrow transplant...genetic counseling
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DGliadin
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protein
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HLA DQ2 & DQ8
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hand off to T cell
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What is the halmark of Paroxysmal Nocturnal Hemoglobinuria?
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dark morning urine
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What drug do you use in paroxysmal nocturnal hemoglobinuria
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soliris
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What EF does early onset diastolic heart failure have?
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> 45%
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actin is a
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globular protein with a myosin binding site which when polymerized forms two twisted strands
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tropomyosin runs along
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the groove of the twisted actin strands and functions to block the myosin binding site
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troponin
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is a globular protein composed of complex of three subunits
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Troponin C
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binds Ca
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when Ca is bound to troponin C, a conformational change occurs
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which removes the tropomyosin inhibition of actin myosin interaction
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cardiac action potential is initiated in the
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myocardial cell membrane and the depolarization spreads to the interior of the cell via the T tubules
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What are the steps of the cardiac action potential
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1. Ca enters cell during plateau
2. Ca induced Ca release from SR 3. Ca binds to troponin C 4. Cross bridge cycling 5 Tension |
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Unique feature of the cardiac action potenital is its
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plateau
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Ca induced Ca released
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inc in intracellular Ca concentration triggers the release or more Ca from stores in the sarcoplasmic reticulum through Ca release channels
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Relaxation occurs when
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Ca is reaccumulated in the sarcoplasmic reticulum by Ca ATPase
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Contractility or inotropism is the
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intrinsic ability of myocardial cells to develop force at a given muscle cell length
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postitive inotropic
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inc contractility
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Contractility correlates directly with
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intracellular Ca concentration
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What is phospholamban
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a protein that regulates Ca ATPase resulting in greater uptake and storage of Ca by the sarcoplasmic reticulum
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Transverse T tubules carry
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action potentials to the cell interior
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heart muscle contracts via
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sliding filament model and cross bridge cycling between myosin and actin
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Increased Ca+ uptake by the sarcoplasmic reticulum will allow for
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a faster relaxation and have a greater amount of storage for the next beat
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circulating catecholamines released during sympathetic innervation increase
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contractility.
Inc peak tension inc rate of tension development faster rate of relaxation |
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sarcolemmal ca channels increase triggers
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Ca current
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phospholamban helps stimulate a greaters amount of
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Ca stored in the SR
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circulating acetylcholine during parasympathetic innvervation of the heart muscle decrease
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contractility on the atria
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acetylcholine decreases the
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Ca current during the plateau phase of the action potential and
shortens the duration of the action potential |
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What is the staircase effect
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heart rate inc then tension increases
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increase in tension causes an inc in
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the amount of calcium during plateau phase and that is stored in the SR until it is at max storage
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Postextrasystolic potentiation
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is an extra beat essentially with inc tension. very next beat less than normal tension but the next beat has more than normal tension
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digoxin is a
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cardiac glycoside
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WHen is digoxin primarily used
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during CHF to improve ventricular contractility
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Digoxin has a
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positive inotropic agent
inhibits Na-K ATPase pump which in turn inhibits the movement of Ca OUT OF THE CELL so if intracellular calcium inc and tension is diretly proportional to the amount of intracellular ca |
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Stimulation of PNS has a
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negative inotropic effect on the atria
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The neg inotropic effect is mediated via the
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muscarinic receptors
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caridac glycosides are a class of drugs that act as
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positive inotropic agents
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when the Na K ATPase is inhibited less Na is pumped out of the cell inc
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intracellular Na concentration
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What is the Frank Starling principle?
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If preload is inc the ventricular fiber length is also inc, resulting in an inc tension of the muscle
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CO is directly related to
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preload (per FS law)
Greater stretch=greater contraction |
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Preload is the
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left ventricular diastolic volume...resting length from which the muscle contracts
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After load for the left ventricle is the
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aortic pressure
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Stroke volume is the
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volume of blood ejected by the ventricle on each beat
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EF is the
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feaction of the end diastolic volume ejected in each stroke volume
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cardiac output is the
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total volume ejected by the ventricle
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Stroke volume =
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end diastrolic volume - end systolic volume
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cardiac output =
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stroke volume x HR
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EF=
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stroke volume/end diastolic volume
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volume work is
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cardiac output
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pressure work is
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aortic pressure
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cardiac minute work
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volume work +pressure work
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pressure work uses more
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oxygen than volume work
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aortic stenosis does what
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inc consumption (pressure work) r/t higher pressures to make it through plaque
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fick principle equation
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CO=O2 consumption/(O2 pulm vein)-(O2 pulm artery)
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TPR-
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Total peripheral resistance
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7 steps of cardiac cycle
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1. atrial systole
2. Isovolumetric ventricular contraction 3. rapid ventricular ejection 4. reduced ventricular ejection 5. Isovolumetric ventricular relaxation 6. rapid ventricular filling 7. reduced ventricular filling *diastole* |
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cardiac and vascular function curves intersect when
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venous return equals cardiac output---steady state
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Un stressed
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blood in veins.
Stressed = blood in arteries |
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a dec in TPR causes
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clockwise rotation of the vascular function curve....for that give right atrial pressure venous return is INCREASED
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a inc in TPR causes
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counterclockwise rotation of the vascular fx curve. for a given right atrial pressure venous return is DECREASED
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Pa or MAP =
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CO x TPR
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The baroreceptor reflex keeps
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arterial pressure constant by changes in the SNS and PNS
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afferent info is integrated from CN
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IX and X at the nucleus tractus sollitarius
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Vasoconstrictor Center
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Efferent neurons of SNS that hit target organs via the spinal cord and cause vasoconstriction in arteries and veins
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Cardiac Accelerator Center
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Efferent neurons of SNS that hit the heart via the spinal cord to increase heart rate by increasing firing of the SA node
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Cardiac Decelerator Center
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Efferent neurons of PNS that travel via CN X and decrease firing of SA node to decrease HR
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microcirculation happens via
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simple diffusion
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Starling forces
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states that fluid movement across a capillary wall is determined by
1. net pressure across the wall hydrostatic +oncotic presssure |
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filtration is movement
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out of the capillary
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absorption is movement
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into the capillary
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hydraulic conductance
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water permeability of the capillary wall
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capillary hydrostatic pressure
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favors filtration out of the capillary.
Highest at arteriolar capillary end and lowest at venous end |
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interstitial hydrostatic pressure
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opposes filtration. should be zero
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capillary oncotic pressure.
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opposesfiltration. determined by protein concentration so inc in protein concentration causes a dec in filtration
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interstitial oncotic pressure is determined by
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interstiltial protein concentration so proteins are usually not in interstitial fluid so this value is low
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myogenic hypothesis
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vascular smooth muscle stretches it contracts. arterial pressure inc leads arteriole stretch and smooth muscle contraction and constriction
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LaPlace
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contracts to return the wall tension of the arterioles back to normal after being stretched
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Active hyperemia
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blood flow is proportional to its activity. if skeletal muscle is exercised it will get more flow
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reactive hyperemia
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inc in flow in reaction to a previous decrease. repaying oxygen debt from an occulsion
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metabolic hypothesis
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O2 delivery to a tissue can be matched to the oxygen consumption of the tissue by altering the resistance of the arterioles
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hormonal control involves vasoactive substance:
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histamine, bradykinin, serotonin, prostaglandins
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histamine and bradykinin are
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vasodilators that inc filtration out of the capillaries and produce local edema
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serotonin is a
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vasoconstrictor also released in response to blood vessel damage
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Coronary blood flow
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Controlled via local metabolites hypoxia and adenosine
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cerebral blood flow control
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Most important vasodilator is CO2
Exhibits autoregulation and reactive hyperemia |
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best way to control body heat
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shivering
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maintainng of body temp is controlled by
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ANTERIOR hypothalamus
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heat stroke
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body temp inc to the point of tissue damage
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malignant hyperthermia caused by
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inhalation anethetics
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Compensatory responses
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Decrease in arterial pressure
Baroreceptor response Renin-Angiotensin II-aldosterone response Capillary response ADH response |
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malignant hyperthermia is characterized by
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massive inc in metabolic rate, o2 consumption and heat production
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Cardiac glycosides block
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Na+K+ ATPase pump and increase contractility or the pumping action. We use this in CHF patients and these are medications like digoxin.
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C. Mechanisms in our body that help control pH are
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a. Buffering of H+ in the ECF and ICF
b. Respiratory compensation c. Renal compensation |
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most important extracellular buffer is
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HCO3/CO2
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a. Two types of acid are produced
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volatitle and fixed
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Arterial pH is slightly alkalotic at
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7.4
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CO2 is a
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volatile acid and is the byproduct of aerobic metabolism
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together with water CO2 makes
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carbonic acid via the enzyme carbonic hydrase
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Proteins generate fixed acid in the form of sulfuric acid and phospholipids generate
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fixed acid in the form of phosphoric acid
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CO2 is called volatile because
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it will be excreted by the lungs. the fixed acids will need to be buffered until the acids can be excretedy by the kidneys.
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Fixed acids can also be as a result of
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pathophysiological processes id DM, ASA OD, strenuous exercise
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A buffered soln will only have a minimally changed pH if
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the hydrogen concetration changes
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acidemia stimulated chemoreceptors in the carotid bodies that produce
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immediate inc in the ventilation rate
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The most significant intracellular buffer is
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hemoglobin
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HCO3 /CO2 is
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the body's first line of defense when hydrogen is gained or lost in the body
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inorganic phosphate
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also serves as a buffer
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To utilize ICF buffers in the acid/base disturbances,
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H+ first must cross the cell membrane by
1. CO2 itself can cross the cell membranes... Co2 rapidly enters the cells, and the H it generates is buffered |
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2 way H can cross the cell membrane
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H+ can enter or leave the cell with an organic anion such as lactate
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3 way H can cross
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H exchanges with K to preserve electroneutralitiy
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In acidemia there is an excess of H in the blood. because more H is bound to plasma proteins,
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less Ca is bound producing free Ca
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in alkalemia, there is a deficit of H in the blood. because less H is bound to plasma proteins, more Ca is bound
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producing a decrease in free Ca concentration
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In respiratory alkalosis symptoms of
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hypocalcemia occus....tingling, numbness and tetany
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the pK of oxyhemoglovin is
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6.7, which is in the range for effective physiologic buffering
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First part of renal buffering
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reabsorption of HCO3...an imortant ECF buffer so we dont want it to be Excreted in urine
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Second part of renal buffering
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excretion of H+ via a titratble acid or as NH4
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The synthesis of new bicarbonate is also important in the ecretion of hydrogen because
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it replenishes the stores that were used to buffer H+ in the first place
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What part of the kidney reabsorbs most of the bicarbonate?
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proximal tubule
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Titratable acid is excreted as H+ with
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urinary buffers throughout the nephron
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the first mechanism for H+ secretion is
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H ATPase, stimulated by aldosterone.
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