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99 Cards in this Set
- Front
- Back
What are the 3 primary mechanisms of control of the circulation
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local, neural, humoral
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hyperemia & autoregulation are associated w/ what type of control mechanism
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local
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what are 3 major sites of control of flow
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very small arteries
arterioles pre-capillary sphincters |
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the primary mechs of control of circulation accomplish their control via
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vasodilation & vasoconstriction
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the primary mechs of control allow for tissues to individually control their respective flow in the face of changes in ___ & ___ by changing the ____
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co, bp, resistance to flow
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THESE MECHANISMS ACT INDEPENDENT OF ANY NERVOUS OR HUMORAL/HORMONAL INPUT; THEY ARE INTRINSIC & RESPOND TO CHANGES IN LOCALIZED FACTORS
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LOCAL CONTROL:
ACTIVE HYPEREMIA FLOW AUTOREGULATION (MYOGENIC RESPONSE) |
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ACTIVE HYPEREMIA:
INC METABOLIC ACTIVITY OF ORGAN>>_ O2, _ METABOLITES IN ORGAN INTERSTITIAL FLUID>>ARTERIOLAR CONST OR DILAT>>_ BLOOD FLOW TO ORGAN |
DEC O2, INC METABOLITES
DILATION INCREASE BLOOD FLOW TO ORGAN |
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FLOW AUTOREGULATION:
DECREASE ARTERIAL PRESS IN ORGAN>>_ BLOOD FLOW TO ORGAN>>_ O2, _METABOLITES, _VESSEL-WALL STRETCH IN ORGAN>>ARTERIOLAR CONST OR DILAT>>RESTORATION OF BLOOD FLOW ___ IN ORGAN |
DEC, DEC, INC, DEC, DILATION, TOWARD NORMAL
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IN ACTIVE HYPEREMIA, THE TISSUE RECEIVES HOW MUCH
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WHAT IT NEEDS, NO MORE, NO LESS
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WHAT ARE 2 MAJOR LOCAL FACTORS INVOLVED IN ACTIVE HYPEREMIA TO INCREASE BLOOD FLOW VIA VASODILATION
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DECREASED O2
INCREASED ADENOSINE |
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FLOW AUTOREGULATION OCCURS B/C OF
ACTIVE HYPEREMIA OCCURS B/C OF |
SIGNIFICANT CHANGE IN BP
INCREASE/DECREASE IN METABOLIC ACTIVITY |
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WHAT IS AN ECONOMICAL CONTROL OF BLOOD FLOW
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FLOW AUTOREGULATION
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WHY DOES REACTIVE HYPEREMIA OCCUR
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BLOOD SUPPLY TO A TISSUE HAS BEEN OCCLUDED
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WHAT BUILDS UP IN REACTIVE HYPEREMIA
WHAT HAPPENS UPON REMOVAL OF THE OCCLUSION |
METABOLIC FACTORS
FLOW TO THE TISSUE IS GREATLY ENHANCED VIA MASSIVE VASODILATION |
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WHAT IS PREDOMINANT ADRENERGIC RECEPTOR IN VASCULAR SYSTEM
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ALPHA RECEPTOR
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WHAT INNERVATES THE FOLLOWING:
MOST SMALL ARTERIES & ARTERIOLES SMALLEST LEVELS OF ARTERIOLES PRE-CAPILLARY SPHINCTERS |
SNS
NONE NONE |
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LOCAL CONTROL IS CONCERNED W/
NEURAL CONTROL IS CONCERNED W/ |
CONTROL OF FLOW TO INDIVIDUAL TISSUES
OVERALL MAINTENANCE OF FLOW, RESISTANCE, & PRESSURE...WHOLE BODY NEEDS |
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WHAT SECRETES EPI INTO THE BLOOD
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ADRENAL MEDULLA
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NOREPI BINDS TO:
CAUSING: EPI BINDS TO: CAUSING: |
ALPHA RECEPTORS MOSTLY
VASOCONTRICTION BETA RECEPTORS MOSTLY VASODILATION |
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WHICH VASOCONSTRICT/VASODILATE?
NOREPI EPI NO PGI2 VASOPRESSIN (AVP) ANGIOTENSIN II (ANG II) ATRIAL NATRIURETIC PEPTIDE (ANP) ENDOTHELIN-1 (ET1) |
BOTH BUT MAINLY CONSTRICT
BOTH BUT MAINLY DILATE DILATE DILATE CONSTRICT CONSTRICT DILATE CONSRICT |
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WHAT CONTROLS:
SHORT-TERM BP LONG-TERM BP |
NERVOUS & HORMONAL
RENAL W/ VOLUME REGULATION |
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this pressure differential created by stored energy in the arteries that moves the blood
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pulse pressure
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map =
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dbp + 1/3 pp
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result of volume of blood in the closed circulatory system w/ normal vascular tone
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diastolic bp
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blood pumped into aorta during ejection phase; becomes potential energy stored in arterial wall due to stretching of elastic arteries
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systolic bp
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WHAT CAUSES SYSTOLIC BP TO INCREASE MORE THAN DIASTOLIC BP IN THE HEALTH GERIATRIC INDIVIDUAL
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LOSS OF COMPLIANCE, VESSELS ARE MORE RIGID; RESULTS IN PP BEING HIGHER
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WHAT HAS BECOME AN IMPORTANT INDICATOR OF CARDIOVASCULAR DZ IN THE ELDERLY & IS CONSIDERED TO BE A POTENTIAL THERAPEUTIC TARGET
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ELEVATED PP, AS A REFLECTION OF AN INCREASE IN SBP
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WHAT IS PREDOMINANT SHORT-TERM NEURAL CONTROL MECH FOR REGULATION OF BP
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BARORECEPTOR REFLEX MECHANISM
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WHAT ARE THE COMPONENTS OF BARORECEPTOR REFLEX MECH
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MEDULLARY CARDIOVASCULAR CENTER
ARTERIAL BARORECEPTORS (MECHANORECEPTORS) AFFERENT & EFFERENT NERVOUS PATHWAYS |
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WHERE ARE THE ARTERIAL BARORECEPTORS LOCATED
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AORTIC ARCH & CAROTID SINUS
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WHAT PART OF MEDULLARY CARDIOVASCULAR CENTER CONTROLS
PARASYMPATHETIC OUTFLOW TO HEART SYMPATHETIC OUTFLOW TO HEART & VASCULATURE |
VAGAL CENTER
VASOMOTOR CENTER |
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AFFERENT NERVOUS PATHWAYS INCLUDE:
WHAT NERVE/S BARORECEPTORS TO WHERE SPECIFICALLY EFFERENT: NERVE/S TO WHERE |
VAGUS & GLOSSOPHARYNGEAL
MEDULLA, NUCLEUS TRACTUS SOLITARIUS (NTS) VAGUS TO HEART, & SYMPATHETIC TO HEART & BLOOD VESSELS |
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WHAT IS THE BIG DRAWBACK OF BARORECEPTOR
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ADAPTATION--VERY RAPIDLY SO IF CHRONIC HIGH BP, WILL SET NORMAL TO HIGHER LEVEL
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CHRONOTROPIC =
INOTROPIC = |
HEART RATE
FORCE OF CONTRACTION (CONTRACTILITY) |
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INC ARTERIAL PRESSURE >> INC ARTERIAL BARO. FIRING >> ____ >> ____ & ____
WHAT HAPPENS W/ SYMP & PARASYMP |
NTS >> VASOMOTOR & VAGAL CENTER
VASOMOTOR: DEC SYMP (NEG INO & CHRONOTROPIC) VAGAL: INC PARA (DEC CHRONO) |
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WHAT ARE THE SHORT-TERM HORMONAL CONTROLERS OF BP
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CATECHOLAMINE
VASOPRESSIN RENIN-ANGIOTENSIN ENDOTHELIN-1 NITRIC OXIDE |
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WHAT ARE THE 2 CATECHOLAMINES
WHERE ARE THEY RELEASED FROM WHAT IS THEIR ACTION |
NE & EPI
SNS TERMINALS; ADRENAL MEDULLA VASOCONSTR; INC HR (CO) |
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WHAT IS VASOPRESSIN
WHERE IS IT SYNTHESIZED WHERE IS IT RELEASED FROM WHY IS IT RELEASED |
PEPTIDE HORMONE
HYPOTHALAMUS POST. PITUITARY IN RESPONSE TO SNS STIMULATION & DIRECTLY THROUGH A DEC IN BP |
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WHAT IS ANG II
ACTION STIMULUS |
PEPTIDE HORMONE
VASOCONS; ALSO MODULATES NE RELEASE DEC IN BP |
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WHAT IS ENDOTHELIN-1
WHERE IS IT SYNTHESIZED WHERE IS IT SECRETED |
PEPTIDE
ENDOTHELIUM ENDOTHELIUM |
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WHAT IS THE MOST POTENT VASOCONSTRICTOR KNOWN
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ENDOTHELIN-1; VERY SMALL AMTS CAUSE SIG. CONSTRICTION
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WHERE IS NO SYNTHESIZED
RELEASED ACTION |
ENDOTHELIUM
ENDOTHELIUM VASODILATOR |
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HOW LONG DO LONG-TERM SYSTEMS TAKE TO ACT
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HOURS TO DAYS TO WEEKS
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THE PRIMARY LONG-TERM RENAL MECH IS BASED ON
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PRESSURE-FILTRATION FX OF THE KIDNEY
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WHAT ARE THE HORMONES INVOLVED IN LONG-TERM BP CONTROL
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RAS, AVP-VASOPRESSIN, & ATRIAL NATRIURETIC PEPTIDE (ANP)
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WHAT DOES ANP DO
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VASODILATES
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WHAT BLOOD VOLUME HAS THE CRITICAL FX OF EXCHANGE OF NUTRIENTS & WASTE PRODUCTS
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5% OF TOTAL VOL IN CAPILLARY NETWORK
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HOW DOES AVP (VASOPRESSIN), ANP, & RAS CONTROL LONG-TERM BP
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AVP & RAS--DEC SODIUM AND WATER EXCRETION, THEREFORE INC BLOOD VOL & INC BP
ANP--INC SODIUM & WATER EXCRETION, THEREFORE DEC BLOOD VOL AND DEC BP |
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WHAT CONTROLS FLOW THROUGH THE TISSUES
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SMALL PRE-CAPILLARY ARTERIOLES & PRE-CAPILLARY SPHINCTERS
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WHERE IS THE CONTROL OF DEVELOPMENT AND GROWTH OF VASCULAR NETWORKS IN TISSUES
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MICROCIRCULATORY LEVEL (CAPILLARY)
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ANGIOGENIC
ANGIOSTATIC |
GROWTH PROMOTING
GROWTH INHIBITING |
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WHAT LEADS TO EXCESSIVE BLOOD VESSEL GROWTH PROVIDING THE BLOOD NEEDED FOR TUMOROUS AND CANCEROUS GROWTH
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THE IMBALANCE OF ANGIOGENIC & ANGIOSTATIC FACTORS
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WHAT IS NOT TRANSPORTED THROUGH ENDOTHELIAL CELLS AT INTERCELLULAR CLEFTS
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PROTEINS
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TRANSPORT MECH FOR WATER, IONS & SMALL WATER-SOLUBLE SOLUTES OF ENDOTHELIAL CELLS ARE
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INTERCELLULAR CLEFTS
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WHAT ARE THE 3 MECH OF TRANSPORT ACROSS MOST CAPILLARY WALLS FROM BLOOD TO TISSUE & VICE VERSA
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DIFFUSION THROUGH CELL MEMBRANE, INTERCELLULAR CLEFTS & VESICLE CHANNELS
VESICLE TRANSPORT UTILIZING CELL MEM (SMALL AMTS OF PROTEIN) BULK FLOW THROUGH INTERCELLULAR CLEFTS |
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WHAT IS THE FX OF BULK FLOW
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MAINTAIN A NORMAL DISTRIBUTION OF FLUID WITHIN THE 2 DIVISIONS OF THE EXTRACELLULAR COMPARTMENT: B/T THE
PLASMA AND INTERSTITIAL FLUID |
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THE INTERSTITIAL FLUID IS ESSENTIALLY THE SAME AS PLASMA EXCEPT IT HAS
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A LOW PROTEIN CONTENT
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WHAT ARE THE 4 STARLING FORCES
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PC-CAP HYDROSTATIC PRESS
PIF-INTERSTITIAL FLUID HYDROSTATIC PRESS PIE P-PLASMA COLLOID OSMOTIC PRESS (ONCOTIC PRESS) PIE IF-INTERSTITIAL FLUID COLLOID OSMOTIC PRESS |
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WHAT IS THE RELATIONSHIP B/T THE STARLING FORCES
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(DEC + DEC) - (INC + INC)
(Pc + PIEif) - (Pif + PIEp) |
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LYMPH CAPILLARIES ARE SIMILAR TO BLOOD CAPILLARIES B/C OF WHAT, BUT DIFFERENT B/C OF WHAT
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COMPOSED OF ENDOTHELIAL CELLS ON A BASEMENT MEMBRANE;
MUCH MORE PERMEABLE TO INTERSTITIAL FLUID SO LARGE PROTEINS & SUBS CAN GET INTO LYMPH VESSEL |
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LYMPH FLUID IS DERIVED FROM
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INTERSTITIAL FLUID
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HOW IS LYMPH FLUID MOVED THROUGH THE LYMPHATIC SYSTEM
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SPONTANEOUS, RHYTHMIC CONTRACTIONS OF THE SMOOTH VESSELS (INTRINSIC)
VALVES TO PREVENT BACKFLOW VESSELS HAVE SOME INNERVATION BY SNS TO FURTHER ENHANCE FLOW BY INC SMOOTH MUSCLE TONE |
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WHAT WILL THE FOLLOWING DO TO NET FILTRATION & THE STARLING FORCES:
HEMORRHAGE ARTERIOLAR VASOCONSTRICTION INCREASE IN PLASMA PROTEINS INC IN OVERALL BP INC IN VENOUS PRESSURE INFLAMMATION OR BURNS LIVER DZ |
DEC NET FILTRATION DEC IN Pc
DEC NET FILTRATION DEC IN Pc DEC NET FILTRATION INC PIEp INC NET FILTRATION INC IN Pc INC NET FILTRATION INC IN Pc INC NET FILTRATION INC PIEif INC NET FILTRATION DEC PIEp |
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AN INCREASE IN NET FILTRATION OF FLUID MAY LEAD TO
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EDEMA
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WHAT ARE THE PRIMARY METABOLIC REGULATORS OF CEREBRAL CIRCULATION
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O2, CO2, H+
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IN AUTOREGULATION, FLOW IS TYPICALLY NOT AFFECTED IN THE MAP RANGES OF WHAT FOR CEREBRAL CIRCULATION
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60-150mmHg
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AUTOREGULATION VIA ___ MECHANISM FOR CEREBRAL CIRCULATION
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MYOGENIC
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WHAT SUPPLIES THE BULK OF BLOOD FLOW TO THE HEART
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2 MAIN CORONARY ARTERIES
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VENOUS RETURN IS TO THE RIGHT ATRIUM VIA
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CORONARY SINUS
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AVG CORONARY BLOOD FLOW IS __ - __% OF TOTAL CO
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4-5%
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WHAT ORGAN IS THE MOST EFFICIENT AT EXTRACTING O2
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HEART
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WHEN IS CORONARY FLOW THE GREATEST
MINIMAL |
DIASTOLE
SYSTOLE WHICH IS OPPOSITE OF THE SYSTEMIC CIRCULATION |
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AORTIC PRESSURE IS GENERATED FROM
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VENTRICULAR SYSTOLE
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WITH INC SNS ACTIVITY TO THE HEART, CORONARY BLOOD FLOW INC B/C OF WHAT 2 THINGS
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DIRECT EFFECTS
INDIRECT EFFECTS |
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WHAT IS NORMAL BLOOD FLOW TO SKELETAL MUSCLE CIRCULATION
HOW MUCH CAN EXERCISE INCREASE THE FLOW |
3-4 ML/MIN/100G OF TISSUE
15-25 TIMES |
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WHAT IS THE FLOW PATTERN LIKE IN SKELETAL MUSCLE
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MUCH LIKE THE HEART WITH LOW FLOW DURING CONTRACTION & HIGH FLOW DURING RELAXATION
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WHAT IS A MAJOR MECH OF INCREASING FLOW IN SKELETAL MUSCLE
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RECRUITMENT OF CAPILLARIES
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SKIN CIRCULATION:
VENOUS PLEXUS & ARTERIOVENOUS ANASTOMOSES FOR REG ARTERIES, CAPILLARIES, VEINS FOR |
CONDUCTION OF HEAT
NUTRITION OF SKIN |
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WHAT CONTROLS FLOW FOR REGULATION OF BODY TEMP
FOR NUTRITION FLOW |
SNS IN CONJUNCTION W/ HYPOTHALAMUS IN CNS
PREDOMINANTLY BY SNS W/ SOME LOCAL METABOLIC & AUTOREGULATORY ACTIVITY |
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BLOOD FLOW TO SPLANCHNIC CIRCULATION IS APPROX
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1400-1550 ML/MIN (25% OF CO)
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FLOW TO HEPATIC IS FROM WHAT SOURCE/S
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HEPATIC ARTERY & PORTAL VEIN
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FOR HEPATIC FLOW:
SNS CONTROLS AUTOREGULATION CONTROLS |
BOTH THE HEPATIC ARTERY & PORTAL VEIN
HEPATIC ARTERY |
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WHAT REGULATES RBC PRODUCTION
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ERYTHROPOIETIN
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WHERE IS ERYTHROPOIETIN:
RELEASED WHAT STIMULATES IT |
KIDNEY
PRIMARY IS REDUCED O2 DELIVERY TO THE KIDNEY; TESTOSTERONE ALSO |
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WHAT IS THE PRIMARY STEP IN THE CLOT FORMATION AND WHAT DOES IT INCLUDE
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MESHWORK OF FIBRIN; PLATELETS & RBC'S
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WHAT IS IMPORTANT FOR THE WHOLE CASCADE TO OCCUR
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REQUIRES ACTIVATED PLATELETS, PLASMA COFACTORS, AND CALCIUM
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CLOTTING INITIATED BY FACTORS ONLY IN THE BLOOD--TEST TUBE CLOTTING
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INTRINSIC PATHWAY
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CLOTTING INITIATED BY TISSUE FACTORS; ESSENTIALLY WHAT OCCURS IN THE BODY
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EXTRINSIC PATHWAY
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WHERE DO BOTH PATHWAYS CONVERGE
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Xa (PROTHROMBIN ACTIVATOR)
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WHAT IS NECESSARY FOR PRODUCTION OF PROTHROMBIN
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VITAMIN K
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WHAT IS PRINCIPAL MECH BY WHICH CLOTS ARE REMOVED
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FIBRINOLYTIC SYSTEM
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TISSUE FACTOR PATHWAY INHIBITOR (TFPI) PREVENTS WHAT
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FORMATION OF FACTOR Xa
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PRIMARY SITE OF CONTROL OF BLOOD FLOW IS WHERE
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ARTERIOLES
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WHAT HAS THE LARGEST TO SMALLEST CROSS SECTIONAL AREA
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CAPILLARIES > VEINS > ARTERIES
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WHAT HAS THE LARGEST TO SMALLES BLOOD VOLUME
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VEINS > ARTERIES > CAPILLARIES
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WHERE IS BP GREATEST
RESISTANCE OCCURS PRIMARILY WHERE FLOW OF BLOOD IS SLOWEST WHERE HOW ARE BLOOD FLOW VELOCITY & CROSS SECTIONAL AREA RELATED |
AORTA
LEVEL OF ARTERIOLES CAPILLARIES BLOOD FLOW = 1/CROSS SECTIONAL AREA |
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STUDY OF THE PHYSICAL CHARACTERISTICS OF THE BLOOD ITSELF & THE PRINCIPLES OF FLOW THROUGH VESSELS
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HEMODYNAMICS
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WHAT IS THE MOST IMPORTANT DETERMINANT FOR CHANGES IN RESISTANCE AND SUBSEQUENTLY FLOW
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RADIUS B/C TPR = 1/R^4
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RESISTANCE TO BLOOD FLOW IS MUCH LESS IN WHAT TYPE OF CIRCUIT
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PARALLEL CIRCUIT
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