Physiology Exam 3

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What are the 3 primary mechanisms of control of the circulation: local, neural, humoral
hyperemia & autoregulation are associated w/ what type of control mechanism: local
what are 3 major sites of control of flow: very small arteries
arterioles
pre-capillary sphincters
the primary mechs of control of circulation accomplish their control via: vasodilation & vasoconstriction
the primary mechs of control allow for tissues to individually control their respective flow in the face of changes in ___ & ___ by changing the ____: co, bp, resistance to flow
THESE MECHANISMS ACT INDEPENDENT OF ANY NERVOUS OR HUMORAL/HORMONAL INPUT; THEY ARE INTRINSIC & RESPOND TO CHANGES IN LOCALIZED FACTORS: LOCAL CONTROL:
ACTIVE HYPEREMIA
FLOW AUTOREGULATION (MYOGENIC RESPONSE)
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
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
IN ACTIVE HYPEREMIA, THE TISSUE RECEIVES HOW MUCH: WHAT IT NEEDS, NO MORE, NO LESS
WHAT ARE 2 MAJOR LOCAL FACTORS INVOLVED IN ACTIVE HYPEREMIA TO INCREASE BLOOD FLOW VIA VASODILATION: DECREASED O2
INCREASED ADENOSINE
FLOW AUTOREGULATION OCCURS B/C OF ACTIVE HYPEREMIA OCCURS B/C OF: SIGNIFICANT CHANGE IN BP

INCREASE/DECREASE IN METABOLIC ACTIVITY
WHAT IS AN ECONOMICAL CONTROL OF BLOOD FLOW: FLOW AUTOREGULATION
WHY DOES REACTIVE HYPEREMIA OCCUR: BLOOD SUPPLY TO A TISSUE HAS BEEN OCCLUDED
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
WHAT IS PREDOMINANT ADRENERGIC RECEPTOR IN VASCULAR SYSTEM: ALPHA RECEPTOR
WHAT INNERVATES THE FOLLOWING: MOST SMALL ARTERIES & ARTERIOLES SMALLEST LEVELS OF ARTERIOLES PRE-CAPILLARY SPHINCTERS: SNS
NONE
NONE
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
WHAT SECRETES EPI INTO THE BLOOD: ADRENAL MEDULLA
NOREPI BINDS TO: CAUSING: EPI BINDS TO: CAUSING:: ALPHA RECEPTORS MOSTLY
VASOCONTRICTION

BETA RECEPTORS MOSTLY
VASODILATION
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
WHAT CONTROLS: SHORT-TERM BP LONG-TERM BP: NERVOUS & HORMONAL

RENAL W/ VOLUME REGULATION
this pressure differential created by stored energy in the arteries that moves the blood: pulse pressure
map =: dbp + 1/3 pp
result of volume of blood in the closed circulatory system w/ normal vascular tone: diastolic bp
blood pumped into aorta during ejection phase; becomes potential energy stored in arterial wall due to stretching of elastic arteries: systolic bp
WHAT CAUSES SYSTOLIC BP TO INCREASE MORE THAN DIASTOLIC BP IN THE HEALTH GERIATRIC INDIVIDUAL: LOSS OF COMPLIANCE, VESSELS ARE MORE RIGID; RESULTS IN PP BEING HIGHER
WHAT HAS BECOME AN IMPORTANT INDICATOR OF CARDIOVASCULAR DZ IN THE ELDERLY & IS CONSIDERED TO BE A POTENTIAL THERAPEUTIC TARGET: ELEVATED PP, AS A REFLECTION OF AN INCREASE IN SBP
WHAT IS PREDOMINANT SHORT-TERM NEURAL CONTROL MECH FOR REGULATION OF BP: BARORECEPTOR REFLEX MECHANISM
WHAT ARE THE COMPONENTS OF BARORECEPTOR REFLEX MECH: MEDULLARY CARDIOVASCULAR CENTER

ARTERIAL BARORECEPTORS (MECHANORECEPTORS)

AFFERENT & EFFERENT NERVOUS PATHWAYS
WHERE ARE THE ARTERIAL BARORECEPTORS LOCATED: AORTIC ARCH & CAROTID SINUS
WHAT PART OF MEDULLARY CARDIOVASCULAR CENTER CONTROLS PARASYMPATHETIC OUTFLOW TO HEART SYMPATHETIC OUTFLOW TO HEART & VASCULATURE: VAGAL CENTER

VASOMOTOR CENTER
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
WHAT IS THE BIG DRAWBACK OF BARORECEPTOR: ADAPTATION--VERY RAPIDLY SO IF CHRONIC HIGH BP, WILL SET NORMAL TO HIGHER LEVEL
CHRONOTROPIC = INOTROPIC =: HEART RATE

FORCE OF CONTRACTION (CONTRACTILITY)
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)
WHAT ARE THE SHORT-TERM HORMONAL CONTROLERS OF BP: CATECHOLAMINE
VASOPRESSIN
RENIN-ANGIOTENSIN
ENDOTHELIN-1
NITRIC OXIDE
WHAT ARE THE 2 CATECHOLAMINES WHERE ARE THEY RELEASED FROM WHAT IS THEIR ACTION: NE & EPI

SNS TERMINALS; ADRENAL MEDULLA

VASOCONSTR; INC HR (CO)
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
WHAT IS ANG II ACTION STIMULUS: PEPTIDE HORMONE

VASOCONS; ALSO MODULATES NE RELEASE

DEC IN BP
WHAT IS ENDOTHELIN-1 WHERE IS IT SYNTHESIZED WHERE IS IT SECRETED: PEPTIDE

ENDOTHELIUM

ENDOTHELIUM
WHAT IS THE MOST POTENT VASOCONSTRICTOR KNOWN: ENDOTHELIN-1; VERY SMALL AMTS CAUSE SIG. CONSTRICTION
WHERE IS NO SYNTHESIZED RELEASED ACTION: ENDOTHELIUM

ENDOTHELIUM

VASODILATOR
HOW LONG DO LONG-TERM SYSTEMS TAKE TO ACT: HOURS TO DAYS TO WEEKS
THE PRIMARY LONG-TERM RENAL MECH IS BASED ON: PRESSURE-FILTRATION FX OF THE KIDNEY
WHAT ARE THE HORMONES INVOLVED IN LONG-TERM BP CONTROL: RAS, AVP-VASOPRESSIN, & ATRIAL NATRIURETIC PEPTIDE (ANP)
WHAT DOES ANP DO: VASODILATES
WHAT BLOOD VOLUME HAS THE CRITICAL FX OF EXCHANGE OF NUTRIENTS & WASTE PRODUCTS: 5% OF TOTAL VOL IN CAPILLARY NETWORK
HOW DOES AVP (VASOPRESSIN), ANP, & RAS CONTROL LONG-TERM BP: 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
WHAT CONTROLS FLOW THROUGH THE TISSUES: SMALL PRE-CAPILLARY ARTERIOLES & PRE-CAPILLARY SPHINCTERS
WHERE IS THE CONTROL OF DEVELOPMENT AND GROWTH OF VASCULAR NETWORKS IN TISSUES: MICROCIRCULATORY LEVEL (CAPILLARY)
ANGIOGENIC ANGIOSTATIC: GROWTH PROMOTING

GROWTH INHIBITING
WHAT LEADS TO EXCESSIVE BLOOD VESSEL GROWTH PROVIDING THE BLOOD NEEDED FOR TUMOROUS AND CANCEROUS GROWTH: THE IMBALANCE OF ANGIOGENIC & ANGIOSTATIC FACTORS
WHAT IS NOT TRANSPORTED THROUGH ENDOTHELIAL CELLS AT INTERCELLULAR CLEFTS: PROTEINS
TRANSPORT MECH FOR WATER, IONS & SMALL WATER-SOLUBLE SOLUTES OF ENDOTHELIAL CELLS ARE: INTERCELLULAR CLEFTS
WHAT ARE THE 3 MECH OF TRANSPORT ACROSS MOST CAPILLARY WALLS FROM BLOOD TO TISSUE & VICE VERSA: DIFFUSION THROUGH CELL MEMBRANE, INTERCELLULAR CLEFTS & VESICLE CHANNELS

VESICLE TRANSPORT UTILIZING CELL MEM (SMALL AMTS OF PROTEIN)

BULK FLOW THROUGH INTERCELLULAR CLEFTS
WHAT IS THE FX OF BULK FLOW: MAINTAIN A NORMAL DISTRIBUTION OF FLUID WITHIN THE 2 DIVISIONS OF THE EXTRACELLULAR COMPARTMENT: B/T THE
PLASMA AND INTERSTITIAL FLUID
THE INTERSTITIAL FLUID IS ESSENTIALLY THE SAME AS PLASMA EXCEPT IT HAS: A LOW PROTEIN CONTENT
WHAT ARE THE 4 STARLING FORCES: PC-CAP HYDROSTATIC PRESS

PIF-INTERSTITIAL FLUID HYDROSTATIC PRESS

PIE P-PLASMA COLLOID OSMOTIC PRESS (ONCOTIC PRESS)

PIE IF-INTERSTITIAL FLUID COLLOID OSMOTIC PRESS
WHAT IS THE RELATIONSHIP B/T THE STARLING FORCES: (DEC + DEC) - (INC + INC)

(Pc + PIEif) - (Pif + PIEp)
LYMPH CAPILLARIES ARE SIMILAR TO BLOOD CAPILLARIES B/C OF WHAT, BUT DIFFERENT B/C OF WHAT: COMPOSED OF ENDOTHELIAL CELLS ON A BASEMENT MEMBRANE;

MUCH MORE PERMEABLE TO INTERSTITIAL FLUID SO LARGE PROTEINS & SUBS CAN GET INTO LYMPH VESSEL
LYMPH FLUID IS DERIVED FROM: INTERSTITIAL FLUID
HOW IS LYMPH FLUID MOVED THROUGH THE LYMPHATIC SYSTEM: 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
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
AN INCREASE IN NET FILTRATION OF FLUID MAY LEAD TO: EDEMA
WHAT ARE THE PRIMARY METABOLIC REGULATORS OF CEREBRAL CIRCULATION: O2, CO2, H+
IN AUTOREGULATION, FLOW IS TYPICALLY NOT AFFECTED IN THE MAP RANGES OF WHAT FOR CEREBRAL CIRCULATION: 60-150mmHg
AUTOREGULATION VIA ___ MECHANISM FOR CEREBRAL CIRCULATION: MYOGENIC
WHAT SUPPLIES THE BULK OF BLOOD FLOW TO THE HEART: 2 MAIN CORONARY ARTERIES
VENOUS RETURN IS TO THE RIGHT ATRIUM VIA: CORONARY SINUS
AVG CORONARY BLOOD FLOW IS __ - __% OF TOTAL CO: 4-5%
WHAT ORGAN IS THE MOST EFFICIENT AT EXTRACTING O2: HEART
WHEN IS CORONARY FLOW THE GREATEST MINIMAL: DIASTOLE

SYSTOLE

WHICH IS OPPOSITE OF THE SYSTEMIC CIRCULATION
AORTIC PRESSURE IS GENERATED FROM: VENTRICULAR SYSTOLE
WITH INC SNS ACTIVITY TO THE HEART, CORONARY BLOOD FLOW INC B/C OF WHAT 2 THINGS: DIRECT EFFECTS
INDIRECT EFFECTS
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
WHAT IS THE FLOW PATTERN LIKE IN SKELETAL MUSCLE: MUCH LIKE THE HEART WITH LOW FLOW DURING CONTRACTION & HIGH FLOW DURING RELAXATION
WHAT IS A MAJOR MECH OF INCREASING FLOW IN SKELETAL MUSCLE: RECRUITMENT OF CAPILLARIES
SKIN CIRCULATION: VENOUS PLEXUS & ARTERIOVENOUS ANASTOMOSES FOR REG ARTERIES, CAPILLARIES, VEINS FOR: CONDUCTION OF HEAT

NUTRITION OF SKIN
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
BLOOD FLOW TO SPLANCHNIC CIRCULATION IS APPROX: 1400-1550 ML/MIN (25% OF CO)
FLOW TO HEPATIC IS FROM WHAT SOURCE/S: HEPATIC ARTERY & PORTAL VEIN
FOR HEPATIC FLOW: SNS CONTROLS AUTOREGULATION CONTROLS: BOTH THE HEPATIC ARTERY & PORTAL VEIN

HEPATIC ARTERY
WHAT REGULATES RBC PRODUCTION: ERYTHROPOIETIN
WHERE IS ERYTHROPOIETIN: RELEASED WHAT STIMULATES IT: KIDNEY

PRIMARY IS REDUCED O2 DELIVERY TO THE KIDNEY; TESTOSTERONE ALSO
WHAT IS THE PRIMARY STEP IN THE CLOT FORMATION AND WHAT DOES IT INCLUDE: MESHWORK OF FIBRIN; PLATELETS & RBC'S
WHAT IS IMPORTANT FOR THE WHOLE CASCADE TO OCCUR: REQUIRES ACTIVATED PLATELETS, PLASMA COFACTORS, AND CALCIUM
CLOTTING INITIATED BY FACTORS ONLY IN THE BLOOD--TEST TUBE CLOTTING: INTRINSIC PATHWAY
CLOTTING INITIATED BY TISSUE FACTORS; ESSENTIALLY WHAT OCCURS IN THE BODY: EXTRINSIC PATHWAY
WHERE DO BOTH PATHWAYS CONVERGE: Xa (PROTHROMBIN ACTIVATOR)
WHAT IS NECESSARY FOR PRODUCTION OF PROTHROMBIN: VITAMIN K
WHAT IS PRINCIPAL MECH BY WHICH CLOTS ARE REMOVED: FIBRINOLYTIC SYSTEM
TISSUE FACTOR PATHWAY INHIBITOR (TFPI) PREVENTS WHAT: FORMATION OF FACTOR Xa
PRIMARY SITE OF CONTROL OF BLOOD FLOW IS WHERE: ARTERIOLES
WHAT HAS THE LARGEST TO SMALLEST CROSS SECTIONAL AREA: CAPILLARIES > VEINS > ARTERIES
WHAT HAS THE LARGEST TO SMALLES BLOOD VOLUME: VEINS > ARTERIES > CAPILLARIES
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
STUDY OF THE PHYSICAL CHARACTERISTICS OF THE BLOOD ITSELF & THE PRINCIPLES OF FLOW THROUGH VESSELS: HEMODYNAMICS
WHAT IS THE MOST IMPORTANT DETERMINANT FOR CHANGES IN RESISTANCE AND SUBSEQUENTLY FLOW: RADIUS B/C TPR = 1/R^4
RESISTANCE TO BLOOD FLOW IS MUCH LESS IN WHAT TYPE OF CIRCUIT: PARALLEL CIRCUIT

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