Pbd Quiz 10

Front 1

How is flow regulated at the whole body level

Back 1

reflex control systems

Front 2

How is flow regulated at the organ level

Back 2

local control systems

Front 3

Vasoactive substances

Back 3

How much blood vessel is constricted or dilated

Front 4

Types of Vasoactive Substances

Back 4

Neurotransmitters (ANS effects)

Hormones (via circulation)

Local mediators (from endothelia or tissue)

Metabolites (O2, CO2, K+, adenosine)

Front 5

Sympathetic Receptors

Back 5

A1

B2

Ach

Front 6

A1 sympathetic receptors

Back 6

Locations: Arterioles in skin, muscle, kidney, splanchnic
Also veins

Effect: Constrict
For veins, constrict and reduce compliance

Front 7

B2 sympathetic receptors

Back 7

Location: Arterioles in skeletal muscle and arterioles

Effect: Dilate

Front 8

Ach sympathetic receptors

Back 8

Location: arterioles in skeletal muscle, skin? (palms, lips, soles)

Effect: Dilate

Front 9

Parasympathetic Receptors

Back 9

Ach

Bradykinin

Front 10

Ach and Bradykinin parasympathetics receptors

Back 10

Location: sweat glands, salivary glands, sex organs

Effect: dilate

Front 11

Local/Endocrine Constrictors

Back 11

From adrenal medulla, 8-% Epi & 20% NE

Front 12

Types of Local/Endocrine Constrictors

Back 12

Epi/NE via A1 receptors

angiotensin II

vasopressin

prostaglandin PGF2 A (potent smooth muscle constrictor)

thromboxane

endothelin

Front 13

Epinephrine as endocrine constrictor

Back 13

Epinephrine from adrenal medulla

FLIGHT OR FIGHT (sympathetic stimulation)

Front 14

Vasopressin as endocrine constrictor

Back 14

Vasopressin from posterior pituitary
Increased with dehydration, blood loss

Front 15

Angiotensin II as endocrine constrictor

Back 15

angiotensin II: product of renin-angiotensin system

Increased with dehydration, blood loss, sympathetic stimulation

Front 16

Making Angiotensin II

Back 16

Liver produces angiotensinogen

SNS to kidney produces Renin

Renin + Angiotensinogen form Angiotensin I

Angiotensin I + ACE in lungs (angiotensin converting enzyme) forms Angiotensin II

Front 17

G Protein Coupled Aq receptors

Back 17

IP3 interacts with RyR

Ca2+ causes constriction

Front 18

Endocrines as local dilators

Back 18

Epi/NE via B2 receptors (only in some places!)-skeletal muscle

Atrial natriuretic peptide
(ANP) - opp of ANG II

prostaglandin PGE2

prostacyclin

nitric oxide

also: CO2, lactic acid, other metabolites

adenosine

Front 19

eNOS

Back 19

Ca2+ dependent enzyme

Front 20

G Coupled Protein Alpha S as a dilator

Back 20

"big" K+ channels. Ca2+ activated. Spatially coupled to SR.

cAMP in, deactivates PLB that's on RyR. K+ out.

cGMP causes decrease in Ca2+, decrease in K+ (hyperpolarize). Effect is dilation

Front 21

G Coupled Protein Alpha S as a Constrictor

Back 21

"big" K+ channels. Ca2+ activated. Spatially coupled to SR

Ca2+ leaks out of SR - calveoli. IP3 in. Ca2+ binds to RyR. Ca2+ causes contriction

Front 22

What determines tone with Alpha A

Back 22

Balance of constriction and dilation

Front 23

Local Control

Back 23

Autoregulation: Intrinsic Control

mediated by LOCAL mediators of tone

This is the most important way blood flow is regulated in the heart and CNS

also important to renal function and with increased activity in muscle and skin

Front 24

CONTROL OF THE CARDIOVASCULAR SYSTEM

Flow to organ

Back 24

FLOW = Driving P/ R

(heart, brain flow determined by Pa, local Resistance)
Pa determined by CO and R elsewhere (TPR)

Front 25

Shunting of flow

Back 25

dilate to keep blood in brain

or increase driving pressure, increase cardiac output, increase resistance elswhere

Front 26

No Autoregulation

Back 26

No local control
Constance Resistance

Front 27

With Autoregulation

Back 27

Constant flow even though pressure has changed

Front 28

Metabolic Control

Back 28

Uses local vasodilators :
CO2, lactate, K+, low O2
(products of metabolism)

Match flow to metabolic needs

Front 29

How this relates to flow?

Back 29

Can increase pressure via shunting

Can increase flow to head during fight or flight

Can decrease resistance to gut after meal.

Front 30

Variations in circulations

Back 30

Neural Control VS Local Control??

Brain (cerebral)
Heart (coronary)
Kidney (renal)
Skin (cutaneous)
Skeletal muscle
GI tract (splanchnic)

Front 31

Cerebral Circulation

Back 31

Circle of Willis (internal carotid artery, middle cerebral artery, basilar artery)

One of few anasomoses in brain

Front 32

Innervation of cerebral circulation

Back 32

Sympathetic Nerves
Cholinergic Nerves
Sensory Nerves

Autoregulation over a range of -mmHg. Depends on O2, CO2, and adenosine

Front 33

Sympathetic Nerves in Cerebral Circulation

Back 33

NE, NPY - neuropeptide (constrict)

Lrg arteries

Front 34

Cholinergic Nerves in Cerebral Circulation

Back 34

Ach (NO formed), VIP - vasoactive intestinal peptide (dilate)

Lrg Arteries

Front 35

Sensory Nerves is Cerebral Circulation

Back 35

substance P, neurokinin, CGRP (dilate)

Front 36

Cerebral Flow Regulated by Metabolites

Back 36

Blood vessels in brains will vasodilate with low O2 or high CO2

Low PO2 then cerebral blood flow increases

Increase PCO2 in tissue then flow increase to get rid of CO2

Front 37

Variations in Cerebral Blood FLow

Back 37

Flow to areas changes with brain activity:

Local metabolic activity alters local flow!

Front 38

Changes in cerebral blood flow with pathology

Back 38

Seizures increase flow locally, decreased flow post seizure in area of focus

Alzheimer's disease decrease flow in superior parietal, then temporal, then frontal cortex
Also changes in Huntington’s, disease manic depression, schizophrenia

Also suggest flow linked to metabolic activity of neurons

Front 39

Coronary circulation

Back 39

Coronary artery branch from aorta near aortic valve
Large arteries travel on surface of heart,
Smaller arterioles must pass from epicardium to endocardium through contracting muscle

Front 40

Coronary circulation - contraction

Back 40

Contraction of heart compresses the arteries, so subendocardial flow only during diastole (mechanical property)

TACHYCARDIA decreases flow to left ventricle

Aortic stenosis decreases flow to left ventricle

Front 41

Control of Coronary Circulation - Innervation

Back 41

Innervation: minimal, but not zero. BC not many Alpha receptor in heart.

Direct α adrenergic constriction on VSM, but
β adrenergic receptors on HR, contractility lead to vasodilation via metabolic effects

Effects of nerve or NE- generally Vasodilation unless β-blocker

Front 42

Control of Coronary Circulation - Autoregulation

Back 42

Autoregulation critical and more important: Range 60-200 mmHg

Calibrates flow to O2 demand. Vasodilation produced by low O2, or high CO2, H+, K, lactate, prostaglandin, adenosine (Oxidative metabolism very important)

Reactive hyperemia present (increased flow after occlusion)

Front 43

Renal Circulation

Back 43

Innervation: sympathetics - very important

Regional autoregulation
Humoral factors can have local regional effects

In cases of severe renal vasoconstriction (hypovolemia) renal vasoconstriction can result in acute renal failure (ex-extreme dehydration)

Front 44

Cutaneous circulation - Innervation and temperature response

Back 44

Innervation : sympathetic, constrictor (Alpha)

Temperature response – shunting between arterial-venous anastomoses (unique to skin)

Front 45

Cutaneous Circulation

Mechanical response and wheal

Back 45

Mechanical response- contraction of precapillary sphincters

Wheal: vasodilation reflex from sensory neurons- substance P

Front 46

Skeletal Muscle

Flow, Innervation

Back 46

Able to increase flow by 20x with exercise - B2 dilation effect

Innervation: sympathetic A adrenergic can decrease flow to ¼ normal (precise use of sym)

Front 47

Skeletal Muscle

Autoregulation, Mechanical Forces

Back 47

Autoregulation: important in the exercising muscle, flow to contracting fibers increases as metabolism increases

BUT mechanical forces- compression of vessels can decrease flow in exercising muscle (downside)

Front 48

GI Tract Circulation

Back 48

Major regulation vs SNS
Contriction when body needs increase BP or flow to heart, brain
Dilation post-prandial

Autoregulation/metabolic effects : probably important in increasing flow to a given segment (eg stomach vs intestine) with digestion

Front 49

Control of CV System

Back 49

Variable sensed

Processing or Intergration

Response

Front 50

Variable Sensed

Back 50

Afferents
What is sensed? How? Where?

Pressure, volume, O2, CO2

Front 51

Response

Back 51

Efferents

What changes, How? Where?

Resistance, Rate, SV

Front 52

Types of Sensory receptors

Back 52

1. Baroreceptors
2. Atrail Receptors
3. Ventricular receptors
4. Central & Peripheral Chemoreceptors
5. Renal Baroreceptors
6. Osmoreceptors in hypothalamus

Front 53

Baroreceptors

Back 53

Stretch receptors in carotid sinus and aortic arch

Firing sends signal to brain: carotid BR via CN IX aortic BR via CN X (Vagus)

Can be reset

Front 54

Atrial Receptors

Back 54

At junction of great veins and atria

Type A fire with atrial contraction

Type B fire with increase venous return. "volume" receptors. Signal from vagus

Front 55

Ventriculat Receptors

Back 55

In wall of ventricle
Respond to stretch of ventricle with increased ventricular pressure.
Can cause reflex devrease heart rate

Aortic stenosis can activate

Front 56

Central & Peripheral Chemoreceptors

Back 56

In aortic arch & carotid sinus

respond to changes in O1 and CO2.
Help increase flow when aortic, carotid, or brain levels of O2 fall or CO2 rise

Front 57

Renal Baroreceptors

Back 57

Renin to ANG II

Respond to intrarenal perfusion pressure

Help maintain renal blood flow and blood volume

Front 58

Osmoreceptors in Hypothalamus

Back 58

Respond to NA+ concentration of ECF.

Cause AVP release and drinking (kidney retain volume)

Front 59

Efferent Mechanisms can be

Back 59

slow (hormonal) or fast (neural)

Front 60

Sympathetic NS

Back 60

Inc HR
Inc Contractility
Inc venous tone - less compliant (inc venous return)
Inc arteriolar resistance - esp to skin, GI, kidney.

Stimulate kidney renin to ANG II

Front 61

Parasympathetic NS

Back 61

Dec HR

Front 62

Hormones Involved

Back 62

epinephrine (adrenal)
AVP (pituitary)
renin-angiotensin- aldosterone (kidney-adrenal)

ACTH-cortisol (pituitary-adrenal), progesterone/estradiol

Front 63

MAP equals

Back 63

Cardiac Output x TPR (total resistance in systemic circulation)

CO equals SV x HR

Front 64

Efferent:

Contractility

Back 64

B1

Front 65

Efferent:

Venous Compliance Return

Back 65

A1

Front 66

Efferent:

Volume

Back 66

Longer term:

kidney, AVP, Ang II, Aldosterone

Front 67

Efferent:

Dec Rate

Back 67

Ach

Front 68

Efferent:

Inc rate

Back 68

B1

Front 69

Efferent:

Vasoconstrict:

Back 69

A1
AVP - if BP very low
ANG II

Front 70

Efferent:

Vasodilate

Back 70

B2

Front 71

Role of arterial BR: What happens if arterial BP falls?

Back 71

Dec BP leads to dec BR firing rate leads to change neuron firing in CNS

Dec Parasympathetic (VAGAL) - Inc HR

Inc Sympathetic firing to: arterioles (esp in GI tract, skin) - A1: Inc Resistance

heart: B1 - Inc HR

veins: A1 - Dec C

Front 72

Result of Above reflex

Back 72

Inc HR - Inc CO

Inc C - Inc SV and Inc CO

Inc Vasoconstriction - Inc R

Inc Venoconstriction (Dec Compliance) - Inc VR, Inc SV, Inc CO - Frank Starling Mech

Inc CO, Inc TPR, Inc BP toward normal

Front 73

Dec in volume (Dec in BP) causes:

Back 73

Dec BR firing rate
Dec afferent firing to MEDULLA

Dec Parasympathetic
Inc Sympathetic

Resistance increases

Compliance decreases

Contractility increases

Transcapillary fluid reabsorption increases
Dec in P in capillary if R in arterioles ince. Less fluid flows out.

Front 74

What may happen at same time as reflexes?

Back 74

At same time reflexes acting local effects may also be acting to change local vascular tone, esp in organs with good autoregulation

Front 75

Inc BP causes:

Back 75

Inc BR firing rate
Inc afferent firing to MEDULLA

Inc Parasympathetic (Dec HR)
Dec Sympathetic

Dec Resistance
Inc Compliance - keep more blood in veins, dec CO, Dec SV

Dec Contractility

Front 76

Injection of Phenylephrine

Back 76

A1 agonist - stimulates A1 receptors
VSM in arterioles cause vasocontriction
Inc BP & slows heart
Dec SV
Dec Contractility

Front 77

Where is NO made?

Back 77

In endothelial calls

Cause vasodilation

Dec BP

Front 78

Atrial pressure and HR

Back 78

As HR inc, Atrial pressure (systolic) Increases

Front 79

Role of Atrial receptors: What happens if blood volume falls?

Back 79

Dec VR
Dec Atrial B firing rate (susceptible to stretch)
change neuron firing to CNS (Dec BR firing)

Inc secretion of hormones vasopressin and renin-ang II - can help body to increase volume

Front 80

Net effect of Fall in blood volume

Back 80

increase retention of fluid
also increase vasoconstriction to SHUNT flow

Inc Sympathetic. A1 effect is vasoconstriction. B1 in kidney stimulates Renin

Front 81

Effects of fluid intake - long term

Back 81

Venous Return

Inc CO
Inc Arterial pressure
Inc to kidney urinary output

Front 82

Effects of fluid intake - short term

Back 82

Dec TPR
Dec CO
Inc Arterial pressure
Inc kidney output

Front 83

Inc Arterial pressure

Back 83

Increases:

HR
vasoconstriction
venoconstriction
contractility

Front 84

Atherosclerosis

Back 84

Form of arteriosclerosis caused by deposition of fat and fibrin over time

increases resistance (narrow vessles)
decreases flow to tissue
leads to complications: clotting, ischemia, etc

Front 85

3 Steps of atherosclerosis

Back 85

1. Fatty Streak
2. Fibrous Plaque
3. Complicated Lesion

Front 86

Fatty Streak

Back 86

Lipid deposition in intima and subintima

Front 87

Fibrous Plaque

Back 87

extends into lumen of vessel, also involves smooth muscle cells and tunica media

Front 88

Complicated Lesion

Back 88

alterations with time and local events: hemorrhage, cell necrosis, calcification, thrombosis

Front 89

Etiology of Atherosclerosis

Back 89

Hypertension: endothelial injury (“shear stress”)
Hyperlipidemia: LDL/HDL ratio
Oxidative damage: aging, diabetes
thrombogenesis and platelet activation

INFLAMMATORY DISEASE OF VESSEL WALL

Front 90

Detailed fatty streak

Back 90

lipid deposition in intima in foam cells

macrophages enter intima
adhesion (VCAMs)

take-up oxidized LDL lipids
oxidation of LDLs

LDL receptors “scavenger receptors”

Front 91

Detailed fatty streak

cont

Back 91

macrophages have fat. Normal intima does not have many macrophages

LDL gets into cells via VCAM

Oxidized LDL's get taken up first

Front 92

Detailed Lesion Intiation

Back 92

LDL oxidation
Oxidized LDL interact with matrix fibers

LDL trapped in matrix before getting taken up by macrophages

Front 93

Detailed Fibrous Plaque

Back 93

involves smooth muscle cells and fibrous tissue

Growth factors and cytokines from T-cells and macrophages induce SMC and matrix accumulation

Front 94

Detailed Fibrous Plaque

cont

Back 94

Cannot dilate and function as normal blood vessel. Can't regulate resistance

Cells that take up fate prone to necrosis. Clump together to necrotic core

Smooth muscle prob engulfs fat

Inc ANG II stimulates smooth muscle proliferation

Front 95

Detailed Complicaed Lesion

Back 95

necrosis, calcification, thrombosis

platelet aggregation (thromboxane A2 macrophages)

infection

Front 96

Detailed Complicated Lesion

cont

Back 96

Resistance further impaired

Luman and wall of vessel now invaded with Ca2+

Macrophages release thromboxane

Wall prone to infection

Front 97

Complications associated with atheroslerosis

Back 97

Increased blood pressure (hypertension) - cause or effect

decreased perfusion
(organ ischemia/damage; peripheral tissue ischemia/damage)

increased risk of thrombosus
(“stroke”)

Front 98

Signs/Symptoms/Complications

Back 98

ischemia- pain

fatigue (esp muscle fatigue)

intermittent claudication

thrombosis/embolism

hypertension

Front 99

Ischmia

Back 99

Restriction in blood supply

Front 100

Intermittent Claudication

Back 100

"limping"; cramplike pains in legs due to poor perfusion

Front 101

Arteriosclerosis Obliterans

Back 101

Plaques with complications

progressive stenosis and obstruction with atherosclerotic plaques

in medium and large sized arteries - esp to limbs

inadequate flow to tissues, results in pain, fatique, claudication

Front 102

Signs/Symptoms

Back 102

bruits - mumur in bv due to turbulent flow

reduction or loss of pulses below site of stenosis

if severe: muscle atrophy, cyanotic (Blue) discoloration, hair loss, gangrene, necrosis

Front 103

Thrombosis

Back 103

intrinsic pathway activated by blood pooling (aneurysms, obstructions), hypotension

extrinsic pathway activated by infection

Front 104

Diseases associated with thrombosus

Back 104

atherosclerosis‑disruption of intima starts clotting cascade

aneurysms‑ pooling of blood

infection‑invasion of intima

on cardiac valves‑ by calcification or bacterial infection (endocarditis)

Front 105

Complications of Thrombosus

Back 105

disseminated intravascular coagulopathy

thromboembolism

thrombophlebitis

Front 106

disseminated intravascular coagulopathy

Back 106

Very Bad! Activates and deactivatesd clotting cascade. Backa nd forth with excessive clotting and internal bleeding.

-childbirth or accident

High fatility rate. Once time episode

Front 107

thromboembolism

Back 107

Clot breaks and problems ensue

Front 108

thrombophlebitis

Back 108

Clot in vein. Want it to stay away from heart and lungs
A lot of pain involved.

Front 109

Signs/Symptoms/Complications of Thrombosis

Back 109

ischemia
(obstruction)‑PAIN

tenderness, swelling ( - Inc R = Inc hydrostatic press = fluid leaking out)

if arterial‑ skin pale (downstream)

if venous‑ skin red to deep blue‑purple

neuralgia‑ with edema(venous) - edema presses on nerves and causes pain

Embolism‑organ disruption, necrosis, sepsis