Mf2 Iii Physiology

Front 1

Angiogenesis

Back 1

Formation of need blood vessels from pre-existing vasculature

Front 2

Vasculogenesis

Back 2

De novo formation of new blood vessels from angiogenic precursor cells during development

Front 3

Stages of wound healing (7)

Back 3

Injury -> hemostasis -> provisional matrix -> inflammation -> apoptosis -> angiogenesis -> re-epithelialization

Front 4

Angiogenic switch

Back 4

Tumors are dormant until angiogenesis is turned on

Front 5

What effect does tumor removal have on angiogenesis?

Back 5

Increases
Primary tumors secrete metalloproteinases that cleave plasminogen

Front 6

Angiostatin

Back 6

Secreted by primary tumors to inhibit angiogenesis

Front 7

Pressures in cardiac chambers

Back 7

Atria - 5
RV - 25/0 (low because of high lung resistance)
LV - 120/0

Front 8

Cardiac output

Back 8

Total volume of blood thru systemic and pulmonary circulation
HEART RATE X STROKE VOLUME

Front 9

Relationship b/w velocity, flow, x-sectional area

Back 9

V = Q/A
Q is constant
Velocity is greater in tubes with lower A
Capillaries have highest A, so velocity of blood is slow there giving time for gas exchange

Front 10

Mean arterial pressure

Back 10

(sys - dias)/3 + dias

Front 11

Poisseuille's law

Back 11

Radius has a fourth power effect on Q
Small increase in radius -> large increase in flow

Front 12

Swan-Ganz catheter

Back 12

Analyze right side of heart
Insert catheter into venous system and inflate balloon at end of vena cava
Measures: RA, RV, PA, pulmonary capillary pressures
Pulmonary wedge pressure = left atrial pressure

Front 13

Left ventricular catheter

Back 13

Insert into femoral artery -> aorta pressure-> LV pressures

Front 14

P wave

Back 14

Depolarization of right and left atria
Causes atrial contraction

Front 15

Q wave

Back 15

Early ventricular septal depolarization
Left bundle depolarizes (is negative first), so positive end of dipole is on right, closer to the negative electrode

Front 16

R wave

Back 16

Depolarization of major portions of ventricular walls

Front 17

S wave

Back 17

Depolarization at ventricular bases

Front 18

T wave

Back 18

Repolarization of ventricles
Proceeds in reverse direction of repolarization: from apex to base

Front 19

What causes the pause between atrial and ventricular contraction?

Back 19

At AV node, cells get narrower
Conduction velocity decreases w/ decreasing lambda which is a function of diameter
Allows for ventricular topping off

Front 20

Which ventricle depolarizes first?

Back 20

Left
Left wall is thicker so this allows for more time for it to depolarize so both ventricles contract at the same time

Front 21

When and how do pacemaker cells depolarize?

Back 21

Spontaneously during diastole
Don't need ANS innervation

Front 22

Ionic basis of pacemaker potential

Back 22

Phase 4 depolarization is due to decrease in K+ permeability
Dominant inward current is by Ca NOT Na

Front 23

Pacemaker potential phase 4

Back 23

Resting phase in cardiac cells

Front 24

Parasympathetic heart rate regulation

Back 24

Ach increases K+ conductance leading to hyperpolarization so that it takes longer for phase 4 depolarization to reach threshold
SLOWS heart rate

Front 25

Sympathetic heart rate regulation (5)

Back 25

NE binds beta1 receptors
-> increase in intracellular Ca
-> decreased conductance in Ca-sensitive K channel
-> increased depolarization rate during phase 4
-> INCREASES heart rate

Front 26

Ionic basis of non-pacemaker myocardiocyte (phase 0-4)

Back 26

Phase 0 -Like neurons, increased Na conductance upon threshold causes depolarization
Phase 1 - partial repolarization due to K+ channel opening
Phase 2 - plateau due to K+ channel closing and voltage-gated Ca channel opening
Phase 3 - repolarization by Ca channel inactivation and K channel activation
Phase 4 - resting potential maintained by K+ channels

Front 27

Consequence of non-pacemaker cell plateau phase

Back 27

Prolonged action potential and plateau phase protects against tetanus
Critical for allowing ventricles to relax and fill

Front 28

Conducting vs respiratory zones

Back 28

Conducting: major piping
Respiratory: alveoli where gas exchange occurs

Front 29

Tidal volume

Back 29

Amount of air normally displaced between inspiration and expiration, with no extra force exerted

Front 30

Minute ventilation

Back 30

Respiratory rate x tidal volume

Front 31

Anatomic dead space and alveolar ventilation

Back 31

Air that does not reach the alveoli for gas exchange
Eg: tidal volume - dead space = volume of air that actually is ventilated
V_A = respiratory rate x this volume that reaches alveoli

Front 32

Two factors that increase tendency for lungs to collapse

Back 32

1/3 from elastic recoil property of lungs
2/3 from alveolar surface tension

Front 33

Law of LePlace (what happens to surface tension as alveoli get smaller?)

Back 33

Pressure to keep a sphere inflated = 2xSurfaceTension / radius
As alveoli deflate, more pressure is required to prevent them from deflating, so tendency to deflate increases

Front 34

Function of surfactant

Back 34

Amphiphilic molecule that separates water molecules
Lowers surface tension, reducing pressure needed to keep alveoli expanded

Front 35

Lung compliance

Back 35

Change in volume as transmural pressure changes
At low volumes, compliance is low due to high alveolar surface tension
As alveoli expand, compliance goes up

Front 36

Inspiratory/Expiratory reserve volumes

Back 36

Volume of air that can be inspired or expired beyond the normal tidal volume

Front 37

Vital capacity

Back 37

Max air moved by IRV + ERV
( = IRV + ERV + TV

Front 38

Residual volume

Back 38

Volume of air that remains in lung after expiratory reserve volume is expired

Front 39

Functional residual capacity

Back 39

RV + ERV

Front 40

How to calculate residual volume?

Back 40

Helium dilution method
C1XV1 = C2XV2

Front 41

FEV1/FVC (normal?)

Back 41

FEV1 = volume of air expired forcefully in first second
FVC = full vital capacity
FEV1/FVC measures the % of vital capacity that can be expired in one second
Normal = 80%

Front 42

Hypoxia in pulmonary circulation

Back 42

Pulmonary vessels constrict in response to hypoxia to divert flow from poorly ventilated alveoli

Front 43

PO2 of mixed venous blood vs pulmonary veins (arterial)

Back 43

Mixed venous - 40
Pulmonary veins - 100

Front 44

PCO2 of mixed venous blood vs pulmonary veins

Back 44

Mixed venous - 46
Pulmonary veins - 40

Front 45

Alveolar pressures

Back 45

Pretty much same as arterial
PCO2 - 40
PO2 - 105
(venous blood approximates tissue concentrations)

Front 46

Calculating dissolved oxygen content of blood

Back 46

solubility coefficient X partial pressure = 1.5% total O2 in blood

Front 47

What shifts the Hb-O2 curve to the right (why?)

Back 47

Right shift means that a given partial pressure, Hb is less saturated which means more dissolved O2 can be given up to tissues
Higher temp
More CO2
Lower pH (from CO2 production -> lactic acid)
More 2-3 DPG

Front 48

Hb oxygen saturation in arterial vs venous blood

Back 48

Arterial - 100%
Venous - 75%
So about one O2 is given up to tissue

Front 49

How is CO2 transported in blood? (3)

Back 49

Dissolved (CO2 has higher solubility than O2)
Bicarbonate (majority, formed in RBC from carbonic anhydrase)
Carbamino compounds (bound to Hb at protein side chains, does not compete w/ O2)

Front 50

Haldane effect

Back 50

[O2] affects Hb-CO2 binding
High O2 (in alveoli) causes unloading of CO2 from Hb
Low O2 (tissue capillaries) causes binding of CO2 to Hb

Front 51

Ventilation perfusion ratio and regional distribution

Back 51

Ideally = 1, rate of bringing air in equals (V_A) rate of perfusion of alveoli
V/Q > 3 at apex
V/Q ~ .6 at base
In prone position they are more uniform

Front 52

Regional distribution of ventilation

Back 52

Alveoli are stretched out at lung apex because lung settles at base and pulls apex away from chest wall
Stretched alveoli have lower compliance so less air is drawn in
V @ apex < V @ base

Front 53

Regional distribution of perfusion

Back 53

Capillaries at apex are compressed by expanded alveoli
Q @ apex < Q @ base