Physiology - Cv Quiz 1

Front 1

What is the relative ion distribution of K, Na, and Ca in a typical cell?

Back 1

K in > K out
Na and Ca in < Na and Ca out

Front 2

Na/K Pump

Back 2

Requires ATP, 2 K in for every 3 Na out

Front 3

Na/Ca Pump

Back 3

1 Ca out for every 3 Na in

Front 4

At rest, the permeability of K is what in relation to Na?

Back 4

PK+ >> PNa+ by 100x

Front 5

What ion's potential determines RMP?

Back 5

K+'s

Front 6

Fast type AP occur where?

Back 6

Atria and Ventricles

Front 7

Slow type AP occur where?

Back 7

SA and AV nodes

Front 8

Phase 0 of Fast Type AP

Back 8

Rapid depolarization (voltage dependent) due to Na+ entry

1. Fast type Na+ channels open
2. Slow close of activation gates

Front 9

Phase 1 of Fast Type AP

Back 9

Small repolarization

1. Outward mov't of K+
2. Inactivation of Na+ channel

Front 10

Phase 2 of Fast Type AP

Back 10

Plateau due to:

1. Ca in through L type Ca channels
2. Slow current of Na in through non-tetrodotoxin Na+ channel
3. K+ permeability decreases

Front 11

Inward Retification

Back 11

Less outward K+ current b/c K permeability decrease

Front 12

Phase 3 of Fast Type AP

Back 12

Repolarization

1. Na and Ca channels inactivated so currents stop
2. Increased permeability of K+

Front 13

Phase 4 of Fast Type AP

Back 13

Stable RMP

Front 14

Absolute Refractory Period

Back 14

Inactivation of Fast Na channels so Ca can enter, contraction of heart

Front 15

Slow vs. Fast AP

Back 15

Slow...

1. Slower initial depolarization, but spontaneous
2. Lower amplitude overshoot
3. Shorter and less stable plateau phase
4. Unstable RMP

Front 16

Phases 0-2 of Slow Type AP

Back 16

Depolarization mainly due to Ca entry

Front 17

Phase 3 of Slow Type AP

Back 17

Repolarization

1. Ca and Na channels inactivated
2. Increased permeability of K

Front 18

Phase 4 of Slow Type AP

Back 18

Spontaneous depolarization due to:

1. Decreasing K permeability
2. Increasing Ca permeability
3. Increasing Na permeability

Front 19

Where is the origin of the heart beat?

Back 19

SA node and potentially AV node

Front 20

What's norepinephrine's effect on heart rate?

Back 20

Increase by causing faster phase 4 depolarization (Ca channel opening enhanced)

Front 21

What's acetycholine's effect on heart rate?

Back 21

Decreases heart rate by causing slower phase 4 depolarization (K channel opening enhanced)

Front 22

Describe spread of excitation w/in heart.

Back 22

1. Atria contract
2. Electrical events reach AV node
3. Conduction slow, ventricular filling
4. Purkinje fibers accelerate excitation to allow for coordinated contraction

Front 23

P Wave

Back 23

Atrial depolarization and contraction

Front 24

QRS Wave

Back 24

Ventricular depolarization and contraction

Front 25

T Wave

Back 25

Ventricular repolarization

Front 26

What happens w/heart failure?

Back 26

1. Blood accumulates behind the heart
2. Not enough blood flows out of the heart into the body

Front 27

Ca enters the cytosol of myocytes from which 2 places?

Back 27

1. Extracellular space
2. Sarcoplasmic reticulum

Front 28

In order for the heart to relax, what must Ca do?

Back 28

Ca must be removed from the cytosol(uphill transport)

Front 29

When Ca enters the cytosol, what kind of protein does it bind?

Back 29

Ca binds high-affinity Ca binding E-F PROTEIN

Front 30

In what kind of cells is diffusion from the extracellular fluid sufficient for contraction?

Back 30

Embryonic muscle and adult smooth muscle

Front 31

The sarcoplasmic reticulum includes what 2 distinct regions?

Back 31

1. Sarcotubular network
2. Subsarcolemmal cisternae

Front 32

Sarcotubular network

Back 32

Pumps Ca OUT of the cytosol

Front 33

Subsarcolemmal cisternae

Back 33

Transmit signals generated by depolarization of the T-tubules

Front 34

Transverse tubulues (t-tubules)

Back 34

Extension of sarcoplasmic reticulum, open to extracellular space, carry AP to inner parts of cell

Front 35

Dyads

Back 35

Special structures formed by t-tubules and subsarcolemmal cisternae

Front 36

How do AP at cell surface trigger Ca release from SR?

Back 36

1. T-tubulues open to and communicate w/extracellular space
2. T-tubule membrane propagates AP

Front 37

Which structures are involved in the external Ca cycle?

Back 37

Ca in from ECF:
1. L-type Ca channel

Ca out to ECF:
2. Plasma membrane Ca Pump
3. Na/Ca Exchanger

-Na/K ATPase: generates small repolarizing current, helps maintain RMP

Front 38

Which structures are involved in the internal Ca cycle?

Back 38

Ca into cytosol from SR:
1. SR Ca Release Channel

Ca into SR from cytosol:
1. SR Ca Pump

Front 39

Plasma Membrane Ca Pump (PMCA)

Back 39

Part of external Ca cycle, pumps Ca out into cytosol, requires ATP

Front 40

Na/Ca Exchanger (NCX)

Back 40

Part of external Ca cycle, 3 Na in for 1 Ca out (depolarizing effect)

Front 41

Which external Ca cycle structure has depolarizing effects? What can it cause clinically?

Back 41

Na/Ca Pump can cause cardiac arrhythmias/sudden cardiac death

Front 42

Which internal Ca cycle structure is aka ryanodine receptors/feet?

Back 42

SR Ca release channels

Front 43

How are SR Ca release channels opened?

Back 43

By Ca entry from L-type Ca channels

Front 44

Troponin C

Back 44

EF protein that binds Ca to initiate muscular contraction

Front 45

Sarcoplasmic Reticulum Ca Pump (SERCA)

Back 45

Part of internal Ca cycle, pumps Ca into SR

Front 46

Phospholamban

Back 46

Regulates SERCA

Front 47

How does phosphlamban regulate Ca uptake?

Back 47

If dephosphorylated, SLOWS Ca uptake into SR

If phosphorylated, SPEEDS UP Ca uptake into SR

Front 48

Calsequestrin

Back 48

Stores CA w/in SR

Front 49

Sarcomere

Back 49

B/w 2 Z lines containing 1 A band and 2 half I-bands

Front 50

Striations in the sarcomere are a result of what?

Back 50

Distribution of thick and thin filaments

Front 51

Cross bridges. How are they in resting vs. active muscle?

Back 51

Project from THICK filaments

Resting muscle: Perpendicular to thick filaments, not bound to thin filaments.

Active muscle: Row thin filaments toward the center

Front 52

Which contractile proteins are involved in muscle contraction?

Back 52

Myosin (thick filament) and Actin (thin filament)

Front 53

Which regulatory proteins are involved in muscle contraction?

Back 53

Tropomyosin, Troponin C, Troponin I, and Troponin T

Front 54

Tropomyosin (TM)

Back 54

Protein that lies in the groove b/w 2 actin strands

Front 55

Troponin I (TN-I)

Back 55

Inhibits actin-myosin interactions when Troponin C is not bound

Front 56

Troponin C (TN-C)

Back 56

E-F hand Ca binding protein, binds CA to activate muscle contraction

Front 57

What happens when TN-C is not bound to Ca?

Back 57

Active sites on actin are blocked so actin cannot interact w/myosin

Front 58

Troponin T (TN-T)

Back 58

Binds TM, TN-C, TN-I to thin filament

Front 59

Preload

Back 59

Load supported BEFORE contraction

Front 60

Afterload

Back 60

Load supported AFTER contraction

Front 61

Maximal Afterload

Back 61

Isometric contraction where muscle can't shorten/no cycling

Front 62

Zero Afterload

Back 62

Cross-bridges cycle at maximal rate

Front 63

What is the effect of increasing the afterload on cardiac efficiency?

Back 63

Cardiac efficiency decreases

Front 64

Muscle length is determined by what?

Back 64

Preload that stretches muscle (direct relationship)

Front 65

Maximal force is determined primarily by what?

Back 65

# of actin sites interacting w/myosin...amount of Ca bound to TN-C

Front 66

Maximal shortening velocity is determined by what?

Back 66

Actin-myosin cross-bridge turnover rate (myosin heavy chain isoform)

Front 67

Resting tension of a muscle

Back 67

Force required to stretch a resting muscle to different lengths

Front 68

Active or developed tension of a muscle

Back 68

Tension developed in a muscle when it is stimulated to contract but the length is held constant (the ends are fixed)

Front 69

At what muscle length is maximum active tension achieved? How does this property affect cardiac muscles?

Back 69

At an intermediate muscle length (Lmax). Little tension is developed at very short or very long lengths. Cardiac muscle usually operates at lengths much lower than Lmax, so increasing muscle length increases active tension during isometric contraction.

Front 70

What is the relationship b/w EDV (preload), SW, SV?

Back 70

Proportional to SW and SV

Front 71

How is EDV related to muscle length?

Back 71

Length varies directly with EDV

Front 72

Afterload can be increased how? What happens to the VFC?

Back 72

1. Increasing PAd, size, pressure

VFC lower

Front 73

What are 2 ways you can increase SV for the same PAd?

Back 73

1. Increase preload
2. Increase contractility

Front 74

Heterometric

Back 74

Heart regulation as a result of changing initial muscle length

Front 75

Homeometric

Back 75

Heart regulation as a result of change in contractility

Front 76

According to the Law of Laplace, afterload depends on what 2 factors?

Back 76

1. pressure
2. size

Front 77

Starling's Law

Back 77

Stroke volume increases as cardiac filling increases