Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardio Entrance > Heart Failure Physiology > Flashcards

Heart Failure Physiology Flashcards

1
Q

Describe
Ventricular myocytes
Atrial Myocytes

A

Ventricular - brickshaped, 150x20x12 um

Atrial - smaller, more spnindle shaped; <10u in diameter; <100um in length

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

The on and off switch for contraction

A

SR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are ryanodine receptors

A

Ca2+ release channels concentrated at the part of SR in close apposition with T tubules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

parts of SR

A

1 terminal cisternae / junctional SR

2 longitudinal/ free/ network SR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is SERCA/ SR Ca-ATPase

A

ATP-consuming Ca2+ pump that faciliates calcium uptake from the sarcoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Calsequestrin

A

Calcium buffering proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Caveolae

Caveolin , RYR

A

small invaginations of sarcolemma

Scaffolding preoteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How many mitochondria in a ventricular myocyte?

A

8000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How is the mitochondira in myocytes during Calcium overload?

A

there is a electrochemical gradient favoring the entry of calcium in the mitochondria - but this is kept to a level by the Na/Ca exhanger to pump calcium out, but this will increase Na inside the mitochondria so the Na/H exchanger regulates this - but there is a consequence since H+ influx uses ATP.
Instead of these protons being used to make more ATP (F0-F1 ATP synthase) they were used to extrude Na and Ca
So in Calcium overload- calcium can diminish gradient at expense of ATP production thus hampering recovery from stress; also elevated Ca facilitate opening of the mitochondrial permeability transistion pore releasing Mmatrix to cytosol and result to death of mitochondria; release of ROS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Two chief contractile proteins

A

actin and myosin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Titin is

A

a giant molecule, largest protein to be described
1 - tethers myosis and thick filaments to Z line; stabilizing sacromere
2- its elasticity contribute to the stress-strain relationship; aid in early diastolic filling
3- limits overstretching of sarcomeres at end diastolic volume
4 - transduces mechanical stretch to growth signals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Musle LIM protein (MLP)

A

attached to z line at end of titin, stretch sensor that transmits signals that result in myocyte growth pattern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

MLP is defective in what condition

A

dilated cardiomyopathies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Crossbridge cycle events

A 
A - Rigor state
B- Weak binding state
C - ATP hydrolysis 
D- strong binding state 
E- Powerstroke;
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Crossbridge cycle: ADP released ; vacant empty pocket

A

Rigor state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Binding of ATP to the pocket produces

A

Weak binding state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

ATP hydrolysis results to

A

alteration of actin binding domain; favoring release from actin, head binds to adjacent actin; “cocked”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Strong binding state

A

Phosphate is released; myosin head strongly attaches to induce powerstroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Troponin C
Troponin I
Troponin T

A
  • Calcium binding
  • binds to actin in thin myofilaments to hold the actin-tropomyosin complex in place
  • binds to tropomyosin, interlocking them to form a troponin-tropomyosin complex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

B myosin heavy chain (B-MHC)

A

slower ATPase rate, predominant in adult humans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Defects in myosin, myosin binding protein C, other myofilament proteins linked to

A

familial hypertrophic cardiomyopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

In vascular smooth muscle, contraction is activated by

A

Calcium dependent myosin light chain kinase (MLCK)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

preload is

A

sarcomere length at end of diastole

24
Q

Frank-Sterling effect

A

the more diastolic filling of the heart, the greater the strength of each heartbeat

A great diastolic end volume would increase contractile strength and increase stroke volume

25
Q

why does the Frank-Starling effect occur

A

as the myocardium is stretched due to greater volume, there is increase in sarcomere length, increase in myofilament calcium sensitiviy - hence stronger contraction

26
Q

what happens in isovolumetric contraction ?

A

sarcomeres do not shorten but cross bridges are developing force

27
Q

main entry of Ca in cells

A

voltage gated L-type calcium channels (3/4) vs Ca influx

28
Q

TOtal SR content is sum of Ca SR plus Ca bound to?

A

calsequestrin - local reservoir of buffered Calcium

29
Q

mediates SR release of calcium

A

RYR channels -functions as ca channel and scaffolding protein

30
Q

Can stabilize RSR gating

A

calmodulin, FKBP, kinases, CAMKII

31
Q

When is SR Calcium release turns off?

A

When calcium in SR drops by approx 50%

32
Q

What breaks the positive feedback of Ca release?

A

1 closure of RYR channels by binding to CaM
2 Ryr2 gating is sensitive to luminal CaSR
3 Calcium flux through RyR falls and junctional Ca also falls

33
Q

Versatile mediator of Calcium signaling

A

Calmodulin

34
Q

Calcium is transported in the SR by

A

SERCA
cardiac myocytes (SERCA2a)
1 ATP - 2 Ca ions

35
Q

A reduction in SERCA expression or function can be sean in

A

heart failure or energetic limitations

slower rates of cardiac relaxation

36
Q

what is PLB

A

Phospolamban - a single transmembrane pass protein that binds directly to SERCA2a -this reduces the affinity of SERCA for cytosolic Ca- weaker uptake

37
Q

What happens when PLB is phosphorylated by CaMKII

A

The inhibitory effect of PLB is relieved leading to increased SERCA uptake - cardiac relaxation (lusitropic effect) and increased SR Ca content - stronger contraction

38
Q

2 types of sarcolemmal Ca channels

A

T-type

L-type - predominate in ventricular myocytes

39
Q

T (transient) type channels

A
  • open at more negative voltage
  • short bursts of opening
  • do not interact with Calcium antagonist drugs
  • doesnt participate in excitation-contraction coupling
  • seen in neonatal ventricular myocytes, purkinje fibers, pacemaker cells
40
Q

L-type / long lasting Calcium channels

A
  • at T-tubules & jSR sites
  • inhibited by Verapamil, Diltiazem, Dihydropyridines
  • facilitates rapid sympathetic activation of changes in Ica
41
Q

Important contributor to plateau phase of cardiac action potential

A

InwardCalcium

42
Q

Voltage gated cardia Na is mainly carried by

A

Nav 1.5 cardiac isoform

near intercalated discs

43
Q

Is sodium participating in the plateau phase?

A

yes - late sodium current - ultra slow voltage independent inactivation / activation

44
Q

Consequence of inrease Na

A

acquired long QT syndrome

Cause sodium and calcium loading of myocytes

45
Q

CaMKII is upregulated and chronically activated in

A

ischemia reperfusion, heart failure , ROS; LQT3 Syndrome;Brugada like syndrome
(Ca overload)

46
Q

NCX is

A

responsible for extruding most of the Ca entered by Ica and NCX;
-reversible

47
Q

Main mechanism for extruding Na from the cell is

A

NaKATPase

48
Q

Order of agonist activity in B1 and B2 receptors

A

B1 isproterenol > E = NE

B2 isoproterenol > E > NE

49
Q

Relative potencies of alpha agonists are

A

NE >E> Isoproterenol

50
Q

Gs - cAMP

Gi - (cholinergic & vagal)

A

Gs- chronotropic, inotropic lusitropic , dromotrophic
Gi - inhibit adenylyl cyclase - slow HR, limit cAMP

AC5 and 6 - cardiac myocytes

51
Q

Potent direct adenylyl cyclase inhibitor-

PDE inhibitor -

A

Forskolin

IBMX

52
Q

5 main determinants of ventricular mechanical performance

A 
preload
afterload
contractility
lusitropy
HR
53
Q

Normal pressure in LA

A

8-15 mmHg

54
Q

physiologic systole

A

-start of isovolumetric contraction to peak of ejection phase

55
Q

Physiologic diastole

A
  • as calcium is taken back to SR , myocyte relaxation dominates; LV starts to fall
56
Q

Cardiologic systole

A
  • longer than physiologic

- M1 to A2

57
Q

When is S3 heard

A

prodiastole

Cardio Entrance (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions