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Advanced human physiology > Exam 2 main flash cards > Flashcards

Exam 2 main flash cards

1
Q

Heart metabolism

A

1) Primary ventricular myosin isoforms is Beta-cardiac myosin (gene MYH7)
2) Primary Atrial isoform Alpha-cardiac myosin (gene MYH6)
3) high metabolic demands
4) Rich in mitochondria

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2
Q

how does the Left ventricle contract?

A

1) Clockwise rotation of the apex
2) Counter clockwise rotation of the base
-this pulls the base downward to the apex during SYSTOLE

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3
Q

What are cell membranes that separate individual muscle from one another
-They are permeable communicating junctions (gap junctions) that allow rapid diffusion of ions —> the AP travel (called syncytium)

A

Intercalated discs

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4
Q

How does cardiac muscle act as a function syncytium?

A

1) Atria separated from ventricles by AV valves
2) The AV bundle allows for the conduction from the atria syncytium to the ventricular syncytium
-This allows the atria to contract before the ventricles

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5
Q

What has endothelial cells and connective tissue and is on the surface of the heart chambers?

A

Endocardium

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6
Q

What is the main part of the heart, comprised of the muscle cells (cardiomyocytes)?

A

Myocardium

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7
Q

What the visceral layer of serum pericardium and connective tissue?

A

Epicardium

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8
Q

What has 2 layers the inner serous pericardium (epicardium) + outer fibrous pericardium?

A

Pericardium

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9
Q

What layer of the heart contains pericardial fluid?

A

pericardial space/cavity

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10
Q

What is the function of the pericardial fluid?

A

It is the mechanical protection for the heart and vessels, reducing the friction during contraction/heartbeat

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11
Q

What is the parietal pericardium?

A

inner layer

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12
Q

What is the Fibrous pericardium?

A

Outer layer of connective tissue

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13
Q

What is the standard transverse components at the Z-lines (rectangular arrays) they also contain longitudinal elements that expands on top of the sarcomeres called?

A

Transver-axial tubule system (TATS)

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14
Q

T-tubules density is _____________ in diabetic HFpEF, _______________ in non-diabetic HFpEF, and ________________ in HFeEF

A

1) Unchanged
2) Increased
3) Decreased

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15
Q

What are the phases in the action potential of the heart?

A

1) phase 0 (depolarization)
2) phase 1 (initial repolarization)
3) Phase 2 (plateau)
4) Phase 3 (rapid repolarization)
5) Phase 4 (resting membrane potential)

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16
Q

Differences in the action potential in cardiac vs skeletal muscle?

A

1) The action potential of skeletal muscle is caused by the sudden opening of large numbers of (FAST Na+ CHANNELS) then abruptly closes leading to re-polarization/ (end of the action potential)

2) Cardiac muscle, the action potential is caused by opening of 2 types of channels:
- The same voltage-activated fast Na+
- L-type calcium channels
-the potassium decrease 5 fold after the AP (this decreases the efflux of K+ during the AP causing the plateau) prevents early return of AP

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17
Q

What is the phase 0 of the cardiac muscle contraction?

A

Depolarization
-Fast sodium channels open (reaching +20 mV before Na+ channels close)

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18
Q

What is phase 1 of the cardiac muscle contraction?

A

Initial repolarization
-The Na+ channels close (repolarization begins)
-K+ leave the cell

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19
Q

What is Phase 2 of the cardiac action potential?

A

Plateau
-Calcium channels open and Fast potassium channels close

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20
Q

What is phase 3 of the cardiac action potential?

A

Rapid repolarization
-Calcium channels close and slow potassium channels open

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21
Q

What is phase 4 of the cardiac action potential?

A

Resting membrane potential

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22
Q

What is the interval of time during which a normal cardiac impulse cannot re-excite an already excited area called?

A

Refractory period

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23
Q

This is more difficult to excite than normal but can be excited by a strong excitatory signal what is this called?

A

Relative refractory period

24
Q

Excitation-contraction coupling:

A

Similar to skeletal muscle
- the AP spreads to the interior of the cardiac muscle fiber along the membranes of the (T)ransverse tubules
-the T-tubule action potential then act on the membrane of the longitudinal sarcoplasm tubules to cause release of Ca2+ from the SR (sarcoplasmic reticulum)
-Ca2+ diffuse into the myofibrils and catalyses the chemical reactions that promote sliding of the actin and myosin filaments along one another, producing muscle contraction

25
Q

What is the receptor that causes the release of calcium through the sarcoplasmic reticulum?

A

ryanodine receptor channels

26
Q

cardiac cycle: each cycle is initiated by the spontaneous generation of an action potential in the _________________

A

sinus node (pacemaker)

27
Q

the atrias is the

A

primar pumps

28
Q

What is the regulation in response to changes in volume of blood flowing into the heart?

A

Intrinsic cardiac pumping

29
Q

What controls the heart rate and the strength?

A

Autonomic nervous system

30
Q

What is important of intrinsic regulation of the heart?

A

1) Venous return: blood flows to the heart from the veins
2) Peripheral control: the peripheral tissue controls its own local blood flow (all go directly to the RIGHT ATRIUM)
3) Heart intrinsic ability: blood is automatically pumped into the arteries
4) Frank-starling mechanism:

31
Q

The more the stretch during filling = the greater is resulting force of contraction = the greater the quanitityh of blood pumped into the aorta this is called?

A

Frank-starling mechanism
“law of the heart”

32
Q

Mechanism of the Frank-Starling:

A

when an extra amount of blood flows into he ventricles, the cardiac muscle is STRETCHED TO A GREATER LENGTH. The SARCOMERE ARE ALSO STRETCHED and the actin and myosin filaments are brought to a MORE OPTIMAL DEGREE OF OVERLAP FOR FORCE GENERATION. therefore, the cardiac muscle can contract with INCREASE FORCE. Therefore, the ventricle, bc of its increased pumping, automatically pumps the extra blood into the arteries

33
Q

Ventricular function curves
STROKE WORK OUTPUT CURVE

A

As atrial pressure increases, the stroke work output for that side increases until it reaches the limit of the ventricles pumping ability

34
Q

Ventricular function curves
VENTRICULAR VOLUME OUTPUT CURVE

A

As the right and left atrial pressures increase, the respective ventricular volume outputs per minute also increase

35
Q

Mechanism of excitation of the heart by the SYMPATHETIC nerves

A

1) Increase heart rate
2) It can force the heart to contract
3) Can increase the MAXIMUM CARDIAC OUTPUT AS MUCH AS 2 to 3 TIMES

36
Q

Inhibition of the sympathetic nerves causes what to happen to the heart?

A

1) Heart will decrease cardiac output
2) Heart rate and strength decrease

37
Q

Control of the heart by the parasympathetic nerves

A

Parasympathetic (vagal) stimulation reduces heart rate and strength
-vagal (vagus nerve) fibers mainly found in the atria not in many in the ventricles

38
Q

Increasing the arterial pressure load…

A

does not decrease cardiac output

39
Q

Effect of K+ on the heart:

A

excess K+ in the extracellular fluid
1) Slows heart rate
2) heart becomes dilated
3) Blocks conduction from the AV bundle
4) DECREASES THE RESTING MEMBRANE POTENTIAL (MEMBRANE POTENTIAL BECOMES LESS NEGATIVE)
5) the intensity of the AP decreases

40
Q

Effect of excess Ca2+ on the heart:

A

it increases contraction

41
Q

Effect of temperature on the heart:

A

1) Increased temperature increases heart rate
2) decreasing temperature decreases heart rate
-Hypothermia: body temperature drops

42
Q

Conductive system of the heart:

A

1) Sinus node (SA node) pacemaker of the heart
2) Internodal pathway: takes impulses from the SA node to the AV node
3) AV node: impulses from the atria are delayed before passing into the ventricles
4) AV bundle: Conducts impulses from the atria into the ventricles
5) Purkinje fibers:Conduct cardiac impulses to all parts of the ventricles

43
Q

Internodal and interatrial pathways

A

1) the ends of the sinus node fibers connect directly with the surrounding atrial muscle fibers
2) AP in the sinus node travel to the atrial muscle fibers and then to the AV node
3) Atrial fibers have bands called anterior interatrial band (Bachman’s bundle: this allows impulses to travel from the right atria to the left atria
4) 3 other bands terminate in the AV node

44
Q

Mechanism of Sinus nodal rhythmicity:

A

1) fast Na+ channels is responsible for the rapid upstroke spike of the AP observed in ventricular muscle
**2) The cause of this lower negativity is that the cell membranes of the sinus fibers are NATURALLY LEAKY to Na+ and Ca2+

45
Q

The pacemaker elsewhere than the sinus node is called an

A

ectopic pacemaker

46
Q

What causes an abnormal sequence of contraction of the different parts of the heart and can cause significant weakening of heart pumping?

A

Ectopic pacemaker

47
Q

Mechanism of the vagal effect:

A

The acetylcholine released at the vagal nerve endings greatly increases the permeability of the fiber membranes to K+
-Rapid leakage of K+ causes increased negativity inside the fiber (hyper-polarization)

48
Q

What is the proportion of blood that is red blood cells called?

A

Hematocrit

49
Q

Increasing hematocrit increases

A

Blood viscosity (more pressure is needed to push the blood)

50
Q

The greater the viscosity the lower the

A

flow in a vessel if all other factors are constant

51
Q

What effects would cause the venous pressure in the feet?

A

gravitational pressure

52
Q

Present in the endothelial cells are many minute plasmealemmal vesicles, also called?

A

calveolae (small caves)

53
Q

Special types of pores in capillaries of certain organs:

A

1) Brain: tight junctions only allows really small molecules
2) Liver: Wide open
3) GI tract: Midway size
4) Kidney: glomerular capillaries have windows called fenestrae allows small molecules in

54
Q

What occurs after tissue blood supply is blocked for a short time?

A

reactive hyperemia

55
Q

What is achieved by rapid changes in local vasodilation or vasoconstriction of the arterioles, metarterioles, and precapillary sphincters that occur within sec to mins to provide rapid maintenance of appropriate local tissue blood flow?

A

Acute control

56
Q

What means slow, controlled changes in flow over a period of days, weeks, or even months (adaptation). These changes provide better control of the flow proportion to the needs of the tissues. Mainly an increase or decrease in the size and number of blood vessels supplying the tissues?

A

Long-term control

57
Q

interstitium and interstital fluid contain to main components what are they?

A

1) collagen fiber bundles
2) Proteoglycan filaments

Advanced human physiology (3 decks)

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