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Phase 1 > CVR 2: Cardiovascular > Flashcards

CVR 2: Cardiovascular Flashcards

1
Q

How do inotropes increase contractility?

A

Increase the plateau of action potential, increase Ca ingress and release from SR, therefore more Ca binds to TnC, increasing contractility of myofibrils.

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2
Q

What is excitation-contraction coupling?

A

Chemical reaction, using chemical energy derived from ATP, resulting in mechanical action (contraction).
Begins with depolarisation and ends when Ca binds to TnC.

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3
Q

“When the heart is relaxing it isn’t resting!”
What does this mean?

A

When the heart is relaxed, it is still working hard, using ATP to pump Ca ions out of the myocytes.

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4
Q

Why is the T-tubule important in myocytes?

A

To allow calcium into the cell closer to the SR and myofibrils.

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5
Q

How does the myocyte remove calcium from the cytoplasm during relaxation?

A

Using ATP, moves Ca into SR stores.

Sodium/calcium exchanger uses electrochemical potential to allow 3x sodium ions into the cell in exchange for 1x calcium ion to leave.
Sodium gradient is then maintained by Na+/K+ ATPase.

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6
Q

Why is titin important and where is it found?

A

Titin is important because it acts as a spring in the myofibrils.
Attaches the myosin to the actin at the Z discs.

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7
Q

What are the three troponins in the troponin complex and what are their individual functions?

A

TnI = inhibits any interaction between actin and myosin.
TnC = binds to calcium, moves TnI and TnT (hence tropomyosin) away from actin, exposes actin binding site to myosin heads.
TnT = binds to tropomyosin to anchor the troponin complex and helps position the tropomyosin on actin, to also prevent myosin binding to actin.

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8
Q

What is a sarcomere?

A

The functional unit of myofibril, the region between two Z-lines.

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9
Q

What is isovolumic contraction?

A

Part of the cardiac cycle where the ventricle contracts without causing any change in the volume of blood in the ventricle.
Occurs after mitral/tricuspid valves close and before aortic/pulmonary valves open.

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10
Q

What pressure does the LV need to reach to open the aortic valve?

A

Diastolic pressure.

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11
Q

What is the ejection fraction in females vs males (percentage of blood ejected with each beat)?

A

Females = 65%
Males = 55%

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12
Q

What do the 1st and 2nd heart sounds correspond to?

A

“Lub dub”
1st = closing of mitral valve “lub” This is just after the start of isovolumic contraction.
2nd = closing of aortic valve “dub” This is also the start of isovolumic relaxation.

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13
Q

What is the early phase of filling?

A

When pressure in the left atrium increases above pressure in the left ventricle, blood rushes into ventricle passively prior to any atrial contraction.

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14
Q

In a young healthy adult, what percentage of blood from the left atrium moves into the ventricle during early phase of filling, and which heart sound can this create in youth/athletes/pregnancy?

A

85%
3rd heart sound (gallop).

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15
Q

When is the 3rd heart sound pathological and what does it suggest?

A

In adults over middle age, suggestive of congestive heart failure.

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16
Q

When does diastasis occur in the cardiac cycle?

A

When pressure in left atrium and left ventricle becomes equalised due to early phase of filling equalising the pressure. Net flow of blood = 0.

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17
Q

What is atrial augmentation?

A

When left atrium contracts and squeezes out the last part of blood in the atria, happens milliseconds after P wave on ECG.

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18
Q

When might you hear the 4th heart sound?

A

Galloping sound of blood being forced into stiff or hypertrophic left ventricle during atrial augmentation. Pathological sign of failing left ventricle.

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19
Q

A patient with AF has developed a hypertrophic left ventricle. Would you hear a 4th heart sound?

A

No! Because they don’t have any atrial augmentation.

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20
Q

Does contraction of the left ventricle (systole) occur before or after the mitral valve closes?

A

Before! Isovolumic contraction starts just before mitral valve closes.

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21
Q

What does preload refer to?

A

The load/volume of blood present before left ventricular contraction has started/degree of stretch of the myocardium.
“Left ventricular end-diastolic pressure”.

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22
Q

What is afterload?

A

The load after the ventricle starts to contract. The amount of pressure the heart needs to exert against pressure caused by aorta and circulation.

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23
Q

How does titin relate to Starling’s law?

A

Titin in myofibril keeps the unit tight. If the heart is overfilled and go beyond the capacity and stretch/elasticity of the titin, the heart is unable to contract efficiently.

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24
Q

What is elasticity of the heart?

A

The ability of the myocardium to recover its normal resting shape after removal of systolic stress.

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25
Q

How is ejection fraction calculated?

A

Stroke volume/end-diastolic volume.

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26
Q

What do pressure-volume loop graphs demonstrate?

A

Changing relationship between LV pressure and LV volume during cardiac cycle.

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27
Q

In embryonic development, from which layer do the coronary arteries develop from?

A

Ectoderm; the cardiac neural crest.

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28
Q

In embryonic development, from which layer does the myocardium develop?

A

Mesoderm (all types of muscle develop from the mesoderm).

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29
Q

What is the heart like at day 15 of embryonic development?

A

Tube-like heart, similar to a fish. First heart field; which will develop into left ventricle & atria, and second heart field; which will develop into right ventricle.

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30
Q

By what day of embryonic development does the heart start to resemble a mammalian heart?

A

Day 50.

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31
Q

What is a transcription factor and how might this relate to embryonic development of the heart?

A

Type of protein which when expressed “turns on/off” many other gene expressions.

If someone has a genetic variant which alters/deletes code for particular transcription factors which regulate embryonic heart development, could cause a malformed heart; congenital heart condition in baby or miscarriage.

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32
Q

What are the three stages of cardiac formation in the embryo?

A
  1. Formation of the primitive heart tube.
  2. Cardiac looping.
  3. Cardiac septation.
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33
Q

Why is Nodal important in embryological development and what is it?

A

Family of proteins, responsible for signalling developing cells to either move away or towards it; determines positioning e.g. left/right positioning of the heart.

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34
Q

What is the atrioventricular canal?

A

The initial gap between the embryonic single atrium and ventricle, which separates into two openings - eventually becoming the openings which situate the mitral & tricuspid valves.

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35
Q

What are the three types of capillaries?

A

Continuous (most common)
Fenestrated (kidney, small intestine, endocrine glands)
Discontinuous/sinusoidal (liver sinusoids, have larger openings than fenestrated)

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36
Q

When do the precursors of blood vessels form in the embryo, what are they called, and where do they form?

A

Day 17
Blood islands
Form in the yolk sac

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37
Q

When does vasculogenesis commence in the embryo?
Briefly describe the process.

A

Day 18
1. Blood islands = core of haemoblasts surrounded by endothelial cells.
2. Develop into angioblasts.
3. Angioblasts coalesce to form angioblastic cords throughout embryonic disc.

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38
Q

When and how does angiogenesis take place in embryonic development?

A

Day 18 onwards.
Driven by angiogenic growth factors.
Takes place by proliferation and sprouting. Other mesodermal cells are recruited to develop into smooth muscle intima media.

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39
Q

In embryonic development, do the 1st and 2nd aortic arch become coronary vessels?

A

No, they become minor head vessels.

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40
Q

In embryonic development, which aortic arch becomes the carotid arteries?

A

3rd aortic arch.

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41
Q

In embryonic development, what vessels derive from the 5th aortic arch?

A

Trick question! There is no 5th aortic arch!

42
Q

In embryonic development, what forms from the left 6th aortic arch?

A

Ductus arteriosus (communication between pulmonary artery and aorta).

43
Q

What is the most rare blood group in ABO?

A

The 5th group: Bombay group.

44
Q

What does a blood group depend on?

A

Antibodies in plasma and antigens on erythrocyte cell surface.

45
Q

Why is ABO the main identifying blood type used?

A

ABO is extremely immunogenic. Very unusual in that even if never exposed to other blood types, you still have antibodies against them.

46
Q

What sort of molecules in the antigen determine what blood group a person has?

A

Sugar molecules.

47
Q

Which blood group means you don’t have A or B antibodies?

A

Group AB

48
Q

What sort of antibodies are A and B antibodies?

A

Mix of IgG and IgM

49
Q

Which blood group is a universal recipient and why?

A

Group AB, because plasma does not contain either anti-A or anti-B antibodies.

50
Q

Which blood group is a universal donor and why?

A

Group O, because does not contain A or B antigens on RBC surface.

51
Q

What sort of reaction and what disease can Rhesus D cause?

A

Haemolytic transfusion reactions.
Haemolytic Disease of the Foetus and Newborn (HDFN).

52
Q

Will a person who is RhD-ve have antibodies against RhD in their plasma if they have never been exposed to Rh+ve blood?

A

No, only will develop RhD antibodies after being exposed by blood transfusion or after pregnancy with a Rh+ve baby.

53
Q

What is anti D and who is it given to?

A

RhD immunoglobulin, given to prevent formation of RhD antibodies in Rh-ve pregnant women prior to delivery, or after sensitising event, and again if baby is confirmed Rh+ve.

54
Q

In reverse typing, what signifies a positive test?

A

Agglutination, where cells clump together in a line on top of gel in tube. Occurs when the sample serum has reacted to the antigen, demonstrating serum has antibodies to the test RBC ABO type.

55
Q

In forward typing, what signifies a positive test?

A

Agglutination, where the cells clump together in a line on top of gel in tube. Occurs when the sample RBC has reacted to the test antibodies, demonstrating RBCs have antigens to the test antibody.

56
Q

What is cross-matching?

A

The intended donor RBCs is combined with the recipient’s serum to see if reaction occurs (indirect Coombs test).

57
Q

When might a direct Coombs test performed?

A

Usually done if a transfusion reaction has occurred.

58
Q

What is apheresis in blood donation?

A

Blood removed and externally separated into plasma and platelets. Unrequired RBCs are returned to patient.

59
Q

Why is plasma from female patients who have donated blood thrown away?

A

Female plasma is thought to be more immunogenic.

60
Q

What is the shelf life of donated RBCs, and how does this compare to the shelf-life of platelets?

A

35 days for RBCs.
7 days for platelets.

61
Q

What are the four potential transfusion reactions?

A

Haemolytic reactions.
Bacterial contamination.
Transfusion-related lung injury (TRALI).
Transfusion-associated circulatory overload (TACO).

62
Q

A blood donor is blood group AB. Recipients with which ABO blood group can be given their packed red blood cells?

A

AB only.

63
Q

Patients with blood group O can be universal donors (their blood can be given to anyone regardless of the recipient’s ABO type). Why?

A

Their erythrocytes have neither A nor B antigens.
But have antibodies to both in plasma so can only receive Group O blood.

64
Q

What are the stages of atherogenesis?

A

Fatty streak -> fibrous plaque -> athero-sclerotic plaque -> atherothrombosis by plaque rupture/fissure -> thrombosis.

65
Q

Why do platelets change their shape when activated?

A

To increase surface area which increases the possibility of cell-cell interactions.

66
Q

What receptors on platelets binds them together?

A

Glycoprotein IIb/IIa receptors on different platelets bind with the same fibrinogen molecule -> platelet aggregation.

67
Q

How do platelets adhere to damaged vessel walls?

A

Receptors on the platelet membrane (e.g glycoprotein Ib/GPIb) attach to collagen via von Willebrand Factor, or directly to collagen itself, which has been exposed in the endothelium basement membrane.

68
Q

Name four agonists that cause platelet activation.

A

Collagen.
Thrombin.
Thromboxane A2.
ADP.

69
Q

What is the difference in affect of COX inhibition between low dose aspirin (75mg & 300mg) and high dose aspirin (>500mg)?

A

Low dose aspirin inhibits COX-1 and high dose aspirin inhibits both COX-1 and COX-2.

70
Q

The heart is supplied by…

A

the left and right coronary arteries.

71
Q

Blood flow to the myocardium occurs during systole or diastole?

A

Diastole.

72
Q

The left coronary artery divides into…

A

the left anterior descending (LAD) and circumflex arteries.

73
Q

Compared to other veins, the oxygen saturation in coronary venous blood is very low (often O2 saturation of only 35%). This is because…

A

oxygen extraction by the heart muscle is very high.

74
Q

What surface of the heart does the right coronary artery supply?

A

The inferior surface of the heart.

75
Q

What is responsible for synthesising coagulation factors and fibrinogen?

A

The liver.

76
Q

What is the precursor for an enzyme that lyses clots?

A

Plasminogen.

77
Q

Describe the coagulation cascade in five words.

A

A series of proteolytic enzymes.

78
Q

What enzyme cleaves fibrinogen to create fibrin?

A

Thrombin.

79
Q

What is released upon cell activation, containing a high concentration of a molecule that acts as an agonist at the platelet P2Y12 receptor? What is the molecule?

A

Platelet dense granules.
They contain ADP.

80
Q

What part of the heart is responsible for the apex beat and where is it palpated?

A

The left ventricle.
Apex beat is palpated in the left 5th intercostal space and midclavicular line.

81
Q

Which part of the ECG represents ventricular repolarisation?

A

T wave.

82
Q

Which part of the ECG has a normal duration of 120-200ms (0.12-0.2 sec)?

A

PR interval.

83
Q

Which leads in a 12-lead ECG assess electrical activity within the lateral myocardial territory?

A

Leads I, aVL, V5, and V6

84
Q

Which lead in a 12-lead ECG yields complexes that are normally inverted compared to the anterior and inferior leads?

A

Lead aVR

85
Q

Which leads in a 12-lead ECG assess electrical activity within the inferior myocardial territory?

A

Leads II, III, and aVF

86
Q

Which part of ECG represents atrial depolarisation?

A

P wave.

87
Q

Which part of the ECG should be less than 120ms in duration?

A

QRS complex.

88
Q

Which receptors on platelet membranes bind to collagen via von Willebrand factor?

A

GPIb, GPIIb, GPIIIa
GP = glycoprotein

89
Q

Which receptors on the platelet membrane bind directly to collagen?

A

alpha 2 beta 1 (AKA, GPIa) and GPVI
GP = glycoprotein

90
Q

Where is von Willebrand factor found?

A

Free in plasma.
Inside Weibel-Palade bodies in endothelial cells.
Inside platelet alpha granules.

91
Q

What is the longest protein found in biology?

A

von Willebrand factor!

92
Q

What happens to von Willebrand factor at high shear rates?

A

It unravels from its usual “ball of wool” shape, exposing more sites for platelet binding, and can join together to form nets to catch platelets in.

93
Q

What does the enzymes Cyclooxygenase 1 and 2 (COX 1 & 2) do to arachidonic acid?

A

Both convert arachidonic acid into prostaglandin H2.

94
Q

What is the difference between prostaglandins (local hormones) made by platelets and endothelial cells?

A

Platelets make thromboxane A2, which triggers platelet aggregation and vasoconstriction.

Endothelial cells make prostacyclin, which inhibits platelet aggregation and can cause vasodilation.

95
Q

ADP binds to both P2Y1 and P2Y2 receptors on platelet membranes. What different affects do these different receptors trigger?

A

P2Y1 activates Gq protein, which initiates aggregation and platelet shape change (platelet activation).

P2Y12 activates Gi protein, which leads to amplification of platelet activation, aggregation, and dense granule release - secreting ADP into plasma; positive feedback loop and activates further platelets.

96
Q

Activated platelets release stored calcium ions into their cytoplasm. Why is this important for cleaving prothrombin in plasma into thrombin?

A

Calcium ions inhibit translocase and activate scramblase, which causes aminophospholipids to be expressed externally on platelet cell membrane.
Aminophospholipids allow assembly of prothrombinase complex; causing prothrombin in plasma to cleave into thrombin.

97
Q

Platelets catalyse thrombin generation from prothrombin. How does this affect coagulation?

A

Thrombin converts fibrinogen into fibrin. Fibrin is needed to stabilise the aggregated platelets into a platelet-fibrin clot.

(Thrombin also as an agonist for platelet activation, activating further platelets.)

98
Q

What are the key enzymes in the fibrinolytic system and what reactions do they catalyse?

A

Tissue plasminogen activator (tPA) catalyses plasminogen (protein) into plasmin (enzyme).
Plasmin catalyses fibrin into fibrin degradation products (such as D-dimer).

99
Q

What inhibitors are important in the anti-fibrinolytic pathway?

A

Plasminogen activator inhibitor-1 (PAI-1) inhibits tPA.
Antiplasmin inhibits plasmin, creates plasmin-antiplasmin complex (inactive).

100
Q

What do platelet alpha granules contain and when are they released into plasma?

A

Contain many different proteins; important coagulation factors and inflammatory mediators, including von Willebrand factor and fibrinogen.
Released following platelet activation.

101
Q

Platelet alpha granules mediate expression of surface P-selectin. Why is this important for the inflammatory response?

A

P-selectin expression on platelet membrane allows platelets to interact with monocytes which bond to P-selectin.
This triggers monocytes to release:
1. Cytokines to attract other leucocytes.
2. Proteolytic enzymes.
3. Tissue factor.

102
Q

In platelets, what drugs inhibit P2Y12?

A

Clopidogrel, prasugrel, ticagrelor.

Phase 1 (11 decks)

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