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Year 1 Medicine > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is the the haemocrit for blood?

A

45% cellular component of blood.

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2
Q

what is the fluid component of blood?

A

55%

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3
Q

What lies between the red blood cell and fluid layers on a haemocrit?

A

it is the white blood cells and platelets.

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4
Q

Where is haemopoesis in utero?

A

the yolk sac, liver and spleen, and bone marrow.

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5
Q

Where is haemopoesis in children?

A

in all bones in the bone marrow

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6
Q

Where in adults is haemopoesis?

A

in the axial skeleton. the spine and skull

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7
Q

What is the name for production of RBCs?

A

Erythropoeisis?

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8
Q

What is the name for production of white blood cells?

A

Myelopoiesis

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9
Q

What is the name for the production of Platelets?

A

Thrombopoesis

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10
Q

What cells does a common myeloid progenitoro lead to?

A

Megakaryocytes, erythrocytes, mast cells, myeloblasts

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11
Q

What do myeloblasts lead to?

A

Basophils, neutrophils, eosinophils, and monocytes.

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12
Q

What do common lympnoid proogenitors lead to?

A

lymphocytes

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13
Q

What growth factor causes RBC production?

A

Erythropoietin

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14
Q

What growth factor causes white blood cell production?

A

Granulocyte-macrophage-colony-stimulating factor

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15
Q

Which growth factor stimulates growth of platelets?

A

Thrombopoietin

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16
Q

Facts about RBCs?

A

simple cells no nucleus, no mitochondria, Biconcave disk around 7.5um contai haemoglobin and glycolysis enzymes.

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17
Q

Describe the haemoglobin molecule

A

quaternary structure. 2 alpha chains 2 beta chains. contain Fe2+ in haem group

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18
Q

What are the types of haemoblobin in an adult and proportions?

A

HbA 2 alpha 2 beta, 96-98%, HbF 2 alpha 2 gamma 0.5-0.8%, HbA2 2 alpha 2 delta 1.5-3.2%

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19
Q

What are the signs and symptoms of anaemia?

A

signs pallor tachycardia, signs related to underlying cause. symptoms tiredness/lethargy shortness of breath on exertion angina claudications symptoms related to underlying cause.

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20
Q

What changes in acute blood loss?

A

Volume of blood no change to haemocrit as all components lost equally.

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21
Q

How long do RBCs last for?

A

120 days aproximately 9 billion in an hour.

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22
Q

Which organs are involved in the removal of RBCs?

A

Spleen, Liver Bone marrow

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23
Q

Define Hypoplastic

A

not enough/ under development

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24
Q

Dyshaemopoietic

A

ineffective production

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25
Q

Haemolytic

A

breaking of red blood cells

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26
Q

What is hypoplastic anaemia?

A

Not enough RBC produced causes renal failure endocctine problems can be inherited or idiopathic.

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27
Q

What are causes of iron deficiency anaemia

A

chronic bleeding poor diet malabsorption or hookworm

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28
Q

Length of life of a neutrophil?

A

6-10 hours

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29
Q

Length of life of a monocytes?

A

20-40 hours

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30
Q

Length of life of a lymphocyte?

A

weeks to years

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31
Q

Length of life of a basophil?

A

days

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32
Q

Length of life of a eosinophils?

A

days

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33
Q

Which white blood cells are the most numebrous?

A

The neutrophils

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34
Q

What is the function of neutrophils?

A

To phagocytose bacterial and foreign material they also release chemotaxins and cytokines which are important in the inflammatory response

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35
Q

What are macrophages?

A

They are cells that phagocytose bacteria and foreign material can differentiat to specific ones in tissues

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36
Q

What are macrophages derived from?

A

Monocytes

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37
Q

What are dendritic cells?

A

they present antigens to the immune system

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38
Q

What are basophils?

A

they migrate to tissues and they are important in immunity and allergic response primarily against bacteria and fungi

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39
Q

Eosinophils what do they do?

A

They have a role in inflammation and allergic response especially in protection against parasites.

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40
Q

What are the two types of lymphocytes?

A

B lymphocytes and T lymphocytes.

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41
Q

What do B lymphocyts do?

A

mature in bone marrow and generate antibodies becoming plasma cells.

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42
Q

What do T lymphocytes do?

A

Mature in the thymus and aid B cells and generate cell mediated immunity.

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43
Q

What is Haemostatis?

A

The balance keeping blood fluid in the vessels and clotting outside the vessels

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44
Q

What acts to cause clotting?

A

Platelets and proteins of coagulation cascade

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45
Q

What acts to prevent clotting?

A

Endothelial cells, the anticoagulant pathway and fibrinolytic pathway.

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46
Q

How are platelets produced?

A

There are megakaryocytes that release platelet precursors from their surface as blebs. they are anucleate and circulate in an inactive state.

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47
Q

What are the stages of action of platelets?

A

They bind to collagen via glycoprotein 1a (GP1a) on the platelet membrane. they can also stick to collagen via factors like von Willebrand factor through GP1b GP2a/b.once the platelets are activated they change shape to help them stick together to make a platelet plug. They release granules. finally GPVI causes stable adhesion and aggregation

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48
Q

What are in electron dense granules of patelets?

A

Calcium ADP and ATP and serotonin

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49
Q

What are in the alpha granules of platelets?

A

Platelet derived growth factor fibrinogen, heparin antagonist PF4 and vonWillebrand factor

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50
Q

What is thrombocytopenia?

A

too few platelets

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51
Q

What is thrombocytosis?

A

having too many platelets which can lead to thrombosis.

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52
Q

What are some of the components of Plasma?

A

Proteins- albumin, carrier proteins coagulation proteins and immunoglobulins.

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53
Q

What does albumin do where is it produced?

A

produced in the liver helps maintain oncotic pressure of the blood to keep fluid in the blood.

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54
Q

What are immunoglobulins?

A

they are proteins produced by B lymphocytes that are in the blood for immune response.

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55
Q

How many clotting factors are there?

A

13 but no 3,4,6

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56
Q

What is haemophillia A?

A

genetic condition males defficiency of clotting factore VII bleeding into muscles and joints

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57
Q

What is haemophillia B

A

Defficiency in factor IX bleeding into muscles and joints

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58
Q

What is an example of acquired bleeding disorder?

A

liver disease because of vitamin K deficiecy(found in vegetables.

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59
Q

What is the shape of IgM antibodies?

A

pentagonal shape

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60
Q

what is the shape of IgA antibodies?

A

two normal stuck to each end.

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61
Q

What causes a transfusion reaction?

A

The production of antibodies whcih react with the antigens on the surface of a foreign RBC

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62
Q

What type of antibodies are usually involved with blood reactions?

A

IgM ones

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63
Q

Which types of antibodies can cross the placenta?

A

IgG

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64
Q

What is the difference between ABO and RhD antbodies?

A

RHd is an immune antibody they are warm agglutins while ABO are naturally present and they are cold agglutanins that means they like to react at colder temperatures.

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65
Q

Why is RhD a problem in pregnancy?

A

When the mother is Rhesus negative so doesn’t have D antigen. If the baby has go D antigens. All pregnant women are tested all who are negative are given antiD antibodies to stop sensitisation Haemolytic disease of the newborn.

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66
Q

What is cross matching in transfusions?

A

mix donor blood and patient to check for agglutination. could have antibodies from previous transfusions.

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67
Q

What are the early transfusion risks?

A

ABO incompatability, allergic reactons pyrogenic reactions bacterial contamination. couagulopathy. circulatory overload, transfusion related lung injury. post transfusion purpura

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68
Q

Late transfusion risks

A

RhD sensitisation, Delayed transfusion reaction, transfusion related iron overload, viral infection, prion infection

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69
Q

What is packed red cells?

A

Blood which has less plasma and higher haematocrit

can be given with diuretic usually over 2-3 hours

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70
Q

What product is used for poor clotting?

A

platelets given over 30mins when have very low platelet count

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71
Q

What is FFP?

A

Fresh frozen plasma. Frozen in less than 6 hours contains proteins and inhibitors useed fro massive transfusion and dilutional coagulopathy liver disease and

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72
Q

What is cryoprecipitate?

A

rich in fibrinogen factor 1 used in massive transfusion.

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73
Q

What is HAS?

A

Human albumin solution plasma expander increases osmotic pressure and reduce oedema.

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74
Q

What layer of the embryo contributes to the arteries and cardiac outflow?

A

The mesoderm

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75
Q

Which layer of the embryo forms the blood and heart?

A

mesoderm

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76
Q

What is the shape of the heart fields?

A

They are sausage shaped sitting on top of each other the first on top of the second the lowest part will form the atria

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77
Q

What does the first heart field give rise to?

A

the left ventricle

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78
Q

What does the second heart field give rise to?

A

The future right ventricle the atria and outflows

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79
Q

What does the truncus arteriosis or bulbus cordis do and where is it?

A

It is at the top of the fused heart tubes and forms the aortic arch and most of the right ventricle

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80
Q

What does the primitive ventricle form?

A

The left ventricle

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81
Q

Where is the primitive atrium?

A

it is below the bulbus cordis and primitibve ventricle like carina. it forms the left and right atria

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82
Q

what are the sinus venosis?

A

they are at the bottom they produce the inferior vena cava and the right atrium

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83
Q

What happens to the heart after the formation of regions?

A

Dextro rotation to the right. the cordis and primitive ventricle moves down and to the front
the primitive atrium moves up the back

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84
Q

What is cardiac septation?

A

formation of septum from the primus

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85
Q

what are the endocardial cushions?

A

they grow up and down to form the separation of the AV canal.

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86
Q

Describe the formation of the interatrial septum.

A

First There is the growth of the septum primum to join with the endocardial cussion making a hole the foramum primum at the bottome, then the foramen primum dissapears then forms foramen secundum at top.then the septum secundum which is thicker and more muscular than the septum secundum contains the foramen ovale. the septum primum acts a valve flap for the atria.

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87
Q

Where is most of the blood in the body?

A

In veins

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88
Q

Where are the elastic arteries?

A

main ones like aorta brachiocephalic carotids subclavian and pulmonary.

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89
Q

What are the three types of capillaries?

A

Continuous which are most common, fenestrated in kidney small intestine and endocrine glands and discontinuous in the liver sinusoids

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90
Q

What advantage does valves give veins?

A

Muscular return of blood can take places.

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91
Q

When does vasculargenesis commence?

A

day 18

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92
Q

Which part of the primitive heart makes the aortic arch?

A

the truncus arteriosis/bulbus cordis

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93
Q

how many arches of the aorta are there?

A

6 main ones but there is no 5th

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94
Q

What does the 1st arch become?

A

part of the maxillary artery

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95
Q

What does the 2nd arch become?

A

the stapedial artery

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96
Q

what does the 3rd arch become?

A

the left or right internal and external carotid

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97
Q

What does the 4th arch become?

A

on left part of the aortic arch on the right the right subclavian.

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98
Q

What does the 6th arch develop into?

A

left the pulmonary artery and ductus arteriosis, on the right the right pulmonary artery

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99
Q

What does the 7th segmental artery become?

A

the left subclavian artery and part of the right subclavian artery

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100
Q

what does the dorsal aorta do?

A

It becomes the decending thoracic aorta on the left and regresees to be part of the right subcavian on the right.

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101
Q

What does the aortic sac become?

A

ascending aorta and part of brachiocephalic trunk.

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102
Q

What is the importance of platelets in pathology?

A

will cause Thrombosis

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103
Q

Describe the stages of Thrombosis

A

A fatty streak builds up on the lining, becomes a fibrous plaque, (atherosclerotic plaque)
then this can rupture or fissure and cause the clot to block that artery or pass to a critical area like the heart or brain.

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104
Q

What happens when a platelet it activated?

A

It changes shape from smooth to spiculates and pseudopodia (legs). increasing SA so increased interactions. more receptors and increased affinity to fibrinogen

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105
Q

Which receptors are used to cause adhesion?

A

attachement via GPIIb/IIIa integrin alphaIIb beta3

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106
Q

What can activate platelets?

A

Thrombin- also cleavs fibrinogen into fibrin. by PAR1 and PAR4
Thromboxane A2- comes from platelets when its bound to collagen, asprin stops this.
Collagen GPVI receptor
ADP- P2Y1

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107
Q

What biochemical changes occur at activation of platelets?

A

Causes more GPIIb/IIIa receptors,

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108
Q

Describe the action of COX1 and 2

A

Cyclooxygenases. both convert arachidonic acid into prostaglandin H2
COX-1 turns into thromboxane A2 in platelets
and COX-1 and COX-2 in endothelial cells convert prostaglandin H2 into prostacyclin

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109
Q

What is the effect of thromboxane A2?

A

causes platelet aggregation, and vasoconstriction.

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110
Q

What is the effect of prostacyclin?

A

Inhibits platelet aggregation and vasoconstriction. it mediates inflamation

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111
Q

What do NSAIDs do?

A

Block COX-1 and 2 to stop prostacyclin being formed meaning a clot is more likely.

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112
Q

What does low dose asprin do?

A

it inhibits COX-1 in platelets which stops thromboxane A2 production which leads to less clotting

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113
Q

What does high dose asprin do?

A

Block COX-1 and 2 to stop prostacyclin being formed meaning a clot is more likely.

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114
Q

What does high dose asprin do?

A

Block COX-1 and 2 to stop prostacyclin being formed meaning a clot is more likely.

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115
Q

What are P2y1 and P2y12?

A

both ADP receptors:
P2Y1 is a Gq receptor which releases PLC and this induces Ca mobilisation and activation of platelets

P2Y12 is a Gi GPCR. This inhibits adenylate cyclase producing cAMP. Normally cAMP would inhibit platelet activation and therefore the inhibition increases platelet activation

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116
Q

What are amplification pathways on the platelet?

A

P2y12 activated by ADP releases dense granules to re stimulate itself.
GPIIb/IIIa causes granule release.
Collagen binding to GPVI causes release of thromboxane A2.
Thrombin activates dense granule release.
thrombin produced on membrane

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117
Q

Describe the changes to lipid bilayer in platelets that faciltate production of thrombin

A

usually has amiophospholibids that are kept on inner layer of plasma membrane by translocase. when activated Ca released which scramblase is activated and translocase inhibited which means amino phospholibids allows prothrombinase can bind to the membrane and convert prothrombin to thrombin factor 2 and 2a

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118
Q

Describe the fibrinolytic system

A

the endothelium releases tPA tissue plasminogen activator. converts plasminogin into plasmin which converts fibrin into degreded productsthere are inhibitors are PAI-1 and antiplasmin

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119
Q

What is the significance of platelete alpha granules?

A

release coagulation factors and inflammatory mediators which help the wound healing with WBCsallow monocytes to bind.

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120
Q

What lies on the right heart border?

A

Superior vena cava, right atrium

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121
Q

Where does the right heart border lie?

A

It is to the right of the sternum

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122
Q

Where is the inferior border of the heart.

A

Sits on the diaphragm and below the xiphoid sternum.

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123
Q

Where is the let heart border?

A

left mid clavicular line

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124
Q

Where is the apex beat?

A

left midclavicular line 5th intercostal space.

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125
Q

What is the pleural refelction?

A

it is an area below the xiphoid sternum it is an area on inferior surface of the heart and is a gap in pleural membrane used to drain fluid from the heart without openning the pleural.

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126
Q

What lies on the left heart border

A

aorta left atrial appendage and most is left ventricle.

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127
Q

what makes the anterior border of the heart?

A

right ventricle and left ventricle

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128
Q

What is the posterior border of the heart?

A

the left atrium.

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129
Q

What is the importance of the sternal angle?

A

2nd costal cartilage, defines the superior and inferior mediastinum. T4/5 level

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130
Q

What is in the anterior mediastinum?

A

the thymus

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131
Q

What is in the middle mediastinum?

A

pericardium and heart

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132
Q

What is in the posterior mediastinum?

A

oesophagus the aorta intercostal arteris bronchial arteries the throacic duct azygous veins and hemiazygous vein sympathetic trunks

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133
Q

What is the pericardium like?

A

Fibrous layer parietal and visceral on the surface of the heart.

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134
Q

which great vessels are at the front of the heart

A

aorta and pulmonary artery.

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135
Q

What are the two areas of the right atrium?

A

the smooth parts and the trabeculated part(with ridges) they are separated by the crista terminalis

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136
Q

Where is the coronary sinus?

A

it drains into the right atrium directly runs in the atrioventricular goove

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137
Q

What is the aortomitral continuity?

A

the aortic and mitral valves are connected by a fibrous area.

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138
Q

What are the branches of the right coronary artery?

A

it runs through the atriventricular sinus then at edge gives right marginal artery, continues to the back potentally giving posterior interventricular artery.

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139
Q

What are the first branches of the aorta?

A

the coronary arteries

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140
Q

describe the branches of the left coronary artery.

A

The circumflect comes off to go in atrioventricular groove to back to give posterior interventricular also gives obtuse marginal artery. the LAD runs between the ventricles. it gives the septal arteries that go into the septum and diagonal across the front.

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141
Q

Explain dominance in terms of coronary arteries

A

what artery suplies the posterior descending. 70% right dominant 20% co dominant and 10% left dominant

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142
Q

How many electrodes are there on an ECG?

A
  1. left arm right arm left leg right leg. then V1-6 V1 on Rhs of sternum 4th intercostal space. V2 right ternal border 4th intercostal space. V3 between V2V4 V4 5th iCS mid clavicular line V5 anterior axillary V6 mid auxillary
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143
Q

What does each small square represent on an ECG?

A

40ms

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144
Q

What does each big square represent?

A

0.2s

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145
Q

Why are there 12 leads but 10 electrodes?

A

different views between them

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146
Q

how many bipolar leads are there?

A

3

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147
Q

how many unipolar leads are there?

A

3 arm 6 chest

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148
Q

Which leads give lateral view?

A

Lead 1 avL V5 V6

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149
Q

which give inferior view?

A

lead 2 lead3 avF

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150
Q

which give septal view?

A

V1 and V2

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151
Q

Which ECG lead gives anterior view?

A

V3 V4

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152
Q

Which lead(s) are P waves negative?

A

aVR

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153
Q

What does a P wave represent?

A

atrial depolarisation(not systole)

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154
Q

How to interpret an ECG?

A 
Rate
Rhythm
Axis
P wave
PR interval
QRS
ST segment
T waves
QT interval
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155
Q

How can you calculate ventricular rate on an ECG

A

300 divided by big squares between 2 QRS complexes

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156
Q

How can you tell if it is sinus rhythm?

A

Pwave morphology suggest its from SA node eg positive in all but aVR and that its followed by a QRS complex

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157
Q

name sone other rhythms?

A

sinus, supraventricular, ventricular heart block

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158
Q

What is a normal cardiac axis?

A

-30 to 90 degrees

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159
Q

How long should the P wave be?

A

3 small squares.

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160
Q

What kind of abnormalities can be present in P waves?

A

Tall peaks, right atrial enlargment.
bifid p wave left atrial enlargement.
inverted non sinus origin

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161
Q

PR interval should be how long?

A

3 to 5 squares long can show poor conduction.

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162
Q

How long should the QRS complex be?

A

3 small squares or 120msec

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163
Q

What does the QRS complex represent?

A

Verntricular depolarisation (not systole)

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164
Q

What are some common QRS comples abnormalities?

A

Broad complex- Ventricular origin, BBB, hyperkalemia, ventricular pacing.
High voltage QRS-ventricular hypertrophy

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165
Q

What does the ST segment show?

A

Interval between depolarisation and repolarisation.

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166
Q

What does T wave show?

A

Ventricular repolarisation

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167
Q

What is a common ST abnormalities?

A

ST segment depression often due to ischemia or digitoxin toxicity hypokalemia ventricular hypertrophy

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168
Q

T wave inversion is caused by what?

A

ischemis pulmonary embolism, ventricuar hypertrophy, often normal like this in children.

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169
Q

What is the QT interval? how long is too long?

A

Time of depolarisation and repolarisation. 440 for men 460 for women

170
Q

Which organs of the body use the most blood(in order)>

A

Liver Kidneys, muscle, brain

171
Q

Where does blood flow the fastest in the circulatory system?

A

in the aorta and vena cava

172
Q

What are the adaptations of the arteries?

A

Elastic to cushion systole and maintain blood flow to organs during diastole.

173
Q

Which blood vessel is the principal site of resistance tovascular flow?

A

the arterioles

174
Q

What is TPR?

A

Total peripheral resistance = total arteriola resistance it can be varied and plays a major role in detrmining arterial pressure and distribution of flow to organs

175
Q

what happens when vascular smooth muscle constricts?

A

radius decreases and resistance increases and flow decreases.

176
Q

Is vascular smooth muscle ever completely relaxed?

A

No this is called the myogenic tone

177
Q

What happens to blood in capillaries?

A

it slows down to allow for blood do drop off nutrients.

178
Q

What is the average pressure of a vein?

A

10mmHg

179
Q

What mediates vasoconstriction?

A

the sympathetic nervous system

180
Q

What is the purpose of lymphatics?

A

To drain excess filtered fluid from capillaries and the tissues

181
Q

Where is the return of the interstitial fluid?

A

The throacic duct at the left subclavian vein.

182
Q

What aids the flow of lymph?

A

respiratory pump skeletal muscle pup smooth muscle in lymphatic vessels?

183
Q

What is cardia output?

A

heart rate x stroke volume

184
Q

Equation for blood pressure?

A

cardiac output x total peripheral resistance

185
Q

What is pulse pressue?

A

systolic- diastolic pressure

186
Q

what is the mean arterial pressure?

A

diastolic +1/3 of the pulse pressure

187
Q

What changes the flow?

A

the pressue and resistance flow= pressure gradient/resistance Ohm’s law

188
Q

Which is poiseullie’s equation?

A

Flow = radius to the power of 4

189
Q

What is the frank starling mechanism?

A

more stretch in ventricle or of muscle the sronger it contracts causing a higher pressure and larger cardiac output

190
Q

What happens whe venous return is higher?

A

end disastolic volume is higher stroke volume is therefore higher and then the cardiac output is higher

191
Q

What is an important factor in long term blood pressure?

A

Blood volume

192
Q

Which systems change blood volume?

A

Renin-angiotensin-Aldosteroe System and ADH

193
Q

why does the circulation need controlling?

A

maintain the flow of blood, maintain pressure

194
Q

What is systolic and diastolic blood pressure?

A

systolic is the highest blood pressure when the ventricles contract. the diastolic is the lowest when the ventricles relax

195
Q

Why do you measure blood pressure using the brachial artery?

A

convenient to compress and it is at the level of the heart.

196
Q

which Korotkoff sounds are important for measuring BP?

A

1 and 5

197
Q

What is myogenic autoregulation?

A

the innate response of a vessel to contract against an expansion.

198
Q

Which organs have good autoregulation which have bad?

A

renal cerebral coronary are very good.
skeletal and splanchnic are moderate
Cutaneous is poor

199
Q

What is intrinsic control?

A

registration of blood flow through the body due to the control from the Autonomic Nervous system and the smooth/cardiac muscle

200
Q

What are the local humoral factors for vasoconstriction?

A

Endothelin-1 and internal blood pressure

201
Q

What are the local humoral factors of vasodilation?

A

Hypoxia Adenosine Bradykinin NO potassium CO2 Hydrogen ions tissue breakdown and prostacyclin

202
Q

What is the role of the endothelium in control of the circulation?

A

Produces NO, prostacyclin and endothelin.

203
Q

What are circulating(hormonal) vasoconstrictors?

A

Adrenaline, Angiiotensin 2, vasopressin(ADH).

204
Q

what are circulating (hormonal) vasodilators?

A

Epinephrine, Atrial natriuretic peptide

205
Q

Where are the primary baroreceptors of the body?

A

Carotid sinus and aortic arch

206
Q

Where are the secondary baroreceptors?

A

in the veins myocardium and pulmonary vessels

207
Q

What are the afferent nerves for baroreceptors?

A

Glossopharengeal 9th

208
Q

What are the efferent nerves for baroreceptors?

A

Sympathetic and Vagus 10th

209
Q

How do arterial baroreceptors affect central control?

A

If pessure increases then they fire more which decreases sympathedic coutflow to the heart and arterioles but increases parasympathetic outflow to the heart

210
Q

Where are the cardiopulmonary baroreceptors found?

A

in the atria and verticals and pulmonary artery.

if they are stimulated they act to reduce BP.

211
Q

What are the main neural influences on the medulla?

A

Baroreceptors, chemoreceptors, hypothalamus, cerebral cortex, skin, canges in O2 and CO2

212
Q

What does stimulation of the hypothalamus do?

A

reduce blood pressure. it can regulate skin blood flow

213
Q

Where are the central chemo receptors?

A

in the medulla.

214
Q

What is excitation- contraction coupling?

A

When the membrane is stimulated it releases calcium which leads to the contraction of the muscle.

215
Q

What type of process does calcium use to move into the muscle cytosol?

A

passie diffusion

216
Q

How is relaxation of the heart initiated?

A

When calcium is pumped out of the cells.

217
Q

What does the heart use for energy?

A

Free fatty acids as this is the most efficient. it can use glucose anaerobically if required.

218
Q

What is the A band?

A

a reigone of the sarcomere that has thick filaments and is dark

219
Q

What is the I band?

A

It is light and is only occupied by thin filaments that extend toward the centre of the sarcomere from the z lines it also contains tropomyosin and troponin

220
Q

Where is the Zline?

A

In the middle of each I band

221
Q

How does the power stroke contraction happen in ECC?

A

Sliding of actin over mysosin by ATP hydrolysis by ATP ase in the myosin heads

222
Q

Describe the structure of myosin

A

2 heavy chains that are responsible for the dual heads and 4 light chains the heads are perpendicular at rest and bend towerds the middle.

223
Q

Describe the structure of actin

A

It is a globular protein with a double stranded macromolecular helix and form F actin

224
Q

Describe the structure of tropomyosin.

A

it is an elongated molecule made of two helical peptide chains. it is in the grooves of the actin strands and regulates the interaction with the other strands

225
Q

What are the components of troponin?

A

I T C

226
Q

What do the components of troponin do?

A

I with tropomyosin inhibit actin and myosin interaction
T binds troponin complex to the tropomyosin
C has a high affinity for calcium. this allows the Tn I to move away from actin allowing interaction.

227
Q

At what angle are all the heads of myosin?

A

40 degree angle

228
Q

What is the ventricular contraction of the heart cycle?

A

LV contraction there is isovolumic contraction where the volume doesn’t change and pressure increases. then maximal ejection where it actually ejects. at the start of relaxation there is reduced ejection. then isovolumic relaxation and it fills passively

229
Q

What is the atrial booster?

A

when the atria contract to fill the ventricle .

230
Q

What is the first heart sound made from?

A

After the atrial booster which closes the mitral valve

231
Q

What is the second heart sound?

A

After the aortic valve closes after relaxation of the ventricle

232
Q

What is the 3th heart sound

A

when the ventricle jitters which coincides with early filling passively of ventricle

233
Q

What is the 4th heart sound

A

Just before mitral valve closes it is pathogenic stenosis.

234
Q

What is diastasis?

A

when the ventricle rises to same pressure as the atrium just before the ventricle contracts again.

235
Q

Where should you feel a pulse for the timing of heart sounds?

A

the carotid pulse pressing against transverse process of C6

236
Q

What is isovolumetric contraction.

A

Ventricular contraction when all valves are closed. This increases ventricular pressure but as the valves are closed the volume remains unchanged.

237
Q

What produces the first heart sound?

A

Closing of the mitral valve.

238
Q

What causes the mitral valve to close?

A

When LVp exceeds LAp. Just before ventricular isovolumetric contraction.

239
Q

Describe systole.

A

Wave of depolarisation arrives, Ca2+ channels open. LVp>LAp and the mitral valve closes.LVp rises, isovolumetric contraction, LVp>aortic p. Aortic valve opens and ejection begins.

240
Q

What produces the second heart sound?

A

Closing of the aortic valve.

241
Q

Describe diastole.

A

LVp decreases and there is a phase of reduced ejection. LVp is less than aortic pressure and the aortic valve closes: isovolumetric ventricular relaxation. LVp is less than LAp and mitral valve opens - ventricles fill with blood. Atria contract - atrial booster. LVp > LAp and mitral valve closes.

242
Q

What is the duration of systole?

A

0.3s.

243
Q

What is the duration of diastole?

A

0.5s.

244
Q

What is end systolic volume?

A

The volume of blood remaining in the LV following systole.

245
Q

Define preload.

A

The volume of blood in the ventricles just before contraction (EDV).

246
Q

Define afterload.

A

The pressure against which the heart must work to eject blood in systole.

247
Q

Define contractility.

A

The inherent strength and vigour of the heart’s contraction during systole.

248
Q

Define elasticity.

A

Myocardial ability to recover it’s original shape after systolic stress.

249
Q

Define compliance.

A

How easily a chamber of the heart expands when it is filled with blood (C=ΔV/ΔP).

250
Q

Define diastolic distensibility.

A

The pressure required to fill the ventricle to the same diastolic volume.

251
Q

Define resistance.

A

A force that must be overcome to push blood through the circulatory system.

252
Q

What is the basic principle of Starling’s law of the heart?

A

Increased EDV = increased SV.

253
Q

Explain Starling’s law.

A

The greater the EDV, the greater the sarcomeres are stretched and the more forceful the contraction.

254
Q

With relation to Starling’s law, what is the effect of an increased venous return?

A

EDV will increase and so SV increases and so Cardiac output also increases as CO=SVxHR.

255
Q

Give the equation for stroke volume.

A

SV=EDV-ESV.

256
Q

Give the equation for cardiac output.

A

CO=SVxHR.

257
Q

Define cardiac output.

A

The volume of blood each ventricle pumps per unit time.

258
Q

Give the equation for mean arterial pressure.

A

MAP = DP + 1/3(SP-DP).(SP - systolic pressure, DP - diastolic pressure).

259
Q

Give the equation for pulse pressure.

A

PP=SP-DP.

260
Q

Give the equation for blood pressure.

A

BP=COxTPR.

261
Q

What is Poiseuille’s equation?

A

Q=r^4.

262
Q

What is Ohm’s law?

A

F=ΔP/R.

263
Q

What are the principle vessels of resistance?

A

Arterioles.

264
Q

What do arterioles respond to?

A

Blood pressure changes. Local, neural and hormonal factors.

265
Q

Name 2 local factors that result in vasoconstriction.

A

Endothelin, internal BP.

266
Q

Name 5 local factors that result in vasodilation.

A

Hypoxia, NO, K+ (accumulate from AP), CO2, H+, adenosine.

267
Q

What neural factors result in vasoconstriction?

A

Sympathetic nerves that release noradrenaline.

268
Q

What neural factors result in vasodilation?

A

Parasympathetic innervation.

269
Q

Name 3 hormonal factors that result in vasoconstriction.

A

Angiotenisn 2, ADH, Adrenaline (binds to alpha-adrenergic receptors in smooth muscle).

270
Q

Name 2 hormonal factors that result in vasodilation.

A

Atrial natriuretic peptide, Adrenaline (binds to beta2 receptors).

271
Q

What is myogenic auto-regulation of blood flow?

A

An intrinsic mechanism in smooth muscle blood vessels. If BP increases the vessel constricts. This is important in regulating blood flow.

272
Q

Myogenic auto-regulation of blood flow: What is the response to an increase in BP?

A

Increased BP will result in vasoconstriction and so blood flow decreases.

273
Q

Myogenic auto-regulation of blood flow: What is the response to a decrease in BP?

A

Decreased BP will result in vasodilation and so blood flow increases.

274
Q

What is hyperaemia?

A

An increased blood flow to tissues.

275
Q

What is the cause of active hyperaemia?

A

When blood flow increases due to an increase in metabolic activity. - Increased metabolic activity = decreased O2 and increased metabolites = arteriolar dilation = increased blood flow.

276
Q

What is the cause of reactive hyperaemia?

A

When blood flow increases following occlusion to arterial flow.

277
Q

Describe excitation-contraction coupling.

A
  1. Na+ depolarises membrane. 2. A small amount of Ca2+ is released from T tubules. 3. Ca2+ channels in sarcoplasmic reticulum open. 4. Ca2+ flows into cytosol. Cytosolic Ca2+ conc raised. 5. Ca2+ binds to troponin C, this pulls tropomyosin and exposes the myosin binding site on actin. 6. Cross bridge cycling begins.7. After depolarisation, Ca2+ is returned to SR. K+ outflow = repolarisation.
278
Q

What effect does myocardial contraction have on the A-band of a sarcomere?

A

No effect, it stays the same length.

279
Q

What effect does myocardial contraction have on the I-band and H-zone of a sarcomere?

A

They get shorter.

280
Q

Describe actin (thin filament).

A

A globular protein, single polypeptide. It polymerises with other actin monomers to form a double stranded helix. Together they form F actin.

281
Q

Describe myosin (thick filament).

A

2 heavy polypeptide chains and 4 light chains. The myosin heads have 2 binding sites; one for actin and one for ATP.

282
Q

Describe tropomyosin.

A

An elongated molecule made of 2 helical peptide chains.

283
Q

What is the function of troponin I?

A

Troponin I, together with tropomyosin, inhibits actin and myosin binding.

284
Q

What is the function of troponin T?

A

Troponin T binds to tropomyosin.

285
Q

What is the function of troponin C?

A

Troponin C has a high affinity for Ca2+. TnC drives away TnI and so allows cross bridge formation.

286
Q

Name 3 effectors in circulation control.

A
  1. Blood vessels - vasoconstrict/dilate and effect TPR.2. The heart - can affect rate or contractility. 3. Kidneys - regulates blood volume and fluid balance.
287
Q

Where are baroreceptors located?

A

Aortic arch and carotid sinus.

288
Q

What activates baroreceptors?

A

Baroreceptors contain stretch receptors that respond to pressure.

289
Q

Are atrial baroreceptors involved in short-term or long-term regulation of BP?

A

Short-term. (Cardiopulmonary = long-term).

290
Q

Where central chemoreceptors located?

A

In the medulla oblangata.

291
Q

What do central chemoreceptors respond to?

A

Changes in pH/(H+). Increased PaCO2 increases H+ and so decreases pH. Increased PaCO2 results in vasodilation.

292
Q

What is the ligamentum teres a remnant of?

A

The umbilical vein.

293
Q

What is the ligamentum venosus a remnant of?

A

The ductus venosus.

294
Q

Briefly describe foetal circulation.

A

Maternal circulation - umbilical vein (oxygenated blood) - ductus venosus - IVC - RA - LA/RV - aorta - umbilical artery (deoxygenated blood) - maternal circulation.

295
Q

What layer of the tri-laminar disc forms the cardiovascular system?

A

The mesoderm.

296
Q

What does the first heart field produce?

A

The left ventricle.

297
Q

What does the second heart field produce?

A

The right ventricle, atria and outflow tracts.

298
Q

What are the 3 stages of heart formation?

A
  1. Formation of primitive heart tube.2. Cardiac looping.3. Cardiac septation.
299
Q

Describe what happens in the formation of the primitive heart tube.

A

Two endocardial tubes form (day 19). The tubes fuse together and the heart beats (day 22).

300
Q

Describe what happens in cardiac looping.

A

Nodes secrete nodal, this circulates to the left due to ciliary movement. Nodal causes a cascade of transcription factors that transduce looping.

301
Q

Describe what happens in cardiac septation.

A

Endocardial cushions form. Fuse at mid-line to form atrio-ventricular septum. Muscular ridge in the floor of the primitive ventricle migrates to endocardial cushions forming interventricular septum.

302
Q

What does the sinus venosus form?

A

The coronary sinus and RA.

303
Q

What does the primitive atrium form?

A

RA and LA.

304
Q

What does the primitive ventricle form?

A

Forms most of LV.

305
Q

What does the bulbus cordis form?

A

Part of the ventricles.

306
Q

What does the truncus arteriosus form?

A

The aorta and pulmonary trunk.

307
Q

What do the 1st and 2nd aortic arches form?

A

Minor vessels in the head.

308
Q

What does the 3rd aortic arch form?

A

The common carotid arteries.

309
Q

What does the left and right 4th aortic arch form?

A

Left - aorta. Right - Right subclavian artery.

310
Q

What does the 5th aortic arch form?

A

There is no 5th arch!

311
Q

What does the left and right 6th aortic arch form?

A

Left - left pulmonary artery and ductus arteriosus. Right - right pulmonary artery.

312
Q

What does the 7th segmental aortic arch form?

A

Left and right subclavian arteries.

313
Q

What does the dorsal aortae form?

A

Left dorsal aortae - descending aorta. Right dorsal aortae - part of right subclavian artery.

314
Q

What are chronotropic effects?

A

Those that change the heart rate. Positive chronotropic = increased heart rate.

315
Q

What are inotropic effects?

A

Those that alter the force of muscular contractions.

316
Q

What affect does parasympathetic stimulation have on heart rate?

A

Decreases heart rate (-ve chronotropic). Cardiac output therefore decreases with parasympathetic stimulation. (CO=HRxSV).

317
Q

What affect does sympathetic stimulation have on force of contraction?

A

Increases force (+ve inotropic).

318
Q

What pump maintains the negative resting potential of a membrane?

A

Na+/K+ pump.

319
Q

What is the purpose of the Nernst equation?

A

It is used to determine a membranes potential.

320
Q

Give the Nernst equation.

A

E = 60log(conc outside/conc inside)

321
Q

What membrane channels are responsible for the plateau period in the cardiac AP?

A

Voltage gated Ca2+ ‘slow’ channels.

322
Q

Briefly describe the cardiac action potential in 5 steps.

A
  1. Na+ channels open; influx of Na+ into cell; depolarisation. 2. When the Na+ channels close, a small number of K+ leave the cell resulting in partial repolarisation. 3. Ca2+ channels open and there is Ca2+ inflow. K+ channels are also open and there is K+ outflow. This results in the plateau period. 4. Ca2+ channels close and K+ channels remain open. K+ leaves the cell resulting in repolarisation.5. Maintaining the resting potential (approx -90mV). Na+ inflow, K+ outflow.
323
Q

Where is the SAN located?

A

In the RA under the crista terminalis.

324
Q

Briefly describe the electrical conduction pathway in the heart.

A
  1. The SAN generates an electrical impulse. 2. This generates a wave of contraction in the atria.3. Impulse reaches AVN.4. There is a brief delay to ensure the atria have fully emptied. 5. The impulse then rapidly spreads down the Bundle of His and Purkinje fibres.6. The purkinje fibres then trigger coordinated ventricular contraction.
325
Q

Why is there rapid conduction in the bundle of his and purkinje fibres?

A
  1. The fibres have a large diameter. 2. There is high permeability at gap junctions.
326
Q

What is the function of the refractory period?

A
  1. It prevents excessively frequent contractions. 2. It allows time for the atria to fill.
327
Q

What does the P wave on an ECG represent?

A

Atrial depolarisation. Duration is less than 0.12s.

328
Q

What does the QRS complex on an ECG represent?

A

Ventricular depolarisation. Duration is 0.08-0.1s.

329
Q

What does the T wave on an ECG represent?

A

Ventricular repolarisation.

330
Q

What might an elevated ST segment be associated with?

A

Myocardial infarction.

331
Q

ECG: where would you place lead 1?

A

Right arm (-ve) to left arm (+ve).

332
Q

ECG: where would you place lead 2?

A

Right arm (-ve) to left leg (+ve).

333
Q

ECG: where would you place lead 3?

A

Left arm (-ve) to left leg (+ve).

334
Q

What is Einthoven’s triangle?

A

An imaginary formation of the 3 limb leads in a triangle shape.

335
Q

ECG: where would you place lead aVR?

A

Left arm and left leg (-ve) to right arm (+ve).

336
Q

ECG: where would you place lead aVF?

A

Right arm and left arm (-ve) to left leg (+ve).

337
Q

ECG: where would you place lead aVL?

A

Right arm and left leg (-ve) to left arm (+ve).

338
Q

ECG chest leads: In which intercostal space would you place V1 and V2?

A

The 4th intercostal space. V1 is right of the sternum and V2 in left.

339
Q

ECG chest leads: In which intercostal space would you place V3-V6.

A

The 5th intercostal space. V3 is left of the sternum, V4 is in the mid-clavicular line, V5 is left of V4 and V6 is under the left arm.

340
Q

What are the average systolic and diastolic pressures for the pulmonary circulation?

A

25 and 10 mmHg.

341
Q

What are the average systolic and diastolic pressures for the systemic circulation?

A

120 and 80 mmHg.

342
Q

Why might someone with liver injury experience prolonged bleeding time?

A

Because the liver produces clotting factors.

343
Q

What is exposed if you damage the endothelium of a vessel?

A

Underlying connective tissue and collagen.

344
Q

What is the role of vWF?

A

vWF binds to collagen and platelets bind to vWF.

345
Q

What happens in platelet activation?

A

The change shape: smooth to spiculated. This increases their surface area. New platelets adhere to old ones = platelet aggregation. This forms a platelet plug.

346
Q

What do activated platelets synthesise?

A

Thromboxane A2.

347
Q

What is the function of Thromboxane A2 (TXA2)?

A

Platelets binding to collagen through GPVI causes the release of TxA2.
This leads to further platelet aggregation by binding to the receptor TPalpha on the platelet

348
Q

What are the platelet receptors for fibrinogen?

A

glycoprotein IIb/IIIa. Fibrinogen forms ‘bridges’ between platelets.

349
Q

What does an undamaged endothelium release in order to prevent platelet activation in undamaged areas?

A

Prostacyclin (inhibits platelet aggregation) and NO (inhibits platelet adhesion).

350
Q

What are platelets made from? and where are they made?

A

In the bone marrow from megakaryocytes.

351
Q

In haemostasis what is prothrombin converted into?

A

Thrombin.

352
Q

Give 3 functions of Thrombin.

A
  1. Converts fibrinogen into fibrin.2. Activates factor XIII into XIIIa.3. Has a positive feedback effect resulting in further thrombin production.
353
Q

What is the essential component of a blood clot?

A

Fibrin.

354
Q

Briefly describe the Fibrinolytic system.

A

Plasminogen is converted into plasmin. Plasmin cuts the fibrin at various places leading to the formation of fragments.

355
Q

What is the purpose of the fibrinolytic system?

A

It acts to prevent blood clots from growing and becoming problematic.

356
Q

What is the structure of Hb?

A

2 alpha and 2 beta chains. 4 haem groups.

357
Q

Describe the composition of blood.

A

Plasma - 55%.Cellular - 45% - RBC: 44%, WBC: 1%.

358
Q

Does blood flow to the heart occur during diastole or systole?

A

Diastole.

359
Q

What does the left coronary artery divide into?

A

The left anterior descending, and the circumflex.

360
Q

Why is the O2 saturation in coronary venous blood very low?

A

O2 extraction by the heart muscle is very high.

361
Q

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

A

The inferior surface (underside) of the heart.

362
Q

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

A

Platelet dense granules.

363
Q

What valve prevents high pressures developing in the jugular veins during ventricular systole?

A

Tricuspid valve.

364
Q

What is the normal duration for the PR interval?

A

0.12-0.2 seconds.

365
Q

What ECG lead yields complexes that are normally inverted compared to the anterior and inferior leads?

A

Lead aVR.

366
Q

Is there a point in the cardiac cycle when both atrial and ventricular diastole occur together?

A

Yes: when the ventricles are relaxing and the atria are filling (before atrial contraction).

367
Q

Why does an increase in LVEDV signify heart failure?

A

Heart failure is the inability to pump blood out of the heart. There is blood remaining at the end of systole. The blood therefore accumulates and so LVEDV increases.

368
Q

Which pressure is most likely to increase in left sided heart failure?

A

LV EDP.

369
Q

Which pressure is most likely to decrease in left sided heart failure?

A

Mean aortic pressure. (Less blood is being pumped into the aorta).

370
Q

What is stenosis?

A

Narrowing.

371
Q

Which pressure is most likely to increase in mitral valve stenosis?

A

Left atrial end-systolic pressure.

372
Q

What does it mean if a heart valve is incompetent?

A

It is regurgitant.

373
Q

Which pressure is most likely to increase when the aortic valve is incompetent?

A

Left ventricular end-diastolic pressure.

374
Q

Pulmonary oedema is a sign of what?

A

Left heart failure.

375
Q

What can severe pulmonary hypertension cause?

A

Right heart failure.The heart has to pump harder to get blood into the pulmonary circulation due to an increased afterload.

376
Q

Shortness of breath, severe peripheral oedema and ascites after a heart attack can indicate what?

A

Biventricular failure.

377
Q

What is ascites?

A

Accumulation of fluid in the peritoneal cavity, this can cause abdominal swelling.

378
Q

How long is the PR interval on an ECG?

A

0.12-0.2 seconds.

379
Q

What does the PR interval represent?

A

The slow conduction between the AVN and the His-Purkinje system.

380
Q

Diastole: what is diastasis?

A

When LVp = LAp. Net movement of blood is zero. This is the time between ventricular suction and atrial contraction.

381
Q

What branch does the right coronary artery give off as it reaches the inferior border of the heart?

A

The right marginal branch.

382
Q

What artery does the RCA anastomose with on the diaphragmatic surface of the heart?

A

The circumflex artery.

383
Q

What does the LAD anastomose with on the diaphragmatic surface of the heart?

A

The posterior inter-ventricular branch of the RCA.

384
Q

Where is the coronary sinus found?

A

Between the LA and LV - left atrio-ventricular sulcus.

385
Q

What does the coronary sinus drain into?

A

The RA.

386
Q

What artery arises from the RCA in 90% of hearts, the circumflex in 30% and in 20% arises from both the RCA and circumflex?

A

The posterior inter-ventricular branch.

387
Q

What equation explains why small changes in the diameter of a blood vessel have a great effect on the resistance to flow of a fluid through that vessel?

A

Poiseuille’s equation. Q=r^4.

388
Q

What is the role of fibrinogen in platelet aggregation?

A

It forms cross-links between aggregating platelets.

389
Q

Give 2 reasons why the liver is important in clotting.

A
  1. The liver produces many clotting factors. 2. The liver produces bile salts that are needed for vitamin K absorption. Vitamin K is needed for clotting factor production.
390
Q

When are the platelet receptors for fibrinogen exposed?

A

During platelet activation.

391
Q

Which of the ABO blood groups is recessive?

A

O, A and B are co-dominant.

392
Q

Why is the O blood group a universal donor?

A

It has no A or B antigens.

393
Q

What are the two ways of determining someones ABO blood group?

A
  1. Test using antibodies. 2. Test for the presence of antibodies against A or B antigens.
394
Q

Describe how testing for the presence of antibodies against A or B antigens will determine someones blood group?

A

The presence of antibodies in the blood will indicate that this person does not have these antigens on their RBC’s. For example, if a persons blood is found to contain antibodies against the B antigen then they can’t be of the AB or B blood groups.

395
Q

Describe how testing using antibodies will determine someones blood group?

A

If the antibodies bind it indicates the presence of a specified antigen. For example, if antibodies against the B antigen bind to the patients RBC then the person must be of either the AB or B blood groups.

396
Q

What are antigens are part of the Rhesus blood group system?

A

C, D and E.(D is the most important).

397
Q

What problems can arise if a pregnant lady is found to be rhesus D negative?

A

If exposed to D RBC’s the lady will have antibodies against the D antigen. The antibodies can cross the placenta and cause haemolysis of the babies red blood cells. This can result in in-utero death.

398
Q

What can be given to rhesus D negative mothers to prevent sensitisation?

A

Anti-D.

399
Q

Describe the arterial baroreceptor reflex in response to an increase in blood pressure.

A
  • Increased parasympathetic outflow to the heart means contractility and heart rate are reduced and so cardiac output is reduced: CO=HRxSV.
  • Decreased sympathetic outflow to the arterioles results in vasodilation and so TPR is reduced.
  • BP=COxTPR and so blood pressure is lowered.
400
Q

Describe the arterial baroreceptor reflex in response to a decrease in blood pressure.

A 
#- Increased sympathetic outflow to the heart means contractility and heart rate are increased and so cardiac output is increased: CO=HRxSV.
- Increased sympathetic outflow to the arterioles results in vasoconstriction and so TPR is increased.
  • BP=COxTPR and so blood pressure is increased.
401
Q

What phase of the cardiac action potential coincides with diastole?

A

Phase 4.

402
Q

What part of the ECG does the plateau phase of the cardiac action potential coincide with?

A

ST segment

403
Q

Give 4 factors that affect the gating of ion channels.

A

Voltage, drugs, hormones, temperature.

404
Q

What is Virchow’s triad?

A

It describes 3 categories thought to contribute to thrombosis.

405
Q

What are the 3 categories of Virchow’s triad?

A
  1. Stasis of blood flow. 2. Endothelial injury.3. Increased coagulation ability.
406
Q

Define ischaemia.

A

A decrease in blood flow to a tissue.

407
Q

Define infarction.

A

No blood flow to a tissue - tissue death.

408
Q

Explain the formation of fluid exudate in inflammation.

A

Chemical mediators cause vasodilation of vessels and an increase in permeability.

409
Q

What are the roles of lymphatics in acute inflammation?

A

Lymphatics drain exudate and carry antigens.

410
Q

What happens in phase 4 of the cardiac action potential?

A

Pacemaker potential - Na+ inflow and slowing of K+ outflow. Slow depolarisation begins = innate contractility.

411
Q

Where is Ca2+ released from in excitation contraction coupling?

A

The T tubules and the sarcoplasmic reticulum.

412
Q

What is the resting potential of the SA node?

A

-55 to -60 mV.

413
Q

How do central chemoreceptors respond to an increase in PaCO2?

A

Vasoconstriction.

414
Q

Why do central chemoreceptors stimulate vasoconstriction in response to an increase in PaCO2?

A

They act to counter the affect of CO2 as a vasodilator and so maintain blood flow to tissues.

415
Q

What reaction does adenyl cyclase catalyse?

A

The conversion of ATP into cAMP.

416
Q

How do muscarinic M2 receptors cause a decrease in cAMP?

A

They inhibit adenyl cyclase.

417
Q

What 2 channels are closed during the refractory period in a cardiac action potential?

A

Fast Na+ and Ca2+ channels.

418
Q

What surface of the heart does the RCA supply?

A

Inferior.

419
Q

What is the normal duration of the PR interval?

A

120-200ms.

420
Q

What would an absent P wave on an ECG be a sign of?

A

Atrial fibrillation.

Year 1 Medicine (25 decks)

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