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EM: > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

how much of the blood is fluid and how much is plasma?

A

45% cellular 55% fluid

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2
Q

what is the lifespan of erythrocytes?

A

120 days but usually regenerated every 30 days

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3
Q

what is the lifespan of platelets?

A

7-10 days

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4
Q

3 important haemopoietic growth factors

A
  • Erythropoietin (EPO)
    • red cells
  • Granulocyte Macrophage Colony Stimulating Factor (GM-CSF)
    • white cells
  • Thrombopoietin
    • platelets
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5
Q

Male and Female normal erythrocyte count

A
  • Female
    • ~4 x 1012 / L
  • Male
    • ~5 x 1012 / L
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6
Q

Haemoglobin structure

A
  • a tetramer of two alpha chains and two beta chains
  • each has a central porphyrin ring with an Fe2+
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7
Q

five types of anaemia

A
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8
Q

what is haematocrit

A

the ratio of the volume of red blood cells to the total volume of blood

often presented as a percentage

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9
Q

what is mean corpuscular haemoglobin

A

a measure of the average mass of haemoglobin per red cell

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10
Q

what is corpuscular volume

A

the measure of the average volume of a red blood cell

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11
Q

Acute anaemia

A

due to blood loss

low haemoglobin but haematocrit remains at 45%

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12
Q

Chronic anaemia

A

due to inflammatory disorders or malignancy

reduced Hb and reduced haematocrit (~20%)

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13
Q

iron deficiency anaemia

A
  • poor diet, malabsorbtion, chronic bleeding
  • low mean corpuscular volume
  • low mean corpuscular haemoglobin
  • hematocrit remains at 45%
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14
Q

Megaloblastic anaemia

A
  • Macrocytosis
  • abnormally large RBCs (high MCV)
  • reduced production of normal RBCs leads to low Hb
  • this can be caused by liver disease, alcohol abuse and hypothyroidism
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15
Q

B12 and Folate

A
  • These are required for DNA synthesis
  • they affect all dividing cells but blood cells first
    • bone marrow is the most active source of dividing cells
  • B12 absorbtion requires intrinsic factor from gastric parietal cells
    • pernicious anaemia is AA disorder where these are destroyed
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16
Q

Haemolytic anaemia

A
  • red blood cell lifespan reduced to <30 days (120 is normal)
  • increased RBC production
  • increases haem turnover leading to jaundice and anaemia
  • can be inherited or congential
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17
Q

Neutrophil lifespan

A

6-10 hours

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18
Q

Monocyte lifespan

A

20-40 weeks

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19
Q

Lymphocyte lifespan

A

weeks to years

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20
Q

Basophil and eosinophil lifespan

A

days

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21
Q

what is the most numerous white blood cell in the blood

A

neutrophils

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22
Q

how many lymphocytes are T cells and how many are B cells?

A
  • 20% of lymphocytes are B cells
  • 80% of lymphocytes are T cells
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23
Q

summarise what all the different types of white blood cells do

A

monocytes also turn into macrophages (phagocytosis) and dendritic cells (APC)

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24
Q

what kind of proteins are soluble in plasma?

A

albumin

immunoglobulins

clotting proteins

carrier proteins

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25
Q

Haemophilia A is the deficiency of which clotting factor

A

VIII

remember 8 sounds like A

treated with recombinant factor VIII

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26
Q

Haemophilia B

A

Deficiency of factor IX

treat with recombinant factor IX

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27
Q

what is haemostasis and what are the three overall steps?

A

the arrest of bleeding

three steps:

  1. vasoconstriction (endothelin 1 and neural control)
  2. formation of platelet plug
  3. coagulation - platelet plug reinforced with a fibrin mesh
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28
Q

what happens following damage to a blood vessel

A
  • blood vessel constricts due to neural control and endothelin-1
  • two endothelial surfaces of the vessell stick together
  • permanent closure due to constriction and contact stickiness only occurs in microvasculature
  • in order to arrest bleeding there must first be the formation of a platelet plug and then the coagulation cascade
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29
Q

Platelet plug formation

A
  1. disrupted endothelium exposes collagen fibres
  2. platelets adhere to these via von willebrand factor
  3. platelet binding causes them to activate and degranulate
    • activation = formation of spines so greater surface area and up-regulation of glycoprotein receptors on their surface
  4. these glycoprotein receptors bind fibrinogen
  5. old platelets bind new ones and they all aggregate
    • they are sort of cross linked by fibrinogen
  6. platelets contain actin and myosin - this allows contraction and strengthening of the plug
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30
Q

what stops the platelet plug expanding into normal endothelium

A
  • healthy endothelium secretes prostaglandin which is a vasodilator and inhibits platelet aggragation
  • healthy endothelium also secretes NO2 which is a vasodilator and an inhibitor of adhesion, activation and aggregation
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31
Q

what is the difference between the intrinsic and the extrinsic pathway of coagulation

A
  • Extrinsic - a cellular component from outside the blood is needed
  • Intrinsic - all factors required are found in the blood
  • the extrinsic pathway is the most common initiator
  • thrombin links the two pathways
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32
Q

Intrinsic pathway of coagulation

A

Roman numerals should be used

  • factor 12 is activated to factor 12a when it is exposed to collagen
  • factor 12a catalyses the activation of factor 11 into 11a
  • factor 11a catalyses the activation of factor 9 into factor 9a
  • factor 9a catalyses the activation of factor 10 into factor 10a
    • here factor 8a is used as a cofactor
  • factor 10a is the factor that converts prothrombin to thrombin
  • thrombin converts soluble fibrinogen to insoluble fibrin fibres ]
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33
Q

Extrinsic pathway of coagulation

A
  • begins with tissue factor which is not a plasma protein but a protein that is located on the outer plasma membrane of various cells outside the endothelium
  • tissue factor binds factor 7 which is activated to factor 7a
  • complex of tissue factor and factor 7a then catalyses the activation of:
    • factor 10 into factor 10a
    • factor 9 into factor 9a
  • factor 9a activates more factor 10
  • factor 10a activates prothrombin into thrombin
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34
Q

give an example of a cell that expresses tissue factor

A

fibroblasts

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35
Q

thrombin feedback

A
  • activates factors 11 and 8 of the intrinsic pathway (positive feedback)
  • thrombin activates platelets
  • the amount of thrombin generated using only the extrinsic pathway is not enough to clot properly
  • possitive feedback is essential for a clot to form
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36
Q

two reasons liver damage causes poor clotting

A
  • the clotting factors ( including prothrombin) are produced in the liver
  • the liver produces bile salts which are essential for the absorbtion of fat soluble vitamins
    • vitamin K is a fat soluble vitamin
    • Vitamin K is needed for post translational modification of clotting factors 2, 7, 9 and 10. (1972)
    • NB factor 2 is prothrombin
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37
Q

draw and annotate a sarcomere

A
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38
Q

what is the I band

A

Only thin filaments

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39
Q

what are the z lines

A

these cross only thin filaments and they define the boundary of one sarcomere

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40
Q

what is the H zone

A

this is the area on the sarcomere with only thick filaments

this reduces with contraction

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41
Q

what is the m line?

A

this is the centre of the H zone - down the middle of the sarcomere

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42
Q

Thin filaments

A
  • actin is globular and monomers plymerise to form two intertwined helical chains
  • each actin molecule has a binding site for myosin
  • tropomyosin lies in the groove between the two actin filaments, covering the myosin binding site
  • troponin is a protein on the tropomyosin
    • it can change shape when it binds to Ca2+ and this moves the tropomyosin, exposing the myosin binding sites
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43
Q

Thick filaments

A
  • myosin
  • two large chains and four smaller chains
  • combine forming a molecule with two globular heads
  • globular heads form cross bridges with the neighbouring actin filament
  • each globular head has two binding sites
    • one for the thin filament and one for binding ATP
  • the ATP binding site is an ATPase that hydrolyses ATP and uses this energy for contraction
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44
Q

what is titin

A

Titin connexts the Z line to the M line

it is an elastic protein

it maintains the alignment of the sarcomere

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45
Q

what is the sarcoplasmic reticulum

A
  • this is a membrane network that surrounds the contractile proteins
  • it is the cell’s internal calcium store and can supply the calcium needed for contraction
  • releases calcium when ca2+ binds to its ryanodine receptor
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46
Q

describe the ion distribution inside and outside of a cardiomyocyte at rest

A
  • the inside of the cell is more negative than the outside (-90mV)
  • there’s more Ca2+ and Na+ outside of the cell
  • there’s more K+ inside of the cell
  • ATPase pumps 3Na+ ions out of the cell for every 2K+ ions pumped in
  • this maintains the membrane potential
  • Ca2+ moves across the membrane through calcium channels
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47
Q

Types of calcium channels in the heart

A

L-type channels and T-type channels

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48
Q

what are t tubules

A
  • these run from the cell’s surface to deep within the cell
  • they are continuous with the membrane
  • in the centre of the cell they form a network
  • they associate with the terminal cisternae
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49
Q

what is the pacemaker of the heart

A

the SA node

The pacemaker cells are modified cardiomyocytes that have lost the ability to contract

50
Q

what speed do electrical impulses travel through the heart?

A

1m/s

51
Q

Pacemaker action potential

A
  • there is no true resting potential in these cells
  • K+ travels out of the cell leading to hyperpolarisation (-60mV)
  • this triggers the hyperpolarisation activated cyclic nucleotide-gated (HCN) channels
  • Na+ slowly enters the cell through these channels causing diastolic depolarisation to (-40mV)
  • at -40mV Ca2+ ion channels open
  • rapid calcium influx depolarises to +20mV
    • this is the action potential
    • the action potential spreads from one cell to the other via gap junctions in intercalated discs
  • K+ then effluxes from the cell causing repolarisation
52
Q

HCN channels

A
  • unique to the heart
  • they are opened by catecholamines like noradrenaline
    • if more are open there’s faster transfer of Na+ into the cell
    • there’s faster reaching of -40mV threshold
    • there’s faster heartrate
  • they are closed by Ach
    • if fewer are open then there’s slower transfer of Na+ into the cell
    • slower reaching of -40mV threshold
    • and the heartrate slows
53
Q

myocardiocyte action potential

A
54
Q

Excitation contraction coupliung

A
  • Influx of calcium from the ECF (during the plateau) is not enough to induce contraction - Ca2+ from the sarcoplasmic reticulum is needed
  • T tubules contain more calcium channels than the rest of the membrane
  • Ca2+ enters the cell at the t tubule and binds the ryanodine receptor on the sarcoplasmic reticulum
  • this causes the SR to release even more Ca2+
    • ​this is calcium induced calcium release
  • Ca2+ binds to troponin causing the conformational change that allows tropomyosin to move and unblick
55
Q

when does contraction of the cardiomyocyte begin and end with reference to the graph

A

half way through the plateau phase and continues until the end of that phase

because of the plateau, cardiac muscle stays contracted longer than skeletal muscle

56
Q

what is the route of cardiac electrical conduction?

A
  • SA node across the atria (bachmann’s bundle)
  • across the atria down to the AV node
  • AV node delays impulse by 100-200 ms to allow the atria to empty
  • impulse travels from AV node down the bundle of His
  • Bundle of His divides into:
    • Left bundle
      • there’s left posterior and left anterior bundles too
    • Right bundle
  • On all sides purkinje fibres project up from the apex
57
Q

How long is the cardiac cycle?

A

0.8 seconds long

58
Q

how much of the cardiac cycle is systole and how much is diastole

A

systole: 1/3
diastole: 2/3

59
Q

when does systole begin with realation to the ECG and when does it end?

A
  • Begins at the peak of the QRS complex (when isovolumetric contraction begins)
  • Ends when the aortic valve closes - this is ~ the end of the T wave
60
Q

when do the atria fill?

A
  • blood is constantly dripping into the atria
  • during ejection they are filling
  • then during the majority of diastole blood is dripping straight through into the ventricles
61
Q

Label the ECG

A
62
Q

ECG normal timings

A
  • P wave: 0.08-0.1
  • QRS complex: 0.08-0.12 seconds
63
Q

how much of the blood’s circulation is in veins at any one point?

A

70%

64
Q

why do veins need a low pressure?

A

so that they can draw arterial blood through the capillaries

this is why being compliant is important for them

65
Q

Blood flow through organs

A
  • Liver - 27%
  • Kidneys - 22%
  • Muscle - 12%
  • Brain - 14%
66
Q

What vessels are the highest pressure

A

arterioles

67
Q

5 systems important for blood pressurea and circulation control

A
  • autoregulation
  • local mediators
  • hormonal factors
  • baroreceptors
  • neural control
68
Q

Myogenic autoregulation

A
  • if pressure increases in resistance vessels (arterioles) and they are stretched they respond by contraction of the smooth muscle cells
  • this reduces the size of the lumen
  • occurs until the diameter is normalised
  • they also dilate when blood pressure is low
  • this system evens out unecessary changes in perfusion pressure
69
Q

which tissues are good at myogenic autoregulation?

A
  • Good
    • Renal, cerebral and coronary
  • Bad
    • skin and muscle
  • so if you need to concerve circulation then it’s the skin that suffers
70
Q

local mediators of circulatory control

A
  • vasoconstrictors
    • endothelin-1
  • vasodilators
    • Hypoxia
    • adenosine
    • NO
    • CO2
    • H+

endothelin and NO are the main ones

71
Q

circulating hormonal factors that control blood pressure and circulation

A
  • vasoconstrictors
    • angiotensin II
    • vasopressin (ADH)
  • vasodilators
    • Arial Natriuretic Peptide
72
Q

where are the Baroreceptors

A
  • Primary
    • aortic arch
    • carotid sinus
  • Secondary are in the
    • veins
    • myocardium
    • pulmonary vessels
73
Q

How do baroreceptors work ?

A
  • their firing rate is proportional to the PP and the MAP
  • increased pressure causes them to fire more
  • these impulses are sent to the medulla and response to lower BP is initiated
    • increased stimulation of parasympathetic innervation of the heart
      • Vagus and Ach
    • decreased stimulation of sympathetic nervous system
  • this causes lowered cardiac output as well as lowered total peripheral resistance
    • BP falls
  • Reverse happens for low blood pressure
74
Q

baroreceptors in hypertensive patients

A
  • after a few days away from normal blood pressure, baroreceptors adapt to normal baseline
  • so baroreceptors are useful in the short term but do little in controlling blood pressure long term
75
Q

Neural control

A
  • most important tool for control of blood pressure
  • main neural influences on the medulla are from baroreceptors
  • The medulla
    • pressor region: sympathetic raising of the blood pressure
      • vasoconstriction
      • increased cardiac output (inc heart rate and stroke volume)
    • depressor region: parasympathetic lowering of blood pressure
      • it does this by inhibiting the pressor region
      • it also parasympathetically innervates the heart via the vagus
76
Q

what is hyperaemia

A

The increase of blood flow

77
Q

what is preload

A
  • the amount of filling of the ventricles
  • increased by anything that increases ventricular filling or stretch of cardiac muscle
    • i.e. aortic stenosis or ventricular systolic failure
  • Decreased by anything that reduces stretch or ventricular filling
    • i.e. mitral or tricuspid valve stenosis or atrial fibrilation
78
Q

what is afterload

A
  • this is the pressure aginst which the heart must work to eject blood during systole
  • increased afterload decreases stroke volume
  • depends on ABP and thickness of the ventricles
79
Q

what is end diastolic volume

A

this is the volume of blood in the ventricles at the end of diastole

80
Q

what is end systolic volume

A
  • end systolic volume is the volume of blood left in the ventricle at the end of systole
81
Q

what is stroke volume

A
  • this is the amount of blood pumped by the left ventricle into the aorta with each ventricular contraction
  • this is about 2/3 of the EDV
  • SV = EDV - ESV
82
Q

Frank Starling’s law of the heart:

A
  • if all other factors remain constant SV will increase in response to an increased EDV
  • this is due to the length tension relationship of muscle
  • so if there’s more blood in the ventricle, the ventricle will be more stretched and as a result will contract more forcefully
  • this doesn’t work forever - sometimes the heart becomes so stretched that it fails
83
Q

what is contractility

A

this is the force of heart muscle contraction - it is independent of sarcomere length

84
Q

what is elasticity

A

the tendancy for the heart to recoil following removal of a distending force (ventricular filling)

it is directly related to compliance

85
Q

what is compliance?

A
  • this is the ability of a tissue to resist recoil to its original dimensions on application of a distending force without allowing the pressure to increase a lot
  • directly related to elasticity
  • C = change in volume / change in pressure
  • blood vessels with a higher compliance are more likely to deform
    • veins
86
Q

what is resistance

A
  • this is the resisting force that must be overcome in order to push blood around the circulation and create flow
87
Q

what is total peripheral resistance

A
  • this is aka systemic vascular resistance
  • it is the total resistance offered by the entire vascular system
88
Q

Cardiac output equation

A
  • Cardiac output = heart rate / stroke volume
89
Q

what is normal cardiac output

A

5L/minute

90
Q

Blood pressure equation

A

blood pressure = cardiac output x total peripheral resistance

91
Q

what is pulse pressure

A

this is the systolic pressure minus the diastolic pressure

92
Q

what is mean arterial pressure

A

MAP = diastolic pressure + 1/3 pulse pressure

MAP = CO x TPR

93
Q

Ohm’s law

A

flow = change in pressure / resistance

94
Q

what is left ventricular filling pressure

A

this is the pressure that builds up in the ventricle as the ventricle is being filled with blood

95
Q

cardiac compensatory mechanisms during heart failure

A
  • frank starling mechanism
  • chronic ventricular dilation or hypertrophy
  • tachycardia
96
Q

autonomic compensatory mechanisms during heart failure

A
  • increased sympathetic adrinergic activity
  • reduced vagal activity to the heart
97
Q

Hormonal compensatory mechanisms during heart failure

A
  • renin - angiotensin - aldosterone system
  • vasopressin (ADH)
  • circulating catecholamines
    • Dopamine, epinephrine (adrenaline), and norepinephrine
  • Natriuretic peptides
98
Q

draw and label the heart tube and its bulges

A
99
Q

what does the bulbus cordis give rise to

A
  • the right ventricle
  • the outflow tracts of the left and right ventricle
    • i.e. the proximal aorta and the pulmonary trunk
100
Q

what does the primordial ventricle give rise to?

A

the left ventricle

101
Q

what does the primordial atrium give rise to?

A
  • left atrium
  • anterior portion of right atrium
  • left and right auricles
102
Q

what does the sinus venosus give rise to ?

A
  • the right atrium
  • the vena cava
  • the coronary sinus
103
Q

what does the aortic sac give rise to

A

the aorta and the pulmonary artery

104
Q

on what day does the heart begin to beat

A

22

105
Q

what is the truncus arteriosus

A

it is the primitive common outflow tract of the heart - it goes on to develop into the ascending aorta and the pulmonary trunk

106
Q

what are the endocardial cushions

A
  • when the heart is basically just a curly tube blood enters the common atria, travels through the atrioventricular canal and exits the ventricles through the truncus arteriosus
  • endocardial cushions grow at the sides of the AV canal and begin to partition it into two seperate openings
  • the right and left AV canals are formed
107
Q

formation of the aorta and the pulmonary artery

A
  • at the end of the 4th week a muscular septum grows up from the floor of the ventricle
  • an opening remains between the top of the septum and the bottom of the fused endocardial cushions
  • this is called the interventricular foramen
  • a spiral shaped septum called the aorticopulmonary septum grows up the truncus arteriosus and divides it
  • this forms the aorta and the pulmonary trunk
  • the aorticopulmonary septum grows down to fuse woth the cushions and the ventricular septum
  • the fusion of these three elements of the septum happens by week 8
108
Q

what do the first and second aortic arches become

A

they become minor arteries in the head

109
Q

what do the 3rd aortic arches become

A

these become the right and left common carotids

110
Q

what do the 4th aortic arches become

A
  • the right becomes part of the right subclavian
  • the left becomes part of the aortic arch
111
Q

what do the 6th aortic arches become

A

they become the pulmonary arteries

112
Q

Foetal circulation

A
  • oxygenated blood from the placenta enters the foetus in the umbilical vein
  • it bypasses the liver in the ductus venosus (later the ligamentum venosum) and enters the inferior vena cava
  • here it combines with deoxygenated blood
  • this blood enters the right atrium (along with SVC)
  • most of this is then shunted into the foramen ovale
  • any remaining blood that does enter the pulmonary artery will then be shunted into the aorta via the ductus arteriosus
  • deoxygenated blood returns to the placenta via the umbiliacal arteries originating from the internal iliacs near the bladder
113
Q

the first breath

A
  • the sudden oxygenation of the lungs causes the vasodilation of the respiratory system
  • this massively reduces the pressure in the pulmonary circulation
  • this causes the pressure in the right side of the heart to drop relative to the left
  • the foramen ovale snaps shut
    • within 3 months it has fused and produced the fossa ovalis
  • the umbilical vein constricts and forms the ligamentum teres
  • umbilical arteris constrict and form the medial umbilical ligaments
  • the ductus arteriosus constricts and forms the ligamentum arteriosum
  • the ductus venosus constrics and forms the ligamentum venosum
114
Q

Where does the SVC drain into

A

the right atrium at the 3rd rib

115
Q

what is the surface marking for the apex of the heart?

A

the 5th intercostal space in the mid-clavicular line

116
Q

how many people are right left and codominant

A
  • 70% right dominant
  • 10% left dominant
  • 20% codominant

dependant on which coronary artery supplies the posterior interventricular artery

117
Q

what does the posterior interventricular artery supply

A

it supplies the AV node

118
Q

papillary muscles

A
  • these attach to codi tendini
  • cordi tendini attach to the cusps of the AV valves
  • the papillary muscles contract during systole to prevent backflow of blood back into the atria
119
Q

how many cusps do the semi-lunar valves have

A
  • they have 3
  • these are the aortic and pulmonary valves
120
Q

what is ANP and what does it do

A
  • atrial natriuretic peptide is secreted by atrial myocytes when they get stretched
  • it promotes the excretion of water and sodium and potassium by the kidney
  • it inhibits the secretion of renin
121
Q

what are the two types of platelet granule

A
  • alpha granules containing:
    • clotting factors including fibrinogen
    • platelet derived growth factor
  • delta granule (aka dense bodies) containing:
    • ADP
    • Calcium
    • Serotonin
    • these are all platelet activating factors

EM: (14 decks)

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