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CV lectures > CV important > Flashcards

CV important Flashcards

1
Q

what is the percentage of plasma in the blood

A

55%

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2
Q

what is in the buffy coat of the blood

A

1%

platelets and leukocytes

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3
Q

what is the percentage of red blood cells in the blood

A

45%

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4
Q

what are the components of the plasma

A

water
electrolytes
hormones
proteins (carrier, immunogloblins, clotting factors)

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5
Q

where are Erythrocytes (RBC’s) made and with what hormone

A

liver in foetus, bone marrow in adults

hormone: erythropoietin

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6
Q

describe the structure of RBC’s

A

biconcave, anucleate

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7
Q

lifespan of RBC’s

A

120 days

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8
Q

what is a haematocrit

A

percentage of blood occupied by RBC’s

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9
Q

what are the 3 sites of haemolysis

A

spleen
bone marrow
lymph nodes

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10
Q

what causes a high haematocrit

A

excessive RBC production and dehydration

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11
Q

what causes a low haematocrit

A

anaemia

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12
Q

what is anaemia and what are the 2 types

A

haemoglobin deficiency
types:
impaired production
increased haemolysis

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13
Q

what are the 2 categories of leukocytes

A

agranulocytes

granulocytes

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14
Q

what are the 3 subtypes of granulocytes

A

basophils
eosinophils
neutrophils

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15
Q

what are the 2 subtypes of agranulocytes

A

monocytes

lymphocytes

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16
Q

what is the role of neutrophils

A

phagocytosis

front-line defence during acute inflammation

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17
Q

what is the role of eosinophils

A

combats parasite infections

neutralises histamine

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18
Q

what is the role of basophils

A

responsible for anaphylaxis

produces histamine

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19
Q

what is the role of monocytes

A

only monocytes when in blood
differentiate into macrophages inside tissue
phagocytoses foreign material
e.g. Kupffer cells

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20
Q

what are the 3 types of lymphocytes

A

T-cells
B-cells
Natural killer cells

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21
Q

how does the structure of platelets change

A

Anucleate & discoid -> become spiculated with pseudopodia once activated

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22
Q

what is the function of platelets

A

haemostasis

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23
Q

how and where are platelets produced

A

liver & kidneys
thrombopoietin
derived from megakaryocytes

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24
Q

what is haemostasis

A

the process to prevent & stop bleeding

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25
Q

describe the stages of primary haemostasis

A 
Platelet plug formation
4 steps (Vessel injury -> Adhesion -> Activation -> Granule release -> Aggregation
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26
Q

what is involved in secondary haemostasis

A

coagulation cascade

fibrin clot formation

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27
Q

how to platelets bind to collagen

A

via vWF using their receptor GP1B

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28
Q

describe the activation stage of haemostasis

A

Once bound to the subendothelium, platelets change shape

Platelets release alpha and electron dense granules, to escalate haemostasis process

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29
Q

name examples of Alpha granules

A

vWF, Thromboxane, fibrinogen

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30
Q

name examples of electron-dense granules

A

ADP, Ca2+, Serotonin

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31
Q

what happens during the aggregation stage of haemostasis

A

Lots of platelets join the party and bind to each other using GP2b/3a receptors and fibrinogen

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32
Q

name 4 important factors in the coagulation cascade

A

IIa: Thrombin
Ia: Fibrin
XIIIa: Fibrin-stabilizing factor
IV: Ca2+

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33
Q

what are the Vitamin-K dependent factors in the coagulation cascade

A

X, IX, VII, II

1972

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34
Q

what are the stages of the fibrinolytic pathway

A

plasminogen -> plasmin -> fibrin breakdown

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35
Q

what are the 2 types of blood transfusion

A

Homologous (emergency transfusion)

Autologous (self-transfusion)

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36
Q

Rh+ facts

A

contains D-antigen, no antibodies
can receive from both Rh+ and Rh-
only donates to Rh+

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37
Q

Rh- facts

A

contains no antigens, and anti-D antibodies
can donate to both Rh- and Rh+
only receives from Rh-

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38
Q

describe week 3/4 formation of the primitive heart tube

A

Visceral Mesoderm -> 2x Heart Tubes -> Fuse (Lateral folding) -> Craniocaudal folding (“Shrimp”) -> Heart tube has divisions now

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39
Q

what are the divisions of the primitive heart tube

A 
truncus arteriosus 
bulbus cordis
primitive ventricle 
primitive atrium 
sinus venosus
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40
Q

what does the truncus arteriosus become

A

> Ascending aorta

> Pulmonary trunk

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41
Q

what does the bulbus cordus become

A

> Smooth (outflow) parts of L & R ventricles

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42
Q

what does the primitive atrium become

A

> both auricular appendages
Entire L atrium
Anterior part of R atrium

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43
Q

what does the primitive ventricle become

A

> Forms majority of ventricles

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44
Q

what does the sinus venosus become

A

> Smooth part of R atrium
Vena cavae
Coronary sinus

45
Q

what does the 1st aortic arch become

A

maxillary

46
Q

what does the 2nd aortic arch become

A

stapedial

47
Q

what does the 3rd aortic arch become

A

common carotids (part of internal carotids)

48
Q

what does the 4th aortic arch become

A

left -> aortic arch

right -> right subclavian

49
Q

what does the 6th aortic arch become

A

pulmonary arteries

left -> ductus arteriosus

50
Q

when does the heart appear and start beating

A

3rd week

beating = day 23

51
Q

what is obstetrical climbing

A

constriction of umbilical vein > ligamentum teres

52
Q

what are the 3 layers of the heart

A

Epicardium – adipose tissue, vessels & nerves underlying the pericardium
Myocardium – thickest layer that contracts
Endocardium – inner layer of the heart, made of endothelial cells

53
Q

what are the 3 layers (tunics) of blood vessels

A 
Tunica intima (endothelial layer)
Tunica media (muscle layer)
Tunica adventitia  (connective tissue)
54
Q

what is myosin comprised of

A

2x heavy chains

4x light chains

55
Q

what is actin

A

polymerised globular protein with troponin and tropomyosin incorporated

56
Q

what is Titin

A

elastic filaments that maintain alignment of sarcomere

57
Q

what is tropomyosin

A

Binds to Actin and blocks its Myosin binding site

58
Q

what is troponin

A

Binds to Tropomyosin, unlocked by calcium

59
Q

describe excitation-contraction coupling

A

AP spreads into myocytes via T-Tubules -> Ca2+ channels open , enters muscle cell -> binds with troponin -> uncovers active site on tropomyosin

60
Q

what is the force of contraction directly proportional too

A

levels of cytosolic Ca2+

61
Q

what do drugs which increase myocardial contractility do

A

increase cytosolic calcium levels e.g. adrenaline

62
Q

what is the first stage of the cardiac cycle (ventricular systole)

A

isovolumetric contraction
ventricular p > atrial p so AV valves close
arterial p>Ventricular p so SL valves closed

63
Q

what is the 2nd stage of the cardiac cycle (ventricular systole)

A

Ejection
ventricular p> arterial p so SL valves open and blood ejected out
atria begin to fill with blood

64
Q

what is the 3rd stage of the cardiac cycle (diastole)

A

isovolumetric relaxation

ventricular p

65
Q

what is the 4th stage of the cardiac cycle (diastole)

A

passive blood flow
atrial p> ventricular so AV valves open
70-80% of blood passively fills the ventricles

66
Q

what is the 5th stage of the cardiac cycle (diastole)

A

atrial booster
Extra kick to move the remaining blood out of the atria
PR interval

67
Q

what are the 3 factors affecting stroke volume

A

preload
afterload
contractility

68
Q

what is the Frank-Sterling law

A

States that stroke volume depends on force of contraction
Increased EDV -> increase stretch of the myocardium -> increase sarcomere length -> increase length of overlapping filaments -> increased force of contraction -> increased stroke volume

69
Q

5 factors that affect preload

A 
atrial contractility 
venous return 
ventricular compliance 
valvular resistance 
heart rate
70
Q

increased contractility

A 
Increases FoC -> increases SV
Positive inotropic agents:
 Sympathethic nervous system
 Hormones: adrenaline, thyroxine
 Drugs: e.g. Digoxin
71
Q

decreased contractility

A

Decreases FoC  Decreases SV
Negative inotropic agents:
Parasympathetic nervous system
Drugs: e.g. β-blockers

72
Q

what is afterload

A

Ventricular wall stress during systole
The amount of resistance the ventricles must overcome during systole
Basically the same as systolic blood pressure
Indirectly proportional to SV (unlike preload)

73
Q

what 3 factors affect afterload

A

valvular diseases
aortic pressure
SVR/TPR

74
Q

what is the pacemaker potential generated by

A

Nodal cells 1%
primary pacemaker - SA node
latent pacemakers - AV node, bundle of His, Purkinje

75
Q

what is the sympathetic stimulation of the pacemaker potential

A

Noradrenaline = increases Ca2+ channel opening = faster depo.
Steeper Phase 0
Increases heart rate and force of contraction

76
Q

what is the parasympathetic stimulation of the pacemaker potential

A

Decreases heart rate
ACh activates potassium channels = Hyperpolarizes membrane = longer to reach TP
Also decreases calcium influx= decreases slope of pacemaker potential

77
Q

what is the absolute refractory period?

A

Period where the cell is completely unexcitable

Longer for cardiomyocytes

78
Q

what is the relative refractory period?

A

when a greater than normal stimulus can depolarise the cell

79
Q

describe the path of action potential

A

SAN → Bachmann’s Bundle (left atria) + RA cardiomyocytes → AVN (only A-V connection) → Bundle of His → Purkinje fibres (R/L)

80
Q

what is AV nodal delay

A

0.1 ms

Allows atrium to fully contract/ventricular filling

81
Q

p wave

A

atrial depolarisation

82
Q

PR segment

A

AVN delay & atrial contraction

83
Q

QRS complex

A

ventricular depolarisation

84
Q

ST segment

A

space between Ventricular depo. and repo.

85
Q

T wave

A

Ventricular repo.

86
Q

mean arterial pressure =

A

CO x TPR

87
Q

what is systolic pressure

A

point when LV pressure during ejection = aortic pressure during ejection

88
Q

what is diastolic pressure

A

Pressure caused by recoiling of arteries during diastole

89
Q

pulse pressure =

A

SP - DP

90
Q

velocity of blood flow =

A

blood flow/area of vessel

91
Q

factors affecting resistance

A

Viscosity
Vessel length
Vessel radius

92
Q

blood pressure =

A

CO x TPR

93
Q

role of baroreceptors

A 
sense changes in BP
Aortic body = increase
Carotid body = both
Signal via CNs to Nucleus tractus Solitarius to CV control centres in Medulla
Negative feedback
94
Q

how changes in CO2 control BP

A

chemical chemoreceptors
Increase CO2 -> diffuses into CSF (react w/ H2O)
H2CO3 > H+ and HCO3-
Decrease pH of CSF
Activation of vasomotor region of medulla (CV control centre)

95
Q

name some major vasoconstrictors

A 
local = endothelin-1
hormonal = adrenaline, ADH, angiotensin 2
neural= cardiovascular control centre
96
Q

name some major vasodilators

A

local= NO, Lactic acid
Hormonal=Adrenaline, ANP
Neural = CV control centres

97
Q

where can the aortic valve be heard

A

2nd intercostal space, right sternal border

98
Q

where can the tricuspid valve be heard

A

5th intercostal space, left sternal border

99
Q

where can the mitral valve be heard

A

5th intercostal space, mid-clavicular line

100
Q

where can the pulmonary valve be heard

A

2nd intercostal space, left sternal border

101
Q

Cardiac output

A

The amount of blood ejected by each ventricle per minute. CO = SV * HR. ~5-6 L/min.

102
Q

stroke volume

A

The volume of blood ejected by each ventricle with each beat ~70 mL.

103
Q

heart rate

A

The number of times the heart beats per minute. 60-100 per minute

104
Q

end-diastolic volume

A

Volume of blood in each ventricle at the end of diastole ~130 mL.

105
Q

ejection fraction

A

Percentage of end-diastolic volume ejected with each beat. SV/EDV. 65%.

106
Q

end-systolic volume

A

Volume of blood remaining in each ventricle at the end of systole ~50 mL.

107
Q

mean arteriole pressure =

A

diastolic pressure + 1/3 PP

108
Q

stroke volume =

A

EDV - ESV

109
Q

Poiseuille’s equation:

A

radius to the power of 4

CV lectures (30 decks)

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