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IK1 - LSS > Cardiovascular System > Flashcards

Cardiovascular System Flashcards

1
Q

Describe the excitation-contraction coupling of the heart including specific receptors.

A

Depolarisation causes the opening of L-type calcium channels. This leads to influx of calcium into the myocyte. The calcium then binds to the Ryanodine receptor and leads to the release of calcium from the sarcoplasmic reticulum.

SERCA then takes the calcium from the cytoplasm back into the SR. The Na/Ca exchanger pumps out as much calcium as entered the cell in the first place.

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2
Q

Compare the length-tension relationship in skeletal and cardiac muscle

A

Cardiac muscle is much more resistant to stretch. Cardiac muscle exerts a lot more passive force.

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3
Q

What are the two types of cardiac contraction? What are the differences between the two?

A

Isometric and isotonic

Isometric contraction is when the muscle length does not shorten and contract.

Isotonic contraction the muscle fibres shorten.

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4
Q

What is preload?

A

The weight that stretches the muscle before it is stimulated to contract

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5
Q

What is afterload?

A

The weight that is not apparent to the muscle in the resting state and is only encountered once the muscle has started to contract

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6
Q

What is the effect of increasing preload? What is the in vivo implications of preload?

A

Increasing preload increases the force exerted by the muscle fibres. In the heart this increases the stroke volume.

End diastolic volume. This is when venous returns stretches the muscle fibres before contraction.

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7
Q

What is the effect of increasing afterload? What is the in Vivo implications of afterload?

A

Increasing afterload decreases the amount of shortening of muscle fibres and decreases the velocity of shortening fibres.

Blood pressure in the vessels leaving the ventricles

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8
Q

State starlings law. What are the 2 factors leading to the law?

A

Increase in diastolic fibre length increases ventricular contraction.

  1. Changes in the number of myofilament cross-bridges
    2 changes in the calcium sensitivity of the myofilaments
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9
Q

What is stroke work and the equation for stroke work? What are impacts the factors of the equation?

A

Stroke work is work done by the heart to eject blood under pressure into the aorta and pulmonary artery.

Stroke work = stroke volume x pressure
SV is greatly affected by preload, afterload and contractility
Pressure is influenced by structure

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10
Q

State the law of Laplace.

A

When the pressure within a cylinder is kept constant, tension increases with increasing radius.

T= PxR
Tension = pressure x radius
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11
Q

What is the physiological relevance of the law of Laplace with regard to the structure of the right and left ventricles? What is the clinical significance?

A

The left ventricle has a smaller radius of curvature than the right ventricle meaning that the left ventricle is able to generate higher pressures with similar wall tension.

In dilated cardiomyopathy, the radius of curvature increases and hence the pressure generated decreases

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12
Q

State the different phases of the cardiac cycle in order

A

Atrial systole ➡️ isovolumic contraction ➡️ rapid ejection ➡️ reduced ejection ➡️ isovolumic relaxation ➡️ rapid ventricular filling ➡️ reduced ventricular filling

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13
Q

What is end systolic volume?

A

Volume left in ventricle at the end of contraction

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14
Q

What is end diastolic volume?

A

Volume in ventricle at the end of the filling phase.
- made up of end systolic volume + amount passively added to ventricle during atrial diastole + amount added by atrial systole

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15
Q

What is stroke volume? What’s the equations for it?

A

Volume of blood ejected by ventricular contraction

Stroke volume = end diastolic volume - end systolic volume

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16
Q

What is the ejection fraction and what is the equation?

A

The ejection fraction is the percentage of the end diastolic volume ejected

Ejection fraction = stroke volume/end diastolic volume

It is dependent on physical state and should normally be around 65% but in heart failure patients may be closer to 35%

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17
Q

What is the cardiac output and what is the equation?

A

Cardiac output is the amount of blood ejected by each ventricle in one minute

Cardiac output = heart rate x stroke volume
Unit = ml/min

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18
Q

What happens during atrial systole? What changes can be seen on an ECG? What abnormal heart sound may be heard and what could the underlying cause be?

A

During atrial systole the blood flows possible throughout open atrio-ventricular valves into the ventricle. Atrial systole (contraction) tops off blood volume. Atrial depolarisation is triggered by SA node.

ECG: P wave indicating atrial depolarisation
Abnormal heart sound: sound S4 may be heard indicating valve incompetency. Causes: pulmonary embolism, congestive heart failure and tricuspid incompetence

  • jugular pulse may be felt as atrial contraction pushes some venous blood into jugular vein
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19
Q

What happens in isovolumic contraction? What changes can be seen on the ECG? What heart sounds can be heard? What are pressure and volume changes occur?

A

The atrioventricular valves are closing and the semi-lunar valves are opening. When valves are closed isometric contraction of ventricles starts (no shortening of muscle fibre lengths) - in this stage known as isovolumic contraction.

There is a rapid increase in pressure heading to aortic pressure, no volume change.
ECG: QRS complex indicates ventricular depolarisation
Heart sounds: S1 is heard due to valves closing - Lub sound

When pressure exceeds aortic pressure (afterload) the aortic valves opens and ejection starts

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20
Q

What is angiogenesis? What is the general process?

A

This is the formation of new blood vessels by sprouting from pre-existing vessels

Hypoxia ➡️ release of chemicals ➡️ EC receptor binding (intracellular signalling) ➡️ EC activation ➡️ EC proliferation ➡️ directional migration ➡️ ECM remodelling ➡️ tube formation ➡️ loop formation ➡️ vascular stabilisation

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21
Q

What happens during rapid ejection? What changes can be seen on an ECG and heart sounds heard?

A

The aortic and pulmonary valves (semi-lunar) open as pressure in ventricles exceeds pressure in vessels. Ventricular contraction leads to a decrease in ventricular volume.

Nothing seen on ECG and no heart sound.
c wave is seen in arterial pressure caused by RV contraction pushing against tricuspid valve leading to small wave in jugular vein.

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22
Q

What happens during reduced ejection? What changes can be seen on an ECG and heart sounds heard?

A

This is the end of SYSTOLE
blood leaves ventricles slowly and ventricular pressure falls till vessel pressure>ventricular pressure and valves begin to close.

T wave seen on ECG as ventricular repolarisation occurs
no heart sounds as valves haven’t closed in this phase

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23
Q

What happens during isovolumic relaxation? What ECG changes and heart sounds can be detected?

A

Beginning of diastole. the pulmonary and aortic valves have shut and AV valves are also shut. The atria are filling with blood increasing in volume and pressure.

v wave in atrial pressure caused by blood pushing on tricuspid valve giving a second jugular pulse.
DICHROTIC NOTCH: small sharp increase in aortic pressure due to rebound of pressure against aortic valve as aorta relaxes

S2 heart sounds heart at valves closing “dub”
no ECG changes

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24
Q

What happens in rapid ventricular filling? What changes on an ECG or heart sounds can be detected during this phase?

A

AV valves open and blood flows rapidly from atria to ventricle. Ventricular volume increases and atrial pressure decreases. PASSIVE FILLING no atrial systole.

ECG: nothing seen
ABNORMAL HEART SOUND: S3 and is a sign of turbulent ventricular filling which may be due to hypertension or mitral incompetance

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25
Q

What happens in reduced ventricular filling? What changes on an ECG or heart sounds can be detected during this phase?

A

Slow filling of ventricle known as diastasis where ventricular volume increases slowly. There are no changes on an ECG and no heart sounds

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26
Q

What is the normal blood pressure in the systemic and pulmonary system?

A

Systemic: 120/80 mmHG
Pulmonary: 25/5 mmHG

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27
Q

What do the points on a pressure-volume loop represent?

A 
Point 1 (bottom right) = end diastolic volume 
Point 2 (top right) = aortic valve opening 
Point 3 (top left) = end systolic volume 
Point 4 (bottom left) = mitral valve opening
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28
Q

on a pressure volume loop, how is the stroke volume represented?

A

The stroke volume is the difference between point 2 and 3

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29
Q

What are the four parts/groups of the heart that enable conduction through the heart?

A 
SA node
Inter-nodal fibre bundles
AV node
Ventricular bundles 
- bundle branches
-purkinje fibres
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30
Q 
How do these things effect an ECG?
Depolarisation towards +ve electrode
Depolarisation away from +ve electrode 
Re-polarization towards +ve electrode
Re-polarization away from +ve electrode
A

Depolarisation towards +ve electrode = upward inflection
Depolarisation away from +ve electrode = downward
Re-polarization towards +ve electrode = downward
Re-polarization away from +ve electrode = upward

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31
Q

Where do the 4 Limb leads of an ECG go?

Where do the Chest leads go?

A

Limb leads: right foot (zero reference point), right foot, left arm, left foot

Chest leads:
V1: 4th intercostal space right of sternum
V2: above but on the left
V3: between V2 and V4
V4: 5th intercostal space at midclavicular line
V5: left anterior axillary line (V4 level)
V6: (V5 level) mid-axillary line left (under armpit line)

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32
Q

How are the augmented limb leads created?

A

aV-R: right arm is positive, negative is halfway between left arm and left foot

aV-L: left arm is positive, negative is halfway between right arm and left foot

av-F: left foot is positive, negative is halfway between right and left arm

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33
Q

What is a normal QRS axis?

A

-30 degrees - +90 degrees

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34
Q

What can the QRS tell you?

A

orientation of the heart, thickness of ventricular muscle and abnormalities in the direction of ventricular depolarisation

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35
Q

What does an increased P wave amplitude and duration indicate?

A

atrial hypertrophy
long with 2 waveforms = left
large amplitude = right

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36
Q

What does ST depression look like on an ECG and what may it signify?

A

ST waveform is below the isoelectric line and may signify drugs, MI, ventricular hypertrophy

development during exercise is due to myocardial ischaemia

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37
Q

What is sinus tachycardia?

A

heart rate over 100. common and is an abnormally fast resting heart rate and is often physiological response to insult e.g. infection

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38
Q

What is atrial fibrillation?

A

220-430 atrial bpm and ventricular rhythm

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39
Q

What is the equation for blood flow?

A

blood flow = difference in pressure/resistance

units = L/min

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40
Q

What are the 2 variable that impact resistance? What is the equation linking them?

A
  • viscosity
  • length of tube
  • inner radius of tube

resistance = 8 x length x viscosity / pie x radius^4

In the body blood viscosity can change but in most situations it is fairly constant, the length is fixed so to change resistance the radius of the vessel is altered

41
Q

What are the 2 ways of calculating MABP

A

MABP = DP + (1/3x PP)
where PP = SP-DP

OR MABP = CO x TPR

42
Q

What types of blood flow exist?

A

Laminar flow and turbulent flow

43
Q

What is laminar flow?

A

this is where blood flows in stream lines which don’t interfere with one another. Laminar flow leads to high shear stress which promotes epithelial survival and quiescence

44
Q

What is turbulent flow?

A

These can be heard and it where the blood is not travelling in stream lines. Turbulent flow can lead to variable velocity which may decrease shear stress contributing to pathophysiology. low shear stress results in endothelium proliferation and apoptosis

turbulent flow found at bifurcations

45
Q

What is shear rate? what is the equation for shear stress?

A

Shear stress = shear rate x viscosity
shear rate = velocity gradient - the difference between the blood in the middle and that slowed by adherence forces by the vessel wall

46
Q

What are the function of vascular endothelium?

A

vascular tone management, thrombostasis, absorption and secretion, barrier and growth

47
Q

What molecules promote vasodilation?

A

nitric oxide and prostacylcin

48
Q

What molecules promote vasoconstriction?

A

thromboxane, endothelin-1 (however can have mild vasodilatory effects), angiotensin II

49
Q

Describe the synthesis of nitric oxide.

A

(ENDOTHELIUM CELL) A stimulant will bind to G protein couple receptor which activated phospholipase C. Phospholipase C converts PIP2 ➡️ IP3 and DAG. IP3 moves to Er where it stimulates calcium efflux. The rise in intracellular calcium uprefulates nitric oxidase synthetase.
this catalyses L-arginine + oxygen ➡️ L-citrulline +NO

50
Q

Describe how NO leads to vasodilation of vessels.

A

NO moves into smooth muscle cells where it up-regulates the activity of guanylyl cyclase which converts GTP ➡️cGMP. cGMP upregulates Protein Kinase G leading to relaxation of smooth muscle and vasodilation

51
Q

Describe how prostacyclin is synthesised.

A

Phospholipid ➡️ arachidonic acid by phospholipase A2.
Arachidonic acid ➡️ prostaglandin H2 by cyclooxygenase enzymes
Prostaglandin H2 ➡️ prostacyclin by prostacyclin synthetase

52
Q

What other molecules can be made from arachidonic acid?

A

leukotrienes via lipooxygenase enzymes
Thromboxane
Prstacyclin

DAG can also be converted into arachidonic acid by DAG lipase

53
Q

How does prostacyclin lead to vasodilation?

A

Binds to IP receptor on smooth muscle which is coupled to adenylate cyclase leading to ATP ➡️ cAMP. this upregulates Protein Kinase A leading to relaxation and therefore vasodilation

prostacyclin is also anti-atherogenic and anti-platelet

54
Q

Describe how thromboxane is synthetised.

A

Phospholipid ➡️ arachidonic acid by phospholipase A2.
Arachidonic acid ➡️ prostaglandin H2 by cyclooxygenase enzymes
Prostaglandin H2 ➡️ Thromboxane A2 via thromboxane synthase

55
Q

How does thromboxane mediates it’s effects?

A

for VASOCONSTRICTION thromboxane binds to beta receptors on smooth muscle. THe beta receptors are couple with phospholipase C which converts PIP2 ➡️ IP3. IP3 mediates contraction ➡️ vasoconstriction

If thromboxane binds to alpha receptors on platelets it leads to platelet activation as well as stimulating further production of thromboxane

56
Q

How is endothelin-1 synthesised?

A

Endothelin precursor is produced in the nucleus and cleaved by endothlin converting enzyme to produce endothelin-1.

57
Q

How does endothelin-1 mediate it’s effects?

A

VASOCONSTRICTION: endothelin-1 binds to alpha and beta receptors on the smooth muscle. The receptors are coupled to phospholipase C which leads to PIP2➡️ IP3 triggers calcium influx which leads to contraction

On bindindg to endothelium cells it triggers the activation of nitric oxidase synthetase enzyme so more NO is produced leading to dilation

antagonists: PGI2, NO, ANP, heparin, HGF, EGF
agonists: adrenaline, ADH, angiotensin II, IL-1

58
Q

Describe angiotensin II synthesis

A

Angiotensinogen is produced by the liver. Juxtaglomerular cells in the kidney will secrete renin in response to signals from the macula densa cells (kidney) in response to salt concentration combined with low BP (detected by juxtaglomerular).

Angiotensinogen ➡️ Angiontensin I via renin
Angiotensin I ➡️ Angiotensin II via ACE (angiontensin converting enzyme)

59
Q

How does angiotensin II mediate it’s effects?

A

Angiontensin II binds to angtiotensin receptor on vascular smooth muscle which activates phospholipase C. PIP2 ➡️ IP3 . IP3 leads to an influx in calcium and contraction triggered

some receptors are G protein coupled and upregulate vascular smooth muscle growth

60
Q

How does bradykinin mediate it’s effects? what degrades bradykinin?

A

bradykinin ➡️ bradykinin receptor-1 ➡️ activate phospholipase C
PIP2➡️ IP3 ➡️ upregulate NO ➡️ vasodilation

ACE breaks down bradykinin

61
Q

What are the effects of angiotensin II?

A
  • rapid pressure response in periphery and slow pressor response in kidney
  • constricts vessels increased TPR
  • enhances peripheral noradrenaline
  • acts on adrenal cortex to release aldosterone
  • stimulates ADH release
  • stimulates cardiac and vascular hypertrophic response
  • increase Na+ reabsorption in the proximal tubule
62
Q

How can you pharmacologically manipulate the renin-angiotensin system?

A 
loop diuretics: prevents renin release
NSAIDS: block renin release
ACE inhibitors
At1 blockers: block vasoconstriction
Alpha 1 and beta 1 blockers: inhibit receptor activity in kidney so no renin release
63
Q

What are the subdivisions of adrenoceptors? What are they coupled to?

A

alpha: excitatory effects on smooth muscle
- couples to G protein linked receptors. Activates phospholipase C so PIP2➡️ IP3, calcium increases and constriction occurs

beta: relaxant effect on smooth muscle, stimualtory effect on heart
- activates adenyl cyclase converting ATP to cAMP and decreasing intracellular calcium

64
Q

What effects on the cardiovascular systen so noradrenaline, adrenaline and isoprenaline have?

A

Noradrenaline: increase SBP, DBP, MABP, decreases heart rate

adrenaline: increases SBP, MABP and heart rate, decreases DBP
isoprenaline: increases SBP and heart rate, decreases DBP and MABP

65
Q

What are the major resistance vessels in the body? What functions does the alteration of radius achieve?

A

Arterioles
Radius changes to accomplish:
1. match of blood flow to metabolic need of tissues
2. help regulate arterial blood pressure

66
Q

What are the 3 types of capillary structures and describe them.

A

Continuous: mostly continuous with small water filled gap junctions allowing movement of small substances

Fenestrated: leakier - slightly larger gaps allowing large substances to pass through

discontinuous: large holes allowing things such as cells to pass through. e.g. needed in bone marrow

67
Q

What are some causes of heart failure?

A

arrhythmias, valve disease, pericardial disease, congenital heart disease, myocardial disease, hypertension, some drugs (over using beta blockers, calcium antagonists)

68
Q

What is heart failure?

A

a clinical syndrome cause by abnormality of the heart and recognised by a characteristic pattern of haemodynamic, renal, neural and hormonal responses.

69
Q

What are causes of dilated cardiomyopathy?

A

genetic, idiopathic, infections, toxins, drugs, collagen disorders, autoimmune, neuro-muscular

70
Q

What are some causes of restrictive cardiomyopathy?

A

associated with fibrosis which may occur due to:

diastolic dysfunction, infiltrative disease, storage disorders, endomyocardial disorders.

71
Q

signs and symptoms of heart failure?

A

ankle swelling, exertional breathlessness, fatigue, nocturia, orthopnoea, tachycardia, oedema, large liver, ascites.

72
Q

What drugs are commonly used to treat heart failure?

what treatment is there for those with severe heart failure?

A

diuretics, ACi inhibitors, beta blockers, aldosterone antagonsists, digoxin (treats AF), internal defibrillator

severe: IV forms of drugs above, fluid control, surgery (cardiomyoplasty), transplant

73
Q

What are the risk factors for cardiovascular disease?

A

smoking, physical inactivity, alcohol, unhealthy diet, hypertension, obesity, diabetes, hyperlipidaemia

74
Q

What 3 things contribute to thrombosis?

A

abnormal vessel wall, abnormal blood flow, abnormal blood constituents.

75
Q

What happens in remodelling of the left ventricle?

A

this can occur from an MI. The heart muscle expands, the scar thins and there is impairment of the heart.

LV dilation, in the non-infarcted area hypertrophy and myofilament dysfunction and there may be issues with conduction of electrical signals
as a result wall tension increases, mitral regurgitation, arrhythmias.

76
Q

What is autoregulation?

A

the intrinsic capacity to compensate for changes in perfusion pressure by changing vascular resistance.

77
Q

What are the 2 theories that could explain why when BP drops there is a gradual decrease in resistance and so flow increases slowly.

A

MYOGENIC THEORY: smooth muscle fibres respond to stretch (stress operated ion channels) as pressure rises, the muscle fibres start contraction to keep flow constant.

METABOLIC THEORY: if vessels supplying a vascular bed contract, the flow to the bed decreases and the bed produces more metabolites. The increase in metabolites it feels back on the vessel supplying the bed stimulating vasodilation therefore allowing more flow.

78
Q

What hormones are involved in systemic regulation of blood flow?

A
  • kinins (interact with renin-angiotensin system)
  • atrial natriuretic peptide (secreted from atria when stretched and leads to vasodilation)
  • circulating vasoconstrictors (e.g vasopressin, angiotensin II, noradrenaline)
79
Q

Where is the vasomotor centre located and what does it consist of?

A

located bilaterally in medulla and lower third of pons

consists of:

  • vasoconstrictor centre
  • vasodilatory centre
  • cardio-regulatory inhibitory area

high centres in the brain can influence the vasomotor centre

80
Q

What leads to change of arteriole radius?

A

The main control is the sympathetic nervous system which releases noradrenaline leading to constriction
- NOTE EXCEPTION: in skeletal muscle vasodilation occurs by cholinergic fibres, the sympathetic nerves actually trigger vasodilation

other things that impact radius:

  • local controls: oxygen, K+, CO2, H+, osmolarity, metabolites, injury agents
  • plasma epinephrine
81
Q

How is the heart innervated and how does this lead to control of heart rate?

A

the heart has dual innervation of sympathetic and parasympathetic - SA node receives signals

sympathetic ➡️ adrenaline and noradrenaline increase gradient potential meaning threshold reached more quickly and heart rate increases

parasympathetic ➡️ acetylcholine decreases gradient of pacemaker potential, harder to reach threshold decrease in HR

82
Q

How does the sympathetic system increase heart contractility?

A

noradrenaline binds to adrenoceptors ➡️ increasing of cAMP ➡️ activated PKA which phosphorylates the L-type calcium channel ➡️ SR release Ca2+ as Ryr receptor activated.

NOTE: parasympathetic has no effect on contraction

83
Q

whbat are the 2 ways of changing the stroke volume?

A

Changing end-diastolic ventricular volume (preload) which increases the contraction of the heart (starlings law)

changing activity of sympathetic activity to the heart altering contraction force as more Ca2+ becomes available and changing the intracellular stores

84
Q

What nerve connects the carotid sinus baroreceptor to the vasomotor centre? What nerve connects the aortic arch baroreceptor to the vasomotor centre?

A

carotid sinus = via glossopharyngeal nerve

aortic arch = via vagus nerve

85
Q

Why does blood pressure drop when standing if no compensatory mechanisms occur?

A

When you stand gravity pulls blood down to vessels in the legs. In the veins venous distension occurs increasing the amount of blood in the venous reserve, this decreases venous return of the heart so stroke volume declines leading to TRANSIENT HYPOTENSION.

86
Q

What compensatory mechanisms occurs when we stand to correct the transient hypotension? what happens if they do not occur?

A

Compensatory mechanisms: carotid baroreceptors decrease firing and cardiopulmonary receptors signal to brainstem the decrease in venous return.

This leads to reduction of parasympathetic activity and increased sympathetic to heart.

  • increases heart rate by 15-20 bpm and increase contractility
  • vasoconstriction in skeletal muscle, splanchic and renal vascular beds so TPR increases by 30-40%

if these fail you may feel dizzy and in some cases faint

87
Q

What happens in haemorrhage? How does the body compensate?

A

The venous return to the heart decreases.

compensatory: reflex tachycardia and peripheral vasoconstriction. HOW?:
- low pressure in kidney ➡️ increased angiotensin activity ➡️ increased aldosterone.
- increased vasopressin secretion
- reduced blood flow to kidney so less urine made and fluid retention
- decreased baroreceptor firing so increased sympathetic
- organ specific vasoconstriction

if capillary pressure falls osmotic pressure of plasma proteins dominates ➡️ intersitial fluid absorbed back into blood preserving BP.

88
Q

How much blood lose can be compensated for?

A

10% can be compensated with up to 30% being manageable. over 30% may lead to shock (very likely to lead to shock)

89
Q

What problems does exercise present to the CVS system?

A

1) increased pulmonary blood flow - enhance gas exchange
2) increasing blood flow to working muscles
3) stable blood pressure maintained

90
Q

What compensatory response occurs during exercise?

A

vasodilation leading to decreased resistance.
increased sympathetic activity increased heart rate/cardiac activity
there is an increase in CO and blood flow to vessels where resistance has reduced (skeletal muscle)

91
Q

What is primary haemostasis?

A

Primary haemostasis is initiated by the exposure of collagen and other matrix proteins to blood when vessel is damaged. Collagen binds to platelets directly and captures platelets leading to the formation of a PLATELET PLUG

92
Q

What is secondary haemostasis?

A

secondary haemostasis occurs when the coagulation cascade is initiated by blood coming into contact with tissue factor. The cascade is a series of enzymes and co-factors resulting in a rapidly increasing concentration of THROMBIN.

thrombin ➡️ soluble fibrinogen ➡️ insoluble fibrin which forms clot holding platelet plug together. Clot is secured by FXII cross-linking to fibrin.

Later the clot is dissolved

93
Q

What is the intrinsic pathway, extrinsic pathway and common pathway of the clotting cascade?

A

INTRINSIC PATHWAY: involves activation of zymogen which is a precursor of protease for factor XII
Factor XII ➡️ factor XIIa (active) ➡️ factor XI activated and the cascade continues

EXTRINSIC PATHWAY: the vessel is damage and the blood comes into contact with tissue factor which binds to factor VII activating it leading to factor X being activated.
- factor Xa converts pro-thrombin ➡️ thrombin

common pathways is where the above converges to the same pathway and this is at factor X ➡️ Xa

94
Q

What are defects of primary haemostasis?

A

ageing weakens the vessel wall which may lead to an unstable platelet plug formation.

Von Willebrand Factor - no VWF means no primary haemostasis

Drugs such as aspirin that can affect platelet activity

95
Q

What are some defects of secondary haemostasis?

A

Haemophilia - factor 8 or 9 due to genetic mutations
liver disease- lots of factors are synthesis in the liver
Drugs: warfarin, inhibition of coagulation factor synthesis
Dilution: results from volume replacement
Consumptive coagulopathy: acquired and leads to generalised activation of coagulation via tissue factor
- associated with sepsis, major tissue damage and inflammation

96
Q

What blood pressure is considered hypertension?

A

above 140/90 mmHg

97
Q

Describe what happens to LDLs after endothelial activation (atherosclerosis)

A

Endothelial activation increases the membrane permeability. LDL enter and are oxidised by free radicals and become stuck in subendothelial layer. Oxidised LDLs are phagocytosed by macrophages to form foam cells. The foam cells accumulate and cause chronic inflammation. The foam cells accumulate fat and die by apoptosis releasing cytotoxic fat and contributing to the lipid necrotic core of the atherosclerotic plaque.

98
Q

What conditions count as coronary artery disease?

A

sudden cardiac death, acute MI, unstable angina, stable angina, heart failure and arrhythmia

IK1 - LSS (5 decks)

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