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zFoundations of Pathophysiology > Topic 8 - CardiovascularDisease > Flashcards

Topic 8 - CardiovascularDisease Flashcards

1
Q

What is atherosclerosis?

A

hardening/thickening of artery walls

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2
Q

What are the causes of atherosclerosis?

A

endothelial damage, platelet adhesion to endothelium, LDL accumulation, oxidation and glycation of LDL, fatty streaks, ulceration, rupture

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3
Q

What is ischemic heart disease?

A

-atherosclerosis affecting coronary arteries and the narrowing of coronary vessels

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4
Q

What is ischemia?

A

cell deprivation of blood and oxygen, symptoms = angina, breathlessness

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5
Q

What is myocardial infarction?

A

complete occlusion of coronary arteries and damage to heart muscle

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6
Q

What is the difference between systemic and pulmonary circulation?

A

Systemic: heart and body
Pulmonary: heart and lungs

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7
Q

What is the cardiac cycle?

A

mechanical and electrical events in one beat

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8
Q

What is diastole?

A

relaxation phase, ventricles untwist, lengthen and unthicken for filling

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9
Q

What is systole?

A

contraction phase, ventricles twist, shorten and thicken for rapid blood ejection

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10
Q

What are the diastolic events of the cardiac cycle? (mechanical)

A
  1. ventricles are relaxed and fill passively
  2. atrial systole - atria contract to eject blood into ventricles
  3. isovolumentric ventricular contraction - ventricles contract but valves are closed
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11
Q

What are the systolic events of the cardiac cycle?

A
  1. rapid ejection of blood from ventricles (semi-lunar valves open)
  2. isovolumetric ventricular relaxation - decreased pressure to close semi-lunar valves
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12
Q

What is the entire process of the cardiac cycle?

A
  1. ventricles are relaxed and fill passively
  2. atrial systole - atria contract to eject blood into ventricles
  3. isovolumentric ventricular contraction - ventricles contract but valves are closed
  4. rapid ejection of blood from ventricles (semi-lunar valves open)
  5. isovolumetric ventricular relaxation - decreased pressure to close semi-lunar valves
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13
Q

Define heart rate

A

number of cardiac cycles per minute

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14
Q

Define stroke volume

A

vol of blood pumped from ventricles in one heart beat

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15
Q

Define cardiac output

A

HR x SV, blood pumped out in one min

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16
Q

Define ejection fraction

A

% end diastolic volume (EDV) pumped in one heart beat

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17
Q

What is preload?

A

workload imposed on ventricle prior to contraction

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18
Q

What is the Frank-Starling mechanism?

A

ability of the heart to change force of contraction, therefore SV, in response to changes in venous return.
-the force of contraction of heart is directly proportional to the initial length of muscle fibres

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19
Q

What is afterload?

A

force required to eject blood from the heart

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20
Q

What does afterload depend on?

A
  • systemic vascular resistance

- ventricular wall tension

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21
Q

What is the difference between positive and negative inotropic agents?

A

+ increase contractility

- decreased contractility

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22
Q

What is blood pressure?

A

pressure exerted on arterial walls

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23
Q

What is the formula for blood pressure?

A

cardiac output x total peripheral resistance

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24
Q

What is systolic BP?

A

pressure during ventricular contraction

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25
Q

What is diastolic BP?

A

pressure during ventricular filling

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26
Q

What is the role of ADH in blood pressure?

A
  • causes retention of water by kidney
  • vasoconstrictor
  • increased blood volume
  • alters permeability of DCT
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27
Q

What is the role of the RAAS system in blood pressure?

A

low Na+ –> renin released by kidneys –> angiotensin I –> angiotensin II by ACE (angiotensin converting enzyme) –> aldosterone released

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28
Q

What is hypertension?

A

constant elevation of systemic arterial blood pressure, resulting from sustained TPR and increased blood volume

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29
Q

What are the three types of hypertension?

A

primary/idiopathic - most common, systolic and diastolic hypertension
secondary - caused by underlying disease
isolated systolic/diastolic

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30
Q

What are some risk factors of hypertension?

A

low K+ in diet, alcohol, diabetes, age, race, family history, gender, high cholesterol, obesity, physical inactivity, smoking, high Na+ intake

31
Q

What are the consequences of hypertension?

A

stiffness of arteries, left heart failure, stroke, kidney failure, blindness

32
Q

What is the use of an ECG?

A

diagnostic tool that detects electrical disturbances and abnormalities in heart rhythm

33
Q

What are the phases of the electrical activity of the heart?

A

depolarisation (Na+ influx)) –> rapid repolarisation (K+ out) –> plataeu (balanced movement) –> repolarisation (overall -ve) –> diastolic depolarisation (resting membrane potential)

34
Q

What is the P wave?

A

atrial depolarisation, contraction

35
Q

What is the QRS complex?

A

ventricular depolarisation, commencement of ventricular systole, masks atrial repolarisation

36
Q

What is the T wave?

A

ventricular repolarisation, -ve membrane potential

37
Q

What are the layers of blood vessels?

A

tunica adventitia: CT –> collagen
tunica media: smooth muscle, elastic fibres
tunica intima: direct contact with blood, endothelium

38
Q

What is the pathogenesis of atherosclerosis?

A
  • intra-aterial fat deposts enter into intima

- it hardens and causes occlusion to blood flow

39
Q

What is pathophysiology of atherosclerosis?

A
  1. injury to tunica media - dysregulated parainflammatory response
  2. macrophages
  3. macrophages oxidise to foam cells
  4. foam cells -> fatty streaks
  5. plaque formation –> blockage, emobolism
40
Q

What are some examples of injurious environments for atherosclerosis?

A

smoking, hypertension, diabetes, increased LDL, decreased HDL, insulin resistance, infection, oxidative stress

41
Q

What is the progression of atherosclerosis?

A

injury - inflammation - macrophages - foam cells - fatty streak - fibrous plaque - complicated plaque or embolism

42
Q

What is coronary artery disease?

A

any vascular disorder which narrows/occludes coronary arteries

43
Q

What are some risk factors of coronary artery disease?

A

hypertension, smoking, diabetes, obesity, sedentary lifestyle, infection

44
Q

What is the process of coronary artery disease?

A

decreased myocardial blood supply - ischaemia - acute coronary syndrome - infarction

45
Q

What is heart failure?

A

inability of the heart to adequately pump blood to meet metabolic requirements

46
Q

Systolic heart failure

A

-inability for heart to pump blood efficiently

47
Q

Left sided heart failure

A

blood backed up to lungs

48
Q

What are the causes of systolic left sided heart failure? left

A

coronary atherosclerosis: plaque buildup - less blood to heart tissue - damage to myocardium - death or scar tissue
long standing hypertension: harder for LV to pump blood into hypertensive state, hypertrophy of LV (greater demand for oxygen), increased bulk squeezes coronary arteries
dilated cardiomyopathy: chamber grows in size, can work for a little while but muscle becomes weaker and thinner until failure, eccentric hypertrophy

49
Q

What is diastolic heart failure? Left

A

concentric hypertrophy, less room for blood, no change in ejection fraction, decreased preload

50
Q

What are the causes of diastolic heart failure?

A
  • aortic stenosis: narrowing of aortic opening
  • restrictive cardiomyopathy - stiffer and less compliant
  • RAAS system - increased preload: increased fluid retention - increased contraction strength (Frank-Starling), BUT fluid leaks into lungs and builds up: difficult gas exchange, increased pressure, pulmonary oedema
51
Q

What is right-sided heart failure?

A
  • often caused by left-sided heart failure
  • inability for RV to provide enough blood to supply pulmonary circulation
  • caused by L to R cardiac shunt (hole between left and right) –> high to low pressure
52
Q

What is diastolic right sided failure?

A

concentric hypertrophy of RV - smaller volume

53
Q

What is systolic right sided failure?

A

chronic lung disease, increased pressure in pulmonary vessels

54
Q

What are the symptoms of right-sided heart failure?

A

liver failure, pitting oedema in legs/sacrum

55
Q

What are risk factors for heart failure?

A

circulating LDL (hyperlipidemia), hypertension, diabetes, insulin resistance, increased sodium intake, smoking, hypertrophic cardiomyopathy

56
Q

What is an aneurysm?

A

excessive, localised enlargement of an artery or balloon-like buldge of blood, caused by weakening of arterial walls

57
Q

Where are aneurysms common?

A

common in areas of weakness, vulnerability, high pressure

58
Q

What are the types of aneurysms?

A

Fusiform: symmetrical
Sacular: hangs off to one side
Extra-vascular haematoma: weakened area, hole in artery

59
Q

What are the signs and symptoms of an aneurysm?

A

severe pain, pulsating mass in area of pain, hypotension in ruptured aneurysm

60
Q

What is a thombosis?

A

coagulated mass of aggregated platelets, RBC and fibrin that form locally

61
Q

What is an embolism?

A

piece of thombus that has broken free inside a vessel and circulates around the body

62
Q

What is haemostasis?

A

process involving platelets and factors in response to blood vessel injury in order to decrease blood loss

63
Q

What is the difference between a primary and secondary haematoma?

A

1: platelet plug creation
2: reinforcement by fibrin

64
Q

What does haemostasis involve?

A

platelets, blood proteins (clotting factors), vasculature

65
Q

What is the role of platelets?

A

contribute to regulation of blood flow (vasoconstriction), initiate interactions (platelet plug), initiate clotting cascade (stabilise plug), initiate repair process

66
Q

How is a platelet activated?

A

when a vessel is damaged, through: adhesion, activation, degranulation, aggregation

67
Q

What is a clot?

A

a meshwork of protein (fibrin) to stabilise a plug and trap other cells

68
Q

What are the purposes of a clot?

A

plug damaged vessel, trap microorganisms, framework for healing

69
Q

What is the process fora clot development?

A
  1. release clotting factors from injured tissue and platelets
  2. formation of thombin
  3. formation of fibrin
70
Q

What are the two parts of the coagulation cascade?

A
  1. intrinsic (contact activation)

2. extrinsic (tissue factor)

71
Q

When do the two parts of the coagulation cascade join?

A

factor X is the common pathway

72
Q

Intrinsic/contact activation

A

activated by presence of abnormal/damaged vessel

73
Q

Extrinsic/tissue factor

A

tissue factor released by damaged endothelium

zFoundations of Pathophysiology (10 decks)

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