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Clinical Ageing > Ageing Heart > Flashcards

Ageing Heart Flashcards

1
Q

How does Calcium transients contribute to raise in mmHg?

A

allows for ca2+ influx

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2
Q

describe the journey of calcium within cardiac myocytes

A
  1. Ca enters the sarcolemma
  2. Ca binds to sarcoplasmic reticulum and becomes an inorganic ion
  3. the inorganic ca binds to troponin c on the myofilament
  4. the molecule becomes SERCa2+ phospholamban
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3
Q

which has faster Ca2+ accumulation, adult cells or SC?

A

adult cells

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4
Q

what needs to be produced in order for the ca2+ to be transported?

A

production of ATP form mitochondrion form lactate, fat, glucose

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5
Q

what does a cardiac mri show?

A

structure and function of the heart

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6
Q

how does a cardiac mri work? (three things)

A
  1. using 31P to calculate PCr/ ATP ratios
  2. high resolution
  3. non invasive MR tagging
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7
Q

what does MR tagging show within a cardiac mri? (3 things)

A
  1. left ventricular mass
  2. blood pool volume
  3. ejection fraction
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8
Q

how do you calculate cardiac output?

A

CO= stroke volume x HR

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9
Q

How do you calculate ejection fraction?

A

EJ = (stroke vol/ end diastolic vol) x 100

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10
Q

how do you work out stroke volume?

A

difference between end-diastolic and end-systolic volume

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11
Q

at what time is the lowest blood pool volume?

A

400ms

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12
Q

what happens with CO with age?

A

it decreases

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13
Q

what happens to systolic bp with age ?

A

it increases

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13
Q

what happens to systolic bp with age ?

A

it increases

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14
Q

what happens to diastolic bp with age?

A

it decreases

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15
Q

what happens to the heart during heart failure

A

there is a reduction in the hearts ability to relax and contract

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16
Q

how many people in the UK have HF?

A

900,000

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17
Q

what percentage does HF relate to A/E admissions in the UK?

A

5%

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18
Q

what expenditure does HF contribute to?

A

2%

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19
Q

what are 4 risk factors for HF - reduced ejection fraction?

A

MI, alcohol, chemo, hypertension

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20
Q

how fast do symptoms of HF- rEF occur?

A

fast

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21
Q

what 3 things are risk factors for HF- pEF?

A
  1. hypertension
  2. diabetes
  3. obesity
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22
Q

how fast do symptoms of HF- pEF present?

A

gradual onset

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23
Q

what do pEF and rEF have in common?

A

similar symptoms which leads to terminal decline and death

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24
Q

in rEF, what occurs within neurohormonal activation?

A
  1. activation of sympathetic NS
  2. initial maintenance of arterial bp due to fall in CO
  3. leads to water retention, progressive LV re-modelling
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25
Q

what is the function of renin- angiotensin- aldosterone system?

A

regulate blood pressure and fluids

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26
Q

what do ACEi do and what does it treat?

A

an inhibitor of renin to angiotensin II

treats hypertension and reduces HF mortality

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27
Q

what is the function of ARB?

A

prevents angiotensin II binding to its receptor

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28
Q

what do beta blockers do?

A

produce negative chronotropic and inotropic effects

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29
Q

what are chronotropic effects?

A

the increase of heart rate

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30
Q

what are inotropic effects?

A

the increase of contractability

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31
Q

what are the adverse affects of using drugs to control RAAS system?

A

mainly only reduce bp - not actually treating HF
highly complex - patient needs to be in full understanding
electrolytes and renal function needs close monitoring
specialist care required - mdt

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32
Q

what causes HF- pEF?

A

rise in hypertension
atrial fibrillation
diabetes
ischaemic heart disease

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33
Q

what is the most common type of HF?

A

left ventricular systolic dsyfunction

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34
Q

what is the basis of HF- REF?

A

unpaired contractions

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35
Q

what is the basis of HF- PEF?

A

muscle thickening

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36
Q

what 3 drug classes are the most optimal way to treat HF?

A
  1. ACE inhib
  2. beta blockers
  3. mineralocorticoid antagonists eg aldosterone
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37
Q

name three ACE inhib

A
  1. ramipril
  2. lisonopril
  3. enalpril
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38
Q

what are the side effects of using ACE inhib?

A

dry cough, hyperkalaemia, renal impairments

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39
Q

where is renin release from?

A

renal juxtaglomerular apparatus

40
Q

what conditions leads to the release of renin?

A
  1. reduced na delivery to dct
  2. reduced perfusion pressure in kidney
  3. sympathetic stimulation of JGA via B1 adrenoreceptors
41
Q

where is angiotensin I produced?

A

liver

42
Q

where is angiotensin II produced?

A

lungs

43
Q

what affects do angiotensin II have on the cardio system

A

increase total peripheral resistance, which increases blood pressure
increases cardiac output

44
Q

what other systemic effects does angiotensin II have?

A

increases ADH secretion
more noradrenaline
increases na reabsorption within dct

45
Q

what does aldosterone do within the RAAS system?

A

increases na channel expression

increases na/k/ ATPase activity

46
Q

what hormone does angiotensin II stimulate the release of?

A

aldosterone

47
Q

according to PHE, 2019, how many global deaths are due to poor cardiovascular health?

A

17.9 million which is approximately 31%

48
Q

of the 17.9 million CVD deaths annually, how many are CHD?

A

9.43 million

49
Q

out of 17.9 million CVD global deaths how many are due to stroke?

A

5.78 million

50
Q

out of 17.9 million how many CVD deaths are from COPD?

A

3.04 million

51
Q

according to the BHF, 2022, how many people are living with heart/ circulatory diseases within the UK

A

7.6 million

52
Q

in the UK (BHF, 2022) how often does someone die from heart/ circ diseases?

A

every 3 mins

53
Q

in the UK (BHF, 2022) how often is someone admitted due to a stroke?

A

every 5 mins

54
Q

what percentage of the UK pop are born with CHD?

A

1-2 %

55
Q

what is the UK survival rate following a heart attack?

A

7/10

56
Q

what factors are responsible for CVD?

A

environment, genetics and ageing

57
Q

name some examples of treatable RF caused by the environment that contributes to the pathogenesis of heart diseases

A
  1. smoking
  2. stress
  3. diet
  4. exercise
58
Q

what medical conditions increases the risk of heart disease?

A

metabolic syndrome, central obesity, hypertension, high triglycerides, low density cholesterol, insulin resistance

59
Q

what is metabolic syndrome

A

cluster conditions that increases the risk of heart disease

60
Q

what are the pathological mechanisms causing heart disease?

A
  1. dysregulation of the cell cycle
  2. oxidative stress
  3. abnormal ca signalling
  4. vascular inflammation
61
Q

how does dysregulation of the cell cycle contribute to heart disease?

A

more senescent cells and no more division to create healthy cells

62
Q

how does oxidative stress contribute to heart disease?

A

the build up of reactive oxygen species and nitrogen species

63
Q

how does abnormal ca signalling contribute to heart disease?

A

linked to Ca inorganic/ K+ signalling

more hyperpolarisation which causes more small resistance arteries

64
Q

how does vascular inflammation contribute to heart disease

A

more endothelial dysfunction, leads to more arterial remodelling

65
Q

what is hyperuricemia and who is affected the most?

A

increased uric levels, highest in older women.

7mg/ dL

66
Q

what does the amount of SC show?

A

can be an independent predictor of mortality

contributes to arterial stiffness

67
Q

what happens to endothelial cells when they age?

A

become flatter/ enlarged with polypoid nucleus

68
Q

what is atherosclerosis?

A

hardening and thickening of the walls of arteries

69
Q

what is the aetiology of atherosclerosis?

A

caused by the buildup of plaque within inner lining of arteries. plaque made up of fatty substances, cholesterol, cellular waste products, ca2+, fibrin

69
Q

what is the aetiology of atherosclerosis?

A
  1. fatty deposits on the inner lining
  2. calcification of walls
  3. thickening of the muscular wall
70
Q

is atherosclerosis an inflam disease?

A

yes - categorised by the increased monocytes, macrophages, dendritic cells

71
Q

how does atherosclerosis result in a thrombus formation?

A

build up of lipid core - fibrous cap produced - rupturing causes platelets and then a thrombus is formed

72
Q

what happens when endothelial and platelets activate?

A

adhesions, differentiation to macrophages, proteolysis and chemotaxis

73
Q

how would you diagnose atherosclerosis?

A
  1. symptoms - angina pectoris, dsypnea
  2. ecg - can show heart attack
  3. echo - shows abnormal wall motion
  4. stress test - shows abnormal chamges in bp/ hr change in rhythm
  5. coronary CT imaging
  6. coronary angiography - maps vessels - identifies coronary stenosis
74
Q

what is the issue with atherosclerosis and treatment?

A

can only treat the symptoms

75
Q

how do you treat a stroke?

A

thrombolysis, embolectomy, medication to reduce blood pressure, break down blood clots

76
Q

how do you treat coronary heart syndrome?

A

if it progresses to acute MI - stent or bypass

77
Q

how do you treat aortic syndrome?

A

stent

78
Q

how do you treat peripheral artery occulsion?

A

anticoagulation, thrombolysis, embolectomy, percutaneous revascularisation, surgery

79
Q

how does AB1 -40 link to CVD?

A

amyloid- beta hypothesis in Alzheimer’s increases CVD risk

80
Q

what is veriguat?

A

a novel soluble granulate cyclase stimulator which enhances guanosine monophosphate pathway

81
Q

how is GMP linked to the heart?

A

GMP is a secondary messenger within nitric oxide pathway and NO is a vasodilator

82
Q

2020 ref, what happens to those with HF-rEF if they require hospitalisation within 1 yr of urgent treatment?

A

poor prognosis

83
Q

2020 ref, what condition is veriguat given for?

A

used for those with reduced EF and gives a better prognosis than the placebo in the study

84
Q

2020 ref, what are the side effects of veriguat?

A

more syncope, dsypnea - due to lower haemoglobin levels

85
Q

what is amyloid beta within cerebrovascular disease?

A

cerebral amyloid angiopathy

86
Q

what is the main amyloid beta peptide within the vascular system?

A

AB1-40

87
Q

where is AB1-40 found in cardiac system?

A

tunica media, smooth muscle cells and adventica, produced in platelets, plaque invading macrophages, endothelial cells

88
Q

what does high density lipoprotein and apolipoprteoiin E clear?

A

AB1-42 not AB1-40

89
Q

what does AB1-40 do to the heart? 2020 ref

A

more vasoconstriction, more ROS, telomere shortening - promotes vascular ageing
stimulates platelets activation and adhesions
predicts coronary artery disease mortality risk
atherothrombosis

90
Q

what NT is responsible for increasing heart rate?

A

acetylcholine

91
Q

what is meant by venous return drops?

A

drop in cardiac output and drop in mean arterial blood pressure

92
Q

what happens to baroreceptors when bp drops?

A

there is less tension applied to them and they are less stretched, so there is less neuronal firing to the medulla

93
Q

where is the vagal nerve that detects the increase in ventricular contractions?

A

it is the main PNS nerve, the mechanoreceptors in the aortic arch relay BP levels via vagal nerve fibres

94
Q

once the medulla has received the signal of drop in blood pressure causing vigorous ventricular contractions, what does the medulla do to increase BP and decrease HR to normal?

A

nucleus of solitary tract then activates neurones in the ventrolateral medulla that controls SNS that innervates neurones to increase HR

95
Q

in atherosclerosis, how does tissue hypoperfusion occur?

A

hypoperfusion is the the shock to tissues which is caused by narrowing of lumen of arteries, which leads to ischamia

96
Q

what is ischaemia?

A

insufficient blood supply

97
Q

in atherosclerosis, what happens if the plaques rupture?

A

acute thrombosis, acute artery occlusion, tissue death, organ failure and then death

Clinical Ageing (10 decks)

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