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Body Systems > L15 Cardiovascular diseases > Flashcards

L15 Cardiovascular diseases Flashcards

1
Q

death rates and stuff with CVD

A

causes biggest amount of deaths
1 in 3 deaths are CVD
been a steady decline in deaths by CVD as treatments and lifestyle changes inc

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2
Q

major diseases that you need to know

A

Affecting the vessels
- hypertension
- stroke
- coronary heart disease
- thrombosis

Affecting the heart
- valvular disease
- arrhythmia
- myocardial infarction
- heart failure

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3
Q

diagram for what diseases affect bwhat part of the cardiac output,
see onenote

A

:)

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4
Q

HYPERTENSION: what bp counts as high blood pressure

A

over 140mmHg/90mmHg

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5
Q

how does hypertension affect afterload and therefore the SV

A

increases the afterload
which increases ESV
and thus decreased SV

see notes on bp regulation

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6
Q

how does hypertension affect filtration

A

increases filtration
can lead to oedema (increase in fluid)
see notes on capillary exchange

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7
Q

how many people on avg are affected by hypertension in UK

A

about 15mil people
and 1/3 of these usually goes undetected

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8
Q

what is the main thing that makes hypertension so dangerous

A

its a big risk factor for many diseases

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9
Q

how does hypertension lead to coronary artery disease & myocardial infarction

A

accelerates ATHEROSCLEROSIS
by increasing damage to endothelial walls of coronary arteries

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10
Q

what is artherosclerosis btw

A

thickening or hardening of the arteries caused by a buildup of plaque in the inner lining of an artery

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11
Q

how does hypertension lead to aneurysms

A

aneurysm is when weakness in blood vessel wall develops
so can bulge under pressure

increased wall stress
leads to aneurysms
and also makes it more liekly to rupture

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12
Q

what vessel is prone to aneurysm

A

aorta

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13
Q

what type of aneurysm can lead to stroke

A

saccular aeurysm - in the cerebral circulation

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14
Q

what are the 2 types of stroke

A

haemorrhagic - when a blood vessel inside the skull bursts and bleeds into and around the brain
and ischaemic - when the blood supply to part of the brain is interrupted or reduced, preventing brain tissue from getting oxygen and nutrients

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15
Q

how does hypertension lead to stroke

A

damage to endothelial cells in the cerebral arteries

increasing atherosclerosis
which can lead to ischaemia by blocking arteries
or hamorragic by aneurysms that may form

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16
Q

how can hypertension damage the kidneys

A

can cause inc vasoconstriction of the renal arteries
and reduce blood supply to kidney

damaged the nephron and kidney function declines

causing chronic kidney disease

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17
Q

how can hypertension cause heart failure

A

chronic hypertension puts more strain on ventricles
by increasing afterload
and reducing cardiac output

the heart tries to compensate by hypertophy (when the organ literally increases in size via bigger cells)
this increases contractility
but it’s temporary and will decrease over time

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18
Q

Causes of hypertension:
2 classifications of causes - what is primary hypertension?

A

primary/essential hypertension:
= when no known cause
probs lots of contributing factors
e.g.
- genetic predisposition
- alcohol
- less excersise
- obesity
- diabetes
- intrauterine environment (maternal high bp can influence developing bp in later life)

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19
Q

Causes of hypertension:
2 classifications of causes - what is secondary hypertension?

A

when known medical cause of hypertension

e.g.

adrenal gland diseases
- pheochromacytoma (a tumour affecting this gland)
- leads to increased catecholamine production
- leads to more adrenaline circulating

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20
Q

how is chronic kidney disease a secondary cause of hypertension

A

chronic kidney disease
- less Na+ excretion
- more fluid retained
- so RAAS system is activated
(see BP reg notes)
- so inc vasoconstriction

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21
Q

how is endocrine disorders a secondary cause of hypertension

A

endocrine disorders
- diabetes (inc fluid, and inc arterial stiffness)
- cushings disease (when pituitary gland releases too much cortisol ie ACTH, and increased RAAS activation)

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22
Q

how is adrenal gland disease a secondary cause of hypertension

A

adrenal gland diseases
- pheochromacytoma (a tumour affecting this gland)
- leads to increased catecholamine production
- leads to more adrenaline circulating

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23
Q

treatment of hypertension: what are the 2 main things that treatments aim to fix for hypertension

A

reducing cardiac output
or
reducing vasocontriction

cuz BP = CO x total peripheral resistance

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24
Q

explain the 3 types of drugs that affect the RAAS system that is used to treat hypertension

A

all lead to RAAS inhibtion

  1. Angiotensin Converting Enzyme inhibitor (ACEi)
  2. Angiotensin II receptor blocker (ARB)
  • these 2 both reduce vasoconstriction cuz angiotensin causes vasoconstric
  1. Aldosterone antagonist (Spironalactone)
  • aldosterone stimulates Na+ and water reabsorption
  • so when this is stopped, this reduces Na+ and water reabsorption
  • reducing cardiac output
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25
Q

in treating hypertension, what do Ca2+ channel blockers do?

A

Ca2+ stiulates muscle contrarction
so this drug inhibits entry of Ca2+ into cardiac and vascular muscle cells

reducing contractility and strok volume
therefore reducing CO

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26
Q

in treating hypertension, what are thiazide diuretics

A

diuretics - effects kidney

this inhibits renal Na+ reabsorption
increasing water loss in uring

thus decreasing venous return
and EDV

reducing CO

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27
Q

in summary, what are the 3 main types of drugs used to treat hypertension

A
  • RAAS inhibitors
  • Ca2+ channel blockers
  • thiazide diuretics
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28
Q

what are the levels and classes of drugs used to treat hypertension

A

1 drug = target angiotensin or Ca2+ blocker

if dont respond,

2 drugs = add in more angiotensin blocker, Ca2+ blocker or a thizide diuretic

if still dont respond,

3 drugs = all 3 classes of drugs

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29
Q

what is it called when the patient doesnt respond to all 3 classes of drugs?

A

resistant hypertension

add in aldosterone antagonist OR a beta blocker (which blocks sympathetic pathway)

this is last step

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30
Q

vascular disorders: ATHEROSCLEROSIS, what is it

A

narrowing of vessels,
fatty plaque narrow the blood vessel

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31
Q

what are the 2 main triggering factors for atherosclerosis

A

endothelial damage (BP, smokeing, diabetes)

high LDL cholesterol

32
Q

describe plaque formation

A

the triggering factors increase the mrisk of inflammatory cells
e.g. macrophages and lipid accumulation
and fibrous tissure forms a little cap
and fatty streak which forms plaque

also thrombus formation because theres high chance of rupturing
this can lead to clot formation

33
Q

see onenote for atherosclerosis diagram

A

:)

34
Q

what ar the 2 circulations where this damage is most common

A

cerebral
coronary

35
Q

Effects of atherosclerosis in coronary circulation

A

redued blood supply to myocardium
causes chest pains = angina pectoris
or
if complete blockage in vessel = ischaemic heart disease

36
Q

Effects of atherosclerosis in cerebral circulation

A

complete cut off = stroke

partial cut off = brain cells die = vascular dementia

37
Q

how do we treat therosclerosis

A

statins

inhibits cholesterol synthesis = lowers LDL

acc the most prescribed drugs in the uk

38
Q

vascular diseases - THROMBOSIS, what is it

A

blood clots

39
Q

what might cause thrombosis

A

static/low blood flow
e.g. immobility and atrial fibrilation (where heart rate is slower than avg)

40
Q

where is thrombosis most likely to occur

A

in legs

cuz mobility helps venous return so immobility means skeletal muscle pumps not working

41
Q

explain formation of thrombosis venous circulation

A

e.g. starts in leg
in immobility
swelling and thrombus forms usually in veins near valves

risk of part of this breaking off and embolise
to form embolus
this goes up minto the circulation back through heart
will be fine on the way to the heart cuz vessels get bigger

but when leaves the heart to the pulmonary circ
will evetually encounter vessel it cant get trhoguh
= pulmonary embolism

blood supply to lungs cut off vry bad

42
Q

explain formation of thrombosis in arterial circulation

A

e.g. if atrial fibrilation - so blood flow in heart is not very good
thrombus happens in atria and breaks off
can go from L atrium to L ventricle
gets pumped into aorta
and get lodged
or could go into cerebral circ and cause stroke

or into coronary circulation and cause myocardial infarction

43
Q

how do we treat thrombosis

A

anticoagulants:
e.g. warfarin

anti platelet therapy:
e.g. aspirin

44
Q

cardiac disorders: CORONARY ARTERY DISEASE and myocardial infarction, what is it

A

biggest killer worldwide

starts with ATHEROSCLEROSIS of coronary artery
can restrict myocardial blood flow
can lead to angina (due to lack of O2)

45
Q

what treatment for angina in CAD

A

GTN spray
basically nitric oxide - leads to vasodilation

46
Q

what can the atheroscleorsis of coronary artey lead to

A

atherothrombosis
where the plaque ruptures or there’s an embolism
this causes the vessel to get completely cut off

leading to MI
any muscle that is supplied by the vessel that’s blocked starts to die pretty quickly

47
Q

whats the most commmon vessel to be affected by this

A

the left anterior descending coronary artey

supplies the left ventricle

48
Q

what is the treatment for myocardial infarction

A

percutaneous coronary intervention
= minimally invasive operation using catheter (inserted via femoral or radial artery)
inserts a stent to reopen blocked artery

and also given thrombolyitcs
= medication to break up clot

49
Q

cardiac disorders - VALVULAR DISEASE, what are the 2 types

A

stenosis
and regurgitation

50
Q

what is stenosis

A

thick/stiff valves that fail to open properky
this increases the afterload, reducing ejection

51
Q

common cause of stenosis

A

rheumatic fever
these symptoms can appear years after infection

52
Q

what can stenosis lead to

A

LV hypertrophy -> eventual heart failure

53
Q

what is regurgitaion

A

valves fail to close properly
so backflow of blood
reduces stroke volume and cardiac output

54
Q

treatments for valvular disease

A

surgery to repair valves
or can replace w/ sythetic valves

55
Q

cardiac disorders- HEART FAILURE, what are the 2 types

A

heart cant keep up with body’s demands

normally is secondary to other diseases, e.g. hypertension or myocardial infarction

diastolic and systolic

56
Q

what is diastolic heart failure

A

caused by thickening or stiff chambers in ventricles
so heart cant relax properly
and can’t fill with blood

this reduces EDV and reduces SV

57
Q

what is sytolic heart failure

A

heart cant pump
stretched thin chambers
arent effecient at contracting

so reduced contractility and reduced SV

58
Q

causes of heart failure

A

is secondary so

diseases that increase workload:
- hypertension
- aortic stenosis
causes pressure overload on ventricle
increases afterload
hypertrophy occurs and you get thinner walls and larger chambers

damage to myocardium -
after myocardial infarction
can happen years after
lose a lot of myocytes
so the rest of heart tissue has to work harder
myocytes arent replaced- instead you get a fibrous scar
leads to heart failure

59
Q

how can heart failure affect pulmonary circulation

A

if left sided heart failure
then not enough blood pumping out of the aorta
causes a backflow through the LA and LV
means the blood in the pulmonary circ gets backed up also
inc pressure in pulmonary veins
causing pumonary oedema
which is why shortness of breath and coughing

60
Q

how can heart failure affect systemic circ

A

right sided failure
blood pools in peripheral as increased pressure in systemic veins
= peripheral oedema

61
Q

what is it caleld when heart failure affects both sides of heart

A

congestive heart failure

62
Q

how does heart failure affect cardiac output and how is this a cycle

A

reduced cardiac output naturally leads to activation of RAAS and SNS
this might be alright short term but
it icreases the amount of fluid, vasoconstriction (thus resistance), and workload increases
this again reduces cardiac output cua the heart cant deal

63
Q

how do we treat heart fialure then, 4 key treatments

A

no curative treatments

damaged myocardiocytes cant be replaced

but can use
> beta blockers

> anti-hypertensives

surgical:
> left ventricular assist device

> heart transplant

64
Q

explain beta blockers in heart failure treatment

A

specifically beta adrenoreceptor antagonists
reduces SNS activity to reduce worload
and to prevent desensitisation (which tends to happen after constant activation of SNS, so this means when SNS is acc needed its sensitive to it)

65
Q

explain anti hypertensives in heart failure treatment

A

same drugs used in hypertension treatment
reduces fluid to relieve symptoms
reduces vasoconstriction
reduces workload

66
Q

explain left ventricular assist device and heart transplant as treatment

A

mechanical heart pump or transplant from healthy donor
but
surgical risks
immunorejection
also heart failure candidates usually older and frail so not good for these high risk surgeries

67
Q

cardiac disorder: ARRHYTHMIAS, what is it

A

devation heart’s normal sinus rhythm
can be asymptomatic
or
palpitations, faitning, heart failure, cardiac arrest, death

68
Q

2 main arrhythmias

A

bradychardia

tachycardia

69
Q

what is bradycardia

A

<60bpm
slow signals from SA node
SINUS BRADYCARDIA

or can be caused by damage to SA node, AV node or conductive tissue
which will block signals

70
Q

treatment for bradychardia

A

pacemaker

71
Q

what is tachycardia

A

> 100bpm

2 type:
> sinus tachycardia
(normal PQRST wave, but quicker)
caused by: drugs, hormones(e.g. thyroid)

> non-sinus tachycardia
= additional abmornal impulses in ECG

72
Q

some types of arrythmia

A

atrial fibrilation (AF)

long QT syndrome (LQTS)

Ventricular tachcardia(VT)

Ventricular fibrilation (VF)

73
Q

what is atrial fibrilation (AF)

A

most common
- rapid impulses
- so it quivers but doesnt quite contract
- can go undetected
- cause palpitations, fatining
- increases risk of stroke (due to the statis in blood flow cuz less contraction)

74
Q

what is long QT syndrome

A

prolongs the QT interval

affects mostly young people under 25

caused by genetic channelopathies (leading to prolonged action potential)

can cause additional ventricular depolarisations

can lead to ventricular tachycardia

75
Q

what is ventricular tachycardia

A

early depolarisation
leads to premature ventricul contraction
and not adequate filling before the heart contracts

prolonged VT can lead to ventricular fibrilation

76
Q

what is ventricular fibrilation

A

ie cardiac arrest
ventricles dont pump
w/o treament - death

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