cardiovascular disease Flashcards

1
Q

what is the natural pacemaker of the heart?

A

Sino-atrial node

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2
Q

2 types of heart valve failure

A
  1. stenosis

2. regurgitation/incompetence

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3
Q

what do DVT embolise to?

A

pulmonary embolisms

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4
Q

5 major sites for atherosclerosis

A
  1. coronary - MI
  2. cerebral - stroke
  3. femoral - claudication
  4. mesenteric - bowels
  5. aorta
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5
Q

4 risk factors for atherosclerosis

A
  1. smoking
  2. diabetes
  3. hypertension
  4. hyperlipidaemia/chloesterol
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6
Q

difference between ischaemia + infarction?

A
ischamia = reduced blood blow
infarction = no blood flow, death of tissue
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7
Q

3 causes of ichaemia/infarction

A
  1. atherosclerosis
  2. thrombosis
  3. embolism
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8
Q

what is heart black?

A

arrhythmia caused by impaired conduction through AV node

ventricular bradycardia but normal atrial activity

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9
Q

what is atrial fibrillation?

A

uncoordinated atrial activity with irregular ventricle activity

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10
Q

why is it important to be aware of patients with arrhythmias?

A

can be on warfarin - AF especially due to thrombus risk

care with adrenaline

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11
Q

3 developmental stages of atheroscleosis

A
  1. fatty streak
  2. fibrolipid plaque
  3. complicated lesion
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12
Q

what is virchows triad?

A

3 major determinants for thrombus formation

  1. changes in intimal surface of vessel
  2. changes in pattern of blood flow
  3. change in blood constituents
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13
Q

AF + mitral stenosis may cause what type of thrombus to form?

A

atrial

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14
Q

rheumatic fever + endocarditis may cause what type of thrombus to form?

A

valvular

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15
Q

previous MI may cause what type of thrombus to form?

A

ventricular

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16
Q

how does ECG show difference between angina + MI

A

ST depression in angina

ST elevation in MI

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17
Q

chronic/late complications of MI

A

arrhythmias, heart failure, angine, recurrent MI

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18
Q

4 cause of valvular heart disease

A
  1. rheumatic fever
  2. congenital
  3. degenerative - aortic stenosis common
  4. infective
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19
Q

3 common symptoms of heart failure

A
  1. breathlessness
  2. tiredness
  3. swelling of ankles
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20
Q

how does blood pressure alter between aortic stenosis + aortic regurgitation

A
AS = low
AR = high
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21
Q

what is rheumatic fever?

A

condition occurs 2-3 weeks after streptococcal URTI
self limiting but recurrent
inflammation at multiple sites - heart, arteries, joint, skin

can cause calcification of heart valves

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22
Q

3 sites IE occurs

A
  1. valve
  2. mural endocardium
  3. congenital defect

focal area

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23
Q

how does IE occur?

A
  1. focal area of abnormal endocardium has collagen exposed
  2. platelets stick + fibrin deposition
  3. bacteraemia occurs from an outside source e.g. dentist
  4. colonise vegetation
  5. more platelets, fibrin, bacteria
  6. vegetation grows - embolism/ischaemia may happen
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24
Q

what does idea blood pressure lie between?

A

120/80 - 90/60 mmHg

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25
Q

what is primary + seconding hypertension

A

primary - diagnosis of exclusion

secondary - caused by renal problems or Endocrinology problems

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26
Q

4 lifestyle choices that increase BP

A
  1. lack of exercise
  2. obesity
  3. salt intake
  4. alcohol

smoking affects cardiovascular risk but not BP

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27
Q

3 major complications of hypertension

A

MI
stroke
peripheral vascular disease

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28
Q

6 risk factors for stroke, from most common to least common

A
  1. hypertension
  2. vascular disease elsewhere
  3. smoking
    4, diabetes
    5, TIA
  4. atrial fibrillation
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29
Q

how does angiotensin II affect BP?

A

increases BP

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30
Q

what converts angiotensin I into angiotensin II?

A

ACE

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31
Q

what BP measurement classfies as hypertension?

A

140/90

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32
Q

for pts under 55, what is the pathway for antihypertensive drugs?

A
  1. ACE inhibitor
  2. ACE + calcium channel blocker
  3. A + C + diuretic
  4. A + C + D + alpha/beta blockers
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33
Q

for pts over 55 or black person, what is the pathway for antihypertensive drugs?

A
  1. calcium channel blocker
  2. C + ACE
  3. C + A + Diuretic
  4. A + C + D + alpha/beta blockers
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34
Q

4 factors contributing to BP

A
  1. HR
  2. contractility
  3. angiotensin II
  4. peripheral resistance
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35
Q

how do thiazide like diuretics work?

A

decrease peripheral resistance

increase secretion of NA, Cl, K in nephron

can cause Na deficiency + gout flare

-Ide

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36
Q

how do beta blockers lower BP?

A

b-adrenoreceptor antagonists

decrease HR + contractility
also inhibit RAS + decrease peripheral resistance

B1 > B2 (resp side effects)

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37
Q

what is atenolol?

A

beta blocker selective to B1 (less respiratory side effects)

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38
Q

how do calcium channel blockers lower BP?

A

block Ca entry into smooth muscle cells = vasodilation

some inhibit ca current into sinus + AV node

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39
Q

which calcium channel blocker causes gingival hyperplasia?

A

amlodipine

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40
Q

how do ACE inhibitors lower BP?

A

inhibit conversion of ang I - ang II
inhibits degradation of bradykinin which is a vasodilator
reduces aldosterone secretion
renal vasodilation

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41
Q

what is aldosterone?

A

secreted by adrenal cortex

controls secretion in kidney, increases retention of water + Na

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42
Q

2 relevant side effects of ACE inhibitors

A

cough - caused by bradykinin

burning mouth syndrome

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43
Q

how do angiotensin receptor blockers work + what used for?

A

inhibit action of Ang II

do not produce cough like ACE

mainly heart failure

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44
Q

how do alpha blockers lower BP?

A

a1 adrenoreceptor blocked - stops vasoconstriction

first dose phenomenon

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45
Q

5 drug therapies for angina?

A
  1. nitrates
  2. beta blockers
  3. calcium channel blokcers
  4. potassium channel activators
  5. ivadridine
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46
Q

how do nitrates treat angina?

A

NO release, reacts with SH group, increases cGMP

causes smooth muscle relaxation

also dilate coronary arteries

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47
Q

what happens to nitrate therapy over a long period of time?

A

effect decreases

8hr gap needed

48
Q

how do beta blockers treat angina?

A

decrease myocardial oxygen demand by decreasing HR + contractility

49
Q

how do potassium channel blockers treat angina?

A

e.g. nicorandil

activate K+ channels, causes vasodilation

50
Q

how does ivabradine treat angina?

A

selectively inhibits If channels in cardiac pacemaker

lower HR

51
Q

adverse effect of ivabradine?

A

visual effects - spots at edges of vision

52
Q

where do 95% of cases of IE affect?

A

left side of heart - mitral + aortic

53
Q

what bacteria is acute IE normally caused by?

A

staphylococcus aureus

54
Q

what causes right sided IE?

A

IV drug abuse

immunosuppressed

55
Q

what oral bacteria causes IE?

A

streptococci

56
Q

signs of IE

A

oslers nodes
finger clubbing
splinter haemorrhage >8
janeway lesions

57
Q

what criteria is used to diagnose IE?

A

DUKE criteria

58
Q

what is a cardiopulmonary bypass?

A

blood removed from heart, oxygenated outside of body, back into aorta

used in CABG

59
Q

what is percutaneous coronary intervention (PCI)?

A

angioplasty +/- stenting

60
Q

3 options for management of coronary artery disease

A
  1. drugs
  2. PCI
  3. CABG
61
Q

2 surgical options for valvular heart disease?

A
  1. TAVI = transcatheter aortic valve implantation

2. SAVR = surgical aortic valve replacement

62
Q

what is claudication?

A

leg pain on walking due to blocked/narrowed artery

70-80% narrowing

pain due to lactic acid build up, as blood can’t take away

63
Q

drug therapy for claudication?

A
BP control
statins
anti-platelets
ACE inhibitor 
control diabetes
64
Q

how does diabetes effect vascular system?

A

accelerated athersclerosis

65
Q

what is critical ischaemia?

A

pain at rest +/ gangrene, ulcers

66
Q

treatment for critical ischaemia?

A

balloon angioplasty +/- stent

bypass surgeries

67
Q

what is acute ischaemia?

A

sudden onset caused mainly due to thrombus or embolism

also caused by trauma/compression/vasoconstrictor drugs

68
Q

what is the critical time for irreversible change in acute ischaemia?

A

4-6hours

69
Q

aortic aneurysms are common in which people?

A

men over 65, smoke, hypertensive

70
Q

when are AA treated?

A

above 5.5cm

71
Q

what is carotid disease?

A

carotid artery stenosis normally at bifurcation of artery

causes TIA/stroke by embolism

72
Q

4 steps of haemostasis

A
  1. contrition of damaged vessel
  2. mechanical blockage of hole by platelet
  3. coagulation cascade
  4. thrombolysis - plasmin breaks down clot
73
Q

what stimulates platelet activation + aggregation?

A

thromboxane A2

aggregation also ADP

74
Q

what is thrombolysis?

A

fibrin mesh prevented from increasing + dissolved by plasmin

75
Q

3 ways drugs treat thrombus disorders

A
  1. antiplatelet
  2. anticoagulant
  3. thrombolytic
76
Q

how is aspirin used long term

A

75mg a day prophylaxis

77
Q

how does aspirin work?

A

cox inhibitor, irreversible inhibitor of platelet thromboxane

78
Q

CI for aspirin use?

A
<12years
active peptic ulceration
recent gastrointestinal bleeding
recent intracranial bleeding
bleeding disorders
severe liver sides
79
Q

what is clopidogrel?

A

ADP receptor antagonist

inhibits ADP receptor on platelets which would otherwise caused aggregation

80
Q

benefits of clopidogrel>aspirin?

A

safer GI bleeding

81
Q

what types of drugs does clopidogrel interact with?

A

PPI

82
Q

what is dipyridamole?

A

adenosine reuptake inhibitor

CI - uncontrolled angina

83
Q

how does heparin cause anticoagulation?

A

vit k antagonist

enhances activity of antithrombin III, inactivates prothrombin, impares platelet function

84
Q

why can heparin only be given parentally?

A

poorly absorbed in gut

85
Q

advantage of LMWHs>heparin?

A

once daily dosing
no need to monitor APTT
reduced risk of thrombocytopenia

used on outpatient

86
Q

what is used to reverse effects of heparin?

A

protamine sulphate

87
Q

unwanted effects of heparin?

A

haemorrhage - GIT
thrombocytopenia
long term - osteoporosis, liver disease

88
Q

how does warfarin cause anticoagulation?

A

vit k antagonist

89
Q

which clotting factors are vit k dependant?

A

2, 7, 9, 10

90
Q

what is used to reverse effects of warfarin?

A

vit k

91
Q

main drug interactions with warfarin

A

aspirin
fluconazole + miconazole
erythromycin
metronidazole - NEVER

92
Q

when to check INR?

A

ideally within 24hrs

if stably anticoagulated then up to 72hrs

93
Q

how does dabigatran cause anticoagulation

A

direct thrombin inhibitor

94
Q

how does rivaroxaban cause anticoagulation

A

direct factor Xa inhibitor

95
Q

if high risk procedure and take apixaban or dabigatran how should you alter dose?

A

miss morning, give evening

> 4hrs post op

96
Q

if high risk procedure and take rivaroxaban how should you alter dose?

A

take once a day

if in morning - delay and >4hrs post op
if in evening - no change >4hrs post op

97
Q

5 common types of drugs used for heart failure

A
  1. inotropes
  2. diuretics
  3. beta blockers
  4. ACE inhibitors
  5. angiotensin receptor blockers
98
Q

how do inotroped treat heart failure?

A

adrenoreceptor agonists - increase contractility

stimulates B1 receptors

99
Q

what are cardiac glycoside e.g. digoxin used for?

A

treat arrhythmias

via vagus nerve

100
Q

2 types of diuretics

A
  1. K+ losing - e.g. thiazide like

2. K+ sparing - use aldosterone

101
Q

how does the vagus nerve effect the heart?

A

decreases HR

102
Q

how does atropine treat bradycardia?

A

blocks vagal inhibition

103
Q

how does isoprenaline treat bradycardia?

A

B1/B2 agonist - increase HR

104
Q

classification for arrhythmia drugs?

A

vaughan williams singh

105
Q

2 types of heart failure

A

acute + chronic

106
Q

2 keys signs of acute heart failure

A

breathlessness + pulmonary oedema

107
Q

4 cardiac causes of heart failure

A
  1. heart muscle disease - ischaemia + cardiomyopathy
  2. xs volume load - valvular incompetence
  3. xs pressure - hypertension + stenosis
  4. arrhythmias
108
Q

3 non-cardiac causes of heart failure

A
  1. xs demand e.g. anaemia, hyperthyroidism, shunts
  2. fluid overloads e.g. IV therapy, renal failure
  3. COPD - cor pulmonale
109
Q

what is the conflicting near-humoral compensatory mechanism 1

A
  1. reduced cardiac output
  2. RAAS activated + vasoconstriction
  3. increase BP
  4. damages heart further
110
Q

what stimulates ACE?

A

renin - secreted by kidney when reduced renal blood flow

111
Q

cardiac cycle

A
  1. SA node
  2. atrial systole
  3. AV node
  4. pause
  5. to ventricle
  6. bundle of his
  7. purkinje fibres
112
Q

what is sinus tachycardia?

A

normal response to exercise/emotion

113
Q

what is ventricular tachycardia associated with?

A

ichaemic heart disease

114
Q

type of fibrillation in cardiac arrest?

A

ventricular fibrillation

115
Q

what are korotkow sounds?

A

systolic when appear

diastolic when disappear

116
Q

what cardiac drug may cause angioedema?

A

ACE inhibitors