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BRS 2 > cardio > Flashcards

cardio Flashcards

1
Q

6 examples of congenital structural heart diseases?

A

ventricular / atrial septal defect
coarctation of the aorta
tetralogy of fallot
patent formane ovale / ductus arteriosis

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2
Q

what are the 4 hallmarks of tetralogy of fallot?

A

vsd
wide aorta (over both ventricles)
right ventricle hypertrophy
pulmonary stenosis

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3
Q

what is coarctation of the aorta?

A

narrowing of aorta → ventricle has to pump much harder - increased afterload

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4
Q

Risk factors for aortic stenosis?

A 
older age
hypertension
LDL levels
smoking
↑ CRP
congenital bicuspid valves 
CKD
radiotherapy
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5
Q

what is aortic stenosis preceded by?

A

aortic sclerosis (thickening without flow limitation)

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6
Q

how is aortic stenosis suspected?

A

early-peaking systolic ejection murmur (shrill)

confirmed with echo

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7
Q

3 causes of aortic stenosis?

A

rheumatic heart disease
calcium build up
congenital heart disease

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8
Q

outline the pathophysiology of aortic stenosis?

A

abnormal blood flow across valve (eg bicuspid) → damage to valvular endocardium → inflammatory response → leaflet fibrosis and calcium deposition on valve → progresses → ↓ aortic leaflet mobility → stenosis

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9
Q

how does rheumatic heart disease lead to aortic stenosis?

A

autoimmune inflammatory reaction triggered by streptococcus infection that targeted valvular endothelium → inflammation → calcification → stenosis

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10
Q

what can be the trigger for rheumatic heart disease?

A

streptococcus infection

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11
Q

what happens to the heart as aortic stenosis progresses?

A

left ventricular hypertrophy as after load increases

stenosis worsens and wall stress increases → systolic function decreases → systolic heart failure

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12
Q

history and presentation of aortic stenosis?

A

exertion dyspnoea
fatigue
ejection systolic murmur
h/o rheumatic fever, high LDL, CKD, over 65

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13
Q

what 4 investigations can be carried out for aortic stenosis?

A

transthoracic echocardiogram
ecg + chest x ray for LVH
catheterisation
mri

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14
Q

what is the primary treatment of symptomatic aortic stenosis?

A

aortic valve replacement

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15
Q

when is aortic valve replacement the first line treatment for aortic stenosis?

A

in symptomatic AS
in asymptomatic with severe AS with LVEF < 50%/undergoing cardiac surgery
severe AS but asymptomatic with rapid progression, abnormal exercise test, elevated BNP

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16
Q

management options for aortic stenosis?

A

AVR
balloon aortic valvuloplasty
antihypertensives
statins

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17
Q

what is aortic regurgitation?

A

the diastolic leakage of blood from the aorta into the left ventricle

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18
Q

what valve incompetencies are more common than AR?

A

AS and MR

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19
Q

what can chronic AR culminate in?

A

congestive heart failure

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20
Q

how can acute AR present?

A

sudden onset of pulmonary oedema, hypotension/cardiogenic shock
= medical emergency

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21
Q

6 causes of aortic regurgitation?

A 
rheumatic heart disease
infective endocarditis
aortic stenosis
congenital mitral bicuspid valve
congenital heart defects
aortic root dilation
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22
Q

5 causes of aortic root dilation?”

A 
marfan's syndrome
connective tissue/collagen vascular diseases
idiopathic
ankylosing spondylitis
traumatic
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23
Q

how does infective endocarditis lead to AR?

A

rupture of leaflets , paravalvular leaks, vegetations → inadequate closure of leaflets

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24
Q

pathophysiology of acute AR?

A

↑ blood volume in LV during systole and ↑ end-diastolic LV pressure → ↑ pulmonary venous pressure → dyspnea and pulmonary oedema → heart failure → cardiogenic shock

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25
Q

pathophysiology of chronic AR?

A

gradual ↑ in LV volume → LV eccentric hypertrophy (dilates to help maintain normal pressure)
initially EF is normal/slightly raised
eventually falls and ESV ↑
SP rises, DP falls
→ dyspnea, lower coronary perfusion→ ischemia, necrosis. apoptosis

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26
Q

how can acute AR present?

A 
tachycardia
cardiogenic shock
cyanosis 
pulmonary oedema
Austin flint murmur
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27
Q

what is the Austin flint murmur?

A

hear at apex of heart in acute AR, caused by blood hitting LV wall
rumbling diastolic murmur

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28
Q

how can chronic AR present?

A

wide pulse pressure
corrigans pulse
pistol shot pulse - Traube sign

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29
Q

what is Corrigan pulse?

A

excessive visible pulsations often seen in chronic AR

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30
Q

4 investigations that can be carried out in AR?

A

transthoracic echo
chest xray
cardiac catheterisation
cardiac MRI/CT

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31
Q

first line management for chronic asymptomatic AR?

A

normal LV function → positive ionotrope and vasodilator drugs

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32
Q

first line management for chronic symptomatic AR?

A

valve replacement with adjunct vasodilator therapy

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33
Q

main cause of mitral stenosis in developing countries?

A

rheumatic fever

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34
Q

what does mitral stenosis progress to?

A

pulmonary hypertension and right heart failure

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35
Q

causes of mitral valve stenosis?

A 
rheumatic fever
carcinoid syndrome
sertotenergic drugs
SLE
mitral annular calcification
amyloidosis
RA
Whipple disease
congenital valve deformity
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36
Q

when does mitral stenosis often present?

A

years after rheumatic fever

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37
Q

why does exertion dyspnoea present in mitral stenosis?

A

increase in left atrial pressure during moderate exercise/tachycardia

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38
Q

how does severe mitral stenosis lead to dyspnoea at rest?

A

very high left atrial pressure → transudation of fluid into lung interstitium

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39
Q

how can haemoptysis occur as a result of mitral stenosis?

A

↑ LA pressure → pulmonary hypertension → brachial vein rupture

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40
Q

how can mitral stenosis present?

A 
dyspnoea
orthopnea
diastolic murmur
loud P2
neck vein distention
hemoptysis
h/o rheumatic fever
40-50 yrs
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41
Q

5 investigations for mitral stenosis?

A 
ECG
chest x ray
cardiac catheteristation
chest CT/MRI
transthoracic echo
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42
Q

management for progressive asymptomatic MS?

A

no therapy

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43
Q

management for severe asymptomatic MS?

A

no therapy

can offer adjuvant balloon valvotomy

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44
Q

management for severe symptomatic MS?

A

first line : diuretic + balloon valvotomy, valve replacement or repair
adjuvant : beta blockers

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45
Q

causes of acute mitral regurgitation?

A 
mitral valve prolapse
rheumatic heart disease
infective endocarditis
post valvular surgery
prosthetic mitral valave dysfucntion
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46
Q

causes of chronic mitral regurgitation?

A 
rheumatic heart disease
scleroderma
SLE
hypertrophic cardiomyopathy
drug related
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47
Q

how does infective endocarditis lead to MR?

A

accesses form leading to vegetations on the valves → ruptured chordae tendinae → leaflet perforation

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48
Q

in chronic MR what changes are seen in the heart?

A

eccentric hypertrophy of LHS
increased preload and end diastolic volume
decreased after load and end systolic volume
→ LV dysfunction

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49
Q

presentation of MR?

A 
dyspnoea, orthopnea
high pitched, blowing murmur
diminished S1
fatigue
chest pain
atrial fibrilaltion
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50
Q

MR investigations?

A 
ECG
chest xray
mri/ct
echo
catheterisation
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51
Q

management for acute MR?

A

emergency surgery adjunct preoperative diuretics and intra-aortic balloon counterpulsation

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52
Q

management for chronic asymptomatic MR

A

1st line CE inhibitors + beta blockers

surgery if LV EF < 60%

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53
Q

management for chronic symptomatic MR

A

surgery + medical treatment if LV EF ≥ 30%

LVEF <30% → medical + intraaortic balloon counterpulsation

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54
Q

3 types of cardiomyoptahies?

A

dilated
hypertrophic
restrictive

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55
Q

causes of dilated cardiomyopathy? primary and secondary?

A

primary - familial , idiopathic w/out fhx

secondary - valve disease, post natal, thyroid disease, myocarditis, alcoholism, autoimmune, drug ingestion, mitochondrial disorders

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56
Q

dilated cardiomyopathy pathophysiology?

A

left ventricle eccentric hypertrophy → ↓ EF and ↑ ESV → ↑ ventricular wall stress
compensation → ↑ HR and ↑ tone of peripheral vascalature, activation of RAAS, ↑ catecholamines, ↑ natriuretic peptides
eventual heart failure

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57
Q

presentation of dilated cardiomyopathy?

A

dyspnoea
systolic murmur, displaced apex beat, s3
fatigue, angina, pulmonary congestion , ↓ CO

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58
Q

investigations for dilated cardiomyopathy?

A 
genetic testing
viral serology
ECG
CXR
catheterisation 
cardiac mri/ct
exercise stress test
echo
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59
Q

management for dilated cardiomyopathy?

A

diet modifications → ↓ fluids and na+
treat underlying cause
acei, b blockers, diuretics, arbs → if ineffective → LVAD/ICD/transplant
anticoags for atrial fibrillation

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60
Q

how could you characterise dilated cardiomyopathy?

A

enlarged ventricle chamber with systolic dysfunction

normal wall thickness in LV

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61
Q

what is the leading causing of sudden cardiac death in adolescents and preadolescents?

A

hypertrophic cardiomyopathy

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62
Q

how is hypertrophic cardiomyopathy characterised?

A

increased left ventricle wall thickness not explained by abnormal stresses
abnormal diastolic function

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63
Q

which area of the lv is most often involved in hypertrophic cardiomyopathy?

A

inter ventricular septum → obstructs outflow from LV

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64
Q

what valve disorders can dcm lead to?

A

mitral and tricuspid valve regurgitation as valves don’t fully close when walls are stretched

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65
Q

how is diastolic function affected in hcm?

A

smaller ventricular chamber and less compliant walls → less filling in diastole →↓ stroke volume → diastolic heart failure

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66
Q

what is the Venturi effect?

A

outflow of lv is obstructed by enlarged interventricular septum → increased blood flow velocity → pulls mitral valve leaflet towards septum → further obstruction

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67
Q

what is often the first clinical manifestation of hcm?

A

death due ventricular tachycardia or arrhythmia - increased muscle requires more oxygen but theres reduced blood flow so tissue becomes ischaemic

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68
Q

commonest cause of hcm?

A

genetic mutation

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69
Q

how can hcm present?

A

sudden cardiac death
syncope
s3 gallop
congestive heart failure
dizziness, palpitations, angina, dyspnea
ejection systolic murmur (crescendo, descendo)

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70
Q

investigations for hcm?

A 
Hb levels 
bnp and troponin t levels 
echo
cxr
cardiac mri
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71
Q

management for hcm?

A

1st : b blockers, verapamil
2nd : disopyramide
3rd : mechanical therapy , septal myectomy, ablation §

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72
Q

how is restricted cardiomyopathy characterised?

A

diastolic dysfunction
enlarged atrium
ventricles are less complaint but have normal wall thickness and volume

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73
Q

pathophysiology of rcm?

A

depositions in heart tissue → stiffer ventricles → less compliant → cannot stretch as much → less diastolic filling → less stroke volume → diastolic heart failure

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74
Q

causes of rcm?

A

genetic
idiopathic
secondary : amyloidosis, sarcoidosis, fabry’s disease, haemochromatosis, radiation → depositions in heart tissue

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75
Q

how can rcm present?

A 
patient prefers sitting 
ascites 
pitting oedema
hepatomegaly , ± painful
weight loss
cardiac cachexia
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76
Q

how can amyloidosis present as in rcm?

A

macroglossia
carpal tunnel syndrome
easy bruising
periorbital purpura

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77
Q

investigations for rcm?

A

fbc, serology, amylodois check

cxr, ecg, echo, catherisation, mri

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78
Q

management for rcm?

A 
heart failure → ACEi, ARBs, diuretics, aldosterone inhibitors 
antiarrhythmic therapies
immunosuppression 
pacemaker
transplant
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79
Q

EF =

A

EDV /SV x 100

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80
Q

CO =

A

HR x SV

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81
Q

MAP =

A

DP + 1/3 (PP)

= DP + 1/3 (SP-DP)

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82
Q

what is infective endocarditis?

A

infection of endocardium or vascular endothelium of heart

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83
Q

what heart structure is most often affected in endocarditis?

A

the valves

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84
Q

what bacteria is most common cause for infective endocarditis?

A

streptococcus

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85
Q

pathophysiology of infective endocarditis?

A

bacteria adhere to damaged endothelium and microthrombi → proliferate → macrophage, neutrophil infiltration → platelets fibrin → vegetation

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86
Q

how can infective endocarditis present?

A

fever, malaise, swetas, unexplained weight loss
heart murmur
anemia, raised infection markers

87
Q

investigations for infective endocarditis?

A

fbc, cultures

echo → vegetation , abscess , valve perforation , regurgitation

88
Q

what type of echo is more sensitive over another in infective endocarditis?

A

transoesophageal better than transthoracic

89
Q

what criteria are used to assess possible infective endocarditis ?

A

Dukes

90
Q

what are dukes criteria?

A

Major :
postive blood culture for typical organisms ≥2 times
echo : vegetation, prosthetic valve dishedence , abscess
new regurgitation murmur
coxiella burnetti infection

Minor:
predisposing heart condition or IV drug use
fever ≥ 38C
vascular - emboli, janeway lesions
immunological - glomerulonephritis, roths spots, oslers nodes, janeway lesions
other +ve blood culture

91
Q

what is required for +ve IE diagnosis?

A

2 major
1 major + 3 minor dukes criteria
5 minor

92
Q

what is required for possible IE diagnosis?

A

1 major + ≥2 minor dukes

3 minor

93
Q

signs and symptoms of cardiac decompensation?

A

SoB, coughing, ascites and ankle swelling , fatigue
↑ JVP , lung crackles, oedema
vascular/embolic phenomena : stroke, janeway lesions, splinter/conjunctival haemorrhages
immunological phenomena : osler nodes , Roth spots

94
Q

what valve is most commonly affected in IE?

A

aortic ≥ mitral ≥ right sided

95
Q

advantages if ecg?

A

cheap and easy
reproducible between people and centres
quick turnaround

96
Q

what cells make up the SAN?

A

autorhythmic myocytes

97
Q

what is seen on ecg when the avn is depolarised?

A

isoelectric line - slows signal transduction

98
Q

why are no deflections seen on ecg when the bundle of his is depolarised?

A

well insulated

99
Q

what is the placement of each limb lead? and direction?

A 
aVr - right arm (210/-150)
aVl - left arm (-30)
avF - left leg (90)
N - right leg
lead I -  (RA → LA) (0)
lead II -  (RA → LL) (60)
lead III - (LA→LL) (120)
100
Q

where are the chest leads placed?

A

V1 - right sternal border, 4th intercostal space
V2 - left sternal border, 4th intercostal space
V3 - between v2 and v4
V4 - mid clavicular line in 5th intercostal space
V5 - ant axillary line at v4 level
V6 - mid axillary line at v4 level

101
Q

what planes do the limb and chest leads look at?

A

limb - coronal

chest - axial

102
Q

which leads are associated with the left circumflex artery?

A

I
aVL
V5
V6

103
Q

which leads are associated with the right coronary artery?

A

II
III
aVF

104
Q

which leads are associated with the left anterior descending artery?

A

V1 - V4

105
Q

5 little squares = how many seconds on ecg?

A

2s

106
Q

what is sinus rhythm?

A

P waves followed by QRS in 1:1
regular rate
normal bpm

107
Q

what can cause sinus bradycardia?

A

can be normal
vagal stimulation
meds

108
Q

what is sinus arrhythmia?

A

each p wave followed by qrs
irregular rate but normal bpm
R-R interval varies with breathing (shortens on inspiration and HR increases)

109
Q

what counteracts the SAN to maintain heart rate?

A

vagus nerve

110
Q

how is atrial fibrillation seen on ecg?

A

oscillating baseline - no isoelectric as atria are contraction asynchronously
irregular rhythm , slow rate

111
Q

atrial fibrillation increases risk of?

A

clotting due turbulent flow

112
Q

how is atrial flutter seen on ecg?

A

regular saw tooth pattern in baseline in leads II, III, aVF

atrial : ventricular beats → 2 : 1 / 3 : 1

113
Q

how is first degree heart block seen on ecg?

A

prolonger P-R interval → slower AV conduction
regular rhythm 1:1 P:QRS
progressive disease of aging

114
Q

how is mobitz I seen on ecg?

A

gradual prolongation of P-R interval until beat skipped - no QRS after p wave
regular irregular rhythm

115
Q

what causes mobitz I?

A

diseased AVN

116
Q

another name for mobitz I?

A

wenckebach

117
Q

how is mobitz II seen on ecg?

A

regular p waves but only some followed by qrs
no p-r elongation
regularly irregular
can rapidly deteriorate into third degree

118
Q

how is third degree heart block seen on ecg?

A

regular p waves and qrs complexes but no relationship
p waves can be hidden in bigger vectors
non-sinus rhythm

119
Q

how is ventricular tachycardia seen on ecg?

A

hidden p waves
regular rate but fast (100-200bpm)
dissociated atrial rhythm

120
Q

give 2 examples of a shockable rhythm?

A

ventricular tachycardia

ventricular fibrillation

121
Q

how is ventricular fibrillation seen on ecg?

A

irregular hr
fast (≥250bpm)
filling and ejection uncoordinated

122
Q

what causes ST elevation?

A

infarction of tissue by hypo perfusion eg obstructed vessel

123
Q

ST elevation is seen in leads II, III and aVF. what does this indicate?

A

obstruction in RCA

124
Q

what causes ST depression?

A

myocardial ischaemia due to coronary insufficiency

125
Q

what is the normal axis range?

A

-30 to 90

126
Q

what can cause an axis change?

A

hypertrophy - deviation to side of hypertrophy

infection/ischaemia - deviation away

127
Q

what happens immediately after damage to endothelial vessel lining?

A

vascular smooth muscle contract → constrict vessel → limit blood flow to vessel

128
Q

outline primary haemostasis?

A

platelets bind to collagen (adhesion)
- indirectly : VWF via GIpIb receptor
-directly : via GIpIa receptor
ADP and thromboxane (from arachidonic acid) released
platelets aggregate using fibrinogen and calcium to connect in GIpIa/b receptors

129
Q

what can cause thrombocytopenia?

A

leukaemia , B12 deficiency (bone marrow failure)
Immune thrombocytopenic purpura , disseminated intravascular coagulation (accelerated clearance)
pooling and destruction in spleen

130
Q

what can cause impaired platelet function?

A

hereditary absence of glycoproteins or granules

drugs such as aspirin, clopidogrel, NSAIDS

131
Q

3 examples of hereditary platelet defects?

A

glanzmanns thrombasthenia
Bernard soulier syndrdome
storage pool disease

132
Q

what does arachidonic acid produce and via what?

A

thromboxane a2 prostaglandin and prostacyclin PGI2 via cyclo-oxygenase

133
Q

how does aspirin work in inhibiting primary haemostasis?

A

irreversibly blocks cyclo-oxygenase so less thromboxane a2 is produced from arachidonic acid → ↓ platelet aggregation

134
Q

what is the function of prostacyclin pgi2?

A

inhibits platelet aggregation

135
Q

where else is prostacyclin pgi2 produced? why is this useful

A

from endothelial cells

even when aspirin blocks COX pgi2 can still be produced and help inhibit platelet aggregation

136
Q

how long do the effects of aspirin last?

A

about 7 days

137
Q

how does clopidogrel work in inhibiting primary haemostasis?

A

irreversibly blocks ADP receptor on platelets

138
Q

what are the functions of VWF?

A

bind to collagen and capture platelets

stabilise f VIII

139
Q

what is the cause of von willebrand disease? types?

A

hereditary - autosomal
type 1 and 3 - deficiency of vwf
type 2 - vwf w abnormal function

140
Q

what disorders cause vessel wall defects that inhibit primary haemostasis?

A

inherited - haemorrhage telangiectasia , Ehlers- Danlos syndrome
acquired - steroids, ageing, vasculitis, scurvy

141
Q

how do disorders of primary haemostasis present?

A 
immediate, prolonged bleeding
nose bleeds ≥ 20 mins
gum bleeding
menorrhagia
easy/spontaneous bruising (ecchymosis)
petechiae
purpura (bigger) , non-blanching
142
Q

what tests are done for disorders of primary haemostasis?

A

platelet count and morphology
vwf assays
clinical observation

143
Q

APPT and PT in disorders of primary haemostasis?

A

normal

except in severe VWD when fVIII is low

144
Q

how can disorders disorders of primary haemostasis be treated?

A 
replace vwf or platelets 
stop drugs like apsirin
immunosuppressuin 
splenectomy for ITP
desmopressin to increase VWF and fVIII
145
Q

what are the causes of coagulation factor deficiency?

A

genetic - haemophilia A/B (f8 & 9)

acquired - liver disease, anticoagulant drugs like warfarin and doacs

146
Q

how can a blood transfusion lead to a coagulation disorder?

A

if there is insufficient plasma in the transfusion then the blood become diluted and there are less coagulation factors

147
Q

what can cause an increased consumption of coagulation factors?

A

disseminated intravascular coagulation

autoantibodies

148
Q

what happens in haemophilia?

A

failure to produce fibrin to stabilise the platelet plug → breaks up → bleeding

149
Q

what is the hallmark of haemophilia?

A

haemarthrosis → spontaneous joint bleeding

150
Q

what should not be given to haemophilia patients?

A

intramuscular injections

151
Q

what coagulation factor deficiency is lethal?

A

factor II (prothrombin)

152
Q

what are the symptoms of a factor XI deficiency?

A

bleeding after trauma

not spontaneous

153
Q

what are the symptoms of a factor XII deficiency?

A

none - no bleeding

154
Q

why does liver failure lead to coagulation dysfunction?

A

most coagulation factors are made in the liver

155
Q

which factors are not synthesised in the liver? where?

A

vWF - endothelial cells

fV - platelets , megakaryocytes

156
Q

outline disseminated intravascular coagulation

A

can be caused by sepsis, major tissue damage, inflammation

generalised coagulation activation via tissue factor → ↑ clots around body → ↓ platelets (thrombocytopenia) and clotting factors , ↓ fibrinogen & ↑ D - dimer → spontaneous bleeding and organ failure as clots interrupt blood supply leading to ischaemia

157
Q

what are the clinical features of 2* haemostasis coagulation disorders?

A 
superficial cuts don't bleed
brushing is common
nosebleeds rare
deep spontaneous bleeding - joints and muscles
trauma bleeding prolonged, delayed 
bleeding restarts after stopping
158
Q

how can you distinguish between bleeding due to platelets and coagulation disorders?

A

platelets

  • superficial bleeding - skin and mucosal membranes
  • bleeding immediately after injury

factors

  • deep bleeding - joints and muscles
  • trauma bleeding delayed but severe and prolonged
159
Q

what are the screening tests for coagulation disorders?

A

full blood count for platelets
prothrombin time
activated partial thromboplastin time

160
Q

differences between PT and APTT?

A

PT - extrinsic pathway -2, 7

APTT - intrinsic pathway - 1, 2, 9, 10, 11, 12

161
Q

prolonged APTT can indicate what?

A

haemophilia A/B

factor XI or XII deficiency

162
Q

prolonged PT can indicate what?

A

factor VII deficiency

163
Q

prolonged APTT and PT can indicate what?

A 
liver disease
warfarin / doacs
DIC
dilution following rbc transfusion
vit k deficiency
164
Q

what are the factor replacement therapy options? (5)

A

fresh frozen plasma - all factors
cryoprecipitate - fibrinogen , 8, vwf, 13
factor concentrates - all except 5
prothrombin complex concentrates - 2, 7, 9, 10
recombinant forms of 8 and 9 - prophylactic or treatment

165
Q

what is the current approved treatment for haemophilia?

A

recombinant clotting factors

166
Q

what are novel treatment options for haemophilia?

A 
gene therapy (A and B)
bispecific antibodies (A) - mimics procaogulant function of fVIII
RNA silencing (A and B) - targets antithrombin
167
Q

additional treatment options for abnormal haemostasis?

A

transexamic acid - antifibrinolytic
desmopressin - vasopressin analogue → increase vwf and fVIII
fibrin glu/spray

168
Q

what can cause increased bleeding via increased fibrinolysis?

A

↑ tissue plasminogen activator - stroke

169
Q

what can cause increased bleeding via increased anticoagulation?

A

heparin

170
Q

how can a pulmonary embolism present?

A 
tachycardia
hypoxia , sob
chest pain
haemoptysis
sudden death
171
Q

how can a dvt present?

A

painful leg
swelling, red, warm
can embolise to lungs

172
Q

what is virchows triad?

A

the 3 contributing factors to thrombosis

  • blood (venous)
  • vessel wall (arterial)
  • blood flow (both)
173
Q

what is thrombophilia? presentation?

A

increased venous thrombosis risk

  • thrombosis at young age, spontaenous
  • multiple thromboses
  • thrombosis while anti coagulated
174
Q

what can cause venous thrombosis? think blood

A

↓ antithrombin , protein c & s
↑ coagulation factors - 2 , 5 leiden , 8
myeloprolifrtaive disorders

175
Q

how do antithrombin and protein c&s deficiencies lead to thrombosis

A

antithrombin normally inactivates fXa and IIa
c and s normally inactivate Va and VIIIa
↓ → ↑ clotting factors

176
Q

how is the vessel wall thought to be involved in thrombosis?

A

coagulation proteins expressed in vessel endothelial cells - altered during inflammation

177
Q

when does blood flow contribute to thrombosis?

A

stasis increases risk

surgery, long flights, pregnancy (compression from foetus)

178
Q

treatment options for venous thrombosis?

A

assess and prevent risks
prophylaxis - anticoagulant therapy, heparin
lower procoagulant factors - warfarin, doacs to reduce risk of recurrence

179
Q

three layers of blood vessels?

A

tunica adventitia - vasa vasorum, nerves
tunica media - smooth muscle
tunica intima - endothelium
(all except venues and capillaries)

180
Q

structures of capillaries and venues?

A

endothelium supportert by mural cells/pericytes and a basement membrane

181
Q

function of microvascular endothelium?

A

promotes tissue homeostasis and organ regeneration via angiocrine release

182
Q

what can dysfunctional endothelium contribute to?

A

cancer
diabetes
ischaemia
chronic inflammatory diseases

183
Q

what kind of properties do endothelial cells have?

A

organ-typic - continuous (fenestrated or non-fensprated) or discontinuous

184
Q

what is contact inhibition?

A

endothelial cells form a monolayer with cdll-cell junctions

185
Q

what blood vessel functions do endothelial cells regulates?

A

tissue homeostasis and regeneration
vascular tone - vasoconstrictors/dilators
angiogenesis - growth factors & matrix products
haemostasis and thrombosis - procoagulant factors/antithrombotic
permeability
inflammation - adhesion molecules

186
Q

what can lead to an activated endothelium?

A 
smoking
oxidised LDL
mechanical stress
viruses
inflammation
high bp
high glucose
187
Q

risk factors for atherogenesis?

A 
hypercholstrolaemia
DM
hypertension
sex hormone imbalance
ageing
188
Q

difference between a capillary and a post capillary senile?

A

PCV has more pericytes

189
Q

outline normal leukocyte recruitment

A

during inflammation leukocytes adhere to endothelium of post capillary venules and transmigrate into tissues

190
Q

outline leukocyte recruitment in atherosclerosis

A

leukocytes adhere to endothelium of large arteries and get stuck in sub endothelial space
monocytes then migrate in and differentiate into macrophages and foam cells

191
Q

how does vascular permeability contribute to atherogenesis?

A

endothelial dysfunction leads to ↑ permeability → lipoproteins can move into subendothelial space and bind to matrix proteoglycans → oxidised LDLs → bind ti macrophages → foam cells

192
Q

where are atherosclerotic plaques most likely to form? why?

A

at bifurcations and curvatures

due to turbulent, nonuniform flow → low wall shear stress → endothelial cell activation

193
Q

benefits of laminar flow?

A

promote antithrombotic and anti-inflammatory factors
endothelial survival, inhibits smc proliferation
NO production

194
Q

disadvantages of disturbed blood flow?

A

thrombosis, inflammation - leukocyte adhesion
endothelial apoptosis and smc proliferation → shape chnage
loss of NO production

195
Q

protective effects of NO on vascular endothelium?

A 
dilates blood vessels
reduces LDL oxidation
reduces release of superoxide radicals 
reduces SMC proliferation
inhibits monocyte adhesion
reduces platelet activation
196
Q

what can promote angiogenesis?

A

hypoxia as in advanced atherosclerosis

197
Q

modifiable risk factors for CHD?

A

smoking, lipids intake, blood pressure, diabetes, obesity, sedentary lifestyle

198
Q

nonmodifiable risk factors for CHD?

A

age, sex, genetics

199
Q

outline the progression of atherosclerosis

A

hypertrophy of smooth muscle in lesion-prone coronary artery (eg at bifurcation) → lesion occurs → macrophages enter and engulfs oxLDLs → foam cells → pools of extracellular lipid → core of extracellular lipid → fibrous thickening (SMC hypertrophy) → fissure , hepatoma & thrombus
type II lesion → preatheroma → atheroma → fibroatheroma → complicated lesion

200
Q

two types of macrophages?

A

inflammatory - kill microorgansisms

resident - homeostatic, suppress inflammation

201
Q

outline how LDLs lead to inflammation in blood vessels?

A

damaged endothelium → LDLs can leak through into sub endothelial space → trapped by proteoglycans → modified bu mechanisms like oxidation (free radicals) → phagocytosed by macrophages → die and become foam cells → chronic inflammation

202
Q

what is familial hypercholestrolaemia?

A

autosomal disease
↑↑↑cholsetrol due to failure to clear LDL from blood
xanthomas
early atherosclerosis

203
Q

statins inhibit ethic enzyme?

A

HMG-CoA reductase

204
Q

what allows macrophages to bind to OxLDLs?

A

macrophage scavenger receptor A and B

205
Q

how do macrophages further oxidise LDLs?

A

NADPH oxidase
myeloperoxidase
= ↑ oxidation = ↑ endothelial damage

206
Q

how do plaque macrophages recruit more monocytes?

A

cytokines - eg IL-1 → ↑ VCAM-1

chemokine MCP-1 → CCR2

207
Q

explain the positive feedback loop in atheroscelrosis

A

oxidised LDLs become phagocytosed by macrophages → macrophages release free radicals to oxidise more LDLs → macrophages phagocytose more → die and become foam cells → release cytokines and chemokine → more monocyte recruitment

208
Q

outline the ‘wound-healing’ role of macrophages in atherosclerosis

A

macrophages release :
-platelet derived growth factor → ↑ VSMC
-transforming growth factor beta → ↑ collagen and matrix deposition
forms fibrous cap around necrotic core
VSMC becomes less contractile and more synthetic

209
Q

outline the role of proteinases released by macrophages

A

release metalloproteinases which activate each other to degrade collagen (w Zn) → plaque erosion → rupture → blood coagulation → occlusive thrombus

210
Q

what are the characteristics of a vulnerable plaque?

A 
thin fibrous cap
large soft eccentric lipid-rich core
increased vsmc apoptosis
reduced collagen content
activated macrophages expressing mmps
211
Q

outline macrophage apoptosis

A

macrophages are overloaded by oxLDLs → die via apoptosis → release macrophage tissue factors and toxic lipids → into necrotic core (central death zone) containing thrombogenic material → walled off by fibrous cap
rupture → thrombosis

212
Q

what is the master regulator of inflammation?

A

nuclear factor kappa b (activates macrophages)

213
Q

how is NFkB activated? what does it do?

A

scavenger receptors, toll-like receptors, IL-1

switches on inflammatory genes (MMPs, inducible nitric oxide synthase, IL-1)

BRS 2 (12 decks)

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