Revision Flashcards

1
Q

what causes a parasternal heave

A

right ventricular hypertrophy

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2
Q

what causes a thrill

A

turbulent blood flow

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3
Q

is stenosis an opening or closing problem

A

opening

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4
Q

is regurgitation an opening or closing problem

A

closing

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5
Q

what valves could cause a stenosis murmur during systole

A

aortic or pulmonary

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6
Q

what valves could cause a regurgitation murmur during systole

A

mitral or tricuspid

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7
Q

what valves could cause a stenosis murmur during diastole

A

mitral or tricuspid

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8
Q

what valves could cause a regurgitation murmur during diastole

A

aortic or pulmonary

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9
Q

what is the normal range for BMI

A

18-25

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10
Q

where do you measure waist circumference

A

halfway in between lower rib and iliac spine

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11
Q

what are the normal ranges for waist circumference

A

102 cm men 82 cm women

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12
Q

what are the normal ranges for cholesterol

A

low 5 LDL, above 1 HDL

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13
Q

what are the normal ranges for blood pressure

A

120/80-140/90

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14
Q

what is the cut of age for suspicion of hereditary disease

A

60 men 65 women

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15
Q

what is the most commonly occluded coronary artery

A

LAD (left anterior descending)

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16
Q

why do veins have a wider lumen

A

as they carry most of the blood- capacitance vessels

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17
Q

what is atherosclerosis

A

a pogressive disease characterised by the build up of plaques within the arteries

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18
Q

describe the pathogenesis of atherosclerotic plaques

A

endothelial damage

Protective response results in production of
cellular adhesion molecules

Monocytes and T lymphocytes attach to
‘sticky’ surface of endothelial cells

Migrate through arterial wall to subendothelial space

Macrophages take up oxidised LDL-C

Lipid-rich foam cells

Fatty streak and plaque

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19
Q

what is the largest class of lipoproteins

A

chylomicrons

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20
Q

are triglycerides good or bad

A

associated with increased risk of CHD events but not as bad as LDL

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21
Q

what does VLDL do in the endogenous pathway

A

transports triglycerides from the liver to the rest of the body

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22
Q

what do chylomicrons do in the endogenous pathway

A

transport triglycerides from the gut to the liver

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23
Q

what is xanthelasma

A

xanthomas of eyelids (may/may not be associated with hyperlipidemia)

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24
Q

what are tendon xanthomas

A

extensor tendons (of Achilles tendon, fingers, patella. elbows) are infiltrated by lipids

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25
Q

what are tuberous xanthomas

A

lipid deposits in the dermis and subcutis

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26
Q

what is eruptive xanthomas

A

small reddish-yellow papules (buttocks, posterior thighs, body folds)

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27
Q

what does hypertension treatment reduce the risk of

A

ischaemic heart disease, stroke, mortality

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28
Q

what is the assign score

A

risk of developing CVD

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29
Q

what is essential/primary hypertension

A

no underlying cause (90%)

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30
Q

what is secondary hypertension

A

underlying cause (caused by another medical conditions)

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31
Q

what is an example of an intrinsic control mechanism of the heart

A

the frank starling curve- EDV and stroke volume

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32
Q

what is ventricular preload

A

degree of stretch cardiac muscle cells before they contract (at the end of diastolic filling)

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33
Q

what is cardiac contractility

A

degree of shortening of cardiac muscle cells from a fixed fibre length

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34
Q

how does pre load affect CO

A

greater the stretch, greater the contractility (up to optimum fibre length)

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35
Q

what affect does SA node stretch have on HR

A

increases HR as caused by increased venous return

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36
Q

what is pressure diuresis

A

increased urine output due to high blood pressure

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37
Q

what is pressure natriuresis

A

increased sodium excretion due to high arterial pressure

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38
Q

what leads to the secretion of the enzyme renin by the juxtaglomerular apparatus

A

in response to reduced blood pressure

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39
Q

what does renin do

A

converts angiotensinogen into angiotensin I

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40
Q

what cornverts angiotensin I to angiotensin II

A

ACE

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41
Q

what is angiotension II

A

potent vasoconstrictor of aterioles and veins and stimulates the adrenal cortex’s release of aldosterone

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42
Q

what does aldosterone do

A

increases sodium reabsorption into the kidneys

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43
Q

what does the reabsorption of sodium by kidneys do

A

increases blood volume as water follows sodium, increasing blood pressure

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44
Q

what does ADH do

A

acts directly on on blood vessels causing vasoconstriction, and increases the permeability of the kidney tubules to water- increasing water reabsorbtion

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45
Q

what stimulates the secretion of ADH

A

increased solute concentration in plasma detected by hypothalamus

decreases in blood pressure and volume detected by baroreceptors

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46
Q

what is atrial natriuretic peptide released from and in response to what

A

released from atrial muscle of heart in response to increased stretch

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47
Q

what is the role of atrial natriuretic peptide (BNP)

A

acts on the kidneys to increase water and sodium secretion. also has vasodilator effect on the arteries and veins

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48
Q

what is masked hypertension (black coat)

A

true normotension with high clinical pressure

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49
Q

what should be offered to all patients who have hypertension

A

test urine for presence of protein
take blood to measure glucose, electrolytes, creatinine, estimated glomerular filtration rate and cholesterol
examine fundi for hypertensive retinopathy
arrange a 12-lead ECG.

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50
Q

what blood pressure should be aimed for in people over 80

A

under 150/90

51
Q

what is Phaeochromocytoma

A

a rare tumor of adrenal gland tissue. It results in the release of too much epinephrine and norepinephrine, hormones that control heart rate, metabolism, and blood pressure

52
Q

what is Fibromuscular Dysplasia

A

a non-atherosclerotic, non-inflammatory disease of the blood vessels that causes abnormal growth within the wall of an artery. common in young woman, curable

53
Q

in treating blood pressure id combination or monotherapy better

A

Initial combination much more effective than optimized initial monotherapy

54
Q

what are the three main treatments used for hypertension

A

A – ACE inhibitor or low-cost angiotensinII receptor blocker (ARB)1
C – Calcium-channel blocker (CCB)
D – Thiazide-like diuretic

55
Q

what can cause resistant hypertension

A
Non-concordance
‘White Coat’ Effect
Pseudo-Hypertension
Lifestyle Factors
Drug Interactions
Secondary Hypertension
True Resistance
56
Q

what is the most effective treatment for resistant hypertension

A

Spironolactone (start low go slow)

57
Q

what hypertension treatment should be used in young women

A

BCD (B=beta blockers)

58
Q

fill out the following

younger (<55 years) and non-Black
Step 1
Step 2
Step 3

A
1= A
2= A + C
3= A + C + D
59
Q

fill out the following

older (>= 55 years) or black
Step 1
Step 2
Step 3

A
1= C
2= C + A
3= A + C + D
60
Q

fill out the following

step 4 (resistant hypertension);

A

A + C + D + consider further diuretic (b), (c) or alpha- or beta-blocker (d)

Consider seeking specialist advice

61
Q

what is the new technology developed to treat hypertension

A

Renal denervation (doesnt work)

Baro-receptor stimulation

Rox Coupler

62
Q

describe the anatomy of the aortic valve

A

usually tricuspid, semi luminar (can be bicuspid congenitally)

63
Q

what are the symptoms of IE

A

fever, clubbing, splinter haemorrhages, janeway lesions, osler nodes and roth spots

64
Q

what can septic emboli cause when infecting tissue

A

micro anuersyms, abscesses

65
Q

what is haemopericardium

A

blood in the pericardial sac, causes tamponade

66
Q

where is pressure acting in the heart felt the most

A

in the RA, as thin walled

67
Q

what can cause a haemopericardium

A

dissecting aneurysm, trauma

68
Q

after an MI when does scar tissue replace dead tissue

A

within a few months

69
Q

what are the two types of inflammation

A

acute and chronic

70
Q

what is the cardinal cell of acute inflammation

A

neutrophils, have granules that have enzymes which break down dead cells

71
Q

when and why does rupture of myocardium after an MI happen

A

5-7 after MI, as dead tissue being broken down before it is replaced by scar tissue

72
Q

what causes co-arctation of the aorta

A

congenital

73
Q

how can hypertrophy lead to arrhythmias

A

as muscle deficient of blood and oxygen so is unstable

74
Q

what can cause hypertrophy

A

hypertension, aortic stenosis (working against resistance)

75
Q

what makes an atherosclerotic plaque bigger

A

cholesterol accumulating within it

76
Q

what is the most common site for coronary artery occlusion

A

proximal third of LAD

77
Q

how can nuclei shoe necrosis

A

when cells die their nucleus breaks down, dead cells have no nucleus

78
Q

when do neutrophils arrive at site of necrosis

A

build up after 48 hrs

79
Q

what is pus

A

dead tissue and dead or dying neutrophils

80
Q

when does a CXR show cardiomegaly

A

when width more than 50% of thoracic width

81
Q

what is the cardiothoracic ratio

A

ratio of maximum diameter of the heart divided by the maximum diameter of the thorax

82
Q

what are the pros and cons of angiography

A

p - excellent coronary arterial depiction, assess anomalies/ plaques/ stenosis/ stents/ CABGs
c - radiation, invasive, complications, may need admission, contrast allergy, kidney damage

83
Q

what plane of CXR can the cardiothoracic ratio be measured

A

PA

84
Q

what are the pros and cos of echocardiography

A

p - immediate, functional/ valvular/ chamber assesment, no radiation
c - operator (inexperienced) and patient (obese, chest deformity) dependant, incomplete cardiac assessment

85
Q

cardiac CT can be done with or without contrast. what is a cardiac CT good and bad at showing

A

non contrast can show presence of calcium in CA but not good at showing vascular lumen to see stenosis

86
Q

what are the pros and cons of cardiac CT with contrast

A

p - excellent depiction, non invasive (as only IV), functional/chamber assesment, looks at vessels and lungs aswell
c- radiation, not as good as catheter angiography, contrast allergy and nephropathy, need specialist equipment and expertise

87
Q

what are the pros and cons of MRI

A

p - no radiation, functional and anatomical assesment- good at soft tissue reolution, GOLD
STANDARD
c - takes long, claustrophobia, MRI contraindications (e.g. pacemaker), not good at coronary arteries

88
Q

what can cardiac MRI calculate

A

cardiac function

89
Q

what is a cine cardiac investigation and what does it show

A

dynamic MRI, shows functionality and any abnormalities

90
Q

what does nuclear cardiology assess

A

myocardial perfusion

91
Q

what may precipitate pulmonary oedema in patients with poor cardiac function

A

atrial fibrillation

92
Q

what can echocardiography and MRI show in patients who have previously had an MI

A

ventricular wall dysnfunction

93
Q

can interventions be done in the same procedure as CT angiography

A

yes

94
Q

what can cause a delay in radial and femoral pulses

A

coarctation of the aorta which classically happen in proximal part of descending aorta, distal to the left subclavian artery (blood struggles to get through narrowing)

95
Q

do MRI or echo investigations have associated radiation

A

no

96
Q

what valve problem is associated with aortic coarctation IMPORTANT

A

congential bicuspid aortic valve which is prone to becoming stenosed

97
Q

what valve problem can cause anginal symptoms

A

aortic stenosis

98
Q

when does atrial septal defect often present and with what symptoms

A

in adulthood- cardiac murmur, exertional dsypnoea

99
Q

what are clinical features of dilated cardiomyopathy

A

pleural effusion, LV chamber dilatation, mid-myocardial enhancement

100
Q

what can delayed enhacement foci be substrates

A

sudden onset arrhythmias

101
Q

when should CTPA be used for PE

A

in patients with ABNORMAL CXR or pre existing lung disease

102
Q

when should a V/Q scan be used for PE

A

when patient has NORMAL CXR or no existing lung disease (no perfusion but normal ventilation)

103
Q

when should CT angiogram be used in in head injury

A

good at finding blood in brain, e,g malformation of vasculature after a bleed from a haemorrhage

104
Q

how long approximately does systole and diastole

A

s 0.3, d 0.5

105
Q

what is masked by the QRS complex

A

atrial repolarisation

106
Q

when do the ventricles contract in an ECG

A

after QRS in ST segment- mechanical activity follows electrical

107
Q

where is the ectopic focus that causes A fib

A

in pulmonary veins

108
Q

does A fib require permanent pacing

A

sometimes

109
Q

when do the ventricles relax in an ECG

A

in the TP interval

110
Q

what does the PR interval represent

A

AV nodal delay

111
Q

is the heart rate in complete heart block irregular or regular

A

regular- ventricles excited by alternative pacemaker which usually has slower rate. Despite ventricles going at slower rate, and slow heart rate, rhythm is still regular just slower. Atrial rate different from ventricle rate (rate of P waves different from rate of QRS, but P waves not getting through so doesn’t affect rhythm)

112
Q

what can slow the heart rate in SVT

A

adenosine

113
Q

what do vagal manoeuvres cause

A

vagal stimulation

114
Q

what is the treatment of complete heart block, bradycardia and haemodynamic instability

A

pacemaker

115
Q

what does the vagus nerve supply in the heart

A

both AV and SA node

116
Q

what does vagal stimulation do to heart

A

increase AV delay by slowing down the firing

117
Q

what does a tachycardia that doesn’t respond to adenosine mean

A

below AV node, ventricular

118
Q

when will vagal manoeuvres not help

A

if below AV node

119
Q

why is the QRS in A fib wide

A

as heart getting excited from within ventricles, not normal pathway

120
Q

can ventricular tachycardia be treated with ICD

A

yes

121
Q

what type of drugs are not effective in VT

A

anti-arrhythmic drugs

122
Q

how does atropine speed up HR

A

as blocks para sympathetic stimulation

123
Q

what is the anagram for heart murmurs

A

MRS DARMS