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RACP Clinical > Clinical > Flashcards

Clinical Flashcards

1
Q

Clubbing

A

Loss of hyponychial angle

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2
Q

Schamroth’s sign

A

Disappearance of the diamond shaped space when nails of two similar fingers are held facing each other

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3
Q

Splinter haemorrhages

A 
Trauma
Infective endocarditis
Vasculitis (e.g. RA, PAN, APLS). 
Haematological malignancy
Profound anaemia
Sepsis
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4
Q

Osler’s nodes

A

Red, raised, tender, palpable nodules

Osler ouch

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5
Q

Janeway lesions

A

Non-tender erythematous maculopapular lesions containing bacteria

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6
Q

Tendon xanthomata

A

Yellow or orange deposits of lipid in the tendons that occur in type II hyperlipidaemia

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7
Q

Palmer and tuboeruptive xanthomata

A

Yellow or orange deposits of lipid are characteristic of type III hyperlipidaemia

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8
Q

Radiofemoral delay

A

Coarctation of the aorta

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9
Q

Radial-radial delay

A

Large arterial occlusion by atherosclerotic plaque or aneurysm
Subclavian artery stenosis
Dissection of the throacic aorta

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10
Q

Pulse of aortic regurgitation

A

Bounding pulse

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11
Q

Pulsus alternans

A

Alternating strong and weak pulse

Advanced LVF

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12
Q

Korotkoff sounds

A

K1: pressure at which the sound is first heard
K2: increase in intensity of sound
K3: sound decreases
K4: sound becomes muffled
K5: sound disappears
? K5 as best measure of diastolic pressure
K4 is more accurate in severe AR

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13
Q

Pulsus paradoxus

A

During inspiration the systolic and diastolic BP normally decrease, if this is exaggerated then is pulsus paradoxus
Abnormal if >10mmHg
Detect: lower cuff pressure slowly until K1 is audible intermittently (expiration), and then at every heart beat. Difference in the two measurements represents the level of the pulsus paradoxus.

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14
Q

Causes of pulsus paradoxus

A

Constrictive pericarditis
Pericardial effusion
Severe asthma

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15
Q

Postural hypotension

A

Fall in BP >15mmHg systolic or 10mmHg diastolic
May or may not be symptomatic
Most common cause is an a-adrenergic antagonist

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16
Q

Xanthelasmata

A

Intracutaneous deposits around the eye
May be a normal variant
May indicate type II or III hyperlipidaemia
Not always associated with hyperlipidaemia

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17
Q

Arcus senilis

A

Half or completegrey circle is seen around the pupil

Probably associated with increased cardiovascular risk

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18
Q

Causes of postural hypotension

A

Hypovolaemia
Addison’s
Neuropathy (DM, amyloidosis, Shy-Drager symdrome)
Drugs (vasodilators, TCAs, antihypertensives, diuretics, antipsychotics)
Idiopathic orthostatic hypotension (rare, progressive degenerative ANS disease seen in elderly men)

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19
Q

Mitral facies

A

Rosy cheeks with a bluish tinge due to dilation of the malar capillaries
Associated with pulmonary hypertension and a low cardiac output

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20
Q

Marfan’s syndrome

A

Congenital heart disease: aortic regurgitation secondary to aortic root dilatation
Mitral regurgitation secondary to mitral prolapse

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21
Q

Anacrotic pulse character

A

Small volume, slow uptake, notched wave on upstroke

Aortic stenosis

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22
Q

Plateau pulse character

A

Slow upstroke

Aortic stenosis

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23
Q

Bisferiens pulse character

A

Aortic stenosis and regurgitation

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24
Q

Collapsing pulse character

A 
Aortic regurgitation
Hyperdynamic circulation
Patent ductus arteriosus
Peripheral arteriovenous fistula
Arteriosclerosis aorta (particularly elderly pts).
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25
Q

Small volume pulse character

A

Aortic stenosis

Pericardial effusion

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26
Q

Alternans pulse character

A

Alternating strong and weak beats

Left ventricular failure

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27
Q

JVP: a wave

A

Coincides with right atrial systole and S1
Precedes carotid pulsation
Due to atrial contraction

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28
Q

JVP: v wave

A

Due to atrial filling

Period when the TV remains closed during ventricular systole

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29
Q

Kussmaul’s sign

A

Rise in JVP on inspiration (opposite of what normally happens)

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30
Q

Abdominojugular reflex

A

Pressure exerted over the middle of the abdomen for 10 seconds will increase venous return to RA and thus JVP will transiently rise
If RV failure or LA pressures are elevated (LVF) then it may remain elevated for duration of compression

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31
Q

Cannon a waves

A

Occur when right atrium contracts against a closed tricuspid valve
Intermittent complete heart block
Paroxysmal nodal tachycardia with retrograde atrial conduction

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32
Q

Giant a waves

A

Occur with each beat
Occur when right atrial pressures are raised because of elevated pressures in the pulmonary circulation or obstruction to outflow (TS)

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33
Q

Causes of an elevated central venous pressure

A 
RV failure
TS or TR
Pericardial effusion or constructive pericarditis
SVC obstruction
Fluid overload
Hyperdynamic circulation
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34
Q

Causes of dominant a wave, JVP

A

TS (also causing a slow y descent)
Pulmonary stenosis
Pulmonary hypertension

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35
Q

Causes of a dominant v wave

A

TR
Large v waves of TR should not be missed
Reliable sign

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36
Q

Causes of an absent x descent

A

Atrial fibrillation

37
Q

Causes of an exaggerated x descent

A

Acute tamponade

Constructive pericarditis

38
Q

Causes of a sharp y descent

A

Severe TR

Constructive pericarditis

39
Q

Causes of a slow y descent

A

TS

Right atrial myxoma

40
Q

Causes of clubbing

A 
Cyanotic congenital heart disease
Infective endocarditis
Lung cancer (usually not small cell)
Chronic pulmonary suppuration (e.g. bronchiectasis, lung abscess, empyema)
Idiopathic pulmonary fibrosis

Uncommon: cystic fibrosis, as estosis, pleural mesothelioma (benign), pleural fibroma, cirrhosis (esp. biliary cirrhosis), inflammatory bowel disease, coeliac disease, thyrotoxicosis

Rare: Neurogenic diaphragmatic tumours, pregnancy, secondary parathryoidism

41
Q

Causes unilateral clubbing

A

Bronchial AV aneurysm

Axillary artery aneurysm

42
Q

Location of normal apex beat

A

Fifth left intercostal space

1cm medial to the midclavicular line

43
Q

Pressure loaded apex beat

A

Heaving, hyperdynamic or systolic overloaded apex
Forceful sustained impulse
Aortic stenosis or hypertension

44
Q

Volume loaded apex beat

A

Thrusting apex beat
Displaced, diffuse, non-sustained impulse
Occurs in advanced MR or dilated cardimyopathy

45
Q

Dyskinetic apex beat

A

Uncordinated impulse felt over a larger area than normal in the praecordium and is usually due to LV dysfunction (e.g. In anterior myocardial infarction)

46
Q

Double impluse apex beat

A

Two distinct impulses felt with each systole

Characteristic of hypertrophic cardiomyopathy

47
Q

Tapping apex beat

A

Felt when the first heart sound is palpable

Indicates mitral or tricuspid stenosis

48
Q

Parasternal impluse

A

Felt with heel of hand is resting just to the left of the sternum with the fingers lifted slightly off chest
If RV enlargement or severe LA enlargement then the RV is pushed anteriorly and the heel of the hand is pushed off the chest wall

49
Q

Palpable P2

A

Palpation with fingers over pulmonary area may reveal the palpable tap of pulmonary valve closure in pulmonary hypertension

50
Q

Thrills

A

Palpable murmurs

Presence of a thrill usually indicates an organic lesion

51
Q

S1

A

Corresponds to closure of mitral and tricuspid valve closure
Mitral valve closes before tricuspid
Indicates beginning of systole

52
Q

S2

A

Softer, shorter, higher pitched
Marks end of systole
Aortic and pulmonary valve closure
The lower pressure in the pulmonary circulation, flow continues into the pulmonary artery after the end of systole and pulmonary valve closes later than aortic valve

53
Q

Loud S1

A

When the MV or TV cusps remain open at the end of diastole and shut forcefully with the onset of ventricular systole
MS: the narrow valve orifice limits ventricular filling so there is no diminution in flow towards then end of diastole
Other causes are due to reduced diastolic filling time
Tachycardia
Short AV conduction time

54
Q

Soft S1

A

Due to a prolonged diastolic filling time (e.g. first degree AV block)
Delayed onset of LV systole (e.g. LBBB)
Failure of the leaflets to coapt normally (e.g. MR)

55
Q

Loud A2

A

Systemic hypertension (forceful valve closure secondary to high aortic pressures). Congenital aortic stenosis

56
Q

Loud P2

A 
Pulmonary hypertension (forceful valve closure due)
Palpable P2 correlates better with raised pulmonary pressure
57
Q

Soft A2

A

Aortic valve calcification and reduced motion if valve leaflets
AR when leaflets do not coast

58
Q

Splitting S1

A

Usually not detectable

Complete RBBB

59
Q

Fixed splitting S2

A

No respiratory variation

ASD

60
Q

Reversed splitting

A

P2 occurs first and splitting occurs in expiration
LBBB (delayedLV depolarisation)
Severe AS, coarctation of the aorta (delayed LV emptying)
Large PDA (increased LV volume load
n.b. this is a large machinery murmur, so S2 is not usually heard).

61
Q

Pathological S3

A

Due to reduced ventricular compliance

Strongly associated with increased atrial and ventricular end diastolic pressure

62
Q

Left ventricular S3

A

Louder at the apex
Louder on expiration
Can be physiological (due to very rapid diastolic filling)
Associated with increased cardiac output (e.g. thyrotoxicosis, pregnancy)
Sign of LVF and dilatation
Also AR, MR, VSD and PDA

63
Q

Right ventricular S3

A

Louder at the LSE
Louder with inspiration
Occurs in RV failure or constructive pericarditis

64
Q

S4

A

Late diastolic sound
Pitched slightly similar to “Tennessee”
Due to high pressure atrial wave reflected back from a poorly compliant ventricle
n.b. Lost when atrial fibrillation, because sound depends on effective atrial contraction
Low pitched. Disappears if the bell of the stethoscope is pressed firmly to the chest.

65
Q

Right ventricular S4

A

RV compliance is reduced (e.g. pulmonary hypertension, pulmonary stenosis)

66
Q

Left ventricular S4

A

LV compliance is reduced (e.g. AS, acute MR, systemic hypertension, IHD, advanced age)

67
Q

Summation gallop

A

S3 and S4 are superimposed
Occurs when heart rate is >120
does not imply ventricular stress unless extra sounds persist when the HR slows or is slowed by carotid sinus massage

68
Q

Quadruple rhythm

A

Occurs when both S3 and S4 are audible

Implies severe ventricular dysfunction

69
Q

Opening snap

A

High pitched sound that occurs in MS at a variable distance after S2
Due to the sudden opening of the mitral valve and is followed by the diastolic murmur of MS

70
Q

Systolic ejection click

A

High pitched sound over aortic or pulmonary area and LSE
May occur in congenital pulmonary or aortic stenosis
Followed by systolic ejection murmur of aortic or pulmonary stenosis

71
Q

Tumour plop

A

RARE
Associated with atrial myxoma
during atrial systole a loosely pedunculated tumour may be propelled into the mitral or tricuspid valve orifice causing an early diastolic plopping sound

72
Q

Diastolic pericardial knock

A

Sudden cessation of ventricular filling because of constrictive pericardial disease

73
Q

Characteristics of a murmur

A

Timing
Area of greatest intensity
Loudness and pitch
Effect of dynamic manoeuvers (e.g. respiration, Valsalva)

74
Q

Causes of pansystolic murmur

A

MR, TR, VSD

75
Q

Causes of mid-systolic ejection murmur

A

Crescendo-decrescendo murmur

AS, PS

76
Q

Causes of a late systolic murmur

A

Mitral valve prolapse

Papillary muscle dysfunction where MR beings in midsystole

77
Q

Early diastolic murmur

A

AR or PR

Murmur is loudest at the beginning when aortic and pulmonary pressures are highest

78
Q

Mid-diastolic murmur

A

MS, TS
Due to impaired flow during ventricular filling when valve is narrowed
Also atrial myxoma (tumour mass obstructs valve orifice)

79
Q

Continuous murmurs

A

Extend throughout diastole and systole
PDA
AV fistula (coronary artery, pulmonary, systemic)
Aortopulmonary connection (congenital, Blalock shunt)
Venous hum
Rupture of the sinus of Valsalva into the right ventricle or atrium (Mammary soufflé: late pregnancy or early postpartum period)

80
Q

Pericardial friction rub

A

Due to movement of inflamed pericardial surfaces
Pericarditis
Louder when sitting forward and on inspiration

81
Q

Mediastinal crunch (Hamman’s sign)

A

Crunching sound heard in time with the heart beat, but with systolic and diastolic components
Due to presence of air in mediastinum

82
Q

Levine’s grading system (murmur)

A

1/6: very soft and not heard at first
2/6: soft, but detected by experienced auscultator
3/6 Moderate, there is no thrill
4/6: Loud, thrill just palpable
5/6: Very loud with a thrill easily palpable
6/6: very, very loud (heard without using stethoscope)

83
Q

Respiration manoeuvers for murmurs

A

Murmurs that arise on R side of the heart become louder during inspiration (increased venous return, blood flow to the R side)
L sided murmurs are unchanged or become softer
Expiration has the opposite effect

84
Q

Deep expiration (murmurs)

A

AR, pericardial friction rub
Have pt. sit up, lean forward and exhale
(brings the base of the heart closer to the chest wall)

85
Q

Valsalva manoeuver (murmurs)

A

LSE: during systole can augment murmur or HCM (becomes louder)
Apex: systolic click of mitral prolapse is heard earlier

86
Q

Standing to squatting manoeuver (murmurs)

A

Pt. squats rapidly, increase in venous return and systemic arterial resistance
Augments most murmurs
Reduces the intensive to the systolic murmur of HCM and delays the midsystolic click and murmur or mitral prolapse
Opposite occurs on standing quickly

87
Q

Isometric exercise (murmurs)

A

Sustained hand grip or repeated sit-ups (20-30sec)
increases systemic arterial resistance, BP and heart size
AS murmur becomes softer
Most other murmurs are louder
HCM murmur is softer
Mitral valve prolapse i9s delayed because of an increase in ventricular volume

88
Q

DDx: carotid artery bruit

A

Carotid artery stenosis
AS murmur radiating to the carotids
Thyrotoxicosis may result in a systolic bruit due to increased vascularity of the gland
If carotid artery stenosis listen in steps back to base of heart, if disappears then carotid stenosis, if continues the AS radiating

RACP Clinical (1 decks)

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