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PACES > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Peripheral signs infective endocarditis

A
  • splinter haemorrhages
  • oslers nodes (finger pulp, tender)
  • Janeway lesions (palm)
  • Roth spots (retina)
  • splenomegaly
  • haematuria
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2
Q

Aortic stenosis Vs sclerosis

A

AS - radiation to carotids, may have slow rising pulse
Sclerosis - murmur only

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3
Q

Aortic stenosis causes

A
  • Age/calcification
  • Congenital (bicuspid) +/- coarctation
  • Rheumatic/streptococcal
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4
Q

Dukes criteria

A

MAJOR
- BCs with typical org
- Echo evidence - abscess/vegetation/dehiscence
MINOR
- Fever >38
- Suggestive echo
- Predisposition e.g. prosthesis
- Embolic phenomena
- Vasculitic phenomena e.g. ESR
- Atypical org on BC

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5
Q

AS signs besides murmur

A
  • Slow rising pulse
  • Narrow pulse pressure
  • => “parvus et tardus” carotid = weak/slow
  • Delayed A2
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6
Q

AS replacement indications

A

Severe +:
- Vmax >5m/s
- Area <0.6cm2
- LVEF<55%
- BNP*2 normal
- Symptoms on exercise
- Gradient > 40mmHg + area <1cm

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7
Q

Aortic Regurg peripheral signs

A
  • Quinkes - nail bed pulsation
  • Corrigan - vegorous neck pulsation
  • De Mussets - head nodding
  • “Pistol shot” femoral pulse sounds
  • Collapsing/waterhammer pulse
  • Wide pulse pressure
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8
Q

AR causes

A

Acute valve:
- Endocarditis
Chronic valve:
- Rheumatic fever
Acute root:
- Type A dissection
- Trauma
Chronic root:
- Marfan’s -dilation
- HTN - dilation
- Syphilis - aortitis
- Ank spond - aortitis
- Vasculitis

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9
Q

AR valve replacement criteria

A
  • Acute
  • pulse pressure>100
  • LVEF<50%
  • ECG changes
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10
Q

Reason for wide S2 splitting in MR

A

Aortic valve shuts sooner as it empties rapidly

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11
Q

Causes MR

A

CTDs (ED/Marfan’s, osteogenisis imperfecta),
Turners
Rheumatic fever
LV dilatation

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12
Q

JVP waves

A

A wave - atrial systole
C - tricuspid closure
X descent - ventricular systole
V wave - atrial filling
Y descent - Tricuspid opening
https://gramproject.com/wp-content/uploads/2021/01/JVP-waveform.png

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13
Q

AS medical management

A

If symptoms, replace.
Follow up:
- Echo every 6/12, 1 year, or 3 years dep on severity
Medications:
- Statins
- BP control, avoiding ACE if haemodynamically significant disease. Avoid vasodilators.
- BB good option in heart failure

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14
Q

Clinical features severe AS

A
  • Slow rising, low volume pulse
  • Narrow pulse pressure
  • Quiet/absent S2
  • High pitch, long duration murmur
  • LV heave
  • S4 in LVH
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15
Q

Mitral stenosis causes

A
  • Rheumatic fever most common
    Rarer:
  • Congenital
  • Carcinoid syndrome
  • SLE
  • Amyloid
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16
Q

HCM inheritance

A

Usually AD
MYH7 (B myosin) or MYBPC3 (myosin binding protein chain)

17
Q

Young cardio patient syncope

A

HCM
Channelopathies (LQT, brugada, WPW)
Other congenital cardiac conditions

18
Q

Broad categories congenital heart disease

A

1 - L-R shunts (acyanotic)
2 - R-L shunts (cyanotic)
3 - Obstructive

19
Q

Eisenmenger’s syndrome

A
  • Any congenital L-R shunt
    -> Increase pulmonary vascular resistance
    -> Pulmonary hypertension
    -> Pulmonary/right heart remodelling
    -> R pressure > L
    -> Shunt reversal and cyanosis, polycythaemia
    Usually around age 20-40
20
Q

Congenital L-R in order of prevalence

A
  • VSD (outlet, inlet, perimembranous, muscular)
  • ASD (sinus venosus, ostium primum, o secundum, unroofed coronary sinus)
  • Patent ductus arteriosus (aorta-pulm circ, bypasses pulm circ as maternal blood entering RA -> lower body cyanosis, machinery murmur)
  • APVC (anomolous pulmonary venous connection) Rare.
21
Q

Causes of VSD

A
  • Congenital (most common CHD)
  • Ischaemic
22
Q

VSD signs

A

Pansystolic murmur LLSE. Loud 2nd HS if pulm HTN

23
Q

ASD signs

A

Systolic murmur at L upper sternal edge
Fixed S2 splitting

24
Q

Why does ASD cause fixed S2 splitting

A

ASD equalises pressures in both ventricles, negating physiological variation of splitting with respiration

25
Q

Explain physiological S2 splitting

A
  • S2 = aortic & pulmonary valves
  • At end of systole, aortic pressure > pulmonary artery pressure (V pressure similar)
  • Therefore A shuts before P
    In inspiration:
  • Flow of blood into R circulation increased
  • Prolonged RV ejection time -> later P2
  • Flow of blood out of L circulation decreased
  • Therefore shorter ejection rime -> A earlier

Leads to increased split on inspiration

26
Q

R-L congenital shunts

A
  • Tetralogy of fallot
  • Transposition of great arteries (presents in hours of life, emergency surgery)
  • Epsteins anomoly (TV misplacement -> RA/LA shunt)
27
Q

Tetralogy of fallot

A
  • Outlet VSD
  • RVOT obstruction
  • RV hypertrophy
  • Overriding aorta

Congenital of life
Presents in childhood with cyanosis, dyspnoea, poor growth

28
Q
A

PACES (4 decks)

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