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Cardio final > Pummy large group > Flashcards

Pummy large group Flashcards

1
Q

What produces a new holosystolic murmur is heard at the apex that does not vary with respiration and radiates to the axilla?

A

mitral regurgitation

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2
Q

What would be the diagnostic workup for a pt with a fever and a new murmur?

A

blood cultures and cardiac ultrasound (echocardiogram)

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3
Q

What is GPC partially hemolytic; optochin-resistant; and produce dextran?

A

streptococci viridans

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4
Q

what is GPC catalase-positive; β-hemolytic; coagulase-positive; have fibronectin-binding proteins?

A

Staph aureus

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5
Q

what is Encapsulated GPC; bile-soluble; optochin-susceptible; α-hemolytic?

A

pneumococci

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6
Q

What is GPC catalase-positive; non-hemolytic; produce glycocalyx “slime layer”?

A

coagulase negative staphylococci

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7
Q

What is the best way to confirm diagnosis of Infectious endocarditis? What are the components of this?

A

Duke Criteria
2 major or one major and 3 minor or 5 minor criteria met

major:

    • blood cultures
  2. evidence of endocardial involvement (+ echo–> could be vegetation, abscess, new regurge)

minor:
1. fever
2. vascular phenomena (janeway lesions, conjuntival petechiae)
3. immunologic phenomena (osler’s nodes, rot’s spots)
4. predisposing heart condition or IDU
5. microbiologic evidence (blood cultures not meeting major criteria)

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8
Q

What allows the bacteria from the mouth to infect the valve?

A

previous injury of the valve

in older person, degeneration of the valve==> aberrant flow ==> NBTE

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9
Q

How do you go from NBTE to IE?

A

need bacteria in the blood

portals of entry:

  • skin: staphylococci
  • oral cavity: viridans
  • Upper resp tract: HACEK organisms
  • GI tract: S. bovis (gallolyticus
  • Urogenital: enteroocci
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10
Q

Which of the following will have the MOST SIGNIFICANT impact on the duration of intravenous penicillin treatment required for streptococcal native-valve endocarditis?

a. The time during which the penicillin serum concentration exceeds the lowest concentration at which active bacterial growth is prevented
b. Inoculum of metabolically inactive bacteria
c. Vascular blood supply to the infected valve
d. Presence or absence of an implantable defibrillator/pacemaker
e. The ratio of the area under the 24-hour serum penicillin concentration-time curve to the lowest concentration at which active bacterial growth is prevented

A

b. Inoculum of metabolically inactive bacteria

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11
Q

In streptococcal IE, with an MIC <0.12, what would you treat with? what is the best way of doing this?

A

PCN G, 2-3 million units IV given frequently (time dependent killer)

or cephtriaxone IV daily x 4 weeks

continuously given IV –> steady state and no troughs (below the MIC)

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12
Q

This patient (old guy with IE from s. viridans) is at highest risk for developing which of the following complications?

a. Myocardial infarction
b. Conduction defects
c. Septic pulmonary emboli
d. Lung abscess with pleural extension
e. Cerebrovascular accident

A

e. Cerebrovascular accident

because the mitral valve vegetation could break off–> can lead to CVA

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13
Q

What 3 things can give a holosystolic murmur?

A
  1. mitral regurge
  2. tricuspid regurge
  3. VSD
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14
Q

what is carvallo’s sign?

A

the maneuver where a murmur gets louder with inspiration

indicates a right sided murmur (tricuspid)

increased venous return on the right side of the heart–> increased right sided murmur

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15
Q

What will make a mitral valve louder?

A

increased after load

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16
Q

What can cause acute vs subacute endocarditis?

A

acute:
s. aureus
beta hemolytic strep
pneumococci

subacute:
viridans streptococci
enterococci 
S. bovis
HACEK group
Coagulase-negative staph
Bartonelle 
Coxiella
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17
Q

Which of the following is MOST LIKELY expressed on the surface of staph aureus?

a. Fimbrial M proteins
b. Hyaluronic acid capsule
c. Glycocalyx biofilm
d. Dextran
e. Clumping factor A

A

e. Clumping factor A

18
Q

pt with s. aureus and tricuspid vegetation is at highest risk for developing which complication?

A

Septic pulmonary emboli

Tricuspid on right–> vegetation break off and go to lungs

19
Q

What is MSSA treated with?

A

naficillin or oxacillin for 4 weeks (unless PCN allergy)

(treat for 6 weeks if left sided)

20
Q

Infection of which valve has the highest likelihood of extension beyond the valve and developing heart block?

What test would you like to order and why?

A

aortic valve

do an EKG to look for heart block==> see if they need just medical or surgical treatment

21
Q

Why is a vasovagal response more dangerous in a patient with aortic stenosis?

A

BP will drop==> decrease coronary flow==> more ischemia

22
Q 
Which exam most suggests severe aortic stenosis?
A. bounding pulse
B. soft P2
C. late peak 
D. loud murmur
A

C. late peak

late peak and longer extends==> worse stenosis

AS will have tarvis Jarvis–> late, weak pulse

23
Q

What are the causes of aortic stenosis in different age populations?

A

elderly==> calcific

<65=bicuspid

outside US can be rheumatic but WILL ALWAYS be combined with mitral valve disease

24
Q

Why is hypertrophy seen with stenosis?

A

decreases the increasing wall stress of Pressure overload

25
Q

When should a pt with Aortic stenosis be referred for surgery?

A

when symptomatic!!!

More severe symptoms–> worse prognosis

26
Q

What is the preceding event in most cases of mitral stenosis?

A

rheumatic fever

27
Q

What is the criteria for Rheumatic fever?

A

Jones criteria

28
Q

Will the opening snap be earlier or later in worse Mitral stenosis? Why?

A

earlier

atrial P will increase
less time for ventricular P< atrial P ==> open valve

29
Q

what is the severity for mitral stenosis? (or any stenosis)

A

Normal 4-6cm2

Mild 1.6-2cm2

Moderate 1.0-1.5cm2

Severe < 1cm2

30
Q

what will the echo of mitral stenosis look like?

A

hockey stick appearance

due to the left atrial enlargement and NORMAL LEFT VENTRICLE

31
Q

How will the left ventricle be affected by mitral stenosis?

A

it won’t!!

will get increase in left atria and pulmonary congestion

32
Q

what are mitral stenosis pts predisposed to get?

how can we treat this?

A

atrial fibrillation

we need to increase time of ventricular filling (because MS is a diastolic disorder)===> want to decrease the HR (beta blocker or calcium channel blocker)

(also, Pulm HTN, stroke, hemoptysis)

33
Q

What will happen to the muscle in mitral regurgitation vs aortic stenosis?

A

aortic stenosis=concentric hypertrophy
-pressure overload

regurgitation =dilated

  • eccentric hypertrophy
  • due to volume overload
34
Q

Who would be more likely to get a bioprosthetic valve?

A

> 65 yo

or woman who is of child bearing age

last about 20 years but don’t need to be on coumadin

35
Q

What does a pt with a mechanical valve need to be on forever?

A

coumadin

–> mechanical valve will last longer than bioprosthetic

-mostly worried about the mitral valve** and clots because it is a low flow system–> more likely to have clots

36
Q

What is another word for “nonbacterial thrombotic endocarditis”?

A

marantic endocarditis

uninfected vegetations in pts with malignancy and chronic disease

37
Q

What is a late finding in aortic stenosis?

A

atrial fibrillation

can precipitate decompensation in AS pts because depend on the atrial kick

38
Q

What are the symptoms seen in severe aortic stenosis?

A

angina, syncope, CHF, atrial fibrillation

39
Q

How are the lungs affected by mitral stenosis?

A
  1. venous P elevation
    - -> pulmonary congestion
  2. arterial P elevation –> fixed pulmonary HTN
    * fixed pulmonary HTN =poor prognosis –> can lead to right sided heart failure
40
Q

What is the first thing you want to do in a pt with mitral stenosis (symptomatic)?

A

keep the HR down
–> beta blocker or Ca2+ channel blocker

more time for ventricular filling

41
Q

Which valve regurgitation is normally NOT an intrinsic valve problem?

A

Tricuspid regurgitation is normally secondary to right ventricular enlargement

Cardio final (15 decks)

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