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Cardiovascular System - 3rd year > Microbiology Review Q's > Flashcards

Microbiology Review Q's Flashcards

1
Q

acute vs subacute endocarditis

who do they usually affect? what organism causes them?

A

acute endocarditis= organism with high virulence (staph aureus) usually affects people with normal hearts

subacute endocarditis= organism with low virulence (strept viridans) usually affects people who are predisposed (ex/ any heart condition that will alter flow)

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2
Q

organsim that causes infective endocarditis in patients with prosthetic heart valves

A

staph epidermidis

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3
Q

organism that causes infective endocarditis in patients with damaged/susceptible heart

A

strept viridans

(50% of people with infective endocarditis)

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4
Q

most common organism that causes acute infective endocarditis

A

staph aureus

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5
Q

Patient with prosthetic heart valve gets infective endocarditis

less than 2 months after heart valve operation VS more than 2 months after

A

less than 2 months after= most common organism that infects prosthetic hearts is staph epidermidis (organism was put in the heart during the surgery)

more than 2 months after= organism infected heart later, most common organism that infects susceptible hearts is strept viridans

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6
Q

Why is mitral valve prolapse a risk factor of infective endocarditis?

A

Mitral valve prolapse is associated with regurgitation, they both cause abnormal blood flow- which allows organisms to be in contact with the endocardium of the heart for a longer time, allowing them to stick and cause damage

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7
Q

Describe the infective endocarditis of IV drug abusers.

A

Mostly on the right side of the heart because they inject organisms along with the drugs in their veins- which then go to the right atrium.

(they may also have multiple organisms present when you test them because they inject a variety of organisms into the blood stream)

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8
Q

Why are cardiac prostheses more likely to cause infective endocarditis?

A

the normal surface of the heart is smooth while the prosthesis surface is rougher, so it attracts platelets and fibrin to stick to it= non-vegetative thrombus

This thrombus then allows organisms in the blood to stick to it and produce a vegetation (thrombus + multiplying organisms)

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9
Q

This shows a vegetation in the heart: acute or subacute infective endocarditis?

A

acute; the bacteria was virulent and was able to stick to the endothelial surface by itself. After that, the thrombus formed.

In subacute, the organism isn’t strong enough to stick by itself, so the heart must have an abnormality causing a non-vegetative thrombus to form first, then the bacteria would stick to the area. (so it would be a thrombus and the bacteria on top/superficial)

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10
Q

What are bacteria properties that help it cause infective endocarditis?

A

dextran

fibrinogen-binding proteins (/peptides)

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11
Q

organism causing infective endocarditis in IV drug users?

A

staph aureus

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12
Q

IV drug user has infective endocarditis. He uses tap water to dilute drugs. What’s the causative organism?

A

pseudomonas

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13
Q

IV drug user has infective endocarditis. He uses lemon juice to dilute drugs. What’s the causative organism?

A

candida spp.

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14
Q

What are the four microrganisms that cause culture-negative infective endocarditis?

A

Mycoplasma pneumoniae

Coxiella burnetii

Chlamydiaspp.

Legionella spp.

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15
Q

earliest manifestation of infective endocarditis?

A

fever + murmur (due to valvular affects)

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16
Q

Osler’s nodes VS Janeway lesion

A

Janeway lesion = nontender, macular lesions in palms & soles, vasculitis… painless!

Osler’s nodes = palpable, painful finger pulp

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17
Q

Which organisms that cause infective endocarditis are also likely to cause embolic events? Why?

A

S. aureus or fungal infective endocarditis

Because they cause big vegetations and thus bits can break off and cause embolic complications (splinter hemorrhage in the nails, or bigger complications like stroke)

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18
Q

What is Roth’s spot?

A

a rash in the retina that may occur as a complication of infective endocarditis

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19
Q

What infective endocarditis patient is more likely to get a lung abscess?

A

a patient where the infection is on the right side of the heart (pulmonary trunk sends it to lungs)

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20
Q

What is a mycotic aneurysm? Why does it occur?

A

it’s a dilation of an artery due to damage of the vessel wall by an infection (septic complication); AKA infected aneurysm.

The term “mycotic” referring to fungal is a misnomer as various organisms including predominantly bacterial can cause the aneurysm.

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21
Q

List some late complications of infective endocarditis

A

clubbing

spelenomagaly

roth’s spot

osler’s nodes

janeway lesion

lung abscess

mycotic aneurysm

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22
Q

How do you diagnose infective endocarditis?

(via Duke criteria, but how?)

A

for the diagnosis of definite infective endocarditis, we have to have

2 major criteria OR

1 major 3 minor criteria OR

5 minor criteria

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23
Q

A very sick patient is suspected of infective endocarditis. How do you confirm the condition by obtaining a blood culture?

A

You can either take 2 cultures, 12 hours apart

OR

4 cultures within 1 hour (15 minutes apart)

this patient is very sick and we have to start antibiotic therapy ASAP so go for the second option

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24
Q

A patient suspected of infective endocarditis has one positive blood culture. is this a major/minor Duke’s criteria?

A

minor

(major has to be 2 cultures, 12 hours apart OR 4 cultures within 1 hour)

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25
Q

Patient suspected of infective endocarditis has Temp >38.0°C, rheumatic heart disease, and a positive blood culture (+ twice, more than 12 hours apart). can you definitively say he has IE?

A

No; he has 2 minor and 1 major criteria.

We need 1 major and 3 minor for it to be definite IE

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26
Q

nosocomial infective endocarditis often occurs as a complication of which condition?

A

A complication of nosocomial bacteremia
Especially if bacteremias persist > 48h

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27
Q

3 organisms that cause aggressive infective endocarditis

A

S. aureus

Pseudomonas aeruginosa

Aspergillus spp.

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28
Q

What percent of people with aggressive infective endocarditis also have anemia?

A

70-90%

(30-60% of people with aggressive infective endocarditis also have RBC’s in urine, so it makes sense)

29
Q

Which type of echocardiography is more likely to diagnose aggressive infective endocarditis?

a. Transthoracic (TTE)
b. Transesophageal (TOE)

A

b. Transesophageal (TOE)

>95% positive

30
Q

Which type of echocardiography has the transducer behind your heart?

a. Transthoracic (TTE)
b. Transesophageal (TOE)

A

b. Transesophageal (TOE)

31
Q

Which type of echocardiography should NOT be used with patients that have heart prosthesis?

a. Transthoracic (TTE)
b. Transesophageal (TOE)

A

a. Transthoracic (TTE)

32
Q

bactericidal antibiotics for sensitive Viridans streptococci

A

penicillin x 4 weeks IV

33
Q

bactericidal antibiotics for resistant Viridans streptococci

A

ampicillin + gentamicin x 4 weeks

34
Q

bactericidal antibiotics for sensitive S. epidermidis

A

flucloxacillin x 4-6 weeks

35
Q

bactericidal antibiotics for resistant S. aureus

A

vancomycin x 4 weeks

36
Q

bactericidal antibiotics to treat Coxiella burnetii

A

doxycycline and ciprofloxacin x 2-3 years

37
Q

how to treat fungal infective endocarditis

A

surgery + antifungal

38
Q

antibiotics to treat Actinobacter

A

ceftriaxone x 4 weeks
for HACEK: (Haemophilus, Actinobacter, Cardiobacter, Eikenella, Kingella)

39
Q

Patient has left sided S. aureus infective endocarditis. treat.

A

surgical intervention because Lt sided S. aureus—> embolization to brain & all the body

40
Q

What causes persistent emboli after the treatment of infective endocarditis?

A

large or mobile vegetations

mobile vegetations is when there a stalk connecting the vegetation to the valve, this causes it to become unstable and embolize

41
Q

Large vegetations usually cause continuing fever. Why?

A

the bacteria is embedded inside the vegetation, so even if we give antibiotics they won’t reach the bacteria within- the patient won’t improve unless we surgically intervene.

42
Q

Why should we/shouldn’t we give prophylaxis to prevent infective endocarditis?

A

we should= because the prophylaxis cost is little and the benefits, if it works, are very high

we shouldn’t= because it’s not proven that it will prevent infective endocarditis (no evidence)

43
Q

When does severe valve dysfunction occur?

A

Seen in uncontrolled infection

44
Q

What is this called? What is it indicative of?

A

Aschoff bodies are nodules found in the hearts of individuals with rheumatic fever. They result from inflammation in the heart muscle and are characteristic of rheumatic heart disease.

45
Q

How is C reactive protein used to diagnose and track the progress of an infective endocarditis patient?

A

C reactive protein (protein made by the liver levels increase when inflammation present) is high initially then it will drop with treatment. if it’s not dropping it means that there is something wrong (complications OR patient is not responding)

46
Q

Explain the sequence of events leading to rheumatic heart disease.

A

1 strep throat

2 acute rheumatic fever

3 rheumatic heart disease (a long term complication of rheumatic fever)

47
Q

Which bacteria causes rheumatic heart disease? What are 2 important characteristics of it?

A

Streptococcus pyogenes (group A strep)

encapsulated

has M protein (which does antigenic mimicry and causes the body to attack itself)

48
Q

How long does it take from a person to go from having an acute throat infection to acute rheumatic fever?

A

2-3 weeks

49
Q

T/F: Rheumatic fever is a suppurative inflammatory disease

A

false it’s non-suppurative

(Suppurative is a term used to describe a disease or condition in which a purulent exudate (pus) is formed and discharged)

50
Q

What are the criteria for diagnosing rheumatic fever? How do you confirm the diagnosis?

A

2 major criteria OR 1 major + 2 minor criteria
PLUS
Evidence of recent Group A streptococcal infection

51
Q

Rheumatic heart disease often occurs in which location type?

A

developing countries, countries with poor living conditions/ overcrowding

52
Q

Streptococcal M protein share antigens with what parts of the body?

A

cardiac myosin

sarcolemmal membrane protein

synovial tissue

cartilage of joints

brain proteins

53
Q

T/F: every person who develops strep throat has an equal chance of developing rheumatic fever

A

false, genetic predisposition plays a role

class II HLA antigens

54
Q

Which HLA genes are more susceptible to rheumatic heart disease? does it differ based on ethnicity?

A

class II HLA antigens

HLA-DR2 in blacks

HLA-DR4 in whites

55
Q

Describe the arthritis associated with rheumatic fever? (5 things)

A

acute and painful

swelling/effusion

in large joints

migratory arthritis (moves around from joint to joint)

no residual change in joints (no permanent damage)

56
Q

What is this? Where does it most likely occur?

A

Erythema marginatum

On trunk or proximal extremities

57
Q

define pancarditis

A

inflammation affecting all tissue of heart (endocardium, myocardium, pericardium)

58
Q

Rheumatic endocarditis usually affects which area?

A

the valves (why not the whole endocardium? because the valves move and add mechanical stress onto the condition)

usually mitral valve

then aortic valve

rarely tricuspid

59
Q

Rheumatic myocarditis clinical symptoms

A

muscle becomes weak due to inflammation (conductivity also affected) so you’ll see a difference in ECG and echocardiogram

May lead to heart failure

60
Q

Rheumatic endocarditis leads the heart to develop which conditions?

A

mitral stenosis and/or regurgitation

stenosis happens because the valve inflamed then when fibrosis occurs it closes the valve via the fibrous tissue. This makes the valve more rigid and also affects chordae tendineae, if it’s affected heavily it will be so tight that it pulls the valves open even during systole- this what causes regurgitation

61
Q

What is Sydenham’s Chorea? Who does it affect?

A

Neurological disorder characterized by emotional liability,
muscular weakness, rapid & involuntary purposeless uncoordinated movement
affects older children, girls (who have rheumatic fever)

62
Q

Describe Erythema marginatum.

(pain? when does it appear? etc.)

A

non-painful erythema with raised margin, changing lesion that waxes and wanes with fever from hour to hour

(appears with fever onset and disappears with fever)

63
Q

Where do the nodules of rheumatic fever appear? are they painful?

A

over tendons on extensor surfaces of arms (on the back of the arms, near the elbow)

Painless

64
Q

Patient has 2 major Jones ciriteria and now we need to find Evidence of recent Group A streptococcal infection to confirm the RF diagnosis. How do we do that?

A
  1. Culture of throat
  2. The rapid strep test (RST)
  3. Streptococcal antibody titer (ASOT=Anti Streptolysin O Titer)
65
Q

How do we prevent valve deformity in kids who keep getting strep throat?

A

give Penicillin until child leaves school (no bacteria, no attack)

if allergic give erythromycin instead

66
Q

19-year-old patient has Rheumatic Fever without carditis. How long is the prevention duration?

A

5 years

(5 yrs or until age 21, whichever is longer)

67
Q

10-year-old patient has Rheumatic Fever with carditis but no valvular disease. How long is the prevention duration?

A

until age 21

(10 yrs or until age 21 whichever is longer)

68
Q

26-year-old patient has Rheumatic Fever with carditis and residual heart disease (persistent valvular disease). How long is the prevention duration?

A

until 40

(10 yrs or until age 40, whichever is longer )

69
Q

What who things increase the mortality rate of rheumatic heart disease?

A

severe chronic heart failure or pericarditis

(low mortality rate otherwise)

Cardiovascular System - 3rd year (23 decks)

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