Cv System - Acute Rheumatic Fever And Infective Endocarditis

Front 1

cardiac damage is most often associated with what?

Back 1

mitral valve stenosis

Front 2

most cases of endocarditis infect what type of tissue?

Back 2

damaged tissue

Front 3

define acute rheumatic fever

Back 3

-delayed nonsupporative disease (no white cells)
-Occurs after an antecedant Group A Strep infection (and the infection must be in the upper respritory tract)
-Characterized by proliferative inflammatory lesions in the connective tissue of joints, heart, skin and central nervous tissue

Front 4

how long after an upper respritory tract infection by a group A strep will we start to antibodies and mitral valve damage from rheumatic fever?

Back 4

2-3 weeks

Front 5

what is the average time between attack and initial Gp A strep infection?

Back 5

18 days

Front 6

what are the ages that acute rheumatic fever are prevalent in?

Back 6

yrs 5-15yr

Front 7

Streptococcus pyogenes

Back 7

gram + cocci in chains
(with Beta Hemolysis)

catalase - (this is how we seperate staph from strep)

Ferment sugars -> lactic acid -> low pH

Front 8

describe the differences between the different hemolyses, alpha, beta, gamma

Back 8

beta - total clearing (always pathogenic)
alpha - some clearing
gamma - no clearing

Front 9

List some of the structural virulence factors of Group A strep

Back 9

- capsule (hyaluronic acid)
- peptidoglycan layer
- group A carbohydrate
- fibrils (consist of M-proteins)
- T-antigen, ect.

Front 10

what is the primary virulence factor for group A strep?

Back 10

M-Protein

Front 11

What are some soluble virulence factors for group A strep

Back 11

- Streptolysin O
- Streptodornase
-NADase
- Streptokinase
- Hyaluronidase
- Chemotoxins
- Erythrogenic toxin (some strains will cause scarlet fever)
-super antigens (may cause streptococcal toxic shock- even though before we only really spoke about staph based toxic shock, this does have the capability of doing that as well)
- SpyCEP - envelops that inactivates IL-8

Front 12

describe the pathogenesis of Acute rheumatic fever

Back 12

- molecular mimicry (the presence of epitopes in human tissue that are immunologically similar to Grp A strep antigens

M protein = Human tropomyosin and myosin

Grp A Carb. = Heart valve glycoprotein

Front 13

is there a genetic component to acute rheumatic fever?

Back 13

yes, only 2-3 % of the population have a ability to acquire acute rheumatic fever

Front 14

Rhwumatic heart valves have been shown to contain what?

Back 14

infiltrates of t-cells

Front 15

If you get rheumatic fever does it reoccur?

Back 15

yes, there is a high probability of it

Front 16

What is the treatment of acute rheumatic fever?

Back 16

Long term antibiotics (long term as in years, like 5 years) this is due to the affinity for re occurrence

Front 17

What is the criteria for the clinical diagnosis of acute rheumatic fever?

Back 17

1.) lab evidence of recent strep infection (usually through ASO titers)

2.) presence of 2 mojor or 1major and 1 minor jones criteria

Front 18

whate are the major jones criteria?

Back 18

-carditis
-polyarthritis
-erythema marginatum
-subcutaneous nodules
sydenham's chorea

Front 19

what are the minor jones criteria?

Back 19

-Arthralgia
-fever
-previous rheumatic fever
-prolonged p-r interval on the ECG
-elevated erythrocyte sed-rate
-c-reactive protein or leucocytosis

Front 20

the most common major jones criteria is what?

Back 20

polyarthritis (80%)
carditis (40-50%)

Front 21

what is the laboratory screening techniques for ARF?

Back 21

steptozyme test, if positive do ASO (>500units = +)

Front 22

treatment of acute rhematic fever

Back 22

salicylates (4-8wks)
-prednizone reserved for pts with severe carditis
-heart failure - usually requires bed rest and valve replacement

Front 23

what is our strategy for the prevention of acute rheumatic fever?

Back 23

- prevent the primary attack, prompt recognition and treatment of strep throat DOC= PCN
- secondary attack, continuous long term prophylaxos with PCN (>5yrs)

Front 24

What is PANDAS?

Back 24

pediatric autoimmune neurologic disorders associated with strep.

they are probably a manifestation of sydenham's chorea (tics, tourette's and OCD and it usually improves with steroid therapy

Front 25

What is Infective Endocarditis (IE)?

Back 25

- An infection of the native or prosthetic valve or endocardium
- it occurs most often in patients with recognized heart disease
- hearts of such Pts undergo an edematous, cellular distortion resulting in non-bacterial thrombocytic endocarditis (NBTE) lesions (these lesions then become something that the bacteria can bind to to crease an IE lesion)

Front 26

can heart cath cause damage to the valves?

Back 26

yes, in about 2%

Front 27

what is seen more, right or left sided endocarditis?

Back 27

Right sided endocarditis, this is due to IV drug usage and invasive procedures done in the hospital

Front 28

Acute Infective endocarditis?

Back 28

comes on rapidly, there is high fevers, and they are brought on by staph a.

Front 29

Subacute infective endocarditis?

Back 29

comes on slowly, maybe you have a fever at night, often caused by alpha hemolytic strep, and they may have already had valve damage (Strep. viridans)

Front 30

IV drug use infective endocarditis?

Back 30

dirty unclean injections into the blood stream can inject bacteria into the blood stream, the endocarditis will be seen on the right side (Staph. aureus)

Front 31

Prosthetic valve endocarditis (PVE)

Back 31

there is an early onset and a late onset both caused by some damage from the prosthetic that the bacteria can then attach to (Staph. epidermidis = early)(Strep. viridans = late onset)

Front 32

What are the damage causing agents in valve disorders?

Back 32

-heart disease
-Drugs
-Toxins

Front 33

What are some of the sources of bacteria for infective endocarditis?

Back 33

dental (Strep. viridans)
IV introduction (tricuspid)
Pulmonary (Mitral Valve)

Front 34

What side, right or left vegitations has lower bacterial density?

Back 34

the right side, this is because there is more neutrophil access (note that both sides usually have the majority of bacteria in the metabolically inactive state, therefore resistant to antibiotics)

Front 35

What valve is the most common for infective endocarditis?

Back 35

Mitral valve endocarditis

Front 36

What is the Venturi effect?

Back 36

Cardiac abnormalities → high pressure area through narrowing to low pressure reservoir → platelet-fibrin aggregate on low pressure side
High velocity jet streams → injury on wall of L atrium, R ventricle, or chordae mitral valve leaflet → platelet-fibrin thrombi → nidus of infection

Front 37

Explain traumatized valves and the role of nonbacterial thrombotic vegetations.

Back 37

endothelial changes leads to the tissue being denuded of collagen, platelets then aggrigate and fibrin deposits. This allows bacteria to colonize and vegetations to form this can then stimulate thrombi (vegetations may enlarge and become a sanctuary for organisms).

Front 38

what are some of the clinical signs of acute infective endocarditis (AIE)?

Back 38

-abrupt onset of fever, rigots, prostration, and leucocytosis
-skin may show evidence of embolitic pustules or hemorrage
- Occassionally there will be janeway lesions
-heart murmer

Front 39

What are janeway lesions?

Back 39

Janeway lesions (nontender, macular lesions most commonly involving the palms and soles). Janeway lesions occur more frequently in endocarditis caused by Staphylococcus aureus. Janeway lesions are caused by septic emboli. Subcutaneous abscesses are found on histologic examination.

Front 40

Subacute infective endocarditis (SIE), what are some clinical signs?

Back 40

- presents as an ill defined wasting disease over a long period of time.
-patirnt not feeling well- often anorexia and weight loss
-heart murmer, splenomegaly and petechiae
-splinter hemorrhages are common
- ocasionally, osler nodes and Roth's spots are present
- slight leukocytosis and anemia
-hematuria

Front 41

What is an Osler node?

Back 41

Osler’s nodes (painful, palpable, erythematous lesions most often involving the pads of the fingers and toes). Caused by immune complexes (they want you to know that for Step 2).

Front 42

What are Roth's spots?

Back 42

Spots in the eye, that are due to immune complexes

Front 43

How do you detect organisms for AIE?

how about for SIE?

Back 43

AIE: Blood draws, draw three cultures during a 1-2 hour period (95%)

SIE: draw 3 bood cultures per day for 2 days (harder to get the organism)

Front 44

How are SIE and AIE treated?

Back 44

- It depends on the organism, but the Antibiotics should be bactericidal, moniter treatment with blood cultures and serum bactericidal levels (should be>1.8)
- If damage is severe, and the infection can not be cleared then we will do valve replacement.