Review Q's Week 7 Flashcards
1. micro: infective endocarditis (1-44) 2. micro: rheumatic heart disease (45-69) 3. pathology valvular heart disease (70-109) 4. patho lab valvular heart disease (110-126) 5. clinical med (127-167)
acute vs subacute endocarditis
who do they usually affect? what organism causes them?
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)
organsim that causes infective endocarditis in patients with prosthetic heart valves
staph epidermidis
organism that causes infective endocarditis in patients with damaged/susceptible heart
strept viridans
(50% of people with infective endocarditis)
most common organism that causes acute infective endocarditis
staph aureus
Patient with prosthetic heart valve gets infective endocarditis
less than 2 months after heart valve operation VS more than 2 months after
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
Why is mitral valve prolapse a risk factor of infective endocarditis?
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
Describe the infective endocarditis of IV drug abusers.
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)
Why are cardiac prostheses more likely to cause infective endocarditis?
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)
This shows a vegetation in the heart: acute or subacute infective endocarditis?
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)
What are bacteria properties that help it cause infective endocarditis?
dextran
fibrinogen-binding proteins (/peptides)
organism causing infective endocarditis in IV drug users?
staph aureus
IV drug user has infective endocarditis. He uses tap water to dilute drugs. What’s the causative organism?
pseudomonas
IV drug user has infective endocarditis. He uses lemon juice to dilute drugs. What’s the causative organism?
candida spp.
What are the four microrganisms that cause culture-negative infective endocarditis?
Mycoplasma pneumoniae
Coxiella burnetii
Chlamydiaspp.
Legionella spp.
earliest manifestation of infective endocarditis?
fever + murmur (due to valvular affects)
Which organisms that cause infective endocarditis are also likely to cause embolic events? Why?
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)
Osler’s nodes VS Janeway lesion
Janeway lesion = nontender, macular lesions in palms & soles, vasculitis… painless!
Osler’s nodes = palpable, painful finger pulp
What is Roth’s spot?
a rash in the retina that may occur as a complication of infective endocarditis
What infective endocarditis patient is more likely to get a lung abscess?
a patient where the infection is on the right side of the heart (pulmonary trunk sends it to lungs)
What is a mycotic aneurysm? Why does it occur?
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.
List some late complications of infective endocarditis
clubbing
spelenomagaly
roth’s spot
osler’s nodes
janeway lesion
lung abscess
mycotic aneurysm
How do you diagnose infective endocarditis?
(via Duke criteria)
for the diagnosis of definite infective endocarditis, we have to have
2 major criteria OR
1 major 3 minor criteria OR
5 minor criteria
A very sick patient is suspected of infective endocarditis. How do you confirm the condition by obtaining a blood culture?
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
A patient suspected of infective endocarditis has one positive blood culture. is this a major/minor Duke’s criteria?
minor
(major has to be 2 cultures, 12 hours apart OR 4 cultures within 1 hour)
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?
No; he has 2 minor and 1 major criteria.
We need 1 major and 3 minor for it to be definite IE
nosocomial infective endocarditis often occurs as a complication of which condition?
A complication of nosocomial bacteremia
Especially if bacteremias persist > 48h
3 organisms that cause aggressive infective endocarditis
S. aureus
Pseudomonas aeruginosa
Aspergillus spp.
What percent of people with aggressive infective endocarditis also have anemia?
70-90%
(30-60% of people with aggressive infective endocarditis also have RBC’s in urine, so it makes sense)
Which type of echocardiography is more likely to diagnose aggressive infective endocarditis?
a. Transthoracic (TTE)
b. Transesophageal (TOE)
b. Transesophageal (TOE)
>95% positive
Which type of echocardiography has the transducer behind your heart?
a. Transthoracic (TTE)
b. Transesophageal (TOE)
b. Transesophageal (TOE)
Which type of echocardiography should NOT be used with patients that have heart prosthesis?
a. Transthoracic (TTE)
b. Transesophageal (TOE)
a. Transthoracic (TTE)
bactericidal antibiotics for sensitive Viridans streptococci
penicillin x 4 weeks IV
bactericidal antibiotics for resistant Viridans streptococci
ampicillin + gentamicin x 4 weeks
bactericidal antibiotics for sensitive S. epidermidis
flucloxacillin x 4-6 weeks
bactericidal antibiotics for resistant S. aureus
vancomycin x 4 weeks
bactericidal antibiotics to treat Coxiella burnetii
doxycycline and ciprofloxacin x 2-3 years
antibiotics to treat fungal infective endocarditis
surgery + antifungal
antibiotics to treat Actinobacter
ceftriaxone x 4 weeks
for HACEK: (Haemophilus, Actinobacter, Cardiobacter, Eikenella, Kingella)
Patient has left sided S. aureus infective endocarditis. treat.
surgical intervention because Lt sided S. aureus—> embolization to brain & all the body
Large vegetations usually cause continuing fever. Why?
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.
Why should we/shouldn’t we give prophylaxis to prevent infective endocarditis?
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)
What causes persistent emboli after the treatment of infective endocarditis?
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
When does severe valve dysfunction occur?
Seen in uncontrolled infection
How is C reactive protein used to diagnose and track the progress of an infective endocarditis patient?
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)
Explain the sequence of events leading to rheumatic heart disease.
1 strep throat
2 acute rheumatic fever
3 rheumatic heart disease (a long term complication of rheumatic fever)
Which bacteria causes rheumatic heart disease? What are 2 important characteristics of it?
Streptococcus pyogenes (group A strep)
encapsulated
has M protein (which does antigenic mimicry and causes the body to attack itself)
What is this called? What is it indicative of?
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.
How long does it take from a person to go from having an acute throat infection to acute rheumatic fever?
2-3 weeks
T/F: Rheumatic fever is a suppurative inflammatory disease
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)
Rheumatic heart disease often occurs in which location type?
developing countries, countries with poor living conditions/ overcrowding
Streptococcal M protein share antigens with what parts of the body?
cardiac myosin
sarcolemmal membrane protein
synovial tissue
cartilage of joints
brain proteins
T/F: every person who develops strep throat has an equal chance of developing rheumatic fever
false, genetic predisposition plays a role
class II HLA antigens
Which HLA genes are more susceptible to rheumatic heart disease? does it differ based on ethnicity?
class II HLA antigens
HLA-DR2 in blacks
HLA-DR4 in whites
What are the criteria for diagnosing rheumatic fever? How do you confirm the diagnosis?
2 major criteria OR 1 major + 2 minor criteria
PLUS
Evidence of recent Group A streptococcal infection
Describe the arthritis associated with rheumatic fever? (5 things)
acute and painful
swelling/effusion
in large joints
migratory arthritis (moves around from joint to joint)
no residual change in joints (no permanent damage)
define pancarditis
inflammation affecting all tissue of heart (endocardium, myocardium, pericardium)
Rheumatic endocarditis usually affects which area?
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
Rheumatic myocarditis clinical symptoms
muscle becomes weak due to inflammation (conductivity also affected) so you’ll see a difference in ECG and echocardiogram
May lead to heart failure
Rheumatic endocarditis leads the heart to develop which conditions?
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
What is Sydenham’s Chorea? Who does it affect?
Neurological disorder characterized by emotional liability,
muscular weakness, rapid & involuntary purposeless uncoordinated movement
affects older children, girls (who have rheumatic fever)
What is this? Where does it most likely occur?
Erythema marginatum
On trunk or proximal extremities
Describe Erythema marginatum.
(pain? when does it appear? etc.)
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)
Where do the nodules of rheumatic fever appear? are they painful?
over tendons on extensor surfaces of arms (on the back of the arms, near the elbow)
Painless
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?
- Culture of throat
- The rapid strep test (RST)
- Streptococcal antibody titer (ASOT=Anti Streptolysin O Titer)
How do we prevent valve deformity in kids who keep getting strep throat?
give Penicillin until child leaves school (no bacteria, no attack)
if allergic give erythromycin instead
19-year-old patient has Rheumatic Fever without carditis. How long is the prevention duration?
5 years
(5 yrs or until age 21, whichever is longer)
10-year-old patient has Rheumatic Fever with carditis but no valvular disease. How long is the prevention duration?
until age 21
(10 yrs or until age 21 whichever is longer)
26-year-old patient has Rheumatic Fever with carditis and residual heart disease (persistent valvular disease). How long is the prevention duration?
until 40
(10 yrs or until age 40, whichever is longer )
What who things increase the mortality rate of rheumatic heart disease?
severe chronic heart failure or pericarditis
(low mortality rate otherwise)
What kind of valvular heart conditions do adolescents most likely have?
congenital
What kind of valvular heart conditions do adults most likely have?
degenerative heart diseases
Which of the following is a valve closing problem?
stenosis or regurgitation
regurgitation
(stenosis is an opening problem while regurgitation is a closing problem)
If no physical symptoms appear due to valvular heart conditions, how do you tell if there’s a problem?
auscultation (physical finding, abnormal sound occurring due to valves closing pathologically)
*the clinical symptoms are fatigue, SOB, and edema (pretty general, so auscultation is an easy way to test for it)
T/F: all valvular diseases have a characteristic murmur
true
Which of the following is more likely to lead to a dilated left ventricle?
stenosis OR regurgitation (in aortic valve)
regurgitation (blood comes back to ventricle and dilates it)
in stenosis of aortic valve, the left ventricle hypertrophies because it’s pushing against an incomplete opening
Which two valves are the main ones affected by valvular heart disease?
Aortic and mitral
Which valve would you expect to be stenotic if the patient has a hypertrophied and dilated left atrium? Describe symptoms of this patient.
mitral valve stenosis
The back pressure that would affect the lungs leading to congestion and edema
+ (in the long run, the pulmonary edema can affect the Rt. ventricle leading to congestive heart failure)
When does calcification of the heart valve start?
when there’s tissue deformity it starts slowly depositing
T/F: all valvular degenerative diseases are clinically important
false, valves degenerate as age increases its a normal process
What’s the most common of all valvular abnormalities?
Calcific Aortic Stenosis
Is there anything wrong with this aortic valve? explain.
yes, it’s a bicuspid aortic valve. So instead of having the normal three leaflet, it is now bicuspid. calcification will set in eariler due to this anomaly.
Whats the population that most commonly get calcific aortic stenosis?
Acquired, Senile/age-associated “wear and tear”
(makes sense because the calcifications take years to build up)
Is there something wrong with this aortic valve?
massive calcific deposits
Why are people in developing countries more likely to get rheumatic fever?
usually after a step throat infection, people are treated with antibiotics to prevent rheumatic fever from developing. But in low socioeconomic areas, that’s not available- that’s why they’re more susceptible.
(also because developing contries are overcrowded and a throat infection spreads more easily)
What’s the likelihood that a child who gets strep throat for the first time (and didn’t get antibiotic treatment) would develop rheumatic fever? How about if he had subsequent infections?
untreated infection once= 3% can develop Rheumatic fever
subsequent infections= 50%
How old are the patients of rheumatic fever? how about valvular heart disease?
rheumatic fever= mostly kids 5-15 years
valvular heart disease= 20’s-30’s because its a chronic complication, which means they got frequent strep infections when they were younger and it lead up to this point
What are two conditions that indicate rheumatic fever by themselves?
Sydenham’s Chorea (an abnormal involuntary movement disorder)
+
indolent carditis (carditis of insidious onset and slow progression)
Which two of JONES criteria disappear within 3 weeks?
polyarthritis + carditis
Patient has acute rheumatic carditis, which layer of heart has Aschoff bodies?
a. endocarditis
b. myocarditis
c. pericarditis
b. myocarditis
Patient has acute rheumatic carditis, which layer of heart has bread and butter appearance?
a. endocarditis
b. myocarditis
c. pericarditis
c. pericarditis
Patient has acute rheumatic carditis, which layer of heart is the most likely not to heal and leave some problems behind?
a. endocarditis
b. myocarditis
c. pericarditis
a. endocarditis
(valves never the same again)
What’s the difference between the vegetations of infective endocarditis and rheumatic endocarditis? which one is shown below?
vegetations in rheumatic endocarditis are along the line of the closure of the valve (edge that closes) but the vegetations in infective endocarditis are anywhere on the valve
What are some cells you find in Aschoff bodies?
Anitschow cells (picture; they have nuclei looking like caterpillars)
+
Aschoff giant cell (macrophages combine to make giant cells)
What results if the valve leaflets heal via fibrosis in chronic rheumatic carditis?
stenosis
the valves are usually loose and will open when blood pushes them, but when fibrotic they become more stiff- causing the stenosis
What results if the chordae tendineae heals via fibrosis in chronic rheumatic carditis?
regurgitation
(they become so tight that they don’t allow the valve to fully close shut. So when systole occurs, blood is able to flow through the remaining gap in the valve.
describe + where does this occur?
fish mouth/button hole stenosis with commissural fusion
occur in Chronic Rheumatic carditis
Chronic Rheumatic carditis
VS
Acute Rheumatic carditis
Chronic= no Aschoff bodies + Diffuse fibrosis and neovascularisation
Acute= valvular vegetation + aschoff bodies + bread and butter
diagnose and explain
Chronic Rheumatic carditis
thickening and shortening of the chordae tendineae
+
neovascularization of anterior mitral leaflet (arrow)
What is mitral valve prolapse? Why does it happen? When is diagnosed? What are the symptoms?
its when the mitral valve leaflet bulges (prolapse) upward into the left atrium. It happens due to connective tissue disorders that causes thick and long leaflets- this is what causes the prolapse.
It mostly has no symptoms and that’s why its incidentally found. Some symptoms are chest pain, dizziness, palpitations.
mitral valve prolapse oscillation
mid-systolic click and murmur
(hear mid-systolic click with or without a late systolic murmur)
T/F: infective endocarditis occur only in people who have previous heart conditions and are susceptible
no, virulent organisms can affect normal valves with infective endocarditis
Which of the following is fatal in 50% of the people?
a. acute infective endocarditis
b. subacute infective endocarditis
a. acute infective endocarditis
Which of the following needs surgery more often?
a. acute infective endocarditis
b. subacute infective endocarditis
a. acute infective endocarditis
Which of the following occurs due to less virulent organisms?
a. acute infective endocarditis
b. subacute infective endocarditis
b. subacute infective endocarditis
How do you diagnose
infective endocarditis VS rheumatic fever
infective endocarditis= Duke Criteria
rheumatic fever= Jones Criteria
Nonbacterial Thrombotic Endocarditis (NBTE) usually affect
Debilitated patients, cancer or sepsis
(in a hypercoagulable state)
Libman-Sacks Endocarditis occurs in
people with SLE
Describe vegetation of Nonbacterial Thrombotic Endocarditis (NBTE) and Libman-Sacks Endocarditis (LSE)
both small and sterile
Describe vegetation of rheumatic heart disease and infective endocarditis
RHD in the border of the valves while in IE its anywhere on the valve
Whats the normal ESR (erythrocyte sedimentation rate)?
Women under age 50 should have an ESR between 0 and 20 mm/hr. Men under age 50 should have an ESR between 0 and 15 mm/hr.
(you need to know this because its a minor JONES criteria- diagnose rheumatic fever)
What makes up the bread and butter appearance?
fibrin deposition
Why are ESR and ASOT high in rheumatic carditis?
ESR and ASOT are elevated during a strep group A infection
Complications of chronic rheumatic heart disease.
(Where do they occur? what are they? explain mechanism.)
It mostly occurs in the mitral valve, so stenosis and regurgitation occurs and leads to the dialtion and hypertrophy of the left atria. This to the blood back flowing into the lungs causing pulmonary edema.
Over a longer time, the right side of the heart (right ventricle) would get tried of pushing blood against the edema of the lungs… so heart failure could also occur
Which disease do these features point to?
Aschoff bodies
small vegetation on valve
bread and butter appearance
nodules
Erythema marginatum
Acute Rheumatic Heart Disease
Which disease do these features point to?
Fibrosis
Neovascularization
Fish mouth/buttonhole appearance
shortened chordae tendinae
Chronic Rheumatic Heart Disease
T/F: patients with a history of Rheumatic Disease are predisposed to infective endocarditis
true (it’s in Duke’s criteria)
What’s a common complication of patients with infective endocarditis?
Patients with infective endocarditis (IE) can develop several forms of kidney disease: a bacterial infection-related immune complex-mediated glomerulonephritis (GN), renal infarction from septic emboli, and renal cortical necrosis.
Whats a syndrome associated with mitral prolapse?
Marfan’s syndrome
(connective tissue)
intravenous drug user comes in with chest pain, fever, high Jugular venous pressure, hepatomegaly, and edema. diagnose.
infective endocarditis
affects right side of heart (tricuspid infective endocarditis)
probably S aureus caused it
patient with exertional dyspnea and episodes of near syncope. Imaging revealed moderate left ventricular hypertrophy and mild pulmonary edema. What do you expect to see in the aortic valve?
aortic stenosis
(The left ventricle works hard to push the blood against the stenotic valve, the atria is also affected so the backed-up blood goes to the lungs and causes edema. if this continues for a long time it may lead to congestive heart failure.)
(dyspnea and syncope because not enough blood going through aortic valve to body)
What is the lesion shown in the aortic valve?
a. rheumatic vegetations
b. infective vegetations
c. marantic vegetations
d. calcification
e. floppy aortic valve
b. infective vegetations
What is the diagnosis of this myocardial lesion? (picture below)
a. viral myocarditis
b. bacterial myocarditis
c. rheumatic myocarditis
d. toxic myocarditis
e. giant cell myocarditis
c. rheumatic myocarditis
What is your diagnosis?
a. rheumatic aortic stenosis
b. bicuspid calcific aortic stenosis
c. senile calcific aortic stenosis
d. atherosclerotic aortic stenosis
c.senile calcific aortic stenosis
Name a pulmonary complication of this condition:
a. pulmonary infection
b. pulmonary stenosis
c. pulmonary edema
d. pulmonary fibrosis
c.pulmonary edema
Name a common complication of this condition:
a. atheromatous embolism
b. fat embolism
c. pulmonary embolism
d. septic embolism
d.septic embolism
diagnose
mitral valve prolapse
(associated with marfan’s syndrome)
T/F: pulmonary congestion starts as soon as the left atrium gets extra blood from the ventricle (due do regurgitation from mitral valve, causing increase in LA pressure)
false, LA adapts to the larger volume by dilating, which increases its compliance. This remodeling helps to limit the increases in LA pressure initially- but after a while it can’t keep up and pulmonary congestion occurs.
How is the annulus affected by Chronic Renal Failure?
It undergos Calcification
What 3 conditions cause Chordae Tendineae rupture?
Rheumatic Fever, Trauma, infective endocarditis
Papillary muscle dysfunction is cause by (2)
Ischemia, LV dilatation
How can mitral regurgitation lead to heart failure?
mitral regurgitation→blood leaks from LV to RV→RV has higher pressure→RV dilates to compensate→LV volume overload→ hyperdynamic LV→progressive LV dilation→ to heart failure
Describe the left atrial pressure and ejection fraction during acute mitral regurgitation.
left atrial pressure= increases because the regurgitated blood causes an increase in volume; since its acute, the right atrium has no time to dilate (to compensate)
ejection fraction= it increases due to the increase in total stroke volume. The regurgitated blood causes an increase in preload, leading to a hyperdynamic state->SV increase
Describe the left atrial pressure and ejection fraction during chronic compensated mitral regurgitation.
left atrial pressure= it’s slightly elevated. The left atria had time to dilate and accommodate the regurgitated blood, leading to a decrease in pressure (LAP is less than LAP in acute regurg.)
ejection fraction= high because the heart is pumping harder to provide adequate blood to body-> high total stroke volume -> high EF
Describe the left atrial pressure and ejection fraction during chronic decompensated mitral regurgitation.
left atrial pressure= high because the atria dilated to it’s max
ejection fraction= low because the ventricle is dilated further due to the high pressure and now has a weak pump
How can you determine the cause/severity of mitral regurgitation?
Echocardiogram
When do you Surgically treat the heart valves?
when patient is Symptomatic and if the valve infection Severe
(2 conditions)
Patient comes in with mitral regurgitation + symptoms. What is the pharmaceutical treatment?
Diuretics, ACE-I, warfarin (AF)
Patient with mitral regurgitation has a severe infection and is symptomatic. What are the 2 surgical options? explain them.
Valve repair= artificial annulus (stop dilation) + stitch leaflets to repair them (this is the preferred surgery)
Valve replacement= remove old and put a new artificial valve
Most mitral stenosis cases are due to
Rheumatic fever (99%)
Whats the normal mitral valve orfice area?
5cm squared
(has to get to 2cm to produce symptoms; if 1cm or smaller then its severe mitral stenosis)
Why is the blood velocity increased in mitral stenosis? What does it look like in echo?
due to stenosis, the blood gradient has to be high between atria and ventricle for the blood to pass through the stenotic valve. higher gradient means increased velocity, and that also means turbulent flow. This has a mosaic appearance in echo.
Mitral stenosis VS regurgitation
which heart chamber gets dilated in each?
Mitral stenosis= only L atria
Mitral regurgitation= both LV and LA
describe ECG of mitral stenosis
The ECG in mitral stenosis is often normal early in disease. The most common finding is left atrial enlargement (p-mitrale)(however this finding disappears if the patient enters atrial fibrillation**) Right heart strain may produce findings of right axis deviation
**=valve stenosis is linked to a higher risk for atrial fibrillation
Patient has AF as a complication of mitral stenosis. how do we treat?
warfarin, control heart rate
Patient has pulmonary hypertension due to mitral stenosis. How so we treat?
by relieving the obstruction
via Trans-septal balloon valvotomy
OR
Mitral valve replacement
How does aortic stenosis affect exercise?
The valve obstruction does not allow CO to increase during exercise
Complications of aortic stenosis
stenosis causes left ventricular hypertophy→thick wall more susceptible to ischemia→ arrythmias→ heart failure
Age related calcific degeneration of aortic valve is more common in which region?
developed countries
Risk factors for the development of calcific Aortic stenosis
similar to those for vascular atherosclerosis:
elevated LDL cholesterol, diabetes , smoking, hypertension
T/F: Calcific aortic stenosis increases risk of cardiovascular death only due to valve obstruction
False, Calcific aortic stenosis has a 50 % increased risk of
cardiovascular death and myocardial infarction even in the absence of valve obstruction
T/F: Bicuspid aortic valve disease is mostly discovered in childhood or adolescence
false, Usually functions normally in childhood. the abnormal structure causes stress which leads to calcifications later on (40’s+)
T/F: Bicuspid aortic valve disease is more common in men
true 4:1 ratio
Vascular complications of bicuspid aortic stenosis
Medial degeneration (damages connective tissue and results in the breakdown or destruction)
Aortic aneurysm
Aortic Dissection (rare)
Patient has Aortic stenosis, aortic regurgitation, and mitral valve problems. What’s a likely diagnosis?
Rheumatic valve disease (can involve all left heart)
(If mitral stenosis alone—> mitral valve disease)
What’s the best indicator of aortic stenosis prognosis?
the symptoms are the best indicator
no symptoms= good prognosis
symptoms=dismal prognosis
symptoms of aortic stenosis. explain them
- chest pain
- no blood in aorta, no blood in coronary arteries
- syncope
- no blood reaching brain
- dyspnea
- indicates heart failure= the worst symptom
How can we determine the severity of the aortic stenosis?
mean pressure gradient
the higher it is, the more severe the stenosis
medical treatment for severe symptomatic aortic stenosis
no medical treatment, just replace the valve via”
Transcatheter Aortic-Valve Implantation (TAVI)
T/F: Transcatheter Aortic-Valve Implantation (TAVI) is an invasive operation used to implant a new, synthetic aortic valve
false, it’s non-invasive (done by catheter)
Management of severe asymptomatic aortic stenosis
adjust lifestyle (no vigorous physical activity)
observe clinically and by echo
prophylaxis for rheumatic fever (penicillin) and infective endocarditis (good hygine)
What are factors that cause aortic regurgitation by affecting the wall of the aortic root?
- age-related (degenerative) aortic dilation
- cystic medial necrosis of the aorta (Marfan’s)***
- Syphilitic aortitis
- Ankylosing spondylitis
*** cystic medial necrosis= accumulation of basophilic ground substance in the media with cyst-like lesions
What structural changes occur due to aortic regurgitation?
for Cardiac Output to be maintained, total volume pumped into aorta must increase, leading to LV dilatation
aortic stenosis→ ? ventricular changes
aortic regurgitation→ ? ventricular changes
aortic stenosis→ hypertrophy
aortic regurgitation→ dilation
When do the murmurs occur in each of the following condition?
Mitral regurgitation
Mitral stenosis
aortic regurgitation
aortic stenosis
Mitral regurgitation and aortic stenosis—> systolic murmurs
Mitral stenosis and aortic regurgitation—> diastolic murmurs
Describe carotid pulsations in
aortic regurgitation VS aortic stenosis
aortic regurgitation= prominent carotid pulsations
aortic stenosis= low/little carotid pulsations
When do we surgically treat aortic regurgitation?
Symptomatic + severe —> surgery
Either repair or replacement but mostly replacement.
pharma treatment of aortic regurgitation
Marfan syndrome: beta-blockers (may slow aortic root dilatation)
Hypertension, LV dysfunction when surgery is contraindicated or LV dysfunction persists: ACE, ARB
