Transcript SGD 2: RHD

SGD 2: RHD
Saldana Emmanuel, Sales Stephanie, Salonga Cryscel, San Diego Phoebe,
San Pedro Rina, Sanez Eric, Sanidad Erica, Santos Emmalene, Santos
Jeniffer, Santos Joel, Santos Karen,Santos Mary Elaine
Elvie, 28 y/o housewife, dyspnea
3 days PTA
Dental Procedure
2 days PTA
• Cough productive of
yellowish sputum
accompanied by colds
• Pricking chest pain radiating
to the back lasting more than
30 minutes occurring even at
rest
• Fever at 38 degrees Celsius
Dyspnea
with joint pain and myalgia
Easy Fatigability
1 day PTA
Admission
• Past Medical History
– (+) frequent
streptococcal throat
infection in childhood
– At age 16, diagnosed to
have valvular heart
disease with monthly
injections of Benzathine
Penicillin
• Family History
(+) hypertension –
grandfather
(+) heart disease - father
Physical Examination
• Drowsy, in respiratory distress, prefers the
semi-sitting position
• BP: 130/60 mmHg PR: 124 beats/min
• CR: 135 beats/min, irregularly irregular
• RR: 40 cycles/min Temp: 38.5°C
Physical Examination
• Cold, clammy extremities, no active dermatoses
• No nasoaural discharge, with alar flaring
• Moist buccal mucosa, hyperemic posterior
pharyngeal wall, tonsils not enlarged
• Supple neck, distended neck veins at 4-5cm at
30°angle
• Symmetrical chest expansion, (+) supraclavicular
retractions, coarse crackles over both lung fields
Physical Examination
•
•
•
•
Dynamic precordium, AB at 6th LICS AAL
(+) heave at the left lower parasternal area
(++) impulse at the 2nd LICS,
On auscultation at the apex, S1 was noted to vary
in intensity, followed by a grade 3/6 holosystolic
murmur that radiates to the axilla, S2 is normal
followed by an opening snap and a grade 3/6
diastolic rumbling murmur
• At the base, the pulmonic component of S2 is
loud with a grade 3/6 diastolic blowing murmur
Physical Examination
• Globular abdomen, liver is palpable
• Extremity: grade 2 bipedal edema
Laboratory and Ancillary Tests
CBC
Patient
Normal Values
Hgb
120
120-158 g/L
Hct
0.40
0.354-0.444
Platelet
305
165-415 x 109/L
WBC
19.9
3.54-9.06 x 109/L
Segmenters 0.91
0.40-0.70
Lympho
0.08
0.20-0.50
ASO
>200
IU/L
ESR
100
0-20mm/hr
Chest X-ray:
• Cardiomegaly with features of mitral valve
pathology
• Pulmonary edema
• Haziness at right paracardiac border
ECG:
• Atrial Fibrillation with rapid ventricular
response
• Non-specific ST-T wave changes
2D-Echo:
• Mitral Stenosis, moderate to severe
• Mitral regurgitation, moderate
• Aortic regurgitation, moderate
• LV and RV dilatation
• Dilated LA and RA with no evidence
of thrombus
• Dilated main pulmonary artery
Diagnosis
• Rheumatic Heart Disease, active
• Mitral stenosis, moderate to severe; Mitral
regurgitation, moderate; Aortic regurgitation,
moderate; LV and RV dilatation; Dilated LA and
RA with no evidence of thrombus; Dilated
Main Pulmonary Artery; Pulmonary
Hypertension; Congestive heart failure in atrial
fibrillation with rapid ventricular response
• Class IV-D
Pathophysiology of Rheumatic
fever/Rheumatic Heart Disease
Organism Factors
• Acute Rheumatic Fever is caused by infection
of the upper respiratory tract with any strain
of group A streptococci.
• A series of preceding streptococcal infections
is needed to "prime" the immune system prior
to the final infection that directly causes
disease.
Host Factors
• Findings of familial clustering of cases &
concordance in monozygotic twins—
particularly for chorea—confirm that
susceptibility to ARF is an inherited
characteristic.
• HLA class II alleles
• ↑levels of circulating MBL & polymorphisms
of TGF-β1 gene and immunoglobulin genes
Immune Response
Immune Response
• Epitopes present in the cell wall, cell
membrane, and the A, B, and C repeat regions
of the streptococcal M protein are
immunologically similar to molecules in
human myosin, tropomyosin, keratin, actin,
laminin, vimentin, and N-acetylglucosamine.
• Human molecules—particularly epitopes in
cardiac myosin—result in T cell sensitization.
Immune Response
• Laminin, another -helical coiled-coil protein
like myosin and M protein, which is found in
cardiac endothelium and is recognized by antimyosin, anti-M protein T cells.
• Antibodies to cardiac valve tissue cross-react
with the N-acetylglucosamine of group A
streptococcal carbohydrate, and there is
some evidence that these antibodies may be
responsible for valvular damage.
Physical examination findings in
MS, MR, AR?
Mitral Stenosis
 Inspection
o malar flush with pinched and blue fascies
 Palpation
 Arterial pulse amplitude decreased
o RV tap along left sternal border signifies enlarged RV, diastolic thrill at
cardiac apex
 Auscultation:
o S1 accentuated and delayed and palpable at left sternal border
o S2 closely split with accented P2
o OS readily audible in expiration
o Follows P2 closely, followed by a low pitched, rumbling diastolic murmur
heard best at apex and does not radiate
o Soft grade 1 or 2/6 murmur heard at apex or left sternal border
 Hepatomegaly, ankle edema, ascites and pleural effusion if with
RV failure
Mitral Regurgitation
• Usually asymptomatic for chronic mild-moderate MR
• Palpation
–
–
–
–
–
Arterial pressure usually normal but may show a sharp upstroke
Systolic thrill at cardiac apex
Palpable rapid filling wave (S3)
Apex beat displaced laterally
In acute severe MR
• Reduced arterial pressure
• Normal or increased jugular venous pressure
• Apical impulse not displaced
• Auscultation
–
–
–
–
–
–
Grade 3/6 holosystolic high-pitched decrescendo, my obliterate S2
Radiates from apex to base or to left axilla
Absent or soft S1
Premature A2 resulting in wide but physiologic splitting of S2
S3 often present
S3-S4 on those with severe MR
Aortic Regurgitation
• Inspection
– Jarring of the entire body and bobbing motion of the head
with each systole
– Abrupt distention (water hammer pulse) and collapse of
large arteries during late sytole and diastole (Corrigan’s
pulse)
– Alternate flushing and paling of the skin at the root of the
nail (Quincke’s pulse)
– Booming sound on femoral artery ( Traube’s sign)
Aortic Regurgitation
• Palpation
– Elevation of systolic pressure (300 mmHg)
– Depression of diastolic pressure
– LV impulse is heaving and displaced laterally and inferiorly
– Palpable diastolic thrill along the left sternal border, systolic
thrill in suprasternal notch transmitted in the carotid arteries
• Auscultation
– Murmur is high pitched, blowing, decrescendo diastolic murmur heard
best in 3rd ICS along the left sternal border
– Low pitched rumbling murmur at the apex (Austin Flint)
– Soft S1, M1 and A2 often intensified
– S3 and systolic ejection sound are audible
– Occasionally S4 can also be heard
– Auscultatory features are intensified by strenous handgrip, which
increases sytemic resistance
AUSCULTOGRAM
MR, MS, AR, AS
AUSCULTOGRAM
Differential Diagnosis for the
Cause of Fever
Differential Diagnosis for the Cause of
Fever
•
•
•
•
•
Myocarditis
Pericarditis
Systemic Lupus Erythematosus (SLE)
Pneumonia
Pulmonary Tuberculosis (PTB)
Myocarditis
Patient
Dyspnea
(+)
(+)
Chest Pain
(+)
(+)
Fever
(+)
(+)
history of recent flulike
syndrome of fevers,
arthralgias or pharyngitis,
or upper respiratory tract
infection.
(+)
(+)
Dilated cardiomyopathy
(+)
(+)
Arrhythmia
(+)
(+)
Heart Failure
(+)
(+)
Myocarditis
Patient
Decompensation of heart
failure (tachycardia, mitral
regurgitation, edema)
(+)
(+)
Leukocytosis
(+)
(+)
Elevated ESR
(+)
(+)
nonspecific ST or T-wave
changes
(+)
(+)
(+) rheumatic fever
(+)
Frequent streptococcal
throat infection in
childhood
Pericarditis
Patient
Males
(+)
(-)
Adults
(+)
(+)
Chest Pain
(+)
(+)
Pericardial friction rub
(+)
(-)
Dyspnea
(+)
(+)
Fever
(+)
(+)
Tachypnea
(+)
(+)
Tachycardia
(+)
(+)
Elevated ESR, segmenters
Frequent streptococcal
throat infection in
childhood
Pericardial effusion
Pericarditis
Patient
(+)
(+)
(+) rheumatic fever
(+)
(+)
(-)
SLE
Patient
Females
(+)
(+)
Childbearing age
(+)
(+)
Fatigue
(+)
(+)
Fever
(+)
(+)
Arthralgia
(+)
(+)
Myalgia
(+)
(+)
edema
(+)
(+)
SLE
Patient
Dyspnea
(+)
(+)
Chest pain
(+)
(+)
Multiple cytopenias
(+)
(-)
Tachypnea
(+)
(+)
crackles
(+)
(+)
Pneumonia
Patient
Fever
(+)
(+)
Productive Cough
(+)
(+)
Dyspnea
(+)
(+)
Pleuritic Chest pain
(+)
(-)
Rales
(+)
(-)
Infiltrates on chest x-ray
(+)
(-)
PTB
Patient
Males
(+)
(-)
Older than 65
(+)
(-)
Productive cough
(+)
(+)
Fever
(+)
(+)
Weight loss
(+)
(-)
Hemoptysis
(+)
(-)
Chest pain
(+)
(+)
Anorexia
(+)
(-)
Fatigue
(+)
(+)
PTB
Patient
Night sweats
(+)
(-)
Chest x-ray: patchy or
nodular infiltrate
(+)
(-)
REVISED JONES CRITERIA
2002-2003 WHO Criteria for the Diagnosis of RF and RHD
Includes preceding streptococcal type A
infection and a combination of major and minor
clinical manifestations
Harrison’s Principles of Internal Medicine, 17th ed.
REVISED JONES CRITERIA
2002-2003 WHO Criteria for the Diagnosis of RF and RHD
MAJOR MANIFESTATIONS:
•
•
•
•
•
Carditis
Polyarthritis
Chorea
Erythema Marginatum
Subcutaneous Nodules
MINOR MANIFESTATIONS:
• Clinical: fever, polyarthralgia
• Labs: elevated ESR, C-reactive
protein (Acute Phase
Reactants)
• ECG: prolonged P-R interval
SUPPORTING EVIDENCE OF A PRECEDING STREPTOCOCCAL
INFECTION W/IN THE LAST 45 DAYS:
• Elevated or rising anti-streptolysin O or other streptococcal antibody, or
•(+) Throat culture, or
• Rapid antigen test for group A streptococcus
Harrison’s Principles of Internal Medicine, 17th ed.
REVISED JONES CRITERIA
2002-2003 WHO Criteria for the Diagnosis of RF and RHD
DIAGNOSTIC CATEGORIES
Primary Episode of Rheumatic Fever
2 Major OR 1 Major + 2 Minor manifestations
Plus evidence of preceding group A streptococcal infection
Recurrent attack of RF in a patient without established RHD
2 Major OR 1 Major + 2 Minor manifestations
Plus evidence of preceding group A streptococcal infection
Recurrent attack of RF in a patient with established RHD
2 Minor manifestations
Plus evidence of preceding group A streptococcal infection
Harrison’s Principles of Internal Medicine, 17th ed.
REVISED JONES CRITERIA
2002-2003 WHO Criteria for the Diagnosis of RF and RHD
DIAGNOSTIC CATEGORIES
Rheumatic Chorea
Insidous onset rheumatic carditis
Other major manifestations or evidence of group A strep.
infection not required
• Infective endocarditis should be excluded.
Chronic valve lesions of RHD
Do not require any other criteria to be diagnosed as having
rheumatic heart disease
• Congenital heart disease should be excluded.
Harrison’s Principles of Internal Medicine, 17th ed.
REVISED JONES CRITERIA
2002-2003 WHO Criteria for the Diagnosis of RF and RHD
“Probable Rheumatic Fever”
– with polyarthritis (or with only polyarthralgia or
monoarthritis) and with several (3 or more) other minor
manifestations, plus evidence of recent group A
streptococcal infection.
– may later turn out to be rheumatic fever
– advise regular secondary prophylaxis, follow up closely and
do regular heart examination (esp. in vulnerable age groups in
high incidence settings)
Harrison’s Principles of Internal Medicine, 17th ed.
The Duke Criteria
The Duke Criteria
• The diagnosis of infective endocarditis is
certain only when vegetations obtained are
examined histologically and microbiologically.
• Duke criteria is based on clinical, laboratory
and echocardiographic findings.
• 2 major criteria, 1 major + 2 minor criteria, or
5 minor criteria allows a definitive diagnosis.
The Duke Criteria
• The diagnosis of infective endocarditis is
rejected if:
– Alternative diagnosis is established
– Symptoms resolve and do not recur within 4 days
or less of antibiotic therapy
– Surgery or autopsy after 4 days or less of
antimicrobial therapy yields no histologic evidence
of endocarditis
The Duke Criteria
• Illnesses not classified as definite endocarditis
or rejected are considered possible cases
when either 1 major + 1 minor citeria or 3
minor criteria are identified.
• To fulfill a major criterion, the isolation of an
organism that causes both endocarditis and
bacteremia in the absence of endocarditis
must take place repeatedly and in the absence
of primary focus of infection.
The Duke Criteria
• Organisms that rarely cause endocarditis but
commonly contaminate blood cultures must
be isolated repeatedly if their isolation is to
serve as a major criterion.
The Duke Criteria
• Major Criteria
– Positive Blood Culture
• Typical microorganisms from two separate blood
cultures*
• Persistently positive blood culture, defined as recovery
of a microorganism consistent w/ infective endocarditis
from:
– Blood cultures drawn >12 hrs apart
– All of three, majority of four or more separate blood cultures,
with first and last drawn at least 1 hr apart
– Single positive blood culture from Coxiella burnetti or phase I
IgG titer > 1:800
The Duke Criteria
– Evidence of Endocardial Involvement
• Positive Echocardiogram
– Oscillating intracardiac mass on valve or supporting structures
or in the path of regurgitant jets or in implanted material, in
the absence of an alternative anatomic explanation
– Abscess
– New partial dehiscence of prosthetic valve
• New valvular regurgitation*
The Duke Criteria
• Minor Criteria
– Predisposition*
– Fever >/= 38°C*
– Vascular phenomena*
– Immunologic phenomena*
– Microbiologic Evidence*
Differential Diagnosis for the
cause of dyspnea
Algorithm for Dyspnea
Pathophysiology
DYSPNEA
RESPIRATORY
CARDIOVASCULAR
Gas Exchanger
Pump
Controller
Low output
Normal output
High output
Pulmonary
embolism
Pneumonia
Interstitial lung
disease
COPD
Asthma
Kyphoscoliosis
Pregnancy
Metabolic
acidosis
Congestive heart
failure
Myocardial
ischemia
Constrictive
pericarditis
Deconditioning
Obesity
Diastolic
dysfunction
Anemia
Hyperthyroidism
Arteriovenous
shunt
PNEUMONIA
• infection of the pulmonary parenchyma
• results from the proliferation of microbial pathogens
at the alveolar level and the host's response to those
pathogens
• the most common way by which microorganisms
gain access to the lower respiratory tract is by
aspiration from the oropharynx
ETIOLOGY
Hospitalized patients
Outpatients
Non-ICU
ICU
Streptococcus pneumoniae
S. pneumoniae
S. pneumoniae
Mycoplasma pneumoniae
M. pneumoniae
Staphylococcus aureus
Chlamydophila pneumoniae
Legionella spp.
C. pneumoniae
H. influenzae
Gram-negative bacilli
Respiratory viruses
Legionella spp.
H. influenzae
Haemophilus influenzae
Respiratory virusesa
CLINICAL MANIFESTATIONS
•
•
•
•
•
•
•
Febrile
Tachycardia
Chills and/or sweats
Cough that is either nonproductive or productive of mucoid, purulent, or bloodtinged sputum
Pleuritic chest pain
Nausea, vomiting, and/or diarrhea
Fatigue, headache, myalgias, and arthralgias
On physical examination:
• increased respiratory rate and use of accessory muscles of respiration
• increased or decreased tactile fremitus
• on percussion note can vary from dull to flat, reflecting underlying consolidated
lung and pleural fluid, respectively
• on auscultation, crackles, bronchial breath sounds, and possibly a pleural friction
rub may be heard on auscultation
CONGESTIVE HEART FAILURE
• Heart failure (HF) is a clinical syndrome that occurs in
patients who, because of an inherited or acquired
abnormality of cardiac structure and/or function,
develop a constellation of clinical symptoms
(dyspnea and fatigue) and signs (edema and rales)
that lead to frequent hospitalizations, a poor quality
of life, and a shortened life expectancy
ETIOLOGY
• any condition that leads to an alteration in LV
structure or function can predispose a patient
to developing HF.
–
–
–
–
–
–
–
–
Coronary artery disease
Hypertension
Faulty heart valves
Cardiomyopathy
Myocarditis
Congenital heart defects
Arrhythmias
Chronic diseases : diabetes, severe anemia, hyperthyroidism, hypothyroidism,
emphysema, lupus, hemochromatosis and amyloidosis
CLINICAL MANIFESTATIONS
Type of Heart Failure
Chronic heart failure
(A long-term condition with signs and
symptoms that persist.)
Signs and symptoms
• Fatigue and weakness
• Rapid or irregular heartbeat
• Shortness of breath (dyspnea) when
you exert yourself or when you lie
down
• Reduced ability to exercise
• Persistent cough or wheezing with
white or pink blood-tinged phlegm
• Swelling (edema) in your legs, ankles
and feet
• Swelling of your abdomen (ascites)
• Sudden weight gain from fluid
retention
• Lack of appetite and nausea
• Difficulty concentrating or decreased
alertness
CLINICAL MANIFESTATIONS
Type of Heart Failure
Acute heart failure
(An emergency situation that occurs when
something suddenly affects your heart's
ability to function.)
Signs and symptoms
• Signs and symptoms similar to those
of chronic heart failure but more
severe, and start or worsen suddenly
• Sudden fluid buildup
• Rapid or irregular heartbeat with
palpitations that may cause the heart to
stop beating
• Sudden, severe shortness of breath
and coughing up pink, foamy mucus
• Chest pain if caused by a heart attack
Enumerate the precipitating
factors of heart failure.
HEART FAILURE
• Pathophysiologic state
wherein the heart loses
its ability to pump
sufficient amount of
blood due to a structural
or functional cardiac
abnormality
HEART FAILURE
• A majority of the patients’
symptoms of heart failure are due
to impairment of left ventricular
function.
•
Hence, a condition that leads to an
alteration in LV structure or
function can predispose a patient
to developing heart failure.
HEART FAILURE
LV dysfunction begins with some
injury to the myocardium, and is
a progressive process, even in
the absence of a new
identifiable insult to the
myocardium.
Cardiac remodelling occurs in
association w/ homeostatic
attempts to decrease wall stress
through increases in wall
thickness.
This would then result in a
change in the geometry of the
LV, hence, the chamber dilates,
hypertrophies and becomes
more spherical
HEART FAILURE
HEART FAILURE
PRECIPITATING CAUSES OF HEART FAILURE:
Reduction in therapy
Hypertension
High salt intake
Cardiac infection and
inflammation
Arrhythmias
High output states
Systemic infection
Physical, environmental
and emotional stress
Pulmonary embolism
Development of an unrelated
illness
Development of a second
form of cardiac disease
Differentiate low and high output failure,
R/L sided heart failure, systolic and
diastolic dysfunction
Systolic Versus Diastolic Failure
Forms of Heart Failure
Sytolic Failure
• Inability of the ventricle
to contract normally
and expel sufficient
blood
• Inadequate cardiac
output with weakness,
fatigue, reduced
exercise tolerance
(hypoperfusion)
Diastolic Failure
• Inability to relax or fill
normally (elevation of
filling pressures)
• Due to increased
resistance to ventricular
diastolic capacity,
impaired ventricular
relaxation, and
myocardial fibrosis and
infiltration
Management
10. How do you manage this patient
on the following conditions?
RF? Tight MS?
Congestive Heart Failure
• Patients With Reduced Left Ventricular
Ejection Fraction
– If with fluid retention:
• Use diuretics (thiazides)
– Medications that should be AVOIDED:
• Anti-arrhythmics
• Calcium channel blockers
• NSAIDs
Circulation; Journal of the AHA http://circ.ahajournals.org/cgi/content/full/119/14/1977
Congestive Heart Failure
• Patients With Reduced Left Ventricular
Ejection Fraction
– Recommendations concerning aldosterone
antagonists:
• carefully selected patients with moderately severe or
severe HF symptoms and recent decompensation or
with LV dysfunction early after MI
Circulation; Journal of the AHA http://circ.ahajournals.org/cgi/content/full/119/14/1977
Congestive Heart Failure
• Patients With Refractory End-Stage Heart
Failure (Stage D)
– Intravenous Peripheral Vasodilators and Positive
Inotropic Agents:
• hospitalized frequently for clinical deterioration, and
during such admissions, they commonly receive
infusions of both positive inotropic agents
(dobutamine, dopamine, or milrinone) and vasodilator
drugs (nitroglycerin, nitroprusside, or nesiritide)
Circulation; Journal of the AHA http://circ.ahajournals.org/cgi/content/full/119/14/1977
Congestive Heart Failure
The Hospitalized Patient
Common Factors That Precipitate
Hospitalization for Heart Failure
• Noncompliance with medical regimen, sodium
and/or fluid restriction
• Acute myocardial ischemia
• Uncorrected high blood pressure
• Atrial fibrillation and other arrhythmias
Circulation; Journal of the AHA http://circ.ahajournals.org/cgi/content/full/119/14/1977
Congestive Heart Failure
The Hospitalized Patient
Common Factors That Precipitate
Hospitalization for Heart Failure
• Recent addition of negative inotropic drugs
(e.g., verapamil, nifedipine, diltiazem, beta
blockers)
• Pulmonary embolus
• Nonsteroidal anti-inflammatory drugs
Circulation; Journal of the AHA http://circ.ahajournals.org/cgi/content/full/119/14/1977
Congestive Heart Failure
The Hospitalized Patient
Common Factors That Precipitate
Hospitalization for Heart Failure
• Excessive alcohol or illicit drug use
• Endocrine abnormalities (e.g., diabetes
mellitus, hyperthyroidism, hypothyroidism)
• Concurrent infections (e.g., pneumonia, viral
illnesses)
Circulation; Journal of the AHA http://circ.ahajournals.org/cgi/content/full/119/14/1977
Rheumatic Fever
• Inflammatory disease that may develop two to
three weeks after a Group A streptococcal
infection (such as strep throat or scarlet
fever).
• Caused by antibody cross-reactivity and can
involve the heart, joints, skin, and brain
Rheumatic Fever
The management of acute rheumatic fever is
geared toward the reduction of inflammation
with anti-inflammatory medications such as
aspirin or corticosteroids.
1.Antibiotics
2.Anti- inflammatory Drug
Antibiotics
Erythromycin
Penicillin V
• Antibiotics that is used to
treat infections such as
respiratory tract and soft
tissue infections.
• Antimicrobial spectrum of
macrolides is slightly wider
than that of penicillin,
macrolides are a common
substitute for patients with a
penicillin allergy.
• Beta-hemolytic streptococci is
usually susceptible to
macrolides
• Phenoxymethylpenicillin is the
orally active form of penicillin.
• Phenoxymethylpenicillin exerts a
bactericidal action against
penicillinsensitive
microorganisms during the stage
of active multiplication.
• Used only for the treatment of
mild to moderate infections, and
not for chronic, severe, or deepseated infections since
absorption can be unpredictable
• Used as primary and secondary
prophylaxis for RF
Anti- inflammatory Drugs
• Corticosteroids and salicylates cannot prevent
or modify the development of subsequent
rheumatic heart disease but are used for
symptomatic relief
• Avoid anti-inflammatory drugs until diagnosis
is confirmed, as they may mask symptoms
essential to the diagnosis
Anti- inflammatory Drugs
NSAIDS
• Act as non-selective inhibitors of the enzyme
cyclooxygenase, inhibiting both the
cyclooxygenase-1 (COX-1) and
cyclooxygenase-2 (COX-2) isoenzymes.
• lowering an elevated body temperature and
relieving pain without impairing
consciousness) and, in higher doses, with antiinflammatory effects.
Aspirin
• Acetylsalicylic Acid
• Acetyl derivative of salicylic acid that is a white,
crystalline, weakly acidic substance, with melting
point 137°C.
• It is useful in the relief of headache and muscle
and joint aches.
• Aspirin is also effective in reducing fever,
inflammation, and swelling and thus has been
used for treatment of rheumatoid arthritis,
rheumatic fever, and mild infection.
Aspirin
Common Side Effects
• Heartburn; nausea; upset
stomach.
Severe Side Effects
• Severe allergic reactions (rash;
hives; itching; difficulty
breathing; tightness in the
chest; swelling of the mouth,
face, lips, or tongue); black or
bloody stools; confusion;
diarrhea; dizziness;
drowsiness; hearing loss;
ringing in the ears; severe or
persistent stomach pain;
unusual bruising; vomiting.
Anti- inflammatory Drugs
Corticosteroid
• Drugs that are closely related to cortisol, a hormone
which is naturally produced in the adrenal cortex.
• Act on the immune system by blocking the production
of substances that trigger allergic and inflammatory
actions, such as prostaglandins.
• They also impede the function of white blood cells
which destroy foreign bodies and help keep the
immune system functioning properly.
• Interference with white blood cell function yields a side
effect of increased susceptibility to infection.
Anti- inflammatory Drugs
Corticosteroids
• Used in severe carditis and CHF and also
prevents the complications of carditis.
• High-dose prednisone is administered for 2-3
wk, then tapered over 3 wk. IV corticosteroids
are reserved for fulminant cases.
• Rebound occurs frequently with
corticosteroids; hence, they require gradual
tapering rather than abrupt cessation.
Prednisone
• Synthetic corticosteroid drug that is
particularly effective as an
immunosuppressant, and affects virtually all
of the immune system.
• Used in severe carditis and CHF.
• High-dose prednisone is administered for 2-3
wk, then tapered over 3 wk. IV corticosteroids
are reserved for fulminant cases.
Prednisone
Minor Side Effects
• stretchmarks;nervousness;
acne ; rash; increased
appetite; hyperactivity;
frequent urination;
diarrhea; removes intestinal
flora; leg pain; sensitive
teeth
Major Side Effects
•
Micrograph of fatty liver, as may be
seen due to long-term prednisone use.;
weight gain; facial swelling; depression,
mania, psychosis or other psychiatric
symptoms; unusual fatigue or
weakness; mental confusion /
indecisiveness; blurred vision;
abdominal pain; peptic ulcer;
infections; painful hips or shoulders;
Steroid-induced osteoporosis; Long
term migraines; insomnia; severe joint
pain; cataracts; anxiety; black stool;
stomach pain or bloating; severe
swelling; mouth sores or dry mouth;
avascular necrosis; hepatic steatosis
Mitral Stenosis
• Mitral stenosis is a condition in which the
mitral valve leaflets become thickened and the
commissures fused along with thickening and
shortening of the chordae tendineae.
• Approximately 40% of all patients with
rheumatic heart disease.
• Goal of medical therapy is to control the rapid
ventricular rate.
Medical Therapy
• Symptom Control
– Beta blockers & Nondihydropyridine CCB
• To slow the ventricular rate of patients w/ AF
– Digoxin (rate control of AF)
– Cardioversion for new onset AF and HF
• Undertaken after patient has had at least 3 consecutive
wks of anticoagulant tx
– Diuretics for HF
Medical Therapy
• Warfarin
– INR of 2-3
– given indefinitely to patients w/ MS who have AF
or a hx of thromboembolism
• Penicillin prophylaxis of Grp A β-hemolytic
streptococcal infection
– Prevent RF
Mitral Valvotomy
Indication:
Symptomatic (NYHA
Functional Class II-IV)
patients w/ isolated MS
whose effective orifice
(valve area) is
<~1.0cm2/m2 body
surface area, or 1.5 cm2 in
normal-sized adults
 Percutaneous mitral
balloon valvotomy
 Surgical valvotomy