Week 9 Flashcards
(172 cards)
1
Q
What is the definition of endocarditis?
A
Endocarditis is inflammation of the heart’s endocardial surface, particularly the valve leaflets, manifesting as vegetations (fibrin–platelet aggregates, microbes, and inflammatory cells).
2
Q
What are the two main types of endocarditis?
A
- Infective Endocarditis (IE)
- Non-infective (Marantic) Endocarditis
3
Q
What characterizes Infective Endocarditis (IE)?
A
Microbial colonization, subtyped by acuity (acute vs. subacute), location (right- vs. left-sided), and prosthetic involvement (early ≤1 year vs. late >1 year).
4
Q
What are sterile vegetations associated with in Non-infective Endocarditis?
A
Hypercoagulable or malignancy states.
5
Q
List the structural valve abnormalities that are risk factors for endocarditis.
A
- Rheumatic heart disease
- Congenital defects
- Degenerative lesions
6
Q
What is a risk factor for endocarditis related to prosthetic materials?
A
Prosthetic valves and cardiac implantable electronic devices (CIEDs).
7
Q
How does intravenous drug use (IVDU) contribute to endocarditis?
A
It leads to repeated skin flora inoculation, predominantly causing right-sided (tricuspid) IE.
8
Q
What host predispositions increase the risk of endocarditis?
A
- Prior IE
- Immunosuppression
- Metabolic comorbidities
9
Q
What are the primary etiologic agents of infective endocarditis (IE)?
A
- Staphylococcus aureus
- Coagulase-negative staphylococci
- Viridans group streptococci
- Streptococcus gallolyticus
- Enterococci
10
Q
Which group of fastidious Gram-negative bacteria is associated with culture-negative endocarditis?
A
HACEK (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella).
11
Q
What are some other Gram-negative and fungal agents that can cause endocarditis?
A
- Pseudomonas aeruginosa
- Escherichia coli
- Candida spp.
- Aspergillus spp.
12
Q
True or False: Culture-negative IE can result from prior antibiotics.
A
True
13
Q
What is the first step in the pathogenesis of infective endocarditis?
A
Endothelial disruption due to high-velocity jets causing microtrauma.
14
Q
What forms after endothelial disruption in the pathogenesis of IE?
A
Sterile thrombus formation (NBTE).
15
Q
Fill in the blank: Microbial adhesion involves surface proteins known as _______.
A
MSCRAMMs
16
Q
What leads to vegetation maturation in infective endocarditis?
A
Bacterial proliferation within a protective biofilm of fibrin and platelets.
17
Q
What are some local and distant sequelae of infective endocarditis?
A
- Valvular destruction
- Annular abscesses
- Septic emboli
- Immune complex deposition
18
Q
What are the constitutional manifestations of infective endocarditis?
A
- Fever
- Chills
- Night sweats
- Weight loss
- Fatigue
19
Q
What cardiac manifestation is associated with infective endocarditis?
A
New/worsening regurgitant murmur and signs of volume overload.
20
Q
List the immunologic manifestations of infective endocarditis.
A
- Osler nodes
- Janeway lesions
- Roth spots
- Splinter hemorrhages
21
Q
What laboratory findings are common in infective endocarditis?
A
- Leukocytosis
- Elevated ESR/CRP
- Normocytic anemia
- Positive RF in some
22
Q
What complications can arise from infective endocarditis?
A
- Perivalvular abscess
- Conduction block
- Heart failure
- Septic metastases
23
Q
What is the sensitivity of blood cultures in native-valve IE?
A
> 95 %
Blood cultures should be taken in three sets from separate venipunctures before starting antibiotics.
24
Q
What is the sensitivity of transthoracic echocardiography (TTE) for vegetations ≥2–3 mm?
A
~ 60 %
TTE is used to visualize heart structures but has lower sensitivity compared to transesophageal echocardiography.
25
What is the sensitivity of transesophageal echocardiography (TEE) for detecting vegetations?
> 90 %
## Footnote
TEE is more effective in identifying abscesses and prosthetic-valve involvement.
26
What are the major criteria of the Modified Duke Criteria for diagnosing endocarditis?
* Typical microorganisms from ≥2 cultures
* Echocardiographic evidence of vegetation, abscess, or new dehiscence
## Footnote
These criteria help establish a diagnosis of endocarditis.
27
What are the minor criteria of the Modified Duke Criteria?
* Predisposition
* Fever
* Vascular/immunologic phenomena
* Single positive culture
* Non-major echo findings
## Footnote
Minor criteria complement the major criteria in diagnosis.
28
What adjunctive investigations can be used for endocarditis?
* CT/MRI for silent emboli
* PET/CT for prosthetic-valve infection
* Serologies/PCR for culture-negative organisms
## Footnote
These investigations can provide additional information when standard tests are inconclusive.
29
What is the initial empirical antimicrobial therapy for endocarditis?
Vancomycin + gentamicin
## Footnote
This combination covers MRSA, enterococci, and HACEK organisms while cultures are pending.
30
What is the targeted treatment for MSSA in endocarditis?
Nafcillin/oxacillin ± gentamicin for synergy in prosthetic-valve cases
## Footnote
Targeted therapy is based on culture results.
31
What is the recommended duration of antimicrobial therapy for native-valve endocarditis?
4 weeks
## Footnote
Duration may vary for prosthetic-valve endocarditis.
32
What are the indications for surgical intervention in endocarditis?
* Heart failure refractory to medical therapy
* Uncontrolled infection (abscess, fistula, persistent bacteremia ≥7 days)
* Prevention of embolism with large (> 10 mm) mobile vegetations after systemic embolus
## Footnote
Surgical intervention is critical in certain severe cases.
33
What is a common complication of endocarditis?
Heart failure
## Footnote
It is the leading cause of death in patients with endocarditis.
34
What is the in-hospital mortality rate for native-valve endocarditis?
~ 15–20 %
## Footnote
This statistic highlights the serious nature of the condition.
35
What are poor prognosticators for endocarditis?
* S. aureus etiology
* Prosthetic material
* Kidney dysfunction
* Heart failure
* Annular invasion
## Footnote
These factors contribute to worse outcomes in endocarditis patients.
36
What is the mortality rate for prosthetic-valve endocarditis?
Up to 40 %
## Footnote
This reflects the increased risk associated with prosthetic devices.
37
Fill in the blank: The sensitivity of TTE is approximately ______ for vegetations ≥2–3 mm.
60 %
38
True or False: The Modified Duke Criteria has both major and minor criteria for diagnosing endocarditis.
True
39
What is the classic prototype virus associated with myocarditis?
Coxsackie B virus
## Footnote
Binds the coxsackie–adenovirus receptor (CAR) on cardiomyocytes.
40
Which virus has a similar binding and lytic potential as Coxsackie B virus?
Adenovirus
## Footnote
Specifically, species C.
41
What type of myocarditis is associated with Parvovirus B19?
Subtle chronic myocarditis
## Footnote
Tropism for erythroid precursors and endothelium.
42
What is the mechanism of Human Herpesvirus 6 in myocarditis?
Integration into host genome
## Footnote
Possible reactivation in immunosuppression.
43
What are the potential effects of Influenza A/B on the heart?
Direct myocardial invasion
## Footnote
Occurs during severe systemic infection.
44
What are the two roles of HIV in myocarditis?
Direct infection and secondary cardiotoxic effects
## Footnote
Includes opportunistic myocarditides.
45
What is the potential cardiac effect of SARS-CoV-2?
Direct viral injury plus cytokine-mediated storm
46
Which bacterium is associated with toxin-mediated myocarditis?
Corynebacterium diphtheriae
## Footnote
Leads to “pseudomembranous” involvement.
47
What cardiac condition is associated with Borrelia burgdorferi?
Lyme carditis
## Footnote
AV block predominates, with myocarditis on biopsy.
48
What type of myocarditis is linked to Mycoplasma pneumoniae?
Immune-mediated component
## Footnote
Often occurs in younger patients.
49
What is the main disease caused by Trypanosoma cruzi?
Chagas disease
## Footnote
Leads to acute necrotizing myocarditis and chronic dilated cardiomyopathy.
50
Which fungi can cause myocarditis in immunocompromised hosts?
Candida albicans, Histoplasma capsulatum, Aspergillus fumigatus
## Footnote
Can lead to granulomatous or abscess-forming myocarditis.
51
What is the role of macrophages and dendritic cells in viral myocarditis?
Detect viral RNA and produce type I interferons, TNF-α, IL-1β
## Footnote
This recruits neutrophils and NK cells.
52
What is the function of CD8⁺ Cytotoxic T Lymphocytes in myocarditis?
Recognize viral peptides on MHC I and kill targeted myocytes
53
What phenomenon may trigger chronic autoimmune myocarditis?
Molecular Mimicry
## Footnote
Viral antigens similar to myosin or β‐adrenergic receptors may trigger autoantibody formation.
54
What are the clinical manifestations during the prodromal phase of myocarditis?
Fever, fatigue, myalgias, headache, gastrointestinal upset
## Footnote
These symptoms occur 1–3 weeks prior.
55
What type of chest pain is associated with myopericarditis?
Pleuritic pain
## Footnote
Sharp pain worsened by inspiration.
56
What are the left-sided heart failure signs in myocarditis?
Dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, bibasilar crackles
57
What arrhythmias can occur due to myocarditis?
Atrial fibrillation/flutter and ventricular PVCs, non-sustained or sustained VT
## Footnote
Increases risk of sudden death.
58
What is the fulminant presentation of myocarditis?
Rapid onset severe ventricular dysfunction leading to cardiogenic shock
## Footnote
Requires inotropes and mechanical circulatory support.
59
What chronic condition can result from myocarditis?
Dilated Cardiomyopathy
## Footnote
Characterized by progressive chamber enlargement and chronic systolic dysfunction.
60
What is a key clinical pearl for suspected myocarditis?
Consider cardiac MRI early for non-invasive tissue characterization
61
In what situation is endomyocardial biopsy reserved?
Unexplained heart failure with hemodynamic compromise or suspected giant cell/eosinophilic etiologies
62
What is the primary management approach for myocarditis?
Supportive heart failure therapy and arrhythmia control
## Footnote
Includes etiology-directed treatments like immunosuppression in giant cell myocarditis.
63
What are the ST–T changes observed in myocarditis on an ECG?
Diffuse or regional ST-segment elevations and T-wave inversions; non-specific repolarization abnormalities.
64
What conduction defects can occur in myocarditis?
First-degree to complete AV block, bundle-branch blocks.
65
What arrhythmias are commonly associated with myocarditis?
Frequent premature ventricular complexes, nonsustained ventricular tachycardia, atrial fibrillation.
66
What cardiac biomarker is elevated in more than 50% of myocarditis cases?
Troponin I/T.
67
How do CK-MB levels in myocarditis compare to troponin?
CK-MB may be mildly elevated; less specific than troponin.
68
What does an elevated BNP/NT-proBNP indicate in myocarditis?
Concomitant ventricular dysfunction or heart failure.
69
What is the significance of reduced LVEF (< 50%) in myocarditis?
Indicates systolic impairment.
70
What does T2-weighted imaging in cardiac MRI reveal in myocarditis?
Myocardial edema—high signal intensity in inflamed areas.
71
What does early gadolinium enhancement in cardiac MRI indicate?
Hyperemia and capillary leak.
72
What does late gadolinium enhancement (LGE) in cardiac MRI suggest?
Patchy mid-wall or subepicardial enhancement indicating necrosis and fibrosis.
73
What are the Lake Louise Criteria for diagnosing myocarditis?
Presence of ≥2 of T2-weighted imaging, early gadolinium enhancement, late gadolinium enhancement yields > 80% sensitivity and specificity.
74
What are the indications for an endomyocardial biopsy (EMB)?
Unexplained new-onset heart failure with hemodynamic compromise, suspected giant cell or eosinophilic myocarditis, sarcoidosis, or Chagas disease.
75
According to the Dallas Criteria, what defines active myocarditis?
Inflammatory infiltrate with adjacent myocyte necrosis not attributable to ischemia.
76
What histologic feature characterizes borderline myocarditis?
Inflammatory infiltrate without clear evidence of myocyte necrosis.
77
What histologic variant of myocarditis shows CD3⁺ T-cell predominance?
Lymphocytic (Viral) myocarditis.
78
What is a key feature of eosinophilic myocarditis?
Prominent eosinophils and often vessel necrosis.
79
What defines giant cell myocarditis histologically?
Multinucleated giant cells and extensive myocyte destruction.
80
What is the role of ACE inhibitors/ARBs in myocarditis management?
Afterload reduction and neurohormonal blockade.
81
What is the purpose of using β-blockers in myocarditis?
Reduce arrhythmogenic risk and improve remodeling.
82
What are common complications of myocarditis?
Dilated cardiomyopathy, thromboembolism, sudden cardiac death.
83
What is the prognosis for fulminant myocarditis?
High in-hospital mortality (30-50%) without mechanical support; excellent long-term recovery if inflammation resolves.
84
What percentage of subacute/chronic myocarditis cases progress to end-stage dilated cardiomyopathy?
20-30%.
85
What does the presence of LGE on MRI indicate for prognosis in myocarditis?
Portends poorer outcomes.
86
What is the recommended activity restriction for athletes with myocarditis?
Complete cessation of competitive sports and strenuous exercise for ≥ 3-6 months.
87
True or False: Endomyocardial biopsy is routinely performed in all myocarditis cases.
False.
88
Fill in the blank: The presence of _______ in myocarditis indicates inflammatory infiltrate with adjacent myocyte necrosis.
Active Myocarditis
89
What is the definition of acute pericarditis?
Acute inflammation of the pericardium, typically <4 weeks’ duration.
## Footnote
Acute pericarditis can arise from various causes and often presents with specific clinical features.
90
List the infectious causes of acute pericarditis.
* Viral (coxsackie B, echovirus, influenza)
* Bacterial (tuberculosis in endemic regions, purulent bacterial)
* Fungal
## Footnote
Infectious causes are a significant category of triggers for acute pericarditis.
91
What autoimmune/inflammatory conditions can cause acute pericarditis?
* SLE
* Rheumatoid arthritis
* Scleroderma
* Dressler syndrome (4–6 weeks post-MI)
## Footnote
Autoimmune and inflammatory conditions are common non-infectious causes of pericarditis.
92
What metabolic condition is associated with acute pericarditis?
Uremia (renal failure)
## Footnote
Metabolic causes are less common but can lead to acute pericarditis.
93
What neoplastic causes can lead to acute pericarditis?
Direct invasion or metastases (lung, breast, melanoma)
## Footnote
Neoplastic causes can be serious and often indicate advanced disease.
94
What types of trauma or radiation can cause acute pericarditis?
* Post-thoracotomy
* Chest wall injury
* Radiation therapy
## Footnote
Trauma and radiation are significant risk factors for developing acute pericarditis.
95
What is the classification for idiopathic causes of acute pericarditis?
Presumed viral when no cause identified
## Footnote
Idiopathic cases often remain unexplained despite thorough investigation.
96
Describe the chest pain associated with acute pericarditis.
Sharp, pleuritic, worse supine, relieved by sitting/leaning forward.
## Footnote
This characteristic pain helps differentiate acute pericarditis from other conditions.
97
What is a pericardial friction rub?
High-pitched, scratchy sound; three components (atrial systole, ventricular systole, early diastole).
## Footnote
The presence of a friction rub is a classic sign of acute pericarditis.
98
List the four stages of ECG changes in acute pericarditis.
* Diffuse ST-segment elevation, PR depression
* Normalization of ST/PR
* Diffuse T-wave inversions
* ECG normalization
## Footnote
ECG changes are crucial for diagnosis and monitoring of acute pericarditis.
99
What are other clinical manifestations of acute pericarditis?
* Low-grade fever
* Dyspnea
* Elevated inflammatory markers
## Footnote
These manifestations can help in the overall assessment of the patient.
100
Compare the pain characteristics of acute pericarditis and myocardial infarction.
Acute Pericarditis: Sharp, pleuritic, improves sitting up; Myocardial Infarction: Crushing, pressure-like.
## Footnote
Differentiating between these types of pain is essential for accurate diagnosis.
101
How does the position affect pain in acute pericarditis compared to pulmonary embolism?
Better sitting/leaning forward in acute pericarditis; No change in pulmonary embolism.
## Footnote
Positional changes can help distinguish between different conditions.
102
What auscultation findings are associated with acute pericarditis?
Friction rub
## Footnote
Auscultation findings can provide significant clues in the evaluation of chest pain.
103
What ECG findings are typical for pulmonary embolism?
Sinus tachycardia, S1Q3T3 (in some)
## Footnote
Recognizing these findings can help in the prompt diagnosis of pulmonary embolism.
104
What biomarkers are mildly elevated in myopericarditis?
Mild troponin ↑
## Footnote
Biomarker levels can assist in distinguishing between pericarditis and other cardiac conditions.
105
What are some other signs associated with pulmonary embolism?
* Tachypnea
* Hypoxia
* Hemoptysis (rare)
## Footnote
These signs can help differentiate pulmonary embolism from other conditions.
106
What signs are indicative of myocardial infarction?
* Diaphoresis
* Nausea
* Risk factors
## Footnote
Recognizing these signs is crucial for timely intervention in myocardial infarction cases.
107
What are the ECG findings in Stage I pericarditis?
Diffuse ST-segment elevation in most leads; reciprocal ST depression in aVR and V1; PR-segment depression in limb leads.
## Footnote
Stage I occurs within hours to days of onset.
108
What characterizes Stage II of pericarditis on an ECG?
Normalization of ST and PR segments.
## Footnote
This stage typically occurs within days.
109
What are the ECG findings in Stage III of pericarditis?
Diffuse T-wave inversions as repolarization abnormalities persist.
## Footnote
Stage III occurs 1 to 3 weeks after onset.
110
What happens to the ECG in Stage IV of pericarditis?
ECG returns to baseline.
## Footnote
This stage can last weeks to months.
111
What indicates the presence of pericardial effusion on echocardiography?
Echo-free space between visceral and parietal layers.
## Footnote
Quantification is done by depth: < 10 mm small, 10–20 mm moderate, > 20 mm large.
112
What are signs of cardiac tamponade observed in echocardiography?
* Right atrial systolic collapse
* Right ventricular diastolic collapse
* Exaggerated respiratory variation in transvalvular Doppler flows
* 'Swinging heart' motion
## Footnote
These signs indicate hemodynamic compromise.
113
What does a chest X-ray show if there is a large pericardial effusion?
Globular ('water-bottle') cardiac silhouette; mediastinal width may increase.
114
What does a pericardial thickness greater than 4 mm suggest?
Constrictive physiology.
## Footnote
This finding is best assessed on CT.
115
What laboratory studies are indicative of active pericardial inflammation?
Markedly elevated ESR and CRP.
## Footnote
These markers help guide therapy duration.
116
What is the first-line medical therapy for pericarditis?
* NSAIDs (Ibuprofen 600–800 mg TID or high-dose aspirin 750–1000 mg TID)
* Colchicine 0.5 mg BID (or 0.5 mg daily if < 70 kg or elderly) for 3 or 6 months
## Footnote
NSAIDs reduce inflammation; colchicine reduces symptoms and recurrence risk.
117
What is the second-line therapy for refractory pericarditis?
* Corticosteroids (Prednisone 0.2–0.5 mg/kg/day)
* Immunosuppressants (azathioprine, anakinra) in rare cases
## Footnote
Corticosteroids are tapered slowly to minimize adverse effects.
118
What is the indication for pericardiocentesis?
Cardiac tamponade with hemodynamic instability.
## Footnote
Symptoms include pulsus paradoxus, hypotension, and jugular venous distention.
119
What are the indications for surgical pericardiectomy?
* Chronic constrictive pericarditis causing heart failure unresponsive to medical therapy
* Loculated effusions inaccessible percutaneously
## Footnote
Procedure involves subtotal pericardial strip via thoracotomy or sternotomy.
120
What is a potential complication of pericarditis that requires urgent intervention?
Cardiac Tamponade.
## Footnote
This condition compresses cardiac chambers and can be life-threatening.
121
What is the typical prognosis for idiopathic or viral pericarditis?
Most recover fully with NSAIDs/colchicine; symptom resolution within days to weeks.
122
What percentage of patients experience recurrence of pericarditis despite therapy?
20–30%.
## Footnote
Risk factors include incomplete initial treatment and early tapering of medications.
123
What is the prognosis for constrictive pericarditis after surgical intervention?
Symptomatic relief in ≥ 80% of patients, but carries perioperative risk.
124
Fill in the blank: Neutrophil predominance in pericardial fluid analysis indicates _______.
bacterial infection.
125
Fill in the blank: High protein and LDH levels in pericardial fluid suggest _______.
exudative effusions.
126
What is Acute Rheumatic Fever (RF)?
An immune‐mediated, multisystem inflammatory syndrome following pharyngeal infection by group A β-hemolytic Streptococcus pyogenes, typically appearing 2–4 weeks after untreated streptococcal pharyngitis.
127
What does Rheumatic Heart Disease (RHD) represent?
The chronic sequelae of one or more episodes of acute RF, characterized by permanent deformity of one or more cardiac valves, most often the mitral valve, leading to stenosis and/or regurgitation.
128
What initiates Acute Rheumatic Fever?
Specific S. pyogenes strains expressing rheumatogenic M-protein epitopes colonize the pharynx.
129
What is the role of molecular mimicry in RF?
Host B cells and CD4⁺ T cells generate antibodies and T-cell responses against streptococcal M-protein, which cross-react with human cardiac myosin, tropomyosin, and valve endothelial proteins due to structural similarity.
130
Describe Pancarditis in the context of RF.
* Endocarditis: sterile verrucous vegetations on valve leaflets
* Myocarditis: Aschoff bodies with central fibrinoid necrosis
* Pericarditis: serofibrinous exudate, often mild and transient.
131
What contributes to systemic inflammation in RF?
Immune-complex deposition contributes to arthritis, chorea, and skin manifestations, while cytokines (IL-1, TNF-α) drive fever and acute‐phase reactants.
132
What are Aschoff Bodies?
Pathognomonic cardiac granulomas with central necrosis, Anitschkow cells, and surrounding lymphocytes/plasma cells.
133
What morphological features characterize Chronic Rheumatic Heart Disease?
* Valve Deformities: fibrous thickening, commissural fusion, shortening/thickening of chordae tendineae, calcification
* Myocardial Scarring: interstitial fibrosis
* Mural Thrombi: in dilated atria due to mitral stenosis.
134
What are the modified Jones criteria for Acute RF?
* Migratory Polyarthritis
* Carditis
* Sydenham Chorea
* Erythema Marginatum
* Subcutaneous Nodules.
135
What are common clinical manifestations of Mitral Stenosis in Chronic RHD?
* Exertional dyspnea
* Orthopnea
* Paroxysmal nocturnal dyspnea
* Loud S1
* Opening snap
* Diastolic rumble.
136
What complications can arise from Chronic RHD related to pulmonary hypertension?
Elevated left atrial pressure leading to pulmonary venous congestion and rupture of bronchial veins, causing hemoptysis.
137
What is the significance of Atrial Fibrillation in Chronic RHD?
It occurs secondary to left atrial enlargement, leading to palpitations and increased risk of thromboembolic stroke.
138
Fill in the blank: Acute Rheumatic Fever typically appears ______ weeks after untreated streptococcal pharyngitis.
2–4
139
True or False: Erythema Marginatum is a pruritic rash commonly associated with Acute RF.
False
140
What is the hallmark of myocarditis in Acute RF?
Aschoff bodies.
141
What are the characteristic features of the rash known as Erythema Marginatum?
Non-pruritic, serpiginous rash with central clearing on trunk and limbs.
142
What are the symptoms of Right-Sided Heart Failure in Chronic RHD?
* Peripheral edema
* Hepatic congestion in advanced disease.
143
What are the major criteria for diagnosing Rheumatic Fever according to the Jones Criteria?
* Migratory polyarthritis
* Carditis and valvulitis
* Sydenham chorea
* Erythema marginatum
* Subcutaneous nodules
## Footnote
Major criteria require at least 2 to be present.
144
What are the minor criteria for diagnosing Rheumatic Fever?
* Fever (≥ 38.5 °C)
* Arthralgia
* Elevated ESR or CRP
* Prolonged PR interval on ECG
* Evidence of recent streptococcal infection (positive throat culture, rapid antigen test, elevated ASO or anti-DNase B titers)
## Footnote
Minor criteria require at least 2 plus evidence of preceding streptococcal infection.
145
How is the diagnosis of Rheumatic Fever established?
Diagnosis is established when either:
* 2 major criteria, or
* 1 major + 2 minor criteria
in the context of recent streptococcal pharyngitis.
## Footnote
Clinical application is crucial for the accurate diagnosis.
146
What is the first-line treatment for the eradication of Streptococci in Rheumatic Fever?
Single dose benzathine penicillin G IM (1.2 million units for adults; weight-based for children) or penicillin V PO × 10 days.
## Footnote
For penicillin-allergic patients, macrolides like azithromycin are recommended.
147
What anti-inflammatory therapy is recommended for arthritis associated with Rheumatic Fever?
High-dose aspirin (80–100 mg/kg/day in divided doses in children; 2–4 g/day in adults) until resolution of joint symptoms.
## Footnote
This approach is critical in managing arthritis symptoms.
148
What is the management protocol for severe carditis or pericarditis in Rheumatic Fever?
Short-course corticosteroids (e.g., prednisone 1–2 mg/kg/day, taper over 2–3 weeks).
## Footnote
Corticosteroids help reduce inflammation in severe cases.
149
What supportive measures are recommended for heart failure management in Rheumatic Fever?
* Diuretics for volume overload
* Afterload reduction with ACE inhibitors if regurgitation is severe
* Bed rest during the acute phase
## Footnote
Supportive care is essential in managing heart failure symptoms.
150
What is the duration of secondary prophylaxis for Rheumatic Fever without carditis?
5 years or until age 21.
## Footnote
Duration varies based on the presence and severity of carditis.
151
What is the duration of secondary prophylaxis for Rheumatic Fever with persistent valvular disease?
10 years or until age 40 (or longer per guidelines).
## Footnote
This is to prevent recurrences and manage long-term risks.
152
What are some complications of Rheumatic Fever?
* Progression to chronic RHD with valve deformities and heart failure
* Persistent arrhythmias (e.g., atrial fibrillation) and risk of thromboembolism
* Cumulative cardiac damage from recurrent RF episodes
## Footnote
Complications can significantly affect long-term health.
153
What is the prognosis for patients with timely treatment for Rheumatic Fever?
Most patients recover fully with timely antibiotic therapy and anti-inflammatory treatment.
## Footnote
However, repeated attacks increase the risk of severe valvular disease.
154
True or False: Repeated attacks of Rheumatic Fever do not affect the likelihood of developing severe valvular disease.
False
## Footnote
Repeated attacks significantly increase the likelihood of severe, potentially disabling valvular disease.
155
What is the cellular origin of sporadic myxomas?
Multipotent mesenchymal (subendocardial) cells
## Footnote
Sporadic myxomas account for approximately 90% of cases.
156
What is the peak incidence age range for myxomas?
30–60 years
## Footnote
There is a female predominance with a ratio of 2:1.
157
Where are myxomas most commonly located?
Left atrium (> 75 %)
## Footnote
They are typically attached to the fossa ovalis region of the interatrial septum.
158
Describe the gross morphology of myxomas.
Pedunculated mass on a slender stalk, gelatinous consistency, smooth or villous surface, gray–white to yellow coloration
## Footnote
Larger tumors correlate with more pronounced obstructive symptoms.
159
What are the histologic features of myxomas?
Scattered polygonal or stellate cells in myxoid stroma, mucopolysaccharide matrix, small capillaries, occasional lymphocytes
## Footnote
Variations include the villous/myxofibroma variant and myxosarcoma.
160
What symptoms are associated with the obstructive phenomenon of myxomas?
Positional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, syncope
## Footnote
These occur due to transient obstruction of left-ventricular inflow.
161
What are the possible embolic manifestations of myxomas?
Acute stroke, flank pain, blue toe syndrome
## Footnote
Left-sided myxomas can cause systemic emboli.
162
What constitutional signs may occur due to myxomas?
Fever, weight loss, malaise, arthralgias
## Footnote
These are due to IL-6 secretion by tumor cells and may precede cardiac symptoms.
163
What is a 'tumor plop'?
A low-frequency, early-diastolic sound 60–150 ms after S2
## Footnote
It is distinct from S3 and indicates the presence of a myxoma.
164
What is the first-line diagnostic tool for myxomas?
Transthoracic Echocardiography (TTE)
## Footnote
It has a sensitivity of approximately 95% for left atrial masses greater than 5 mm.
165
What role does Transesophageal Echocardiography (TEE) play in diagnosing myxomas?
Superior resolution for smaller tumors or atypical locations
## Footnote
It also guides intraoperative planning.
166
What is the primary treatment for myxomas?
Surgical excision
## Footnote
This involves median sternotomy with cardiopulmonary bypass.
167
What is the prognosis for sporadic myxomas after surgical excision?
Excellent long-term survival; < 5 % recurrence
## Footnote
This is contingent on negative margins during excision.
168
What genetic mutation is associated with familial myxomas?
Germline mutations in PRKAR1A on chromosome 17q
## Footnote
Familial myxomas account for approximately 7% of cases.
169
What is the core triad of Carney Complex?
1. Cardiac Myxomas 2. Cutaneous Pigmented Lesions 3. Endocrine Overactivity
## Footnote
The endocrine issues may include Cushing syndrome and acromegaly.
170
Fill in the blank: Myxomas are typically ________ in consistency.
gelatinous
171
True or False: Right-sided myxomas are more common than left-sided myxomas.
False
172
What follow-up is recommended after myxoma excision?
Echocardiography at 6 months, then annually for 3–5 years
## Footnote
This is to monitor for recurrence.
