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1 STEP Uworld cardio > Myopericarditis > Flashcards

Myopericarditis Flashcards

1
Q

…… and …… chest pain indicates pericardial involvement

A

Sharp and pleuritic

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2
Q

If acute pericarditis and pain exacerbated with swallowing, ………….. pericardium may be involved.

A

Posterior

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3
Q

If acute pericarditis and pain radiates to the neck, ………….. pericardium may be involved. Why?

A

Inferior.

This region is adjacent to phrenic nerve

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4
Q

Viral pericarditis usually follows an antecedent ………………………….

A

Upper respiratory infection

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5
Q

What two types of pericarditis can manifest after MI?

A

Peri-infarction pericarditis (PIP);

Dressler syndrome

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6
Q

When develops PIP?

A

10-20proc MI patients; between 2 - 4 days after TRASMURAL MI

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7
Q

What type of MI may result in PIP?

A

Transmural

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8
Q

Why pericarditis manifest after MI?

A

It is a reaction to necrosis of myocardium in adjacent pericardium.

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9
Q

Inflammation is spread or local in PIP?

A

Localized - inflammation of the visceral and parietal pericardium overlying the necrotic myocaridial segment.

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10
Q

Treatment of PIP?

A

Resolves with several days of supportive care, sometimes may need high-dose aspirin.

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11
Q

How may be called Dressler syndrome in other name?

A

Postcardiac injury syndrome

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12
Q

Pathophysiology of Dressler syndrome?

A

Autoimmune mediated pericarditis - likely provoked by antigens exposed or created by infarction and necrosis of cardiac muscle.

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13
Q

What may manifest Dressler syndrome?

A

Week to months

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14
Q

Inflammation in pericardium is spread or local in Dressler syndrome?

A

Spread (autoimmune origin)

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15
Q

Myocardial ischemia vs pericarditis pain

A

Pericarditis - sharp and pleuritic, may be exacerbated by swallowing or coughing
Ischemic - constant, substernal and ,,crushing”

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16
Q

Acute pericarditis pleuritic chest pain decreases when …………..

A

When sitting up

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17
Q

ECG in acute pericarditis?

A

Diffuse ST elevation

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18
Q

Pericardial effusion ECG?

A

Decr. QRS voltage +/- electric alterans

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19
Q

Pericarditis may complicate into ………….

A

Pleural effusion

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20
Q

What type of inflammations cause pericardial effusion?

A

Fibrinous or serofibrinous pericardial inflammation

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21
Q

What causes dyspnea on exertion in pleural effusion?

A

Decreased diastolic ventricular filling –> decreased SV

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22
Q

Tachycardia in pleural effusion is to …………….

A

To compensate for decreased ventricular filling.

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23
Q

Low voltage QRS in pleural effusion is due to ………..

A

Pericardial fluid accumulation increasing the distance between the heart and the ECG leads

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24
Q

Why diminished heart sounds in pericardial effusion?

A

Pericardial fluid accumulation increasing the distance between the heart and stethoscope

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25
Q

Why there are electrical alternans on ECG in pericardial effusion?

A

Swinging motion of the heart

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26
Q

How is called a variation in the QRS axis in pleural effusion?

A

Beat to beat variation

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27
Q

2 x-ray characteristics of pleural effusion?

A

Enlarged, globular cardiac silhouette;

Clear lungs

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28
Q

Enlarged cardiac silhouette occur over …….. to …….. (ie ………. course)

A

Due to progressive pericardial stretching over days to weeks (Subacute course).

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29
Q

What volume of fluid may accumulate in subacute pericardial effusion course?

A

up to 1-2L

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30
Q

Why there are clear lung in pericardial effusion?

A

high pericardial pressure affects the low pressure chambers ie right-sided heart chamber more than left –> right sided blood flow obstruction therefore lung are clear. If left-sided obstruction would be more prominent than right-sided - then would be fluid in lungs.

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31
Q

Reason of DCM?

A

Direct insult to the myocardium –> decreased contractile function of both ventricles.

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32
Q

Why left ventricular structural changes are dangerous for patients with DCM?

A

Sudden death due to ventricular arrhythmia.

Bet ir trombai jeigu labai issiplete skilveliai? (tsg klausimas buvo apie structural changes)

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33
Q

When patients are considered are idiopathic DCM?

A

When no apparent cause is identified

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34
Q

Idiopathic DCM –> likely familial (inherited) cause. What structures (2) can be affected by mutations?

A

Sarcomere (ie contractile apparatus) or nonsarcomere proteins.

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35
Q

What gene is most commonly affected in DCM? What it encodes?

A

TTN gene. Sarcomere protein titin.

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36
Q

What is the function of titin protein?

A

It is elastin protein that anchors the beta-myosin heavy chain with Z disc –> contributes to passive myocardial tension

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37
Q

What is the inheritance of TTN gene mutation?

A

Autosomal dominant

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38
Q

Why there may be delayed or absent clinical manifestation of TTN gene DCM?

A

TTN gene mutations have incomplete penetrance

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39
Q

Takotsubo cardiomyopathy is characterized by ………………. of the mid and apical and ………………… of basal segments. It lead to ………….. dysfunction.

A

Hypokinesis;
Hyperkinesis.
LV systolic dysfunction –> reduced EF

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40
Q

What is pathophysiological factor causing takotsubo?

A

Physical/emotional stress –> catecholamine surge –> microvascular spasm –> ischemia or myocardial stunning or direct myocardial dysfunction

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41
Q

What is seen on echocardiography in takotsubo?

A

Balloon shape of LV

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42
Q

What population is mostly affected by takotsubo?

A

Postmenopausal women

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43
Q

Symptoms and diagnostic features of takotsubo?

A

MI and HF symptoms + ECG show ischemia BUT NO CAD ON ANGIOGRAPHY

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44
Q

Treatment of takotsubo?

A

The condition usually resolves within several weeks with supportive treatment only.

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45
Q

How IV drugs affect valves and increase the risk of vegetation formation?

A

Particulate material denudes the surface of the valves –> variegated surface for m/os attachement.

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46
Q

Why right-sided valves are at high risk of damage in IV drugs use?

A
  1. Venous infection –> venous blood reaches right-heart.

2. Pulmonary capillaries prevent large particulate matter from reaching the left side of the heart

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47
Q

Tricuspid valve IE in IV drugs users manifestation?

A

Right sided HF and/or septic pulmonary emboli

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48
Q

Who are seen septic pulmonary emboli on x-ray in IV drugs users?

A

Multiple pulmonary nodules

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49
Q

Why there are crackles and rhonchi in IV drug users?

A

Due to septic emboli

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50
Q

What shows echocardiography in IV drug users?

A

Valvular vegetations which result in regurgitation (due to incomplete valve closure)

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51
Q

Murmur in IV drug users. Location on the chest?

A

Blowing, holosystoli mumur;

Along left lower sternal border

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52
Q

What intenses and what reduces holosystolic mumur in IV drug users?

A

Intensified during inspiration;

Reduced with standing

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53
Q

Why septic pulmonary emboli are less common in aortic/mitral valve IE?

A

Septic thrombi lodge in capillary beds eg cutaneous prior to returning to the right-side of the heart

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54
Q

Conditions that decrease compliance if LV lead to ……………………… (pressure volume)

A

Increased LVEDP at the same LVED volumes

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55
Q

Why there will be increased pulmonary vasculature pressures in restrictive cardiomyopathy?

A

Higher LV filling pressures are transmitter back to pulmonary vasculature –> pulmonary edema

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56
Q

What protein plays important role in restrictive cardiomyopathy?

A

Transthyretin (TTR)

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57
Q

Where is produced transthyretin (TTR)?

A

In liver as tetramer.

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58
Q

What is a carrier function of transthyretin?

A

Carries thyroxine and retinol

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59
Q

Why mutations in the transthyretin (TTR) gene may result in restrictive cardiomyopathy?

A

Mutation –> TTR misfold –> amyloid protein –> infiltration of the myocardium = infiltrative cardiomyopathy

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60
Q

What CT features suggest restrictive pericarditis? (2)

A

Thickening and calcification of pericardium.

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61
Q

What is normal pericardium thick and what is in constrictive pericarditis?

A

Normal: 1-2mm

In CP: 4-20mm

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62
Q

What 3 symptoms typically have patients with constrictive pericarditis?

A

Progressive dyspnea + chronic edema + ascitis

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63
Q

What abnormality is seen in jugular venous pressure tracing in case of constrictive pericarditis?

A

Rapid y-descent that becomes both deeper and steeper during inspiration

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64
Q

What are the possible causes of constrictive pericarditis?

A

Radiation therapy to the chest, cardiac surgery, tuberculosis

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65
Q

Cardiac arrhythmia leads to ….. and ….. –> SCD

A

Markedly decreased CO and impaired coronary artery perfusion

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66
Q

What causes SCD in older adults and younger adults?

A

Older adults - CAD
Younger adults - undelying structural heart disease - hypertrophic cardiomyopathy is one of the most common precipitating diseases

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67
Q

Histology of hypertrophic cardiomyopathy? (3)

A

Cardiomyocyte hypertrophy + myofiber disarray + interstitial fibrosis

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68
Q

What causes ventricular arrhythmia in hypertrophic cardiomyopathy?

A

Structural disarray lead to conduction abnormalities

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69
Q

Patient has pneumonia which complicates into purulent pericarditis. M/o?

A

Streptococcus pneumoniae

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70
Q

How staph. aureus can reach pericardium and cause purulent pericarditis? (2)

A
  1. Portals from skin to bloodstream (eg tunneled dialysis catheter)
  2. From skin to pericardium eg in chest injury, cardiothoracic surgery
  3. Hematologic spread of distant infection
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71
Q

Fungal pericarditis m/o?

A

Candida albicans

72
Q

What patient population with catheters have increased risk of purulent pericarditis by staph. aureus?

A

End-stage renal disease patients who have vascular catheters

73
Q

What 3 patient population have increase risk for candidemia which may complicate into purulent pericarditis due to fungi?

A

parenteral feeding, prolonged corticosteroid use, immunosuppression due to malignancy

74
Q

What is an important diagnostic method and features to detect purulent pericarditis?

A

Pericardiocenthesis: turbid pericardial effusion with high number of leukocytes/frank pus

75
Q

What are the primary mediators of organized cardiac conduction?

A

Intercalated discs

76
Q

2 mechanisms that cause ventricular arrhythmia in hypertrophic cardiomyopathy

A

Conduction system impairment due to disarray (remodeling);
Myocardial ischemia due to a) increased oxygen demand due to hyperthrophied myocardium + b) microvascular impairement in coronary system and obstructed blood outflow due to septal predominance

77
Q

How can be reduced sharp and pleuritic pain in acute pericarditis?

A

By leaning forward –> decreased pressure on parietal pericardium

78
Q

What is the most specific physical finding in acute pericarditis?

A

Pericardial friction rub (high pitch, leathery, scratchy)

79
Q

HCM effect on the coronary capillary network?

A

Poorly developed in hypertrophied regions + microvascular dysfunction

80
Q

What is hyperthrophy in athletes heart?

A

Predominant concentric –> incr. LV cavity size + small degree eccentric –> uniformly increased LV wall thickening

81
Q

What type of cardiomyopathy and what features manifest due to CAD?

A

CAD –> Ischemic cardiomyopathy = manifest as dilated cardiomyopathy –> enlarged LV ventricle cavity + thin LV wall –> systolic dysfunction

82
Q

Anabolic steroid abuse can cause pathologic …………………… LV hypertrophy

A

Concentric

83
Q

What type of collagen are in scar post MI?

A

Type 1

84
Q

histopathology of acute myocarditis?

A

Myocyte necrosis/degeneration + inflammatory mononuclear cell infiltrate

85
Q

Acute myocarditis can lead to what cardiomyopathy?

A

Dilated cardiomyoapthy

86
Q

Cardiac adaptation in athlete’s: CO and afterload

A

Increased CO due to increased load on the heart (MOSTLY)

Slightly increased pressure load (incr. afterload)

87
Q

How changes right heart in athletes?

A

The right ventricular cavity slightly increased to support an increase in CO

88
Q

Athlete’s heart. Effect on coronary arteries and resting heart rate?

A

Enhanced coronary capillary development;

Decreased resting HR due to improved efficiency of cardiac pumping

89
Q

Overall result of high-intensity endurance exercises on heart. (4)

A

Increase in LV mass; enlarged LV cavity size; slightly increased LV wall thickness;
decreased resting heart rate.

90
Q

What function impairment in dilated cardiomyopathy leads to thrombus formation?

A

Global hypokinesis of the left ventricle leads to stagnation of blood flow and the possible development of LV mural thrombus and subsequent systemic embolization

91
Q

Where can radiate pleuritic chest pain?

A

Radiate to the bilateral scapulae posteriorly.

92
Q

When does pleuritic chest pain worsen?

A

When lying flat

93
Q

Why there is an ST elevation in acute pericarditis?

A

Due to ventricular myocardium inflammation

94
Q

In what cardiac cycle stages occurs pleuritic friction rub?

A

During atrial systole, ventricular systole, and early ventricular diastole

95
Q

What vital signs alterations are seen in ARF carditis?

A

Tachycardia, hypotension, tachypnea

96
Q

What valve is damaged and what murmur occurs in pancarditis due to ARF?

A

Acute mitral valve regurgitation –> holosystolic murmur.

97
Q

Anitchkoff cells in myocarditis in ARF are ……………. with ,,………….” chromatin

A

Macrophages with characteristic ,,caterpillar” chromatin

98
Q

Aschoff body consist of (3) cells?

A

Macrophages + lymphocytes + scattered multinucleated giant cells.

99
Q

Eventually aschoff bodies are replaced by …………… and results in ……………..

A

Fibrous scar tissue;

Mitral valve stenosis and regurgitation

100
Q

Dilated cardiomyopathy due to chemotherapeutic agents. Biopsy findings?

A

Patchy fibrosis with vacuolization and lysis of myocytes.

101
Q

Who aschoff bodies are called in other way?

A

Interstitial myocardial granulomas

102
Q

What amount of blood can drastically increase pressure in pericardial space in cardiac tamponade?

A

Pericardial space is not compliant, therefore even small amount eg 100-200ml can significantly compress heart

103
Q

Why there is JVD in cardiac tamponade?

A

Because right-sided ventricle is low-pressure and is easier to compress –> results in decreased diastolic function –> distended jugular veins

104
Q

Why there is hypotension in tamponade despite tachycardia?

A

Due to compressed right ventricle there is decreased diastolic filling –> decreased outflow volume.

105
Q

Why there is dyspnea and tachypnea in tamponade?

A

Due to decreased blood outflow there is impaired peripheral perfusion –> unmet oxygen demand –> dyspnea, increased respiratory drive and tachypnea

106
Q

Which heart side symptoms predominantly occurs in constrictive pericarditis?

A

Right

107
Q

What are seen biopsy changes in case of constrictive pericarditis?

A

Thick, fibrous tissue in pericardial space

108
Q

What is pericardial knock in constrictive pericarditis?

A

Early diastolic sound that occurs before S3

109
Q

What 3 pathophysiological features will be seen in constrictive pericarditis?

A

Pulsus paradoxus;
Pericardial knock;
Kussmaul sign

110
Q

2 ways how malignancy can cause pleural effusion?

A

Direct tumor extension or metastatic spread via blood and lymphatics

111
Q

How progresses subacute pericardial effusion eg in malignancy?

A

Pressure is stable in pericardial space + it gives time to stretch for pericardium –> patients have nonspecific symptoms eg dyspnea and chest discomfort. Impaired cardiac function when larger volumes exceed pericardial stretch capability.

112
Q

What are pericardiocentesis characteristics in malignancy pleural effusion?

A

Hemorrhage - due to bleeding from irrigated vessels.

Cytology –> atypical malignant cells

113
Q

Fibrinous pericarditis is the most common type of pericarditis and consists of …………………

A

Pericardial inflammation with serous fluid and fibrin-containing exudate in the pericardial space.

114
Q

Why there is friction rub in pericarditis?

A

Due to fibrin depositions that result in rough visceral and parietal pericardium

115
Q

Pleural friction rub can be heard during atrial systole, ventricular systole, and early ventricular diastole, therefore is called ………………

A

triphasic friction rub

116
Q

When pericardial friction rub can be absent in case of pericarditis?

A

If significant pleural effusion occurs

117
Q

What is the most common type of inflammation in case of pericarditis?

A

Fibrinous

118
Q

In what cases hemorrhagic pericarditis can occur?

A

Most commonly in malignancy, but can occur in TB and cardiac surgery, or underlying coagulopathy

119
Q

Hemorrhagic pericarditis consists of …..

A

Blood mixed with fibrinous exudate

120
Q

Fibrinous pericarditis consists of ……

A

Serous exudate with fibrin

121
Q

How dilation of the heart helps in pregnancy?

A

Heart accommodates to increased end-diastolic volume

122
Q

In what time period manifests peripartum dilatation?

A

Dilated cardiomyopathy occurs during the last month of pregnancy or within 5 months after delivery.

123
Q

Pathogenesis of peripartum dilatation. What may predispose?

A

May be related to impaired function of angiogenic growth factors (eg, vascular endothelial growth factor) during the peripartum period. In addition, certain individuals may have genetic mutations affecting cardiac structural proteins that predispose to the development of peripartum cardiomyopathy.

124
Q

How is thickened LV wall in cardiac amyloid?

A

Uniformly

125
Q

What exacerbates LVOT obstruction?

A

The systolic anterior motion of the mitral valve toward the interventricular septa this way blocking aortic valve

126
Q

What murmur occurs due to LVOT obstruction? What causes it?

A

Harsh crescendo-decrescendo systolic murmur at the apex and left lower sternal border; the murmur is caused by blood flow through the narrowed LVOT

127
Q

what types of ventricular arrhythmia can occur in HCM? (2)

A

Ventricular tachycardia or ventricular fibrillation

128
Q

What m/o causes chagas disease? What is a vertor?

A

Trypanosoma cruzi; vectos - triatomine (,,kissing”) bug

129
Q

Endemic regions for trypanosoma cruzi?

A

Central and South America

130
Q

Why in chagas disease manifest cardiac damage? (2)

A

Chronic parasite-induced and immune-mediated myocarditis –> dilated cardiomyopathy

131
Q

What are the structural changes in the heart due to chagas disease?

A

Localized apical wall thinning with a large apical aneurysm.

132
Q

Why aneurysma in chagas disease is dangerous?

A

Can predispose formation of mural thrombus which may systemically embolize and cause stroke

133
Q

What rhytmic changes can manifest in chagas disease? why?

A

Damage to the conduction system can also trigger ventricular arrhythmias (ventricular tachycardia/fibrillation)

134
Q

What can lead to sudden death in chagas disease?

A

Ventricular arrhythmias

135
Q

What can lead to dilation and dysfunction of the esophagus and colon in chagas disease?

A

Destruction of the myenteris plexus

136
Q

What is peripheral pulse in case of MI?

A

Weak or undetectable peripheral pulse

137
Q

Hereditary hemochromatosis is assoc. with mutation in …………. gene

A

HFE

138
Q

What does HFE protein? What disease mutation cause?

A

Causes hereditary hemochromatosis.

Hfe protein binds to the tranferin receptor and regulates intestinal and hepatic iron uptake

139
Q

What type of injury causes the accumulation of iron in the heart?

A

Oxidative damage

140
Q

What are early and late changes in the heart in hemochromatosis?

A

Early - diastolic LV dysfunction (restrictive)

Late - dilated cardiomyopathy

141
Q

What 3 features due to conduction system changes can be seen in hemochromatosis?

A

Atrial and ventricular arrhythmias;
sudden cardiac death;
Sinus node dysfunction (sick sinus syndrome)

142
Q

How can be called sinus node dysfunction in hemochromatosis in other name?

A

Sick sinus syndrome

143
Q

What leads to progression of dilated cardiomyopathy in hemochromatosis?

A

progressive ventricular remodeling

144
Q

Sinus node dysfunction can lead to ……….. or ………

A

Presyncope or syncope

145
Q

What is seen in microscopy in cardiac hemochromatosis?

A

Brown, granular deposits in cardiomyocytes that stain strongly with Prussian blue

146
Q

What is a treatment of hemochromatosis?

A

Therapeutic phlebotomy

147
Q

What is the onset time of acute cardiac transplant rejection?

A

Within 6 months

148
Q

How to diagnose acute cardiac transplant rejection?

A

Endomyocardial biopsy

149
Q

What mediates acute transplant rejection?

A

Predominantly - cell mediated;

less commonly - antibody mediated

150
Q

What are microscopic changes in acute cardiac transplant rejection? (2)

A

Interstitial lymphocytic infiltrate (primarily T lymphocytes) and damaged myocytes

151
Q

What is mechanism of immune activation in acute heart transplant rejection?

A

Host T lymphocytes are sensitized against HLA in cardiac allograft –> inflammation and injury to the transplant organ

152
Q

What are the symptoms of progressive cardiac transplant rejection?

A

Systolic dysfunction (eg dyspnea on exertion)

153
Q

What leads to cardiac allograft vasculopathy?

A

Concentric intimal thickening of the coronary arteries

154
Q

Cardiac allograft vasculopathy can lead to …………. (2)

A

Ischemic damage and long-term graft dysfunction

155
Q

What induces concentric intimal thickening of the coronary arteries?

A

Release of cytokines –> smooth muscle cell proliferation in the vessel wall

156
Q

Patchy necrosis with granulation tissue is indicative of ……….. to the donor heart

A

ischemic damage

157
Q

What indicates (microchages) ischemic damage in donor heart?

A

Patchy necrosis with granulation tissue

158
Q

When can occur ischemic damage in donor heart? (3)

A

Resuscitation, transportation from donor to recipient, during initial perfusion after transplantation

159
Q

What causes hypersensitivity myocarditis?

A

it is immunologic response to a newly initiated drug

160
Q

What are the changes in the myocardium in hypersensitivity myocarditis?

A

Perivascular infiltrate with abundant eosinophils

161
Q

What mediates chronic rejection of transplant?

A

Host T lymphocytes as well as antibodies

162
Q

What is changes in transplanted organ in chronic rejection?

A

Interstitial fibrosis with scant inflammation

163
Q

It is believed that an ……………………… to the viral infection allows virus to infect and persist inside cardiomyocytes.

A

Inadequate immune response

164
Q

By which 2 mechanisms does viral myocarditis damages myocardium?

A

Direct cytotoxic effect or a destructive autoimmune reaction

165
Q

What changes in myocardium in viral myocarditis leads to systolic dysfunction?

A

Depletion of cardiomyocytes with subsequent fibrosis –> weakened myocardial contractility (systolic dysfunction) + volume overload + ventricular dilation

166
Q

Regional wall motion abnormality is suggestive of …………….

A

ischemic heart disease (eg MI)

167
Q

Where is impaired myocardial function in MI?

A

Contractile function is impaired in the damaged portion of myocardium,

168
Q

What are 2 clinical features of hyperthrophic cardiomyopathy?

A

Clinical features of hypertrophic cardiomyopathy include exercise-induced syncope (due to outflow obstruction) and sudden cardiac death (due to ventricular arrhythmia) in young athletes

169
Q

How is called systolic ejection murmur in hypertrophic cardiomyopathy?

A

Harsh crescendo-decrescendo

170
Q

What maneuvers/conditions decreased LV preload?

A

Abrupt standing, Valsalva strain phase, dehydration

171
Q

What maneuvers/conditions decreased LV afterload?

A

Administration of vasodilators

172
Q

What 2 changes in LV increase the intensity of hypertrophic cardiomyopathy murmur?

A

Decreased LV preload and decreased LV afterload

173
Q

What maneuvers/conditions increase LV preload?

A

Passive leg raising, squatting

174
Q

What maneuvers/conditions increase LV afterload?

A

arterial vasoconstrictors or sustained handgrip

175
Q

What 2 conditions in LV alleviate hypertrophic cardiomyopathy murmur?

A

increased LV preload and increased LV afterload

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