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CARDIOVASCULAR > CARDIOLOGY- Pathology > Flashcards

CARDIOLOGY- Pathology Flashcards

1
Q

Characteristics “Blue babies”

A

Right to left shunt, Early cyanosis

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2
Q

When is often diagnose right to left shunt?

A

Prenatally or become evident immediatly after birth

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3
Q

What is the treatment for right to left shunt?

A

Ussually require urgent surgical correction and/or maintenance of a Patent Ductus arterious

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4
Q

Right to left shunt diseases

A

The 5Ts:

  1. Truncus arteriosus (1 vessel)
  2. Tansposition (2 swithced vessels)
  3. Tricuspid atresia (3= Tri)
  4. Tetralogy of Fallot (4=Tetra)
  5. TAPVR (5 letters)- Total Anomalous Pulmonary Venous Return
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5
Q

What happens in Persistent truncus arteriosus?

A

Failure of truncus arteriosus to divide into pulmonary trunk and aorta

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6
Q

What do most patients with persistent truncus arteriosus have?

A

Ventricular Septal Defect

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7
Q

What is wrong in D transposition of great vessels

A

Aorta leaves RV (anterior) and pulmonary trunk leaves LV (posterior)

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8
Q

What is the result of D transposition of great vessels?

A

Separation of systemic and pulmonary circulations

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9
Q

This is the prognosis of D transposition of great vessels?

A

Not compatible with life unless a shunt is present to allow mixing of blood (eg VSD, PDA, or patent foramen ovale)

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10
Q

Which is the reason of D transposition of great vessels?

A

Due to failure of the aorticopulmonary septum to spiral

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11
Q

Without treatment how is the life expectancy for D transposition of great vessels?

A

Without surgical intervention, most infants die within the first few months of life

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12
Q

Which problems are found in Tricuspid atresia?

A

Absence of tricuspid valve and hypoplastic RV

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13
Q

What is required in Tricuspid atresia for viability?

A

Both Ventricular Septal Defect and Atrial Septal Defect

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14
Q

What causes Tetalogy of Fallot?

A

By anterosuperior displacement of the infundibular septum

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15
Q

Most common cause of early childhood cyanosis

A

Tetralogy of Fallot

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16
Q

Characteristics of Tetralogy of Fallot

A

Pulmonary infundibular stenosis
Right Ventricular Hypertrophy
Overriding aorta
Ventricular Septal Defect

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17
Q

What is most important determinant for prognosis in Tetralogy of Fallot?

A

Pulmonary infundibular stenosis

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18
Q

In Tetrallogy of Fallot what causes right to left flow across Ventricular Septal defect?

A

Pulmonary stenosis

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19
Q

Clinical manifestation of Pulmonary stenosis causing right to left flow across Ventricular Septal defect

A

Early cyanotic “tet spells,” Right Ventricular Hypertrophy

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20
Q

What does Squatting manuever causes in patients with Tetrallogy of Fallot?

A

↑ systemic vascular resistance, ↓right to left shunt, improves cyanosis

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21
Q

Treatment for Tetrallogy of Fallot

A

Early surgical correction

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22
Q

What happens in Total Anomalous Pulmonary Venous Return?

A

Pulmonary veins drain into right heart circulation (SVC, coronary sinus)

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23
Q

Which cardiac anomallies are associated to Total Anomalous Pulmonary Venous Return? which is the benefit?

A

Atrial Septal Defect, and sometimes Patent Ductus arteriosus

Allow for right to left shunting to maintain cardiac output

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24
Q

Characteristics “blue kids”

A

Left to right shunt- Late cyanosis

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25
Q

Name all Left to right shunt diseases

A

Ventricular Septal Defect
Atrial Septal Defect
Patent Ductus arteriosus

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26
Q

In order, which are the most frequent causes of Left to right shunt diseases

A

Ventricular Septal Defect >Atrial Septal Defect >Patent Ductus arteriosus

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27
Q

Most common congenital cardiac defect

A

Ventricular Septal Defect

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28
Q

Which are the clinical manifestations of Ventricular Septal Defect?

A

Asymptomatic at birth, may manifest weeks later or remain asymptomatic thoughout life

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29
Q

Which is the prognosis of Ventricular Septal Defect?

A

Most self resolve

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30
Q

Which is the risk of Larger lessions of Ventricular Septal Defect?

A

May lead to LV overload and heart failure

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31
Q

During ausculation what is heard in Atrial Septal defect?

A

Loud S1: wide , fixed split S2

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32
Q

Where does Atrial Septal defect ussualy occurs?

A

In septum secundum

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33
Q

Which could be the symptoms of Atrial Septal defect?

A

Range from none to Heart Failure

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34
Q

This is the difference between Atrial Septal defect and Patent foramen ovale

A

Distinct form patent foramen ovale in that septa are missing tissue rather than unfused

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35
Q

In Fetal period which shunt is consider normal?

A

Right to left

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36
Q

What happens in neonatal period if there is a patent ductus arteriosus?

A

↓ Lung resistance → shunt becomes left to right → progressive Right Ventricular hyperthrophy and /or Left Ventricle Hypertrophy and heart failure

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37
Q

Which murmur is associated to Patent ductus arteriosus?

A

Machine like murmur

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38
Q

What maintains patency in patent ductus arteriosus?

A

PGE synthesis and low O2 tension

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39
Q

What could be the result of uncorrected Patent ductus arteriosus?

A

Can result in late cyanosis in the lower extremities (differential cyanosis)

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40
Q

Which drug helps in Patent ductus arteriosus?

A

Indomethacin

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41
Q

When is recommended to administer PGE to keep open a Patent ductus arteriosus?

A

May be necessary to sustain life in conditions such as transposition of great vessels

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42
Q

When is Patent Ductus consider normal? When does it close?

A

PDA is normal in utero and normally closes only after birth

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43
Q

What is Eisenmenger syndrome?

A

Uncorrected left to right shunt (VSD, ASD, PDA)

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44
Q

Which is the pathophysiology of Eisenmenger syndrome?

A

↑ Pulmonary blood flow → pathologic remodeling of vasculature → pulmonary arteriolar hypertension → Right ventricle Hypertrophy occurs to compensate → Shunt becomes rigth to left

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45
Q

What does Eisenmenger syndrome clinicaly causes?

A

Late cyanosis, clubbing and polycythemia

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46
Q

At what age does Eisenmenger syndrome onsets?

A

Varies

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47
Q

Which types of coarctation of the aorta exist?

A

Infantile type

Adult type

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48
Q

In which associated situations is coarctation of the aorta seen?

A

Associated with bicuspid aortic valve, other heart defects

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49
Q

What is wrong in Coarctation of the Aorta infantile type?

A

Aorta narrowing is proximal to insertion of the ductus arteriosus (preductal)

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50
Q

Which pathology is associated to Coarctation of the Aorta?

A

Turner Syndrome

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51
Q

What happens in Coarctation of the aorta in adult type?

A

Aorta narrowing is distal to ligamentum arteriosum (postductal)

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52
Q

Coarctation of the aorta can be associated to these findings

A

Notching of the ribs (collateral circulation), hypertension in upper extremities, and weak, delayed pulses in lower extremities (radiofemoral delay)

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53
Q

Which genetic disorders and diseases have congenital cardiac defect associated?

A 
22q11 syndrome
Down syndrome
Congenital Rubella
Turner Syndrome
Marfan Syndrome
Infant of Diabetic Mother
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54
Q

Which congenital cardiac defect might 22q11 syndrome have?

A

Truncus arteriosus, Tetralogy of Fallot

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55
Q

Down syndrome patients they could have these congenital cardiac defect

A

ASD, VSD, AV septal defect (endocardial cushion defect)

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56
Q

Congenital Rubella might present with these congenital cardiac defect

A

Septal defects, PDA, pulmonary artery stenosis

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57
Q

Which congenital cardiac defect are associated to Turner Syndrome?

A

Bicuspid aortic valve, coarctation of aorta (preductal)

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58
Q

Name congenital cardiac defect associated to Marfan syndrome

A

Mitral valve prolapse, thoracic aortic aneurysm and dissection, aortic regurgitation

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59
Q

Which congenital cardiac defect is associated to Infant of Diabetic mother?

A

Transposition of great vessels

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60
Q

What is hypertension?

A

Defined as a systolic BP > 140 and or diastolic BP > 90 mmHg

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61
Q

Name risk factors for Hypertension

A

↑ Age, obesity, diabetes, smoking, genetic, black> white> asian

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62
Q

Most common cause of Hypertension

A

Is 1º (essential)

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63
Q

What is related to Essential Hypertension?

A

Related to ↑ Cardiac Output or ↑Total Peripheric Resistance

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64
Q

Which is the cause of the remaining 10% of hypertension?

A

Mostly 2º to renal disease, including fibromuscular dysplasia in young patients

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65
Q

What is Hypertensive emergency?

A

Severe hypertension (> 180/120 mmHg) with evidence of acute, ongoing target organ damage (eg papilledema, mental status changes)

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66
Q

What does Hypertension predisposes?

A 
Atherosclerosis
Left Ventricle Hypertrophy
Stroke
Cardiac Heart Failure
Renal Failure
Retinopathy
Aortic dissection
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67
Q

Which is a cause of hypertension in younger patients?

A

“String of beads” apperance of the renal artery in fibromuscular dysplasia

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68
Q

What is seen in Hypertensive nephrophaty?

A

Renal Arterial Hyalinosis

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69
Q

Hyperlipidemia Signs

A

Xanthomas
Tendinous Xanthoma
Corneal Arcus

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70
Q

What are Xanthomas?

A

Plaques or nodules composed of lipid laden histiocytes in the skin

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71
Q

What is Xanthelasma?

A

Xanthomas especially the eyelids

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72
Q

What are Tendinous xanthoma?

A

Lipid deposit in tendon

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73
Q

Which tendon is the most common to have Tendinous xanthoma?

A

Achilles

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74
Q

What is the corneal arcus?

A

Lipid deposit in cornea

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75
Q

If Corneal arcus appears early in life, you must suspect…

A

Hypercholesterolemia

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76
Q

Which patients is common to see Corneal Arcus?

A

In eldery (Arcus senilis)

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77
Q

Which are the types of Arteriosclerosis?

A

Monkeberg

Arteriolosclerosis

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78
Q

Which is the common type of Arteriosclerosis?

A

Arteriolosclerosis

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79
Q

How else is Monkeberg Arteriosclerosis known?

A

Medial calcific sclerosis

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80
Q

What happens in Monkeberg Arteriosclerosis?

A

Calcification in the media of the arteries

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81
Q

Which arteries are more common affected in Monkeberg Arteriosclerosis?

A

Radial

Ulnar

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82
Q

How are Monkeberg Arteriosclerosis classified?

A

Ussually benign

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83
Q

How are Monkeberg Arteriosclerosis visualized? What do you see?

A

Pipestem arteries on the x ray

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84
Q

Why is Monkeberg Arteriosclerosis benign?

A

Because intima is not involved

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85
Q

Which are the types of Arteriolosclerosis

A

Hyaline

Hyperplastic

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86
Q

What could be seen in microscope with Hyaline Arteriolosclerosis?

A

Thickening of small arteries

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87
Q

Which diseases are associated to Hyaline Arteriolosclerosis?

A

Essential hypertension or Diabetes

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88
Q

Hyperplastic Arteriolosclerosis presents this characteristic in microscope

A

Onion Skinning

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89
Q

When is Hyperplastic Arteriolosclerosis seen?

A

Severe hypertension

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90
Q

What ha[[ems om Atherosclerosis?

A

Disease of Elastic Arteries and large and medium sized muscular arteries

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91
Q

How are the risk of Atherosclerosis classified?

A

Modifiable

Non modifiable

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92
Q

Which are modifiable Atherosclerosis risk factors?

A

Smoking, hypertension, hyperlipidemia, diabetes

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93
Q

Non modifiable Risk factors of Atherosclerosis

A

Age, sex (Increased in men and postmenopausal women) and family history

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94
Q

What is important in the progression of Atherosclerosis in its pathogenesis?

A

Inflammation

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95
Q

Which is the progression of Atherosclerosis?

A

Endothelial cell dysfunction → macrophage and LDL accumulation → foam cell formation → fatty streaks → smooth muscle cell migration (involves PDGF ans FGF), proliferation , and extracellular matrix deposition → fibrous plaque → complex atheromas

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96
Q

Complications of Atherosclerosis

A

Aneurysms, ischemia, infarctsm peripheral vascular disease, thrombus, emboli

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97
Q

Frequent locations of Atherosclerosis

A

Abdominal Aorta > coronary artery > popliteal artery > carotid artery

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98
Q

Symptoms of Atherosclerosis

A

Angina, Claudication, but can be asymptomatic

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99
Q

What is an Aortic Aneurysm?

A

Localized pathologic dilation of the Aorta

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100
Q

When does a Aortic Aneurysm causes pain?

A

Sign of leaking, dissection or imminent rupture

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101
Q

Which factor is associated to Abdominal aortic aneurysm?

A

Atherosclerosis

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102
Q

With which patients is more frequently seen Abdominal Aortic aneurism?

A

Occurs more frequently in hypertensive male smokers > 50 years old

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103
Q

Which diseases are associated to Thoracic aortic aneurysm?

A

Asociated with cystic medial degeneration due to hypertension (older patients) and Marfan syndrome (younger patients)

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104
Q

Historically with which diseases is Thoracic aortic aneurysm associated?

A

With 3º syphilis (obliterative endarteritis of the vasa vasorum)

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105
Q

What is Aortic dissection?

A

Longitudinal intraluminal tear forming a false lumen

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106
Q

What is associated to Aortic dissection?

A

Hypertension, bicuspid aortic valve, and inherited connective tissue disorders (eg. Marfan, syndrome)

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107
Q

Which clinical manifestations does Aortic dissection has?

A

Tearing chest pain, of sudden onset, radiating to the back +/- markedly unequal BP in arms

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108
Q

Which study helps to see Aortic Dissection? What does it shows?

A

CXR shows mediastinal widening

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109
Q

Where is the false lumen found in Aortic dissection?

A

Can be limited to the ascending aorta, or propagate from the descending aorta

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110
Q

Which could be the complications of Aortic dissection?

A

Pericardial tamponade, aortic rupture and death

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111
Q

Possible Ischemic heart disease manifestations

A 
Angina
Coronary steal syndrome
Myocardial infarction
Sudden cardiac death
Chronic ischemic heart disease
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112
Q

What is Angina?

A

Chest pain due to ischemic myocardium secondary to coronary artery narrowing or spasm; no myocyte necrosis

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113
Q

How is Angina classified?

A

Stable
Variant Angina
Unstable/crescendo

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114
Q

Which is the usual cause of Stable angina?

A

Usually secondary to atherosclerosis

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115
Q

How is stable angina manifested? How does it get better?

A

Exertional chest pain in classic distribution, resolving with rest

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116
Q

What is ussually seen in ECG in Stable angina?

A

Ussually with ST depression on ECG

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117
Q

How else is Varina angina known?

A

Prinzmetal

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118
Q

When does variant angina starts? why?

A

Occurs at rest secondary to coronary artery spasm

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119
Q

What is seen on the ECG in variant angina (Prinzmetal)?

A

Transient ST elevation on ECG

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120
Q

Which are the possible triggers of Prinzmetal angina?

A

Tobacco, cocainem triptans, but trigger is often unknown

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121
Q

Which is the treatment for Variant angina (Prinzmetal)?

A

With calcium channel blockers, nitrates and smoking cessation

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122
Q

Which is the cause of Unstable/ crescendo angina?

A

Thrombosis with incomplete coronary artery occlusion

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123
Q

What is seen in ECG in Unstable/ crescendo angina?

A

ST depression

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124
Q

Clinical presentation of Unstable/ crescendo angina

A

Increased in frequency or intensity of chest pain; any chest pain at rest

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125
Q

What happens in Coronary steal syndrome?

A

Distal to coronary stenosis, vessels are maximally dilated at baseline

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126
Q

What is the treatment for Coronary steal syndrome?

A

Administration of vasodilators

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127
Q

Name vasodilators use for Coronary steal syndrome

A

Dypiridamole

Regadenoson

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128
Q

Which is the purpose to give Vasodilators in Coronary steal syndrome?

A

Dilates normal vessels and shunts blood toward well perfused areas → ↓ flow and ischemia in the poststenotic region

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129
Q

What helps to study Coronary steal syndrome?

A

Pharmacologic stress test because (Dilates normal vessels and shunts blood toward well perfused areas → ↓ flow and ischemia in the poststenotic region)

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130
Q

What happens during a myocardial infarction?

A

Most often acute thrombosis due to coronary artery atherosclerosis with complete occlusion of coronary arteryand myocyte necrosis

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131
Q

Which are the possible findings in ECG in myocardial infarction?

A

If transmural, ECG will show ST elevations; if subendocardial, ECG may show ST depressions

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132
Q

What makes the diagnosis of myocardial infarction?

A

Cardiac biomarkers

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133
Q

When do we consider Sudden cardiac death?

A

Death from cardiac causes within 1 hour of onset of symptoms

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134
Q

Most common reason of Sudden cardiac death

A

Lethal arrhytmia (eg vantricular fibrilation)

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135
Q

Causes associated to Sudden cardiac death

A

CAD- coronary artery disease (up to 70% of cases)
Cariomyopathy (hypertrophic, dilated)
Heredtary ion channelopathies (eg Long QT syndrome)

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136
Q

What could be the result of Chronic ischemic heart disease?

A

Progressive onset of CHF over many years due to chronic ischemic myocardial damage

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137
Q

Which is the order of frequency of occluded coronary arteries?

A

LAD (left anterior descending) > RCA > circumflex

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138
Q

Symptoms of Myocardial infarction

A

Diaphoresis, nausea, vomiting,severe retrosternal pain, pain in the left arm and/ or jaw, shortness of breath, fatigue

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139
Q

Which are the gross and light microscopic changes in MI during the first 4 hours?

A

None

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140
Q

Compliations of MI during the first 4 hours

A

Arrythmia, HF, cardiogenic schock, death

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141
Q

During the first 24 hours these are gross changes in MI

A

Ocluded artery
Infarct
Dark mottling; pale with tetrazolium stain

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142
Q

Light microscope changes in MI during the 4- 12 hrs

A

Early Coagulative necrosis, release of necrotic cell contents into blood: edema, hemorrhage, wavy fibers

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143
Q

Which are the risk of MI during the first 24 hours?

A

Arrythmia, HF, cardiogenic schock, death

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144
Q

When do MI changes start?

A

From the 4th hour

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145
Q

What happens in MI during the 12-24 hours in light microscope?

A

Neutrophil migration starts

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146
Q

Which risk does reperfusion has during MI?

A

Reperfusion injury may cause contraction bands (due to free radical damage)

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147
Q

At this point of MI happens extensive coagulative necrosis

A

1-3 days

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148
Q

What else is found in ligth microscope during MI in day 1-3?

A

Tissue surrounding infarct shows acute inflamation with neutrophils

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149
Q

Possible complications of MI found in 1-3 days

A

Fibrinous pericarditis

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150
Q

Hyperemia is the gross finding seen during which day of MI?

A

1-3 days

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151
Q

What is seen in gross in days 3-14 in MI?

A

Hyperemic border; central yellow brown softening

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152
Q

When is commonly seen Maximal yellow and soft in MI?

A

By 10 days

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153
Q

Macrophages, then granulation tissue at margins are present during these days of MI

A

3-14 days

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154
Q

Possible Complications of MI during day 3-14

A

Free wall rupture → tamponade papillary muscle rupture → mitral regurgitation ; interventricular seotal rupture due to macrophage- mediated structural degradation

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155
Q

Which MI complication found in days 3-14 is consider “time bomb”?

A

LV pseudoaneurys (mural thrombus “plugs” hole in myocardium)

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156
Q

Gross findigs in MI after 2 weeks to several months

A

Recanalized artery

Gray white myocardial zone

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157
Q

When do we expect to see Contracted scar completed in MI?

A

2 weeks to several months

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158
Q

Complication of MI during 2 weeks to several months

A

Dressler syndrome
HF
Arrythmias
True ventricular aneurysm (outward bulge during contraction, dyskinesia)

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159
Q

What is Dressler syndrome?

A

Is a type of pericarditis, inflammation of the sac surrounding the heart (pericardium)
Autoimmune phenomenom resulting in fibrinous pericarditis

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160
Q

Which is the gold standard of MI during the first 6 hours?

A

ECG

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161
Q

When does Cardiac Troponin I rises?

A

After 4 hours

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162
Q

How much time does Troponin I stays elevated durin MI?

A

7- 10 days

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163
Q

Which is the most specific protein marker during MI?

A

Cardiac Troponin I

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164
Q

Biomarker predominantly found un myocardium but can also be released fro skeletal muscle

A

CK-MB

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165
Q

Which is the use for CK-MB?

A

Diagnosing reinfarction following acute MI

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166
Q

Why is CK-MB usefull in Diagnosing reinfarction following acute MI?

A

Because levels return to normal after 48 hours

167
Q

Which ECG changes could be seen in MI?

A

ST elevation
ST depression
Pathologic Q waves

168
Q

MI that present ST elevation

A

ST segment elevation myocardial infarction

Acute Transmural infarct

169
Q

Which MI is presented with ST depression?

A

Subendocardial infarct

170
Q

When do we find Pathologic Q waves?

A

Evolving or old transmural infarct

171
Q

Types of infarcts

A

Transmural infarcts

Subendocardial infarcts

172
Q

Characteristics of Transmural infarcts

A

↑ necrosis

Affects entire wall

173
Q

How is Transmural infarct found in ECG?

A

ST elevation

Q waves

174
Q

When is consider a Subendocardial infarct?

A

Due to ischemic necrosis of < 50% of ventricle wall

175
Q

Which structure of heart is especially vulnerable to ischemia?

A

Subendocardium

176
Q

Which ECG is found in Subendocardium Infarct

A

ST depression

177
Q

Which artery is related to Anterior wall infarction?

A

Left Anterior Descending Artery

178
Q

Lead that show Q waves in Anterior wall infarction

A

V1-V4

179
Q

Artery that irrigates Anteroseptal structure

A

Left Anterior Descending Artery

180
Q

Leads hat show Anteroseptal infarction

A

V1-V2

181
Q

Who irrigates Anterolateral wall of the heart?

A

Left Anterior Descending Artery

Left Circumflex

182
Q

If there is a Anterolateral infarction which leads indicate the infarction?

A

V4-V6

183
Q

Which artery irrigates Lateral wall of the heart?

A

Left circumflex

184
Q

These leads indicate a Lateral wall infarction

A

I, aVL

185
Q

Which wall does Right Coronary artery irrigates?

A

Inferior wall

186
Q

Which leads indicate a right coronary territory infarction?

A

II, III, aVF

187
Q

MI complications

A 
Cardiac Arrythmia
LV failure and pulmonary edema
Cardiogenic shock
Ventricular free wall rupture
Ventricular pseudoaneurysm formation
Postinfarction fibrinous pericarditis 
Dressler syndrome
188
Q

Important cause of death before reaching hospital as MI complication

A

Cardiac Arrhythmia

189
Q

When is common to see Cardiac Arrhythmia as MI complication?

A

In first few days

190
Q

When can cardiogenic shock happen as MI complication?

A

Large infarct- high risk of mortality

191
Q

Which is the pathogenic of Ventricular free wall rupture as MI complication?

A

Ventricular free wall rupture→ Cardiac tamponade; papilary muscle rupture→ several mitral regurgitation; and interventricular septum rupture → VSD

192
Q

When is the greatest risk of Ventricular free wall rupture as MI complication?

A

6-14 days postinfarct

193
Q

Which are the complications of Ventricular pseudoaneurysm formation?

A

↓ Cardiac output, risk of arrhytmia, embolus form mural thrombus

194
Q

When is the greatest risk of Ventricular pseudoaneurysm formation after MI?

A

1 week post MI

195
Q

When can Postinfarction fibrinous pericarditis happens?

A

1-3 days post MI

196
Q

What is Dressler syndrome?

A

Autoimmune phenomenom resulting in fibrinous pericarditis

197
Q

When is expected to possible see Dressler syndrome?

A

Several weeks post MI

198
Q

Which is the most common cardiomyopathy

A

Dilated cardiomyopathy

199
Q

From all cardiomyopathies which percentage represents Dilated cardiomyopathy?

A

90% of cases

200
Q

Which are the often causes of Dilated cardiomyopathy?

A

Idiopathic or congenital

201
Q

Other etiologies of Dilated cardiomyopathy are…

A 
Alcohol abuse
Wet Beriberi
Cosackie B virus myocarditis
chronic Cocaine use
Chagas disease
Doxurubicin toxicity
hemochromatosis
peripartum cardiomyopathy
202
Q

Which are the findings of Dilated cardiomyopathy?

A

Heart failure
S3
Dilated heart on echocardiogram
Ballon apperance of heart on CXR

203
Q

Which is the treatment for Dilated cardiomyopathy?

A

Na+ restriction, ACE inhibitors, β blockers, diuretics, digoxin, implatable cardioverter defibrilator (ICD), heart transplant

204
Q

Which are possible consequences of Dilated cardiomyopathy?

A 
Systolic dysfunction ensues
Eccentric hypertrophy (sarcomers added in series)
205
Q

Which is the most common cause of Hypertrophic cardiomyopathy?

A

60-70 % of cases are familial

206
Q

The familial cases of Hypertrophic cardiomyopathy which inheritance mode do they follow?

A

Autosomal dominant

207
Q

Which is the possible cause of Autsomal dominant Hypertrophic cardiomyopathy?

A

commonly a β- myosin heavy chain mutation

208
Q

Rarely with which other disease is Hypertrophic cardiomyopathy associated?

A

Friedreich ataxia

209
Q

Cause of sudden death in young athletes

A

Hypertrophic cardiomyopathy

210
Q

Which is the cause of sudden death in young athletes due to Hypertrophic cardiomyopathy?

A

Ventricular arrhytmia

211
Q

Possible findings in Hypertrophic cardiomyopathy

A

S4, systolic murmur

212
Q

Treatment for Hypertrophic cardiomyopathy

A

Cessation of high intensity athletics, use of β blocker or non dihdropyridine calcium channel blockers

213
Q

If a patient is at high risk for Hypertrophic cardiomyopathy what is the alternative treatment?

A

Implantable cardioverter defibrillators

214
Q

What occurs afterwards Hypertrophic cardiomyopathy?

A

Diastolic dysfunction ensues

215
Q

Which are possible consequences of Hypertrophic cardiomyopathy?

A

Marked ventricular hypertrophy, often septal predominance. Myofibrillar disarray and fibrosis

216
Q

Pathogenesis of Obstructive Hypertrophic cardiomyopathy (subset)

A

Hypertrophied septum too close to anterior mitral leaflet → outflow obstruction → dyspnea, possible syncope

217
Q

Which kind of hypertrophy is seen in Hypertrophic cardiomyopathy?

A

Concentric Hypertrophy

218
Q

How else is Restrictive cardiomyopathy known?

A

Infiltrative

219
Q

Name the major causes of Restrictive/Infiltrative cardiomyopathy

A 
Sarcoidosis
Amyloidosis
Postradiation Fibrosis
Endocardial fibroelastosis
Loffler syndrome
Hemochromatosis
220
Q

Which patient are at higher risk to develope Endocardial fibroelastosis?

A

Young children

221
Q

What is the Loffler syndrome?

A

Endomyocardial fibrosis with a prominent eosinophilic infiltrate

222
Q

Hemochromatosis is associated to these cardiomyopathies

A

Restrictive/ infiltrative cardiomiopathy

Dilated cardiomiopathy

223
Q

What occurs afterwards Restrictive/ infiltrative cardiomyopathy?

A

Diastolic dysfunction

224
Q

Which ECG problem is seen in Restrictive/ infiltrative cardiomiopathy?

A

Low voltage ECG despite thick myocardium (especially amyloid)

225
Q

Clinical syndrome of cardiac pump dysfunction

A

Congestive Heart failure

226
Q

Symptoms of Congestive Heart failure

A

Dyspnea, orthopnea and fatigue

227
Q

Signs of Congestive Heart failure

A

Rales, JVD, and pitting edema

228
Q

Which manifestations can Congestive Heart failure has?

A

Systolic dysfunction

Diastolic dysfunction

229
Q

What is found in Systolic dysfunction of Congestive heart failure?

A

Low EF, poor contractility

230
Q

Which is the often cause of Systolic dysfunction in Congestive Heart failure?

A

Secondary to ischemic heart disease or Dilated cardiomyopathy

231
Q

Which are the findings in diastolic dysfunction of Congestive heart failure?

A

Normal EF and contractility

Impaired relaxation, Decrease compliance

232
Q

Which is the common cause of Right heart failure?

A

Most often results from left heart failure

233
Q

Which is the caused of isolated Right heart failure?

A

Ussually to cor pulmonale

234
Q

Which drugs decreased the risk of mortality in Congestive Heart failure?

A

ACE inhibitors, β blockers, angiotensin II receptor blockers, and spironolactone

235
Q

Which drugs don’t help during decompensated Congestive Heart Failure?

A

ACE inhibitors and β blockers

236
Q

Whic is the cause of Cardiac dilation in Congestive Heart Failure?

A

Greater ventricular end diastolic volume

237
Q

Cause of dyspnea on exertion in Congestive Heart Failure

A

Failure of Cardiac Output to ↑ during excercise

238
Q

Characteristics of Left heart failure

A

Pulmonary edema
Orthopnea
Paroxysmal nocturnal dyspnea

239
Q

Which is the pathogenesis in Pulmonary edema caused by left heart failure?

A

↑ pulmonary venous pressure → pulmonary venous distention and transudation of fluid

240
Q

Which microscopic characteristic does Pulmonary edema caused by left heart failure has?

A

Presence of hemosiderin laden macrophages (“heart failure cells”) in the lungs

241
Q

Clinical manifestation of Orthopnea

A

Shortness of breath when supine

242
Q

Pathogenesis in Orthopnea caused by left heart failure

A

↑ Venous return from redistribution of blood (immediate gravity effect) exacerbates pulmonary vascular congestion

243
Q

Clinical manifestation of Paroxysmal nocturnal dyspnea

A

Breathless awakening from sleep

244
Q

Pathogenesis in Paroxysmal nocturnal dyspnea caused by left heart failure

A

↑ Venous return from redistribution of blood, reabsorption of edema, etc

245
Q

Manifestations of right heart failure

A

Hepatomegaly (nutmeg liver)
Peripheral edema
Jugular distention

246
Q

Pathogenesis of Hepatomegaly caused by right heart failure

A

↑ Central venous pressure → ↑ resistance to portal flow. Rarely leads to “cardiac cirhosis”

247
Q

Which is the explantion of Peripheral edema caused by right heart failur?

A

↑ Venous pressure→ Fluid transudation

248
Q

Why does Yugular venous distention occurs in right heart failure?

A

↑ Venous pressure

249
Q

Which drugs just give symptomatic relief in CHF?

A

Thiazide or loop diuretics

250
Q

Which is the most common symptom of Bacterial endocarditis

A

Fever

251
Q

Symptoms of Bacterial endocarditis

A 
Fever
New murmur
Roth spots
Osler nodes
Janeway lesions
Anemia
Splinter hemorrgages on nail bed
252
Q

What are the Roth spots?

A

Round white spots on retina surrounded by hemorrhage

253
Q

What are the Osler nodes?

A

Tender raised lesions on finger or toe pads

254
Q

What are the Janeway lesions?

A

Small, painless , erythematous lesions on palm or sole

255
Q

What is needed to diagnos Bacterial endocarditis?

A

Multiple blood cultures necessary

256
Q

How is Bacterial endocarditits classified?

A

Acute
Subacute
Culture negative

257
Q

Which bacteria causes acute Bacterial endocarditis?

A

S. Aureus (high virulence)

258
Q

How is Acute Bacterial endocarditis caused by S. Aureus seen?

A

Large vegetations on previously normal valves

259
Q

How is the onset of Acute Bacterial endocarditis caused by S. Aureus?

A

Rapid onset

260
Q

Who causes Subacute Bacterial endocarditis ?

A

Viridians Streptococi (low virulence)

261
Q

Which are the damage caused by Subacute Bacterial endocarditis ?

A

Smaller vegetations on congenital abnormal or diseased valves

262
Q

In which cases do we see Subacute Bacterial endocarditis?

A

Sequela of dental procedures

263
Q

Which complication can be seen as sequela of dental procedures?

A

Subacute Bacterial endocarditis

264
Q

How is the onset in subacute Bacterial endocarditis ?

A

Gradual onset

265
Q

Who causes culture negative Bacterial endocarditis?

A

Most likely Coxiella burnetii and Bartonella spp

266
Q

Name other non bacterial causes of Endocarditis

A

Malignancy
Hypercoagulable state
Lupus (marantic/ thrombotic endocarditis)

267
Q

Which bacteria is present in cancer colon?

A

S. bovis

268
Q

Which bacteria could be found in prosthetic valves?

A

S. epidermidis

269
Q

Which valve is most frequently involved in Bacterial endocarditis?

A

Mitral valve

270
Q

If tricuspid valve endocarditis is seen, what is associated?

A

IV drug abuse

271
Q

Which valve suffering endocarditis is associated to IV drug abuse?

A

Tricuspid

272
Q

Bacterias Associated to Tricuspid valve endocarditis?

A

S. aureus
Pseudomonas
Candida

273
Q

Complications of Bacterial endocarditis

A

Chordae rupture
Glomerulonephritis
Suppurative pericarditis
Emboli

274
Q

How is Rheumatic fever adquired?

A

A consequence of pharyngeal infection with group A β hemolytic streptococci

275
Q

Which is the risk of Rheumatic Fever?

A

Early deaths due to myocarditis

276
Q

Late sequale of Rheumatic Fever

A

Rheumatic heart disease

277
Q

In Rheumatic heart disease, in order who are the most affected valves?

A

Affects heart valves- mitral > aortic» tricuspid

(high pressure affected most

278
Q

Early lesion seen in Rheumatic Fever

A

Mitral Regurgitation

279
Q

Late lesion in Rheumatic Fever

A

Mitral Stenosis

280
Q

Which findings are associated to Rheumatic Fever?

A

Aschoff bodies
Anistschkow cells
↑ ASO titers

281
Q

What are Aschoff bodies?

A

Granuloma with giant cells

282
Q

What are the Anistschkow cells?

A

Enlarged macrophages with ovoid, wavy, rod like nucleus

283
Q

Which are the causes of Rheumatic fever?

A

A consequence of pharyngeal infection

Immune madiated not a direct effect of Bacteria

284
Q

Who is responsable of immune mediated Rheumatic fever?

A

Type II hypersensitivity

285
Q

Which is the pathogenesis in Immune mediated who Rheumatic fever?

A

Antibodies to M protein cross react with self antigens

286
Q

Findings in Rheumatic fever

A 
FEVERSS
Fever
Erythema marginatum
Valvular damage (vegetation and fibrosis)
ESR ↑
Red hot joints (migratory polyarthritis)
Subcutaneous nodules
St. Vitus' dance (Sydenham chorea)
287
Q

In which disease do we see St. Vitus’ dance?

A

Sydenham chorea

288
Q

Clinical presentation of acute pericarditis

A

Commonly presents with sharp pain, aggravated by inspiration, and relieved by sitting up and leaning forward

289
Q

How is Acute pericarditis presented?

A

Friction Rub

290
Q

ECG changes in Acute pericarditis

A

Widespread segment elevation and/or PR depression

291
Q

Types of Acute pericarditis

A

Fibrinous
Serous
Supurative/ purulent

292
Q

Who are the cause of Fibrinous Acute pericarditis

A

Dressler syndrome, uremia, radiation

293
Q

How is Fibrinous Acute pericarditis presented?

A

Loud friction rub

294
Q

Causes of Serous Acute pericarditis

A

Viral pericarditis

Noninfectious inflammatory diseases

295
Q

How is viral pericarditis treated?

A

Often resolves spontaneously

296
Q

Causes of Noninfectious inflammatory diseases of Serous pericarditis

A

Rheumathoid arthritis

SLE

297
Q

Who causes Supurative/ purulent Acute pericarditis?

A

Ussually caused by bacterial infections (eg. Pneumococcus, Streptococcus)

298
Q

Why is Supurative/ purulent Acute pericarditis nowdays rare?

A

Rare now with antibiotics

299
Q

What is cardiac tamponade?

A

Compression of heart by fluid in pericardium

300
Q

Which fluids can cause cardiac tamponade?

A

Blood, effussions

301
Q

Which is the result of Cardiac tamponade?

A

Leading to ↓ Cardiac Output

302
Q

What happens during cardiac tamponade?

A

Equilibration of diastolic in all 4 chambers

303
Q

Findings in Cardiac tamponade

A

Beck triad
↑ Heart Rate
Pulsus paradoxus
Kussmaul sign

304
Q

What does Beck triad has?

A

Hypotension
Distended neck veins
Distant heart sounds

305
Q

What does ECG in Acute pericarditis?

A

Shows low voltage QRS and electrical alternans (due to “swinging” movement of the heart in large effusion)

306
Q

What is the Pulsus paradoxus?

A

↓ amplitude of systolic blood pressure by > 10 mmHg during inspiration

307
Q

Which cases present pulsus paradoxus?

A 
Cardiac Tamponade
Asthma
Obstructive sleep apnea
Pericarditis
Croup
308
Q

Which syphilis causes syphilitic heart disease?

A

3º syphilis

309
Q

Which is the pathogenesis of 3º syphilis in syphilitic heart disease?

A

Disrupts the vasa vasorum of the aorta with consequent atophy of the vessel wall and dilation of the aorta and valve ring

310
Q

What can be seen in syphilitic heart disease?

A

Calcification of the aortic root and ascending aortic arch

311
Q

What does syphilitic heart disease leads to?

A

“Tree bark” appearance of the aorta

312
Q

Which could be the results of syphilitic heart disease?

A

In aneurysm of the ascending aorta or aortic arch and aortic insufficiency

313
Q

Which are the most common heart tumors?

A

Is a metastastis (eg. from melanoma, lymphoma)

314
Q

Most common primary cardiac tumor in adults

A

Myxomas

315
Q

Where is the most common site of heart myxomas

A

90% occur in the atria (mostly left atrium)

316
Q

How are cardiac myxomas described?

A

As a “ball valve” obstruction in the left atrium

317
Q

Clinical findings caused by cardiac myxomas

A

Associated with multiple syncopal episodes

318
Q

Most frequent primary tumor in children

A

Rhabdomyomas

319
Q

Which disease is associated to Rhabdomyomas heart tumor?

A

Tuberous sclerosis

320
Q

What is identified in Kussmaul sign?

A

↑ in Jugular venous pressure on inspiration instead of a normal ↓

321
Q

How is Jugular Vein distenssion produced with inspiration?

A

Inspiration → negative intrathoracic pressure not transmitted to heart → impaired filling of right ventricle → blood backs up into venae cavae→ Jugular Vein Distenssion

322
Q

When is Kussmaul sign seen?

A

Constrictive pericarditis
Restrictive cardiomyopathies
Right atrial or ventricular tumors

323
Q

What is Raynaud phenomenon

A

↓ blood flow to skin due to arteriolar vasospasm in response to cold temperature or emotional stress

324
Q

Where are the most often sites of Raynaud phenomenon presentation?

A

Most often in the fingers and toes

325
Q

When do we call Raynaud disease?

A

When Primary (Idiopathic)

326
Q

When is called Raynaud syndrome?

A

When secondary to a disease process

327
Q

Which diseases are related to Raynaud syndrome?

A

Such as mixed connective tissue disease, SLE or CREST (limited form of systemic sclerosis) syndrome

328
Q

Which vessels are affected in Raynaud phenomenon?

A

Affects small vessels

329
Q

Vascular tumors

A 
Strawberry hemangioma
Cherry hemangioma
Pyogenic granuloma
Cystic hygroma
Glomus tumor
Bacillary angiomatosis
Angiosarcoma
Lymphangiosarcoma
Kaposi sarcoma
330
Q

Characteristics of Strawberry hemangioma

A

Benign capillary hemangioma of infancy

331
Q

Which is the incidence of Strawberry hemangioma?

A

1/200 birhts

332
Q

When is the age of apperance of Strawberry hemangioma?

A

Appears in first few weeks of life

333
Q

Which is the normal evolution of Strawberry hemangioma?

A

Grows rapidly and regresses spontaneously at 5-8 years old

334
Q

Benign capillary hemangioma of the elderly

A

Cherry hemangioma

335
Q

Expected evolution of Cherry hemangioma

A

Does not regress. Frequency increases with age

336
Q

Characteristics of Pyogenic granuloma

A

Polypoid capillary hemangiomathat can ulcerate and bleed

337
Q

What is associated to Pyogenic granuloma?

A

With trauma and preganancy

338
Q

Cavernous lymphangioma of the neck

A

Cystic Hygroma

339
Q

Which disease is associated to Cystic Hygroma?

A

Turner syndrome

340
Q

What is Glumous tumor?

A

Benign, painful, red blue tumor under fingernails

341
Q

From where does Glomus tumor arises?

A

Arises from modified smooth muscle cells of glomus body

342
Q

Benign capillary skin papules found un AIDS patients

A

Bacillary angiomatosis

343
Q

Who causes Bacillary angiomatosis?

A

Bartonella henselae infections

344
Q

With wich other Vascular tumor is Bacillary angiomatosis mistaken?

A

Kaposi sarcoma

345
Q

What is Angiosarcoma?

A

Rare blood vessel malignancy

346
Q

Typical Sites of Angiosarcoma apperance

A

In the head, neck, and breast areas

347
Q

Who are at higher risk for Angiosarcoma?

A

Usually in eldery, on sun exposed areas

348
Q

What is associated to Angiosarcoma?

A

Associated with radiation therapy and arsenic exposure

349
Q

Why does Angiosarcoma has very bad prognosis?

A

Verry agresive and dificult to resect due to delay in diagnosis

350
Q

What is Lymphangiosarcoma?

A

Lymphatic malignancy associated with persistent lymphedema

351
Q

Example of Lymphangiosarcoma patients who are at higher risk

A

Post radical mastectomy

352
Q

What is Kaposi sarcoma? where does it commonly appear?

A

Endothelial malignancy most commonly of the skin, but also mouth, GI tract and respiratoy tract

353
Q

Viruses associated to Kaposi sarcoma

A

HHV-8 and HIV

354
Q

Which vascular tumor is frequently mistaken with Kaposi sarcoma?

A

Bacillary angiomatosis

355
Q

How are Vasculitis classified?

A

Large vessel vasculitis
Medium vessel vasculitis
Small vessel vasculitis

356
Q

Large vessel vasculitis

A

Temporal (giant cell) arteritis

Takayasu arteritis

357
Q

Who are mainly affected by Temporal (giant cell) arteritis?

A

Eldery females

358
Q

Clinical manifestation of Temporal arteritis

A

Unilateral headache (temporal artery), jaw claudication

359
Q

Which is the highest risk of Temporal arteritis?

A

May lead to irreversible blindness

360
Q

Which is the reason of irrevesible blindness caused by Temporal arteritis?

A

Due to opthalmic artery occlusion

361
Q

Which disease is associated to Temporal arteritis?

A

Polymyalgia rheumatica

362
Q

Which are the most commonly affected arteries in Temporal arteritis?

A

Branches of carotid artery

363
Q

In light microscope what is seen in Temporal arteritis?

A

Focal granulomatous inflammation

364
Q

Which labs are affected in Temporal arteritis?

A

↑ ESR

365
Q

Which is the treatment for Temporal arteritis?

A

Treat with high dose corticoesteroids prior to temporal artery biopsy to prevent vision loss

366
Q

Main affected by Takayasu arteritis

A

Asian females < 40 years old

367
Q

Clinical presentation of Takayasu arteritis

A

“Pulseless disease” (weak upper extremity pulses), fever, night sweats, arthtis, myalgias, skin nodules, ocular disturbances

368
Q

Pathology findings in Takayasu arteritis

A

Glanulomatous thickening and narrowing of aortic arch and proximal great vessels

369
Q

Treatment for Takayasu arteritis

A

Corticoesteroids

370
Q

Lab studies altered in Takayasu arteritis

A

↑ ESR

371
Q

Medium vessel vasculitis

A

Polyarteritis nodosa
Kawasaki disease
Buerger disease

372
Q

Group of age who present Polyarteritis nodosa?

A

Young adults

Hepatitis B seropositivity in 30% of patients

373
Q

Clinical presentation of Polyarteritis nodosa

A

Fever, weight loss, malaise, headache
GI: abdominal pain, melena
Hypertension, neurologic dysfunction
Cutaneous eruptions, renal damage

374
Q

Which are the commonly vessels affected by Polyarteritis nodosa?

A

Typically involves renal and visceral vessels, no pulmonary arteries

375
Q

How is Polyarteritis nodosa consider?

A

Immune complex mediated

376
Q

Pathology of Polyarteritis nodosa

A

Transmural inflammation of the arterial wall with fibrionid necrosis

377
Q

In Polyarteritis nodosa what is found on arteriogram?

A

Innumerable microaneurysms and spasm

378
Q

What is the treatment for Polyarteritis nodosa?

A

Corticoesteroids, cyclosphosphamide

379
Q

Kawasaki disease principally affects…

A

Asian children <4 years old

380
Q

Which are clinical manifestations of Kawasaki disease?

A

Fever, cervical lymphadenitis, conjunctival injection, changes in lips/oral mucosa (“stawberry tongue”), hand foot erythema, desquamating rash

381
Q

Which are the risk of Kawasaki disease?

A

May develop coronary artery aneurysms, thrombosis → MI, rupture

382
Q

How is Kawasaki disease treated?

A

Treat with IV immunoglobulin and aspirin

383
Q

Alternative name for Buerger disease

A

Thromboangiitis obliterans

384
Q

Patients how have increased rik for Buerger disease

A

Heavy smokers, males <40 years old

385
Q

Clinical presentation of Thromboangiitis obliterans

A

Intermittent claudication may lead to gangrene, autoamputation of digits, superficial nodular phlebitis

386
Q

What else is often present in Buerger disease?

A

Raynaud phenomenom

387
Q

Pathology of Thromboangiitis obliterans

A

Segmental thrombosing vasculitis

388
Q

How is Buerger disease treated?

A

Smoking cessation

389
Q

Small cell vasculitis

A

Granulomatosis with polyangiitis
Microscopic polyangiitis
Churg Strauss syndrome
Henoch Schonlein purpura

390
Q

Alternative name for Granulomatosis with polyangiitis

A

Wegner

391
Q

Lower respiratory tract manifestations of Wegner disease

A

Hemoptysis, cough, dyspnea

392
Q

Upper respiratory tract of Granulomatosis with polyangiitis

A

Upper respiratory tract: perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis

393
Q

Renal manifestations of Wegner disease

A

Hematuria, red cell casts

394
Q

Triad in Granulomatosis with polyangiitis

A

Focal necrotizing vasculitis
Necrotizing granulomas in the lung and upper airway
Necrotizing glomerulonephritis

395
Q

Which labs help in the diagnosis of Wegner disease?

A

PR3- ANCA/ cANCA (anti-proteinase 3)

396
Q

Which other study helps to study Wegner disease?

A

CXR

397
Q

What could be found in CXR in Granulomatosis with polyangiitis?

A

Large nodular densities

398
Q

How is Wegner disease treatred?

A

Cyclophosphamide, corticoesteroids

399
Q

What is Microscopic polyangiitis?

A

Necrotizing vasculitis

400
Q

Which orgnas are commonly involved in Microscopic polyangiitis?

A

Lung, kidneys, and skin

401
Q

What could be found in Microscopic polyangiitis?

A

Pauci immune glomerulonephritis and palpablepurpura

402
Q

Which is the presentation of Microscopic polyangiitis?

A

Similar to granulomatosis with polyangiitis but without nasopharyngeal involvement

403
Q

Labs for Microscopic polyangiitis

A

MPO-ANCA/p-ANCA (antimyeloperoxidase)

404
Q

Treatment for Microscopic polyangiitis

A

Cyclophosphamide and corticosteroids

405
Q

Clinical presentation of Churg Strauss syndrome

A

Asthma,sinusitis, palpable purpura, peripheral neuropathy (eg. wrist/foot drop)

406
Q

What else can Churg Strauss syndrome present?

A

Involve heart, GI, kidneys (pauci immune glomerulophritis)

407
Q

Pathologic findings in Churg Strauss syndrome

A

Granulomatous, necrotizing vasculitis with eosinophilia

408
Q

Labs in Churg Strauss syndrome

A

MPO- ANCA/ p-ANCA, ↑ IgE level

409
Q

Most common childhood systemic vasculitis

A

Henoch Schonlein purpura

410
Q

Commonly what precedes Henoch Schonlein purpura

A

Upper Respiratory tract Infection

411
Q

Classic triad of Henoch Schonlein purpura

A

Skin: palpable purpura on buttocks/ legs
Arthralgias
GI: abdominal pain, melena, multiple lesions of same age

412
Q

What is the cause of Henoch Schonlein purpura?

A

Vasculitis secondary to IgA complex deposition

413
Q

Which disease is associated to Henoch Schonlein purpura?

A

With IgA nephropathy

CARDIOVASCULAR (6 decks)

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