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pathology > Heart Disorders > Flashcards

Heart Disorders Flashcards

1
Q

Why does increased pre load/after load cause ventricular hypertrophy

A

Increased preload/after load–>Increased wall stress–>increased gene expression in muscle–>duplication of sarcomeres

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2
Q

Why is there concentric thickening of the ventricle with an increase in after load?

A

Increased after load- increased resistance against which ventricle contracts–>sarcomeres duplicate parallel to long axis–>increase thickness of myofibril–>greater pressure

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3
Q

What are some causes of concentric LVH?

A

Essential hypertension(MC), Aortic stenosis, hypertrophic cardiomyopathy

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4
Q

What are some causes of concentric RVH?

A

Pulmonary HTN, pulmonary valve stenosis

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5
Q

Why is there eccentric hypertrophy with increase in preload?

A

Increase in preload–>increase in stretching of myocytes due to high EDC–> duplication of sarcomeres end to end–>dilation

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6
Q

Causes of eccentric LVH?

A

Regurgitations-aortic, Mitral valve

Left-right shunting of blood-greater blood in LV since RV cannot handle increased volume

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7
Q

Causes of eccentric RVH?

A

Regurgitations-pulmonary, tricuspid

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8
Q

Why is there left and right sides heart failure with increase in preload and after load?

A

Preload increase-dilation-by Laplace law, with increase in radius, greater wall tension req for same ventricular pressure

After load increase-increase in thickness-decreased compliance-diastolic dysfunction-systolic dysfunction

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9
Q

Why is there angina pectorals with exercise in LVH (concentric)

A

HR increases with exercise-decreased filling

Construction hypertrophy-increased mechanical compression of subendocardial vessels-decreases O2 supply

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10
Q

Why is s4 sound present with LVH/RVH?

A

S4-atrial contraction late diastole against a non compliant ventricle (atrial gallop)

Concentric hypertrophy-non compliant ventricle.
Eccentric hypertrophy-volume overload -non compliant ventricle

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11
Q

Why is S3 present in a LV/RV eccentric hypertrophy?

A

Due to blood entering overloaded chamber in early diastole

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12
Q

Why does ventricular hypertrophy occur?

A

Increase in preload/ increase in after load

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13
Q

Causes of left heart failure?

A

Decreased contraction-systolic failure

Non compliant ventricle- diastolic failure

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14
Q

What are the causes for systolic left heart failure?

A

Ischemia due to coronary atherosclerosis (MC)

Myocarditis, post-MI, dilated cardiomyopathy

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15
Q

What are causes for diastolic left ventricular failure?

A

Non compliant ventricle-concentric hypertrophy-HTN (MC), AV stenosis, hypertrophic cardiomyopathy, restrictive cardiomyopathy(amyloidosis, glycogenesis)

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16
Q

Why are heart failure cells present in LVF?

A

Heart failure cells- macrophages that phagocytosis hemosiderin.

Pressure on pulmonary cap-rupture-RBC enter alveoli-iron excess binds to ferritin-degrades into hemosiderin-rust sputum

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17
Q

Why is there dyspnea in LVF?

A

Blood backs up in lung- pulmonary congestion- interstitial fluid stimulates Juxtacapillary receptors-inner voted by vagus nerve-inhibit full inspiration

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18
Q

Why is there pulmonary edema in LVF?

A

Increase in LVEDV-increase hydrostatic pressure in LV transmitted to pulmonary capillaries- transudate

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19
Q

Why is there cardiac asthma in LVF?

A

Peri bronchial edema-narrowing of airways-expiratory wheeze

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20
Q

Why is there bibasilar respiratory crackles & rust coloured sputum in LVF?

A

Crackles-expanding fluid in alveoli

Rust coloured sputum-macrophages phagocytose hemosiderin

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21
Q

Why is there function MV regurgitation in LVF?

A

Stretching of MV ring by increased LVEDV-regurgitant murmur

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22
Q

Why is there PND in LVF?

A

W/o gravity-insterstial fluid moves into vascular compt-increased VR-LV unable to handle VR-pulmonary edema and dyspnea-relieved by standing or pillows (quantitate)

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23
Q

Why is there elevated serum BNP & ANO in LVF?

A

BNP-neurohormone from dilated left ventricle-diagnoses LVF & prognosis
ANP-produced by dilated atrium

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24
Q

What are the changes in volume & pressure of ventricle LVF?

A

Ejection volume

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25
Q

What are the causes of RVF?

A

Increased preload
Increased afterload
Decreased contraction
Non compliance

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26
Q

Causes for increased RV afterload in RVF?

A

LHF(MC), PH, PV stenosis, saddle embolus

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27
Q

Why is there painful hepatomegaly & ascites in RVF?

A

Venous blood back up in hepatic vein-distended sinusoids-zone 3 hepatic cell necrosis-increased AST & ALT

Sinusoids of liver transmit increased pressure to portal vein-PH-ascites

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28
Q

Why is there dependent pitting edema in RVF?

A

Increase in venous hydrostatic pressure

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29
Q

Why is there cyanosis of mucous mem in RVF?

A

Back of blood in venous system-more time-increased O2 extraction-decreased O2 saturation-cyanosis

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30
Q

Why is there functional TV regurgitation in RVF?

A

Stretching of valve ring due to volume

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31
Q

Why is there prominence of IJ vein in RVF?

A

Increased pressure in RA

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32
Q

How does decreased blood viscosity States cause high output cardiac failure?

A

Decreased viscosity-decreased PVR-increased VR eg. Anaemia

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33
Q

How does vasodilation and AV fistulas lead to high output cardiac failure?

A

Vasodilation-increases VR eg. Thiamine deficiency, endotoxins shock

AV fistulas-bypass micro circulation- increased VR eg. Trauma by knife, shunt in hemodialysis, mosaic bone in pagers disease

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34
Q

What are the types of IHD?

A

Angina pectoris
Chronic ischemic heart disease
Sudden cardiac death
Acute MI

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35
Q

What are the risk factors for IHD?

A

Most impt-age: men>45yrs, women >55yrs
Family history-stroke/IHD
Lipid abnormal-LDL>160mg/dl, HDL60mg/dl)
Smoking, HTN, DM

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36
Q

Causes of stable angina?

A

Decreased supply-atherosclerotic CAD (stenosis>70%), cocaine induced vasoconstriction

Increased demand-concentric thickening of ventricle

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37
Q

Why is there exercise induced substernal chest pain relived on resting/nitrates in angina pectoris?

A

Exercise- increased heart rate & contractility. Hr-decreased diastolic filling. Decreased supply, increased demand-reversible myocardial ischemia

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38
Q

Why is there shortness of breath, diaphoresis in angina?

A

Shortness of breath-backing up of blood in lungs

Diaphoresis-ANP

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39
Q

Why is there intermittent coronary vasospasm at rest in prinzmetal angina?

A

Increase in platelet thromboxane A2-from thrombus material

Increase in endothelin

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40
Q

What is unstable angina?

A

Severe fixed multi vessel atherosclerotic disease -disrupted plaques w/ w/o platelet non occlusive thrombi

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41
Q

Diagnostic tests for angina pectoris?

A

ECG at rest & exercise
Stress echocardiography with perfusion imaging
Coronary angiography
Multi detector CT scan

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42
Q

Why is balloon angioplasty & intracoronary stents done in angina?

A

Re vascularisation technique- balloon angioplasty- dilates & ruptures atheromatous plaque to improve blood flow (re stenosis common)

Intracoronary stents-bypass the obstruction

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43
Q

What grafts are used for CABG?

A

Internal mammary artery-best graft patency for 10 yrs

Saphenous vein-arterialisation in 10yrs

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44
Q

What Pts are reserved for CABG?

A

Left CAD, symptomatic three vessel disease

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45
Q

What is chronic ischemic heart disease?

A

Long term ischemic damage-non contractile scar-progressive CHF

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46
Q

Clinical findings of CIHD?

A

Bi ventricular CHF, angina, evolution into dilated cardiomyopathy

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47
Q

Risk factors for SCD?

A

IHD (impt)
Obesity, glucose intolerance, hyperlipidemia
LVH, HTN, smoking
NSTEMI

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48
Q

Non coronary artery causes of SCD?

A

Cardiomyopathy
AV stenosis
Mitral valve prolapse, WPW syndrome, cocaine, myocarditis

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49
Q

Most common cause of SCD in children?

A

AV stenosis

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50
Q

Why is there SCD with cardiomyopathy, AV stenosis and conduction defects in adults?

A

Coronary atherosclerosis with disrupted plaques

Lethal arrhythmia

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51
Q

How does an atheromatous plaque lead to AMI?

A

Atheromatous plaque disrupted-subendo collagen & thrombogenic necrotic material exposed-occlusive platelet thrombus-TXA2 (platelet aggregation & vasoconstriction)

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52
Q

What are some less common causes of AMI?

A
  1. Cocaine use
  2. Vasculitis (polyarteritis nodosa, Kawasaki disease)
  3. Embolization
  4. Thrombosis syndrome-PV, antithrombin 3 deficiency
  5. Dissection of coronary artery
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53
Q

Types of MI depending on thickness of myocardium involved?

A

Transmural-full thickness STEMI

Non STEMI-1/3 of inner thickness

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54
Q

Why does reperfusion limit size of infarct in AMI?

A

Irreversibly damaged myocytes-death
Ischemic myocardial cells-salvaged

Limit size of infarct

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55
Q

What is the effect of reperfusion

A

Ischemic tissue-salvaged

Irreversibly damaged cells-death & formation of contraction bands

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56
Q

Why do reperfusion arrhythmias occur when reperfusion is done

A

Ischemic tissue-salvaged-interferes with function for a few days/longer-predisposes tissue to arrhythmias-myocardial stunning

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57
Q

Why does reperfusion

A

Irreversibly damaged cells-death-increased cytosolic calcium-hyper contraction of myocytes-contraction bands

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58
Q

Why is reperfusion >3hrs from cessation of blood flow in an AMI not recommended?

A

Reperfusion injury

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59
Q

Why is there irreversible damage in AMI?

A

Superoxide (FR) by xanthine oxidase-irreversible damage
Acute inflammation- neutrophils decrease blood flow, neutrophils release proteome tic enzymes-oxygen FR
Platelet activation, complement activation, apoptosis

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60
Q

Why is day 3-7 most dangerous for rupture in AMI?

A

Coagulation necrosis took place in first 24hrs
Neutrophils lyse dead myocardial cells from day 1-3

Necrosis & inflammation cause softening of myocardium & granulation tissue & collagen well developed day 7-10

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61
Q

Why do changes that occur during the first 2 months of an AMI predispose to CIHD?

A

White patchy non contractile scar tissue formed in first 2 months-CIHD

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62
Q

Differentiate between pain due to angina & AMI

A

Angina pain-retrosternal pain lasting 30s-30min, relieved by rest/nitroglycerin

AMI pain-severe,crushing retrosternal pain, lasting >30min, not relieved by nitroglycerin

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63
Q

Why does pain radiate to epigastrium and inner arm and shoulder in AMI?

A

Heart supplied by T1-T5
Arm and shoulder-T1 distribution
Epigastrium-T4-T5 distribution

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64
Q

Why do silent AMI occur?

A

Elderly, DM- neuropathic so cannot feel pain

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65
Q

What types of AMI have increased risk of re infarction & SCD post MI?

A

NSTEMI

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66
Q

Why does cardiogenic shock occur as a complication in STEMI? What improves survival?

A

Systolic dysfunction-decreased perfusion of tissues

Re vascularisation

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67
Q

Why do arrhythmias occur post MI?

A

Infarct-conduction disturbances

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68
Q

Most common cause of death due to arrhythmia in AMI?

A

Ventricular fibrillation

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69
Q

Most common arrhythmias in AMI?

A

Ventricular premature contractions

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70
Q

Why do ruptures occur 3-7days post AMI?

A

Coagulation necrosis, neutrophil if infiltrate & lysis of myocardial tissue-weakening

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71
Q

What ruptures are associated with thrombosis of LAD artery?

A

Anterior rupture- cardiac tamponade

Inter ventricular septum rupture-Left to right shunt-RHF

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72
Q

What rupture is associated with thrombosis of RCA?

A

Posteromedial papillary rupture- acute onset severe MV regurgitation

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73
Q

Why does mural thrombus occur in AMI?

A

LAD artery thrombus-systolic dysfunction-stasis

Endothelial damage

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74
Q

Why does fibrinous pericarditis occur post AMI?

A

Inflammation of underlying myocardium

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75
Q

Why is precordial friction rub auscultated in fibrinous pericarditis?

A

Increased vascular permeability-exudate

76
Q

Why does Dressler’s syndrome occur post MI?

A

Autoimmune pericarditis-autoantibodies formed against damaged pericardial antigens-type 2 hypersensitivity reaction-fever and precordial friction rub

77
Q

Differentiate between a false aneurysm & true ventricular aneurysm that occurs post MI?

A

False aneurysm- (3-7days)rupture-parietal pericardium adheres to epicardium

True aneurysm- (4-8weeks)precordial bulge during systole, all layers of ventricular wall present,rupture uncommon

78
Q

Why is there SHF in ventricular aneurysm?

A

Increased radius, by Laplace law, with increased radius wall tension increases to maintain pressure

79
Q

Why is there hypotension & RHF with RCA thrombosis?

A

Right ventricular AMI-causes backing up of blood in venous system

80
Q

Why is serial testing of CK-MB used to diagnose AMI?

A

CK-MB levels elevated 4-8hrs post MI, peak at 24hrs and disappear within 1.5-3days

High specificity and sensitivity

81
Q

Why is CK-MB used to detect re infarction?

A

Reappearance of CK-MB in 3 days indicates re infarction(CK-MB disappears within 1.5-3 days)

82
Q

Why is serial testing of troponin I & T used to diagnose AMI?

A

Regulate calcium mediated muscle contraction.
Appear within 3-12hrs, peak at 24hrs, disappear within 7-10days

High sensitivity and specificity

83
Q

Why are serial studies of cardiac enzymes done to diagnose AMI?

A

Do not consistently appear in blood in first 6 hrs post MI

84
Q

What congenital heart disease occurs in a child of maternal DM is poorly controlled?

A
  1. Left ventricular outflow obstruction-AV stenosis, hypertrophied IVS
  2. Transposition of great vessel
  3. VSD
85
Q

What congenital heart disease does alcohol intake during pregnancy cause?

A

VSD PV stenosis

86
Q

What congenital heart disease is associated with rubella infection during pregnancy?

A

PDA, PV stenosis

87
Q

What congenital heart disease is associated with aspirin intake during pregnancy?

A

Persistent PH syndrome

88
Q

What congenital heart disease is associated with maternal SLE?

A

Heart block, myocarditis, endomyocardial fibrosis

89
Q

What congenital heart disease is associated with diphenylhydantoin intake?

A

AV stenosis & PV stenosis

90
Q

Why is there secondary polycythemia Vera with clubbing in cyanosis heart disease?

A

Decreased PO2-erythropoietin release-increased RBC production from BM

91
Q

How can cyanotic heart diseases be differentiated from non cyanotic heart diseases? (Left to right shunts &I right to left shunts)

A

Oxygen saturation
L->R shunts- oxygenated blood (95%saturation) mixed with deoxygenated blood (75%)-saturation of oxygen in right increase(80%)

R->L shunts-deoxygenated blood mixed with oxygenated blood-saturation of oxygen decreases(85%)

92
Q

In L-R shunts why is there concentric RVH?

A

Volume overload-pulmonary hypertension-increased after load-increased wall stress-increased gene expression-duplication of sarcomeres parallel to long axis

93
Q

Why is there LVH eccentric in L-R shunt?

A

Increased LV volume-increased wall stress-increased gene expression-duplication of sarcomeres in series

94
Q

Why can cyanosis and clubbing of fingers develop in L-R shunt?

A

Reversal of shunt-eisenmengers syndrome-late onset cyanosis (tar five cyanosis

95
Q

What is the most common congenital heart disease?

A

Ventricular septal defect

96
Q

Ventricular septal defects are more common in which part of the septum?

A

Membranous>trabecular

97
Q

VSD are associated with which other defects in decreasing order of frequency?

A

ASD>PDA>coarctation of aorta>sub valvular AV stenosis

98
Q

What other congenital diseases is VSD associated with?

A

Feral alcohol syndrome
Cri-du-chat syndrome
Multiple VSD-tetralogy of fallot

99
Q

Why does VSD occur post MI?

A

Post MI-rupture of inter ventricular septum

100
Q

Why are antibiotics prescribed to VSD patients?

A

Lifetime risk of infective endocarditis between 5%-30%

101
Q

What is the most common congenital heart disease in adults?

A

ASD

102
Q

What type of ASD is more common?

A

Secundum type -patent foramen ovale>septum primum defect

103
Q

What congenital disease is ASD associated with?

A

Fetal alcohol syndrome

Down syndrome-primum type

104
Q

How do you differentiate between ASD & VSD based on auscultation of heart?

A

VSD-harsh pan systolic murmur along lower left eternal border

ASD-soft mid systolic murmur along upper stern all border

105
Q

What is the most common congenital heart disease after age 1?

A

Tetralogy of fallot

Accounts for majority of cyanotic CHD in children & adults

106
Q

Defects in tetralogy of fallot?

A

Pulmonary valve stenosis
Overriding aorta
Inter ventricular septal defect
Hypertrophy of right ventricle secondary to septal defect

107
Q

Why is there a harsh systolic crescendo/de crescendo murmur in tetralogy of fallot?

A

RV outflow obstruction

108
Q

Cyanosis in tetralogy of fallot patients indicates what?

A

Cyanosis-oxygen saturation-

109
Q

Why is ASD a cardio protective shunt that increases oxygenation in tetralogy of fallot?

A

ASD-L->R shunt-increases oxygen saturation of deoxygenated blood

110
Q

Why is PDA a cardio protective shunt increasing oxygenation in tetralogy of fallot?

A

Blood shunts from aorta->PA-increased oxygenation of blood

111
Q

Why do tet spells occur in tetralogy of fallot?

A

Hypoxic spells due to increased RV flow obstruction associated with anaemia, crying, hypotension

112
Q

How can tet spells in tetralogy of fallot be relieved?

A

Squatting-increases PVR-increased afterload-reversal of R-L shunt-increased blood to oxygenation

113
Q

Why is ASD a cardio protective shunt in transposition of great vessels?

A

ASD:L-R shunt-increased oxygen saturation of RV blood-increased saturation of oxygen in aorta

114
Q

Why is VSD a cardio protective shunt in transposition of great vessels?

A

R-L shunt-increased blood for oxygenation

115
Q

Why is PDA a cardio protective shunt in transposition of great vessels?

A

Increased blood from aorta to PA for oxygenation

116
Q

Types of Cyanotic CHD?

A 
Tetralogy of fallot
Transposition of great vessels
Tricuspid atresia
Persistent truncus arteriosus 
Total anomalous pulmonary venous return
117
Q

What are the types of IHD?

A

Angina pectoris
Chronic ischemic heart disease
Sudden cardiac death
Acute MI

118
Q

What are the risk factors for IHD?

A

Most impt-age: men>45yrs, women >55yrs
Family history-stroke/IHD
Lipid abnormal-LDL>160mg/dl, HDL60mg/dl)
Smoking, HTN, DM

119
Q

Causes of stable angina?

A

Decreased supply-atherosclerotic CAD (stenosis>70%), cocaine induced vasoconstriction

Increased demand-concentric thickening of ventricle

120
Q

Why is there exercise induced substernal chest pain relived on resting/nitrates in angina pectoris?

A

Exercise- increased heart rate & contractility. Hr-decreased diastolic filling. Decreased supply, increased demand-reversible myocardial ischemia

121
Q

Why is there shortness of breath, diaphoresis in angina?

A

Shortness of breath-backing up of blood in lungs

Diaphoresis-ANP

122
Q

Why is there intermittent coronary vasospasm at rest in prinzmetal angina?

A

Increase in platelet thromboxane A2-from thrombus material

Increase in endothelin

123
Q

What is unstable angina?

A

Severe fixed multi vessel atherosclerotic disease -disrupted plaques w/ w/o platelet non occlusive thrombi

124
Q

Diagnostic tests for angina pectoris?

A

ECG at rest & exercise
Stress echocardiography with perfusion imaging
Coronary angiography
Multi detector CT scan

125
Q

Why is balloon angioplasty & intracoronary stents done in angina?

A

Re vascularisation technique- balloon angioplasty- dilates & ruptures atheromatous plaque to improve blood flow (re stenosis common)

Intracoronary stents-bypass the obstruction

126
Q

What grafts are used for CABG?

A

Internal mammary artery-best graft patency for 10 yrs

Saphenous vein-arterialisation in 10yrs

127
Q

What Pts are reserved for CABG?

A

Left CAD, symptomatic three vessel disease

128
Q

What is chronic ischemic heart disease?

A

Long term ischemic damage-non contractile scar-progressive CHF

129
Q

Clinical findings of CIHD?

A

Bi ventricular CHF, angina, evolution into dilated cardiomyopathy

130
Q

Risk factors for SCD?

A

IHD (impt)
Obesity, glucose intolerance, hyperlipidemia
LVH, HTN, smoking
NSTEMI

131
Q

Non coronary artery causes of SCD?

A

Cardiomyopathy
AV stenosis
Mitral valve prolapse, WPW syndrome, cocaine, myocarditis

132
Q

Most common cause of SCD in children?

A

AV stenosis

133
Q

Why is there SCD with cardiomyopathy, AV stenosis and conduction defects in adults?

A

Coronary atherosclerosis with disrupted plaques

Lethal arrhythmia

134
Q

How does an atheromatous plaque lead to AMI?

A

Atheromatous plaque disrupted-subendo collagen & thrombogenic necrotic material exposed-occlusive platelet thrombus-TXA2 (platelet aggregation & vasoconstriction)

135
Q

What are some less common causes of AMI?

A
  1. Cocaine use
  2. Vasculitis (polyarteritis nodosa, Kawasaki disease)
  3. Embolization
  4. Thrombosis syndrome-PV, antithrombin 3 deficiency
  5. Dissection of coronary artery
136
Q

Types of MI depending on thickness of myocardium involved?

A

Transmural-full thickness STEMI

Non STEMI-1/3 of inner thickness

137
Q

Why does reperfusion limit size of infarct in AMI?

A

Irreversibly damaged myocytes-death
Ischemic myocardial cells-salvaged

Limit size of infarct

138
Q

What is the effect of reperfusion

A

Ischemic tissue-salvaged

Irreversibly damaged cells-death & formation of contraction bands

139
Q

Why do reperfusion arrhythmias occur when reperfusion is done

A

Ischemic tissue-salvaged-interferes with function for a few days/longer-predisposes tissue to arrhythmias-myocardial stunning

140
Q

Why does reperfusion

A

Irreversibly damaged cells-death-increased cytosolic calcium-hyper contraction of myocytes-contraction bands

141
Q

Why is reperfusion >3hrs from cessation of blood flow in an AMI not recommended?

A

Reperfusion injury

142
Q

Why is there irreversible damage in AMI?

A

Superoxide (FR) by xanthine oxidase-irreversible damage
Acute inflammation- neutrophils decrease blood flow, neutrophils release proteome tic enzymes-oxygen FR
Platelet activation, complement activation, apoptosis

143
Q

Why is day 3-7 most dangerous for rupture in AMI?

A

Coagulation necrosis took place in first 24hrs
Neutrophils lyse dead myocardial cells from day 1-3

Necrosis & inflammation cause softening of myocardium & granulation tissue & collagen well developed day 7-10

144
Q

Why do changes that occur during the first 2 months of an AMI predispose to CIHD?

A

White patchy non contractile scar tissue formed in first 2 months-CIHD

145
Q

Differentiate between pain due to angina & AMI

A

Angina pain-retrosternal pain lasting 30s-30min, relieved by rest/nitroglycerin

AMI pain-severe,crushing retrosternal pain, lasting >30min, not relieved by nitroglycerin

146
Q

Why does pain radiate to epigastrium and inner arm and shoulder in AMI?

A

Heart supplied by T1-T5
Arm and shoulder-T1 distribution
Epigastrium-T4-T5 distribution

147
Q

Why do silent AMI occur?

A

Elderly, DM- neuropathic so cannot feel pain

148
Q

What types of AMI have increased risk of re infarction & SCD post MI?

A

NSTEMI

149
Q

Why does cardiogenic shock occur as a complication in STEMI? What improves survival?

A

Systolic dysfunction-decreased perfusion of tissues

Re vascularisation

150
Q

Why do arrhythmias occur post MI?

A

Infarct-conduction disturbances

151
Q

Most common cause of death due to arrhythmia in AMI?

A

Ventricular fibrillation

152
Q

Most common arrhythmias in AMI?

A

Ventricular premature contractions

153
Q

Why do ruptures occur 3-7days post AMI?

A

Coagulation necrosis, neutrophil if infiltrate & lysis of myocardial tissue-weakening

154
Q

What ruptures are associated with thrombosis of LAD artery?

A

Anterior rupture- cardiac tamponade

Inter ventricular septum rupture-Left to right shunt-RHF

155
Q

What rupture is associated with thrombosis of RCA?

A

Posteromedial papillary rupture- acute onset severe MV regurgitation

156
Q

Why does mural thrombus occur in AMI?

A

LAD artery thrombus-systolic dysfunction-stasis

Endothelial damage

157
Q

Why does fibrinous pericarditis occur post AMI?

A

Inflammation of underlying myocardium

158
Q

Why is precordial friction rub auscultated in fibrinous pericarditis?

A

Increased vascular permeability-exudate

159
Q

Why does Dressler’s syndrome occur post MI?

A

Autoimmune pericarditis-autoantibodies formed against damaged pericardial antigens-type 2 hypersensitivity reaction-fever and precordial friction rub

160
Q

Differentiate between a false aneurysm & true ventricular aneurysm that occurs post MI?

A

False aneurysm- (3-7days)rupture-parietal pericardium adheres to epicardium

True aneurysm- (4-8weeks)precordial bulge during systole, all layers of ventricular wall present,rupture uncommon

161
Q

Why is there SHF in ventricular aneurysm?

A

Increased radius, by Laplace law, with increased radius wall tension increases to maintain pressure

162
Q

Why is there hypotension & RHF with RCA thrombosis?

A

Right ventricular AMI-causes backing up of blood in venous system

163
Q

Why is serial testing of CK-MB used to diagnose AMI?

A

CK-MB levels elevated 4-8hrs post MI, peak at 24hrs and disappear within 1.5-3days

High specificity and sensitivity

164
Q

Why is CK-MB used to detect re infarction?

A

Reappearance of CK-MB in 3 days indicates re infarction(CK-MB disappears within 1.5-3 days)

165
Q

Why is serial testing of troponin I & T used to diagnose AMI?

A

Regulate calcium mediated muscle contraction.
Appear within 3-12hrs, peak at 24hrs, disappear within 7-10days

High sensitivity and specificity

166
Q

Why are serial studies of cardiac enzymes done to diagnose AMI?

A

Do not consistently appear in blood in first 6 hrs post MI

167
Q

What congenital heart disease occurs in a child of maternal DM is poorly controlled?

A
  1. Left ventricular outflow obstruction-AV stenosis, hypertrophied IVS
  2. Transposition of great vessel
  3. VSD
168
Q

What congenital heart disease does alcohol intake during pregnancy cause?

A

VSD PV stenosis

169
Q

What congenital heart disease is associated with rubella infection during pregnancy?

A

PDA, PV stenosis

170
Q

What congenital heart disease is associated with aspirin intake during pregnancy?

A

Persistent PH syndrome

171
Q

What congenital heart disease is associated with maternal SLE?

A

Heart block, myocarditis, endomyocardial fibrosis

172
Q

What congenital heart disease is associated with diphenylhydantoin intake?

A

AV stenosis & PV stenosis

173
Q

Why is there secondary polycythemia Vera with clubbing in cyanosis heart disease?

A

Decreased PO2-erythropoietin release-increased RBC production from BM

174
Q

How can cyanotic heart diseases be differentiated from non cyanotic heart diseases? (Left to right shunts &I right to left shunts)

A

Oxygen saturation
L->R shunts- oxygenated blood (95%saturation) mixed with deoxygenated blood (75%)-saturation of oxygen in right increase(80%)

R->L shunts-deoxygenated blood mixed with oxygenated blood-saturation of oxygen decreases(85%)

175
Q

In L-R shunts why is there concentric RVH?

A

Volume overload-pulmonary hypertension-increased after load-increased wall stress-increased gene expression-duplication of sarcomeres parallel to long axis

176
Q

Why is there LVH eccentric in L-R shunt?

A

Increased LV volume-increased wall stress-increased gene expression-duplication of sarcomeres in series

177
Q

Why can cyanosis and clubbing of fingers develop in L-R shunt?

A

Reversal of shunt-eisenmengers syndrome-late onset cyanosis (tar five cyanosis

178
Q

What is the most common congenital heart disease?

A

Ventricular septal defect

179
Q

Ventricular septal defects are more common in which part of the septum?

A

Membranous>trabecular

180
Q

VSD are associated with which other defects in decreasing order of frequency?

A

ASD>PDA>coarctation of aorta>sub valvular AV stenosis

181
Q

What other congenital diseases is VSD associated with?

A

Feral alcohol syndrome
Cri-du-chat syndrome
Multiple VSD-tetralogy of fallot

182
Q

Why does VSD occur post MI?

A

Post MI-rupture of inter ventricular septum

183
Q

Why are antibiotics prescribed to VSD patients?

A

Lifetime risk of infective endocarditis between 5%-30%

184
Q

What is the most common congenital heart disease in adults?

A

ASD

185
Q

What type of ASD is more common?

A

Secundum type -patent foramen ovale>septum primum defect

186
Q

What congenital disease is ASD associated with?

A

Fetal alcohol syndrome

Down syndrome-primum type

187
Q

How do you differentiate between ASD & VSD based on auscultation of heart?

A

VSD-harsh pan systolic murmur along lower left eternal border

ASD-soft mid systolic murmur along upper stern all border

pathology (6 decks)

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