Ce-Cardiac 1-Liners

Front 1

1. What 3 questions should be asked in every focused cardiac examination history of the patient’s present illness?

Back 1

Chest pain, shortness of breath and syncope

Front 2

2. What three pulmonary symptoms could be asked in the history of present illness to help separate pulmonic from cardiac induced shortness of breath?

Back 2

Orthopnea, PND and productive sputum

Front 3

3. What parameter based questions can you ask the patient to separate episodes of stable angina pectoris from unstable angina?

Back 3

Changes in frequency and duration. Pain at rest. If episode of angina last 20 min, the damage process starts

Front 4

4. What is the most common cause of death in both men and women in this country?

Back 4

Atherosclerosis

Front 5

5. How long does myocardial ischemia have to last before myocardial damage (myocardial infarction) begins to occur?

Back 5

20 min

Front 6

6. List 5 major risk factors for the development of coronary artery disease.

Back 6

Age, smoking, age, diabetes, cholesterol, family history, obesity, hypertension

Front 7

7. Where in the history, other than family history, would be the place to list the atherosclerotic risk factors in a patient with suspected coronary artery disease

Back 7

HOPI

Front 8

8. In what part of the history would you list cardiac review of systems in a patient with a cardiac problem?

Back 8

HOPI

Front 9

9. What is the most common diagnosis for episodic syncope upon standing?

Back 9

Orthostatic hypotension/ vasovagal syncope

Front 10

10. How would you describe a Stokes Adams attack?

Back 10

Sudden block in AV conduction leads to syncope, once ventricles establish their own rhythm, patient regain consciousness

Front 11

11. Define congestive heart failure.

Back 11

The heart is unable to pump blood at a sufficient rate to meet the metabolic demands or can do so at elevated filling pressure

Front 12

12. What relatively rare congenital life threatening conditions should you consider in a 20 year old with suspected cardiac induced syncope?

Back 12

Wolf-parkinson disease, hypertrophic cardiomyopathy, Long QT

Front 13

13. What is the usual chief complaint when mitral regurgitation is severe?

Back 13

No symptoms until end stage heart failure. Shortness of breath at end stage

Front 14

14. What are the 3 presenting symptoms of a patient with severe aortic stenosis?

Back 14

Chest pain, syncope, shortnesss of breath

Front 15

15. Which of these 3 complaints in a patient with aortic stenosis is compatable with the shortest life span?

Back 15

Shortness of breath

Front 16

16. What is the usual chief complaint of patient with severe mitral stenosis?

Back 16

Dyspnea

Front 17

17. What is the usual presenting symptom of chronic severe AR?

Back 17

Shortness of breath

Front 18

18. What is the presentation in the emergency department of acute severe AR or MR?

Back 18

Pulmonary edema/shock

Front 19

19. What is the range of pressure we call prehypertensive?

Back 19

120-140 systolic, 80-90 diastolic

Front 20

20. What is the normal pulse pressure?

Back 20

40

Front 21

21. What is the significance of pulsus alternans in a patient?

Back 21

Is the finding of an alternating plse volume. Its indicative of congestive heart failure, LV systolic deficiency

Front 22

22. What is the significance of a 12 mm or greater paradoxical pulse?

Back 22

Paradoxical pulse means that the amplitude decreases with inspiration greater than 10 mm Hg and indicates cardiac tamponade, COPD and pericarditis

Front 23

23. What is the finding on carotid palpation in severe aortic stenosis?

Back 23

The carotid pulse will register parvus at tardus (weak and late) relative to heart beat. Delay between first heart sound and corresponding pulse in carotid artery.

Front 24

24. A patient presents with a murmur, bounding pulses and a pulse pressure of 80. What is your diagnosis?

Back 24

Hyperthyroid, truncus arteriousus, post exercise

Front 25

25. What is top normal size for a point of maximal impulse (PMI)?

Back 25

1-2 cm (5th intercostal space)

Front 26

26. In a patient with normal cardiac anatomy, which chamber are you palpating when feeling the PMI?

Back 26

Left ventricle

Front 27

27. What would be the underlying pathology behind a paradoxical or rocking component of the apical impulse?

Back 27

An uncordinate (dyskinetic) apex beat involving a larger area than normal. Ventricular dysfunction possibly post aneurysm or post MI

Front 28

28. Which venous pulse can you use to estimate right atrial filling pressure?

Back 28

The jugular venous pressure (internal jugular) can be assessed to estimate RA filling pressure

Front 29

29. What is the explanation for the a wave seen in the internal jugular pulses?

Back 29

Due to atrial contraction

Front 30

30. In what heart rhythm abnormality would the a wave disappear?

Back 30

In atrial fibrillation

Front 31

31. Which heart sound signifies the onset of systole?

Back 31

First heart sound (S1)

Front 32

32. Diastole begins with what heart sound?

Back 32

S2

Front 33

33. Why is the S1 sound usually much softer than S2

Back 33

AV valves leaflets are not as taught as the aortic and pulmonary valves (semilunar valves)

Front 34

34. Where would P2 be most easily heard?

Back 34

2 nd intercostal space on the left

Front 35

35. Why is A2 louder than P2?

Back 35

More pressure in the systemic circulation (pushing back against the aortic valve) than in the pulmonary circulation, the aortic closes with more force

Front 36

36. What cardiac event occurs to cause the S4 sound?

Back 36

Atrial kick is caused by contraction of the atria to force extra blood into the ventricles prior to systole

Front 37

37. When does an S3 gallop occur and what does it signify in an adult?

Back 37

Is caused by the flutter of the ventriclular walls as blood rushes in from the atria. It may signify mitral regurgitation or CHF. Decrease ventricular compliance

Front 38

38. What abnormalities could cause reverse splitting of A2P2?

Back 38

Aortic stenosis, hypertrophic cardiomyopathy, left bundle branch block, ventricular pacemakers

Front 39

39. What valves are responsible for early systolic clicks?

Back 39

Semilunar

Front 40

40. What valve is responsible for mid systolic clicks?

Back 40

Opening of a stiffened mitral valve

Front 41

41. What is the pathophysiologic explanation of a diastolic snap?

Back 41

Opening of stenotic mitral valve

Front 42

42. Where, and with what part of your stethoscope, do you listen for left sided cardiac gallops?

Back 42

Listen with bell, S3/S4 apeax with patient in left lateral decubitis

Front 43

43. What is the response of gallops when you increase pressure on the bell of your stethoscope?

Back 43

They dissapear

Front 44

44. At what heart rate does the patient develop a summation gallop?

Back 44

120. Less time to fill. Diastole is shortened happening all in the same time

Front 45

45. How loud does a murmur have to be to cause a thrill?

Back 45

Grade 4-6

Front 46

46. In addition to the cardiac examination, what other areas of physical examination would be of most interest to you in a cardiac problem? List 4

Back 46

Pulmonary, GI, extremities, thyroid, eyes

Front 47

47. What other factors or major organ dysfunction can cause peripheral edema?

Back 47

Liver failure, RHF, lymphatic obstruction, DVT, kidney failure

Front 48

48. What leg statistically swells first in edema?

Back 48

Left leg because of iliac vein

Front 49

49. What differentiates lymphedema from edema secondary to fluid retention?

Back 49

Pitting (fluid, no protein) vs non pitting (lymphedema)

Front 50

50. Describe an aortic stenosis mumur.

Back 50

Harsh thrill, non-holosystolic, crescendo-decrescendo

Front 51

51. In what auscultation site and what position would aortic stenosis be expected to be loudest?

Back 51

Right 2nd IC space

Front 52

52. What is the radiation pattern of an aortic stenosis murmur?

Back 52

Right carotid, clavicle and sternum

Front 53

53. Does loudness of AS usually correlate with severity?

Back 53

Yes, congestive heart failure

Front 54

54. What has occurred when the murmur of severe aortic stenosis decreases?

Back 54

CHF

Front 55

55. The etiology of dilated cardiomyopathy is:

Back 55

Alcohol, defects in cytoskeletal proteins (dystrophin and alpha-actin), volume overload, myocarditis

Front 56

56. Describe the murmur of mitral regurgitation and it’s location?

Back 56

Pansystolic, radiates to axilla, hear in at PMI 5th IC midclavicular line

Front 57

57. Does loudness of MR correlate with severity?

Back 57

No

Front 58

58. What skeletal abnormalities are associated with mitral valve prolapse?

Back 58

Marfans

Front 59

59. What maneuver will move the click of mitral valve prolapse later into systole?

Back 59

Valsava maneuver (more volume so it will occur later). Squatting increases venous return. Standing decreases ledt ventriclualr volume froom decreased venous return to heart

Front 60

60. The murmur of mitral regurgitation will radiate toward the high sternum with an abnormality of which leaflet of the mitral valve?

Back 60

Posterior or anterior

Front 61

61. What are the other sounds associated with a murmur in mitral valve prolapse?

Back 61

Mid systolic click

Front 62

62. What would you expect to find on palpation of the PMI of a patient with severe chronic MR

Back 62

Shift to the left (increase in diameter)

Front 63

63. What is the usual causative factor in the development of mitral stenosis?

Back 63

Rheumatic heart disease and congenital

Front 64

64. If someone presents with mitral stenosis in their teens, what can you surmise?

Back 64

Rheumatic heart disease

Front 65

65. Which sex far predominates in the development of mitral stenosis?

Back 65

Female

Front 66

66. What is the best position and location to hear the murmur of mitral stenosis?

Back 66

Left 5th IC space, left lateral position at apex

Front 67

67. Which head of the stethoscope do you use to hear mitral stenosis?

Back 67

Bell

Front 68

68. Describe the mitral stenosis murmur.

Back 68

Low pitched rumble, decrescnedo in diastole

Front 69

69. What would happen to mitral stenosis murmur if the patient developed atrial fibrillation?

Back 69

Presystolic sound dissapears and all you hear is a midsystolic rumble

Front 70

70. What is the response of mitral stenosis to exercise?

Back 70

Increased. Murmur increased demand of blood. So more has to be pumped through the stenosed valve

Front 71

71. Describe the position of the patient and the locations where the murmur of aortic regurgitation is best heard.

Back 71

2nd to 4th left interspaces. Patient siting, leaning forward, with breath held after exhalation

Front 72

72. What is implied if the murmur of chronic aortic regurgitation is heard best on the right of the sternum?

Back 72

A severe murmur, dilation of the root, ventricular hypertophy

Front 73

73. Why is the murmur of AR decreshendo?

Back 73

Less pressure difference, less blood flow, less sound

Front 74

74. In AR and MR what is the best indication of severity.

Back 74

Length of murmur

Front 75

75. Hypertrophic cardiomyopathy in 50% of people has a familial transmission, describe:

Back 75

Massive myocardial hypertrophy without ventricular dilation. Mutations in any of several genes that encode sarcomeric proteins increases the mass and size of the ventricular walls which reduces diastolic filling capacity of the heart

Front 76

76, 77, 78 What areas of physical examination and what maneuver will help you differentiate aortic stenosis from Hypertrophic Obstructive Cardiomyopathy on physical examination?

Back 76

Carotid: Delayed carotid upstroke in aortic stenosis. The carotid pulse rise quickly in hypertrophic cardiomyopathy
Cardiac:Lateral displacement from cardiac enlargement in hypertrohic cardiomyopathy.  No lateral displacement in aortic stenosis
Maneuvers:  Aotic stenosis murmur heard best with patient sitting and leaning forward.  Hypertrophic cardiomyopathy decreases with squatting

Front 77

79. What physical examination sign is pathognomic of atherosclerotic heart disease?

Back 77

There isn't one

Front 78

80. Which vessel is the most likely cause of an inferior wall MI?

Back 78

Posterior interventricular

Front 79

81. Which vessel is the most likely cause of a lateral MI?

Back 79

Left circumflex artery

Front 80

82. Which vessel is the most likely cause of an anterior wall MI?

Back 80

LAD left anterior descending

Front 81

83. What is the most common abnormality in congenital heart disease?

Back 81

VSD, could be bicuspid aortic valves

Front 82

84. What is the most common form of congenital heart disease in adults?

Back 82

Bicuspid aortic valve

Front 83

85. What is the most common cause of an extracardiac shunt?

Back 83

PDA

Front 84

86. Which congenital heart disease is more common in women:

Back 84

ASD, mitral valve prolapse, patent ductus arteriosis, common atrium (one atrium)

Front 85

87. Which congenital heart diseases occur most commonly in males?

Back 85

Coarction, aortic valve stenosis, tetralogy of Fallot, transposition

Front 86

88. Which congenital heart disease has the largest male predominance?

Back 86

Bicuspid valve

Front 87

89. Which conditions demonstrate increased incidence of patent ductus arteriosus?

Back 87

Girls affected more than boys, genetic defect (down syndrome) predispose to PDA, rubella infection, premature infants

Front 88

90. Describe the murmur and location of a PDA murmur.

Back 88

Harsh machinery-like murmur over left 2 interspace

Front 89

91. What will occur in a child with a patent ductus arteriosus with elevated pulmonary vascular resistance?

Back 89

It can cause a reversal of flow and switch from a left to right shunt to a right to left shunt

Front 90

92. In older children and adults, what is the relationship between the size of a VSD and the murmur?

Back 90

The smaller the size, the smaller the leakage, the louder the sound, the bigger the size,the softer the sound

Front 91

93. On examination of a newborn, how does a small VSD present?

Back 91

Usually asymptomatic unless large. Not heard until a few days

Front 92

94. What is the term used to describe the development over time of pulmonary hypertension in congenital heart disease?

Back 92

Eisenmenger syndroem: Pulmonary vascualr resistance and right heart pressures reach systemic levels and a right shunt can become a right to left shunt

Front 93

95. In the fetus where is the highest percentage oxygen saturation?

Back 93

Umbilical vein

Front 94

96. What is the most common congenital cardiac defect as a cause of early post birth presentation of congestive heart failure?

Back 94

Tetralogy of fallot

Front 95

97. Hypoxemia at birth resulting in pulmonary vascular disease, usually presents first as:

Back 95

Cyanosis “blue baby syndrome”. Retracted breathing

Front 96

98. If this condition persists it presents later with:

Back 96

Clubbing of toes and fingers as well as polyctyhemia

Front 97

99. A male child presents to clinic with dysmorphic facies, mental retardation, bleeding and pulmonic stenosis. Your diagnosis is:

Back 97

Noonan syndrome

Front 98

100. Define Kartagener’s syndrome:

Back 98

Autosomal recessive disorder of cilia (ciliary dyskinesia) that cuase a respiratory tract problems and may cause congenital heart defects

Front 99

101. You are examining a young female patient who is of short stature , has low set ears, broad chest with wide nipples, and a early systolic ejection click and a systolic ejection murmur. What is your diagnosis?

Back 99

Turner's syndrome

Front 100

102. What is the chromosomal abnormality associated with this condition?

Back 100

XO (only one x chromosome

Front 101

103. What heart lesions are often associated with this condition?

Back 101

Coarction of the aorta, bicuspid aortic valve (40%)

Front 102

104. We are seeing a child in pediatric cardiology with a short, flattened facies, upslanted palpebral fissures and mental retardation. What is your diagnosis?

Back 102

Down syndrome (trisomy 21)

Front 103

105. What is the most significant risk factor for the development of this condition?

Back 103

Maternal age over 40

Front 104

106. What are the cardiac conditions most often associated with this condition?

Back 104

Endocardial cushion defects (AAD, VSD, AV defect)

Front 105

107. A thirty five year old man is in your office with chest pain. He is tall, with long limbs, loose ligaments, arachnodactyly, lens dislocation, and aortic regurgitation. What is your diagnosis?

Back 105

Marfans syndrome

Front 106

108. What is the term for a clot that arises from the veins, passes usually thru an ASD to lodge arterial circulation?

Back 106

Paradoxical emobolism

Front 107

109. What congenital syndrome is most commonly associated with endocardial cushion defect (atrioventricular canal defect)?

Back 107

Down syndrome

Front 108

110. What 2 structures does the patent ductus usually connect and in what location?

Back 108

Patent ductus arteriosus connects aorta and pulmonary artery

Front 109

111. What condition would you suspect in a child when you hear a systolic murmur best posteriorly between the scapulae?

Back 109

Coarctation of the aorta

Front 110

113. What would you expect upon blood pressure readings in this child?

Back 110

High BP in the upper body, low bp in the lower body

Front 111

114. What congenital abnormality has a high incidence of this condition?

Back 111

Turner syndrome

Front 112

115. What happens to a newborn baby born with severe coarctation of the aorta if the associated PDA closes?

Back 112

Asymptomatic

Front 113

116. What is the underlying pathology in a 40-70 year old man who presents with symptoms of severe aortic stenosis?

Back 113

Aortic stenosis, calcification (due to aging)

Front 114

117. Where would you expect to hear the murmur of a VSD?

Back 114

Tricuspid are of the left sternal edge

Front 115

118. What is the correlation between loudness of a VSD murmur and VSD size?

Back 115

Louder=small size

Front 116

119. What is the term used for the VSD when a loud murmur is present?

Back 116

Rogers murmur

Front 117

120. What is the mother’s underlying condition in a baby born with Ebstein’s anomaly?

Back 117

Wolf parkinson-white

Front 118

121. What agent has been thought to increase the development of

Back 118

Ebstein’s?; Development of Ebstein's anomaly is common with women who take lithium

Front 119

122. How would you describe the anatomical problem in Ebsteins?

Back 119

a) Tricuspid displaced into R ventricles, b) anomalous attachment of leaflets, c) dysplastic valve tissue, d) regurgitation related to wolf parkinson-white

Front 120

123. What is the usual early presentation of the severe form of this condition

Back 120

a) paroxysmal cyanosis, b) tricuspid regurgitation, c) atrial tachycardia

Front 121

124. Why should pregnancy be avoided in a female patient with congenital heart disease with Eisenmenger’s physiology?

Back 121

Mothers health is at risk if she has pulmonary vascular disease and pulmonary hypertension. Risk of heart failure and arrhythmia

Front 122

125. What is the gender of a child born with Noonan syndrome? What is the associated cardiac abnormality?

Back 122

Male, pulmonary valve stenosis

Front 123

126. What are the four congenital lesions which can present with cyanosis at birth and are considered cardiac emergencies in a new born?

Back 123

Tetralogy of fallot, transposition of great arteries, truncus arteriosus, tricuspid atresia

Front 124

127. Which condition listed above is the most common?

Back 124

Tetralogy is mort common

Front 125

128. Describe the heart shape of truncus arteriosis on X-ray:

Back 125

Large heart, increased vascularity, right arch

Front 126

129. What is expected on examining an X-ray of a patient with tricuspid atresia?

Back 126

Square heart, pulmonary oligenia

Front 127

130. Transposition is noted by the rapidity of 5the development of what post birth. They usually have:

Back 127

Cyanosis, cardioprotective shunts, loud S2, Right ventricular hypertrophy

Front 128

131. Closure of any of PDA, VSD or patent foamen ovale in complete transposition induces

Back 128

Cyanosis, death

Front 129

132. Transposition x-ray appearance:

Back 129

Egg on a side

Front 130

133. Where is the connection of the pulmonary veins in total anomalous pulmonary venous return if a baby is presenting 12 hours after birth with cyanosis and tachycardia and no murmur

Back 130

Subdiaphragmatic, into portal or hepatic vein. Supracardiac into bronchiocephalic vein or supeiror vena cava. Cariac into cardiac sinus or right atrium. mixed

Front 131

134. Describe the heart shape on X-ray of tetrology of Fallot:

Back 131

Boot shaped heart

Front 132

135. What are the components of Tetrology of Fallot?

Back 132

VSD, pulmonary stenosis, RVH, overriding aorta

Front 133

136. What is the usual cause behind the development of ventricular fibrillation and death?

Back 133

Sudden cardiac death, hypercoagulability

Front 134

137. What underlying conditions cause ventricular tachycardia in the absence of structural heart disease?

Back 134

Monomorphic VT or idiopathic VT, more common in women, induced by exercise, stress, caffeine, homorne. Long QT, brugada syndrome

Front 135

138. The 3 main types of non-structural induced ventricular tachycardia are predominantly what type of traits?

Back 135

Polymorphic VT, induced by acute ischemia, myocarditis, changes in QT interval

Front 136

139. Three findings that should suggest a possible diagnosis of infective endocarditis:

Back 136

Major-postive culture or evidence of endocervical involvment (echo or regurgitation) and minor-predisposition, fever, vascualr phenomenon, immunologic phenomenon, microbia evidence

Front 137

140. Which form occurs most commonly is on previously abnormal valves?

Back 137

Strep epidermis is most common after insertion of prosthetic valves. Subacute endocarditis

Front 138

141. What cardiac abnormality is the most common one to develop endocarditis?

Back 138

MVP= mitral valve prolapse

Front 139

142. What is the most common presentation of a patient with severe acute endocarditis?

Back 139

Fever, chest pain, SOB

Front 140

143. Characterize the fever pattern in subacute endocarditis.

Back 140

Low grade fever

Front 141

144. Endocarditis occurs predominately on left sided valves with one exception:

Back 141

Tricuspid valve in drug abusers (S. aureus); Tricuspid valve in drug abusers (S. aureus)

Front 142

145. What is the most common organism which causes acute endocarditis?

Back 142

S. aureus (acute), S. viridans (subacute)

Front 143

146. What is the organism most likely responsible for subacute bacterial endocarditis?

Back 143

S. viridans (native or S. epidermidis (prosthetic)

Front 144

147. What are 2 major criteria for making a diagnosis of endocarditis?

Back 144

Blood culture +, echo ID of valve damage

Front 145

148. What is the recommended number of and timing of obtaining blood cultures:

Back 145

3 cultures, 1 hour apart

Front 146

149. What dermatologic findings can be seen on physical examination in endocaditis?

Back 146

Janeway lesions, osler nodes, roth spots, splinter hemorrhage

Front 147

150. At what age range does acute rheumatic fever usually present?

Back 147

Age 6-15

Front 148

151. What are the major criteria for acute rheumatic fever?

Back 148

Immune response to group A streptococci. Appear 10 day-6 weeks after an episode of pharyngitis, migratory polyarthrits, pancreatitis, subcutaneous nodules, erythema marginatum and syndenham chorea

Front 149

152. Which of the major ARF criteria is the most common?

Back 149

Carditis

Front 150

153. What are the characteristics of the polyarthritis in acute rheumatic fever?

Back 150

In which one large joint after another becomes painful and swollen for a period of days and then subsides spontaneously leaving no residual disability

Front 151

154. List at least 2 of the findings on physical exam that indicate acute rheumatic carditis.

Back 151

Pericardial friction rubs, weak heart sounds, tachy and arrhythmias

Front 152

155. What layers of the heart are involved with rheumatic carditis?

Back 152

All 3 layers (pericardium, myocardium and endocardium)

Front 153

156. What is the pathologic hallmark of rheumatic carditis?

Back 153

Aschoff bodies, also Anitschkow cell

Front 154

157. What part of the body is typically spared in erythema marginatum?

Back 154

Face is spared

Front 155

158. What exam finding develops late, but is characteristic of ARF?

Back 155

Sydenhams chorea

Front 156

159. What does the onset of Sydenham’s chorea and or mitral stenosis have in common

Back 156

occur after latent period

Front 157

160. What valve murmurs would you expect in the acute phase of rheumatic fever?

Back 157

Mitral regurg/stenosis

Front 158

161. What organism is responsible for the development of ARF?

Back 158

Group A,beta hemolytic strep pyogenes

Front 159

162. What is the current antibiotic regimen in the treatment of ARF?

Back 159

Course of penicillin to eradicate S. pyogenes

Front 160

163, 164. After an episode of ARF, what valve is the most likely to be significantly damaged long term and what population subset will present with symptoms in the 30-50 age range?

Back 160

Mitral valve. People with cardiovascualr disease, arthritis, drug abuse, trauma or skin ulcer, alcoholism or drug abuse, malignancy, use of corticosteroids, diabetes mellitus

Front 161

165. Pressure in the LA is higher than LV pressure during

Back 161

mitral stenosis

Front 162

166. What would be the lifestyle modifications you would suggest to a patient with high risk for the development of atherosclerosis?

Back 162

Diet low fat, high fiber, exercise 30 min/day, 3-4 times a week, distress, smoking, alcohol cessation

Front 163

167. What drug is administered during an episode of angina?

Back 163

Nitroglycerin

Front 164

168. side effect of Amiodarone

Back 164

pulmonary fibrosis

Front 165

169. side effect of Procainamide

Back 165

hypotension, pericarditis

Front 166

170. side effect of Ace inhibitors

Back 166

Dry cough

Front 167

171. side effect of Cocaine

Back 167

Coronary spasm, MI

Front 168

172. side effect of Digitalis

Back 168

Heart block

Front 169

173. side effect of Nitro

Back 169

Hypotension

Front 170

174. side effect of B blockers

Back 170

Heart block and CHF, AV block

Front 171

175. side effect of Daunorubicin

Back 171

Cardiomyopathy

Front 172

176. side effect of Methyl dopa

Back 172

hypotension