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Cardiology > Cardiology part 5 > Flashcards

Cardiology part 5 Flashcards

1
Q

Mitral Valve Regurgitation (MR)

A

x

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2
Q

chronic primary mitral valve regurgitation (MR)

A

x

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3
Q

define

A

x

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4
Q

what is primary mitral valve regurge?

A

intrinsic defect of the mitral valve apparatus (eg leaflets, chordae tendinae),

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5
Q

what is secondary (functional) mitral valve regurge?

A

occuring from disease process involving the left ventricle (eg MI, dilated cardiomyopathy)

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6
Q

cause

A

x

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7
Q

most common cause of primary mitral regurge?

A

myxomatous degeneration of the mitral valve leading to mitral valve prolapse (evidence by a systolic click in this patient).

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8
Q

chronic mitral regurgitation

A

x

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9
Q

syx

A

x

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10
Q

how do you define syx of chronic mitral regurge?

A

DOE, heart failure

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11
Q

dx

A

x

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12
Q

what are echo findings of chronic mitral regurge?

A

left atrial and left ventricular enlargement, regurgitant jet prominence

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13
Q

management

A

x

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14
Q

in patients with severe chronic primary MR and LVEF <= 60% , they are considered to have imparie LV systolic fxn, next step?

A

mitral valve repair or replacement

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15
Q

complications

A

x

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16
Q

in patients with chronic MR, LVEF of what is considered abnormal?

A

LVEF <= 60%

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17
Q

Acute Mitral Regurgitation

A

x

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18
Q

causes

A

x

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19
Q

what are the causes of acute mitral regurgitation ?

A

ruptured mitral chordae tendinae from:

  • MVP (marfan syndrome, Ehlers-Danlos Syndrome)
  • infective endocarditis
  • Rheumatic heart disease
  • Trauma
  • MI

papillary muscle rupute due to MI or trauma

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20
Q

syx

A

x

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21
Q

what are the clinical features of acute mitral regurgitation ?

A
  • rapid onset of pulmonary edema (SOB, Diaphoresis)
  • biventricular heart failure
  • hypotension, cardiogenic shock
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22
Q

PE

A

x

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23
Q

what are physical exam findings?

A
  • Diaphoresis, cool extremities
  • Jugular venous distension, pulmonary crackles
  • Hyperdynamic cardiac impulse
  • Apical decrescendo systolic murmur (often absent) at the cardiac apex
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24
Q

dx

A

x

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25
Q

what does CXR show for Acture Mitral Regurgitation?

A

bilateral alveolar infiltrates and hilar prominence are present

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26
Q

management

A

x

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27
Q

what is the management of acute mitral regurgitation?

A
  • bedside echo

- emergent surgical intervention

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28
Q

Infective Endocarditis (IE)

A

x

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29
Q

pathophys

A

x

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30
Q

what is the pathophys of Infective Endocarditis?

A

if it involves the mitral valven can lead to acute MR due to inadequate leaflet coaptation, leaflet perforation, or papillary muscle involvement

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31
Q

syx

A

x

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32
Q

what are the syx of infective endocarditis?

A

preceding fever, combined with velvety skin with scar formation and previous bilateral hernias (suggestive of underlying CTD)

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33
Q

Abx prophylaxis

A

x

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34
Q

in what situations generally speaking should patients receive appropriate Abx therapy?

A

Only patients with a high-risk cardiovascular condition and ongoing GI or GU infection should receive appropriate antibiotic therapy, including an agent active against enterococci (eg, ampicillin, vancomycin), prior to the procedure.

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35
Q

what are high risk cardiac conditions that require Abx prophylaxis?

A
  • prosthetic heart valve
  • previous infective endocarditis
  • structural valve abnormality in transplanted heart
  • unrepaired cyanotic congenital heart disease
  • repaired congenital heart disease with residual defect
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36
Q

what are indicated procedures and appropriate Abx coverage for IE?

A
  • Gingival manipulation or respiratory tract incision: Viridans group Streptococcus coverage (eg, amoxicillin)
  • GU or GI tract procedure in setting of active infection: Enterococcus coverage (eg, ampicillin)
  • Surgery on infected skin or muscle: Staph
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37
Q

Compartment Syndrome (CS)

A

x

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38
Q

syx

A

x

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39
Q

what are common syx of compartment syndrome?

A
  • pain out proportion to injury
  • pain increase on passive stretch
  • rapidly increasing and tense swelling
  • paresthesia (early)
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40
Q

what are uncommon syx of compartment syndrome?

A
  • decrease sensation
  • motor weakness (within hours)
  • paralysis (late)
  • decrease distal pulses (uncommon)
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41
Q

risk

A

x

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42
Q

what are risk of compartment syndrome?

A

MVA, fractured humerus, T2DM,

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43
Q

PE

A

x

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44
Q

what are physical exam findings?

A

increased edema, cold extremity, absent pulses

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45
Q

pathophys

A

x

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46
Q

what is the pathophys of compartment sydnrome?

A

arterial and venous occlusion in the extremity results in anoxic muscle necrosis (rhabdomylosis). The released myoglobin is filtered and degraded in the kidney.

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47
Q

complications

A

x

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48
Q

what are the complicatoins of compartment syndrome?

A

acute renal failure

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49
Q

pathophys of acute renal failure in compartment syndrome?

A

Heme pigment from myoglobin degradation;

  • is directly toxic to proximal tubular cells
  • combines with Tamm-Horsfall protein to form tubular casts
  • induces vasoconstriction, reducing medullary blood flow
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50
Q

what other complications less commonly can occur from compartment syndrome of the leg?

A

arterial shearing resulitng in intimal tear from blunt trauma, and the arterial lumen can be paritally or completely occluded by the intimal flap

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51
Q

causes

A

x

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52
Q

what are other causes after crush injury causing compartment syndrome?

A

leg hematoma

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53
Q

dx

A

x

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54
Q

how do you diangose leg hematoma?

A

dropping hemaglobin in setting of increased swelling in the leg

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55
Q

what measurement do you use to assess compartment pressures?

A

tissue pressures. Pressure >30mm Hg

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56
Q

when it comes compartment pressures the delta pressure is also an excellent assesment. How do you calculate it?

A

DBP-Compartment Pressure <20-30 mm Hg indicates significant CS

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57
Q

trx

A

x

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58
Q

what ist he treatment for compartment syndrome?

A

fasciotomy

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59
Q

what other intervention can you do in the meantime to maintain perfusion pressure to limb?

A

keep limb at torso level and treat hypotension

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60
Q

prognosis

A

x

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61
Q

what is the most important determinatn of patients prognosis with Compartment syndrome?

A

timing of surgical intervention

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62
Q

does absence of arterial pulses indicate poor prognosis?

A

no, because not a consistent finding

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63
Q

are patients with motor or sensory deficits indicative of poor prognosis?

A

no, usually can be relieved early in disease process

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64
Q

Ehlers Danlos Syndrome (EDS) vs Marfans Syndrome

A

x

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65
Q

Features

A

x

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66
Q

what are skin manifestations of EDS vs Marfans Syndrome?

A

EDS: Transparent and hyperextensible, easy bruising, poor healing, velvety with atrophy and scarring
Marfan: No features other than striae

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67
Q

what are MSK manifestations of EDS vs Marfans Syndrome?

A

EDS: Joint hypermobiltiy, pecus excavatum, scoliosis, high arched palate
Marfan: Joint hypermobiltiy, pecus excavatum or carinatum, scoliosis, tall with long extremities

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68
Q

what are cardiac manifestations of EDS vs Marfans Syndrome?

A

EDS: MVP, acute MR
Marfan: Progressive aortic root dilation, MVP, acute MR

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69
Q

what are other manifestations of EDS vs Marfans Syndrome?

A

EDS: Abdominal and inguinal hernias, uterine prolapse, cervical insufficiency
Marfan: Lens and retinal detachment, spontaneous pneumothorax

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70
Q

what are the genetic manifestations of EDS vs Marfans Syndrome?

A

EDS: COL5A1 and COL5A2 mutation, autosomal dominant
Marfan: FBN1 mutation, autosomal dominant

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71
Q

Marfan Syndrome (MFS)

A

x

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72
Q

genetics

A

x

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73
Q

what type of genetics is it?

A

autosomal dominant defect in fibrillin 1

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74
Q

pathophys

A

x

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75
Q

where is fibillin 1 found that contributes to defects in connective tissues?

A

MSK, Cardiovascular (eg aorta, heart valves) as well zonular fibers that suspend the ocular lens in place

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76
Q

PE

A

x

77
Q

what is a hallmark physical exam finding of Marfans?

A

ectopia lentis (lens subluxation) in the upward direction

78
Q

what are PE findings?

A

tall stature, increased arm span to height ratio, myopia

79
Q

comorbidity

A

x

80
Q

what is the most concerning comorbidity of MFS?

A

aortic root dilation which can lead to life threatening aortic dissection

81
Q

complications

A

x

82
Q

what is a common complicatoin of marfan patients?

A

SCD due to intense excercise

83
Q

dx

A

x

84
Q

what diagnostic imaging of choice is needed prior to participation in sports?

A

Echocardiogram.

85
Q

management

A

x

86
Q

if aortic root disease and/or a fam hx of aortic dissection or SCD is present, patients are counseled on what?

A

avoid strenuous physical activity, with intense/contact sports (eg track, basketball, football) generally restricted

87
Q

Gigantism

A

x

88
Q

causes

A

x

89
Q

what is the cause of gigantism?

A

growth hormone secreting pituitary adenoma

90
Q

syx

A

x

91
Q

what are the syx of gigantism?

A

tall stature, glucose resistance

92
Q

PE

A

x

93
Q

what are typical exam findings?

A

coarse facial features, frontal bossing, bitemporal hemianopsia

94
Q

Retinoblastoma

A

x

95
Q

PE

A

x

96
Q

what is the physical exam finding of retinoblastoma?

A

leukocoria

97
Q

Homocystinuria

A

x

98
Q

genetics

A

x

99
Q

what is the genetics of homocystinuria?

A

autosomal recessive disorder

100
Q

syx

A

x

101
Q

what are the findings of homocystinuria?

A

marfinoid habitus, myopia, ectopia lentis

102
Q

findings

A

x

103
Q

what are findings unique to homocystinuria?

A

intellectual disability, venous thromboembolism, downward displaced lens

104
Q

Acute Rheumatic Fever

A

x

105
Q

cause

A

x

106
Q

what is the most common cause of Acute Rheumatic Fever?

A

group A strep infection

107
Q

syx

A

x

108
Q

what are the major manifestations of acute rheumatic fever?

A

migratory arthritis, carditis, or valvulitis, CNS involvement with sydenham chorea, erythema marginatum, and subcutaneous nodules.

109
Q

complications

A

x

110
Q

what is a common sequelae of rheumatic fever?

A

chronic MR (not usually acute MR)

111
Q

Digoxin Toxicity

A

x

112
Q

syx

A

x

113
Q

what are symptoms of digoxin Toxicity?

A

n/v, anorexia, fatigue, confusion, visual disturbances, and cardiac abnormalities

114
Q

cause

A

x

115
Q

what is the most likely cause of digoxin toxicity?

A

verapamil , quinidine, amiodarone, and spiranolactone

116
Q

pathophys

A

x

117
Q

how does verapmil cause digoxin toxicity?

A

inhibits renal tubular secretion of digoxin in almost 70-100% leading to increase in serum digoxin levels

118
Q

Infants of Diabetic Mother

A

x

119
Q

Complications

A

x

120
Q

what are the complications of maternal hyperglycemia in first trimester?

A

Congenital Heart Disease, Neural Tube Defecs, Small Left colon syndrome, spontaneous abortion

121
Q

what are the complications of maternal hyperglycemia in second and third trimester?

A

fetal hyperlycemia and hyperinsulinemia leading to polycythemia (increased metabolic demand, fetal hypoxemia, increased EPO and leading to PCV), organomegaly, neonatal hypoglycemia, shoulder dystocia (brachial plexopathy, clavicle fraacture, perinatal asphyxia), hypertrophic cardiomyopathy

122
Q

prevention

A

x

123
Q

how do you prevent complications of gestational diabetse?

A

strict glycemic control throughout pregnancy (ideal fasting blood glucose <=95 mg/dL)

124
Q

Hypertrophic Interventricular Septum

A

x

125
Q

syx

A

x

126
Q

what are the syx of hypertrophic interventricular septum?

A

asyx, but if left ventricular outfolow is obstructed you see CHF manifestations (respiratory distress, tachycardia, hypoxia, FTT)

127
Q

PE

A

x

128
Q

what are physical exam findings?

A

crackles, tachypnea, nasal flaring, retractions, heart murmur

129
Q

Dx

A

x

130
Q

what confirms the diagnosis?

A

Cardiomegaly on CXR, Echo

131
Q

pathophys

A

x

132
Q

what is the pathophys of hypertrophic interventricular septum?

A

insulin trigger glycogen synthesis and excess glycogen and fat are deposited within the myocardium, particularly the interventricular septrum. Increased oxidative stress of the interventricular septum may contribute to this selective thickening

133
Q

management

A

x

134
Q

what is the trx of transient hypertrophic cardiomyopathy if asyx?

A

no treatment is required, after birth infant not exposed to maternal hyperglycemia and plasma insulin levels normalize

135
Q

what is the trx of transient hypertrophic cardiomyopathy if syx?

A

propranolol and appropriate fluid management

136
Q

when is surgery a requirement in heart abnormalities?

A

tetralogy of fallot, transposition of the great arteries

137
Q

Ebstein Anomaly

A

x

138
Q

pathophys

A

x

139
Q

what is the pathophys of ebstein anomaly?

A

atrialization of the right ventricle due to a malformed tricuspid valve

140
Q

PE

A

x

141
Q

what are the physical exam findings of Ebstein Anomaly?

A

tricuspid regurg and cyanosis

142
Q

Hypoplastic Left Ventricle (hypoplastic left heart syndrome)

A

x

143
Q

timing

A

x

144
Q

when does hypoplastic left ventricle occur?

A

embryologic malformation that occurs early in the first trimester in infants of mothers with pregestational diabetes

145
Q

Neonatal Coarctation of the Aorta

A

x

146
Q

associations

A

x

147
Q

what disease is it associated with?

A

turners syndrome

148
Q

PE

A

x

149
Q

what are the physical exam findings of neonatal coarctation of the aorta?

A

weak femoral pulses and decreased postductal oxygen saturation

150
Q

dx

A

x

151
Q

what are the CXR findings of neonates with coarctation of the aorta?

A

aortic arch indentation (“3 sign”) is seen on radiography

152
Q

Congenital Pumonary Valve Stenosis

A

x

153
Q

pathophys

A

x

154
Q

what are the pathophys findings of congenital pulm valve stenosis?

A

obstruction of the pulm valve

155
Q

association

A

x

156
Q

what disease is it associated with?

A

Noonan Syndrome

157
Q

pathophys

A

x

158
Q

what does pulm valve stenosis result in?

A

right to left shunting

159
Q

Ductal Dependent Lesions

A

x

160
Q

types

A

x

161
Q

what are subtypes of ductal dependent lesions ?

A

hypoplastic left heart, transposition of the great arteries

162
Q

trx

A

x

163
Q

what are the treatments for ductal dependent lesions?

A

Prostaglandins, then await surgery

164
Q

Cardiac Catheterization

A

x

165
Q

complications

A

x

166
Q

what are complications of cardiac catheterizations?

A

hematoma, pseudoaneurysm, AV fistula

167
Q

Retroperitoneal Hematoma

A

x

168
Q

PE

A

x

169
Q

what are the physical exam findings ?

A

may or may not have a mass, no bruit, ipsilateral pain

170
Q

dx

A

x

171
Q

what is best way to dx retroperitoneal hematoma?

A

CT Abd and Pelvis

172
Q

Pseudoaneurysm

A

x

173
Q

risk

A

x

174
Q

what is the risk of pseudoaneurysm?

A

inadequate post procedural manual compression to achieve arterial hemostasis

175
Q

trx

A

x

176
Q

how do you treat small pseudoaneurysms?

A

U/S guided compression or thrombin injetion into the pseudoaneurysm cavity

177
Q

how do you treat large pseudoaneurysms?

A

surgical repair

178
Q

pathophys

A

x

179
Q

how does a pseudoaneurysm occur?

A

when bleeding from an inadequately sealed arterial puncture site remains confined wthin the periarterial connective tissue, resulting in a contained hematoma. Diastolic pressure equalizes between the artery adn the confined hematoma, resulting in blood flow in and out of the hematoma cavity with systole

180
Q

PE

A

x

181
Q

what are the physical exam findings ?

A

bulging, pulsatile mass, pain, swelling, and accenuated pulsation near the access point, systolic bruit

182
Q

Dx

A

x

183
Q

what is the best dx tool to confirm pseudoaneurysm?

A

U/S

184
Q

AV Fistula

A

x

185
Q

PE

A

x

186
Q

what are the physical exam findings?

A

no mass, continuous bruit, localized pain

187
Q

dx

A

x

188
Q

if U/S is negative, what is the next best diagnostic approach?

A

angiography

Cardiology (7 decks)

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