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CardioPulmonary Vascular Disease > Cardiopathies > Flashcards

Cardiopathies Flashcards

1
Q

What is the most common valve assoc. w/ valvular disease?

A

mitral valve

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2
Q

what is the most common valvulopathy?

A

bicuspid aortic valve

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3
Q

What are the most common causes of calcific aortic stenosis?

A

atherosclerosis, natural wear & tear assoc. w/ age

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4
Q

congenital bicuspid aortic valve is very prone to calcific deposits; it is caused by an incomplete commissural separation into 3 valves; what is this structure called?

A

raphe: this is most common location of the calcific deposits

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5
Q

what is the pathogenesis of congenial bicuspid aortic valve?

A

mutations of the NOTCH1 protein

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6
Q

List the cascade of physiological consequences assoc. w/ calcific aortic stenosis?

A

obstruction & narrowing - increases pressure gradient - increases LV pressure - leading to LVH - and eventually HF

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7
Q

what are conditions assoc. w/ Mitral valve prolapse (MVP)?

A

marfan syndrome, EDS, PKD, fragile X syndrome

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8
Q

Describe the morphology of MVP?

A

dilated LA sugesstive of long-standing valvular insufficiency & volume overload; dysplasia of the fibrosa & spongiosa layers caused by decreased integrity of supporting collagens & proteoglycans

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9
Q

Mitral annular calcification is commonly seen in what populations?

A

women > 60 yrs.

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10
Q

What is the only cause of acquired mitral stenosis?

A

rheumatic heart disease

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11
Q

Describe the morphology of MAC?

A

stony hard ulcerated nodules at the base of the mitral leaflets

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12
Q

Describe the pathogenesis of ARF?

A

immunological response to strep A. antigens that cross-react w/ host proteins

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13
Q

ARF is most common in what pt. population & how long after the infection does it appear?

A

ped. pts. b/t 5-15 yrs.; typically appears 10 days to 6-weeks after infection

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14
Q

what dermatological findings are indicative of ARF?

A

subcutaneous nodules on bony prominences; sydenham chorea (involuntary dancing); erythema marginatum

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15
Q

Describe the different morphological features of ARF?

A

diffuse inflammation in all 3 layers of the heart: pericarditis, myocarditis, endocarditis; aschoff bodies composed of T & B lymphocytes and activated macrophages called antischlow cells; caterpillar like cells

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16
Q

What is the main valve involved in chronic RHD

A

mitral valve

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17
Q

Acute infective endocarditis is commonly caused by which pahtogen?

A

Staphy. A.; worse prognosis

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18
Q

Subacute IE is commonly assoc. w/ what pathogen?

A

viridans streptococci; better prognosis

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19
Q

What is in almost all cases, going to be found in the PE of a pt. w/ IE?

A

heart murmurs

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20
Q

What pathogens are pts. most susceptible to 1 to 2 months after placement of a prosthetic valve?

A

Staphy. A. & epidermidis

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21
Q

What pathogens are pts. most susceptible 1 year after placement of a prosthetic valve?

A

streptococci

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22
Q

what are the most common sites for IE?

A

aortic & mitral valves

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23
Q

Describe the morphologies of AIE & SIE?

A

SIE: large friable vegetations; AIE: extensive cuspal destruction and ring abscess

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24
Q

Describe the different manifestations seen w/ post-IE migratory vegetation

A

janeway lesions: erythematous lesions seen in terminal vessels of the palms; Roth spots: orbital hemorrhage w/ pale center; nail bed hemorrhages; osler nodes: develop in the pulp of interphalangeal joints

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25
Q

Describe the Etiology of nonbacterial thrombotic endocarditis.

A

Prerequisites include mucinous adenocarcinomas, sepsis, hyper coagulopathies, endocardial trauma

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26
Q

Describe the pathogenesis of libman-sacks endocarditis

A

specifically seen in pts. w/ SLE; vegetations seen on valve surface, chordae, or along the endocardium; vegetation caused by immune complex deposition w/ activation of complement

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27
Q

Describe the morphology of Libman-Sacks endocarditis.

A

intense valvulitis and fibrinoid necrosis; fibrosis, scarring

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28
Q

what is the qualitative definition of HF?

A

heart unable to pump blood at a rate sufficient to meet metabolic demands

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29
Q

What are the classifications of left-side induced HF?

A

HFrEF (systolic) HF w/ reduced EF; HFpEF (diastolic): HF w/ preserved EF

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30
Q

What are the criteria for Stage A HF:

A

pts. w/ assoc. risk factors of CVD but no h/o HF specifically

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31
Q

what is the criteria for Stage B HF:

A

pts. w/o h/o HF but w/ evidence of a structural heart disease

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32
Q

what is the criteria for stage C HF:

A

pts. presenting w/ symptoms of HF and h/o similar signs

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33
Q

at what point does HF progress to Stage D?

A

HF symptoms that interfere w/ daily with recurrent hospitalizations

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34
Q

Define the 4 stages of NYHA classes for HF?

A

Class 1: asymptomatic; Class 2: mild symptoms & comfortable at rest; Class 3: only comfortable at rest w/ marked decrease in physical activity; stage IV: discomfort even at rest

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35
Q

What are diseases that cause HF?

A

amyloidosis & sarcoidosis

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36
Q

Overstimulation of what neurohormonal pathways put pts. at increased risk for HF?

A

Adrenergic nervous system; RAAS; ADH

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37
Q

What would you expect to find on CXR of a pt. presenting w/ left-sided HF?

A

congestion in the pulmonary veins assoc. w/ orthopnea

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38
Q

Left-sided HF is also referred to as what?

A

forward heart failure

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39
Q

Right sided HF is also referred to as what?

A

backward HF3

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40
Q

Right-sided HF is usually always secondary to Left-sided HF; What are its clinical manafestations?

A

JVD; hepatomegaly; peripheral edema

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41
Q

Besides Left-sided HF, what are some of the other causes of right-sided HF?

A

pulmonary parenchymal disease including COPD, Interstitial lung disease (eg. sarcoidosis) or chronic lung infections; pulmonary vascular diseases including PE and PHTN; cardiac causes include pulmonic valve stenosis & right ventricular infarction

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42
Q

What are biomarkers for indication of HF and not other pulmonary disease?

A

BNP & NT proBNP

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43
Q

what is the significance of BNP in the context of HF?

A

BNP is released from ventricular myocytes when ventricular DBP is raised

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44
Q

What are important factors to consider in the pt’s. history when testing BNP levels?

A

BNP is naturally lower in obese pts.; And elevated in pts. w/ anemia, renal failure, women, & elderly pts.

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45
Q

what are some distinctions that can be made to determine if it is RVH or LVH?

A

RVH: amplified QRS complex; both can have inverted T-waves

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46
Q

What can be seen on the CXR of a pt. w/ HF?

A

kerley lines: interstitial edema

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47
Q

What is the most common acute decompensated HF?

A

warm & wet

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48
Q

What types of ADHF are assoc. w/ orthopnea, elevated JVP, S3 gallops, & edema?

A

warm & wet; Cold & wet

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49
Q

Which types of ADHF are not assoc. w/ orthopnea, elevated JVP, S3 gallops, & edema?

A

warm & dry; Cold & dry

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50
Q

which types of ADHF are assoc. w/ cool extremities & hypotension?

A

Cold & Dry; Cold & wet

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51
Q

which types of ADHF are not assoc. w/ cool extremities & hypotension?

A

warm & dry; warm & wet

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52
Q

What would be the most appropriate plan for warm & dry ADHF?

A

optimization of oral medications

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53
Q

What would be the most appropriate plan for warm & wet ADHF?

A

pts. w/ this usually present w/ hypervolemic shock so the best plan would be to administer IV diuretics and vasodilators

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54
Q

What would be the most appropriate plan for cold & dry ADHF?

A

pts. typically present w/ hypoperfusion: treatment for these would be IV fluid, dobutamine, or Inotrope

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55
Q

What would be the most appropriate plan for cold & wet ADHF?

A

these pts. present w/ both hypoperfusion & hypervolemia: IV diuretics, dobutamine, or inotrope

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56
Q

What are the treatment recommendations for pts. w/ HFpEF assoc. w/ preserved LVEF at > 50%?

A

diuretics; SGLT2i, ARNi, MRA, ARB

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57
Q

What are the treatment recommendations for pts. w/ HFmrEF assoc. w/ mildly reduced LVEF at 41-49%?

A

same as for HFpEF with the addition of ACEi, ARNI, & BBs for HFrEF

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58
Q

what are the 3 main types of cardiomyopathies?

A

Dilated (DCM); Hypertrophic (HCM); Restrictive (RCM)

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59
Q

What are the main effects of DCM?

A

Frank-Starling forces:
Increased myofiber stretch: Increased end diastolic volume, increased inotropy & increased SV
Neurohormonal activation: decreased CO stimulates SNS to increase HR & inotropy leading to increased CO
RAAS Activation: decreased CO due to decreased renal perfusion will increase renin release; this will increase systemic vascular resistance & increased intravascular volume

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60
Q

Increased Angiotensin II induced by DCM will result in what physiological consequences?

A

ANT II increases SVR which will increase afterload; when the afterload becomes toO high the LV cannot pump against the increased resistance leading to HF

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61
Q

Increased Aldosterone induced by DCM will result in what physiological consequences?

A

Aldosterone will increase intravascular volume leading to pulmonary & systemic congestion

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62
Q

chronic elevation of aldosterone and ANT II will eventually cause what?

A

cardiac remodeling & fibrosis

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63
Q

What PE findings indicate DCM?

A

low arterial pressure, cool extremities, pulmonary venous congestion (crackles), left & upward displacement of PMI assoc. w/ enlarged heart; S3

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64
Q

If the RV were to fail, what would be possible PE findings?

A

JVD, hepatomegaly, ascites, peripheral edema

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65
Q

What viruses can cause DCM?

A

coxsackievirus A & B; adenovirus, CMV, parvovirus B19

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66
Q

Chronic use of what substances can cause DCM?

A

chronic alcohol ingestion; chronic cocaine use; chemotherapeutic agents

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67
Q

What medical conditions are assoc. w/ DCM?

A

sarcoidosis; hemochromatosis; muscular dystrophy

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68
Q

List genetic causes of DCM.

A

TTN gene mutation: reduces cytoskeleton integrity; X-linked DCM: assoc. w/ MD; Mitochondrial gene deletions: problems w/ FA oxidation & oxidative phosphorylation

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69
Q

What parasitic infections can cause DCM?

A

Trypanosoma cruzi (Chagas Disease); Trichinella spiralis; Toxoplasma gondii; borrealia burgdorferi; corynebacterium diphtheriae

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70
Q

LVH is associated w/ what myocardiopathy?

A

Hypertrophic cardiomyopathy (HCM)

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71
Q

What physiological consequences are assoc. w/ HCM w/o obstruction?

A

reduced LV chamber size; decreased LV compliance

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72
Q

Decreased LV compliance will result in what physiological consequences?

A

decrease in both SV & CO; increased DBP in LV which will cause retrograde blood flow back up into the LA & pulmonary veins

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73
Q

What is the pathophysiology of HCM w/ obstruction?

A

dysfunction of the Mitral valve leaflets leading to partial blockage of blood flow through the LV and general diastolic dysfunction; results in septal hypertrophy as well and mitral regurgitation may also be present

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74
Q

What are the physiological consequences of having a hypertrophic ventricle?

A

increased wall stress & O2 demand can lead to angina & focal ischemia; Increased ventricular pressure can result in mitral regurgitation which will further elevate LA & PV pressures

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75
Q

What are the physiological consequences of having a smaller chamber of the LV?

A

a decrease in this space will naturally move the mitral leaflets & septum closer together resulting in reduced venous return, volume depletion

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76
Q

What are the physiological consequences of having a larger chamber of the LV?

A

mitral leaflet & septum will become more separated resulting in increased venous return, volume increase

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77
Q

What are some distinctive histological features seen w/ HCM?

A

ventricular cavity has a “banana like” configuration; haphazard arrangements of myocyte bundles w/ myofibril disarray w/ interstitial fibrosis

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78
Q

What are some of the known mutations that cause Primary HCM that you need to know?

A

beta-myosin heavy chain (most common); cardiac troponins; myosin binding protein C; alpha-tropomyosin; ALL OF THESE PROTEINS MAKE UP THE SARCOMERE

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79
Q

What insults result from mutated proteins within the sacromere?

A

contractile impairment increaseS myocyte stress; this will result in compensatory hypertrophy, secretion of GF (leading to myofiber disarray), & fibroblast proliferation (interstitial fibrosis)

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80
Q

What are possible PE findings that would be found for HCM?

A

S4; if outflow obstruction is present: harsh systolic ejection murmur at left lower sternal border; crescendo, de-crescendo

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81
Q

Describe the pathophysiology of ARVC (AKA arrhythmogenic RV Dysplasia)

A

genetic: point mutation deletions in genes that encode for desmosomal junctional proteins; loss of myocytes and myocyte replacement w/ fatty tissue and severe thinning of RV wall

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82
Q

What are the symptoms of Naxos syndrome?

A

ARVC + hyperkeratosis of plantar & palmar surfaces; assoc. w/ mutations in plakoglobin (desmosome-associated protein)

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83
Q

What are the 4 most common types of amyloidosis?

A

light chain multiple myeloma, diseases of chronic inflammation (type Ab2M assoc. w/ dialysis complications), hereditary & senile are assoc. w/ transthyretin amyloid overproduction

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84
Q

What are distinctive features of the MM type of amyloidosis?

A

glossomegaly, periorbital purpura

85
Q

What are findings assoc. w/ wild-type ATTR amyloidosis?

A

bilateral carpal tunnel syndrome, lumbar spinal stenosis, biceps tendon rutures, small fiber neuropathies, autonomic dysfunction

86
Q

what is the main organ involved in senile amyloidosis?

A

the heart

87
Q

what are histological findings of cardiac amyloidosis?

A

gross appearance: pale & pallor discoloration; hyaline eosinophilic amyloid plaque deposits in several different layers of the heart

88
Q

What is the distinctive histochemistry of cardiac amyloidosis?

A

congo red stain shows salmon pink deposits w/ apple green birefringence upon polarization microscopy

89
Q

What is the qualitative definition of restrictive cardiomyopathy (RCM)?

A

decrease in ventricular compliance resulting in impaired ventricular filling during diastole; abnormally rigid but not thickened

90
Q

What are clinical findings of CHF & RCM?

A

decreased CO, JVD, peripheral edema, ascites, large liver, pulmonary rales; on CXR: normal-sized heart w/ pulmonary congestion

91
Q

What is the clinical significance of tropical endomyocardial fibrosis?

A

most prevalent in children & young adults in Africa & tropical regions; very rare in North America; Characteristics: fibrosis of ventricular endocardium extending from apex to AV valves; pathogenesis: unknown but thought to be due to loeffler endocarditis (eosinophilic endomyocardial fibrosis)

92
Q

What are the histological findings of Loeffler endomyocarditis?

A

type of RCM; large mural thrombi, increased blood eosinophils in periphery & multiple organs

93
Q

What disease is loeffler endomyocarditis assoc. with?

A

chronic myeloproliferative disorders of PDGFR alpha/beta genes

94
Q

What do you need to know about endocardial fibroeastosis?

A

fibroelastic thickening usually of the mural LV endocardium; usually presents within first 2 yrs. of life; assoc. w/ aortic valve obstruction & congenital cardiac anomalies; mutation of tafazzin which affects mitochondrial inner membrane integrity

95
Q

What is happening during an S2 sound and where can you hear it best?

A

occurs at beginning of diastole and closure of semilunar valves; louder at base

96
Q

What is happening during an S1 sound and where can you hear it best?

A

occurs at beginning of systole: closure of AV valves; louder at apex

97
Q

describe the process of physiological splitting of S2?

A

splits w/ inspiration: decreased intrathoracic pressure, increased venous return, increased Blood volume in RV; S2 splits into A2 & P2; A2 is heard before P2 and best heard in pulmonic area

98
Q

What CVDs can cause wide-splitting of the A2 & P2 sounds?

A

PHTN; RBBB; pulmonary stenosis

99
Q

What CVDs cause fixed splitting of A2 & P2?

A

atrial septal defects

100
Q

what CVDs cause paradoxical (reversed splitting) of A2 & P2?

A

aortic stenosis; LBBB

101
Q

What are the characteristics of grade 1 murmurs?

A

very faint unusual sounds

102
Q

What are the characteristics of grade 2 murmurs?

A

quiet but heard very clearly w/ stethoscope placed on chest

103
Q

What are the characteristics of grade 3 murmurs?

A

moderately loud

104
Q

What are the characteristics of grade 4 murmurs?

A

loud w palpable thrill

105
Q

What are the characteristics of grade 5 murmurs?

A

grade 4 + heard w/ stethoscope is only partially placed on the chest

106
Q

What are the characteristics of grade 6 murmurs?

A

grade 4 + heard w/ stethoscope entirely off the chest

107
Q

what kind of heart murmur can be heard at the aortic area?

A

systolic murmur

108
Q

What are the main causes of systolic murmurs?

A

aortic stenosis, aortic valve sclerosis

109
Q

what kind of heart murmur can be heard at the pulmonary area?

A

systolic ejection murmur

110
Q

what are common causes of systolic ejection murmurs?

A

pulmonic stenosis; atrial septal defect

111
Q

what kind of heart murmur can be heard at the tricuspid area?

A

holosystolic & diastolic murmurs

112
Q

what diseases are assoc. w/ holosystolic murmurs?

A

holosystolic: tricuspid regurgitation, ventricular septal defect; tricuspid stenosis (diastolic)

113
Q

what kind of heart murmur can be heard at the mitral area?

A

holosystolic, systolic, & diastolic murmurs

114
Q

what cardiac dysfunctions are assoc. w/ murmurs heard at the mitral area?

A

holosystolic: mitral regurgitation; systolic: mitral valve prolapse; diastolic: mitral stenosis

115
Q

what kind of heart murmur can be heard along the left sternal border?

A

diastolic & systolic murmurs

116
Q

what cardiac dysfunctions are assoc. w/ murmurs heard along the left sternal border?

A

diastolic: aortic or pulmonic regurgitation; systolic: HCM

117
Q

Right-sided murmurs can be heard the best during which part of respiration?

A

Inspiration due to increased RV preload

118
Q

Left-sided murmurs can be heard the best during which part of respiration?

A

expiration where LV preload will be greatest

119
Q

Standing reduces the sound of all murmurs except……..

A

MVP & HOCM

120
Q

leg raising & squating worsen most murmurs except……..

A

MVP & HOCM

121
Q

Hand grip makes what kind of murmurs heard more & herad less?

A

AFFECTS L-SIDED MURMURS ONLY: worse: mitral & aortic regurgitation, mitral stenosis; Improve: aortic stenosis

122
Q

List the clinical presentations of aortic stenosis?

A

crescendo-decrescendo murmur; sound intensity increased when preload is decreased and decreased when afterload is increased; syncope, angina, & dyspnea on exertion; radiates to the carotids

123
Q

List the clinical presentations of pulmonic stenosis?

A

c-d murmur; radiates to left shoulder & neck; increasing in intensity w/ inspiration; wide splitting of S2; causes are usually congenital (tetralogy of Fallout & congenital rubella)

124
Q

List the clinical presentations of a Mitral regurgitation?

A

blowing; radiates to the left axilla; increased intensity w/ increase in both pre & after loads; Causes: post MI (acute papillary muscle rupture); MVP; infective endocarditis (RHD); LV dilation secondary to HF

125
Q

List the clinical presentations of MVP?

A

c-murmur; increased intensity w/ decreased preload; causes: weakening of valve leaflets and/or chordae tendineae w/ leaflets ballooning into the LA; marfan syndrome; myxomatous degeneration

126
Q

List the clinical presentations of tricuspid regurgitation?

A

blowing; increased intensity w/ inspiration; causes: PHTN, ebstein’s anomaly, RHD

127
Q

List the clinical presentations of aortic regurgitation?

A

blowing w/ d murmur; radiates to apex; increased intensity with increased after & pre load; water hammer pulse, widened pulse pressure; causes: congenital bicuspid aortic valve, aortic root dilation (aneurysm)

128
Q

List the clinical presentations of pulmonic regurgitation?

A

blowing w/ d murmur; radiates along left sternal border; increased intensity w/ inspiration; caused mainly by PHTN

129
Q

List the clinical presentations of mitral stenosis?

A

NON-RADIATING d murmur w/ opening snap caused by abrupt halt of stiffened leaflets; increased intensity upon expiration & left lateral decubitus; causes: chronic RHD

130
Q

List the clinical presentations of Tricuspid stenosis?

A

NO-RADIATING d murmur w/ opening snap; increased intensity w/ inspiration

131
Q

Why is RA pressure > LA pressure in a developing fetus?

A

lungs are not being used

132
Q

neural crest & endocardial cells become what adult structures?

A

ascending aorta & pulmonary trunk

133
Q

what is the purpose of the ductus venosus?

A

bypasses liver (umbilical vein to IVC); umbilical vein supplies O2 & nutrients to the liver

134
Q

what is the purpose of the foramen ovale:

A

bypasses lungs (RA to LA)

135
Q

What is the purpose of the ductus arteriosus?

A

bypasses lungs (PA to aorta)

136
Q

What physiological changes happen to the lungs shortly after birth?

A

lungs expand driving down pulmonary vascular resistance & pressure to increase pulmonary blood flow which will subsequently increase LA pressure

137
Q

The ductus venosus become what adult structure?

A

ligamentum venosum

138
Q

What causes the ductus venosus to close?

A

clamping of umbilical cord terminates its blood flow leading to closure

139
Q

The foramen ovale becomes what adult strucutre?

A

fossa ovalis

140
Q

what causes the foramen ovale to close?

A

with increasing LA pressure will cause interatrial septums to fuse

141
Q

What adult structure does the ductus arteriosus become?

A

ligamentum arteriosum

142
Q

what causes the ductus arteriosus to close?

A

increased O2, decreased PGs

143
Q

What happens w/ persistent truncus arteriosus?

A

the aorticopulmonary septum fails to separate the Aorta & PA

144
Q

What are the clinical hallmarks of DiGeorge Syndrome?

A

cardiac trunk anomaly (typically tetralogy of fallot or PTA), hypocalcemia (SZ, tremors); absent thymus (immune defects), low set ears, cleft palate, Ch22q11.2 deletion

145
Q

Transposition of the great vessels results in what?

A

PA is connected to LV and Aorta is connected to RV; caused by malsprial rotation of aorticopulmonary septum

146
Q

What is associ. w/ transposition of the great vessles?

A

Diabetic mom; CXR: narrow mediastinum w/ globular heart

147
Q

What happens in tricuspid valve atresia?

A

absence of tricuspid valve and a RA/RV septum instead leading to right atrial dilation

148
Q

What is the pathophysiology of Tetralogy of Fallot?

A

anterosuperior displacement of the infundibular septum

149
Q

What kind of defects can be present in Tetralogy of fallot?

A

pulmonary artery stenosis leading to RVH; overriding aorta (shifts b/t right & left sides of the heart; ventricular septal defect

150
Q

what are symptoms of tetralogy of fallot?

A

exacerbation of RV outflow obstruction during exercise, crying & stress causing R to L shunt and cyanosis; relieved by squatting due to increased SVR and reduced RL shunt, increased pulmonary BF & increased oxygenation

151
Q

what are the most common causes of tetralogy of fallot?

A

alcohol exposure in utero, maternal rubella, DeGeorgie syndrome; Down syndrome

152
Q

What medications can be given to treat tetralogy of fallot?

A

increased SVR w/ phenylephrine & PG E if PDA is also present

153
Q

What happens in total anomalous pulmonary venous returen?

A

pulmonary veins drain into right heart circulation depriving left side of the heart of oxygen

153
Q

what is the pathophysiology of hypoplastic left heart syndrome?

A

nonfunctional left side of the heart

154
Q

What is an Ebstein anomaly?

A

Displacement of Tricuspid leaflets into RV causing RV pressure to exceed LV pressure leading to a right to left shunt

155
Q

what teratogen is assoc. w/ ebstein anomaly?

A

lithium exposure in utero

156
Q

What is the clinical significance of a Stills murmur?

A

usually asymptomatic and non-pathologic; murmur sounds musical and vibratory and increases in intensity while laying down

157
Q

What is a venous hum?

A

disappears when supine; assoc. w/ venous return to the heart

158
Q

What are the clinical hallmarks of ASDs?

A

LR shunt; acyanotic in most cases; loud S1 w/ fixed split of S2; assoc. w/ fetal alcohol syndrome

159
Q

What are the clinical hallmarks of VSD?

A

LR shunt; holsystolic murmur; assoc. w/ Down syndrome

160
Q

What is the pathogenesis of Eisenmenger Syndrome?

A

result of uncorrected LR shunt over time; volume overload in right side of heart with increased R sided pressure; reversal to a RL shunt & cyanosis

161
Q

complete atrioventricular septal defects are most assoc. w/ what?

A

Down syndrome

162
Q

AV canal & endocardial cushion defects if not corrected can lead to what?

A

eisenmenger syndrome

163
Q

Patent Ductus Arteriosus results in what?

A

LR shunt; assoc. w/ congenital rubella

164
Q

what medication can be given to correct PDA?

A

indomethacin (antiPG agent)

165
Q

Coarctation of the Aorta can result in what LE symtoms?

A

Claudication; hypotension; absent femoral pulse; cyanosis

166
Q

coarctation of the aorta can result in what symptoms of the upper body?

A

berry aneurysm; HF; rib-notching

167
Q

coarctation of the aorta is assoc. w/ what congenital disease?

A

bicuspid aortic valve, Turner’s syndrome

168
Q

Long QT syndrome in infants is assoc. w/ what syndrome?

A

Sudden Infant death

169
Q

congential 3rd degree Heart blocks are assoc. w/ what maternal conditions?

A

SLE; sjogren syndrome; autoimmune injury to fetus by IgG; Anti-SSA/Ro, anti SSB/La

170
Q

Define vasovagal syncope?

A

interruption of normal central vasomotor tone leading to arteriolar vasodilation, hypotension, & decreased cerebral perfusion pressure

171
Q

Vasovagal syncope is most common in what situations?

A

fasting, anxiety, fright, surprise

172
Q

Define cardiac syncope?

A

heart lesions that cause obstruction of L-side BF

173
Q

what is cardiac syncope commonly assoc. with?

A

aortic stenosis

174
Q

what is assoc. w/ arrhythmogenic syncope?

A

long QT syndrome

175
Q

Define orthostatic syncope?

A

failure of vascular compensatory responses to postural changes leading to decrease in BP & cerebral perfusion

176
Q

orthostatic syncope is most commonly assoc. w/ what?

A

dehydration

177
Q

Why is DCM assoc. w/ decreased contractility?

A

myocyte atrophy of LV

178
Q

What prescribed drug is known to cause DCM?

A

Doxorubicin & extasy

179
Q

HCM is usually asymptomatic so why is it still a serious condition?

A

HCM is the most common cause of sudden cardiac death typically occurring w/ sport induced arrhythmia

180
Q

what are the differences b/t DCM, HCM, & RCM?

A

HCM & RCM are diastolic dysfunctions; DCM is a systolic dysfunction; RCM & DCM have similar features except for RCM, ventricular thickness & volume is normal

181
Q

kawasaki disease is more prevelant in ped pts. of what race?

A

asian

182
Q

What are lab findings of suspected kawasaki disease?

A

elevated WBC, anemia, thrombocytosis

183
Q

What occurs for phase 1 of kawasaki disease?

A

first 2 weeks; acute vasculitis of coronary arteries

184
Q

What are major concerns for stage 2 kawasaki disease?

A

2-4 wk. after onset; persistent vasculitis increases risk of aneurysms; thrombosis in coronary arteries

185
Q

What should be a concern for stage 3 kawasaki disease?

A

4-8 wk. after onset; inflammation subsides but aneurysms persist

186
Q

What happens after 8 weeks from onset of kawasaki disease?

A

stage 4: scar formation, calcification of arteries w/ stenosis & myocardial fibrosis

187
Q

What are buzz words for different heart defects?

A

Transposition of vessels: egg on a string; Tetralogy of Fallot: Boot Shaped; TAPVR: snowman

188
Q

Congenital bicuspid aortic valve is most commonly assoc. w/ what type of murmurs?

A

Aortic stenosis & regurgitation

189
Q

RHD & chronic RHD as most commonly assoc. w/ what types of murmurs?

A

Mitral regurgitation & stenosis

190
Q

Down syndrome is most commonly assoc. w/ what congenital heart defects and what are some clinical hallmarks of down syndrome?

A

VSD, ASD; upslanting palpebrate, brachydactyly, single palmar creases

191
Q

What are some of the clinical hallmarks of Edwards syndrome?

A

rocker-bottom feet

192
Q

what are some of the clinical hallmarks of patau syndrome?

A

holoprosencephaly, polydactyly, midline cleftings, omphalocele

193
Q

what congenital heart defect is most commonly assoc. w/ turner syndrome?

A

coarctation of aorta, bicuspid AV

194
Q

DiGeorge syndrome is most commonly assoc. w/ what congenital heart defect and what are some clinical hallmarks?

A

80% cases are assoc. w/ tetralogy of fallot; other clinical manifestations: thymic hypoplasia, clefting & hypocalcemia

195
Q

What is the pathogenesis of Williams syndrome and what are common clinical manafestations?

A

supravalvular aortic stenosis for 80% of cases; cocktail party personality; hypercalcemia; 7q11.23 microdeletion

196
Q

What is the most common mutation assoc. w/ noonan syndrome?

A

PTPN11; autosomal dominant

197
Q

what are the most common clinical manifestations of noonan syndrome?

A

pulmonary valve stenosis & HCM; low set ears, downslanting eyes w/ ptosis, triangular face

198
Q

What is the pathogenesis of CHARGE syndrome and what are common clinical hallmarks?

A

autosomal dominant CHD7 gene mutations; atresia choanae, retarded growth & development, genital & ear defects

199
Q

What is the RR for a woman w/ the 22q11.2 microdeletion?

A

50%

200
Q

A pediatric pt. w/ disproportionately long limbs, scoliosis and skin striae presents to the clinic. What is the most likely diagonosis?

A

marfan syndrome

201
Q

How would your marfanoid DDx change if a bifid uvula was present?

A

most likely cause would be loeys-dietz syndrome

202
Q

How would your marfanoid DDx change if a mental impairment was present?

A

most likely: homocystinuria

203
Q

How would your marfanoid DDx change if a congenital joint contractures were also noted?

A

Beal’s syndrome: mutation of fibrillin 2

204
Q

What drug can be given for a marfan pt. to decrease aortic wall stress?

A

BBs

205
Q

what drug can be prescribed to a marfan pt. to slow and prevent progression of HD?

A

losartan (ARB): inhibition of TGF-B

206
Q

Vascular EDS is assoc. w/ a defect of which collagen type?

A

III

207
Q

Genetic HCM is assoc. w/ defects in what type of proteins and list examples?

A

sarcomere proteins; ex. include noonan, pompe, & Friedreich’s ataxia

208
Q

Genetic acquired DCM is assoc. w/ defects in what proteins?

A

cytoskeletal protein genes

CardioPulmonary Vascular Disease (7 decks)

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