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Cardiology > Cardiovascular Development > Flashcards

Cardiovascular Development Flashcards

1
Q

How many live births have congenital heart disease?

A

-~1% -most common congenital disorder

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2
Q

3 rationales fro studying CV development

A
  1. inherent scientific knowledge 2. understanding the pathogenesis of CHD: dx and prognostic tool development, develop therapies 3. hypothesis: mlc pathways important for CV development are recapitulated during CV disease pathogenesis
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3
Q

5 major processes in cardiac development

A
  1. normal cardiac morphogensis 2. left-right patterning 3. valve formation 4. angiogenesis vs vasculogensis 5. contribution of extra-cardiac cells to heart: epicardium and NC
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4
Q

6 parts of normal cardiac morphogenesis

A

-myocardial specification -formation of linear heart tube -looping -septation -patterning of great vessels -circulatory changes at birth

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5
Q

where is the cardiogenic (heart-forming) region located in embryo? What is this called?

A

-initially located at the anterior rim of the embryonic disc very early in development -called the cardiac cresent: epithelial layer of cardiac MULTIpotent progenitor cells that make up myocardium, endocardium, pericardium

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6
Q

As the embryo grows, the developing heart assumes a position where? Then what happens?

A

-ventral to forming forebrain and foregut; as 2 side tubes -heart progenitors migrate ventrally and medially to form a linear heart tube; attached to rest of embryo by dorsal mesocardium

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7
Q

3 events happening at linear heart tube phase

A
  1. heart begins to beat: intrinsic pacemaker activity (caudal >rostral) 2. blood flow commences: single circulation in series caud to rostral (remember atria on bottom of linear tube) 3.chamber specification due to molecular determination
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8
Q

Atrium location within linear tube

A

-caudal end! under LV and RV

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9
Q

Chamber-specific transcriptional programs of linear heart tube

A

-dHAND is RV and eHAND is LV -hey1 is atria and OFT and hey2 is ventricles

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10
Q

T/F: Advanced cariac morphogenesis does not require midline fusion.

A

-true

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11
Q

Secondary Heart Field

A

-large parts of RV and OT derived from secondary field of cardiac precursors -these cells migrate into OT and differentiate into muscle from pharynx -diff gene expressions of these cells within cardiac crescent

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12
Q

Secondary Heart Field is associated with ______ and ______ signaling.

A

-LiCl (Wnt agonist) -Wnt signalling

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13
Q

Secondary Heart Field defects are attributable to ______ variants in 11-18% cases.

A

-Islet 1 variants

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14
Q

3 events occurring during cardiac looping

A

-linear heart tube bends to right and anteriorly, thought to be driven by regional differences in myocardial growth rate–first sign of assymetry in heart!! -begin septation: endocardial cushions (OFT and AV canal) and interventricular septum -myocardial trabeculation

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15
Q

2 end results of cardiac looping

A

-atria assume a more rostral and posterior orientation -advanced regional specification: bulbis cordis (conus cordis becomes cardiac OFT, truncus arteriosus becomes PA and Ao), AV canal (maturation of AV canal and formation of endocardial cushions)

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16
Q

4 septation events

A

-AV canal septation -Interventricular septation -Interatrial septation -outflow tract septation (TA and CC)

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17
Q

steps of atrial septation

A
  1. septum primum grows from dorsal wall of atrium toward AV cushions 2. initially incomplete (passive): ostium primum= residual connection 3. eventually completely (actively) closed by fushion with cushions 4. new opening in septum primum occurs= ostium secundum (smaller performations up higher) 5. new septum = septum secundum grows from superior atrial wall 6. septum secundum passively closes the ostium secundum
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18
Q

In embryonic circulation, ostium secundum allows for flow from right to left atrium (little pulm circulation). In the adult, septum secundum closes the ostium secundum. Ostium secundum later ______ closes in most, but not all people. What is a variant of this called when the ostium secundum does not close?

A

-actively -Patent Foramen Ovale: 20-25% of people and potential stroke risk

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19
Q

Ostium Secundum Atrial Septal Defect

A

-most common type of ASD (larger, constantly lets blood thru) -occurs in center of the septum between LA and RA -due to incomplete formation of septum secundum or incomplete active closure of ostium secundum -variant of this type of ASD is PFO and is very small!

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20
Q

Ostium Primum ASD

A

-2nd most common ASD -located in lower portion of atrial septum -due to incomplete active closure of ostrium primum -often associated with a cleft or slit-like defect in anterior leaflets in MV

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21
Q

-Ostium Primum cause and association

A

-due to incomplete active closure of ostrium primum -often assoc with cleft or slit-like defect in anterior leaflet of MV

22
Q

Sinus Venosus ASD

A

-least common of ASD -located in upper portion of atrial septum -due to defect in formation of septum primum -often has an abnormal pulmonary vein connection associated with in -one of PVs abnormally connect to the RA instead of the LA (anomalous PV)

23
Q

-Location of ASDs in atrial septum from top to bottom

A
  1. top: sinus venosus ASD 2. middle: ostium secundum ASD 3. bottom: Ostium primum ASD
24
Q

Rank 3 main ASD in order of how common they are

A

-Ostium secundum is most common -Ostium primum ASD -Sinus venosus ASD

25
Q

Nkx2.5

A

-homeobox gene expressed as soon as heart muscle precursors are specified (paraxial mesoderm) -required from dorsal aorta in flies, looping in mice, and heterozygous mutations in humans with CHD

26
Q

______ is expressed prior to formation of the midline cardiac tube.

A

-Nkx2.5

27
Q

Nkx2.5 mutations in flies, mice, humans

A

-flies: no dorsal aorta -mice: fatal looping defect -humans: conduction defects (potential link to A. fib/heart block), ASD, tetralogy of fallot

28
Q

Patterning of the great vessels

A

-initially, 5 pairs of symmetric aortic arch arteries -some regress while others grow, resulting in the mature asymmetric vascular pattern -signals from pharyngeal endoderm and migrating neural crest are required for this remodeling

29
Q

What is required for the correct remodeling of the great vessels?

A

-signals from pharyngeal endoderm and migrating neural crest

30
Q

Other issues associated with neural crest cell migration

A

-skin discoloration (melanocytes), parathyroid and thymus issues, facial deformities

31
Q

Abnormal remodeling of branches may lead to interruption of the __________.

A

-aortic arch

32
Q

DiGeorge Syndrome

A

-most common human chromosome deletion syndrome -del 22q11 -CHD, parathyroid deficiency, thymus defect -phenotype similar to animal models of NC ablation -many children with CHD along and nothing else have this deletion

33
Q

An important gene found within the region deleted within DiGeorge?

A

-Tbx1 -deletion of 22q11 in DiGeorge

34
Q

3 main events that are changes in circulatory system at birth

A

-closure of ductus arteriosus -closure of ductus venosus -closure of foramen ovale

35
Q

Abnormalities of L-R axis

A

-mirror image: dextrocardia -discordance between organs: heterotaxy

36
Q

L-R axis is established very early, as seen by ____________.

A

-asymmetric expression of signalling mlcs at primitive streak stage -persistence of this program results in asymmetric expression in the developing heart (eHAND vs dHAND)

37
Q

Defects in sidedness can be due to defects in what process? What in particular is thought to be an etiology of this?

A

-looping -nodal ciliar abnormalities early in development–reminiscent of Kartagener’s which has dextrocardia and immotile cilia

38
Q

Valve formation

A

-endothelial cells migrate into “cardiac jelly” (ECM between initial 2 layers of cells) between endothelium and myocardium -undergo a phenotypic switch= epithelial-mesenchymal transformation (EMT) -cellular swellings within cardiac jelly are the endocardial cushions, that mature into valve leaflets

39
Q

Reciprocal inductive interactions in valve formation

A

-signals from myocardium required from EMT -signals from endothelium required for myocardium to mature -cross-talk between opposing tissues is a common theme in developmental biology

40
Q

Where are the endocardial cells that form cushions located?

A

-AV canal and OFT (think of where the valves are normally formed!!)

41
Q

What pathway was seen to be important in EMT in valve formation?

A

-Ras pathway

42
Q

Angiogenesis vs Vasculogenesis

A

-angiogenesis: formation of new blood vessels from pre-existing blood vessels -vasculogenesis: formation of new blood vessels from endothelial precursors (angioblasts)–usually only occurs in embryo

43
Q

T/F: VEGF is only player in vascular development.

A

-false: it is potent angiogenic stimuli -but also Notch ligand and semaphorin ligands too

44
Q

Semaphorins

A

-mediate REPULSIVE signals involved in axon guidance and growth cone collapse -secreted ligands bind to plexin/neuropilin receptors -expressed broadly outside CNS

45
Q

Epicardium arises from and required for ?

A

-from proepicardial organ, a derivative of the septum transversum (also gives rise to diaphragm, liver) -EMT again -required for coronary artery development and for myocardial maturation (inductive signals)

46
Q

Neural crest cells migrate from ________ to _____ and ______.

A

-dorsal neural tube -pharynx and heart

47
Q

What do neural crest cells form?

A

-arterial SMCs, nerve, bone, skeletal muscle, melanocytes, cells of thymus, thyroid, parathyroid

48
Q

2 things NC cells are required for in heart development. Defects result in?

A
  1. SMC layers of PA, Ao, DA, carotid arteries 2. septation of truncus arteriosus and OFT (Ao and PA) -defects result in cardiac outflow tract defects
49
Q

What is one possible thought on where aortic dissection entrance and exit points occur?

A

-embryologic border zones -ascending aortic SMC from NC cells -descending SMCs diff origin

50
Q

4 broad steps important in normal morphogenesis

A
  1. crescent –> linear tube –> looping –> septation

Cardiology (27 decks)

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