Anatomy + Embryology Flashcards

1
Q

What structure is critical for the vitelline system (Blood cell development)?

A

The yolk sac

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2
Q

Venous drainage to primordial heart is through what structure?

A

Sinus venosus

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3
Q

Where does fetal erythropoiesis occur and in which stages?

A

Young Liver Syhthesizes Blood

Yolk sac (3-8 weeks)

Liver (6 weeks-birth)

Spleen (10-18 weeks)

Bone marrow (18 weeks- adult)

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4
Q

subunits of adult vs. fetal hemoglobin

A

HbF: alpha2gamma2

HbA: alpha2beta2

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5
Q

Pattern of globulin protein subunits of hemoglobin from fetal to adult

A

Alpha Always, Gamma Goes, Becomes Beta

Alpha is produced early and stays high until adulthood. Gamma subunit is produced high early but decreases after birth, which is replaced by beta subunits. Beta subunits rise after birth. Epsilon and zeta subunits are produced very early in fetal development but decreases to 0 before 12 weeks.

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6
Q

What does it mean when zeta/episilon subunits are seen in adult Hgb?

A

It means that there is something wrong with the adult Hgb, and they have to rely on making fetal Hgb (zeta and epsilon) subunits

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7
Q

When is delta subunit of Hgb produced and what does its presence in adult Hgb indicate?

A

Delta subunit comes on at birth but its level stays very low. Presence of delta subunit in HbA means that there is something wrong.

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8
Q

What type of oxygen dissociation curve shift is seen for HbF compared to HbA and why?

A

There is a leftward curve shift of the sigmoidal curve. This is because HbF has a higher affinity for oxygen than HbA because HbF has less avid binding to 2,3-BPG. As a result, HbF is able to extract O2 from maternal hemoglobin across the placenta.

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9
Q

What is 2,3-BPG?

A

Byproduct of glycolysis; when this molecule binds Hgb, Hgb has less affinity for oxygen. HbF doesn’t bind this molecule and therefore has a greater affinity for oxygen than HbA.

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10
Q

What shape is oxygen dissociation curve for Hb compared to myoglobin and why?

A

Hb displays a sigmoidal curve due to cooperativity, in which binding of oxygen to one heme group increases affinity of oxygen for the next heme groups. Myoglobin displays a hyperbolic curve because it has no cooperativity.

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11
Q

What does the intra-embryonic coelom turn into?

A

Pericardial, pleural, and peritoneal cavities

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12
Q

Where does the heart tube (primordial heart) begin relative to the motuh and intra-embryonic coelom?

A

Begins superior to the mouth and ventral to the intra-embryonic coelom.

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13
Q

How does the heart end up below the head/mouth?

A

As head grows, the heart tubes fold ventrally along with the pericardial cavity (anterior to the heart tubes). Thus, the head and mouth are superior to the head and mouth.

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14
Q

Where is the fetal foregut relative to the two dorsal aorta?

A

It is trapped anteriorly by the paired dorsal aorta.

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15
Q

What structure is the primordium of central tendon of diaphragm and separate the heart and lungs from the peritoneal cavity?

A

Septum transversum

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16
Q

Structure of endocardial tube from top to bottom

A

Aortic sac → truncus arteriosus → bulbus cordis → primitive ventricle → primitive atrium → sinus venosus

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17
Q

What does aortic sac give rise to?

A

Pharyngeal arches

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18
Q

What does the truncus arteriosus give rise to?

A

Ascending aorta and pulmonary trunk

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19
Q

What does the bulbus cordis give rise to?

A

Outflow tract (smooth parts) of left and right ventricles

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20
Q

What does the primitive ventricles give rise to?

A

Trabeculated part of both ventricles

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21
Q

What does the primitive atrium give rise to?

A

Trabeculated part of both atria

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22
Q

What does left horn of sinus venosus give rise to?

A

Coronary sinus

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23
Q

What does right horn of sinus venosus give rise to?

A

Smooth part of right atrium (sinus venarum)

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24
Q

What does the primitive pulmonary veins (which grow into left atrium) give rise to?

A

Smooth part of left atrium

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25
Q

What gives rise to SVC?

A

Right common cardinal vein and right anterior cardinal vein

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26
Q

What veins come drain into the sinus venosus?

A

Common cardinal vein, vitelline vein, and umbilical vein

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27
Q

What gives rise to hepatic vein?

A

Right vitelline vein

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28
Q

What are the venous structures from the sinus venosus that degrades?

A

Left vitelline vein and right umbilical vein

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29
Q

What happens to the left umbilical vein?

A

Remains

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30
Q

What does the anterior cardinal vein give rise to?

A

Jugular vein (drains head), subclavian vein (drains arms), and SVC (drains from both)

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31
Q

What does the posterior cardinal veins give rise to?

A

IVC and azygos system

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32
Q

What is the first functional organ in vertebrate embryos?

A

Heart

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33
Q

When does the heart begin to beat spontaneously?

A

By week 4 of development

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34
Q

How does the primary heart loop initially, when does it do this, and what is the purpose?

A

The atrial portion rotates up and end up behind the heart; however, it is higher than where it started out. This begins at week 4 of gestation and establishes left-right polarity.

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35
Q

What structure is important in primary heart rotation to establish L-R polarity?

A

Cilia

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36
Q

What does the AV endocardial cushions do and what is their purpose?

A

They are located between the primordial atria and ventricle. They are invaded by neural crest cells and fusein the ventral-dorsal direction, dividing the AV canal into left and right canals. The purpose is to seaprate the primordial atrium from the primordial ventricle (not left and right).

Additionally, they contribute to the membranous portion of interventricular septum.

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37
Q

What type of cells are neural crest cells derived from, and where do they migrate?

A

They are formed from neuroectodermal tissue. They migrate to the outflow tract and cardiac endocardial cushions. They also organize tissue movement.

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38
Q

Derivatives of neural crest cells

A

PNS (dorsal root ganglia, CNs, autonomic ganglia, Schwann cells), melanocytes, chromafrin cells of adrenal medulla, parafollicular (C) cells of thyroid, pia and arachnoid, bones of the skull, odontoblasts, articopulmonary septum, endocardial cushions

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39
Q

Kartagener’s syndrome inheritance pattern, pathophysiology, symptoms

A

Type of primary ciliary dyskinesia

Autosomal recessive

Pathophysiology: Defects in dyein → ciliary dysfunction → L/R asymmetry due to defect in primary heart tube rotation (e.g. rotation wrong way)

Triad sx: Situs inversus (heart in wrong side of chest), chronic sinusitis (cavities have drainage that cannot be drained due to impaired cilia), bronchiectasis (bronchi are damaged bc they’re not properly drained by cilia)

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40
Q

Steps in atrial septum development (7)

A

1) Septum primum grows toward endocardial cushions, narrowing foramen primum
2) Foramen secundum forms in septum primum as small holes and foramen primum disappears (via fusion of septum primum and endocardial cushion)
3) Septum secundum develops as foramen secundum maintains right to left shunt
4) Septum secundum expands and covers most of foramen secundum. Residual foramen is foramen ovale.
5) Remaining portion of septum primum forms valve of foramen ovale.
6) Septum secndum and septum primum fuse to form the atrial septum
7) Foramen ovale usually closes soon after birth due to increase in LA pressure

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41
Q

Why does foramen ovale close after birth?

A

The lung works in the newborn and therefore blood from the lungs goes to LA → increased LA pressure (L>R)

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42
Q

Why does the foramen ovale stay open during fetal life?

A

Higher pressure on the right than left atrium

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43
Q

Ostium secundum vs. ostium primum

A

Type of ASD

Ostium secundum (90%) is caused by abnormal growth (not enough) of septum primum or secundum.

Ostium Primum (5%) is when septum primum doesn’t fuse with endocardial cushion. It is also associated with AV valve defects.

44
Q

What atrial septal defect is commonly seen in down syndrome?

A

Ostium primum

45
Q

How can an embolus from the leg or pelvis lead to an embolic stroke? What is this called?

A

Paradoxical emboli; embolus from leg or pelvis → passes through atrial septal defect → enters LA →LV → CNS → stroke

46
Q

What is paradoxical emboli and what conditions are commonly associated with this?

A

Venous thromboemboli that enters the systemic arterial circulation.

Commonly seen in ASD or patent foramen ovale

47
Q

Eisenmenger syndrome cause, pathophysiology, sx

A

Cause: Uncorrected left to right shunt (ASD, VSD, PDA)

Pathophys: Left to right shunt increases pulmonary blood flow → pathologic remodeling of vasculature → pulmonary arterial HTN → RVH occurs to compensate → reversal of shunt R to L

Sx: Late cyanosis, clubbing, polycythemia

48
Q

Formation of ventricular septation (2 steps)

A

1) Muscular interventricular septum forms to form interventricular foramen
2) Aorticopulmonary septum rotates and fuses with muscular ventricular septum to form membranous niterventricular septum, closing interventricular formaen.

49
Q

What is the most common congenital cardiac anomaly?

A

Ventricular septal dfect

50
Q

Where do ventricular septal defects usually occur?

A

In membranous septum

51
Q

Why do ventricular septal defects usually asymptomatic at birth, manifest weeks later, or remain asymptomatic throughout life?

A

Because it maintains a Left to right shunt

52
Q

Why do valsalva maneuvers (e.g. shitting) a common cause of embolic strokes in pts with hole in the heart?

A

This transiently increases pressure on the right side of the heart → opens up hole transiently, allowing clot to go through → travel up to systemic circulation → stroke

53
Q

What are conotruncal abnormalities caused by, how do they present (blue babies vs. blue kids), and what are examples (3)?

A

Caused by failure of neural crest cells to migrate to the heart, affecting primary heart tube rotation. Presents as blue babies or early cyanosis.

Ex: Transposition of great vessels, Tetralogy of Fallot, Truncus arteriosus

54
Q

Persistent truncus arteriosus

A

Truncus arteriosus fails to divide into pullmonary trunk and aorta due to lack of aorticopulmonary septum formation.

55
Q

What defect is usually seen in pts with persistent truncus arteriosus?

A

VSD

56
Q

Arrangment of aorta and pulmonary trunk as it exits out of ventricles

A

Aorta exits out of left ventricle, goes behind the pulmonary trunk and comes out to the right. Pulmonary trunk exits from the right ventricle and goes in front of aorta to the left side.

57
Q

Transposition of great vessels cause

A

Caused by failure of aorticopulmonary septum to spiral. Aorta leaves RV anteriorly and pulmonary trunk leaves LV posteriorly, resulting in separation of systemic and pulmonary circulations.

58
Q

Prognosis of baby with transposition of great vessels

A

Not compatible with life unless a shunt i present to allow mixing of blood (VSD, PDS, or patent foramen ovale). Most infants die within first few months of life

59
Q

Cause of tetralogy of fallot

A

A type of conotruncal abnormality (failure of neural crest cells to migrate to the heart, resulting in defective rotation of primary heart tube). Specifically, anteriosuperior displacement of infundibular septum.

60
Q

Sx/findings of tetrology of fallot (4)

A

1) Pulmonary infundibular stenosis
2) Right ventricular hypertrophy (RVH)/ boot shaped heart on CXR
3) Overriding aorta
4) VSD

61
Q

What is the most important determinant prognosis for tetrology of fallot and why?

A

Pulmonary infundibular stenosis because this decreases circulation to the lungs. This stneosis forces R to L flow across VSD, resulting in RVH. The blood to the left ventricle will go to aorta → hypoxia.

62
Q

Why does squatting help sx of tetrology of Fallot?

A

Squatting increases systemic vascular resistance, making it harder for LV to unload the blood and therefore increasing the volume of blood in left ventricle. This ultimately makes it harder for blood to go from RV to LV (reduce R → L shunt), improving cyanosis.

63
Q

Cause of late cyanosis/ blue kids

A

Left to Right shunts (ASD, CSD, PDA). Eisenmenger syndrome develops, in which left to right shunts eventually overwhelms the lungs, which increases pulmonary vascular resistance, which then reverses the shunt to right to left (like blue baby). This is a late cyanosis because in the beginning, L to R shunt isn’t bad because blood is still oxygenated; however, once the shunt reverses, the child will become cyanotic.

64
Q

Aortic Arch derivatives

A

1st: Part of maxillary artery (1st is maximal)
2nd: Stapedial artery and hyoid artery (Second= Stapedial)
3rd: Common Carotid Artery and proximal part of internal carotid artery
4th: On left, aortic arch; on right, proximal part of right subclavian artery
5th: vestigial
6th: Proximal part of pulmonary artery and left only ductus arteriosus

65
Q

Positioning of left recurrent larygeal nerve vs. right recurrent laryngeal nerve.

A

Left recurrent laryngeal nerve is hooked underneath the ductus arteriosus, which turns into the ligamentum arteriosum after birth. Right recurrent laryngeal goes around the right subclavian artery because the 6th arch on the right side degrades after forming pulmonary artery (no ductus arteriosus)

66
Q

Types of coarctation of aorta (3) and cause

A

Cause: There is some contractile muscle in DA. Some of this muscle can go to aortic arch and contract, resulting in coarctation.

Types:

1) Postductal coarctation
2) Preductal coarctation
3) Juxtaductal coarctation

67
Q

How are the aortic/pulmonary valves developed?

A

Derived from endocardial cushions of outflow tract

68
Q

How are mitral and tricuspid valves developed?

A

Derived from fused endocardial cushions of AV canal

69
Q

Types of valvular anomalies

A

Atretic, stenotic, regurgitant, or displaced (e.g. Ebstein anomaly)

70
Q

Epstein anomaly

A

Displacement of tricuspid valve leaflets downwarrd into RV, “artrializing” the ventricle (very small RV and big RA)

71
Q

What type of treatment is associated with Ebstein’s anomaly?

A

Lithium treatment for bipolar disorder in mothers

72
Q

PO2 of blood in umbilical vein and % oxygen saturation

A

PO2= 30 mm Hg with 80% oxygen saturation

73
Q

Do umbilical arteries have high or low oxygen saturation?

A

Low

74
Q

3 shunts in fetal development

A

1) Ductus venosus: blood conducted from umbilical vein is conducted into IVC via ductus venosus, bypassing hepatic circulation.
2) Foramen ovale: Between RA and LA; most of highly oxygenated blood reaching heart via IVC is directed here, allowing oxygenated blood to pump into aorta and supply head and body.
3) Patent ductus arteriosus: Deoxygenated blood from SVC passes through RA → RB → main pulmonary artery → patent ductus arteriosus → descneidng aorta.

75
Q

Why is patent ductus arteriosus necessary in fetal circulation?

A

SThis shunt is present due to high fetal pulmonary artery resistance (since lung is filled with amniotic fluid, there is high resistance), so the blood in pulmonary trunk bypasses the lungs and instead goes to descending aorta.

76
Q

What causes closure of foramen ovale after birth?

A

At birth, infant takes a breath, which decreases resistance in pulmonary vasculature →increase in left atrial pressure vs. right atrial pressure → foramen ovale closes.

77
Q

What causes closure of ductus arteriosus after birth?

A

1) Increase in O2
2) Decrease in prostaglandins

78
Q

What causes decrease in prostaglandins after birth

A

Placental separation

79
Q

What drug causes PDA closure and why?

A

Indomethacin- blocks PG syntehsis.

80
Q

What keeps PDA open?

A

Prostaglandins E1 and E2.

81
Q

What structure directs oxygenated blood from IVC straight to the foramen ovale and into LA?

A

Valve of inferior vena cava

82
Q

3 Highest oxygen value in fetal circulation?

A

Umbilical vein → inferior vena cava → right atrium

83
Q

Post-natal derivative of umbilical vein

A

Ligamentun teres hepatis (contained in falciform ligament)

84
Q

Post-natal derivative of umbilical arteries

A

Medial umbilical ligament

85
Q

Post-natal derivative of ductus arteriosus

A

Ligamentum arteriosum

86
Q

Post-natal derivative of ductus venosus

A

Ligamentum venosu

87
Q

Post-natal derivative of foramen ovale

A

Fossa ovalis

88
Q

Post-natal derivative of allantois

A

Urachus-median umbilical ligament

89
Q

Structures supplied by RCA

A

Right atrium, right ventricle, posterior 1/3 of interventricular septum, portion of Left ventricle, SA and AV nodes

90
Q

4 branches of RCA

A

SA nodal, right marginal, AV nodal, posterior interventricular (posterior descending artery)

91
Q

Branches of LCA (2)

A

LAD (left anterior descending), circumflex

92
Q

Structures supplied by LCA

A

Left atrium, left ventricle, portion of right ventricle, anterio 2/3 of interventricular septum, portion of right ventricle

93
Q

Right dominant circulation (85%)

A

PDA arises from RCA

94
Q

Left dominant circulation (8%)

A

PDA arises from LCX (Left circumflex artery)

95
Q

Codominant circulation (7%)

A

PDA arises from both LCX and RCA

96
Q

Which artery usually supplies the SA and AV nodes?

A

RCA

97
Q

Coronary artery occlusion most commonly occurs in which artery?

A

LAD

98
Q

When does the heart muscle receive blood?

A

During diastole because that is when coronary blood flow peaks.

99
Q

How does myocardium receive more oxygen vs. skeletal muscle?

A

Myocardium receives more oxygen by getting more blood flow. Skeletal muscle can get more oxygen by increasing its extraction.

100
Q

Tricuspid valve

A

In between the right atrium and right ventricle

101
Q

Mitral valve

A

2 cusps; in between left atrium and left ventricle

102
Q

What is parietal pericardium?

A

Outer layer of the pericardium

103
Q

Where is parietal pericardium localized and why? What type of pain does it convey and why

A

It is referred to the shoulder/lateral neck area, which are dermatomes for spinal cord segments C3, C4, and C5. This is because pain is carried by somatic afferent fibers in the phrenic nerves. The pain is sharp because they are somatic afferents.

104
Q

Where is cardiac pain localized and why?

A

Cardiac pain is in the chest but it’s very nonspecific/ nonlocalized/ dull pain because the pain is carried by visceral pericardial afferents (autonomics) which return to T1-T5 via SNS.

105
Q

Why can enlargement of the left atrium cause dysphagia or hoarseness?

A

It can cause dysphagia due to compression of the esophagus. It can cause hoarseness due to compression fo the left recurrent laryngeal nerve.