Week 8 Flashcards
(134 cards)
1
Q
What is the primary germ layer responsible for the heart’s cellular origins?
A
Cardiogenic mesoderm from the splanchnic layer of lateral plate mesoderm
This layer gives rise to the heart and its associated structures.
2
Q
When does the First Heart Field (FHF) arise?
A
Around day 15–16
The FHF contributes to the formation of the linear heart tube.
3
Q
What structures does the First Heart Field (FHF) differentiate into?
A
- Left ventricle
- Atrioventricular canal
- Parts of both atria
These structures are essential components of the heart’s anatomy.
4
Q
Where does the Second Heart Field (SHF) emerge in relation to the FHF?
A
Medially and posteriorly to the FHF
The SHF is crucial for further heart development.
5
Q
What structures does the Second Heart Field (SHF) contribute to?
A
- Right ventricle
- Outflow tract (conus arteriosus and truncus arteriosus)
- Rest of the atria
This contribution is vital for proper heart function.
6
Q
What are Cardiac Neural Crest Cells derived from?
A
Neuroectoderm
These cells play a critical role in heart development.
7
Q
What is the role of Cardiac Neural Crest Cells?
A
- Participate in outflow tract septation
- Formation of the aorticopulmonary septum
- Smooth muscle of great arteries
Maldevelopment of these cells can lead to conotruncal anomalies.
8
Q
What is the Proepicardial Organ (PEO) located near?
A
Sinus venosus
The PEO is important for forming several heart structures.
9
Q
What does the Proepicardial Organ (PEO) form?
A
- Epicardium
- Smooth muscle
- Fibroblasts
- Endothelium of coronary vessels
These components are essential for heart structure and function.
10
Q
What are the three layers of the heart tube?
A
- Endocardium
- Myocardium
- Epicardium
Each layer has a distinct role in heart function and structure.
11
Q
What is the function of the endocardium?
A
Inner endothelial lining—precursor of valves and septa
This layer is critical for maintaining proper blood flow.
12
Q
What does the myocardium develop into?
A
Contractile cardiac muscle layer—develops trabeculae and conduction tissue
This layer is essential for the heart’s pumping action.
13
Q
What is the role of the epicardium?
A
Outer mesothelial layer—source of coronary vasculature and fibroelastic tissue
This layer supports the heart’s structure and function.
14
Q
When does the earliest electrical activity in the heart occur?
A
Around Day 22
This activity is crucial for initiating heart function.
15
Q
What drives the spontaneous depolarization of primitive pacemaker cells?
A
Ion channel expression (e.g., HCN channels)
This process is fundamental for the heart’s electrical activity.
16
Q
Where does pacemaker activity localize during sinus venosus maturation?
A
Right sinus horn, forming the sinoatrial (SA) node
The SA node is essential for regulating heart rhythm.
17
Q
When does the SA node become fully functional?
A
Around week 5–6
This development marks a key milestone in heart maturation.
18
Q
What are the two types of conduction regions in the heart?
A
- Slow-conducting regions: AV canal, annulus fibrosus
- Fast-conducting regions: Future atrial and ventricular myocardium with Purkinje-like fibers
These regions are crucial for coordinated heart contractions.
19
Q
What is the location of the SA Node?
A
Right atrium near SVC
The SA node is the primary pacemaker of the heart.
20
Q
What is derived from the AV canal myocardium?
A
AV Node and His Bundle
These structures are integral to the heart’s conduction system.
21
Q
Where do Bundle Branches & Purkinje Fibers develop from?
A
Trabecular myocardium
These components are essential for maintaining coordinated contraction.
22
Q
What is the process of AV canal partitioning?
A
Endocardial cushions swell and fuse centrally, dividing the single canal into right and left AV orifices
Abnormal fusion can lead to atrioventricular septal defects (AVSDs)
23
Q
What forms the foramen primum during atrial septation?
A
Septum primum grows toward endocardial cushions
This leaves an opening known as the foramen primum
24
Q
What is the role of apoptosis in atrial septation?
A
Before closure, foramen secundum forms via apoptosis
This process is crucial for the formation of the atrial septum
25
What does the septum secundum grow adjacent to during atrial septation?
The right side
## Footnote
This forms the foramen ovale, facilitating a right-to-left shunt
26
What is the significance of the right-to-left shunt in fetal circulation?
Allows oxygenated placental blood to bypass fetal lungs
## Footnote
This is critical for fetal development as the lungs are not used for oxygen exchange in utero
27
How does the muscular interventricular septum form?
It rises from the apex of the heart
## Footnote
This is part of the ventricular septation process
28
What structures contribute to the formation of the membranous portion of the interventricular septum?
Fusion of endocardial cushions, conotruncal ridges, and muscular septum
## Footnote
These components are essential for proper ventricular septation
29
What is the outcome of a failure of fusion in the interventricular septum?
Ventricular septal defect (VSD), most commonly in the membranous region
## Footnote
VSDs can lead to significant clinical issues if not addressed
30
What are the AV valves sculpted from?
Endocardial cushion tissue
## Footnote
This tissue is crucial for the formation of both the tricuspid and mitral valves
31
What is the origin of the chordae tendineae and papillary muscles?
Derived from underlying myocardium
## Footnote
These structures play a key role in valve function
32
What do the semilunar valves arise from?
Conotruncal swellings (aorticopulmonary septum)
## Footnote
This development is essential for proper blood flow from the heart
33
What cells contribute to valvular interstitial tissue and cusps in the semilunar valves?
Neural crest cells
## Footnote
Their contribution is vital for the structural integrity of the valves
34
What gives rise to the aortic sac in aortic development?
The truncus arteriosus
## Footnote
The aortic sac bifurcates into paired aortic arches.
35
How do the aortic arches connect to the descending aorta?
They connect to the dorsal aortae, which fuse caudally
## Footnote
This fusion forms the descending aorta.
36
What does the first aortic arch remodel into?
Maxillary artery
37
What adult structures are derived from the second aortic arch?
Stapedial and hyoid arteries
38
What does the third aortic arch develop into?
Common carotid and proximal internal carotids
39
What do the fourth aortic arch remodel into on the right and left sides?
Right: proximal right subclavian; Left: aortic arch
40
Which aortic arch gives rise to the proximal right pulmonary artery and ductus arteriosus?
Sixth aortic arch
41
From where are the cranial arteries derived?
Largely from the internal carotid arteries formed by the third aortic arch and dorsal aorta
42
Where do coronary arteries originate?
From the epicardium (proepicardial organ)
## Footnote
They invade the aortic root and connect to the aortic sinuses via ingrowths.
43
What do cardinal veins form in the venous system?
SVC, brachiocephalic, azygos, and renal systems
44
What is the function of vitelline veins?
Drain the yolk sac and form the portal venous system
45
What do umbilical veins carry from the placenta?
Oxygenated blood
## Footnote
The left umbilical vein persists as the main channel.
46
How do pulmonary veins form?
As an outgrowth from the left atrial wall
## Footnote
This establishes a connection with the lung buds.
47
What does the lymphatic system develop from?
Venous endothelial outgrowths forming primary lymph sacs
48
What are the primary lymph sacs in the lymphatic system?
Jugular, retroperitoneal, cisterna chyli
49
What do lymphatic vessels form from the primary lymph sacs?
Thoracic duct and peripheral lymphatics
50
What is the primary method of oxygenation in fetal circulation?
Blood is oxygenated via the placenta, not lungs.
51
Which organs are bypassed in fetal circulation to prioritize oxygen delivery?
Lungs and liver.
52
What happens to pulmonary circulation at birth?
With the first breath, lungs expand, and pulmonary circulation becomes functional.
53
What occurs to the shunts during postnatal circulation?
Shunts close, redirecting blood to the lungs and liver.
54
What is the pathway of oxygenated blood in fetal circulation?
Placenta → umbilical vein → ductus venosus (bypasses liver) → IVC → right atrium.
55
Where does the most oxygenated blood go after the right atrium?
Foramen ovale → left atrium → left ventricle → ascending aorta (brain and coronary arteries).
56
What is the pathway of deoxygenated blood in fetal circulation?
From SVC → right atrium → right ventricle → pulmonary artery → diverted through ductus arteriosus → descending aorta → umbilical arteries → placenta.
57
What is the oxygenation level in the umbilical vein, ductus venosus, and IVC?
Highly oxygenated.
58
What is the oxygenation status in the right heart and pulmonary artery?
Mixed.
59
What is the oxygenation level in the left heart and ascending aorta?
More oxygenated.
60
What is the oxygenation status in the descending aorta and umbilical arteries?
Less oxygenated.
61
What is the function of the foramen ovale in fetal circulation?
Directs blood from right → left atrium.
62
What is the role of the ductus venosus?
Bypasses hepatic circulation.
63
What does the ductus arteriosus connect?
Connects pulmonary artery → aorta, bypassing lungs.
64
What anatomical change occurs with the closure of the foramen ovale?
Closes functionally within hours due to increased LA pressure.
## Footnote
LA stands for left atrial pressure.
65
How does the ductus arteriosus close?
Closes via smooth muscle contraction in response to oxygen tension and prostaglandin withdrawal.
## Footnote
Prostaglandins are hormones that play a role in maintaining the ductus arteriosus during fetal life.
66
What triggers the closure of the ductus venosus?
Closes with loss of umbilical flow.
## Footnote
The ductus venosus is a blood vessel that carries oxygenated blood from the placenta to the fetus.
67
What happens to the umbilical arteries and vein after birth?
Constriction occurs and they become ligaments, such as the ligamentum teres hepatis.
68
What is the significance of the first breath taken at birth?
Expands alveoli, decreases pulmonary resistance, and increases pulmonary blood flow.
69
What effect does increased left atrial pressure have at birth?
Functionally closes the foramen ovale.
70
What role does increased oxygen tension play in the closure of the ductus arteriosus?
Inactivates prostaglandins, leading to closure.
71
What physiological change occurs due to umbilical cord clamping?
Terminates placental circulation and closes the ductus venosus.
72
What is the outcome of the anatomical changes that occur at birth?
Establishes adult pattern of circulation: all blood now passes through lungs and liver.
73
What are congenital heart defects?
Structural defects present at birth.
74
What factors determine the clinical significance of congenital heart defects?
Depends on shunt direction, location, and severity.
75
What is the pathophysiology of Patent Ductus Arteriosus (PDA)?
Persistent connection → aortic blood enters pulmonary circulation → pulmonary overcirculation.
## Footnote
PDA can lead to increased blood flow to the lungs, causing various complications.
76
What are the clinical features of Patent Ductus Arteriosus (PDA)?
Continuous murmur, widened pulse pressure, respiratory distress.
## Footnote
These symptoms are indicative of increased blood flow to the lungs.
77
What is the treatment for Patent Ductus Arteriosus (PDA)?
Indomethacin (NSAID) to promote closure; surgery if persistent.
## Footnote
Indomethacin is often used in premature infants to help close the ductus arteriosus.
78
What is the most common congenital heart defect?
Ventricular Septal Defect (VSD).
## Footnote
VSDs can vary in size, affecting their impact on heart function.
79
What happens to small Ventricular Septal Defects (VSDs)?
Often close spontaneously.
## Footnote
Many small VSDs do not require intervention.
80
What are the consequences of large Ventricular Septal Defects (VSDs)?
Cause heart failure, failure to thrive, risk of Eisenmenger syndrome if untreated.
## Footnote
Eisenmenger syndrome is a serious condition that can develop from long-standing left-to-right shunts.
81
What is the most common type of Atrial Septal Defect (ASD)?
Secundum ASD.
## Footnote
Secundum ASD occurs in the middle of the atrial septum.
82
What complications can arise from Atrial Septal Defect (ASD) in adulthood?
Volume overload of the right heart → may lead to arrhythmias or paradoxical emboli.
## Footnote
Paradoxical emboli can occur when a clot crosses from the right to the left atrium.
83
What percentage of adults have a Patent Foramen Ovale (PFO)?
Present in 25–30% of adults.
## Footnote
PFO is a remnant of fetal circulation that may not cause issues unless other conditions are present.
84
What potential complication can arise from a Patent Foramen Ovale (PFO)?
May allow paradoxical embolism (e.g., cryptogenic stroke).
## Footnote
Cryptogenic strokes are those with no identifiable cause, and PFO can be a contributing factor.
85
What are the four features of Tetralogy of Fallot (TOF)?
Pulmonary stenosis, overriding aorta, VSD, RV hypertrophy
## Footnote
VSD stands for ventricular septal defect, and RV hypertrophy refers to right ventricular hypertrophy.
86
What causes Tetralogy of Fallot?
Anterior malalignment of conal septum (neural crest)
## Footnote
This malalignment affects the development of the heart structures.
87
What is the primary clinical manifestation of Tetralogy of Fallot?
Cyanosis due to reduced pulmonary flow
## Footnote
Cyanosis indicates a lack of oxygen in the blood, leading to a bluish appearance.
88
How are 'Tet spells' relieved in patients with Tetralogy of Fallot?
'Tet spells' are relieved by squatting, which increases systemic vascular resistance (SVR)
## Footnote
Squatting helps to redirect blood flow and improve oxygenation.
89
What is the cause of Transposition of the Great Arteries (TGA)?
Failure of spiraling of the aorticopulmonary septum
## Footnote
This failure leads to the aorta and pulmonary artery arising from the wrong ventricles.
90
What are the circulatory implications of Transposition of the Great Arteries?
Parallel circuits: systemic and pulmonary circulations do not mix
## Footnote
This condition creates two separate blood flow circuits that do not allow for oxygenation of blood.
91
What is required for survival in patients with Transposition of the Great Arteries until surgery?
PDA, ASD, or VSD
## Footnote
These shunts allow for mixing of oxygenated and deoxygenated blood.
92
What is the initial management for Transposition of the Great Arteries?
Prostaglandin E1 and surgical arterial switch
## Footnote
Prostaglandin E1 helps maintain ductal patency until surgical intervention can be performed.
93
What is Coarctation of the Aorta (CoA)?
A congenital narrowing of the aortic lumen, typically near the insertion of the ductus arteriosus, resulting in obstructed systemic outflow.
## Footnote
CoA can lead to significant clinical complications if not diagnosed and managed promptly.
94
What embryological abnormalities lead to Coarctation of the Aorta?
Abnormal remodeling of the aortic arch and its branches, underdevelopment of the left fourth aortic arch, or abnormal involution of ductal tissue.
## Footnote
These factors contribute to the constriction of the aorta upon ductal closure.
95
What are the two anatomic types of Coarctation of the Aorta?
1. Infantile Type (Preductal Coarctation)
2. Adult Type (Postductal Coarctation)
## Footnote
Each type has distinct clinical presentations and management strategies.
96
What characterizes Infantile Type Coarctation of the Aorta?
Narrowing occurs proximal to the ductus arteriosus, which remains patent to provide distal perfusion until it closes after birth.
## Footnote
Symptoms can worsen significantly after ductal closure.
97
What are the associated conditions with Infantile Type Coarctation of the Aorta?
* Hypoplastic aortic arch
* Ventricular septal defect (VSD)
* Turner syndrome
## Footnote
Turner syndrome is found in approximately 30% of affected females.
98
What symptoms present in infants with Coarctation of the Aorta?
* Cardiogenic shock
* Tachypnea
* Metabolic acidosis
* Possible differential cyanosis
## Footnote
Differential cyanosis indicates varying perfusion in different body regions.
99
What characterizes Adult Type Coarctation of the Aorta?
Narrowing is distal to the ductus arteriosus, with well-developed collateral circulation compensating over time.
## Footnote
This type is often discovered incidentally during evaluations for hypertension.
100
What are the clinical findings associated with Adult Type Coarctation of the Aorta?
* Hypertension in upper extremities
* Hypotension or reduced pulses in lower extremities
* Radiofemoral delay
* Brachial-femoral BP gradient >20 mmHg
* Systolic murmur
* Rib notching on CXR
* 'Figure 3' sign on CXR
## Footnote
These findings are crucial for diagnosis and management.
101
How is Coarctation of the Aorta diagnosed?
* Echocardiography (TTE)
* CT or MR Angiography
* Pulse oximetry and BP measurements in four limbs
## Footnote
Echocardiography is the first-line diagnostic tool for neonates and infants.
102
What is the initial management for infants with critical Coarctation of the Aorta?
* Prostaglandin E1 (PGE1) infusion
* Stabilization with fluids, inotropes
* Surgical repair
## Footnote
Immediate intervention is critical to maintain ductal patency and stabilize the infant.
103
What are the management strategies for older children/adults with Coarctation of the Aorta?
* Surgical resection
* Balloon angioplasty with or without stenting
* Lifelong follow-up
## Footnote
Ongoing monitoring is necessary due to risks of re-coarctation and other complications.
104
What is Pulmonary Stenosis (PS)?
A narrowing of the right ventricular outflow tract (RVOT), typically at the valvular level, with possible subvalvular or supravalvular forms.
## Footnote
PS can lead to significant hemodynamic changes if severe.
105
What embryological factors contribute to Pulmonary Stenosis?
Incomplete or abnormal resorption of the conotruncal ridges or maldevelopment of the pulmonary valve leaflets.
## Footnote
These factors can lead to various clinical presentations.
106
How does Pulmonary Stenosis affect the right ventricle?
Obstruction increases right ventricular afterload, resulting in right ventricular hypertrophy.
## Footnote
Severe forms can lead to cyanosis due to right-to-left shunting.
107
What are the clinical features of severe Pulmonary Stenosis?
* Fatigue
* Dyspnea on exertion
* Cyanosis if shunting occurs
* Systolic ejection murmur
* Ejection click
## Footnote
These symptoms can vary based on severity and presence of shunting.
108
What is the first-line diagnostic tool for Pulmonary Stenosis?
Echocardiography.
## Footnote
It shows valve thickening, doming, and right ventricular hypertrophy.
109
What is the management for isolated valvular Pulmonary Stenosis?
Balloon valvuloplasty.
## Footnote
Surgical repair may be required for subvalvular or complex forms.
110
What is Pulmonary Atresia?
A complete obstruction of the pulmonary valve, preventing any flow from the right ventricle to the pulmonary arteries.
## Footnote
This condition presents significant challenges in neonatal care.
111
What are the two variants of Pulmonary Atresia?
* With intact ventricular septum (PA/IVS)
* With VSD
## Footnote
Each variant has distinct anatomical and physiological implications.
112
What are the clinical features of Pulmonary Atresia?
* Severe cyanosis
* Tachypnea without respiratory distress
* Single second heart sound
* No audible murmur if PDA-dependent
## Footnote
These features typically present in the neonatal period.
113
How is Pulmonary Atresia diagnosed?
* Echocardiography
* Pulse oximetry
* CXR
## Footnote
Echocardiography is crucial for assessing flow and RV morphology.
114
What is the initial management for Pulmonary Atresia?
Prostaglandin E1 infusion to maintain ductal patency.
## Footnote
Surgical strategies will depend on individual anatomy and physiology.
115
What is the primary reason for cardiovascular adaptations during pregnancy?
To support fetal growth and development, uteroplacental circulation, maternal metabolic demands, expansion of maternal tissues, and protection against hemorrhage.
## Footnote
Increased perfusion is necessary for placental exchange of oxygen, nutrients, and waste.
116
By what percentage does cardiac output (CO) increase during pregnancy?
30–50%
## Footnote
Begins early in the first trimester and peaks in mid-pregnancy.
117
What mechanisms contribute to the increase in cardiac output during early and late pregnancy?
* Early: Increased stroke volume from plasma volume expansion
* Late: Increased heart rate (~10–20 bpm above baseline)
118
How much does plasma volume increase during pregnancy?
40–50%
## Footnote
Driven by estrogen and RAAS activation, leading to sodium and water retention.
119
What is a clinical implication of increased plasma volume during pregnancy?
Causes physiological (dilutional) anemia as RBC mass increases only ~20–30%.
120
What happens to systemic vascular resistance (SVR) during pregnancy?
SVR decreases by ~20–30%.
## Footnote
This is due to progesterone-mediated vasodilation and the development of low-resistance uteroplacental circulation.
121
When does the nadir of blood pressure occur during pregnancy?
In the second trimester.
122
What structural changes occur in the heart during pregnancy?
* Cardiac enlargement
* Left axis deviation
* Apical displacement of the heart
123
What ECG findings are common during pregnancy?
* Right axis deviation
* Sinus tachycardia
* Benign arrhythmias (PACs, PVCs)
124
What role does estrogen play in cardiovascular changes during pregnancy?
* Upregulates nitric oxide synthase → vasodilation
* Promotes hepatic synthesis of RAAS components
125
What are the defining characteristics of pre-eclampsia?
* New-onset hypertension (≥140/90 mmHg on two occasions)
* Proteinuria (≥300 mg/24h) or signs of end-organ dysfunction
126
What are some maternal risk factors for pre-eclampsia?
* Primigravida
* Advanced maternal age (>35 years)
* Pre-existing hypertension or renal disease
* Diabetes mellitus
* Obesity
* Multiple gestation
* Family history
127
What is a pathophysiological cause of pre-eclampsia?
Abnormal placentation leading to shallow trophoblastic invasion and ischemia.
128
What are common clinical manifestations of pre-eclampsia?
* Hypertension
* Proteinuria
* Edema
* Neurological symptoms
* Hepatic pain
* Renal dysfunction
* Pulmonary dyspnea
129
What is the management approach for mild pre-eclampsia?
Close monitoring of BP, urine protein, fetal well-being, and antihypertensives like labetalol, nifedipine, and hydralazine.
130
What is the definitive treatment for severe pre-eclampsia?
Delivery, especially with signs of maternal/fetal deterioration.
131
What are potential complications of pre-eclampsia?
* Eclampsia
* HELLP Syndrome
* Placental Abruption
* Fetal Growth Restriction
* Pulmonary Edema
* Maternal Organ Failure
132
What is HELLP Syndrome?
Hemolysis, Elevated Liver enzymes, Low Platelets.
133
What symptoms may precede eclampsia?
Visual or neurological symptoms.
134
Fill in the blank: A multisystem hypertensive disorder unique to pregnancy is called _______.
pre-eclampsia
