Embryology Flashcards
(258 cards)
1
Q
What are cardiomyocytes?
A
Heart muscle cells originating from cardiac progenitor cells in mesodermal tissue
They are responsible for the contractile function of the heart.
2
Q
What is the origin of endocardial cells?
A
Endocardial lineage from mesodermal mesenchyme
They line the interior of the heart chambers and form the endocardium.
3
Q
What do epicardial cells cover?
A
The surface of the heart
They also contribute to coronary vessel development and cardiac fibroblasts.
4
Q
What is the role of cardiac fibroblasts?
A
Provide structural support and ECM production
They mainly originate from epicardial-derived cells and also from circulating mesenchymal cells.
5
Q
From which cells are vascular cells derived?
A
Epicardial cells and mesodermal angioblasts
They form coronary vessels supplying the heart tissue.
6
Q
What is the origin of the cardiac conduction system?
A
Common embryonic cardiac mesenchymal tissue from primitive heart tube mesodermal cells
This tissue differentiates into components like the SA node and AV node.
7
Q
What develops from the sinus venosus tissue?
A
The sinoatrial (SA) node
This region is part of the primitive venous inflow tract.
8
Q
Which genes regulate the differentiation of pacemaker cells?
A
T-box transcription factors (e.g., Tbx3), Islet-1, and Tbx18
These genes influence the development of the SA node.
9
Q
Where does the AV node form?
A
Near the conduction tissue that separates atrial and ventricular myocardium
It develops from mesenchymal cells under genetic influence.
10
Q
What develops from specialized cardiac muscle fibers?
A
The bundle of His and bundle branches
These structures extend into the ventricles as part of the conduction pathway.
11
Q
What characterizes conduction cells in the embryonic myocardium?
A
Specific electrophysiological properties
They develop prominent conduction fibers with high conduction velocity but reduced contractile capacity.
12
Q
What guides the patterning of the conduction system?
A
Complex molecular signaling pathways (e.g., Notch, BMP, Wnt)
These pathways coordinate the precise arrangement of conduction tissues.
13
Q
What are the key processes involved in partitioning the heart during embryogenesis?
A
- Partitioning of the Atrial and Ventricular Chambers 2. Partitioning of the AV Canal 3. Additional Structures
These processes are crucial for the proper formation of the heart’s anatomy.
14
Q
What is the role of the septum primum in atrial partitioning?
A
It partially divides the atrium into right and left chambers
The septum primum is formed by a crescent-shaped membrane that grows downward.
15
Q
What happens during the formation of the foramen secundum?
A
Perforations appear in the upper part of the septum primum as it fuses with the endocardial cushions
This leads to the creation of an opening for blood flow.
16
Q
What is the function of the septum secundum?
A
It develops to the right of septum primum, creating an opening (foramen ovale) that allows right-to-left shunting of blood during fetal life
This structure is crucial for fetal circulation.
17
Q
How is the interventricular septum formed?
A
The muscular septum grows upward from the ventricular floor and merges with endocardial cushions
It has two parts: muscular (first) and membranous (second).
18
Q
What is the role of endocardial cushions in the partitioning of the AV canal?
A
They swell in the AV canal and grow towards each other to form the septum endocardiale
This is essential for dividing the AV canal into two orifices.
19
Q
What is the outcome of the AV septum formation?
A
The cushions fuse and grow to divide the AV canal into right and left AV orifices
This ensures each atrium connects to its respective ventricle.
20
Q
What contributes to the development of the atrioventricular valves?
A
The cushions and surrounding tissue contribute to the septation process
This results in the formation of the tricuspid and mitral valves.
21
Q
Fill in the blank: Atrial septation involves growth of _______ and secundum, forming the foramen ovale.
A
septa primum
This highlights the importance of both septa in fetal heart development.
22
Q
True or False: Ventricular septation involves muscular growth from the atria.
A
False
Ventricular septation involves muscular growth from the ventricles.
23
Q
What is the significance of the foramen ovale?
A
It allows right-to-left shunting of blood during fetal life
This is crucial for proper fetal circulation before birth.
24
Q
What is the primary function of valve formation in the heart?
A
Ensures proper flow of blood between chambers and into the arteries
25
What are endocardial cushions?
Swellings of cellular tissue consisting of mesenchymal cells derived from endocardial cells and neural crest cells
26
Where do endocardial cushions form during early heart development?
In the atrioventricular (AV) canal and outflow tract (conotruncal region)
27
What process allows endocardial cells to become mesenchymal cells?
Endocardial-to-mesenchymal transition
28
What happens during the cushion growth and fusion stage?
Cushions expand and fuse to partition the AV canal into right and left orifices, forming the AV valves
29
What valves are formed from the cushions in the outflow tracts?
Aortic and pulmonary valves
30
What is the role of cell proliferation and ECM deposition in valve formation?
Critical for shaping the valve leaflets
31
What do mesenchymal cells differentiate into within the cushions?
Valvular interstitial cells
32
What is the structure of the mature valve leaflets?
Thin, flexible leaflets with core connective tissue covered by endocardial endothelium
33
What contributes to the stability and flexibility of the valves during maturation?
Vascularization and fibrous tissue deposition
34
What structures are formed to anchor the valves?
Chordae tendineae and papillary muscles
35
Fill in the blank: The formation of chordae tendineae and papillary muscles occurs from the _______.
ventricular myocardium
36
True or False: The cushions do not play a role in the formation of valves.
False
37
What forms during early embryogenesis around the 4th-5th week?
Six pairs of pharyngeal (branchial) arch arteries
## Footnote
These arches form symmetrically from the aortic sac.
38
What do the aortic arches connect ventrally and dorsally?
The aortic sac and the paired dorsal aortae
## Footnote
Initially, the arches are parallel vessels.
39
What does the left 4th arch transform into?
Part of the aortic arch
## Footnote
This is part of the transformation into definitive major arteries.
40
What does the right 4th arch form?
The proximal right subclavian artery
## Footnote
This is one of the outcomes of the remodeling of the aortic arches.
41
What does the left 6th arch develop into?
The ductus arteriosus
## Footnote
This fetal vessel later becomes the ligamentum arteriosum.
42
What does the right 6th arch partly contribute to?
The right pulmonary artery
## Footnote
This illustrates the selective regression and persistence of the aortic arches.
43
What arises from the aortic sac?
The ascending aorta
## Footnote
The aortic sac is a key structure in the formation of major vessels.
44
What do the common carotid arteries form from?
The 3rd arches paired with the dorsal aorta
## Footnote
This is part of the sequence of events in the transformation of aortic arches.
45
Where does the brachiocephalic trunk originate from?
The aortic sac
## Footnote
This trunk is a major vessel formed during embryogenesis.
46
What does the right subclavian artery arise from?
The right 4th arch and right dorsal aorta
## Footnote
This is part of the development of cranial arteries.
47
From which structures do the left common carotid and subclavian arteries develop?
The 3rd arch and left dorsal aorta
## Footnote
This highlights the embryonic development of cranial arteries.
48
What do coronary arteries originate from?
Proepicardial cells
## Footnote
These cells contribute to the epicardium.
49
What develops on the surface of the heart to form the coronary ostia?
Coronary vascular plexus
## Footnote
This structure grows into the aorta.
50
What are the last vessel structures to develop?
Coronary arteries
## Footnote
They connect nascent coronary vessels with the ascending aorta.
51
What do common cardinal veins drain?
The head, neck, and body
## Footnote
This is part of the embryonic venous system.
52
What do anterior cardinal veins drain?
The upper body
## Footnote
They are part of the embryonic venous structures.
53
What do posterior cardinal veins drain?
The lower body
## Footnote
This is another component of the embryonic venous system.
54
What do common iliac veins drain?
Lower limbs and pelvis
## Footnote
They are part of the developing venous system.
55
What do subcardinal veins form parts of?
The IVC and renal veins
## Footnote
This is part of the venous system development.
56
What do supracardinal veins contribute to?
Azygos and hemiazygos veins
## Footnote
These veins are part of the embryonic venous structures.
57
What do vitelline veins drain?
The yolk sac
## Footnote
They form the portal system and hepatic veins.
58
What do umbilical veins carry?
Oxygenated blood from the placenta
## Footnote
The right umbilical vein regresses, while the left persists as the ligamentum teres.
59
True or False: The left cardinal vein mostly persists during development.
False
## Footnote
The left cardinal vein mostly regresses.
60
What do the right anterior and posterior cardinal veins form?
The superior vena cava
## Footnote
This is a significant outcome in the development of the venous system.
61
What do the subcardinal and supracardinal veins develop into?
The IVC and azygos system
## Footnote
This illustrates the transformation of embryonic veins into definitive structures.
62
What is the origin of the lymphatic system?
The lymphatic system develops from lymphatic sacs and vessels that arise during embryogenesis from venous structures.
63
What are the primary sources for the development of lymphatic endothelial cells?
Venous endothelial cells.
64
How do lymphatic vessels develop?
Lymphatic vessels develop from lymph sacs that form by centripetal budding from existing veins.
65
Where do jugular lymph sacs form?
Near the junction of the external jugular and internal jugular veins.
66
Where do retroperitoneal and iliac lymph sacs form?
In the abdominal cavity.
67
What is the cisterna chyli?
A prominent lymph sac in the abdomen, serving as a conduit for lymph from the lower limbs and abdomen.
68
What do lymphatic sacs sprout to form?
Lymphatic channels that extend and connect to form the entire lymphatic network.
69
When do the initial lymphatic vessels start forming during fetal development?
Around 6-7 weeks.
70
What does the lymphatic network grow to drain?
Tissue fluid, immune cells, and fat.
71
What is the thoracic duct?
The main lymphatic vessel, developed from the left lymphatic duct and the cisterna chyli.
72
What does the right lymphatic duct drain?
Lymph from the right side of the head, neck, upper limb, and thorax.
73
Where do lymph nodes develop?
Along lymphatic vessels at junctions for immune surveillance.
74
What is the site of oxygenation in fetal circulation?
Oxygenation occurs in the placenta, not the lungs.
75
What is the site of oxygenation in postnatal circulation?
Oxygenation occurs in the lungs.
76
What is the function of the Ductus Venosus?
Connects the umbilical vein to the inferior vena cava, bypassing the liver.
77
What is the purpose of the Foramen Ovale in fetal circulation?
Allows blood to bypass the non-functional fetal lungs.
78
What does the Ductus Arteriosus connect?
Connects the pulmonary artery to the aorta, diverting blood from the lungs.
79
What is the pathway of oxygenated blood in fetal circulation?
Oxygenated blood from the placenta → Umbilical vein → Ductus venosus → Inferior vena cava → Right atrium.
80
In fetal circulation, what happens to deoxygenated blood?
It returns via the umbilical arteries to the placenta for oxygenation.
81
What are the pressure differences between fetal and postnatal circulation?
Fetal circulation has higher pressure on the right side of the heart; postnatal circulation has higher pressure on the left side.
82
What changes occur in the circulatory system after birth?
Closure of Foramen Ovale, Ductus Arteriosus, Ductus Venosus, and constriction of umbilical vessels.
83
What is the functional significance of fetal circulation?
Prioritizes delivery of oxygenated blood to vital organs while bypassing the non-functional lungs.
84
What is the first segment of the fetal blood flow pathway?
Placenta → Umbilical Vein.
85
Fill in the blank: The _______ allows most oxygenated blood to bypass the liver.
Ductus Venosus
86
What type of blood does the Inferior Vena Cava carry in fetal circulation?
A mixture of oxygenated and deoxygenated blood.
87
What type of blood is carried by the Superior Vena Cava in fetal circulation?
Deoxygenated blood.
88
What happens to the Foramen Ovale after birth?
It closes and becomes the fossa ovalis.
89
What is the purpose of the Ductus Venosus in fetal circulation?
To ensure that the most oxygenated blood reaches the heart and brain without significant oxygen loss in the liver.
90
What happens to the Ductus Arteriosus after birth?
It closes and forms the ligamentum arteriosum.
91
What is the primary pathway for oxygenated blood from the right atrium?
Through the Foramen Ovale to the left atrium.
92
What is the function of the Ductus Arteriosus?
Diverts blood from the right ventricle away from the non-functional fetal lungs.
93
What type of blood does the Ductus Arteriosus carry?
Mixed blood.
94
What type of blood do the Umbilical Arteries carry?
Deoxygenated blood from the fetus back to the placenta.
95
What is the role of the Ductus Venosus in bypassing the liver?
Allows oxygenated blood from the placenta to go directly to the heart.
96
What type of blood enters the left atrium via the Foramen Ovale?
Oxygenated blood.
97
What is the purpose of the Foramen Ovale in prioritizing blood flow?
To ensure that highly oxygenated blood reaches the brain and heart.
98
True or False: The fetal lungs are functional.
False
99
What happens to the blood flow from the right ventricle in the fetal circulatory system?
It is pumped into the pulmonary artery, most bypassing the lungs via the Ductus Arteriosus.
100
What anatomical change occurs to the foramen ovale at birth?
Closure of the foramen ovale, forming the fossa ovalis.
## Footnote
This prevents mixing of oxygenated and deoxygenated blood.
101
What is the function of the foramen ovale before birth?
Allows oxygenated blood from the inferior vena cava to bypass the right ventricle and go directly to the left atrium.
## Footnote
This ensures oxygen-rich blood reaches the brain and upper body.
102
What causes the functional closure of the foramen ovale at birth?
Increased left atrial pressure due to blood returning from the lungs.
## Footnote
The septum primum presses against the septum secundum.
103
How long does it typically take for the foramen ovale to anatomically close?
Weeks to months after birth.
104
What is the ductus arteriosus and its function before birth?
Connects the pulmonary artery to the aorta, allowing blood to bypass the lungs.
## Footnote
This protects the non-functional fetal lungs from excessive blood flow and pressure.
105
What triggers the closure of the ductus arteriosus at birth?
Onset of breathing increases oxygen levels and decreases prostaglandin levels.
## Footnote
This causes constriction and closure of the ductus arteriosus.
106
When does the ductus arteriosus functionally close after birth?
Within 24-48 hours.
107
What does the ductus arteriosus become after anatomical closure?
The ligamentum arteriosum.
108
What is the ductus venosus and its role before birth?
Carries oxygenated blood from the umbilical vein to the inferior vena cava, bypassing the liver.
109
What happens to the ductus venosus at birth?
It ceases blood flow once the umbilical cord is clamped and eventually becomes the ligamentum venosum.
110
What occurs to the umbilical vessels at birth?
The umbilical vein becomes the ligamentum teres hepatis, and the umbilical arteries become the medial umbilical ligaments.
111
What physiological changes occur in circulatory dynamics at birth?
Pulmonary vascular resistance decreases, and systemic vascular resistance increases.
112
What causes decreased pulmonary vascular resistance at birth?
Inflation of the lungs during the first breath, causing pulmonary arterioles to dilate.
113
What is the purpose of the closure of the foramen ovale?
Prevents mixing of oxygenated and deoxygenated blood.
114
What is a congenital heart defect (CHD)?
A structural abnormality of the heart or great vessels present at birth.
115
What are the two main categories of congenital heart defects?
* Cyanotic Defects
* Acyanotic Defects
116
What is an Atrial Septal Defect (ASD)?
An opening in the atrial septum allowing blood flow from the left atrium to the right atrium.
117
What are the symptoms of a Ventricular Septal Defect (VSD)?
Heart murmur, dyspnoea, failure to thrive.
118
What is Patent Ductus Arteriosus (PDA)?
Persistence of the ductus arteriosus, allowing blood flow from the aorta to the pulmonary artery.
119
What combination of defects constitutes Tetralogy of Fallot (TOF)?
* Ventricular septal defect (VSD)
* Pulmonary stenosis
* Overriding aorta
* Right ventricular hypertrophy
120
What occurs in Transposition of the Great Arteries (TGA)?
The aorta and pulmonary artery are swapped in position.
121
What is Coarctation of the Aorta?
Narrowing of the aorta, typically near the ductus arteriosus.
122
What is Hypoplastic Left Heart Syndrome (HLHS)?
Underdevelopment of the left side of the heart, including the left ventricle and aorta.
123
What is the most common cause of patent ductus arteriosus (PDA)?
Prematurity
## Footnote
The immature ductal muscle does not respond well to oxygenation.
124
Which maternal factor increases the risk of patent ductus arteriosus?
Rubella infection during pregnancy
## Footnote
Other risk factors include premature birth and low birth weight.
125
What genetic syndromes are associated with patent ductus arteriosus?
* Congenital rubella syndrome
* Trisomy 21 (Down syndrome)
* Familial inheritance or associated with other congenital heart defects.
126
What environmental factors can contribute to the development of PDA?
* High altitude births due to hypoxia
* Prenatal exposure to certain drugs (like phenytoin)
127
What is the sex predilection for patent ductus arteriosus?
More common in females (about 2:1 ratio)
128
Describe the pathophysiology of patent ductus arteriosus.
In PDA, closure of the ductus arteriosus fails, resulting in a left-to-right shunt, increasing pulmonary blood flow and pulmonary vascular resistance.
129
What are the clinical features of a small patent ductus arteriosus?
Asymptomatic, often detected incidentally by a murmur on routine examination.
130
What murmur is characteristic of moderate to large patent ductus arteriosus?
Continuous 'machine-like' murmur heard at the left infraclavicular area (Gibson’s murmur)
131
What are the symptoms of congestive heart failure in infants with PDA?
* Tachycardia
* Hepatomegaly
* Failure to gain weight
132
What imaging technique is the gold standard for diagnosing patent ductus arteriosus?
Echocardiography (Echo)
## Footnote
It visualizes the patent ductus, estimates shunt volume, and assesses cardiac function.
133
What is the primary medical management for preterm infants with patent ductus arteriosus?
* Indomethacin
* Ibuprofen (Prostaglandin Inhibitors)
134
What are the indications for closure of a patent ductus arteriosus?
* Symptomatic infants with heart failure
* Asymptomatic PDA with significant left-to-right shunt
* Risk of endocarditis
135
What is the most common congenital heart defect?
Ventricular Septal Defect (VSD)
136
What percentage of congenital heart defects does Ventricular Septal Defect account for?
About 20-30%
137
What genetic syndromes are associated with Ventricular Septal Defect?
* Down syndrome (Trisomy 21)
* Trisomy 18 (Edwards syndrome)
* DiGeorge syndrome (22q11.2 deletion)
138
What environmental factors can lead to Ventricular Septal Defect?
* Maternal infections (e.g., rubella)
* Maternal diabetes
* Teratogens (alcohol, certain medications)
139
What is the pathophysiology of Ventricular Septal Defect?
Left-to-right shunt due to higher pressure in the left ventricle, leading to increased pulmonary blood flow and potential pulmonary hypertension.
140
What are the clinical features of a small Ventricular Septal Defect?
* Asymptomatic or mild symptoms
* Loud, harsh, holosystolic murmur at the left lower sternal border
141
What symptoms indicate a moderate to large Ventricular Septal Defect?
* Tachypnea
* Tachycardia
* Poor feeding
* Failure to thrive
142
What is the characteristic murmur of Ventricular Septal Defect?
Holosystolic murmur at the left lower sternal border
143
What is the gold standard for diagnosing Ventricular Septal Defect?
Echocardiography (Echo)
144
What are the indications for surgical management of Ventricular Septal Defect?
* Symptomatic infants with heart failure
* Large VSDs with pulmonary hypertension
* Failure to thrive
145
What is the prognosis for small Ventricular Septal Defects?
Often close spontaneously within the first few years.
146
What is an Atrial Septal Defect (ASD)?
A congenital heart defect characterized by an opening in the interatrial septum, allowing blood to flow between the right and left atria.
147
What are the genetic factors associated with Atrial Septal Defect?
* Familial inheritance (autosomal dominant)
* Associated with genetic syndromes (e.g., Down syndrome, Holt-Oram syndrome)
148
What are the developmental factors contributing to Atrial Septal Defect?
Failure of septal tissue fusion during embryogenesis.
149
What is the pathophysiology of Atrial Septal Defect?
Left-to-right shunt due to higher pressure in the left atrium, leading to increased blood volume in the right atrium and potential pulmonary hypertension.
150
What are the clinical features of Atrial Septal Defect?
* Asymptomatic in small defects
* Exercise intolerance
* Fatigue and dyspnea on exertion
151
What is the characteristic auscultation finding in Atrial Septal Defect?
Wide, fixed splitting of S2
152
What is the gold standard for diagnosing Atrial Septal Defect?
Echocardiography (Echo)
153
What is a common management approach for small, asymptomatic Atrial Septal Defects?
Observation
## Footnote
Small ASDs may close spontaneously, especially in infants.
154
What are the indications for closure of an Atrial Septal Defect?
* Right heart dilation due to significant shunt
* Paradoxical embolism risk
155
What is the preferred approach for most ostium secundum ASDs?
Cardiac catheterization using closure devices (e.g., Amplatzer)
## Footnote
This method is minimally invasive and effective for many patients.
156
When is surgical repair indicated for atrial septal defects (ASDs)?
For large ASDs or when catheter closure is not feasible
## Footnote
Surgical techniques include primary suture closure for small defects and patch closure for large defects.
157
List the indications for closure of atrial septal defects (ASDs).
* Right heart dilation due to significant shunt
* Paradoxical embolism risk
* Pulmonary hypertension
* Symptomatic patients (e.g., dyspnea, arrhythmias)
## Footnote
These conditions highlight the potential complications of untreated ASDs.
158
What is the prognosis after closure of an ASD?
Excellent, particularly if done before pulmonary hypertension develops
## Footnote
Untreated large ASDs can lead to serious complications like right heart failure and atrial arrhythmias.
159
What percentage of the general population has a Patent Foramen Ovale (PFO)?
About 25%
## Footnote
PFO is usually asymptomatic but can become significant under certain conditions.
160
What causes a Patent Foramen Ovale (PFO)?
Incomplete fusion of the septum primum and septum secundum after birth
## Footnote
This condition is considered a normal fetal structure that fails to close postnatally.
161
What are the physiological factors that can reopen a PFO?
* Conditions increasing right atrial pressure
* Pulmonary hypertension
* Valsalva maneuvers
## Footnote
These factors can lead to right-to-left shunting through the PFO.
162
What is the pathophysiology of a Patent Foramen Ovale (PFO) at birth?
Increased left atrial pressure and decreased right atrial pressure usually cause the foramen ovale to close
## Footnote
Failure of the septum primum and septum secundum to fuse leaves a potential passageway.
163
What is a paradoxical embolism in relation to PFO?
A venous thrombus can pass through the PFO and enter systemic circulation, potentially leading to stroke
## Footnote
This condition is more likely during episodes of right atrial hypertension.
164
What are the common clinical features of PFO?
* Asymptomatic (most common)
* Cryptogenic stroke
* Transient Ischemic Attack (TIA)
* Migraine with aura
* Platypnea-orthodeoxia syndrome
* Decompression sickness in divers
## Footnote
These features can vary widely among individuals.
165
What is the gold standard for diagnosing a PFO?
Transesophageal Echocardiography (TEE)
## Footnote
TEE provides superior visualization and can detect shunt flow using contrast studies.
166
What is the initial medical management for symptomatic PFO?
* Antiplatelet therapy (e.g., aspirin, clopidogrel)
* Anticoagulation (e.g., warfarin, DOACs)
* Migraine management
## Footnote
These treatments aim to reduce the risk of stroke and manage symptoms.
167
When is catheter-based closure indicated for PFO?
* Recurrent cryptogenic stroke despite optimal medical therapy
* Severe platypnea-orthodeoxia syndrome
* Paradoxical embolism with high recurrence risk
## Footnote
This minimally invasive procedure reduces the risk of recurrent paradoxical embolism.
168
What is the prognosis for asymptomatic PFO?
Generally benign, requiring no intervention
## Footnote
Most individuals with asymptomatic PFO do not experience complications.
169
What are the potential outcomes after closure of a symptomatic PFO?
* Reduced stroke recurrence
* Possible reduction in migraine symptoms
## Footnote
Closure is particularly beneficial for patients with a history of paradoxical embolism.
170
What is Tetralogy of Fallot (TOF)?
The most common congenital cyanotic heart disease, characterized by four distinct cardiac anomalies.
171
What are the four cardinal features of Tetralogy of Fallot?
* Right Ventricular Outflow Tract Obstruction (RVOTO)
* Ventricular Septal Defect (VSD)
* Overriding Aorta
* Right Ventricular Hypertrophy (RVH)
172
What causes Tetralogy of Fallot?
Abnormal anterior and cephalad deviation of the infundibular septum during cardiac development.
173
Which genetic conditions are associated with Tetralogy of Fallot?
* Chromosomal abnormalities: 22q11 deletion (DiGeorge syndrome), trisomy 21 (Down syndrome)
* Environmental factors: Maternal diabetes, maternal phenylketonuria, fetal alcohol syndrome.
174
What is the pathophysiological consequence of Right Ventricular Outflow Tract Obstruction (RVOTO) in TOF?
Increased right ventricular pressure.
175
What leads to hypoxemia and cyanosis in Tetralogy of Fallot?
Right-to-Left Shunt due to high right ventricular pressure shunting deoxygenated blood through the VSD into the aorta.
176
What are the clinical features of Tetralogy of Fallot?
* Cyanosis
* Clubbing
* Dyspnea on exertion
* Hypoxic (Tet) spells
* Squatting behavior
* Harsh systolic ejection murmur
177
What is the gold standard for diagnosing Tetralogy of Fallot?
Echocardiography.
178
What are the initial management strategies for Tet spells?
* Knee-chest position
* Oxygen
* Beta-blockers (e.g., Propranolol)
* Morphine
* IV Fluids
* Sodium Bicarbonate
179
What is the preferred surgical management for Tetralogy of Fallot?
Primary Repair within the first year of life.
180
What are the potential complications of Tetralogy of Fallot?
* Heart Failure
* Arrhythmias
* Brain Abscesses/Stroke
* Polycythemia
181
What defines Transposition of the Great Arteries (TGA)?
Anatomical reversal of the aorta and the pulmonary artery, resulting in two parallel circulations.
182
What are the major causes of Transposition of the Great Arteries?
* Abnormal development of the truncal and aortopulmonary septa
* Genetic factors (e.g., DiGeorge syndrome)
* Maternal conditions (e.g., diabetes)
* Environmental factors (e.g., prenatal exposure to alcohol or infections)
183
What is the significance of mixing points in TGA?
Survival depends on the mixing of oxygenated and deoxygenated blood, typically through ASD, VSD, or PDA.
184
What are the clinical features of Transposition of the Great Arteries?
* Cyanosis
* Tachypnea
* Tachycardia
* Heart murmur
* Clubbing and Polycythemia
185
What imaging findings are characteristic of Transposition of the Great Arteries?
* Egg-on-a-string appearance on chest X-ray
* Increased pulmonary vascular markings
186
What is the initial stabilization treatment for TGA?
* Prostaglandin E1 infusion
* Balloon Atrial Septostomy (Rashkind Procedure)
187
What is the definitive surgical treatment for Transposition of the Great Arteries?
Arterial Switch Operation (ASO) performed in the first few weeks of life.
188
What are the complications associated with Transposition of the Great Arteries?
* Coronary artery obstruction
* Arrhythmias
* Heart failure
* Residual shunts
189
What is the prognosis for patients with TGA after timely surgical intervention?
Good prognosis with excellent long-term survival.
190
What is coarctation of the aorta (CoA)?
A congenital narrowing of the aorta, typically occurring near the insertion of the ductus arteriosus.
191
What are the common congenital associations with coarctation of the aorta?
* Turner syndrome (45,X)
* Bicuspid aortic valve (50% of cases)
* Other congenital heart defects (VSD, PDA, aortic stenosis)
192
What are the acquired causes of coarctation of the aorta?
* Takayasu arteritis
* Atherosclerosis (rare in adults)
193
Where does the narrowing in coarctation of the aorta typically occur?
Most commonly at the juxtaductal region near the ductus arteriosus.
194
What are the hemodynamic consequences of coarctation of the aorta?
* Increased afterload on the left ventricle
* Hypertension proximal to the coarctation
* Hypotension and decreased perfusion distal to the coarctation
* Development of collateral vessels
195
What clinical features are seen in infants with severe coarctation of the aorta?
* Tachypnea
* Poor feeding
* Lethargy
* Differential cyanosis
* Shock
196
What are the clinical features of older children and adults with coarctation of the aorta?
* Hypertension in upper extremities
* Lower extremity claudication
* Decreased or absent femoral pulses
* Brachio-femoral delay
* Headache, epistaxis
197
What are the complications associated with coarctation of the aorta?
* Heart failure
* Aortic rupture or dissection
* Infective endocarditis
* Stroke
198
What is the key diagnostic finding in physical examination for coarctation of the aorta?
Elevated blood pressure in upper limbs and low blood pressure in lower limbs.
199
What imaging findings are characteristic of coarctation of the aorta on chest X-ray?
* Rib notching
* Figure 3 sign
200
What is the management for neonates and infants with coarctation of the aorta?
* Prostaglandin E1 infusion
* Inotropic support
* Urgent surgical repair
201
What is the preferred management for older children and adults with coarctation of the aorta?
* Percutaneous balloon angioplasty with stent placement
* Surgical repair for complex cases
202
What is the prognosis for patients with coarctation of the aorta after successful intervention?
Most patients have a good long-term prognosis, but residual hypertension may occur.
203
What are the key features of pulmonary stenosis?
* Narrowing of the pulmonary valve
* Increased right ventricular pressure
* Right ventricular hypertrophy
204
What are the associated syndromes with pulmonary stenosis?
* Tetralogy of Fallot
* Noonan Syndrome
* Congenital Rubella Syndrome
205
What distinguishes pulmonary atresia from pulmonary stenosis?
Pulmonary atresia involves complete obstruction with no blood flow from the right ventricle to the pulmonary artery.
206
What are the clinical features of severe pulmonary stenosis?
* Cyanosis
* Exertional dyspnea
* Right-sided heart failure
207
What is the diagnostic tool of choice for pulmonary stenosis?
Echocardiography.
208
What is the first-line treatment for moderate to severe pulmonary stenosis?
Balloon valvuloplasty.
209
What is the management for pulmonary atresia in neonates?
* Prostaglandin E1 infusion
* Oxygen support
210
What is a common surgical procedure for pulmonary atresia to increase pulmonary blood flow?
Blalock-Taussig shunt.
211
What is the prognosis for pulmonary stenosis with early intervention?
Good prognosis with lifelong follow-up required.
212
What can occur at the site of repair in coarctation of the aorta?
Aneurysm formation.
213
What are the primary reasons for cardiovascular changes during pregnancy?
To ensure adequate blood flow to the placenta, support maternal tissues, accommodate increased blood volume, and prepare for blood loss during delivery.
214
How much does total blood volume increase during pregnancy?
Increases by 30-50% (about 1.5 liters).
215
What is the physiological effect of increased blood volume during pregnancy?
Physiological Anemia due to disproportionate increase in plasma compared to RBCs.
216
By what percentage does cardiac output increase during pregnancy?
Increases by 30-50%.
217
What causes the increase in stroke volume during pregnancy?
Increased preload from higher blood volume.
218
What happens to heart rate during pregnancy?
Increases by 10-20 bpm.
219
What is the peak cardiac output period during pregnancy?
Around 20-24 weeks gestation.
220
What is a potential effect of increased cardiac output on women with preexisting cardiac conditions?
They may experience decompensation.
221
How does the heart position change during pregnancy?
Heart is displaced upward and slightly left due to the elevated diaphragm.
222
What causes decreased systemic vascular resistance (SVR) during pregnancy?
Peripheral vasodilation due to progesterone and nitric oxide.
223
What is the typical blood pressure trend during the trimesters of pregnancy?
Slight decrease in 1st trimester, lowest in 2nd trimester, gradual increase in 3rd trimester.
224
What is supine hypotensive syndrome?
Compression of the inferior vena cava by the gravid uterus, decreasing venous return and causing hypotension.
225
What causes increased venous pressure in lower extremities during pregnancy?
IVC compression by the growing uterus and decreased venous return.
226
What are common effects of increased venous pressure in lower extremities?
* Varicose veins * Hemorrhoids * Edema * Increased risk of deep vein thrombosis (DVT)
227
By what percentage does oxygen consumption increase during pregnancy?
Increases by 20-30%.
228
What are the key hormones influencing cardiovascular changes during pregnancy?
* Estrogen * Progesterone * Relaxin * Human Chorionic Gonadotropin (hCG) * Placental Growth Hormone
229
What role does estrogen play in cardiovascular changes during pregnancy?
Increases vascular endothelial growth factor (VEGF) and nitric oxide (NO) production leading to vasodilation.
230
What is the effect of relaxin during pregnancy?
Increases arterial compliance and cardiac output by dilating systemic arteries.
231
What is pre-eclampsia?
A pregnancy-specific hypertensive disorder characterized by new-onset hypertension and proteinuria after 20 weeks of gestation.
232
What are some maternal risk factors for pre-eclampsia?
* First pregnancy (nulliparity) * Advanced maternal age (>35) * Obesity * Pre-existing hypertension * Diabetes * Renal disease
233
What are the theories related to the etiology of pre-eclampsia?
* Abnormal placental development * Endothelial dysfunction * Immunological factors * Genetic predisposition * Vascular dysfunction
234
What are the clinical features of pre-eclampsia?
* Blood pressure ≥140/90 mmHg after 20 weeks gestation * Proteinuria * Possible signs of multisystem involvement
235
What is the significance of increased sFlt-1 in pre-eclampsia?
It binds to VEGF, reducing endothelial repair and contributing to hypertension.
236
What is HELLP syndrome?
A severe form of pre-eclampsia characterized by Hemolysis, Elevated Liver enzymes, Low Platelets.
237
What happens during the pathophysiology of pre-eclampsia related to placentation?
Failure of Spiral Artery Remodeling leading to narrow, high-resistance arteries.
238
What is a common cardiovascular complication associated with pre-eclampsia?
Hypertension and left ventricular hypertrophy.
239
What is the management approach for pre-eclampsia?
Monitoring, potential medication for blood pressure control, and delivery if severe.
240
What can be a consequence of failure to accommodate cardiovascular changes during pregnancy?
Pregnancy complications such as preeclampsia or heart failure.
241
What is proteinuria and oliguria associated with?
Glomerular damage
## Footnote
These are renal complications often seen in pre-eclampsia.
242
What does HELLP syndrome stand for?
Hemolysis, Elevated Liver enzymes, Low Platelets
## Footnote
A hepatic complication of severe pre-eclampsia.
243
What neurological symptoms are associated with severe pre-eclampsia?
Cerebral edema, eclampsia (seizures)
## Footnote
Eclampsia is a serious condition that can occur in the context of pre-eclampsia.
244
What hematological condition is characterized by low platelet count?
Thrombocytopenia
## Footnote
Thrombocytopenia can occur in pre-eclampsia and HELLP syndrome.
245
What is the blood pressure diagnostic criterion for pre-eclampsia?
≥140/90 mmHg after 20 weeks gestation on 2 occasions at least 4 hours apart
## Footnote
This criterion helps in the diagnosis of pre-eclampsia.
246
How is proteinuria defined for the diagnosis of pre-eclampsia?
≥300 mg/24-hour urine collection or urine protein/creatinine ratio ≥0.3
## Footnote
Proteinuria is a key indicator in diagnosing pre-eclampsia.
247
What can confirm the diagnosis of pre-eclampsia in the absence of proteinuria?
* Thrombocytopenia: Platelets <100,000/mm³
* Renal Insufficiency: Serum creatinine >1.1 mg/dL or doubling of baseline
* Liver Dysfunction: Elevated liver transaminases
* Pulmonary Edema
* Neurological Symptoms: Headache, visual disturbances
## Footnote
These criteria are important for accurate diagnosis.
248
What are common symptoms of pre-eclampsia?
* Persistent and severe headache
* Blurred vision or scotoma
* Epigastric or Right Upper Quadrant Pain
* Generalized or localized edema
* Rapid weight gain due to fluid retention
* Hyperreflexia and clonus
## Footnote
Recognizing these symptoms is crucial for early intervention.
249
What is the initial screening test for proteinuria?
Dipstick Test
## Footnote
This is commonly used as a first step in assessing protein levels in urine.
250
What laboratory tests are important in diagnosing pre-eclampsia?
* CBC: Anemia, thrombocytopenia
* Liver Function Tests: Elevated AST/ALT
* Renal Function Tests: Elevated creatinine
* Coagulation Profile
* LDH: Elevated in HELLP syndrome
## Footnote
These tests help evaluate the overall health of the mother and fetus.
251
What fetal monitoring techniques are used in pre-eclampsia?
* Ultrasound: Fetal growth restriction, oligohydramnios
* Doppler Studies: Uteroplacental insufficiency
* Non-Stress Test (NST): Fetal well-being
## Footnote
These techniques are vital for assessing the fetal condition.
252
What is the management for mild pre-eclampsia?
* Monitoring: BP, urine protein, fetal growth
* Lifestyle: Rest and reduced activity
* Antihypertensives: Labetalol, methyldopa, nifedipine
## Footnote
Outpatient management is essential for mild cases.
253
What is the primary treatment for severe pre-eclampsia?
* Magnesium Sulfate: To prevent seizures
* Antihypertensive Therapy: Labetalol, hydralazine, or nifedipine
* Corticosteroids: If <34 weeks for fetal lung maturity
* Fluid Management: To avoid pulmonary edema
## Footnote
Hospitalization is often necessary for severe cases.
254
What is the definitive treatment for pre-eclampsia?
Delivery
## Footnote
The timing and mode of delivery depend on the gestational age and maternal or fetal compromise.
255
What is the prognosis for mothers with pre-eclampsia if managed early?
Good; risk of long-term hypertension
## Footnote
Early management can significantly improve outcomes.
256
What is the fetal prognosis dependent on?
Gestational age at delivery and severity
## Footnote
Outcomes can vary widely based on these factors.
257
What preventive measure is recommended for high-risk women starting from 12 weeks?
Low-Dose Aspirin (75-150 mg/day)
## Footnote
This is suggested to help reduce the risk of developing pre-eclampsia.
258
What supplementation is advised for women with low dietary intake?
Calcium Supplementation
## Footnote
This may help in the prevention of pre-eclampsia.
