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UWORLD > Embyology > Flashcards

Embyology Flashcards

1
Q

What is the triple test? When should it be performed?

A

Triple test: AFP, hCG, estriol

Should be performed btw weeks 16-18

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2
Q

What is AFP?

A

Alpha-fetoprotein is synthesized by fetal liver, GI tract, and yolk sac (early gestation only). Maternal serum AFP levels increase with gestational age.

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3
Q

What is the most common cause of elevated AFP? What are some other causes?

A

Most common: dating error aka underestimation of gestational age–> confirm by fetal u/s
Other causes: neural tube defects, anterior abdominal wall defects (omphalocele, gastroschisis), multiple gestation.

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4
Q

What is estriol? What are decreased levels of estriol suggestive of?

A

Estriol levels: placental and fetal function, both are necessary for synthesis.
Decreased estriol suggest placental insufficiency or IUGR

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5
Q

What is hCG? What are increased levels of hCG associated with?

A

Human chorionic gonadotropin is synthesized by trophoblastic tissue.
Increased levels associated with multiple gestation, hydatidiform mole, choriocarcinoma.

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6
Q

Cranial nerve and bone/cartilage derivatives of pharyngeal (branchial) arch 1

A

CN V (trigeminal)
Mandible, maxilla, zygoma, incus, malleus
Muscles: muscles of mastication (masseter, temporalis, etc)

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7
Q

Cranial nerve and bone/cartilage derivatives of pharyngeal arch 2

A

CN VII (facial nerve)
Stapes, styloid process, lesser horn of hyoid
Muscles: muscles of facial expression

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8
Q

Cranial nerve and bone/cartilage derivatives of pharyngeal arch 3

A 
CN IX (glossopharyngeal)
Greater horn of hyoid
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9
Q

Cranial nerve and bone/cartilage derivatives of pharyngeal arch 4 and 6

A

Vagus (X)
Laryngeal cartilages: cricoid, thyroid cartilages
Dysfunction= laryngeal and pharyngeal paralysis and autonomic dysfunction (eg, esophageal motility, gastric acid secretion, heart rate variability)

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10
Q

What are pharyngeal arches?

A

Developing embryo has 6 pharyngeal (branchial) arches. All but 5th arch contribute to adult structures. Mesoderm forms muscular and vascular elements, neural crest cells form bony/cartilaginous structures. Each arch gives rise to specific CN.

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11
Q

What is Treacher-Collins syndrome (TCS)?

A

Genetic disorder (usually AD) resulting in abnormal development of 1st and 2nd pharyngeal arches. Mutation affects production of “treacle” a protein integral to normal neural crest migration. Resulting craniofacial abnormalities: mandibular and zygomatic bone hypoplasia, microtia (underdeveloped pinna), downward slanting palpebral fissures, lower eyelid colobomas. Typically require extensive craniofacial surgery in childhood due to airway compromise and feeding difficulty.

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12
Q

What is the pathophysiology behind duodenal atresia?

A

Failure of recanalization at 8-10 weeks gestation. Sx. bilious or nonbilious emesis. Double-bubble sign on x-ray. Associated with Down syndrome.

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13
Q

What is the pathophysiology behind jejunum/ileum/proximal colon (midgut) atresia?

A

Vascular injury/occlusion in utero. Diminished intestinal perfusion leads to ischemia of segment of bowel with subsequent narrowing (stenosis) or obliteration (atresia) of lumen. Sx. Bilious emesis and abdominal distension. Associated with gastroschisis.

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14
Q

What is “apple-peel” or “Christmas tree” atresia?

A

If SMA occluded in utero, the area of intestinal necrosis is large leading to a proximal segment that ends in a blind pouch followed by an area of absent small bowel and associated dorsal mesentery. Finally, distal segment of ileum assumes spiral configuration around an ileocolic vessel.

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15
Q

Hirschsprung disease

A

Failure of NC cells to migrate into the distal colonic wall. Submucosal and myenteric plexi do not develop and distal colon becomes nonfunctional. Infant has intestinal obstruction, abdominal distention, and failure to pass meconium.

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16
Q

How does neural system form?

A

During 3rd week of life ectoderm on dorsal surface of embryo thickens to form neural plate. Neural plate deepens in the center to create the neural groove that is bound on both sides by neural folds. The folds fuse to create a neural tube with openings at the ends called neuropores. Anterior and posterior neuropores close during 4th week of fetal life. Failure to close leads to neural tube defects. Folic acid supplementation early in pregnancy significantly decreases risk of these defects.

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17
Q

What is fetal alcohol syndrome?

A

Most common cause of mental retardation. Caused by alcohol consumption during pregnancy. Associated with cardiac defects (VSD), brain defects (microcephaly, holoprosencephaly) and abnormal facies (short palpebral fissures and smooth/long philtrum).

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18
Q

How does smoking during pregnancy affect infant?

A

Can cause fetal hypoxia, IUGR, low birth weight, premature delivery. Not associated with NTDs.

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19
Q

What are the embryologic derivatives of surface ectoderm?

A

Rathke’s pouch (anterior pituitary); lens, cornea; inner ear sensory organs; olfactory epithelium; nasal/oral epithelial linings; epidermis; salivary, sweat/mammary glands

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20
Q

What are the embryologic derivatives of neural tube?

A

Brain, spinal cord, posterior pituitary, pineal gland, retina

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21
Q

What are the embryologic derivatives of neural crest cells?

A

Autonomic, sensory, celiac ganglia (PNS); Schwann cells; pia mater, arachnoid mater; aorticopulmonary septum, endocardial cushions; branchial arches (bones and cartilage); skull bones; melanocytes; chromaffin cells of adrenal medulla; thyroid parafollicular C cells

MOTEL PASS: Melanocytes, Odontoblasts, Tracheal cartilage, Enterochromaffin cells, Laryngeal cartilage, Parafollicular cells of thyroid, Adrenal medulla, Schwann cells, Spiral membrane

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22
Q

What are the embryologic derivatives of mesoderm?

A

Muscles (skeletal, cardiac, smooth), connective tissues, bone and cartilage, serosa linings, CV system, blood, lymphatic system, spleen, internal genitalia, kidney and ureters, adrenal cortex

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23
Q

What are the embryologic derivatives of endoderm?

A

GI tract, liver, pancreas, lungs, thymus, parathyroids, thyroid follicular cells, middle ear, bladder and urethra

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24
Q

What is gastrulation and when does it occur?

A
  1. 3 primary germ layers are formed during week 3 of embryogenesis during gastrulation.
  2. Initiated by formation of primitive streak, a thickening of epiblast cell layer that appears at caudal end of embryo and grows cranially.
  3. Epiblast cells undergo epithelial-to-mesenchymal transition, causing them to lose cell-cell adhesion properties.
  4. Allows them to migrate downward through the primitive streak to form the mesoderm and endoderm layers.
  5. Remainder of epiblast layer forms ectoderm.
    * *********
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25
Q

What is the notochord and how does it form?

A

The notochord becomes the nucleus pulposus of the intervertebral disk in adults. 2 days after gastrulation begins, some epiblast cells migrate cranially through primitive node to form a midline cellular cord, the notochord, which induces the overlying ectoderm to differentiate into neuroectoderm and form the neural plate.

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26
Q

What is a true diverticulum?

A

Contains all layers of GI tract (mucosa, submucosa, muscularis, serosa) i.e. Meckel’s diverticulum, appendix.

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27
Q

What is a pseudodiverticulum?

A

A false diverticulum. Only contains mucosa and submucosa layers as the diverticulum herniates through defects in the muscularis. ie. Zenker’s diverticulum, colonic diverticula

28
Q

What is a Meckel’s diverticulum?

A

Remnant of the omphalomesenteric (vitelline) duct that previously connected lumen of midgut to yolk sac and normally obliterates during 7th week of fetal life. In Meckel’s diverticulum there is partial failure of this duct to obliterate.

29
Q

What is the rule of 2s?

A

2% of population, 2 feet from ileocecal valve, 2 inches long, 2% symptomatic, males 2x more likely to have one.

30
Q

What is the Potter sequence?

A
  1. Potter sequence is caused by a renal anomaly that leads to decreased urine output by the fetus.
  2. Classically 2/2 bilateral renal agenesis, but can be 2/2 to posterior urethral valves or ARPKD.
  3. Urinary tract anomaly–> anuria/oliguria in utero–> oligohydramnios–> pulmonary hypoplasia 2/2 decreased stretching of alveoli by amniotic fluid (breath sounds markedly diminished bilaterally), flat facies (flattened nose), and limb deformities (bilateral club feet) b/c no buffer between fetus and uterine wall.
  4. Umbilical cord often compressed and fetal heart rate anomalies are common during labor.
  5. Respiratory failure 2/2 to severe pulmonary hypoplasia is the most common cause of death among infants with Potter sequence.
    * *********
31
Q

Congenital diaphragmatic hernia

A

Severe respiratory disease, pulmonary hypertension, absent breath sounds unilaterally.

32
Q

Transposition of the great arteries (TGA)

A
  1. Echocardiogram showing an aorta lying anterior to and to the right of the pulmonary artery is diagnostic of transposition of the great arteries (TGA).
  2. TGA results from failure of fetal aorticopulmonary septum to spiral normally during septation of the truncus arteriosus.
  3. Aorta connected to the right ventricle and a pulmonary artery connected to the left ventricle causing separation of pulmonary and systemic circulations and life-threatening cyanosis at birth.
  4. Incompatible with life in absence of accompanying connection (eg, PFO, septal defect, PDA) to allow mixing of oxygenated pulmonary circulation with systemic circulation.
    * *********
33
Q

Continuous machine-like murmur

A

Patent ductus arteriosus (can be found with TGA or on its own)

34
Q

Failed embryonic fusion examples

A
  1. Ex 1. Ostium primum atrial septal defect (failure of endocardial cushion fusion)
  2. Ex 2. Hypospadias (failure of urethral folds to fuse)
  3. Ex 3. Neural tube defect (failure of fusion of neural rube at cranial or caudal neuropores)
    * ****
35
Q

What can be seen on amniocentesis with a neural tube defect?

A

If neuropores do not fuse appropriately, there is an opening between the neural tube and the amniotic cavity. Due to the leakage of fetal CSF, AFP and acetylcholinesterase may appear in amniotic fluid. AFP crosses placenta and level elevated in maternal serum.

36
Q

Primary oocytes

A

A woman’s full complement of primary oocytes (46, 4N) is developed in female embryos by fifth month of gestation, at which point they are arrested in prophase of meiosis I until puberty.

37
Q

Secondary oocyte

A
  1. FSH stimulation during the ovarian cycle (puberty) causes some oocytes to complete meiosis I, forming secondary oocytes and polar bodies (both 23, 2N).
  2. Secondary oocytes (23, 2N) begin meiosis II (the polar body degenerates) but halt in metaphase II.
  3. At day 14 of menstrual cycle, secondary oocyte released from ovarian follicle in response to high estrogen concentrations and paradoxical LH surge (estrogen typically causes feedback inhibition of LH and FSH).
  4. Secondary oocyte remains frozen in metaphase II until fertilization occurs, at which point it divides into a mature oocyte and second polar body.
    * *********
38
Q

Gametogenesis in female

A
  1. Begins early in embryonic development (4 weeks) when primordial germ cells migrate from yolk sac region to developing gonadal region.
  2. PGCs differentiate into oogonia (46, 2N), before beginning meiosis I.
  3. Now called primary oocytes (46, 4N), these cells arrest in prophase of meiosis I and remain until puberty.
  4. At puberty, ovulatory cycles begin. FSH stimulation during the ovarian cycle causes some oocytes to complete meiosis I, forming secondary oocytes and polar bodies (both 23, 2N).
    * *********
39
Q

Derivative of common cardinal veins

A

Superior vena cava (SVC) derived from common cardinal veins. On CT- posterolateral to ascending aorta, anterior to right pulmonary artery, just below level of carina.

40
Q

Veins of early embryonic development

A

Veins fall into 3 main groups: vitelline veins (form portal system), umbilical veins (degenerate), cardinal veins (form veins of systemic circulation).

41
Q

Pulmonary trunk/aorta formation

A

Neural crest cells migrate to partition the truncus arteriosus into the two great arteries by causing fusion and twisting of the truncal and bulbar ridges. Process results in the normal spiral relation between the aorta and pulmonary artery. Failure = TGA and tetralogy of Fallot

42
Q

Amniotic fluid lecithin (phosphatidylcholine) to sphingomyelin ratio

A

Marker of fetal lung maturity. Values above 1.9 indicative of mature fetal lungs. Outward flow of pulmonary secretions from fetal lungs into amniotic fluid maintains the level of lecithin and sphingomyelin equally until 32-33 weeks. Then lecithin concentration begins to increase significantly as surfactant production by mature type II pneumocytes increases. Phosphatidylcholine (lecithin) is component of pulmonary surfactant. Sphingomyelin is common membrane phospholipid and only a minor component of pulmonary surfactant.

43
Q

Multiple Endocrine Neoplasia (MEN) type 2

A

Associated with germ line mutations in RET proto-oncogene and characterized by pheochromocytomas (catecholamine-producing tumor of chromaffin cells of adrenal medulla), medullary thyroid cancer (malignancy of parafollicular C cells), parathyroid hyperplasia (MEN 2A) or mucosal neuromas and marfanoid habitus (MEN 2B)

44
Q

Imperforate anus

A

Spectrum of disorders associated with abnormal development of anorectal structures that manifests as inability to pass meconium or meconium discharge from urethra or vagina. Absence of anal opening most often associated with urorectal, urovesical, urovaginal fistulas. Imperforate anus commonly associated with genitourinary tract malformations (renal agenesis, hypospadias, epispadias, bladder extrophy).

45
Q

VACTERL

A

Vertebral defects, Anal atresia, Cardiac anomalies, Tracheoesophageal fistula, Esophageal atresia, Renal anomalies, Limb anomalies. Much less common than isolated urogenital anomalies associated with imperforate anus.

46
Q

What are the hormones that regulate L/S ratio?

A
  1. Hormones that regulate synthesis of fetal surfactant: glucocorticoids, prolactin, insulin, estrogens, androgens, thyroid hormones, catecholamines.
  2. Glucocorticoids have greatest effect on increasing surfactant production.
  3. Both maternal and fetal cortisol help accelerate fetal lung maturation by stimulating surfactant production.
  4. Production of fetal cortisol gradually increases later in gestation from dormant adult zone of adrenal gland and in response to high placental CRH secretion (which is up-regulated by maternal cortisol).
    * *********
47
Q

Spleen blood supply

A

Spleen derived from mesoderm of dorsal mesentery. Spleen blood supply derives from foregut derivative (splenic artery off the celiac trunk). Venous return from spleen courses through the splenic vein to return to portal circulation rather than systemic circulation.

48
Q

What are the 3 arteries off of the celiac trunk?

A

Left gastric artery, splenic artery, common hepatic artery (which branches into proper hepatic and gastroduodenal artery)

49
Q

Hirschsprung disease

A
  1. Neural crest cells start migrating to intestinal wall early in embryonic developmnent, giving rise to ganglion cells of submucosal (Meissner) and myenteric (Auerbach) plexi of the bowel wall, responsible for intestinal peristalsis.
  2. NC cells move caudally along vagal nerve fibers and are present in proximal colon at 8th week of gestation and in the rectum by 12th week of gestation.
  3. If migration interrupted during 12th week, rectum most likely to be affected.
  4. Absence of ganglion cells in colonic wall causes affected segment to be narrowed b/c cannot relax causing passage through area difficult with compensatory dilatation of proximal areas of the colon (megacolon).
  5. Newborns with Hirschsprung disease fail to pass meconium within 48 hours of birth, as well as bilious vomiting and abdominal distention.
  6. Sigmoid colon involved in Hirschsprung disease 75% of cases, rectum and anus always involved.
    * *********
50
Q

Foregut

A

Gives rise to esophagus, stomach, liver, gallbladder, pancreas, upper duodenum. These organs are supplied by the celiac trunk.

51
Q

Midgut

A

Gives rise to lower duodenum, small intestine, ascending colon, proximal 2/3 of transverse colon. These organs are supplied by the superior mesenteric artery (SMA).

52
Q

Hindgut

A

Gives rise to distal 1/3 of transverse colon, descending and sigmoid colon. These organs are supplied by the inferior mesenteric artery (IMA).

53
Q

Malrotation of midgut

A

Abnormal rotation and fixation of midgut early in fetal life results in intestinal malrotation causing intestinal obstruction (2/2 compression of duodenum by adhesive Ladd’s bands) and midgut volvulus with intestinal gangrene and perforation (2/2 intestinal ischemia due to twisting of intestine around SMA causing impaired perfusion).

54
Q

Midgut development

A
  1. Midgut herniates through umbilical ring during week 6 of embryogenesis to allow rapid growth of intestine and liver despite slower growth of abdominal cavity.
  2. Midgut returns to abdominal cavity during week 10, simultaneously completing a 270-degree turn counterclockwise around SMA.
  3. Rotation allows for proper placement and fixation of intestine in abdominal cavity.
  4. If abnormal–> intestinal malrotation occurs, where cecum found in RUQ fixed with fibrous bands (Ladd’s bands) to second portion of duodenum. Entire midgut fixed to SMA.
    * *********
55
Q

Pancreas divisum

A

Failure of ventral and dorsal pancreatic buds to fuse during week 8 of embryogenesis. Usually incidental finding.

56
Q

Hindgut development

A

Hindgut descent along IMA occurs after midgut returns to abdominal cavity. As intestine grows, ascending and descending loops of colon are pressed against posterior wall of abdomen and are fixed in this position.

57
Q

Vitelline duct abnormalities

A

Persistent vitelline duct (fistula to umbilicus), vitelline sinus, vitelline duct cyst (enterocyst connected to ileum and abdominal wall by fibrous bands), Meckel’s diverticulum. Omphalomesenteric duct connects midgut lumen with yolk sac cavity until it obliterates during week 7 of development.

58
Q

Patent foramen ovale (PFO)

A

PFO occurs in approximately 25% of normal adults. Usually remains functionally closed, but transient increases of right atrial pressure above left atrial pressure (eg, Valsalva) can product a right-to-left shunt, leading to paradoxical embolization of venous clots into systemic arterial circulation.

59
Q

Foramen ovale

A

Used to shunt oxygenated fetal blood from the IVC across the right atrium and into the left atrium. After delivery, umbilical cord clamping and the suddenly decreased pulmonary vascular resistance lower right atrial pressure and raise left atrial pressure, changing the pressure gradient and pushing the flap of the septum primum against the septum secundum and closing the foramen ovale. Over time, fibrosis and remodeling fuses the flap closed.

60
Q

Atrial septal defect (ASD)

A

Open defect of atrial wall. Occurs 2/2 aplasia of the atrial septum secundum or septum primum during development. Over time, patients with unrepaired ASD can get heart failure, pulmonary hypertension, or Eisenmenger syndrome. Fixed splitting of S2 is characteristic of ASD. PFO (25%) is much more common than ASD (~0.1%).

61
Q

Truncus arteriosus

A

Incomplete development of the aorticopulmonary septum results in a single great vessel leaving the heart. Defect causes cyanosis in the newborn and requires early surgical repair.

62
Q

Horseshoe kidney

A

Conjoined kidneys connected at the lower pole, most common congenital renal anomaly. Kidney develops in pelvis and ascends to the abdomen during embryogenesis. Horshoe kidney gets caught on IMA root and is abnormally located in the lower abdomen.

63
Q

Unilateral renal agenesis

A

Leads to hypertrophy of the other existing kidney. Hyperfiltration through this kidney increases the risk of renal failure later in life.

64
Q

Dysplastic kidney

A
  1. Non-inherited, congenital malformation of the renal parenchyma characterized by cysts and abnormal tissue such as cartilage.
  2. Low risk for any subsequent pregnancy to have dysplastic kidney as not inherited.
  3. Usually unilateral. When bilateral must be distinguished from inherited polycystic kidney disease.
    * *******
65
Q

Polycystic kidney disease (PKD)

A
  1. Inherited defect leading to b/l enlarged kidneys with cysts in the renal cortex and medulla.
  2. AR form presents in infants as worsening renal failure and hypertension; newborns may present with Potter sequence.
  3. ARPKD associated with congenital hepatic fibrosis (leads to portal hypertension) and hepatic cysts. Baby with signs of portal HTN–> think ARPKD.
  4. AD form presents in young adults as hypertension (2/2 increased renin), hematuria, worsening renal failure.
  5. ADPKD 2/2 mutation in APKD1 or APKD2 genes, cysts develop over time.
  6. ADPKD associated with berry aneurysms, hepatic cysts and mitral valve prolapse –> “cysts in the brain, cysts in the liver, cysts in kidneys”.
    * *********
66
Q

Medullary cystic kidney disease

A
  1. Inherited AD defect leading to cysts in the medullary collecting ducts.
  2. Parenchymal fibrosis results in shrunken kidneys and worsening renal failure.
    * ****

UWORLD (8 decks)

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