Anatomy Aid Anatomy Aid [86592]

ANATOMY Embryology Embryonic Period: Weeks 3-8, organ system development simultaneous I.

The Heart A. Development (MESODERM) 1. Primitive heart tube - pair of endocardial heart tubes (mesoderm) form within cardiogenic region -EHT fuse during lateral folding to form primitive heart tube = endocardium -surrounding mesoderm develops into myocardium and epicardium -PHT forms five dilations (First Aid p. 94) 2. AP septum (aorticopulmonary) -divides truncus arteriosus into aorta and pulmonary trunk -neural crest cells migrate into truncal and bulbar ridges -grow and twist in spiral, fuse to form AP septum 3. AV septum (atrioventricular) -partitions AV canal into right and left AV canals -dorsal and ventral AV cushions fuse to form AV septum 4. Atrial septum -septum primum grows toward AV septum -foramen primum between edges of septum primum and AV septum; obliterated when SP fuses with AV cushions -septum segundum (crescent-shaped) forms to right of SP and fuses after birth with SP to form atrial septum -foramen ovale is opening between upper and lower parts of SS; shunts blood from right atrium to left atrium -functional closure soon after birth due to pressure changes; anatomical fusion incomplete in 25% of population; incidental (Image, see High-Yield Embryo)

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IV septum (interventricular) -muscular IV septum develops into floor of ventricle and grows toward AV septum; stops short to create IV foramen

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-membranous IV septum forms following fusion of right and left bulbar ridges and AV septum; closes IV foramen 6. Aortic Arches (First Aid p. 92) B. Congenital Anomalies 1. AP septal defects a. Tetralogy of Fallot -improper alignment of AP and AV septums -overriding Aorta, Pulmonary stenosis, VSD (poor AV fusion), right ventricular hypertrophy (right-to-left shunting, cyanosis) b. TGA (transposition of great arteries) -AP septum fails to spiral -right-to-left shunting, cyanosis c. Persistent truncus arteriosus -abnormal neural crest cell migration, incomplete development of AP septum -usually accompanied by defect in IV septum -cyanosis 2. Atrial septal defects a. Patent foramen ovale -foramen secundum defect, excessive resorption of SP or SS -symptoms may manifest as late as age 30 -most common ASD 3. VSDs a. Membranous VSD -most common VSD -fails to develop -left-to-right shunting, pulmonary hypertension -sx: excessive fatigue on exertion 4. Circulatory anomalies a. Coarctation of aorta -abnormally constricted inf. to ductus arteriosus -increased BP in upper extremities, lack of femoral pulse, high risk of cerebral hemorrhage and bacterial endocarditis b. PDA (patent ductus arteriosus) -common in premature infants, mothers with rubella during pregnancy -causes L>R shunting, O2 rich blood back into pulm. circulation -can treat with indomethacin (prostaglandin synthesis inhibitor; I remember it by saying, Take yo’ PDA indo’, man! Also used for acute gout, as in stay indo’ or go-out) The Lungs A. Development -laryngotracheal diverticulum forms in ventral wall of foregut -tracheoesophageal septum divides foregut into esophagus and trachea -distal end of LTD enlarges to form lung bud -lung bud > 2 bronchial buds > primary, secondary, tertiary bronchi = bronchopulmonary segments -4 stages 1. Glandular (Weeks 5-17) -respiration not possible, premature fetuses cannot survive 2. Canalicular (Weeks 13-25) -respiratory bronchioels and terminal sacs; vascularization increases 3. Terminal Sac (Weeks 24-birth) -Type I and II pneumocytes, respiration possible -Premature fetuses weeks 25-28 can survive 4. Alveolar (Birth-year 8) -resp. bronchioles, terminal sacs, alveolar ducts and alveoli increase in number B. Congenital anomalies 1. Tracheosophageal fistula

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-abnormal communication b/t trachea and esophagus; malformation of septum -sx: gagging and cyanosis after feeding, abd. distention after crying, reflux of gastric contents into lungs Respiratory distress syndrome -deficiency of surfactant -common in premature infants, infants with diabetic mothers, fetuses with prolonged IU asphyxia -tx: thyroxine and cortisol to mother Pulmonary hypoplasia -secondary to congenital diaphragmatic hernia (into pleural cavity) and bilateral renal agenesis

Liver A. Development -hepatic diverticulum (endoderm of foregut) forms in septum transversum (surrounding mesoderm, also plays part in development of diaphragm) -HD sends hepatic cell cords into ST -Cell cords surround vitelline veins, which form hepatic sinusoids Kidney A. Development -Intermediate mesoderm forms elevation along dorsal body wall = urogenital ridge -portion of UG ridge, called nephrogenic cord, forms 3 sets of kidneys 1. Pronephros completely regresses 2. Mesonephros forms mesonephric (wolffian) duct 3. Metanephros develops from metanephric mesoderm and ureteric bud (outgrowth of mesonephric duct); becomes definitive adult kidney -ascends during development from sacral region to adult location at T12-L3 B. Congenital anomalies 1. Renal agenesis - failure of ureteric bud to develop 2. Horseshoe kidney – inferior poles fuse, kidney trapped behind inf. mesenteric artery 3. Wilm’s tumor – malignant tumor in children, probably of embryonic origin, good prog 4. Urachal cyst – remnant of allantois, urine drainage from umbilicus 5. Pheochromocytoma – chromaffin cell tumor, generally along migratory path of neural crest cells CNS A. Development 1. Notochord induces overlying ectoderm to differentiate into neuroectoderm to form neural plate; notochord becomes nucleus pulposus 2. Neural plate folds to form neural tube -some cells diff. into neural crest cells -craniocaudal folding 3. Vesicles B. Congenital anomalies 1. Spina bifida (high AFP levels) 2. Anencephaly (high AFP levels) -1/1000 births -most common serious birth defect in stillborns 3. Arnold-Chiari – herniation of cerebellum into foramen magnum 4. Dandy-Walker – hydrocephalus from atresia of foramena of Luschka and Magendie 5. Hydrocephalus – most commonly from stenosis of cerebral aqueduct 6. Fetal alcohol syndrome – most common cause of MR; microcephaly, heart disease 7. Craniopharyngioma – congenital cystic tumor, remnants of Rathke’s pouch Gut (ENDODERM & MESODERM) A. Development 1. Foregut: celiac artery -esophagus, stomach, liver, gallbladder, pancreas, upper duodenum 2. Midgut: superior mesenteric artery -lower duodenum, jejunum, ileum, cecum, appendix, ascending colon, proximal 2/3 transverse colon 3. Hindgut: inferior mesenteric artery

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-distal 1/3 of transverse colon, descending colon, sigmoid colon, upper anal canal 4. Lower anal canal = surface ectoderm (think squamous cell carcinoma) B. Congenital anomalies 1. Esophageal atresia – malformed tracheoesophageal septum 2. Hypertrophic pyloric stenosis – hypertrophy of muscularis externa; projectile vomiting and small, palpable mass at right costal margin 3. Extrahepatic biliary atresia – incomplete canalization > occlusion of biliary duct; jaundice, pale feces, dark urine 4. Annular pancreas – ventral and dorsal pancreatic buds form ring around duodenum; obstruction 5. Duodenal atresia – failed recanalization; polyhydramnios, bile-containing vomit, stomach distention 6. Omphalocoele – midgut loop fails to return to abd. cavity; light gray sac at base of umbilical cord 7. Meckel’s diverticulum – remnant of yolk sac b/t umbilicus and ileum; drainage of meconium from umbilicus 8. Hirschsprung’s – failure of neural crest cells to form myenteric plexus in sigmoid colon and rectum; loss of peristalsis, fecal retention, abd. distention Other congenital anomalies A. Head and neck 1. First arch syndrome – various facial anomalies -lack of migration of neural crest cells into pharyngeal arch 1 -Treacher-Collins, Pierre Robin 2. DiGeorge – pharyngeal pouches 3 & 4 fail to diff. into parathyroids and thymus; “first arch” facial anomalies with cardiovascular anomalies 3. Cleft palate and cleft lip (First Aid p. 94) Skeletal System A. Development -lateral folding -three sources: paraxial mesoderm, lateral plate mesoderm, neural crest cells 1. Paraxial mesoderm -gives rise to somiteres 1-7 in head region -gives rise to somites in postcranial region a. dermatomes – give rise to dermis b. myotomes – give rise to all skeletal muscles below head c. sclerotomes – give rise to bones of axial skeleton -abnormal induction results in spinal defects (scoliosis) B. Congenital Anomalies (not any obvious ones relating directly to somite migration) 1. Caudal dysplasia -refers to constellation of syndromes ranging from minor lesions of lower vertebrae to complete fusion of lower limbs -is caused by abnormal gastrulation, in which migration of mesoderm is disturbed -can be associated with various cranial anomalies: a. VATER – vertebral defects, anal atresia, tracheoesophageal fistula, renal defects b. VACTERL – similar to VATER, includes cardiovascular defects and upper limb defects 2. Sacrococcygeal teratoma -arises from remnants of primitive streak (see below); normally degenerates -derived from pluripotent cells, develop into various tissue types (hair, bone, nerve) -more common in female infants, usually malignant, must be removed by 6 months Fetal Circulation A. Pattern Aorta > R, L umbilical arteries (deoxy) > Left umbilical vein (oxy) > ductus venosus > Inf. vena cava > Right atrium > foramen ovale > Left atrium > Left ventricle > Aorta Right atrium > Right ventricle > Pulmonary artery > Ductus arteriosus > Aorta B. Three main shunts 1. Ductus arteriosus: pulmonary trunk to aorta 2. Ductus venosus: bypass liver

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3. Foramen ovale: right atrium to left atrium C. Remnants (First Aid p. 92) D. After first breath 1. Alveoli are oxygenated 2. Decreased pulmonary resistance (lungs expand) 3. Increased pulmonary blood flow 4. Increased left atrial pressure 5. Functional closure of foramen ovale 6. Ductus arteriosus closes via smooth muscle contraction within a few hours of birth 7. Ductus venosus closes within a few days, mechanism unknown Embryonic Plate: Weeks 2-3 (First Aid p. 91) A. Week Two 1. Embryoblast (bilaminar disk) a. Epiblast b. Hypoblast c. Amniotic cavity d. Yolk sac 2. Trophoblast (Placenta) a. Syncytiotrophoblast b. Cytotrophoblast

B. Week Three 1. Gastrulation -establishes three germ layers: ectoderm, mesoderm, endoderm (trilaminar disk by day 21); give rise to all tissues and organs -primitive streak first indication -all derived from epiblast

Gross Anatomy 1.

Direct hernia: leaves abdominal cavity medial to inferior epigastric vessels Indirect hernia: leaves abdominal cavity lateral to inferior epigastric vessels Femoral hernia: protrusion of abdominal viscera through femoral ring into femoral canal Lumbar puncture: needle into lumbar cistern between spinous processes L3/L4 or L4/L5 Pericardiocentesis: wide bore needle inserted through 5th or 6th intercostal space near sternum. Careful not to puncture internal thoracic artery 2. Thyroid C5 Sternal notch T2 Bifurcation of trachea T4-T5 Heart: Base T6-T9 Apex 5th left intercostal space 3.

Duodenum T12-L1 Kidneys T12-L3 Conus medularis L1-L2 adult, L3 newborn Umbilicus L4

Knee: 1. Patellar ligament- damage to femoral nerve or spinal cord L2-L4. Loss of patellar reflex 2. MCLtear also tears medial meniscus. Passive abduction of extended leg at knee joint. 3. LCL- passive adduction of extended leg at knee joint. 4. ACL- anterior drawer sign. 5. PCL- posterior drawer sign. 6. Terrible triad- MCL, medial meniscus and ACL tears.

Hip: 1. Posterior dislocation- head of femur moves posterior to the iliofemoral ligament. Presents with lower limb that is flexed at hip joint, adducted, medial rotated and shorter than opposite limb. 2. Fracture of neck of femur presents laterally rotated and shortened.

Shoulder: 1. Dislocation- may be anterior or posterior. If anterior then axillary nerve may be damaged. 2. Separation- results in a downward displacement of clavicle. Clavicle: 1. Fracture- most common at medial 1/3. Results in upward displacement of proximal fraagment and downward displacement of distal fragment 4.

Brachial Plexus: 1. Axillary n- dislocation of shoulder, abduction (deltoid) and lateral rotation (teres minor) are compromised. 2. Long thoracic n- winging of scapula (serratus anterior). 3. Radial n- wrist drop (extensors of forearm). 4. Median n- ape hand (thumb muscles) and flexors of forearm if damage is at elbow or above. 5. Ulnar n- claw hand and radial deviation of hand, loss of some flexors if at elbow or above.

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Peripheral nerves: 1. Common peroneal n- foot drop (tibialis anterior m) and inversion (peroneus muscles). 2. Deep peroneal n. entrapment- Compression of anterior compartment muscles of the lower leg by ski boot or athletic shoes that are too tight. Causes pain in the dorsum of the foot that radiates to the space between the first two toes.

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Hands: 1. Carpel Tunnel Syndrome- compression of median nerve by inflammation, weakend flexion and abduciton and opposition of thumb, loss of extension of index and middle fingers, sensory loss of index, middle and half of ring fingers and palmar part of thumb. 2. Cubital tunnel syndrome- sorry I was not able to find this one. 3. Dupuytren’s contracture- progressive fibrosis of palmar aponeurosis, pulls digits into marked flexion at MCP joints.

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Blood-testes barrier: There is a barrier that exists between the blood vessels that supply the testes (branches of the testicular artery and vein) and the duct system in which spermatozoa are produced and transported. The testis is derived partly from celomic mesoderm and partly from intermediate mesoderm with the blood vessels migrating in around the duct system.

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Abdominal arteries: 1. Celiac trunk(CT)-FOREGUT-left gastric a., splenic a., hepatic a. 2. Superior messenteric a.(SMA)- MIDGUT- part of duodenum through proximal 2/3 of transverse colon. 3. Inferior mesenteric a.(IMA)-HINDGUT- distal 1/3 of transverse colon to upper rectum

Collaterals: 1. Internal thoracic a. to superior epigastric a. to inferior epigastric a. 2. Superior pancreaticoduodenal a.(from CT) to inferior pancreaticoduodenal a. (from SMA) 3. Middle colic a. (from SMA) to left colic artery (from IMA) 4. Marginal a. (from SMA and IMA) 5. Superior rectal a. (from IMA) to middle rectal a. (from internal iliac a.) 9. Bone: 1. Metaphysis: between epiphysis and diaphysis. 2. Epiphysis: growth plate responsible for linear bone growth. 3. Diaphysis: long part of bone responsible for annular bone growth. (Add histology and neuroanatomy 1-2)

Neuroanatomy 3. Hearing -Unlike other sensory systems, the central auditory pathways have bilateral representation of sounds (sound from 1 ear reaches auditory cortex in both hemispheres). -Pathway -first neruons in spiral ganglion synapse in cochlear nucleus -second neurons synapse bilaterally in superior olivary nuclei -third neurons travel in the lateral lemniscus to synapse in the inferior colliculus -fourth neurons then synapse in the medial geniculate nucleus -the fibers then go to the transverse temporal gyrus of the cortex -Conduction and nerve deafness -Weber test (forehead)

-lateralizes to the affected ear with conduction deafness and to the unaffected ear with nerve deafness -Rinne test (mastoid process) -distinguishes between better bone or air conduction of sound 4. Extraocular muscles (see First Aid pg. 111 and table 10.1 pg. 118 in Basic Clinical Neuroanatomy) -Movements and innervation -Medial Rectus – CN III – adduction (in) -Superior Rectus – CN III – elevation (after abduction) (up) -Inferior rectus – CN III – depression (after abduction) (down) -Inferior oblique – CN III – elevation and adduction (up and in) -Superior oblique – CN IV – depression and adduction (down and out) -Lateral rectus – CN VI – abduction (out) -Lesions -CN III – eye turned down and out, ptosis, mydriasis -CN IV – eye slightly up and in – diplopia going down stairs – tilting head away from the affected side to correct the diplopia -CN VI – eye deviates medially (abductor paralysis) 5 and 6. Chemical synapse, neurotransmitters, receptors, second messengers, effects BRS phys. 13-18 -Chemical synapse (BRS phys pg. 13-14) -Presynaptic cell -action potential – depolarization of presynaptic terminal – Ca2+ enters presynaptic terminal – release of neurotransmitter into cleft -Postsynaptic cell -neurotransmitter binds to receptors causing a change in permeability to ion -inhibitory neurotransmitters hyperpolarize – excitatory depolarize -Receptor types (BRS phys pg.35-38) -alpha 1 receptors – excitatory – epi and norepi – IP3 and increase intracellular Ca2+ -alpha 2 receptors – inhibatory – inhibit adenylate cyclase and decrease cAMP -beta 1 receptors – excitatory – epi and norepi – activate adenylate cylcase – cAMP -beta 2 receptors – relaxation – epi and norepi – activate adenylate cyclase – cAMP 7. Blood supply to brain (see First Aid pg. 112, BRS Path pg. 356-357) -Embolism – most frequently to middle cerebral artery leading to contralateral paralysis, motor defects, sensory defects, aphasias -Thrombosis – from atherosclerosis of carotids, vertebral and basilar aa., and middle cerebral aa. -Hemorrhage – hypertension and coagulation disorders – most often in basal ganglia, pons, frontal lobe, cerebellum 8. Basal Ganglia (globus pallidus, caudate, putamen) (First Aid pg. 109) -initiation of voluntary movements and control of postural adjustments -Pathology of the basal ganglia -Negative signs: akinesia, bradydinesia, abnormal postural adjustments -Positive signs (dyskinesia at rest): hypertonicity (rigidity), tremors, chorea, athetosis, ballismus -Huntington disease – degeneration of striatal neurons (putamen and caudate) -Parkinson disease – degeneration of the dopamine neurons in the substantia nigra -Tardive dyskinesia – exposure to manganese and drugs – hypersensitivity to dopamine agonists -Hemiballismus – lesions in contralateral subthalamic nucleus 9. Pituitary associations -Optic chiasm sits on top of pituitary – bilateral hemianopsia -Sits in the sella turcica - local pressure effects hypopatuitarism 10. Brain MRI and CT

-Abcess or cysticercosis CT and MRI – ring enhancing lesion -Multiple sclerosis MRI – multiple focal areas of demyelination (plaques) in brain and spinal cord -Huntington’s disease – atrophy of the caudate nucleus, putamen, and frontal cortex – looks like ventricles have enlarged 11. Pupillary light reflex - doesn’t involve cortex -Direct response – afferent pathway is optic nerve of eye tested – efferent pathway is CN III to the eye tested -Consensual response – afferent pathway is optic nerve of eye tested – efferent pathway is CN III of opposite eye -Accomodation – pupils constrict, eyes converge, lense more convex – depends on CN III and visual association cortex