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KRISHNA INSTITUTE OF MEDICAL SCIENCES - ANATOMY PAPER II

Complete Analysis, Question Bank & Answers

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PAPER ANALYSIS

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SECTION A — Q.NO.1: Case Scenario-Based MCQs

• Answer: (B) Obturator nerve - supplies all adductors of the medial compartment (L2-L4)

• Answer: (B) Obturator canal - within the obturator foramen, formed by obturator membrane

• Answer: (A) Omphalocele - failure of physiological gut return to abdomen

• Answer: (C) Adductor magnus - obturator nerve (adductor part) + sciatic nerve/tibial (hamstring part)

• Answer: (A) Zero - Barr body = X chromosomes - 1 = 1-1 = 0

• Answer: (B) Syncytiotrophoblast

• Answer: (A) Inner cell mass (embryoblast)

• Answer: (C) Direct inguinal hernia - medial to inferior epigastric artery

• Answer: (D) Adrenal cortex - (adrenal medulla IS a neural crest derivative; cortex is mesoderm)

• Answer: (B) Type I epithelial cells (epithelioreticular cells), basement membrane, and endothelial cells of continuous capillaries

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SECTION B

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Q.NO.2: LONG ESSAY — Obturator Nerve (10 marks) [2+3+3+2]

a) Origin and Root Value (2 marks)

• The obturator nerve is a branch of the lumbar plexus
• Root value: L2, L3, L4 (anterior divisions/ventral rami)
• It is one of the largest branches of the lumbar plexus
• It is a mixed nerve (both motor and sensory)

b) Course and Relations (3 marks)

• Arises within the substance of the psoas major muscle
• Emerges from the medial border of psoas major
• Crosses the pelvic brim / passes behind the common iliac vessels
• Runs along the lateral wall of the pelvis, anterior to the obturator vessels
• Travels towards the obturator foramen

• Runs along the lateral pelvic wall
• Anterior to obturator vessels (obturator artery and vein)
• Medial to the internal iliac vessels

• Enters the obturator canal (formed within the obturator foramen by the obturator membrane) through its superior aspect
• Passes through the obturator canal and enters the medial compartment of the thigh
• Just after passing through the canal, it divides into anterior and posterior branches, separated by the adductor brevis muscle

c) Branches and Distribution (3 marks)

• Descends on the anterior surface of adductor brevis
• Lies behind pectineus and adductor longus
• Motor supply: adductor longus, adductor brevis, gracilis (and sometimes pectineus)
• Sensory supply: cutaneous branches to skin on medial side of the thigh
• Articular branch to hip joint

• Descends behind adductor brevis, on the anterior surface of adductor magnus
• Motor supply: obturator externus, adductor brevis (when anterior branch is absent), adductor magnus (linea aspera part)
• Articular branch to the knee joint (perforates adductor magnus)

1. Adductor longus
2. Adductor brevis
3. Adductor magnus (pubic/adductor part - to linea aspera)
4. Gracilis
5. Obturator externus

Note: The ischiocondylar (hamstring) part of adductor magnus (to adductor tubercle) is supplied by the tibial portion of the sciatic nerve, NOT the obturator nerve - making adductor magnus a hybrid muscle.

• L2, L3, L4 ventral rami
• Psoas major (within which nerve forms)
• Common iliac vessels (posterior)
• Lateral pelvic wall
• Obturator foramen / obturator canal
• Obturator membrane
• Anterior branch
• Posterior branch
• Adductor brevis (separates branches)
• Adductor longus, adductor magnus, gracilis, obturator externus

d) Applied Aspects (2 marks)

1. Obturator nerve damage - most commonly during childbirth (forceps delivery, prolonged labour) on the lateral pelvic wall. Results in:
   • Weakness of adduction of the thigh
   • Sensory loss on medial aspect of the thigh
   • Adductor spasmis tested by Howship-Romberg sign (pain in medial thigh on extension/abduction - due to obturator hernia compressing the nerve)
2. Obturator hernia - herniation through the obturator canal (more common in thin, elderly women). The hernia sac compresses the obturator nerve causing pain along the medial thigh - Howship-Romberg sign
3. Adductor tenotomy - obturator nerve block used in spasticity
4. Obturator nerve block - done for adductor spasm in patients with hip fractures, TURP surgery, bladder procedures, and pain management

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Q.NO.3: REASONING QUESTIONS (5 x 3 = 15 marks)

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(a) Name the hybrid muscles in lower limb and why they are called hybrid muscles?

• They are formed by the fusion of muscle primordia from two different embryological origins
• Adductor magnus: the adductor part originates from the pubic/medial muscle mass (hence obturator nerve) and the hamstring part originates from the ischial/posterior muscle mass (hence sciatic nerve)
• Biceps femoris: the short head arises from the linea aspera (femoral origin - anterior compartment derivation) while the long head is from ischial tuberosity (posterior/hamstring origin)
• Because they have dual embryological origin and dual nerve supply, they are called hybrid muscles - just like a hybrid vehicle uses two different power sources

• Adductor part: origin - inferior pubic ramus + ischiopubic ramus; insertion - linea aspera; nerve - obturator
• Hamstring part: origin - ischial tuberosity; insertion - adductor tubercle; nerve - tibial (sciatic)

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(b) A tendon injury heals slowly compared with a muscle injury. Explain the reason.

1. Vascularity:
   • Muscles are highly vascular - rich blood supply brings oxygen, nutrients, and repair cells rapidly
   • Tendons are relatively avascular - blood supply is mainly from the peritenon (outer sheath) and musculotendinous junction; the mid-substance of a tendon has very poor blood supply
   • Slow delivery of nutrients = slow repair
2. Cellular composition:
   • Muscles contain myosatellite cells (satellite cells) - stem cells that proliferate after injury and regenerate muscle fibers
   • Tendons contain primarily tenocytes (tendon fibroblasts) - these are quiescent, spindle-shaped cells with low metabolic activity and slow proliferation rate
   • Fewer actively dividing cells = slower repair
3. Tissue composition:
   • Tendons are composed of dense regular connective tissue - tightly packed type I collagen fibers
   • After injury, the disorganized type III collagen (scar collagen) must be gradually replaced by type I collagen over months
   • This remodelling takes 6-12 months; muscle scar replaces faster
4. Oxygen tension:
   • Central tendon substance is relatively hypoxic - tenocytes are adapted to low oxygen
   • Slow metabolic rate = slow repair
5. Inflammatory response:
   • Muscle injury produces a brisk inflammatory response - macrophages, growth factors arrive fast
   • Tendons have a more subdued inflammatory response due to poor vascularity

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(c) An old man suffering from carcinoma of prostate develops vertebral metastasis - justify?

1. Anatomy of Batson's plexus:
   • The vertebral venous plexus (Batson's plexus) is a valveless, thin-walled, low-pressure venous network that runs along the entire length of the vertebral column - both inside (internal) and outside (external) the spinal canal
   • It freely communicates with the prostatic venous plexus (through the pelvic veins)
2. Why prostate cancer specifically spreads here:
   • Prostate cancer cells enter the prostatic venous plexus
   • This plexus communicates directly with the internal vertebral venous plexus (Batson's plexus)
   • Because Batson's plexus is valveless, blood (and tumor emboli) can flow retrograde (backwards) against normal blood flow - especially during increased intra-abdominal pressure (straining, coughing)
   • Tumor cells travel along this route and seed the vertebral bodies - which are highly vascular with red marrow
3. Rich red marrow in vertebrae:
   • Vertebral bodies contain abundant red (haematopoietic) bone marrow rich in sinusoids
   • These sinusoids act as a "trap" for circulating tumor cells
   • Prostate cancer cells express receptors that bind to bone marrow stromal cells (CXCR4/SDF-1 axis)
4. Osteoblastic metastasis:
   • Prostate cancer typically causes osteoblastic (sclerotic) metastases - appears as dense white areas on X-ray
   • The cancer cells stimulate osteoblasts to produce new bone (unlike breast cancer which causes osteolytic lesions)
5. Why vertebrae preferentially?
   • The lumbar and thoracic vertebrae are in the direct drainage territory of the pelvic venous plexus
   • This explains the characteristic distribution: lumbar spine > thoracic spine > sacrum > pelvis

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(d) A male develops an X-linked recessive disorder even though only one mutant allele is present. Explain why?

1. Sex chromosome complement of males:
   • Males have XY sex chromosome constitution
   • They have only ONE X chromosome (and one Y)
2. Hemizygosity:
   • Males are said to be hemizygous for X-linked genes
   • They have only ONE copy of each gene on the X chromosome (no second X to provide a normal allele)
   • There is no corresponding allele on the Y chromosome to "mask" or compensate for a defective allele on X
3. Why recessive disorders express in males:
   • In females: need TWO mutant copies (homozygous: X^a X^a) to express the disease, because one normal allele (X^A) can compensate - carrier females are phenotypically normal
   • In males: having even ONE mutant allele (X^a Y) is sufficient to express the disease because there is NO second X chromosome to provide the normal functional gene product
   • One mutant allele = disease expressed because there is NO backup
4. Examples:
   • Haemophilia A (factor VIII deficiency)
   • Haemophilia B (factor IX deficiency)
   • Red-green colour blindness (OPN1LW/OPN1MW gene)
   • Duchenne Muscular Dystrophy (dystrophin gene)
   • G6PD deficiency
5. Why it is called "recessive":
   • The term "recessive" means the allele only expresses when the dominant normal allele is absent
   • In females, one normal allele suppresses expression
   • In males, there is no second allele at all - so even a "recessive" allele always expresses

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(e) A newborn is diagnosed with omphalocele where abdominal contents remain within the umbilical cord. Explain the embryological event that failed to occur.

1. Physiological gut herniation (weeks 6-10):
   • Between the 6th and 10th week of development, the midgut elongates rapidly and herniates through the umbilical ring into the extraembryonic coelom (within the umbilical cord) - this is normal physiological herniation
   • The gut rotates 270 degrees anti-clockwise during this period (around the superior mesenteric artery axis)
2. Return of gut to abdomen (week 10):
   • By the 10th week, the abdominal cavity grows large enough (due to growth of the embryo and regression of the mesonephros/liver)
   • The herniated intestinal loops return to the abdominal cavity through the umbilical ring
   • As they return, they complete their rotation
   • The umbilical ring then closes/narrows around the umbilical cord structures
3. What failed in Omphalocele:
   • Failure of the physiological return of midgut loops back into the abdominal cavity at week 10
   • The bowel loops remain outside in the extraembryonic coelom (within the umbilical cord)
   • The umbilical ring fails to close
   • The abdominal wall fails to form properly around the midline

• Failure of lateral body wall folding (in some views of omphalocele)
• Failure of the somatic mesoderm to close the ventral abdominal wall

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Q.NO.4: SHORT NOTES (3 x 5 = 15 marks)

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(a) Describe Neural Crest Cells and Their Derivatives

• Neural crest cells originate at the junction between the neural ectoderm and the surface ectoderm (the neural folds/dorsal neural tube)
• When the neural groove closes to form the neural tube, cells at the lateral margins undergo an epithelial-to-mesenchymal transition (EMT) and migrate away
• They migrate extensively throughout the embryo via defined pathways

1. Dorsolateral pathway - between ectoderm and somites - gives rise to melanocytes
2. Ventromedial pathway - through somites, anterior half only - gives rise to DRG, sympathetic ganglia

• Hirschsprung's disease - failure of neural crest cells to migrate to colon = absence of enteric ganglia = megacolon
• Waardenburg syndrome - defect in neural crest migration = deafness, white forelock, heterochromia iridis
• CHARGE syndrome - neural crest related
• Treacher-Collins syndrome - craniofacial neural crest defect
• Neuroblastoma - malignant tumor of neural crest-derived sympathetic neuroblasts
• Melanoma - malignant tumor of melanocytes (neural crest origin)
• Pheochromocytoma - tumor of adrenal medulla (neural crest origin)
• DiGeorge syndrome (22q11.2 deletion) - affects 3rd and 4th pharyngeal arch neural crest migration = absent thymus and parathyroids

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(b) Describe Development of the Urinary Bladder

• The cloaca is divided by the urorectal septum (a wedge of mesoderm growing caudally between the allantois and hindgut) into:
  • Anteriorly: Urogenital sinus
  • Posteriorly: Anorectal canal
• The urorectal septum meets the cloacal membrane by the 7th week, dividing it into the urogenital membrane (anterior) and the anal membrane (posterior)

1. Vesical part (superior/cranial) - forms the urinary bladder (continuous with allantois superiorly)
2. Pelvic part (middle) - forms the urethra (in females: entire urethra; in males: prostatic + membranous urethra)
3. Phallic part (inferior) - forms the penile urethra in males; vaginal vestibule in females

• The mucosa (transitional epithelium/urothelium) of the bladder is derived from endoderm of the urogenital sinus
• The muscular wall (detrusor) and connective tissue are derived from splanchnic mesoderm

• The lower ends of the mesonephric (Wolffian) ducts are absorbed into the developing bladder wall
• This absorption creates the trigone of the bladder
• The ureteric buds (which bud from the mesonephric ducts) come to open separately into the bladder - forming the ureteral orifices at the posterolateral angles of the trigone
• The trigone epithelium (derived from mesonephric duct - mesoderm) gradually becomes replaced by endodermal urothelium

• The superior part of the bladder is continuous with the allantois (which runs in the umbilical cord)
• After birth, the allantois involutes and becomes the urachus (median umbilical ligament)
• Persistence of urachus leads to:
  • Patent urachus - urine drains from umbilicus
  • Urachal cyst
  • Urachal sinus

• Exstrophy of bladder - failure of fusion of lateral mesodermal folds in the anterior abdominal wall - the bladder opens to the exterior
• Patent urachus - allantois fails to close
• Bladder diverticulum - focal weakness in bladder wall

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(c) Draw and Neatly Label a Diagram of the Micro-anatomical Features of the Liver

1. Central vein (terminal hepatic venule) - at center of lobule
2. Portal tract/Portal triad - at each corner of the hexagon, containing:
   • Branch of portal vein
   • Branch of hepatic artery
   • Bile ductule (interlobular bile duct)
   • Lymphatics
3. Hepatocytes - arranged in radial plates (hepatic plates/cords) extending from central vein to periphery; one to two cells thick
4. Hepatic sinusoids - blood channels between hepatic cords; lined by fenestrated endothelium
5. Space of Disse (perisinusoidal space) - between hepatocytes and sinusoidal endothelium; contains hepatic stellate cells (Ito cells/lipocytes - store vitamin A)
6. Kupffer cells - macrophages lining the sinusoids; phagocytic
7. Bile canaliculi - tiny channels between adjacent hepatocytes; formed by modifications of hepatocyte plasma membranes; bile flows towards the portal tract (opposite direction to blood flow)
8. Limiting plate - single layer of hepatocytes surrounding the portal tract
9. Periportal hepatocytes (Zone 1) - most oxygenated; first affected by toxic injury
10. Midzonal hepatocytes (Zone 2)
11. Centrilobular hepatocytes (Zone 3) - least oxygenated; first affected by ischemic injury; site of fatty change in alcohol
12. Rappaport's acinus - functional unit of liver (ovoid, based on blood supply)

• Blood flows FROM portal tract → THROUGH sinusoids → INTO central vein → INTO hepatic veins → INTO inferior vena cava

• Bile flows FROM hepatocytes → INTO bile canaliculi → INTO bile ductules (of Hering) → INTO interlobular bile ducts (at portal tract) → OPPOSITE to blood flow

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Q.NO.5: SHORT NOTES APPLIED ASPECTS (4 x 5 = 20 marks)

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(a) Case: 65-year-old man with reducible groin swelling, medial to inferior epigastric artery, disappears on lying down, does not descend into scrotum

• Direct inguinal hernia bulges through the floor of the inguinal canal (transversalis fascia) at the site of Hesselbach's triangle
• It does NOT pass through the deep inguinal ring (which is lateral to the inferior epigastric artery)
• It presents as a direct anterior bulge through the posterior wall of the inguinal canal
• Because it does not follow the inguinal canal, it does not descend into the scrotum

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(b) Case: 28-year-old woman - day-5 embryo transfer - fluid-filled cavity, inner cell mass at one pole, outer layer of flat cells - hCG becomes positive 5 days later

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(c) Differentiate Duodenum and Ileum Histologically

• See Brunner's glands in submucosa = Duodenum
• See Peyer's patches in submucosa/mucosa = Ileum
• Jejunum = neither Brunner's glands nor Peyer's patches (distinguishes it from both)

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(d) Histological features of Elastic Cartilage vs Hyaline Cartilage

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Q.NO.6: SHORT NOTES (4 x 5 = 20 marks)

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(a) Describe the Methods of Disposal of Bio-medical Waste

1. Incineration:
   • High-temperature burning (850-1100°C) in a dedicated incinerator
   • Used for: anatomical waste (body parts), cytotoxic waste, pathological waste
   • Destroys pathogens completely
   • Produces ash + flue gases (requires pollution control)
2. Autoclaving (Steam sterilization):
   • 121°C at 15 psi for 30-60 minutes
   • Kills all microorganisms including spores
   • Used for: sharps, red category waste after decontamination
   • After autoclaving: waste can be sent for recycling or landfill
3. Microwave Treatment:
   • Electromagnetic radiation at 2450 MHz
   • Effective for contaminated waste (except anatomical/cytotoxic)
   • Waste is first shredded then microwaved
4. Deep Burial:
   • For anatomical waste in remote/rural areas without incinerators
   • Pit must be: at least 2 meters deep, lined with lime, 50 metres from water source, 25 metres from public places
   • Pit is closed when 3/4 full and a new pit is opened
5. Chemical Disinfection:
   • For liquid waste (blood, secretions, body fluids)
   • Using sodium hypochlorite (bleach), formaldehyde, or glutaraldehyde
   • Treated liquid can then be discharged into drains
6. Shredding/Mutilation:
   • After sterilization, sharps and plastics are shredded to prevent reuse
   • Shredded material is then sent for recycling
7. Encapsulation:
   • Sharps placed in containers with cement/clay/sand and sealed
   • Used when incineration/autoclaving not available

• Yellow = Incinerate (dangerous anatomical/pathological/chemical)
• Red = Autoclave then Recycle (contaminated plastics)
• White = Sharps (autoclave + shred + metal recycle)
• Blue = Glassware

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(b) Classify Synovial Joints with Examples

• 1 axis: Hinge, Pivot
• 2 axes: Condyloid, Saddle
• Multiple axes: Ball and Socket
• No axis: Plane (gliding)

• Simple joint - two articular surfaces (e.g. interphalangeal)
• Compound joint - more than two articular surfaces (e.g. elbow - humeroulnar + humeroradial + proximal radioulnar)
• Complex joint - has intra-articular disc or meniscus (e.g. knee, TMJ, sternoclavicular joint, acromioclavicular joint)

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(c) Lyon Hypothesis - Barr Bodies Calculation and Clinical Significance (2+2+1 = 5 marks)

1. Only one X chromosome is genetically active in each somatic cell
2. The other X chromosome(s) undergo heteropyknosis (condensation) and become genetically inactive
3. Inactivation is random - it can be either the maternal or paternal X chromosome in each cell
4. Inactivation occurs at the blastocyst stage (~day 16, or around day 5.5-16 of embryonic life)
5. Once inactivated, the same X chromosome remains inactive in all daughter cells (clonal perpetuation)

• The inactive X is "coated" by the XIST (X-Inactive Specific Transcript) lncRNA
• XIST initiates chromatin silencing via histone modification and DNA methylation
• The inactive X is visible as the Barr body (sex chromatin) at the nuclear periphery in interphase cells
• First identified in neurons of female cats by Murray Barr and Ewart Bertram in 1949

Number of Barr bodies = Number of X chromosomes - 1

1. Explains dosage compensation: Males (XY) and females (XX) have the same effective dose of X-linked gene products because one X is inactivated in females
2. Explains mosaicism in females: Female carriers of X-linked disorders (e.g. haemophilia, Hunter syndrome) show variable expression because some cells express the normal X and some express the mutant X (e.g. patchy hair growth, patchy skin lesions in X-linked disorders)
3. Barr body for sex determination: Buccal smear or cells from amniotic fluid can be examined for Barr bodies to determine chromosomal sex (used before karyotyping was available; still useful in forensics)
4. Explains Turner syndrome: 45,X0 females have severe somatic defects despite having "one X" like males - this is because some genes on the normally inactive X escape inactivation and are needed for normal development
5. X-linked gene therapy: Understanding X-inactivation is important for treating X-linked disorders (e.g. haemophilia) - the inactivated normal allele in carrier females can potentially be reactivated
6. Calico cats: The classic example - female cats heterozygous for X-linked coat color genes are calico (patches of orange and black) due to random X-inactivation in different skin cells

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(d) Micro-anatomical Features of the Thymus and Blood-Thymus Barrier (3+2 = 5 marks)

• Bilobed organ in the superior mediastinum anterior to the great vessels
• Surrounded by a fibrous capsule
• Divided by capsular trabeculae into incomplete lobules

• Densely packed with T-lymphocytes (thymocytes) undergoing development
• Contains Type I epithelioreticular cells (at the corticomedullary junction - barrier cells) and Type II and III epithelioreticular cells (within cortex - form scaffolding, produce thymosin)
• Macrophages - phagocytose dead thymocytes (those failing positive/negative selection - ~95% die here)
• Blood vessels are continuous capillaries (tight junctions) - form part of blood-thymus barrier
• Lymphocytes being "educated" here = positive and negative selection

• Less densely packed; lymphocytes here are mature T cells ready to leave
• Contains Type IV, V, VI epithelioreticular cells
• Hassall's corpuscles (thymic corpuscles) - concentrically arranged, keratinized squamous epithelial cells (degenerated epithelioreticular cells) - hallmark of thymus medulla; their function is debated (possibly involved in Treg development)
• Blood vessels here are NOT part of the blood-thymus barrier (fenestrated in medulla? - actually medulla is accessible to antigens)

1. Fibrous capsule
2. Trabecula
3. Cortex (dark - lymphocyte dense)
4. Medulla (pale)
5. Hassall's corpuscle (in medulla)
6. Epithelioreticular cells (Type I at CMJ, Type II-III in cortex, Type IV-VI in medulla)
7. Thymocytes (immature T lymphocytes)
8. Macrophages
9. Blood vessel (continuous capillary) - part of blood-thymus barrier
10. Corticomedullary junction

1. Endothelial cells of continuous (non-fenestrated) capillaries with tight junctions (zonula occludens)
2. Endothelial basement membrane
3. Perivascular space (contains macrophages that phagocytose any antigens that breach the endothelium)
4. Basement membrane of epithelioreticular cells (Type I)
5. Type I epithelioreticular cells (at corticomedullary junction - send sheet-like processes that surround cortical capillaries)

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ADDITIONAL QUESTION BANK BY CATEGORY

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ADDITIONAL REASONING QUESTIONS (Like Q3 pattern)

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ADDITIONAL SHORT NOTES (Like Q4/Q5/Q6)

• Anterior wall: External oblique aponeurosis (full length) + internal oblique (lateral 1/3)
• Posterior wall: Transversalis fascia (full length) + conjoint tendon (medial 1/3)
• Floor: Inguinal ligament (Poupart's) + lacunar ligament medially
• Roof: Arching fibers of internal oblique + transversus abdominis

• Spermatic cord (vas deferens, testicular artery, pampiniform plexus, cremasteric artery, artery of vas, genital branch of genitofemoral nerve, sympathetic fibers, lymphatics)
• Ilio-inguinal nerve (runs within canal but not in spermatic cord)

• Round ligament of uterus
• Ilio-inguinal nerve

• Synovial membrane: lines the joint cavity EXCEPT over articular cartilage; produces synovial fluid (dialysate of plasma + hyaluronic acid)
• Articular cartilage: hyaline cartilage (no perichondrium, avascular, relies on diffusion from synovial fluid)
• Joint capsule: outer fibrous layer + inner synovial membrane
• Accessory structures: bursae, tendons, fat pads, discs/menisci, labra

• Located in: submucosa of duodenum (unique to duodenum)
• Type: compound tubulo-alveolar glands
• Secretion: alkaline mucus (rich in bicarbonate, glycoproteins)
• Function: neutralize acidic chyme entering duodenum from stomach; protect duodenal mucosa
• In Zollinger-Ellison syndrome: Brunner's gland hyperplasia due to excess gastrin stimulation

• Located in: mucosa and submucosa of ileum (anti-mesenteric wall)
• Type: aggregated lymphoid follicles (secondary lymphoid organ)
• Covered by: M cells (microfold cells) - specialized epithelial cells that transport antigens
• Function: immune surveillance of gut lumen antigens; part of MALT (mucosa-associated lymphoid tissue)
• Clinically: site of Salmonella typhi attachment in typhoid fever; can cause intestinal perforation

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HISTOLOGY DIAGRAM LABELS

• Central vein, Portal triad (portal vein branch + hepatic artery branch + bile ductule), Hepatocytes in cords, Sinusoids, Space of Disse, Kupffer cells, Bile canaliculi, Zones 1-2-3 (acinar zones), Rappaport's acinus

• Capsule, Trabecula, Cortex, Medulla, Hassall's corpuscle, Epithelioreticular cells, Thymocytes, Blood vessels, Corticomedullary junction

• Duodenum: Brunner's glands in submucosa, tall villi, few goblet cells, plicae circulares prominent
• Ileum: Peyer's patches, M cells, more goblet cells, shorter villi

• Elastic: lacunae, chondrocytes, elastic fibers throughout matrix (visible), perichondrium
• Hyaline: lacunae, chondrocytes in isogenous groups, homogeneous matrix (glass-like), territorial matrix (dark) vs interterritorial matrix (lighter), perichondrium

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