Locomotor wk3-4

Question 1

What are the four layers of the epidermis (from deepest to superficial) and what type of epithelium is it made up of?

Answer 1

Stratum basale → spinosum → granulosum → (lucidum)→ corneum

Epidermis epithelium= stratified squamous epithelium

Stratum corneum is made up of corneocytes (dead keratinocytes so have no nuclei)

Question 2

What is the role of keratinocytes?

Answer 2

Major cell type; produce keratin, form barrier, and undergo differentiation from basal to corneum

keratinocytes are most abundant in stratum corneum, hair and nails (54 subtypes)

exist as acidic (type I) and basic (type II) pairs e.g. K5/K14

Question 3

What is filaggrin’s role?

Answer 3

(Stratum granulosum) Binds keratin, aids in barrier function. Loss-of-function mutations linked to eczema.

Question 4

What anchors the epidermis to the dermis?

Answer 4

Basement membrane/ BM (consists of laminin 332, collagen IV+ VII) via hemidesmosomes which link keratin to cytoskeleton of BM

Question 5

What are the two dermal layers and their key features?

Answer 5

Papillary: Thin collagen III, capillaries, sensory nerves.

Reticular: Thick collagen I, provides strength/elasticity

Question 6

What do fibroblasts produce?

Answer 6

Collagen, elastin, proteoglycans

N.B. fibroblasts are the main cell type found in the dermis

Question 7

What are the two hair types and their locations?

Answer 7

Vellus: Fine body hair.

Terminal: Scalp/pubic hair (androgen-sensitive)

Question 8

Compare eccrine vs. apocrine sweat glands

Answer 8

Eccrine: Watery sweat, thermoregulation, widespread.

Apocrine: Odorless secretion (axilla/pubic area), broken down by bacteria → body odor.

Question 9

What are Langerhans cells?

Answer 9

Epidermal macrophages; present antigens to T-cells (first-line immune defense)

Question 10

What do mast cells release?

Answer 10

Histamine → inflammation (e.g., allergies, wound healing)

Question 11

What is melanin’s role?

Answer 11

UV protection (eumelanin: brown/black; pheomelanin: red)

Question 12

What is unique about Merkel cells?

Answer 12

Neuroendocrine; linked to touch sensation (basal layer)

Question 13

What are the three phases of wound healing?

Answer 13

Inflammation: Clot, neutrophils/macrophages (ILs, TNFα).

Proliferation: Fibroblasts (collagen III), angiogenesis, re-epithelialization.

Maturation: Collagen remodeling (I replaces III), scar formation

Question 14

What causes chronic wounds (e.g., diabetic ulcers)?

Answer 14

Poor perfusion, neuropathy, infection → stalled in inflammation/proliferation

Question 15

What is a keloid?

Answer 15

Overhealing → excess collagen (type I) beyond wound margins

Question 16

What is epidermolysis bullosa (EB)?

Answer 16

Genetic defect in anchoring proteins of basement membrane (e.g., collagen VII/IV or laminin 332 ) →

Without proper anchoring, the skin layers easily separate (FRAGILE SKIN), causing blisters, erosions, and wounds even with minimal mechanical stress.

N.B.
Dystrophic EB= Collage VII mutated
Junctional EB= Laminin 332 mutated

Question 17

Why is psoriasis a barrier dysfunction?

Answer 17

Hyperproliferation of keratinocytes → thick, scaly plaques (immune-mediated)

Question 18

Compare cemented vs. uncemented prostheses

Answer 18

Cemented: PMMA/ polymethylmethacrylate filler; better for elderly/poor bone quality! so Cemented is much better for elderly

Uncemented: Porous/hydroxyapatite coating; attracts OSTEOBLASTS into outercasing to fix the prosthetic into place with real bone but needs good bone ingrowth (pore size 100–200 μm).

Hybrid: Combines both ( cemented stem + uncemented cup). (reverse hybrid is cemented cup and uncemented stem but very rare)

Question 19

When is spinal fusion indicated?

Answer 19

Spinal stenosis, vertebral fractures, tumors, deformity correction (e.g., scoliosis

Question 20

What tendon is used for ACL reconstruction?

Answer 20

Hamstring tendons (semitendinosus/gracilis) or patellar ligament

Question 21

What is the gracilis muscle used for in reconstructive surgery?

Answer 21

Free muscle transfer (e.g., elbow flexion in brachial plexus injury)

Question 22

How is Achilles tendon lengthening performed?

Answer 22

Surgical elongation to treat contractures (e.g., hypertonia in cerebral palsy)

Question 23

Define non-union vs. malunion

Answer 23

Non-union: bone not fully healed by 2x expected time (atrophic/hypertrophic).

Malunion: bone heals but in misalignment (rotation/angulation/shortening)

Question 24

What are treatment options for non-union?

Answer 24

Bone graft, osteotomy, Ilizarov technique (distraction osteogenesis)

Question 25

What is the Ilizarov technique?

Answer 25

External fixator for gradual bone lengthening/realignment

Question 26

Bone graft mechanism

Answer 26

1) Osteogenesis ("Seeds"): Graft's live cells (osteoblasts) form new bone directly. 2) Osteoconduction ("Trellis"): Scaffold for host cells to grow into (e.g., calcium phosphate). 3) Osteoinduction ("Fertilizer"): Growth factors (BMPs) recruit host stem cells → osteoblasts. 4) Osteopromotion: Enhances osteoinduction (e.g., growth factors + scaffold). Mnemonic: "SFFT" = Seeds, Fertilizer, Framework, Trellis.

Question 27

What are the hallmark autoantibodies in RA?

Answer 27

Rheumatoid factor (anti-IgG) and anti-citrullinated peptide antibodies (ACPAs)

Question 28

Which immune cells are central to RA pathology?

Answer 28

B cells (produce autoantibodies). T cells (especially CD4+ Th1/Th17; linked to HLA-DR4). Macrophages (secrete TNF-α, IL-1, IL-6)

Question 29

What cytokines drive RA inflammation?

Answer 29

TNF-α, IL-1, IL-6, IL-17 (promote synovitis and bone erosion)

Question 30

How does HLA-DR4 predispose to RA? What is the "shared epitope" in HLA-DR4?

Answer 30

Alters antigen presentation → activates autoreactive T cells. (Accounts for 50% of genetic risk.) What is the "shared epitope" in HLA-DR4? Specific amino acids in MHC-II that bind self-antigens (e.g., citrullinated peptides)

Question 31

What are the stages of joint damage in RA?

Answer 31

Smoking, silica dust, low vitamin D, high sodium/red meat intake

Question 32

How do TNF-α inhibitors (e.g., infliximab) work?

Answer 32

Block TNF-α → reduce IL-1/IL-6, suppress inflammation, and halt joint damage

Question 33

What is ACR20/50/70 for RA?

Answer 33

Measures of treatment response (20/50/70% improvement in symptoms)

Question 34

Define closed vs. open (compound) fractures

Answer 34

Closed: Bone fragments do not pierce skin. Open: Fragments pierce skin (↑ infection risk)

Question 35

What causes a spiral fracture?

Answer 35

Twisting force (e.g., sports injury). Imaging: Oblique line on X-ray

Question 36

Which fracture is common in osteoporosis?

Answer 36

Compression/crush fractures (e.g., vertebral body

Question 37

What is a Colles’ fracture?

Answer 37

Fall onto outstretched hand. Distal radius fracture with dorsal displacement ("dinner fork" deformity)

Question 38

What is a greenstick fracture?

Answer 38

Incomplete fracture in children (bone bends)

Question 39

What distinguishes an avulsion fracture?

Answer 39

Tendon/ligament pulls off a bone fragment (e.g., ASIS avulsion by sartorius)

Question 40

What is a torus (buckle) fracture?

Answer 40

Buckling of pediatric bone (axial load; heals quickly A Torus fracture, aka buckle fracture is the most common fracture in children. It is a common occurrence following a fall, as the wrist absorbs most of the impact and compresses the bony cortex on one side and remains intact on the other, creating a bulging effect.

Question 41

Why are epiphyseal fractures concerning?

Answer 41

May disrupt growth plate → limb length discrepancy

Question 42

Fracture Healing Stages

Answer 42

1. Hematoma (0-48h): Clot forms; inflammation clears debris. 2. Fibrocartilaginous callus (3wks): Fibroblasts/chondrocytes form soft callus (collagen bridge). 3. Bony callus (3-4mo): Osteoblasts create woven bone. 4. Remodeling (months-years): Osteoclasts convert woven → lamellar bone. factors that delay healing; Infection, poor blood supply, mobility, smoking

Question 43

What is pseudoarthrosis?

Answer 43

False joint from failed healing (excess callus/fibrosis)

Question 44

cell-cell adhesions; difference between - adherens junction - desmosome - tight junction - gap junction

Answer 44

Adherens Junctions: Function: Cell adhesion. Proteins: Cadherins (linked to actin). Example: Epithelial cells. Desmosomes: Function: Strong mechanical adhesion. Proteins: Desmoglein, desmocollin (linked to KERATIN/ intermediate filaments). Example: Skin, heart muscle. Tight Junctions: Function: Barrier to prevent paracellular movement. Proteins: Claudins, occludins (linked to actin). Example: Blood-brain barrier, intestines. Gap Junctions: Function: Cell communication (ions/molecules). Proteins: Connexins (form connexons, channels). Example: Heart, neurons.

Question 45

🧬 Difference between Central and Peripheral Tolerance

Answer 45

Central Tolerance: happens during development (in thymus/bone marrow) deletes dangerous cells early; Mechanism: Deletion (apoptosis) or receptor editing (B cells). Purpose: Eliminate self-reactive lymphocytes during development. Peripheral Tolerance: happens after development (in tissues) to control any cells that have escaped Mechanism: Anergy, suppression by Tregs, or deletion. Purpose: Control self-reactive lymphocytes after maturation.