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: (superficial layer of skin) 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. Fracture Hematoma (6-8h): Clot forms; inflammation clears debris. 2. Fibrocartilaginous callus (3wks): New cappillaries organise fracture hematoma into granulation tissue 'procallus'. Fibroblasts/chondrocytes form soft callus (collagen bridge). 3. Bony callus (3-4mo): Osteoblasts make 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.

Question 46

What is the pathophysiology of gout?

Answer 46

Deposition of monosodium urate (MSU) crystals in joints due to chronic hyperuricemia (>6.8 mg/dL). Crystals trigger inflammation when uncoated or concentration changes abruptly.

Question 47

What are classic symptoms of an acute gout attack?

Answer 47

Sudden, severe monoarticular pain (often 1st MTP = podagra), redness, warmth, tenderness. Peak intensity in 8–12 hours; resolves in <2 weeks untreated

Question 48

Name 3 risk factors for gout.

Answer 48

Male sex, purine-rich diet (red meat/seafood/alcohol), renal insufficiency, diuretics, hypertension

Question 49

How is gout definitively diagnosed?

Answer 49

Synovial fluid analysis showing needle-shaped, negatively birefringent MSU crystals

Question 50

What are first-line treatments for acute gout?

Answer 50

NSAIDs (high dose, tapered), corticosteroids (if NSAIDs contraindicated), or IL-1 biologics e.g. Rilonacept, Canakinumab, Anakinra (severe cases)

Question 51

What is chronic gout management?

Answer 51

Urate-lowering therapy: allopurinol (xanthine oxidase inhibitor) or probenecid (uricosuric). Goal: serum uric acid <6 mg/dL

Question 52

What crystals cause pseudogout?

Answer 52

Calcium pyrophosphate dihydrate (CPP) crystals (rhomboid-shaped, weakly positively birefringent)

Question 53

How does pseudogout typically present?

Answer 53

Acute mono/polyarticular arthritis (knee most common), mimics gout but often in older adults (>85yo). May mimic OA (pseudo-OA) much less painful then gout; mostly just uncomfortable What triggers pseudogout attacks? Trauma, rapid calcium reduction, or metabolic stress

Question 54

How is pseudogout treated?

Answer 54

NSAIDs, intra-articular corticosteroids, or colchicine for prophylaxis

Question 55

Compare crystal morphology in gout vs. pseudogout.

Answer 55

Gout: Needle-shaped, negatively birefringent (MSU). Pseudogout: Rhomboid, weakly positive birefringent (CPP).

Question 56

Which joints are most affected in gout vs. pseudogout?

Answer 56

Gout: 1st MTP (podagra), lower extremities. Pseudogout: Knee, wrist, but any joint. Gout: "GOUT" = Great toe, Overnight pain, Urate crystals, Tophi. Pseudogout: "PSEUDO" = Pyrophosphate, Seniors, Elderly knees, Ultrasound (cartilage calcification), Double (rhomboid) crystals, Osteoarthritis mimic.

Question 57

What are cholesterol/lipid crystals associated with?

Answer 57

Rheumatoid arthritis; cholesterol = notched plates, lipids = Maltese cross birefringence.

Question 58

What imaging detects early gout?

Answer 58

DECT (dual-energy CT) identifies MSU deposits (64% sensitivity in early gout)

Question 59

What are radiographic signs of chronic gout?

Answer 59

"Rat bite" erosions with overhanging edges, preserved joint space, tophi (soft tissue deposits).

Question 60

neck of femur fracture signs

Answer 60

external rotation of leg/ foot shortening of leg

Question 61

What are the classic synovial fluid findings in septic arthritis?

Answer 61

Turbid/purulent fluid, WBC >50,000/mm³ (neutrophils), low glucose (<25 mg/dL), Gram stain +ve in 1/3. N.B. gold standard imaging modality for septic arthritis is joint aspiration and synovial fluid analysis

Question 62

Which joints are most commonly affected in septic arthritis?

Answer 62

Knee > hip/ankle/elbow > shoulder/fingers (polyarticular in 10%)

Question 63

What are the two main routes of infection in osteomyelitis?

Answer 63

Hematogenous spread (children) or contiguous spread (adults, e.g., trauma/diabetes) n.b. iatrogenic causes like synovial fluid sampling or corticosteroid injections in OA, RA

Question 64

What imaging is gold standard for osteomyelitis?

Answer 64

MRI (bone scintigraphy if MRI unavailable)

Question 65

What are key predisposing factors for osteomyelitis?

Answer 65

Diabetes, sickle cell disease, trauma, immunosuppression, extremes of age

Question 66

How is chronic osteomyelitis treated?

Answer 66

Surgical debridement (remove dead bone) + 4–6 weeks antibiotics (e.g., vancomycin, flucloxacillin)

Question 67

What triggers reactive arthritis?

Answer 67

Post-infection (STIs like Chlamydia or enteric pathogens e.g., Salmonella). HLA-B27 linked

Question 68

Is the joint sterile in reactive arthritis?

Answer 68

Yes—sterile inflammatory process

Question 69

What is the most successful treatment for prosthetic joint infection?

Answer 69

Remove prosthesis → 6 weeks antibiotics → reimplant (90% success)

Question 70

Which organism causes septic arthritis in neonates/young children?

Answer 70

Haemophilus influenzae (pre-vaccine era)

Question 71

What organism is associated with human bites?

Answer 71

Eikenella corrodens

Question 72

What blood markers are elevated in bone/joint infections?

Answer 72

ESR/CRP (neutrophilia in acute cases). Blood cultures +ve in 1/3–2/3 of septic arthritis

Question 73

What is the most common causative organism in septic arthritis?

Answer 73

Staphylococcus aureus (>90% of cases) Gram reaction: Gram-positive (retains the crystal violet stain, appearing purple under a microscope) Shape: Cocci (spherical), arranged in clusters (like grapes) Catalase: Positive Coagulase: Positive (this distinguishes it from other Staphylococcus species)

Question 74

If septic arthritis is suspected, its a medical emergency. Take the blood results and synovial fluid sample + culture, start them on antibiotics BEFORE u get results. What is the guideline? Then explain treatment post results

Answer 74

IV Flucloxacillin is first-line, unless there is: MRSA risk → use Vancomycin Severe penicillin allergy → use Vancomycin Concern for Gram-negative organisms (e.g., elderly, immunocompromised) → add Ceftriaxone or Gentamicin Tx post results; - drainage and wash out (with sterile saline) every few days - adjust antibiotics depending on gram and patient background

Question 75

What is the first step in managing suspected acute osteomyelitis? (According to NICE)

Answer 75

Start empirical IV antibiotics immediately after blood cultures and imaging/aspiration. Do not delay treatment if signs of sepsis. Usually: Flucloxacillin (or Vancomycin if MRSA or penicillin allergy). - 2–4 weeks IV, then switch to oral if improving

Question 76

chronic osteomyelitis treatment NICE

Answer 76

Chronic osteomyelitis usually needs: Surgical debridement to remove dead bone Longer antibiotics (often >6 weeks) Possible antibiotic-loaded (e.g. vancomycin) beads or spacers

Question 77

What are the steps of the ATLS primary survey?

Answer 77

Airway with C-spine control Breathing & ventilation Circulation & hemorrhage control Disability (neurological status: AVPU) Exposure & environment control

Question 78

What’s the difference between major and minor trauma?

Answer 78

Major: polytrauma, life-threatening injuries Minor: isolated, non-life-threatening injuries

Question 79

Why are pelvic fractures dangerous?

Answer 79

High blood loss (up to 2000 mL) 85% bleeding is venous (posterior plexus) Mortality up to 50% in polytrauma cases

Question 80

What is PRICE and when is it used?

Answer 80

Protect, Rest, Ice, Compression, Elevate — used for early soft tissue injury management.

Question 81

What are signs of fat embolism syndrome (possible complication of fractures that effect bone marrow)?

Answer 81

fat embolism syndrome= when bone marrow (fatty) gets out + travels in blood to brain or lungs ABG= mild hypoxemia, CXR normal MRI: white matter lesions symptoms: Altered consciousness, Hypoxemia, Petechial rash on chest skin/ widespread Tx= fluids to flush fat out, n.b. this is a serious condition + requires monitoring

Question 82

What are the 6 P’s of compartment syndrome?

Answer 82

Pain, Pallor, Pulselessness, Paresthesia, Paralysis, Poikilothermia (inability to maintain a constant core temperature)

Question 83

What is the emergency threshold for compartment pressure?

Answer 83

EMERGENCY= >30 mmHg → Requires urgent fasciotomy normal= 0-10mmHg elevated= 20-30mmHg

Question 84

What are the key symptoms, diagnostic features, and treatment approaches for systemic sclerosis (scleroderma) according to NICE

Answer 84

🟨 Symptoms: Skin: Thickening, tightness, sclerodactyly, telangiectasia, calcinosis Vascular: Raynaud’s phenomenon, digital ulcers GI: Dysphagia, reflux, bloating Lungs: Shortness of breath, pulmonary fibrosis, pulmonary hypertension Renal: Scleroderma renal crisis (hypertension + renal failure) MSK: Joint stiffness, myalgia 🟨 Diagnosis: Clinical features: Raynaud’s + skin thickening = high suspicion Autoantibodies: ANA (positive in >90%) Anti-centromere Ab (limited cutaneous type) Anti-Scl-70 / anti-topoisomerase I (diffuse type) Nailfold capillaroscopy: Capillary dropout, dilated loops Organ assessment: HRCT (lung), echocardiogram (PAH), BP & renal function (renal crisis) 🟨 Treatment (per NICE): Raynaud’s: First-line: Nifedipine (or other CCB) Severe: IV iloprost Digital ulcers: Protection and wound care Consider bosentan for recurrent severe cases General care: Early referral to rheumatology Monitor for organ involvement Refer to relevant specialties for lung, renal, GI issues

Question 85

what superficial muscle is usually used in skin/muscle graft

Answer 85

latissimus dorsi

Question 86

What is an avulsion fracture, and which muscles are commonly involved in pelvic avulsion injuries?

Answer 86

An avulsion fracture occurs when a muscle or ligament forcefully pulls a piece of bone off its attachment site, often during sudden or forceful movement (e.g. sprinting or kicking). Iliac crest -- abdominal muscles Anterior superior iliac spine (ASIS) -- sartorius Anterior inferior iliac spine (AIIS) -- rectus femoris Greater trochanter -- gluteus medius + minimus Lesser trochanter -- iliopsoas Ischial tuberosity -- hamstrings Pubic symphysis -- adductors

Question 87

Medical Research Council (MRC) muscle strength grade meaning

Answer 87

Grade 0= No Movement Grade 1= flicker only Grade 2= full movement without gravity Grade 3= full movement against gravity only Grade 4= full movement against moderate resistance Grade 5= full movement against max resistance

Question 88

What is antalgic gait?

Answer 88

Antalgic gait is a type of abnormal walking pattern that develops as a way to avoid pain while walking; characterized by a shortened stance phase on the affected limb and a relatively longer swing phase of the same limb. This pattern minimizes the time the painful leg bears weight. Key Features: - Shortened step length on the painful side - Limping appearance - Patient often shifts weight quickly off the painful leg - Usually due to pain in the lower limb (e.g., hip, knee, ankle, or foot)