Locomotor 2 wk1+2 Flashcards

Question

What nerve is damaged in a lisfranc fracture + what sign will u see?

Answer 1

deep peroneal/fibular n. (L4-S1) OR tibial n. (L4-S3) Deep Fibular Nerve Injury (Anterior Tarsal Tunnel Syndrome): - Numbness or tingling in the first web space (between the big toe and second toe). - Weakness in toe extension - Pain on the dorsum of the foot that worsens with pressure or wearing tight shoes. - In severe cases= foot drop

Answer 2

deep peroneal nerve (L4-S1) - foot drop - anterior compartment of leg effected; no longer dorsiflex foot nor extend digits

Answer 3

SCIATIC NERVE (L4-S3) Signs its sciatic nerve: - foot drop - weak plantarflexion - weak toe flexion - foot slap gait Sometimes, but v rarely femoral nerve (L2-L4) because it lies protected within the pelvis and posterior to the femur Signs its femoral nerve: Weak knee extension (quad riceps) + anterior thigh numbness.

Answer 4

surgical neck fracture of humerus (common in elderly); axillary nerve (C5-C6)

Answer 5

midshaft fracture of humerus (as it travels down radial groove) radial n. C5-T1= wrist drop

Answer 6

supracondylar fracture of humerus (common in kids)= increased risk of volkmaan's ischemic contractures median/ radial n. + brachial artery most at risk!

Answer 7

medial epicondyle; ulnar n. (C8-T1) = claw hand

Answer 8

lateral epicondyle radial n. (C5-T1)= wrist drop

Answer 9

loss of sensation to dorsum of foot

Answer 10

short saphenous vein is on the lateral aspect of leg great saphenous on the medial aspect of leg

Answer 11

anterior dislocation= FEMORAL nerve (L2-L4) injury

Answer 12

sciatic nerve

Answer 13

the scapulo-humeral rhythm moves 1:2 ratio. When arm is abducted 180 degress, 60 degrees occurs by rotation of scapula and 120 degrees by rotation of humerus at shoulder joint

Answer 14

wingning of the scapula is due to damage to long thoracic nerve serratus anterior dysfunction

Answer 15

regimental badge= deltoid innervated by axillary n. (C5-C6)

Answer 16

spinal accessory nerve (CN XI)

Answer 17

The Allen test (and MAT) assess adequate collateral circulation in hand and the presence of a complete palmar arch before performing any any procedure that could potentially disrupt blood flow in the radial or ulnar arteries. Positive modified Allen test – If the hand flushes within 5-15 seconds it indicates that the ulnar artery has good blood flow; this normal flushing of the hand is considered to be a positive test. Normal test (Positive Allen test): Hand flushes pink within 5–7 seconds, indicating good ulnar artery collateral flow. Abnormal test (Negative Allen test): Hand remains pale >7–10 seconds, suggesting insufficient ulnar artery circulation.

Answer 18

cartillage= type II collagen bone= type I collagen smooth muscle= type III collagen

Answer 19

275 bones at birth (lots of cartillage in babies) then become 206 bones (less cartillage) at adulthood baby's bones will fuse together as they grow kids have a lot of WOVEN bone (their bones are bendy + disorganised layers)

Answer 20

trabecular bone remodels 3-10 times faster than cortical bone

Answer 21

Pott's Disease, also known as tuberculosis spondylitis (rare) caused by mycobacterium tuberculosis infecting the spine= arthritis + vertebral osteomyelitis (infection in bone) symptoms: - Vertebral damage leading to an increased kyphotic deformity and subsequent back pain. - Excessive spinal curvature can also compress spinal nerves which may lead to paraplegia. - Systemic symptoms, such as malaise, fever, appetite loss. haemoptysis, night sweats and weight loss. Infection results in the vertebral bodies collapsing, compressing and damaging the neural tracts travelling through the spine. The anterior corticospinal tracts are typically affected first resulting in an increase in spasticity which is denoted by exaggerated reflex responses as well as extension of the big toes (Babinski sign). Subsequently, the anterior and lateral spinothalamic tracts are affected leading to loss of crude touch, temperature, and pain detection. Finally, the dorsal column medial lemniscus located posteriorly is damaged causing loss of fine touch and proprioception in the upper and lower body. Sphincter control over the bladder and the bowel is also affected. The complete compression of the spinal cord results in a transition from spastic paralysis to flaccid paralysis. The stages of neurological deficit are broken down in the modified Tuli classification.

Answer 22

A characteristic feature of Diffuse Idiopathic Skeletal Hyperostosis (DISH) is ossification of the anterior longitudinal ligament. DISH is a type of arthritis that is characterised by abnormal calcification and ossification of the entheses of the spine. DISH causes the tendons and ligaments around the spine to calcify and form abnormal new bone growth called bone spurs at their attachment points to the bone. It causes the ligaments to harden in areas where they attach to the spine. This is caused by the buildup of calcium salts in these areas causing calcification and overgrowth of bone. DISH can also affect the appendicular bones like the hips, knees, shoulders, and feet, and hands, and is more common in elderly men.

Answer 23

Necrotising autoimmune myopathy (NAM) is an inflammatory condition resulting in the degeneration of muscle fibers. Statins (e.g. Atorvastatin) are one of the main medications that can cause this type of myopathy Other associated medications include colchicine (anti-gout), phenytoin (sodium channel blocker), cimetidine (histamine H2 receptor antagonist) and chloroquine (anti-malarial).

Answer 24

hematopoeitic stem cells -> monocytes -> osteoclasts (bone resorption)

Answer 25

mesenchymal cells (embryonic mesoderm) -> osteoprogenitor cell -> osteoblast (bone formation) -> osteocyte (maintain bone)

Answer 26

Osteoclasts need the following for activation: M-CSF (macrophage colony stimulating factor) RANKL (Receptor activator of nuclear factor kappa-B ligand)

Answer 27

Romosozumab (stimulates bone formation while suppressing bone resorption; treatment for osteoporosis) n.b. Sclerostin is a SOST gene product that reduces osteoblastic bone formation by inhibiting canonical Wnt/β-catenin signaling. Investigational monoclonal antibodies to sclerostin have been to shown to increase bone formation markers and decrease bone resorption markers, with an increase in bone mass

Answer 28

Bone Metabolism: Promotes osteoclast formation, activation, and survival, enabling bone resorption. Balanced by Osteoprotegerin (OPG), which inhibits RANKL. Immune System: Influences dendritic cell survival and T cell responses, linking bone and immune systems (osteoimmunology). Physiological Roles: Essential for mammary gland development, thermoregulation, and fever response. Pathology: Overexpression leads to osteoporosis, rheumatoid arthritis, and bone metastases in cancers. Targeted by denosumab for therapeutic purposes.

Answer 29

Calcium Homeostasis Regulating Hormones: Parathyroid Hormone (PTH): Increases blood calcium via bone resorption, kidneys, and vitamin D activation. Calcitriol (Vitamin D): Enhances intestinal absorption of calcium. Calcitonin: Lowers blood calcium by inhibiting osteoclasts. FGF23: Regulates phosphate elimination, decreasing calcium indirectly. Calcium Distribution: 99% in bones/teeth, 1% in blood and fluids Daily Requirement: 500-1300 mg/day Excretion: Kidneys (~200 mg/day), Gut (600-800 mg/day)

Answer 30

In the four parathyroid glands located behind the thyroid. half-life; About 4 minutes.

Answer 31

short term: By making the kidneys excrete phosphate/ PO4 and reabsorb Ca2+ from the distal tubule. long term: By activating osteoclasts to release CA2+ from bone and by increasing active vitamin D (via 1-α hydroxylase) to enhance intestinal CA2+ absorption.

Answer 32

It decreases PTH production.

Answer 33

It treats secondary hyperparathyroidism in kidney failure patients by binding to calcium-sensing receptor (CaSR), making it more sensitive to calcium, thus reducing PTH secretion. effect cinacalcet has on CaSR response curve: shifts the curve leftward, meaning less extracellular calcium is needed to suppress PTH secretion.

Answer 34

They reduce phosphate excretion and vitamin D activation, causing low blood Ca2+ and high phosphate, which stimulates PTH release.

Answer 35

FGF23 is produced by osteocytes and osteoblasts. Its secretion is stimulated by calcitriol (active vitamin D3) and dietary phosphate loading.

Answer 36

Phosphate: Reduces renal phosphate reabsorption by decreasing Na/phosphate cotransporters in the proximal tubule (similar to PTH). Calcium: Inhibits 1α-hydroxylation of vitamin D → lowers calcitriol → reduces intestinal Ca²⁺ absorption.

Answer 37

In CKD-MBD, FGF23 levels rise due to impaired phosphate excretion and calcitriol deficiency. This further suppresses calcitriol, exacerbating secondary hyperparathyroidism (↑ PTH) and bone demineralization.

Answer 38

Cause: Mutations in the PHEX gene (a phosphate-regulating peptidase) lead to unchecked FGF23 activity → excessive renal phosphate wasting. deficiency= hyperactive FGF23 leads to renal phosphate loss! Effect in children: Causes vitamin D-resistant rickets. Treatment: Burosumab, a monoclonal antibody that neutralizes FGF23. n.b. u cant give them vitamin D supplement because kidney (FGF23) is inhibiting 1α-hydroxylase enzyme so conversion to 1,25 dihydroxyvitamin D not taking place

Answer 39

Shared effect: Both increase renal phosphate excretion. Opposing effects: PTH stimulates 1α-hydroxylase → ↑ calcitriol → ↑ intestinal Ca²⁺ absorption. FGF23 inhibits 1α-hydroxylase → ↓ calcitriol → ↓ intestinal Ca²⁺ absorption.

Answer 40

Source: Secreted by parafollicular C-cells of thyroid in response to high serum Ca²⁺ (>2.25 mmol/L). Effects: - Bone: Inhibits osteoclasts → ↓ bone resorption (weak effect). - Kidney: ↑ Ca²⁺ excretion (inhibits reabsorption). - Intestine: ↓ Ca²⁺ absorption. Clinical Use: Second-line treatment for osteoporosis (limited efficacy cuz calcitonin effects on bone metabolism v minimal). vs. PTH: - Calcitonin lowers blood Ca²⁺ (short-term, mild). - PTH raises blood Ca²⁺ (dominant, via bone/kidney/vitamin D MNEMONIC: Calcitonin Tones Down Calcium (T= thyroid)

Answer 41

GH stimulates hepatocytes to produce IGF-1 and directly promotes growth in cartilage/bone. IGF-1 acts on: Chondrocytes (epiphyseal plate) → longitudinal bone growth. Osteoblasts → proliferation and bone formation.

Answer 42

Targets: Chondrocytes, osteoblasts, osteoclast precursors, and bone marrow stromal cells. Hypothyroidism (children): Dwarfism (impaired bone growth). Hyperthyroidism: Secondary osteoporosis (excessive bone resorption).

Answer 43

Estrogens: ↑ Intestinal Ca²⁺ absorption. Directly stimulate osteoblasts and inhibit osteoclasts (↓ M-CSF, IL-1, IL-6, TNFα). Progesterone: Adds to bone density (used in osteoporosis therapy). FSH: Stimulates osteoclasts, but estrogens compensate anabolically.

Answer 44

Converted to estrogens (via aromatase) → bone-protective effects are largely estrogen-mediated.

Answer 45

↓ Bone formation: Kill osteoblasts and shorten their lifespan. ↑ Bone resorption: Induce RANKL → activates osteoclasts.

Answer 46

GH/IGF-1 (strong anabolic). Estrogens (net anabolic via osteoblast stimulation). PTH (mixed: catabolic in chronic high doses, anabolic in pulses). Cortisol (strongly catabolic). Mnemonic for bone-resorbing hormones: "Cortisol PTHs FSH" (Catabolic: Cortisol, PTH-high, FSH).

Answer 47

Internal (medial) rotation of the shoulder is facilitated by subscapularis (chief internal rotator), teres major, latissimus dorsi, pectoralis major and deltoid. Subscapularis is an anterior rotator cuff muscle, and it is the most important muscle with regards to internal rotation of the shoulder.

Answer 48

External (lateral) rotation of the shoulder is facilitated by infraspinatus (chief external rotator), teres minor and deltoid muscles. Infraspinatus and teres minor are posterior rotator cuff muscles.

Answer 49

"Trigger finger" or stenosing tenosynovitis is typically caused by inflammation of the flexor digitorium tendon and its sheath Stenosing tenosynovitis typically occurs in young adults to middle-aged patients who have occupations or hobbies that involve repetitive and prolonged gripping and grasping Trigger finger can be caused by other things that disrupt the gliding of the tendon within the sheath, such as a leiomyoma.

Answer 50

Extension of the elbow is carried out by triceps brachii and anconeus, flexion of the elbow is carried out by biceps brachii, brachialis, and brachioradialis.

Answer 51

Pain and tenderness upon palpation of the anatomical snuffbox may indicate a scaphoid bone fracture.

Answer 52

alkaline phosphatase is made by osteoblasts (marker of how active osteoblasts are) + by the liver

Answer 53

T-score= number of standard deviations from the mean young (30yr) same gender + ethnicity Z-score= number of standard deviations from same age, gender + ethnicity (used when u have osteoporosis in a young person) n.b. WHO-T score is 25% lower than average= osteoporosis diagnosis

Answer 54

precursor to osteoporosis is osteopenia (low bone density)

Answer 55

- neck of the femur - lumbar vertebra (L1-L4) - distal radius at wrist

Answer 56

iliac crest

Answer 57

Osteoporosis= metabolic bone disease causing porous bone that can lead to fractures 1) Primary Osteoporosis: Age-related (postmenopausal women and elderly men) 2) Secondary Osteoporosis: Due to chronic conditions or medications (e.g., glucocorticoids, hyperthyroidism, malabsorption) Risk Factors: - Female gender, advanced age, family history - Low body weight, smoking, alcohol abuse - Vitamin D or calcium deficiency, sedentary lifestyle Symptoms: - Often asymptomatic until fracture occurs - Common fractures: Hip, spine, wrist - Chronic pain, loss of height, kyphosis (hunchback) Diagnosis: - DEXA scan (T-score ≤ -2.5 confirms osteoporosis) - Lab Tests: Calcium, vitamin D, thyroid, renal function Treatment: - Adequate calcium (1200 mg/day) and vitamin D (800-1000 IU/day) - 1ST LINE MED: Bisphosphonates (e.g., Alendronate, Risedronate): First-line for reducing fracture risk - Denosumab injection every 6 months: Monoclonal antibody binds to RANKL ; For patients intolerant to bisphosphonates - Selective Estrogen Receptor Modulators (SERMs): For postmenopausal women - Teriparatide (PTH analog) & Romosozumab: For severe cases - Strontium ranelate (increases expression of Wnt proteins, activates CaSR= increased collagen type I synthesis)

Answer 58

Osteomalacia= a metabolic bone disease characterized by defective bone mineralization leading to soft, weak bones. Causes/Risk Factors: - Vitamin D Deficiency: Most common cause (dietary lack, malabsorption, lack of sunlight) - Chronic Kidney Disease (CKD): Impaired vitamin D activation - Hypophosphatemia: Renal phosphate wasting or poor intake Medications: Anticonvulsants (phenytoin), aluminum-containing antacids Genetic Disorders: Rare forms (e.g., hereditary hypophosphatemic rickets) Symptoms: - Bone pain and tenderness (especially hips, legs, and ribs) - Muscle weakness (proximal myopathy) - Difficulty walking, waddling gait - Fractures and bone deformities Diagnosis: Laboratory Tests: - Low serum calcium and phosphate, high alkaline phosphatase (ALP) - Low vitamin D (25-hydroxyvitamin D < 20 ng/mL) Radiology: Looser's zones or pseudofractures on X-rays Treatment: -Vitamin D Supplementation: Cholecalciferol (D3) first-line (n.b. use Ergocalciferol (D2) for vegans) Calcitriol in CKD or hypoparathyroidism Calcium and Phosphate Supplements: As needed Treat Underlying Causes: CKD management, phosphate binders Lifestyle Modifications: Sunlight exposure, dietary adjustments Prevention: - Adequate vitamin D and calcium intake - Regular sunlight exposure

Answer 59

intermittent exposure to PTH activates osteoblasts more than osteoclasts

Answer 60

Definition: A chronic bone disorder characterized by excessive bone remodeling, where bone becomes enlarged, weak, and structurally abnormal Causes/Risk Factors: Genetic Factors: SQSTM1 gene mutations (codes for protein p62/ sequestosome 1) linked to increased osteoclast activity Viral Hypothesis: Possible link to paramyxovirus infection (e.g., measles virus remnants in osteoclasts) Age & Gender: More common in older adults (>55 years), men > women Ethnicity: Higher prevalence in European populations Pathology: Excessive osteoclastic resorption Compensatory disorganized osteoblastic formation Symptoms: - Often asymptomatic, diagnosed incidentally on imaging or labs - Bone pain (pelvis, spine, skull, long bones) - Bone deformities (bowing of legs, skull enlargement) - Increased risk of fractures Diagnosis: Laboratory Tests: - Elevated serum alkaline phosphatase (ALP) with normal calcium and phosphate Imaging: - X-ray: Cortical thickening, bone expansion, lytic and sclerotic lesions Treatment: - Bisphosphonates (First-line therapy): - Zoledronic acid (most effective, single-dose infusion) - Alendronate, risedronate (oral options) - Pain Management: NSAIDs, analgesics - Calcium & Vitamin D Supplementation: To prevent secondary deficiencies monitor ALP levels regularly through life

Answer 61

1) Lytic Phase (Initial) - Excessive bone resorption due to giant, hyperactive osteoclasts (possibly triggered by viral infection/genetics). 2) Mixed Phase (Compensatory/Proliferative) - Disorganized bone formation attempts to compensate for resorption → "Mosaic" pattern of woven bone. 3) Sclerotic Phase ("Burnt Out") - Dense, sclerotic "Pagetic bone" with: - Thickened, irregular trabeculae - Fibrovascular marrow replacement - Prominent cement lines

Answer 62

Legg-Calvé-Perthes disease, also known as Perthes disease, is a childhood hip disorder where the blood supply to the femoral head (the ball of the hip joint) is temporarily disrupted, leading to bone death, collapse, and potential long-term hip problem

Answer 63

DO NOT PERFORM THOMAS' TEST ON PATIENT WITH HIP REPLACEMENT! (risk of dislocation) Purpose: Detects fixed flexion deformity of the hip (e.g., iliopsoas tightness or contracture). Contraindication: Do not perform in patients with hip replacements. Steps: - Place hand under the patient’s lumbar spine (assesses lordosis). - Passively flex one hip maximally toward the chest. - Observe the contralateral (opposite) hip. Normal: Contralateral/other hip should remain on the bed (no deformity). Abnormal: Contralateral/other hip raises off the bed → fixed flexion deformity (e.g., iliopsoas tightness). Key Insight: - The test eliminates lumbar lordosis to isolate hip flexion deformity. - Lifting of the opposite hip indicates loss of extension in that hip. (so u are lifting leg on 'healthy side' and looking at hip on other side to see if its fucked)

Answer 64

Purpose: Assesses sciatic nerve compression (L4–S1), commonly due to: - Lumbar radiculopathy (e.g., herniated disc). - Piriformis syndrome (sciatic nerve entrapment). Technique: - Patient lies supine. - Passively raise the straightened leg (30°–70° range). - Observe for reproduction of radicular pain (shooting down the leg). if there is pain ask them to dorsiflex at the height they feel the pain and if it gets worse this will confirm its sciatic (Braggard) Confirmatory maneuvers: Bragaard’s Test: Dorsiflex the foot during SLR → ↑ sensitivity. Pain relief on knee flexion → supports neurogenic etiology. Interpretation: Normal: No pain, full ROM (Range Of Motion) Abnormal: Radicular pain (suggests nerve root irritation).

Answer 65

Method: Patient raises arm sideways (0-180°). Positive: Pain between 60-120° = subacromial impingement. Pain after 120° = AC joint issue.

Answer 66

Method: Examiner lifts patient’s straight arm up while holding the scapula. Positive: Pain at top = subacromial impingement (causes shoulder pain, occurs when rotator cuff muscles' tendons are compressed as they pass through the area beneath the acromion bone aka subacromial space)

Answer 67

Method: Arm bent 90° at shoulder/elbow, palm down. Examiner twists arm inward. Positive: Pain = supraspinatus tendon impingement.

Answer 68

Method: Arms at 90°, thumbs down (like emptying a can). Resist upward movement. Positive: Pain/weakness = supraspinatus tear.

Answer 69

Method: Hand on lower back, push backward against resistance. Positive: Pain/weakness = subscapularis tear.

Answer 70

Method: Bring arm across chest (like a scarf). Positive: Pain = AC joint problem (e.g., arthritis).

Answer 71

Method: Arm forward, palm up. Resist downward push. Positive: Pain = biceps tendonitis or labral tear.

Answer 72

pagets= IV Zoledronic acid 5mg infusion (bisphosphonate) osteoporosis= alendronate or risedronate (bisphosphonate) osteomalacia= Vitamin D Supplementation – Cholecalciferol (Vitamin D3)

Answer 73

Normal articular cartillage is avascular (no blood supply) and aneural (no nerve supply) normal articular cartillage: Hyaline cartilage: 2–4 mm thick, avascular/aneural, low-friction surface. ECM composition: Type II collagen (strength) + proteoglycans (resilience/squishy), maintained by chondrocytes. Tidemark: Boundary between uncalcified and calcified cartilage.

Answer 74

bone= OSTEOBLASTS make the ECM in bone by producing; - organic matrix (called osteoid); made of type I collagen, osteocalcin, osteonectin, and proteoglycans - Once the osteoid is laid down, osteoblasts help mineralize it with calcium and phosphate cartillage= CHONDROCYTES make the ECM in cartillage by producing; - Type II collagen - Proteoglycans (like aggrecan)

Answer 75

Fibrillation (surface splits). Erosion/cracking (deep fissures). Eburnation (bone exposure, polishing).

Answer 76

With age or injury, HMGB2 levels decrease → chondrocytes start to die off. HMGB2 (high-mobility group protein 2) loss=> Superficial chondrocyte death + progenitor cell loss → Reduced ECM synthesis → Cartilage disruption. HMGB2 helps maintain the survival of chondrocytes in the superficial zone of articular cartilage. summary: ↓ HMGB2 ↓ Chondrocyte survival ↑ Cartilage degradation ↑ Risk of developing OA

Answer 77

MMP-13 should NOT be present in normal cartilage Osteoarthritis (OA): MMP-13 overexpression: Primary collagenase targeting type II collagen → catastrophic ECM degradation. Driven by: - Pro-inflammatory cytokines (IL-1β, TNF-α). - Mechanical stress. - Chondrocyte senescence. Results in: Cartilage fibrillation → eburnation. Shift to weak type I collagen (fibrocartilage). Clinical Relevance: MMP-13 is a therapeutic target (e.g., inhibitors in trials).

Answer 78

1) Cartilage erosion → Exposed bone (eburnation). 2) Microfractures of trabeculae due to abnormal loading. 3) Subchondral sclerosis: Increased osteoblast activity → thickened, dense bone. 4) Cyst formation: Focal pressure necrosis → "subarticular cysts." 5) Vascular changes: Engorgement + slowed blood flow → bone marrow edema (painful!). Mechanism: - Biomechanical stress + inflammation → bone remodeling imbalance. Clinical: - Sclerosis/cysts visible on X-ray/MRI; marrow edema correlates with pain.

Answer 79

Molecular Drivers: TGF-β↑: Drives osteoblast activity → sclerosis RANKL/OPG imbalance: ↑RANKL → Osteoclast activation → microfractures ↓OPG (osteoprotegerin) → Unchecked bone resorption VEGF↑: Vascular invasion → edema & cysts Pro-inflammatory cytokines (IL-1β, TNF-α): Stimulate MMPs (e.g., MMP-13) → degrade cartilage-bone interface Wnt/β-catenin pathway: Dysregulation → abnormal bone formation Clinical Link: - Sclerosis/cysts seen on X-ray; marrow edema on MRI (pain correlate). - Therapeutic targets: Anti-TGF-β, anti-RANKL (e.g., denosumab).

Answer 80

tendons (a little less elastic than ligaments) attach Muscle ➝ Bone ligaments attach Bone ➝ Bone

Answer 81

✅ Tendinitis * 🔥 Acute inflammation of a tendon * Caused by microscopic tears * No permanent structural damage to the tendon * 📍 Common sites: - Lateral epicondyle (tennis elbow) - Achilles tendon - Supraspinatus tendon * ⚠️ Causes: - Overuse - Collagen disorders - Renal dialysis (rare but recognized risk) * 🧰 Treatment: - RICE (Rest, Ice, Compression, Elevation) - NSAIDs and analgesia - Stretching and physiotherapy - Surgery in refractory cases - NICE management is often conservative, focusing on inflammation control and rehab. 🧱 Tendinosis * 🕒 Chronic, degenerative condition from failed healing * Histology: Disorganized collagen fibers * Tendon appears thickened, rubbery, and scarred * ❗️May lead to partial or full-thickness tendon tears * Less responsive to anti-inflammatory treatment (as there is minimal inflammation) Studies show altered cell morphology and increased matrix metalloproteinase (MMP) activity in tendinosis tissue. 🧠 Clinical Tip: If symptoms have persisted for >6 weeks and imaging shows degenerative changes, think tendinosis, not tendinitis.

Answer 82

Etodolac is a nonsteroidal anti-inflammatory drug (NSAID) used to treat mild to moderate pain, and helps to relieve symptoms of arthritis (eg, osteoarthritis and rheumatoid arthritis), including inflammation, swelling, stiffness, and joint pain. Etodolac MoA= works by inhibiting cyclooxygenase (COX) enzymes, specifically COX-2, which reduces the synthesis of prostaglandins, thereby alleviating pain, inflammation, and fever

Answer 83

Direct Enthesis: - Insertion shows a gradual transition (as in fibrocartilage) - Better for high-stress areas; allows smooth force transfer Indirect Enthesis: - tendon/ligament attaches to periosteum or diaphysis, often via Sharpey's fibers - More abrupt; common in fibrous entheses

Answer 84

heterotopic ossification: Pathologic bone formation in soft tissues (e.g., muscles, tendons) after trauma, surgery (e.g., hip arthroscopy), or neurologic injury. Example: Seen in a 20-year-old post-hip arthroscopy (left side developed HO; right side had NSAID prophylaxis). COX-2 2 contribution: COX-2 → Prostaglandins (PGE₂) → Promotes: Chondrocyte differentiation/hypertrophy (via VEGF, RANKL). Angiogenesis & osteoclast recruitment → Fracture bridging. Why are NSAIDs used to prevent HO? NSAIDs (e.g., Etodolac) inhibit COX-2 → Reduce PGE₂ → Block: Mesenchymal stem cell differentiation into osteoblasts. Inflammatory signals (IL-1, IL-6) that drive HO. Dose: Etodolac 600 mg daily for 2 weeks post-op (per case example).

Answer 85

They are strong collagen fibers (mainly type I collagen) Anchor tendons, ligaments, and periosteum to bone Insert deep into the cortical bone, ensuring stable attachment Often found in indirect entheses (e.g. where the tendon inserts into the bone via the periosteum)

Answer 86

1) Mechanical injury at the enthesis (bone-tendon junction) triggers stress sensing. 2) Inflammation: Transcortical vessels (TCVs) dilate, allowing immune cell efflux (e.g., neutrophils). 3) Mesenchymal stem cells (MSCs) proliferate and differentiate into osteoblasts. 4) New bone formation: Osteoblasts deposit bone at the enthesis, driven by inflammation and mechanical stress. Key Players: - Transcortical vessels (TCVs; small blood vessels crossing cortical bone at the enthesis): Activate vasodilation and immune cell recruitment. - Mesenchymal stem cells (MSCs; Multipotent cells in bone marrow/entheseal tissues) → Osteoblasts: Drive pathologic bone formation. Hypertrophic chondrocytes: May contribute to entheseal thickening. Clinical Link: Seen in spondyloarthritis (e.g., ankylosing spondylitis). CAUSES OF ENTHESITIS: - recurring stress/ microdamage - associated with HLA B27 anthropathies

Answer 87

- Enthesophytes: Origin: Form at the insertion site of tendons, ligaments, or joint capsules into bone. Location: Do not involve the articular border (joint surface). Associated with: Mechanical stress, enthesitis (e.g., spondyloarthritis). - Osteophytes: Origin: Arise from the articular cartilage border (joint margin). Location: Project into the joint space. Associated with: Osteoarthritis (OA), joint degeneration. Key Distinction: Enthesophytes = Tendon/ligament insertion (non-articular). Osteophytes = Joint margin (articular cartilage). Visual Clue: Enthesophyte: "Where tendon meets bone." Osteophyte: "Where cartilage degenerates."

Answer 88

1. Mechanical/Traumatic Enthesitis - RICE (Rest, Ice, Compression, Elevation) - NSAIDs (e.g., Ibuprofen, Naproxen) – First-line for pain/inflammation. 2. Inflammatory/Autoimmune Enthesitis (e.g., Spondyloarthritis, Ankylosing Spondylitis) - Disease-Modifying Anti-Rheumatic Drug (DMARDs): Sulfasalazine or Methotrexate (for peripheral joint involvement). - Biologics: Anti-TNF therapy (e.g., Adalimumab, Infliximab) For severe, refractory cases. - Local Therapies: Corticosteroid injections (short-term relief). Hyperosmolar dextrose injections (prolotherapy, experimental). Radiotherapy (rare, for resistant cases). Key Points: Anti-TNF can resolve inflammation and halt osteoproliferation (e.g., visible improvement in ankylosing spondylitis at 24 weeks). HLA-B27+ patients often require systemic treatment (linked to autoimmune pathogenesis). Visual Summary: Mechanical → NSAIDs/RICE Inflammatory → DMARDs → Anti-TNF Clinical Pearl: If enthesitis is part of ankylosing spondylitis, prioritize anti-TNF over local therapies.

Answer 89

DMARD = Disease-Modifying Anti-Rheumatic Drug Purpose: Slows disease progression in inflammatory enthesitis (e.g., ankylosing spondylitis, psoriatic arthritis) by targeting the underlying immune dysfunction. Types Relevant to Enthesitis: Conventional DMARDs: - Methotrexate (first-line for peripheral joint involvement). MoA; folate antagonist that inhibits dihydrofolate reductase (DHFR) -> this stops tetrahydrofolate production-> stops DNA synthesis/cell division - Sulfasalazine (especially in axial spondyloarthritis with peripheral symptoms). Biologic DMARDs: Anti-TNF agents (e.g., Adalimumab, Infliximab) – For severe, refractory enthesitis. Key Difference: - NSAIDs (e.g., Ibuprofen) only reduce symptoms. - DMARDs modify the disease course by suppressing inflammation. Clinical Context: DMARDs are used when enthesitis is part of systemic autoimmune disease (e.g., HLA-B27-associated spondyloarthritis).

Answer 90

SLE= a chronic autoimmune disease causing multi-system inflammation due to immune complex deposition and autoantibodies (e.g., anti-dsDNA, anti-Sm). clinical presentation of joint pain and stiffness, fatigue, headache, fever, weight loss, and a distinct rash on face common presentation. Classic Triad: 1) Malar rash (butterfly rash). 2) Photosensitivity. 3) Non-erosive arthritis (Jaccoud arthropathy, 90% of patients). Systemic Involvement: - Renal: Glomerulonephritis. - Hematologic: Anemia, thrombocytopenia. - Neuropsychiatric: Cognitive dysfunction. - Mucocutaneous: Oral ulcers, discoid rash, alopecia. SLE is associated with alopecia, arthralgia, glomerulonephritis, and pleurisy.

Answer 91

1) ANA positivity (>95% sensitive, but nonspecific). 2) Specific antibodies: - Anti-dsDNA (SLE-specific). - Anti-Smith (Sm) (highly specific). N.B SLE is associated with alopecia, arthralgia, glomerulonephritis, and pleurisy. arthritis= Jaccoud's arthritis/arthropathy is a type of non-erosive arthritis seen in SLE MNEMONIC; SOAP BRAIN MD; Serositis → pleuritis, pericarditis Oral ulcers Arthritis → e.g. Jaccoud's arthritis Photosensitivity Blood Disorders → anaemia, thrombocytopenia, leucopenia, lymphopenia Renal Disorder → proteinuria, glomerulonephritis, Antinuclear Antibodies (ANA) - positive Immunological disorder → Anti-dsDNA, Anti-Sm, Antiphospholipid antibodies Neurological disorder → seizures, psychosis Malar (Butterfly) Rash Discoid Rash

Answer 92

Belimumab (fully human): Inhibits B-cell survival (BAFF/BLyS blocker). Rituximab (chimeric i.e. mouse/human): Depletes B-cells (anti-CD20). n.b. both are monoclonal antibodies (mAbs)

Answer 93

Fibers become small/angulated; remaining motor axons sprout to re-innervate them, forming enlarged motor units. If re-innervation fails → group atrophy.

Answer 94

Infantile Hypotonia ("floppy baby"): - 15% are myopathic (e.g., CFTD). - Biopsy shows small/round fibers + rare hypertrophic fibers. CFTD comes in 2 Types: - Classic (common): Small type 1 fibers, normal/large type 2. - Rare form: Large type 1 fibers, small type 2. Note: Hypotonia causes: 68% CNS, 15% muscle/nerve (e.g., CFTD), 17% unknown.

Answer 95

Age-related muscle loss (0.5–5%/year after 50); type II fibers atrophy more. By 70, 40% mass may be lost.

Answer 96

Polymyositis and dermatomyositis are both autoimmune diseases causing muscle inflammation and weakness, but dermatomyositis also involves characteristic skin changes, like a rash, while polymyositis primarily affects muscles Presentations: - Proximal weakness, elevated CK, lymphocyte infiltration (CD8+ T cells in polymyositis). - Dermatomyositis: Rash (heliotrope eyelids), anti-Jo1antibodies, subcutaneous calcifications. TREATMENT IS HIGH DOSE CORTICOSTEROID (PREDNISOLONE) TILL CREATINE KINASE GOES BACK TO NORMAL

Answer 97

Vacuoles, amyloid-like inclusions (β-amyloid, hyperphosphorylated tau proteins, apoliprotein E, presenillin 1, prion protein) deposited in muscles; affects finger/wrist flexors more than extensors. IBM is the most common muscle disease of elderly it has poor prognosis; more common in males; mild elevation in creatine kinase, muscle weakness, dysphagia, loss of quadriceps reflex

Answer 98

Duchenne muscular dystrophy (DMD) is a genetic disorder characterized by progressive muscle degeneration and weakness caused by a mutation in the DMD gene which leads to the deficiency of the structural protein, dystrophin. X-linked recessive; 1:3,500 males; proximal weakness by age 2; death by 30s; fibrosis/fat replace muscle; elevated CK. histology: variation in myofibre size, with small fibres and large, rounded fibres. Furthermore, there is also increased fatty replacement of myofibres and regeneration and increased endomysial connective tissue between muscle fibres. N.B. Dystrophin is key to the structural and functional integrity of the muscle fibres. The absence of dystrophin leads to damage of muscle cells followed by degeneration of muscle cells. The muscle regenerates new fibres which lead to the formation of many small muscle cells and replacement of muscle tissue by connective tissue.

Answer 99

Statins: Rhabdomyolysis (type II fibers). Corticosteroids: Type II atrophy. Alcohol: Acute/chronic proximal weakness.

Answer 100

Widespread pain + 11/18 tender points; CNS sensitization (neurotransmitter/HPA axis dysfunction). - 50% patients positive for antipolymer antibodies 80–90% female; treated with antidepressants (TCAs; amitriptyline first line) + exercise.

Answer 101

Spondyloarthritis (SpA) is a group of inflammatory rheumatic diseases that primarily affect: - The spine (especially the sacroiliac joints) - Entheses (where ligaments and tendons attach to bone) - Peripheral joints (in some subtypes) It’s a seronegative arthritis group (negative for rheumatoid factor, RF), often associated with the HLA-B27 gene. Key Features of SpA: - Inflammatory back pain (better with exercise) - Morning stiffness >30 minutes - Enthesitis (e.g., Achilles tendon) - Dactylitis ("sausage digits") - Extra-articular: uveitis, psoriasis, IBD - HLA-B27 positivity (not always, but common)

Answer 102

Type I fibers: - slow twitch - aerobic metabolism - red (darker when stained with NADH stain) - With an ATPase stain at a pH of 9.4, type I fibers stain lightly compared to type II - fatigue slowly - contain large numbers of mitochondira type II fibers (u lose these faster with age): - fast twitch - anaerobic metabolism - white (paler when stained with NADH) - With an ATPase stain at a pH of 9.4 type II fibers stain darker than type I - fatigue rapidly - contain low numbers of mitochondria

Answer 103

popliteal artery entrapment clinical symptom is cold feet following exercise, paraesthesia of the leg, calf numbness

Answer 104

Nucleus pulposus; - Composition: predominantly type II collagen - Abundant in chondrocytes Outer ring of annulus fibrosus; - Composition: predominantly type I collagen - Appearance: oblong-shaped Inner ring of annulus fibrosus; - Composition: predominantly type II collagen - Appearance: round-shaped

Answer 105

Exercise!! (local muscle strengthening, aerobic fitness) Weight loss (aim for 5% loss if BMI ≥25) Use of aids (walking sticks, orthopaedic insoles) TENS for pain relief Thermotherapy (heat/cold) Mediterranean diet (anti-inflammatory foods)

Answer 106

Paracetamol and/or topical NSAIDs. If ineffective, switch to oral NSAID/COX-2 inhibitor e.g. celecoxib (lowest dose, shortest duration) + PPI. Avoid long-term use due to comorbidities/side effects.

Answer 107

When pain/stiffness significantly impact quality of life (e.g., night waking because of pain will send them to orthopoedic team!). Options include: - Arthroscopic lavage/debridement - Joint replacement (last resort; 15–20-year lifespan) - microfracture (drill holes into subchondral bone + drill the bone marrow pluripotent stem cells; stimulates repair of articular cartilage)

Answer 108

IL-1/TNF inhibitors (e.g., adalimumab) – Limited by variable low-grade inflammation. TNF inhibition; Adalimumab (cost a lot) Platelet-rich plasma (PRP) injections Nerve Growth Factor (NGF) – Used in dogs and cats lol; awful adverse effects limit human use.

Answer 109

viscosupplementation: Mechanism: Hyaluronic acid injections restore synovial fluid viscosity. Pros: Pain reduction, delays joint replacement. Cons: NHS rarely covers it; less effective in severe OA.

Answer 110

Syndesmophytes are bony outgrowths, or calcifications, that form within the spinal ligaments (osteophytes of the spine basically)

Answer 111

Polyarticular osteoarthritis, aka polyarthritis, refers to osteoarthritis affecting five or more joints simultaneously, characterized by pain, stiffness, and potentially inflammation, and can be either inflammatory or non-inflammatory inherited type II collagen defects cause premature polyarthritis

Answer 112

because women have wider pelvis so femur has to angle more to get to knee joint; more weight on medial compartment of knee in females! This is calculated as the q-angle: - a is line drawn from ASIS to center of patella - a is line drawn from the tibial tuberosity to center of patella normal q angle: between 15-20 (angle is bigger in females than males) normal q angle male between 8-12

Answer 113

distal interpharengeal/DIP joint= Herberden's node proximal interpharengeal/PIP joint= Bouchard's node mnemonic: Heberden’s = High up (DIP) Bouchard’s = Below (PIP)

Answer 114

🦴 Erosive Osteoarthritis (EOA) (a rare type of OA): - Affects DIP & PIP joints (causes bony nodules) - Central erosions → "Gull-wing" sign on X-ray - No systemic symptoms - Sudden joint pain/swelling - linked to dyslipidemia and metabolic syndrome 🧬 Rheumatoid Arthritis (RA): - Affects PIP & MCP joints (causes soft tissue swelling) - Marginal erosions, joint space narrowing - Systemic symptoms (fatigue, morning stiffness >1 hr) - Autoimmune disease 🔍 Why are they often confused with eachother? - Both cause joint pain, swelling, and erosions - Both can affect hand joints N.B. EOA is LOCALISED INFLAMMATION OF HANDS WHEREAS RA IS SYSTEMIC INFLAMMATION

Answer 115

Inhibit cyclooxygenase (COX) enzymes, blocking prostaglandin synthesis from arachidonic acid. COX-1 inhibition= ↓ Clotting (↓ TXA2), ↑ GI risk COX-2 inhibition= ↓ Inflammation, pain, fever

Answer 116

NSAIDs: - Inhibit cyclooxygenase (COX) enzymes pathway (COX-1/COX-2). - Block prostaglandin (PG) synthesis from arachidonic acid → reduce pain, fever, inflammation. Example: Ibuprofen (reversible COX inhibition), aspirin (irreversible COX-1 inhibition). Steroids (e.g., glucocorticoids): - Bind intracellular receptors → regulate gene transcription. - Downregulate phospholipase A2 (PLA2) → reduce arachidonic acid release → suppress both cyclooxygenase pathway which produces prostaglandins AND lypoxygenase pathway which produces leukotriene production. - Broad anti-inflammatory effects: inhibit cytokines (IL-1, TNF-α), immune cell migration, and COX-2 expression. Key Difference: NSAIDs target downstream PG production (COX only), while steroids act upstream (PLA2 inhibition) and have broader immunosuppressive effects.

Answer 117

Non-selective (COX-1 & COX-2): Ibuprofen, naproxen, aspirin → GI/CV risks. COX-2 selective: Celecoxib, etoricoxib → lower GI but ↑CV risk (e.g., rofecoxib withdrawn). Aspirin: Irreversibly inhibits COX-1 (antiplatelet effect).

Answer 118

Reversible competitive: Ibuprofen (short-acting). Time-dependent reversible: Diclofenac (high affinity, slow dissociation). Irreversible: Aspirin (covalent modification; platelet COX-1 inhibition lasts 7–10 days).

Answer 119

Low-dose aspirin is cardioprotective (unique among NSAIDs). (only inhibits COX-1 i.e. antiplatelet at 75mg) High-dose aspirin (300mg) behaves like other NSAIDs (↑ CV/GI risks) inhibits COX-2 i.e. anti-inflammatory as well. Not a first-line painkiller due to bleeding risks (use paracetamol/NSAIDs instead).

Answer 120

PGE₂: Vasodilation (renal), immunosuppression (↓ lymphocytes), pain sensitization, ↓ gastric acid, FEVER, uterine relaxation. PGD₂: Vasodilation, bronchoconstriction (10× higher in asthma). PGI₂ (Prostacyclin): Vasodilation (renal), antiplatelet, bronchodilation, ↓ gastric acid, pain sensitization. PGF₂α: Mixed vascular effects, bronchoconstriction, uterine contraction. TXA₂ (Thromboxane A₂): Vasoconstriction, pro-thrombotic (platelet aggregation), bronchoconstriction, uterine contraction. mnemonics: PGE₂ = FEVER" (Fever, Uterine relaxation, Gastric protection). "PGI₂ vs. TXA₂" (Yin-Yang): - PGI₂: Vasodilate + Antiplatelet. - TXA₂: Vasoconstrict + Pro-thrombotic. Asthma Triggers: PGD₂, PGF₂α, TXA₂ → bronchoconstriction.

Answer 121

the subrstrate= arachidonic acid COX catalyses the formation of prostaglandins from arachidonic acid

Answer 122

Paracetamol (acetaminophen)= non-opioid analgesic & antipyretic (NOT NSAID) Mechanism: - Central COX-2/COX-3 inhibition in brain/spinal cord → ↓ PGE₂ in hypothalamus (antipyretic/analgesic) Alternative pathways: - TRPV1 channel modulation (pain) - Serotonergic (5-HT) system effects - Endocannabinoid system activation - Weak/no peripheral COX inhibition → No GI/platelet effects Key Distinction: Unlike NSAIDs: No significant COX-1 inhibition → safer for GI/bleeding risks Unlike opioids: No μ-opioid receptor activity → no respiratory depression

Answer 123

Synovium: 1-3 cell layers (Type A macrophages + Type B fibroblasts) Subintima: Loose connective tissue with fenestrated capillaries Synovial fluid: Ultrafiltrate of plasma + hyaluronan/lubricin Functions: Lubrication ("weeping"), nutrient diffusion, low friction

Answer 124

Pannus formation: Invasive synovial tissue (Th17 cells → IL-17 → RANKL → osteoclasts) Autoantibodies: RF/ACPAs → osteoclast activation + NETosis Cytokines: TNF-α/IL-1/IL-6 → MMPs → cartilage/bone erosion Dkk-1/sclerostin → inhibits osteoblasts

Answer 125

IL-17: Th17/ CD4+ T cells → synovitis → RANKL expression RANKL: Osteoclast differentiation → bone erosion ACPAs: Bind osteoclasts → IL-8 → pain/neutrophil recruitment NETosis: Neutrophil death → autoantigen release → more ACPAs

Answer 126

pannus= (like a tumour) abnormal, hyperplastic synovial tissue that forms in RA joints (caused by chronic synovitis activating osteoclasts) Contains Th17 cells, plasma cells, fibroblasts Secretes: - MMPs (cartilage/bone degradation) - RANKL (osteoclast activation) - Dkk-1 (blocks bone repair) Invades bone at synovium-bone interface n.b. pannus is destructive (secretes cytokines, autoantibodies) + is involved in the erosion of articular cartilage + bone, eventually destroying the joint

Answer 127

Normal Synovial Fluid: - Appearance: Clear, pale yellow - WBC count: <200/mm³ (mostly phagocytes) - Viscosity: High (intact hyaluronan) - Mucin clot test: Forms a firm clot RA Synovial Fluid: - Appearance: Cloudy/yellow (inflammatory) - WBC count: >2000/mm³ (neutrophil-predominant) - Viscosity: Low (hyaluronan degraded by free radicals) - Mucin clot test: Friable or no clot (due to inflammation)

Answer 128

lining fibroblasts= bone erosions subintimal fibroblasts= cytokines + inflammation

Answer 129

Invasive synovial tissue fueled by Th17 cells (→ IL-17 → RANKL → osteoclasts). Activated synovial fibroblasts stimulate osteoclasts and MMPs (→ cartilage/bone erosion).

Answer 130

RF/ACPAs → osteoclast activation + NETosis (neutrophil death → autoantigen release → more ACPAs). ACPAs bind osteoclasts → IL-8 → pain/neutrophil recruitment.

Answer 131

TNF-α/IL-1/IL-6 → MMPs → cartilage/bone erosion. IL-17 (Th17 cells) → synovitis + RANKL → osteoclasts.

Answer 132

Dkk-1/sclerostin block Wnt signaling → suppress osteoblasts.

Answer 133

B-cells → produce RF/ACPAs. T-cells (Th17) → pro-inflammatory cytokines (IL-17, TNF-α). Macrophages → cytokines + can become osteoclasts. Neutrophils → NETosis (→ autoantigens) + ROS damage.

Answer 134

NETosis: Releases citrullinated proteins (via PAD4) → triggers ACPAs. Synovial fluid neutrophils are activated, prolonged survival, and secrete inflammatory mediators. Links: Smoking/infection → NETosis → autoantigen exposure → ACPA production.

Answer 135

Bind osteoclasts → promote bone erosion. Enhance NETosis → perpetuates autoantigen release. Activate complement → chronic inflammation.

Answer 136

ACPAs: 98% specific for RA; predict progression (90% of ACPA+ asymptomatic patients develop RA within 3 years). Rheumatoid Factor (IgM): Less specific (60-80% of RA patients); correlates with severity. Anti-CarP: Associated with smoking; 96% specificity. Triple positivity (RF/ACPA/A-CarP): Nearly pathognomonic for RA. PAD4 autoantibodies= associated with more severe, erosive RA that persists despite treatment with TNF inhibitors

Answer 137

1) Methotrexate/MTX (DMARD): Works in seropositive/negative RA; higher doses may be needed for ACPA+ patients. 2) Triple therapy: MTX, cyclosporine (immunosuppresant) + prednisolone (corticosteroid) Biologicals: - B-cell/T-cell targeted (e.g., rituximab) → better for seropositive RA. - Cytokine inhibitors (anti-TNF/IL-6) → effective in both subtypes. Relapse risk: Increases with number of AMPAs (≥5 AMPAs → 55% relapse risk).

Answer 138

Anaemia of chronic disease: Normocytic → hypochromic (blunted EPO, iron dysregulation). Rheumatoid nodules: Subcutaneous, non-tender (20% of patients; linked to severe disease). Systemic effects: Fatigue, osteoporosis, thrombocytosis (due to IL-1/IL-6/TNF-α).

Answer 139

PAD4 inhibitors (e.g., GSK484, Cl-amidine). DNase I, myeloperoxidase (MPO) inhibitors. Goal: Reduce autoantigen release and inflammation.

Answer 140

Quantitative measure of RA activity (tender/swollen joints, ESR/CRP, patient GH). Scores: ≤2.6 = remission; >5.1 = high activity. Use: Guides treatment decisions and monitors therapy response.

Answer 141

Most babies have flat feet (fat pad); arches develop with walking. Persistent cases: "weak ankles," weight on medial foot. Tx: Orthotics or surgery if severe.

Answer 142

Normal in toddlers; resolves by age 2. Pathologic if persistent: Cerebral palsy, DMD, or idiopathic. Tx: Casting, physiotherapy, or calf muscle surgery.

Answer 143

Presentation: Fixed varus (inward) and equinus (downward) deformity of the foot. Often with calf underdevelopment. Involves adduction and plantarflexion of one or both feet. Epidemiology: - Fairly common - Twice as common in males ~50% bilateral Associations: - Breech presentation - Oligohydramnios - Trisomy 18 (Edwards syndrome) Mnemonic – CAVE: - Cavus – High medial arch due to plantarflexed 1st metatarsal - Adductus – Forefoot turns inward (midfoot) - Varus – Hindfoot turns inward (calcaneus) - Equinus – Ankle in plantarflexion (toes point downward) Treatment: ! Ponseti method: Serial casting and manipulation over ~5 weeks Near 100% success rate if started early

Answer 144

Risk factors: Female, breech, oligohydramnios, family history, 1st born. Tests: Barlow (adduct + push; dislocate hip), then do Ortolani (abduct hips to try and relocate hip), ultrasound (Graf grading= 60 degrees or more is normal Grad I graf... anything below 60 degrees is pathological). GALEAZZI SIGN= one knee is longer than other when you bend leg Tx: Most spontaneuosly resolve by 2-8wks, Pavlik harness puts bby in abduction + hip flexion) (0-6 months); spica (plaster cast in abduction + hip flexion)/open reduction if older. if all this doesn't work= osteotomy

Answer 145

AVN of femoral head, ages 4-8, ♂ >♀. Tx: Observation (<5yo), braces, or osteotomy (older).

Answer 146

What are the key points about SUFE (Slipped Upper Femoral Epiphysis) Who: Obese adolescents/ puberty (♂ >♀), often bilateral, more common on left hip Etiology: Salter-Harris type I fracture. Tx: Surgical fixation (screws), prophylactic pinning. memory tip: its like the ice cream fell off the cone

Answer 147

Causes tibia varus/ Tibia vara from growth plate dysfunction (obesity risk) Tx: Bracing (early), osteotomy (if progressive).

Answer 148

Traction apophysitis of tibial tubercle (10-15yo). Tx: Rest, NSAIDs, physiotherapy (self-limiting).

Answer 149

Calcaneal apophysitis (painful inflammation of the growth plate in the heel bone/ aka calcaneus) from running/jumping. Sx: Heel pain worsened by activity. Tx: Rest, heel pads, stretching.

Answer 150

Kohler’s: AVN of navicular (foot bone) (4-7yo, ♂ >♀). Kienbock’s: AVN of lunate (wristbone) (wrist pain, ↓grip).

Answer 151

A Boutonniere Deformity is a clinical sign characterised by: - Proximal Interphalangeal (PIP) → flexion - Distal interphalangeal (DIP) → hyperextension Mechanism: A tear of the central slip of the extensor tendon over the PIP joint. Causes: - Rheumatoid Arthritis - Trauma - Genetic Conditions (Ehlers-Danlos Syndrome)

Answer 152

Calcaneal avulsion fractures are caused by the contraction of gastrocnemius and soleus muscles

Answer 153

Pain in the posterior aspect of the leg (the sacroiliac joint, the hip and the posterolateral parts of the thigh and the leg) Numbness in the posterior aspect of the leg (the calf and the lateral part of the heel) Atrophy of the gastrocnemius and soleus muscles Loss of plantar flexion Loss of the Achilles reflex

Answer 154

Overview Collectively known as "the hamstrings". 3 Muscles: - Biceps Femoris - Semitendinosus - Semimembranosus Function: - Flexion of the Knee Joint - Extension of the Hip Joint - Reinforcement of Collateral Ligaments of Knee Origin & Insertion: All hamstring muscles (except for the short head of the biceps femoris) originate from the ischial tuberosity in the hip. The common origin and insertion points on the medial and lateral aspects of the knee mean that the hamstrings form the superior part of the diamond shape surrounding the popliteal fossa.

Answer 155

The ulnar nerve is most susceptible to injury at the medial epicondyle.

Answer 156

Clavicular elevation is a pathognomonic sign of acromioclavicular joint dislocation.

Answer 157

Clostridium perfringens is a bacterium responsible for causing gas gangrene.

Answer 158

Septic arthritis is an inflammatory condition caused by infection of the joint. In the majority of people, the causative organism is Staphylococcus aureus

Answer 159

fall on an outstretched hand when the wrist is in extension = Colles' fracture; this patient will have a dinner-fork deformity A fracture of the distal radius (metaphysis part), 2-3cm from the articular surface. It is the most common wrist fracture (75% of wrist injuries). fall on an outstretched hand when the wrist is in flexion= Smith's Fracture. A fracture of the distal radius caused a fall on an outstretched hand whilst the wrist is flexed, whereby the forearm becomes angled anteriorly (volar) relative to the wrist.

Answer 160

Boxer's Fracture → a fracture of the 5th metacarpal bone (or sometimes the 4th metacarpal bone) of the hand. Galeazzi Fracture →a fracture of the distal part of the radius with dislocation of the distal radioulnar joint. Pott's Fracture → a fracture affecting one or both of the malleoli. Smith's Fracture → a fracture of the distal radius caused a fall on an outstretched hand whilst the wrist is flexed, whereby the forearm becomes angled anteriorly (volar) relative to the wrist.

Answer 161

Pseudogout is a type of arthritis that is caused by the accumulation of calcium pyrophosphate crystals, which deposit in soft tissues and joints. This results in inflammation of the joints, causing joint damage and pain. Joint involvement is typically symmetrical and a layer of calcification can often be seen between articulating surfaces (as shown in this image), which will cause narrowing of the joint space. Subchondral cysts, can also be seen on an X-ray as radiolucent regions within the bone. Key Note: The knee joint is the most commonly affected site in pseudogout.

Answer 162

caused by bacteria; Borrelia Burgdorferi The classical sign of Lyme disease is an expanding target-like/bull's eye rash, known as 'Erythema migrans'. The Borrelia genus of bacteria is the causative agent of Lyme disease.

Answer 163

conjunctivitis, urethritis (or cervicitis in women), and arthritis CAN’T SEE, CAN’T PEE, CAN’T CLIMB A TREE usually caused by Sterile inflammation post-GI/GU infection (Salmonella, Chlamydia). HLA-B27 linked (60-80%). differentials from septic arthritis: in reactive arthritis there is NO FEVER, normal blood glucose. Whereas in septic arthritis patient has fever and low blood glucose

Answer 164

septic arthritis: - Bacterial infection (S. aureus, N. gonorrhoeae). Medical emergency - Monoarthritis (knee/hip), fever, hot/swollen joint, systemic symptoms - WBC >50,000/mm³ (often >100K), culture+ (50-70%), low glucose - ↑CRP/ESR, blood cultures+ (50%). MRI: Bone edema/abscess - IV antibiotics (vancomycin + ceftriaxone) + urgent drainage mnemonic "SEPTIC": Sudden, Elevated WBC, Purulent, Temperature, Immunocompromised, Culture+

Answer 165

Conventional: Methotrexate, sulfasalazine, hydroxychloroquine, leflunomide (aka A77 1726) . Biologicals: TNF-α inhibitors, IL-1/6 blockers, B/T-cell modulators, JAK inhibitors

Answer 166

1st-line, weekly oral (start 5-10mg → max 20-25mg). PREGNANCY TEST BEFORE U START; KNOWN TERATOGEN comes as tablet or IV MOA: Folic acid antagonist → inhibits DHFR which stops tetrahydrofolate production → inhibits DNA/RNA synthesis, ↓IL-1/NF-κB. SEs: Hepatotoxicity, myelosuppression (monitor LFTs/CBC q1-3mo). Pregnancy contraindicated.

Answer 167

Gut bacteria split it into sulfapyridine (systemic) + 5-ASA (gut anti-inflammatory). MOA: ↓Superoxide radicals, cytokines (IL-8), IgM/IgG. used in leaky gut syndrome; e.g. in patients with ulcerative colitis + also treats ulcerative colitis.

Answer 168

Anti-malarial; ↑lysosomal pH → blocks TLR9 (↓dendritic cell activation). Slow onset (12 weeks); used for mild RA/SLE.

Answer 169

Etanercept: Fusion protein (TNF-R2 + IgG1), weekly SC. Infliximab: Chimeric mAb, IV q2-6wks. Adalimumab: Human mAb, SC q2wks. SEs: ↑Infection risk (TB reactivation).

Answer 170

Anakinra: IL-1 receptor antagonist, daily SC. Canakinumab: mAb vs. IL-1β, off-label for gout/autoimmune

Answer 171

Anti-CD20 mAb → B-cell depletion (lasts 6-12mo). Used with MTX; effects seen at 3 months.

Answer 172

CTLA-4-Ig fusion → blocks CD80/86 on APCs, preventing T-cell co-stimulation. IV monthly; slower onset than TNF inhibitors

Answer 173

Tocilizumab: Anti-IL-6R mAb, IV monthly. JAK inhibitors (tofacitinib): Oral, rapid onset, comparable to TNF blockers.

Answer 174

Neutralizing: Block drug action. Non-neutralizing: ↑Clearance (immune complexes).

Answer 175

Total score ≥6/10 points = RA 1) Joint Involvement (0-5 points) - 1 large joint= 0 - 2-10 large joints = 1 point - 1-3 small joints = 3 points - >10 joints (at least 1 small joint) = 5 points 2) Serology (0-3 points) - Negative RF + negative ACPA = 0 - Low positive RF or low positive ACPA= 2 - High positive RF or high positive ACPA= 3 3) Acute Phase Reactants (0-1 point) - Normal CRP/ESR = 0 - Elevated CRP/ESR = 1 4) Duration of Symptoms (0-1 point) <6 weeks = 0 ≥6 weeks = 1

Answer 176

Leflunomide is metabolized to its active form A77 1726, which inhibits dihydroorotate dehydrogenase (DHODH) — a key mitochondrial enzyme in the de novo pyrimidine synthesis pathway. ➡️ This inhibition reduces uridine monophosphate (UMP) synthesis, leading to: Decreased proliferation of activated T and B lymphocytes Reduced production of autoantibodies and inflammatory cytokines ➡️ Overall, this results in immunomodulatory and anti-inflammatory effects in autoimmune diseases like rheumatoid arthritis.

Answer 177

1) Hydroxychloroquine (anti-malarial) safe in pregnancy others: prednisolone, MTX, azathioprine (steroid-sparing), Belimumab (NICE only fund if pregnant, kidney or liver damaged)

Answer 178

Mechanism of Action: 🔹 Abatacept is a fusion protein (CTLA-4 linked to IgG1 Fc region) 🔹 Binds to CD80/86 on APCs, blocking interaction with CD28 on T-cells 🔹 Inhibits the second co-stimulatory signal required for full T-cell activation 🔹 Result: Decreased T-cell activation, reduced autoimmune inflammation Dosage: 💉 IV infusion (30 min–1 hr), once monthly; weight-based ⏱ Onset of effect: ~3 months Clinical Use: 🦠 Moderate to severe rheumatoid arthritis (RA) 🧒 Juvenile idiopathic arthritis (JIA)/ oligoarthritis ➡️ Used in patients with inadequate response to DMARDs Related Drug: 🔹 Belatacept – similar structure, used in transplant rejection; blocks T-cell costimulation

Answer 179

Avascular tissue, few reserve chondrocytes, poor nutrient supply

Answer 180

Anemia of chronic disease: blunted EPO, iron dysregulation, shortened RBC lifespan (normocytic → microcytic in severe cases)

Answer 181

OA: asymmetric, weight-bearing joints (knees/hips). RA: symmetric, small joints (PIPs/MCPs).

Answer 182

Pannus= (CD4+) Inflamed synovial tissue invading cartilage/bone , driven by cytokines (TNF, IL-17, RANKL)

Answer 183

Chronic joint damage from inflammation accelerates degenerative changes

Answer 184

TNF (adalimumab), IL-6 (tocilizumab), IL-17 (secukinumab)

Answer 185

The HLA-DRB1 gene, specifically alleles containing the "shared epitope" (SE), is the strongest known genetic risk factor for rheumatoid arthritis (RA)

Answer 186

Janus kinase (JAK) inhibitors can be taken orally

Answer 187

Lymphocytes (CD8⁺)

Answer 188

Growth Plate (Epiphyseal Plate) Located between the metaphysis and epiphysis in children Responsible for longitudinal bone growth Closes after puberty → becomes the epiphyseal lin

Answer 189

No! Bursa: A tiny, fluid-filled sac; acts like a cushion between bones, tendons, and muscles. Purpose: Reduces friction (e.g., stops your shoulder from grinding when you lift your arm). Problem: Bursitis = swollen/painful bursa. Synovial Joint: The actual joint where bones meet (e.g., knee, shoulder). Contains synovial fluid for smooth movement. Problem: Arthritis = joint inflammation. Analogy: Bursa = Grease packet near a hinge (prevents rubbing). Synovial joint = Hinge itself (allows movement). Why It Matters: Bursitis hurts the cushion (bursa), while arthritis hurts the joint (synovial membrane). Example: Shoulder Bursitis: Pain when raising your arm (bursa inflamed). Shoulder Arthritis: Pain even at rest (joint cartilage worn out)

Locomotor 2 wk1+2 Flashcards

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