Locomotor 2 wk1+2 Flashcards
what nerve innervates gluteus maximus
inferior gluteal nerve (L5,S1,S2) innervates gluteus maximus
what nerve innervates gluteus medius, gluteus minimus and tensor fascia latae
superior gluteal nerve (L4,L5,S1) innervates gluteus medius, gluteus minimus and tensor fascia latae
what does a positive trendelenburg sign mean?
A positive Trendelenburg sign= when you ask patient to stand on 1 leg, the pelvis drops on the unsupported side
A person may present with a waddling gait or Trendelenburg gait where the trunk leans toward the weakened side during walking to compensate for the muscle weakness.
+ve Trendelenburg indicates damage to superior gluteal n. or weakness in the hip abductor muscles (gluteus medius and gluteus minimus)
n.b. a normal person= -ve Trendelenburg= when asked to stand on 1 leg, gluteus medius + minimus on other side contract to stop pelvis from dropping
Causes of a Positive Trendelenburg Sign:
- Superior gluteal nerve injury (innervates gluteus medius and minimus)
- Hip abductor weakness (due to muscle atrophy, hip osteoarthritis, or muscle tears)
- Hip joint pathology (e.g., hip dysplasia, hip dislocation)
- Post-surgical complications (e.g., after hip replacement)
what is the blood supply + innervation of anterior compartment of the thigh
anterior thigh:
femoral nerve (L2-L4)
femoral artery
main action is extension of knee + flexion of hip
what is the blood supply + innervation of posterior compartment of the thigh
posterior thigh:
sciatic nerve (L4-S3)
inferior gluteal artery + deep femoral artery
main action is flexion at knee; and extension at hip
what is the blood supply + innervation of medial compartment of the thigh
medial thigh:
obturator nerve (L2-L4)
obturator artery
main action is hip adduction
what muscle is the landmark for the sciatic nerve
piriformis is the landmark for the sciatic nerve
what is the blood supply + innervation of posterior deep compartment of the leg
posterior deep leg:
tibial nerve (L4-S3)
posterior tibial artery
main actions:
- a little plantarflexion
- mainly INVERSION of foot
- flexion of digits (toe curl)
what is the blood supply + innervation of anterior compartment of the leg
anterior leg:
deep fibular/peroneal nerve (L4-S2)
anterior tibial artery
main actions;
- dorsiflex foot
- extend digits
what is the blood supply + innervation of lateral compartment of the leg
lateral leg:
superficial fibular/peroneal nerve (L5-S1)
fibular artery
main actions;
- EVERT foot
what is the blood supply + innervation of posterior superficial compartment of the leg
posterior superficial leg:
tibial nerve (L4-S3)
posterior tibial artery
main actions:
- plantarflexion
- inversion of foot
What does a femoral nerve palsy present as? + some causes
femoral nerve palsy (L2,L3,L4)= damage to anterior compartment of thigh i.e.
- paralysis of quadriceps (no extension or flexion of knee)
- sensory loss of anterior thigh + medial leg
causes:
- compression (resulting from congenital hip dysplasia treatment)
- pelvic fractures
- anterior hip dislocation (V RARE)
What paralysis + sensory loss will you see in a tibial nerve palsy (+ causes)
tibial nerve palsy (L4-S3)= damage to posterior deep + superficial compartment of leg i.e.
- paralysis of plantarflexion + foot inversion
- sensory loss to back of leg + sole of foot
causes:
- fracture of tibia
- compression of tarsal tunnel
What paralysis + sensory loss will you see in a common fibular/peroneal nerve palsy
common fibular/peroneal nerve palsy (L4,L5,S1,S2)= damage to lateral + anterior compartment of leg i.e. unopposed plantarflexion= FOOT DROP!
- paralysis of dorsiflexion, eversion + can’t extend digits
- sensory loss to foot dorsum
What paralysis + sensory loss will you see in a sciatic nerve palsy
sciatic nerve palsy (L4-S3)= damage to posterior thigh + all sensations below knee except medial compartments of leg + foot i.e.
- paralysis of hamstrings + calves= loss of dorsiflexion + plantarflexion
- loss of Achilles reflex
- weak knee flexion
- foot drop
- all sensations below knee lost EXCEPT medial leg + foot
What is the role of the anterior cruciate ligament (ACL) + what sign will u see if damaged
ACL= prevents the femur from sliding posterior on the tibia
Rupture of ACL= anterior drawer sign
What is the role of the posterior cruciate ligament (PCL) + what sign will u see if damaged
PCL= prevents the femur from sliding anteriorly on the tibia
Rupture of PCL = posterior drawer sign
what movements can the ball+socket joint of the hip perform?
ball+socket synovial hip joint can do:
- flexion
- extension
- abduction
- adduction
- circumduction
What type of hip dislocation is more common?
posterior hip dislocations are more common because anterior ligaments are stronger (iliofemoral ligament located anteriorly= strongest ligament in the body)
posterior hip dislocations cause sciatic nerve palsy (L4-S3)
Which fracture of the neck of the femur is more at risk of avascular necrosis
INTRACAPSULAR FRACTURES= occurs within capsule of hip joint
can damage medial femoral + circumflex artery= can cause avascular necrosis (AVN) of femoral head
n.b. whereas extracapsular fractures (occur outside the joint capsule) so blood supply to head of femur intact (v rare complication AVN)
what are the nerve roots and what plexus do the following nerves belong to:
- femoral n.
- superior gluteal n.
- inferior gluteal n.
- obturator n.
- sciatic n.
ALL part of lumbosacral plexus
femoral n. (L2-L4)
superior gluteal n. (L4-S1)
inferior gluteal n. (L5-S2)
obturator n. (L2-L4)
sciatic n. (L4-S3)
What nerve is damaged in a ankle fracture + what sign will u see?
ankle fracture= common peroneal n. (L4-S2)
💡 Clinical Sign:
If deep fibular nerve is damaged:
- Foot Drop:
Inability to dorsiflex the foot (toes drag when walking).
- Loss of sensation in the first web space (between the first and second toes).
If superficial fibular nerve is damaged:
- Numbness or tingling over the dorsum of the foot.
- Weakness in foot eversion (turning the foot outward).
What nerve is damaged in a calcaneus fracture + what sign will u see?
calcaneus fracture= tibial n. (L4-S3)
💡 Clinical Sign:
If tibial nerve or its branches are damaged, the key signs are:
1) Tarsal Tunnel Syndrome:
- Pain, burning, or tingling along the sole of the foot.
- Numbness or paresthesia in the heel, arch, and toes.
- Weakness of intrinsic foot muscles (affecting toe flexion and foot stability).
2) Loss of Plantarflexion & Toe Flexion (Severe Cases):
- If the tibial nerve is severely damaged, loss of plantarflexion (pointing toes down) and toe flexion may occur.
- Rare but significant weakness in the calf muscles (gastrocnemius and soleus).
What nerve is damaged in a metatarsal fracture + what sign will u see?
plantar nerves (medial + lateral) (L4-S3) aka Digital Nerves
Clinical signs of Digital Nerve Injury (Plantar Nerves):
- Burning or shooting pain in the toes.
- Numbness on the plantar surface of the toes.
- Morton’s Neuroma can mimic these symptoms if caused by nerve compression rather than fracture.
What nerve is damaged in a lisfranc fracture + what sign will u see?
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
What nerve is damaged in a tibia fracture + what sign will u see
deep peroneal nerve (L4-S1)
- foot drop
- anterior compartment of leg effected; no longer dorsiflex foot
nor extend digits
What nerve is damaged in a femoral shaft fracture + what sign will u see?
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.
what structures are most at risk in a surgical neck fracture of humerus
surgical neck fracture of humerus (common in elderly);
axillary nerve (C5-C6)
what structures are most at risk in a midshaft fracture of humerus
midshaft fracture of humerus (as it travels down radial groove)
radial n. C5-T1= wrist drop
what structures are most at risk in a supracondylar fracture of humerus
supracondylar fracture of humerus (common in kids)= increased risk of volkmaan’s ischemic contractures
median/ radial n. + brachial artery most at risk!
what structures are most at risk when the medial epicondyle (of humerus) is damaged
medial epicondyle;
ulnar n. (C8-T1) = claw hand
what structures are most at risk when the lateral epicondyle (of humerus) is damaged
lateral epicondyle
radial n. (C5-T1)= wrist drop
a patient fractures their fibular neck + has foot drop. What altered sensation would they have?
loss of sensation to dorsum of foot
how do you tell short and great saphenous apart
short saphenous vein is on the lateral aspect of leg
great saphenous on the medial aspect of leg
anterior dislocation of hip is rare, but when it does happen what nerve most at risk
anterior dislocation= FEMORAL nerve (L2-L4) injury
posterior dislocation of hip damages which nerve?
sciatic nerve
the scapulo-humeral rhythm moves in what ratio?
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
winging of the scapula is caused by damage to what nerve + muscle dysfunction
wingning of the scapula is due to damage to long thoracic nerve
serratus anterior dysfunction
what nerve innervates the ‘regimental badge’ and what muscle is this
regimental badge= deltoid
innervated by axillary n. (C5-C6)
damage to what nerve causes shoulder drop?
spinal accessory nerve (CN XI)
what is the Allen test used to assess
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.
What type of collagen is
- cartillage
- bone
- smooth muscle e.g. blood vessels
made up of?
cartillage= type II collagen
bone= type I collagen
smooth muscle= type III collagen
how many bones do we have at birth vs how many bones do adults have
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)
what type of bone remodels faster; trabecular or cortical
trabecular bone remodels 3-10 times faster than cortical bone
What is Pott’s disease
Pott’s Disease, also known as tuberculosis spondylitis, is a rare condition in which mycobacterium tuberculosis infects the spine, causing arthritis and damage to the vertebrae
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.
what is a characteristic feature of Diffuse Idiopathic Skeletal Hyperostosis (DISH)
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.
Which meds can cause necrotising autoimmune myopathy (NAM)
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).
what cell lineage are osteoclasts derived from?
hematopoeitic stem cells -> monocytes -> osteoclasts (bone resorption)
what cell lineage are osteoblasts, osteocytes and osteoprogenitor cells derived from?
mesenchymal cells (embryonic mesoderm) -> osteoprogenitor cell -> osteoblast (bone formation) -> osteocyte (maintain bone)
what 2 things do osteoclasts need for activation
Osteoclasts need the following for activation:
M-CSF (macrophage colony stimulating factor)
RANKL (Receptor activator of nuclear factor kappa-B ligand)
What monoclonal antibody inhibits sclerostin; how does sclerostin work?
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
What is the role of RANKL in the body?
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.
Calcium Homeostasis - Key Medical Details
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)
Where is parathyroid hormone (PTH) produced? What is the half-life of PTH?
In the four parathyroid glands located behind the thyroid.
half-life; About 4 minutes.
How does PTH increase blood levels in the short term vs the long term?
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.
What happens when free CA2+ binds to the calcium-sensing receptor CaSR on parathyroid chief cells?
It decreases PTH production.
What is the drug cinacalcet used for, and how does it work? What effect does cinacalcet have on the CaSR response curve?
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.
Why do failing kidneys lead to increased PTH secretion?
They reduce phosphate excretion and vitamin D activation, causing low blood Ca2+ and high phosphate, which stimulates PTH release.
What is the primary source of Fibroblast growth factor-23 (FGF23), and what stimuli trigger its production?
FGF23 is produced by osteocytes and osteoblasts. Its secretion is stimulated by calcitriol (active vitamin D3) and dietary phosphate loading.
How does Fibroblast growth factor-23 (FGF23) regulate phosphate and calcium levels in the body?
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.
What role does FGF23 play in chronic kidney disease-mineral and bone disorder (CKD-MBD)?
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.
Explain the pathophysiology of X-linked hypophosphatemia (XLH) and its treatment.
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
Compare and contrast the effects of FGF23 and PTH on phosphate and vitamin D metabolism.
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.
What are the sources, triggers, and physiological effects of calcitonin? How does it compare to PTH in calcium regulation?
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)
How do GH and IGF-1 promote bone growth, and what are their target cells?
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.
What are the effects of thyroid hormone on bone, and what pathologies arise from its imbalance?
Targets: Chondrocytes, osteoblasts, osteoclast precursors, and bone marrow stromal cells.
Hypothyroidism (children): Dwarfism (impaired bone growth).
Hyperthyroidism: Secondary osteoporosis (excessive bone resorption).
How do estrogens and progesterone protect bone, and what is FSH’s role?
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.
How do androgens (e.g., testosterone) influence bone health?
Converted to estrogens (via aromatase) → bone-protective effects are largely estrogen-mediated.
Why do glucocorticoids cause osteoporosis?
↓ Bone formation: Kill osteoblasts and shorten their lifespan.
↑ Bone resorption: Induce RANKL → activates osteoclasts.
Rank these hormones from most anabolic to most catabolic for bone: GH, estrogens, cortisol, PTH
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).
Internal (medial) rotation of the shoulder is facilitated by which muscles? (think of it like going to reach your bra strap)
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.
External (lateral) rotation of the shoulder is facilitated by which muscles?
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.
what is ‘trigger finger’ caused by
“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.
what muscles carry out
- extension of elbow
- flexion of elbow
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.
Pain and tenderness upon palpation of the anatomical snuffbox may indicate a fracture to what bone?
Pain and tenderness upon palpation of the anatomical snuffbox may indicate a scaphoid bone fracture.
what cells is alkaline phosphatase made by and what does its level indicate?
alkaline phosphatase is made by osteoblasts (marker of how active osteoblasts are) + by the liver
Bone mineral density can be expressed as either the T or Z score. What does each mean?
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
what is the precursor to osteoporosis?
precursor to osteoporosis is osteopenia (low bone density)
Dual energy X-ray absorptiometry/ DEXA scans are performed on areas of the body with high levels of trabecular bone (because high turnover rate means pathological changes seen here first); what 3 areas are the scans performed?
- neck of the femur
- lumbar vertebra (L1-L4)
- distal radius at wrist
bone biopsies are usually taken from what bone?
iliac crest
Osteoporosis; causes, symptoms, treatment
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)
Osteomalacia; causes, symptoms, treatment
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:
Ergocalciferol (D2) or Cholecalciferol (D3)
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
intermittent exposure to PTH activates – more than —
intermittent exposure to PTH activates osteoblasts more than osteoclasts
Pagets disease
Definition: A chronic bone disorder characterized by excessive bone remodeling, leading to structurally abnormal, enlarged, and weakened bones.
Causes/Risk Factors:
Genetic Factors: SQSTM1 gene mutations 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
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
3 phases of Pagets disease
Legg-Calvé-Perthes disease
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
What is Thomas’ Test used to assess, how is it performed, and what are the key interpretations? What patients cant have the test performed on them?
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)
What is the purpose, technique, and interpretation of the Straight Leg Raise (SLR) test?
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).
How is the Painful Arc Test performed and what does it indicate?
Method: Patient raises arm sideways (0-180°).
Positive: Pain between 60-120° = subacromial impingement. Pain after 120° = AC joint issue.
What does Neer’s Test check, and how is it done?
Method: Examiner lifts patient’s straight arm up while holding the scapula.
Positive: Pain at top = impingement.
Describe the Hawkins-Kennedy Test.
Method: Arm bent 90° at shoulder/elbow, palm down. Examiner twists arm inward.
Positive: Pain = supraspinatus tendon impingement.
What does the Empty Can Test assess?
Method: Arms at 90°, thumbs down (like emptying a can). Resist upward movement.
Positive: Pain/weakness = supraspinatus tear.
What muscle does Gerber’s test target?
Method: Hand on lower back, push backward against resistance.
Positive: Pain/weakness = subscapularis tear.
What does the Scarf Test check?
Method: Bring arm across chest (like a scarf).
Positive: Pain = AC joint problem (e.g., arthritis).
What does the Speed Test diagnose?
Method: Arm forward, palm up. Resist downward push.
Positive: Pain = biceps tendonitis or labral tear.
