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Explore the complexities of musculoskeletal pathology through focused assessments. This educational tool enhances your understanding of bone and soft tissue disorders, offering insights crucial for medical professionals and...

Questions: 27 | Attempts: 10 | Last updated: Aug 4, 2025

Sample Question 1
Why do patients with Achondroplasia have a larger head compared to limbs?

Due to excessive growth hormone secretion

As a result of maternal age effects

Because of a mutation in the IGF1 gene

*Because Chondrocyte proliferation inhibition due to Overactive FGFR3 leads to Defective ENDOCHONDRAL OSSIFICATION -Long bone growth=Longitudinal bone (Limbs) needs this type of ossification at epiphyseal growth plates,so they have short,thick,tubular long bones in appendicular skeleton(Limbs), while head,chest,flat bones of wrist,AXIAL skeleton(SPINE)don't need endochondrial ossification/cartilage mediator as they undergo Membranous ossification, thus their length can be normal.*Achondroplasia is MCC of Short-limbed dwarfism*Note PTH,GH,IGF1 are usually normal.*Boards also freakin WANT you to know that risk of Achondroplasia in progeny increases with Increased PATERNAL age(Contrast this with maternal age in down's)-achondroPPlasia-PPaternal.*Mental function, life span, and fertility not affected(Questions love to describe guy who has short limbs but becomes scientist or some cool guy with bunch of children lol)*Once again LINEAR growth at epiphyseal growth plate is inhibited.*+UW wants u to know that they can have some craniofacial abnormalities like depression of the nose root,forehead bulging.u should also contrast this short stature that preferentially affects Appendicular skeleton to Short stature caused by GH/IGF1 deficiency where appendicular skeleton(limbs) and Axial skeleton(Spine) are proportionate.

Sample Question 2
Contrast Cancellous bone=trabecular (Spongy) bone with Compact bone(CORTICAL Bone) by locations/Diseases affecting them?

C. Osteoporosis mainly involves compact bone whereas hyperparathyroidism mainly affects cancellous bone.

B. Cancellous bone is primarily affected by osteomalacia. Compact bone is primarily affected by rickets.

*Cancellous bone is found in VERTEBRAL BODIES,Ends of Long bones.*Compact bone(Cortical Bone) is found in Most of the appendicular skeleton, provides support and MUSCLE ATTACHMENT sites.*Hyperparathyroidism(High PTH) usually results in SUBPeriosteal thinning as bone resorption takes place in Cortical(Compact bone)*Osteoporosis on the other hand mainly involves Spongy(Trabecullar,cancellous) bone>VERTEBRAL FRACTURES(MC),Fractures at the neck of the femur(50% is trabecular).Note that Osteoporosis does also affect Compact(Cortical bone) withOUT altering mineralization process, but yet spongy bone(More metabolically active) is preferentially affected.*know that LABS will be all normal in osteoporosis(Calcium,phosphate,PTH,ALP) but Calcium/ALP will be increased and Phosphate will be decreased in primary hyperparathyroidism.*If they make u choose lab abnormal in osteoporosis it is likely cortisosl(Hypercortisolism-like in cushing's syndrome can cause/potentiate osteooporosis)

A. Cancellous bone is found in the skull bones. Compact bone is found in the ribs.

Sample Question 3
Why do we have histologic findings of primary unmineralized spongiosa in medullary canals in osteopetrosis?

*Remember in osteopetrosis OsteoCLASTS can't do their job of bone resorption and unmineralized spongiosa can't be broken down/Replaced.*Thickened, dense bones can't adopt to stress properly and are prone to FRACTURE.*Hepatosplenomegaly is common finding due to extramedullary hematopoiesis(Instead of bone marrow which would normally give us blood cells,we have "Bone in Bone" leading to myelophthisic process), but compensation is not enough and often patients can have anemia,thrombocytopenia,leukpenia(RISK OF INFECTION).*Remember that defect at molecular level is Defective Carbonic Anhydrase2(Which would normally promote Creation of Acidic environment by OsteoCLASTS)*Thickened bone>Narrowing of foramina>Patients often present with Cranial nerve palsies(Can manifest as VISION or HEARING changes)*Treatment is Bone marrow transplant as you give new osteoclasts(Come from Bone marrow monocytes) which don't have that defect and can break down bone when needed.**Mutation in Carbonic anhydrase can lead to Renal tubular acidosis as this enzyme is needed for HCO3 reabsorbtion.*Patient can have Hydrocephalus due to narrowing of Foramen magnum.(Hydrocephalus can manifest with urinary incontinence,Cognitive impairment,Ataxia)

In osteopetrosis, there is an excess production of OsteoCLASTS leading to accumulation of unmineralized spongiosa in medullary canals.

The defect in osteopetrosis lies in OsteoBLASTS, which fail to create new bone matrix leading to unmineralized spongiosa.

Osteopetrosis is characterized by decreased Calcitonin levels, which results in accumulation of unmineralized spongiosa in medullary canals.