Musculoskeletal-Muscles+Bone

Question 1

Embryonic origin of osteoblasts is?

Answer 1

Come from the mesenchymal stem cells periosteum of bone. (CAN BE ASKED)

So, which part of the bone has stem cells for bone production? The periosteum!

Question 2

What can be used to determine the activity of osteoblasts?

Answer 2

ALP
Osteocalcin
Propeptides of Type 1 procollagen (Type can be asked)

Question 3

In short-limbed dwarfism, which cells are not working?

Answer 3

Short-limbed dwarfism/large head relative to limbs—–> FGF3 mutation causes impaired ENDOCHONDRAL OSSIFICATION.
Endochondral ossification is only possible if we have working chondrocytes. So chondrocytes are defective.

Question 4

Which nerve is most like damaged when an old woman falls on her outstretched hand and fractures her radius?

Answer 4

Fall on outstretched hand in osteoperosis–> distal radius fracture–> colle’s fracture–> Median Nerve damaged,

(High yield- will be asked)

Question 5

Treatment of osteopetrosis (underlines are very high-yield concept)?

Answer 5

Osteopetrosis—> is treated by Bone Marrow transplant because osteoclasts (that are defective in this disease) are derived from monocyte-macrophage linage.

These osteoclasts are defective because they lack Carbonic Anhydrase 2–> no acidic environment for osteoclasts to work!

Question 6

Osteomalacia’s pathophysiology is?

Answer 6

DEFECTIVE mineralization of osteoid due to Vitamin D deficiency.

Important co-relation is this that is osteoporosis–> the bone mineralization is normal, and hence, serum vitamin D and Ca levels are also normal!

Question 7

Dense bones/thickened bones are seen in 2 important bone conditions? Do a comparison

Answer 7

Thickend bones/Reduced foramen spaces are seen in:
Osteopetrosis
Osteitis deformas/Paget’s disease.

Osteopetrosis—> osteoclasts are not working so the bones keep on becoming thicker and denser.

Osteitis deformans/Paget’s disease—> osteoclasts are OVER-WORKING so the osteoblasts jump into the matter in such a hurry and make an awful mosaic patterned/woven bone!
(Because the osteoblasts jump into it–> ISOLATED INCREASE OF ALP

Question 8

2 bone conditions that are associated with thin bones—> compare pleassse?

Answer 8

Osteoperosis, and osteomalacia/rickets–> both have thin bones.

Osteoporosis—-> Normal bone mineralization and lab
values (serum Ca2+ and PO4), but there’s increased bone resorption.

Osteomalacia—> Defective mineralization of the osteoid due to Vitamin D deficiency. So on Lab values, everything is decreased but there’s INCREASED PTH, ALP as osteoblasts come for help.

Question 9

Levels of the following labs in Ricket’s disease:

1—> Serum Ca
2—> Serum PO4
3–> ALP
4—> PTH

Answer 9

Paget’s disease—–> means VITAMIN D deficiency.
Level of Vitamin D is directly proportional to levels of serum and calcium.

So, serum ca and PO4 will be decreased.
Ca+ levels affect—> PTH
Low ca+ means elevated PTH.
(PTH is always inversely proportional to Ca, except in primary hyperparathyroidism)

Elevated PTH—> elevated ALP.
(PTH levels are directly proportional to ALP–> except in Paget’s disease of Bone where osteoblasts jump in due to emergency that is not warned about by PTH)

Question 10

Benign Bone tumours?
Name characteristics of 
Osteochondroma
Osteoma
Osteoid Osteoma
Osteoblastoma.

Answer 10

Osteochondroma–> continuous with the Bone marrow space!

Osteoma–> OMMM.–> People doing Yoga in the Garden, always sitting–> associated with Gardner syndrome, COLON cancer.

Osteoid Osteoma—> OO (Double OO)–> We say OO in pain, so a very painful tumor but pain is responsive to NSAIDS.

Osteoblastoma–> SAME histo as Osteoid Osteoma (Central osteoid deposition is seen)–> but pain is not responsive to NSAIDS.

Question 11

How do you remember the location of Bone tumours?

Answer 11

Epiphysis–> Giant Cell tumor (Epic Giant Soap Bubble)—> called Giant cell because has Giant multinucleated cells that overexpress OSTEOCLASTIC ACTIVITY.

Metaphysis–> Osteochondroma, Osteosarcoma
(Mushroom field for RB teenagers.)

Question 12

Which tumor has neoplastic cells admixed in an osteoid background?

(They love these kind of questions with backgrounds on histo)

Answer 12

Osteosarcoma.

Question 13

Which bone tumour’s histo needs to be confirmed by a chromosomal translocation?

Answer 13

Ewing’s–> histologically it looks like a lymphoma or chronic osteomyelitis.

(High-yield—> can be a testing point)

Question 14

Difference between joint erosion that occur in OA vs RA?

Answer 14

OA–> only cartilage ulcerates/erodes.

RA–> Bone and cartilage BOTH erode!!

Question 15

Abnormal overgrowths seen in OA vs RA?

Answer 15

In OA–> overgrowths of bone is seen–> osteophytes, sclerotic bone, subchondral bone cyst.

In RA—> Synoval fluid INCREASE, Synovial pannus formation

Question 16

Histo of dermal manifestation of RA?

Answer 16

RA nodules show fibrinoid necrosis with palisading histiocytes.

(HIGH-YIELD–> Granulomatous skin nodules)

Question 17

In which joint condition would you see calcification of the cartilage on x-ray?

Answer 17

Calcium pyrophosphate deposition disease/ pseudogout.

Cartilage calcification is also called chondrocalcinosis.

Question 18

Which crystals are positively birefringent and which are negatively birefringent?

Answer 18

Gout—> needle shaped crystals and needles are so negative–> so negatively birefringent–>

(A yellow car on road is so negative)–> Negatively birfringent appear yellow in parallel light, and blue in perpendicular light.

Opposite for CRPP deposition which are crystals of rhomboid shape.

Question 19

Prophylactic treatment drug for pseudogout?

Answer 19

Colchicine!

Question 20

Mechanism of action of colchicine?

Answer 20

Inhibits microtubular polymerization—> impairing

neutrophil chemotaxis and degranulation.

Question 21

How will you treat a 15 year old child who presents with painful joint, salmon-rash and daily spiking fever?

Answer 21

Systemic juvenile idiopathic arthritis (which will occur in children less than 16 years of age–> age was below 12 in old FA, below 16 is given in new FA so will be tested)

Treated with NSAIDS, steroids.

Question 22

Which Antibodies do you need to know about Sjogren’s disease?

Answer 22

Anti-SSA or Anti SSB—>Anti-ribonucleoprotein antibodies. (antibodies against ribosomes!!)

Anti-SSA/Anti- Ro cause Neonatal lupus which will present as Congenital Heart block.
(Anti-SSA can cross placenta)

Sjogren’s can have RF even without RA, but it is strongly associated with RA.

Question 23

Which tissue biopsy will you take for Sjogren’s syndrome and what will it show?

Answer 23

Lip biopsy to see minor salivary glands. (We need to exclude other causes of dry eyes and dry mouth–> sarcoidosis, amyloidos)
It’d show LYMPHOCYTIC SIALADENITIS.

In uworld it was written that the histology in Sjogren’s syndrome will show–> periductal lymphocytic infiltration of labial glands.
So labial glands mean–> Biopsy of lip shows lymphocytic infilterate in LIP SALIVARY GLANDS.
Periductal lymphocytic infilterate–> around ducts, makes lymphycytes often with germinal centres.

Question 24

Sjogren’s disease is associated with which neoplasm?

Answer 24

B-cell lymphoma (Presents late in disease—> when one parotid is much more enlarged than the other one.)

parotid enlargement–>B cell lymphoma= Non-Hodgekin’s lymphoma= Marginal Zone Lymphoma= MALT (mucosa associated lymphoid tissue)

Question 25

Septic arthritis signs and symptoms and its causative agents?

Answer 25

Swollen knee joint, purulent synovial fluid. | S aureus, Streptococcus, and Neisseria gonorrhoeae

Question 26

In uworld the question said, Physical examination shows facial edema over the left mandible.  Multiple teeth have decay and gingival recession, and gentle tapping of the left second molar elicits pain.  This patient's current disease process is most likely due to which disease?

Answer 26

Sjogren's syndrome---> recurrent dental infections because of reduced saliva. Facial edema over left mandible means--->osteomyelitis of the mandible (yesss, remember this pleasse)

Question 27

SLE antibodies?

Answer 27

Antibodies directed against host nuclear material--->Antigen-antibody complexes get deposited in various tissues----> this causes complement activation in the tissues---> Reduced CH50, C3, C4 levels. Some keratinocytes undergo apoptosis---> fragments of shrunken/pieces of nuclear material are in the skin---> Self-reactive B cells comes and forms antibodies against this nuclear material----> Antigen-antibody complexes are formed but in low quantity---> Next time, again keratinocytes undergo apoptosis and leave a little nuclear material in the tissue, the antibodies comes and bind to nuclear antigens and make antigen-antibody complexes again---> These antigen-antibody complexes are taken up by dendritic cells via TLR------> This amplify the immune response and now B cells will produce so many antibodies. ANA antibodies, Anti-dsDNA-->(This tells the involvement of Renal tissue---> Renal damage is a common cause of death in SLE patients) (Dramay waali ANA has a malar rash--> abb double ho chuki hai-- Anti-double stranded DNA)

Question 28

SLE is a type ___ HSR but if the patient presents with anemia, thrombocytopenia and leukopenia this is due to type ____ HSR.

Answer 28

SLE is a TYPE 3 HSR. But blood manifestations are due to antobodies directly destroying the blood cells--> Hence, that'll be due to Type 2 HSR. Because AIHA occurs in SLE and that's a type 2 HSR!

Question 29

Classic endocardial finding in SLE?

Answer 29

Libbmann-Sack endocarditis which is actually vegetations on BOTH sides of the AV valve. (Wow, so strange!!) Produced platelet-rich/sterile thrombi in the blood.

Question 30

What test will you do to diagnose syphilis in an SLE patient?

Answer 30

FTA-ABS. In FTA-ABS--> antibodies against the bacterial treponemal antigen is added--> once those antibodies bind, fluorescence is added--> so that we can see those antigen-antibody complexes under microscope. FTA-ABS remains postive for a lifetime, even after syphillis is treated.

Question 31

Which antibody causes falsely-elevated PTT in SLE? | And this antibody is found in which other disease?

Answer 31

Lupus coagulant antibody. | Antiphospholipid Syndrome.

Question 32

Which antibody causes a false positive VLDRL in lupus and antiphospholipid syndrome?

Answer 32

Anticardiolipin antibodies can cause falsepositive VDRL/RPR.

Question 33

What Antibodies are found in antiphospholipid syndrome?

Answer 33

lupus anticoagulant, anticardiolipin, anti-β2 glycoprotein 1 antibodies.

Question 34

Antibodies seen in mixed connective tissue disease?

Answer 34

1, ANA (Antinuclear antibodies) 2. Antibodies against U1 ribonucleoprotein (RNP) ( Don't confuse it with Anti-SM antibodies of SLE which are against snrps--> SNRPS are also called U-RNA because they are full of Uridine)

Question 35

In systemic sclerosis, the antibodies are basically against ____________?

Answer 35

Mesenchymal Antigens. ( When mesenchymal/ CT damage below a blood vessel occurs-----> there's endothelial dysfunction----> this causes increased expression of adhesion molecules of endothelial cells---> immune response triggered!!) ↑ Endothelin---> Hence, vasoconstriction. ↑ PDGF, TGF-B----> causes fibrosis!

Question 36

Antibodies seen in Diffuse and limited scleroderma?

Answer 36

Diffuse Scleroderma--> Anti DNA polymerae 1 and Anti RNA polymerase 3. Limited Scleroderma---> CREST so Anti-centromere antibodies.

Question 37

Antibodies seen in Rheumatoid arthritis?

Answer 37

Rheumatoid factor--> They are IgM antibodies against IgG's Fc portion (high-yield) Anti- ccp--> anti-cyclic citrullinated peptide antibody

Question 38

RA is associated with HLA-____?

Answer 38

HLA-DR4 (4-walled “rheum”)

Question 39

MHC class 1 overexpression in seen in which musculoskeletal conditions?

Answer 39

``` >Seronegative spondyloarthritis-PAIR--> Strong association with HLA-B27 (MHC class I serotype) >Polymyositis--> endomysial inflammation with CD8+ T- cells so MHC class 1 overexpression (Asked in uworld) ```

Question 40

Difference between Aspirin and Acetominophen?

Answer 40

Aspirin is an ASS--> so it is strong enough to ahev ANTI-INFLAMMATORY PROPERTIES. Acetominophen---> only works in CNS because it is inactivated peripherally and hence, has no anti-inflammatory effects. Can be used in children to avoid Reye's syndrome.

Question 41

Name an NSAID which won't cause gastric ulcers?

Answer 41

Celecoxib (selective COX-2 inhibitor) | spares COX-1, which helps maintain gastric mucosa.

Question 42

Bisphosphonates S/E are high-yield?

Answer 42

->Esophagitis (if taken orally, patients are advised to take with water and remain upright for 30 minutes), ->osteonecrosis of jaw, ->atypical femoral stress fractures.