uworld rheumatology/orthopedics/MSK Flashcards
explain the etiology of RA @ the joint, step by step
- activation of T lymphocytes in response to rheumatoid Ags (i.e. citrullinated peptides, type II collagen)
- activated T cells release cytokines that cause synovial hyperplasia w recruitment of additional mononuclear cells
- accelerated metabolic rate of the inflammed synovial tissue –> local hypoxia + inc production of HIF-1 (hypoxia induced factor)
- inc VEGD by local møs and fibroblasts –> synovial angiogenesis (neovascularization)
- w progression of ds, inflammed synovium expands into a rheumatoid pannus = invasive mass composed of fibroblast-like synovial cells, granulation tissue, and inflammatory cells
- over time, pannus encroaches into joint space and can destroy the articular cartilage and erode the underlying subchondral bone
- ossification of the pannus can lead to fusion of the bones across the affected joint = bony ankylosis
what is the etiology of osteoarthritis at the joint
what are the perarticular findings in OA vs RA
progressive fibrillation (fissuring and fracturing) and erosion of articular cartilage due to inc biomechanical stress
extensive bone remodelling –>perarticular osteophyte formation and subchondral sclerosis
vs RA = perarticular bone erosions
what structures derived from the 4 pharyngeal pouches
pharyngeal membrane?
pharyngeal groove?
pharyngeal pouch 1:
-epithelium of middle ear and auditory tube
(pharyngeal membrane ==> tympanic membrane: pharyngral groove= epithelium of external ear canal)
pharyngeal pouch 2:
-epithelium of palatine tonsil crypts
pharyngeal pouch 3:
=thymus, inferior parathyoid glands
pharyngeal pouch 4:
=superior parathyroid glands, ultimobranchial body
when is colchicine the preferred trx of choice for acute gouty arthrirtis
be specific
what is the MOA of colchicine
when NSAIDs are contraindicated
=mild to moderate renal failure, peptic ulcer ds,
MOA colchicine= anti-infl via binding intracellular tubulin to prevent polymerization = x leuokocyte migration and phagocytosis
leukocyte adhesion deficiency
etiology + presentation
LAD = AR absence of CD18 ag = x formation of integrins
- x integrins –> x leukocyte adhesion to endothelial surfaces, x migration to peripheral tissues in response to infection and inflammation
present w
- recurrent skin and mucosal bacterial infections (of umbilical stump, periodontitis) ∝ staph aureus, G- rods
- lack of pus (x purulence) bc no nøs in peripheral tissues + poor wound healing
- delayed umbilical cord seperation (>21 days)
- marked, persistant leukocytosis w neutrophilia (bc leukocytes cannot migrate out the BVs)
inability to form the complement MAC complex, results from a deficiency in what
predisposes to recurrent infections by what
x C5b-C9 –> x MAC formation
recurrent Neisseria infections
which joints are involved in RA? be specific?
x-ray findings?
small joints: PIP, MCP, MTP — spare DIP joints
cervical spine subluxation, cord compression
xray–> ST swelling, joint space narrowing, bony erosions
decreased sensation over 5th digit, flattened hypothenar eminence with no change in triceps function suggests a lesion of what
where is the N lesion? be specific
ulnar N (C8-T1)
@ Guyon’s canal
N enters Guyon’s canal: between the hook of the hamate and the pisiform bone, = fibroosseous tunnel
but most comonly injured @ elbow due to trauma or N compression
what drugs have been implicated for causing drug induced lupus
what genetic abnormality is associated
how does this ds present
labs?
causes of drug induced lupus: procainamide, hydralazine (vasodilator used in HTN), isoniazid, micocycline, TNF-α inhibitors (etanercept)
-inc risk in patient’s with slow/abn liver acetylation (N-acetyltransgerase): esp of isoniazid-related sx
= lupus, but usually w/o the skin, neuro, or renal sx
∝ fever/fatigue, arthralgias/arthritis, serositis
labs= anti-histone Abs in >95% of pts : anti-dsDNA Abs are rare (v specific for SLE NOT DLE)
what is osteomyelitis and how does it happen
list the typical pathogen and location of osteomyelitis in
- children
- sickle cell ds
- Potts ds
- DM
- recumbant pts w impaired mobility
- recent trauma or orthopedic surgery
osteomyelitis= infection of bone and BM :
- hematogenous seeding 2° to episode of bacteremia
- spread from a contiguous focus of finection, i.e. infected DM foot wound
- direct inoculation of bone, i.e. compound frx
- children
- Staph aureus: long bones : **2° to bacteremia**
- sickle cell ds
- Salonella, Staph aureus : long bones : **hematogenous from infarcted bone**
- Potts ds
- Mycobacterium tuberculosis : vertebrae: **hematogenous seeding from lungs**
- DM
- polymicrobial : bones of the feet : contiguous from infected foot ulcer
- recumbant pts w impaired mobility
- polymicrobial : sacrum and heels : contiguous from pressure sores
- recent trauma or orthopedic surgery
- polymicrobial : variable **from direct inoculation**
what is the function of MMPs (matrix metalloproteinases)
what occurs when there is too many MMPs
MMP is imporant in wound healing – encourage both myofibroblast accumulation @ wound edges + scar tissur remodeling
-amassed myofibroblasts intiate wound contraction during healing by second intention
too many MMPs –may–> contractures
= excessive wound contractures = short and hard Ms, tendons, and other tissues -> rigid tissue and joints
keloids formed from what
= a hypertrophic scars = excessive collagenous scar tissue deposited by fibroblasts permanently extends beyond the margins of the original wound
what are the causes/risks of gout
be specific
increased urate production
- primary gout (idiopathic)
- myeloproliferative ds: i.e. polycythemia vera, inc platelets, inc eosinophilia, systemic mastocytosis
- lymphoproliferative ds: i.e. multiple myeloma/waldenstroms macroglobulinemia, EBV associated lymphoproliferative ds, CLL/ALL/hair cell leukemia/ B-cell lymphoma/ T-cell lymphoma/ follicular lymphoma
- tumor lysis syndrome
- hypxanthine guanine PB-transferase deficiency
dec urate clearance
- CKD
- thiazide/loop diuretic
pathology and sx of Duchenne Muscular dystropgy
= X linked recessive xdystrophin
sx:
- clumsy, slow, wadding gait : can’t keep up w peers
- Gower’s sign: progressive wknss in proximal Ms= use hands to support weight on standing
- cald pseudohypertrophy = initialy calf M hypertrophy in response to proximal M wknss, later replaced by fat and CT
- asymmetric weakening of paraspinal Ms –> kyphoscoliosis –> restrictuve pulmonary function (dec vital capacity and total lung capacity)
- most pts are wheelchair bound by age 12
what are the structures that make up the rotator cuff: what is the purpose of the rotator cuff
which structure within the rotator cuff is most commonly affected/injured, and why
rotator cuff= contribute to stability and motion of glenohumeral joint
**SITS**= tendons of supraspinatus, infraspinatus, teres minor, and subscapularis
most commonly affected: supraspinatous tendon
=vulnerable to chronic repated trauma from impingement between head of the humerus and acromion during ABduction
what drugs are TNF-alpha inhibitors
when are TNF-alpha inhibitors indicated
how do they work
what possible sideeffect requires proactive screening before starting on a TNF inhib
i.e. etanercept, infliximab, adalimumab
=trx mod to severe RA in patients who’ve failed methotrexate therapy
= a fusion protein of IgG1-Fc portion and TNF-receptor 2 = act as decoy receptor for TNF-alpha
-can promote reactivation of latent TB and increase the risk of disseminated ds : all potential pts need to TB skin test/ IFN-y release assay to screen for latent TB furst
when is methotrexate indicated
what baseline tests are should be given before starting a patient on methotrexate
methotrexate = RA, psoriasis, + CA
-can cause lung or liver toxicity, so baseline CXR and liver function tests are recommended
what are the indications for hydroxychloroquine use?
MOA?
what irreversible possible AE of the drug requires baseline tests and regular monitoring?
- hydroxychloroquine is indicated in malaria and rheumatoid arthritis/SLE (without organ involvement)
MOA
- antimalarial: forms a heme-chloroquine complex that is highly toxic to plasmodium, causing membrane damage and killing the parasite
- anti-rheumatic: decrease the formation of peptide-MHC protein complexes –> downregulate immune response against autoantigenic peptides
can cause irreversible retinal damage w long term use
– rrequire baseline and regular follow up w opthalmology
what baseline tests should be performed before starting a [atient on amiodarone
PFTs due to AE of pulmonary fibrosis
fecal occult blood testing should be done when in patients taking NSAIDs?
bc of inc risk of peptic ulcers, do a FOBT with any suspicion of GI bleed
Pott’s Ds
pathology
presentation
Potts ds= hematogenous seeding of TB-bacteremia into highly vacular organs (spleen, liver, bones)
- esp likely in vertebrae bc of extensive venous plexus : frequently, infection spreads to adjacent vertebrae fron behind the ant. L. and IV disk space –> contigious bone destruction and abscess formation
clin
- present months to years after the primary pulmonary infection seen w TB
- ∝ intermittant fevers and slowly worsening lumar/lower thoracic back pain with vertebral bone destruction and adjacent fluid collection (abscess)
what is the most common cause of spinal epidural abscess
how does it present
S. aureus = most common cause of spinal epidural abscess
most cases present in IV drug users, from a hematogenous spread of distant infection (i.e. endocarditis) or direct inoculation during a spinal procedure
increased serum markers indicate increased osteoblast activity?
- inc alk phos = expressed by osteoblasts (tho nonspecific)
- N-terminal propeptide of Type 1 collagen = PINP = released during maturation process of type 1 collagen fibrils during bone matrix synthesis
increase urine levels of what are indicative of osteoclast activity
- hydroxyproline
- collagen telopeptides
both seen in inc bone resorption
what is achondroplasia
etiology
presentation
AD xFGFR3 (90% de novo, 10% inherited)
- abn endochondral ossification of long bones and portions of skull/face
- constitutive FGFR3 –> exxagerated inhibition of chondrocyte proliferation –> bone shortening and craniofacial abn
clin:
-short limbs w normal torso length, frontal facial bossing w madfast hypoplasia, macrocephaly, genu varum
what medications are associated inc risk of osteoporotic frx
by what MOA?
- inc Vit D breakdown ∝ anticonvulsants that induce CYP450 = phenytoin, phenobarbital, carbamazepine
- dec estrogen ∝ aromatase inhibitors and medoxyprogesterone
- dec T and estrogen ∝ GnRH agonists
- dec Ca absorption ∝ PPIs
- dec bone formation ∝ glucocorticoids
what system preventsthe overstretching / overburden of Ms
given an example of when this system would be used
golgi tendon organs: sensory receptors located @ junction of Ms+tendons that are innervated by group Ib sensory axons, and are conected w contracting extrafusal sk. M fibers
- when a M actively contracts against resistance, the increase in tension activates the GTO –> Ib sensory axons in the GTO contact inhibitory interneurons in the SC -> synapse on the α-motor neurons that innervate the same M –> if the M exerts too much force, the GTO will inhibit contraction and cause sudden M relaxation
- GTO is NOT sensitive to change in length
i.e. when you lift a heavy load and your arms involuntarily give way and drop the weights to the ground
paget ds
etiology
presentation
labs
diagnostic findings
- =osteitis deformans = chronic ds from excessive and disordered bone formation
- bone weaknes –>bone pain–> bowing, frx, or arthritis of adjacent joints
- xOPG(osteoprotogen-physiologic regulator of osteoclasts)–> juvenile pagets
- sk pain and deformities, focal warmth or bruits at areas of pagetic bone lesions
- can sometimes lead to high out heart failure
- pain and new protuberances of the long bones
- change in hearing due to abn skeletal bone changes
- labs = elevated serum alk phos ∝ inc bone formation
- BUT n Ca, Phosphate, and PTH as homeostasis stays intact
- diagnostic findings
- x-rays showing mixed lytic-sclerotic lesions, thickening of corticol and trabecular bone, bony deformities
- biopsy of bone will show enlarged osteoclasts, w up to hundreds of nuclei
thin myofilament = __
thick myofilament= ____
what are each of the labelled areas seen
what structures are each of the monofilaments bound to
thin myofilament = actin
thick myofilament= myosin
actin in I band are bound to Z-line structural proteins
myosin filaments in A band are bound to structural proteins at M-line
displaced supracondylar dracture of the humerus may injure what BV and N
brachial A, radial N
what BV runs with the radial N at the humerus, mid shaft
deep brachial A and radial N : run behind the midshaft of the humerus
the axillary N travels in close proximity to what BV, and what kind of frx can hit them both
- axillary N runs with the posterior circumflex A, and a frx to the surgical neck of the humerus may damage them
what is the most commonly frx carpal bones, and how does it often happen?
this can lead to what? how does it present
scaphoid frx
from falling on an outstretched hand (FOOSH)
x dorsal scaphoid branch of radial A –> avascular necrosis of the scaphoid bone with , which presents as pain in the anatomic snuffbox (dorsal lateral wrist)
what components make up the anatomic snuffbox of the hand
what are the contents of the snuffbox
what is the clinical significance
triangle @ dorsoradial wrist
medial side= extensor pollicis longus tendon
lateral side= ABductor pollicus longus and extensor pollicis brevis tendons
proximal= styloid process of radius
floor= scaphoid and trapezium bones
contents
- radial A
- branch of radial N
- cephalic V
this is where most of the blunt force of a FOOSH goes, which is why the scaphoid is the most frx bone in the hand
a patient comes in with progressive M wkns (climbing stairs, reaching overhead) and unexpecte weight loss. the pt also has abd discomfort and wknss of the shoulder and hip girdle Ms..
- likely diagnoses, with the etiology?
- what PE finding is seen in this picture what would be seen on M biopsy?
- compare and contrast the etiology and biopsy findings w the related versions of this ds that don’t not have skin sx..
dx: Dermatomyositis
- anti-Mi2 Abs, anti-Jo1 Abs, anti-PI55/PI40 Abs
- as a paraneoplastic syndome, most commonly to an adenocarcinoma of the ovary, lung, or pancreas
Gottron papules = raised, erythematous plaques over the joints and bony prominences of the hand
M biopsy= daignostic finding: perifascicular inflammation and atrophy of the M @ the periphery of the fascicle
vs. polymyositis
- also can be paraneoplastic to adenocarcinoma of the ovary, lung, or pancreas
- biopsy= endomysial and perimysial inflammation and inc CT
vs inclusion body myositis
- no Abs, no respond to trx, is the most common form of inflammatory Abs in 65+, can be associated w IBD
- endomysial inflammation, with “rimmed vacuoles”, w tubulofilamentous inclusions in themyofibrils –> chronic ds=fatty replacement of M
what is the function of an osteocyte
cytoplasmic processes of osteocytes lie w/in cannaliculi that span throughout the bone matrix
via gap junctions btwn these processes, osteocytes can..
- send signals
- exchange nutrients and waste products
- serve their function to maintain the structure of the matrix and maintain Ca homeostasis
- plasma concentration of Ca will directly the metaboic activity of osteocytes
- PTH and calcitonin indirectly signal to osteocytes
- also regulate osteoblasts in response to changes in mechanical stress
what is the cubital fossa and what runs through it
what are the consequences of injury to this area
the cubital fossa = proximal forearm, just lateral to the medial epicondyle (the inside of the elbow)
- medial border= pronator teres M
- lateral border =brachioradialis M
- base= line between medial and lateral epicondyle
running through are the median N and the brachial A (right before it splits into the ulnar and radial As)
injury to median N =
- sensory loss over median N pattern
- loss of forearm pronation
- loss of proximal IP joint flexion (x flexor digitorum superficialis innervation)
what M is innervated by the thoracodorsal N
what is its function
the latissimus dorsi
humerus extension, ADduction, + IR
=C on the picture
in the knee, the ACL and PCL prevent what movements, respectively
the ACL = prevent anterior movement of the tibia relative to the femur
the PCL= prevent posterior movement of the tibia relative to the femur
*in injury of either, you’ll see excessive movement that it was supposed to prevent (too much anterior tibia= x acl)
what Ms exert forces on the clavicle
proximal clavicle: pulled superior by SCM and trap
distal clavicle: pulled inferolateral by deltoid
polyarteritis nodosa
- clin presentation
- biopsy findings
- etiology
=episodes of systemic, muscular, and GI sx
biopsy=
- transmural inflammation of segments of midsized arteries, w areas of amorphous eosinophilic necrosis of the arterial wall
- internal elastic lamina disruption
- if associated w HepB, can see ab-ag complexes in the affected tissue
=usually idiopathic BUT 30% are secondary to HepB (i.e. hx of IV drug use..)
what abn is seen in this CT
what nerve can be affected from this abn
- retroperitoneal hematoma (associated w chronic warfarin use)
- pts present w acute, severe groin, lower abd, or back pain
- the femoral N can also be injured: femoral neuropathy = quadriceps wknss, dec patellar wknss, sensory loss over the anterior and medial thigh and leg
differentiate between presentation of sciatic N injury at the
- femoral head
- fibular neck
- anterior leg (shin)
and also the presentations seen w …
- anterior compartment syndrome (leg)
- lateral compartment syndrome (leg)
- femoral head
- x knee flexion
- fibular neck
- x common fibular N
- x dorsiflexion, eversion : x sensation to lateral leg and dorsal foot
- anterior leg (shin)
- x tibial N
- xplantar flexion, inversion
- x sensation to plantar surface of foot
- x achilles reflex
compartment syndrome: initially present w pain out of proportion to the degree of injury –> wknss and sensory loss
- anterior compartment syndrome (leg)
- x deep branch of fibular N
- x dorsiflexion, sensory loss btwn first and second toes,
- lateral compartment syndrome (leg)
- x superficial branch of fibular N
- x eversion
- x sensation of lateral shin and dorsum of foot
which Ms are innervated by the
- recurrent laryngeal N
- external laryngeal N
