Anatomy Flashcards
Order of neurovasculature in femoral triangle
vein, artery, nerve (medial to lateral)
location of cricothyroid membrane (for cricothyroidotomy if someone is choking)
superior to cricoid cartilage inferior to thyroid cartilage (vignettes 22)
paraesophageal hernia
Fundus protrudes into thoracic cavity. GEJ remains fixed below diagram unlike in sliding hiatal hernia.
Femoral nerve palsy: 1) common scenario 2) dysfunction
1) Pelvic fracture
2) weakness in right leg and lack of sensation in anterior area of thigh + weakness with extension of right knee + weak hip flexion
klumpke vs erb palsy
klumpke is an abduction injury; Erb palsy is an adduction injury
Jugular foramen (Vernet) syndrome
lesion to jugular foramen, thus CN 9, 10, 11 affected
Jugular foramen (Vernet) syndrome presentation
dysphagia + hoarseness + dysarthria + loss of gag reflex on ipsilateral side + deviation of uvula toward normal side + atrophy of sternocleidomastoid muscle and trapezius.
unhappy triad
ACL + MCL + medial meniscus
compartment syndrome presentation
Persistent leg pain + swollen, tense, and warm region + decreased anterior tibial pulse.
causes of compartment syndrome
crush injury + fracture + chronic vigorous exercise
FDS vs. FDP
- FDS wraps around PIP.
- FDP goes all the way to the end and flexes wrist + MCP + interphalangeal joints.
ACL location
lateral femoral condyle –> anterior tibia.
PCL location
medial femoral condyle –> posterior tibia.
Lachman test
Tests for ACL injury, at 30 degree angle
valgus/varus
lateral force/medial force
McMurray test
1) pain, “popping” on external rotation –> medial meniscal tear.
2) pain, “popping” on internal rotation –> lateral meniscal tear.
Baker cyst
Popliteal fluid collection in gastrocnemius-semimembranous bursa, commonly communicating with synovial space and related to chronic joint disease.
most common rotator cuff injury?
supraspinatus
test for supraspinatus tear?
“empty/full can” test.
infranspinatus innervation
suprascapular nerve
Most common pitching injury
infraspinatus
teres minor innervation
axillary
subscapularis innervation
upper and lower subscapular nerves
SITS muscle innervated by
C5-C6
bone palpated in anatomic snuff box
scaphoid
lunate dislocation
Can cause carpal tunnel syndrome
damage to hook of hamate
ulnar nerve injury (common with fall on outstretched hand).
axillary innervation
C5-C6
musculocutaneous innervation
C5-C7
loss of supination suggests…
musculocutaneous damage
decreased grip strength suggests
radial nerve injury (wrist extension necessary for maximal action of flexors)
Median innervation
C5-T1
supracondylar fracture of humerus damages
median
location of radial nerve deep branch
supinator canal, where it can be injured with repetitive pronation/supination (such as using a screwdriver).
ulnar innervation
C8-T1
radial deviation of wrist upon flexion indicates…
ulnar injury
Nerve responsible for abduction and adduction of fingers
Interossei muscle, innervated by ulnar.
recurrent branch of median nerve innervation
C5-T1
recurrent branch of median nerve 1) scenario 2) presentation
1) superficial laceration of palm
2) “ape hand”, loss of thenar muscle group: oppostion, abduction, and flexion of thumb. *no loss of sensation
medial antebrachial cutaneous nerve distribution
FA 442
Damage to posterior cord causes…
Wrist drop
erb palsy muscle deficit
deltoid, supraspinatus, infraspinatus, biceps brachii
klumpke palsy nerve damage
C8-T1
lumbricals function
Flex MCP joints, extend DIP and PIP joints.
klumpke palsy muscle deficit
intrinsic hand muscles; lumbricals, interossei, thenar, hypothenar
TOS functional deficit
atrophy of instrinsic hand muscles; ischemia, pain, and edema due to vascular compression.
pope’s blessing seen with
proximal median nerve injury
hand presentation for proximal ulnar nerve injury
“OK gesture” (digits 1-3 flexed)
dorsal vs. palmar interossei
Dorsal abduct fingers, palmars adduct (DAB PAD)
Obturator innervation
L2-L4
Pelvic surgery nerve at risk
obturator
femoral innervation
L2-L4
Nerve at risk with pelvic fracture
femoral
femoral injury presentation
decreased thigh flexion and leg extension
common peroneal roots
L4-S2
tibial roots
L4-S3
tarsal tunnel syndrome
distal lesion to tibial nerve
tibial nerve damage presentation
Inability to curl toes and loss of sensation on sole of foot.
tibial nerve proximal lesion
Foot everted at rest with loss of inversion and plantarflexion.
superior gluteal nerve roots
L4-S1
localizing trendelenburg
lesion is contralateral to side of hip that drops, ipsilateral to extremity on which patient stands
Inferior gluteal roots
L5-S2
nerve at risk with posterior hip dislocation
inferior gluteal
inferior gluteal lesion presentation
difficulty climbing stairs + rising from seated position + loss of hip extension
superior gluteal innervates..
gluteus medius, minimus + tensor fascia latae.
inferior gluteal nerve innervates…
gluteus maximus
sciatic nerve roots
L4-S3
sciatic path and innervation
innervates posterior thigh, splits into common peroneal and tibial nerves.
pudendal roots
S2-S4
Best location for IM gluteal injection
superolateral quadrant
Presentation of L3-L4 herniation
Weakness of knee extension, decreased patellar reflex.
Presentation of L4-L5 herniation
weakness of dorsiflexion, difficulty in heel-walking
Presentation of L5-S1 herniation
weakness of plantarflexion, difficulty in toe-walking + decreased achilles reflex
long thoracic nerve travels with…
lateral thoracic artery
axillary nerve travels with
posterior circumflex artery
radial nerve travels with
deep brachial artery
median nerve location
distal humerus/cubital fossa
median nerve travels with
brachial artery
tibial nerve travels with
popliteal artery
distal tibial nerve location
posterior to medial malleolus
tibial nerve travels with
posterior tibial artery
skeletal muscle triad
1 T-tubule + 2 terminal cisternae
cardiac muscle dyad
1 T-tubule + 1 terminal cisterna
release Ca effect in muscle cell physiology…
Binds to TROPONIN C, causing conformational change that moves tropomyosin out of the myosin-binding groove on actin filaments.
Muscle cell physiology
tropomysin complex mooves out of myosin-binding groove —> myosin releases bound ADP and Pi –> displacement of myosin on actin filament (power stroke) –> contraction results in shortening of H and I bands between Z lines but A band remains the same (A band Always same length).
Next step after contraction in muscle cell?
Binding of a new ATP molecule causes detachment of myosin head from actin filament. Hydrolysis of bound ATP –> ADP, myosin head adopts high-energy cocked position for the next contraction cycle.
Type 1 vs type II muscle fibers
codebook
NO synthase
activates L-arginine to nitric oxide
smooth muscle relaxation pathway
agonist binds to receptor –> calcium released –> calcium activates NO synthase –> NO diffuse through endothelial cell and into smooth muscle cell –> NO activates GTP to cGMP –> cGMP activates myosin-light-chain phosphatase (MLCP) –> MLCP dephosphorylates myosin II causing relaxation.
myosin-light-chain phosphatase (MLCP)
Enzyme that initiates smooth muscle cell relaxation
smooth muscle contraction pathway
Membrane depolarization –> Ca enters through L-type voltage gated channels –> forms calcium-calmodulin complex –> activates myosin-light-chain-kinase (MLCK) –> phosphorylates Myosin
endochondral ossification bones
codebook
defective process in achondrplasia
endochondral ossification
intramembranous ossification bones
codebook
endochondral ossification process
cartilaginous model –> woven bone –> lamellar bone
woven bone found in…
1) fractures
2) Paget disease
membranous ossification process
woven bone formed directly –> lamellar bone
origin of osteoblasts
differentiate from mesenchymal stem cells in periosteum
osteoclast mechanism
dissolves bone by secreting H+ and collagenases
osteoclast origin
Differentiates from a fusion of monocyte/macrophage lineage precursor.
PTH action
1) At low, intermittent levels, exerts anabolic effects (builds bone) through indirect mechanism.
2) chronic high PTH levels cause catabolic effects (osteitis fibrosa cystica)
osteitis fibrosa cystica
Presentation of primary hyperparathyroidism. Characteristic findings = subperiosteal erosions/thinning of phalanges + granular “salt-and-pepper” skull + osteolytic cysts in long bones.
estrogen mechanism in relation to bone.
Inhibits apoptosis in bone-forming osteoblasts and induces apoptosis in bone resorbing osteoclasts.
estrogen deficiency in relation to osteoporosis
Causes excess cycles of remodeling. Bone resoprtion leads to osteoporosis.
achondroplasia mechanism
Constitutive activation of fibroblast growth factor receptor (FGFR3) inhibits chondrocyte proliferation. So it’s actually a gain of function mutation.
achondroplasia genetics
> 85% occur sporadically; autosomal dominant with full penetrance (homozygosity is lethal).
trabeuclar bone
spongy bone
osteoporosis bone pathophys
There’s normal mineralization and lab values but trabecular and cortical bone lose mass and interconnections.
levothyroxine SE
osteoporosis
osteoporosis diagnosis
Bone mineral density scan (dual energy x-ray absorptiometry) with a T-score of less than or equal to -2.5 OR fragility fracture of hip or vertebra.
osteoporosis treatment
Bisphosphonates + teriparatide + SERMS + rarely calcitonin + denosumab.
Colles fracture
Fracture of distal radius; classic sign of osteoporosis.
Osteopetrosis
1) etiology
2) presentation
3) treatment
o Coded character: walls made out of sponges/persistence of the primary spongiosa in the medullary cavity with no mature trabeculae. Dead zombies lining perimeter + page is weaving + woven bones all along back wall/caused by defective osteoclastic bone resorption, which results in accumulation of woven bone and diffuse skeletal thickening. /autosomal recessive and dominant forms. Skeleton with really thick bones on couch + covered in casts/causes thickened and dense bones that are prone to fracture. Skeletons bones look like below + big Erlenmeyer flasks on table/ends of long bones are misshapen and bulbous (“Erlenmeyer flask deformity”). Casts all over skeleton/although bone turnover is decreased, tissue becomes weak and predisposed to fractures. /cranial foramen decrease in size, leading to CN palsies. Huge spleen to the left of the couch + huge hippo on couch/hepatosplenomegaly. He has a pan on top of his head/bone fills marrow space pancytopenia + extramedullary hematopoiesis. /mutations (eg carbonic anhydrase II) impair ability of osteoclast to generate acidic environment necessary for bone resorption. Big pile of bones on top with Jo-Jo sitting on top/treatment = bone marrow transplant (osteoclasts derived from monocytes).
osteoid
unmineralized, organic portion of bone matrix that forms prior to maturation (mineralization) of bone.
lab profile in osteomalacia/rickets
lab profile = low levels of vitamin D and phosphate + low or normal level of calcium + elevated alkaline phosphatase
“looser zones”
pseudofractures, found in osteomalacia.
lab profile in paget’s
normal Ca, phosphorus, PTH, + increased ALP.
fractures in paget’s
long bone chalk-stick fractures
stages of paget’s
lytic (osteoclasts) –> mixed (osteoclasts + osteoblasts) –> sclerotic (osteoblasts) –> queiescent (minimal osteoclast or blast activity)
causes of avascular necrosis
1) corticosteroids
2) alcoholism
3) sickle cell disease
4) trauma
5) the bends “caisson/decompression disease)
6) Legg-Calve-Perthes disease (idiopathic)
7) Gaucher disease
8) Slipped capital femoral epiphysis
Osteopetrosis lab values
everything normal except low/normal serum Calcium
Paget lab values
everything normal except increased ALP
“Brown tumors”
characteristic finding in osteitis fibrosa cystica due to fibrous replacement of bone, subperiosteal thinning.
Primary hyperparathyroidism lab values
calcium, ALP, PTH up, phosphate down
secondary hyperparathyroidism lab values
decreased serum calcium, increased phosphate, ALP, PTH
Hyperphosphatemia in secondary hyperparathyroidism pathophys
pathophys = phosphate clearance declines due to fall in GFR increased phosphate binds free serum Ca2+, further exacerbating hypocalcemia.
lab profile in osteomalacia/ricktes
low serum ca + phosphate, high ALP, high PTH
Causes of hypervitaminosis D
1) Oversupplementation
2) Granulomatous disease (eg sarcoidosis)
lab profile in hypervitaminosis D
High serum calcium and phosphate, normal ALP, high PTH.
osteochondroma epidemiology
Most common benign bone tumor. Males
osteochondroma characteristics
Bony exostosis with cartilaginous (chondroid cap). rarely transforms to chondrosarcoma.
Giant cell tumor epidemiology, location, other name
20-40 years old, epiphyseal end of long bones, often around knee, “osteoclastoma.” Locally aggressive benign tumor.
osteosarcoma –> epidemiology, RF’s, location, management, characteristic findings
o Code: Evan Olmstead/Bimodal distribution: Peak incidence between 13 and 16, greater than 65 years old. Evil Dr. Hink in suit along wall + evil page/Rb + SIS oncogenes. Taryn with parrot on her shoulders slacklining above/teriparatide is a risk factor. Big devil behind Evan/malignant mesenchymal neoplasm of bone origin (osteoblasts). Aggressive. /second peak of incidence occurs in older adults + is associated with Paget + bone infarcts + ionizing radiation. Masses on his knees + femor/usually arise around knee + distal femur or proximal tibia. Bone stuck in ground with arrow through metaphyseal region/metaphyseal region. Tumors on shoulder + jaw/may also arise in shoulder + proximal femur + jaw. Evil anna petroveks attacking him/histology = anaplastic cells forming osteoid matrix. Below pattern as wallpaper/x-ray = “sunburst” pattern. Codman’s triangle in front of door/Codman’s triangle. /Other predisposing factor = bone infarcts. Surgeon cutting out evan’s back + he’s in a chemo chair/Treat with surgical en bloc resection (with limb salvage) + chemotherapy.
Fusion protein in Ewing’s
EWS-FLI i
Giant cell tumor location
Epiphysis
osteoarthritis presentation/symmetry
- asymmetric
- knee cartilage loss begins medially (“bowlegged”)
synovial fluid in osteoarthritis
non-inflammatory (WBC
joints involved in osteoarthritis
DIP, PIP, 1st CMC, NOT MCP.
osteoarthritis treatment
acetaminophen + NSAIDs + intra-articular glucocorticoids
pannus
proliferative granulation tissue seen in RA
RA RF’s
smoking + silica exposure + female + HLA-DR4
DMARDS
methotrexate, sulfasalazine, hydroxychloroquine, leflunomide
Joint findings in RA
Bone and cartilage erosions + juxtaarticular osteopenia + joint space narrowing + soft tissue swelling + subchondral cysts + pannus formation + increased synovial fluid.
synovial fluid in RA
inflammatory (WBC>2000)
fibrinoid necrosis
necrosis arising from immune complex deposition.
fibrinoid necrosis occurs in..
polyarteritis nodosa, malignant hypertension, preeclampsia, hyperacute transplant rejection
rheumatoid nodule histology description
fibrinoid necrosis with palisading histiocytes. Occurs in subcutaneous tissue.
extraarticular manifestations of RA
ILD, pleuritis, pericarditis, anemia of chronic disease, neutropenia, splenomegaly, amyloidosis, Sjogren’s, scleritis, carpal tunnel syndrome.
Felty syndrome
splenomegaly + RA
Joint findings in OA
thickened capsule + slight synovial hypertrophy + osteophytes + ulcerated cartilage + sclerotic bone + joint space narrowing + subchondral bone cyst
RA deformities
Deformities include subluxation, fingers with ulnar deviation, swan neck, boutonniere’s.
what mediates degradation and inadequate repair in OA?
chondrocytes
Gouty nephropathy pathophys
Urate crystals are deposited in the renal medullary interstitium where they can form intratubular precipitates, inflammatory tophi, or uric acid renal stones. Tubular obstruction leads to cortical atrophy and scarring, so 20% of people with chronic gout eventually die of renal failure
Hyperuricemia in gout epidemiology and pathophys
1) 90% caused by underexcretion of uric acid–largely idiopathic; can be exacerbated by meds.
2) overproduction of uric acid (10% of patients)–Lesch-Nyhan, PRPP excess, increased cell turnover (tumor lysis syndrome), von Gierke’s.
Tophi, etiology and location
Gout –> Accumulation of crystals in soft tissues), most commonly on external ears. Also olecranon bursa + achilles tendon.
What precipitates gout?
Alcohol consumption or large meal.
alcohol and gout pathophys
alcohol metabolites compete for same excretion sites in kidney as uric acid leading to decreased uric acid secretion.
Other name for pseudogout
calcium pyrophosphate deposition disease.