Q4 MSK Flashcards
80% of bone is _______
Cortical or compact
Osteoporosis is a _____ not a ______ problem.
Quantity
Not Quality problem.
Low bone mineral density.
Risk factors for the development of Osteoporosis
White, female, sedentary lifestyle, smoking, Phenytoin, low Ca and Vit D diet, family Hx, premature menopause, Hx of breastfeeding.
Type I Osteoporosis (contrast with TII)
Post menopausal (age related >75)
Estrogen deficiency (poor Ca absorption)
Affects trabecular bone (spongy/ trabecular and cortical bone)
Distal radius and vertebral fx (hip pelvic fx more common)
(You hit menopause befor you get to 75 so type I comes before type II)
Type II Osteoporosis (contrast with TI)
Age-related
>75yo
Trabecular and cortical bone
Poor Ca absorption
Hip and pelvis most affected
Osteopenia = ____ peak bone mass?
Bone density is 1.0-2.5 SD LESS than the mean peak bone mass of a health 25-yo
T-score vs Z-score
T-Score = compare you to healthy 30yo of same gender. Use for DIAGNOSTIC.
Z-Score = compare to average for same AGE and gender.
“ThirT year old” “diagnosTic”
Who needs Osteoporosis screenings?
Women >= 65 and men >= 70yo.
Post menopausal women and men 50-69 based on risk profile
Postmenopausal women and men age >=50yo with history of adult-age fracture.
Osteoclasts vs blasts
Clasts - eat away (the letter C is like an open mouth pacman)
Blasts - Build up the new bone. Remodel.
Slide 16 - draw on FreeForm
RANKL is expressed by _____. It binds to _____ activating them and suppressing ______.
OPG is secreted by _____. It binds to _____ preventing ______
Osteoblasts
RANK on osteoclasts
Suppressing apoptosis - live longer!
Osteoblasts.
RANKL.
Prevents osteoclast activation.
Osteoblasts are the Boss!
Patients who have a T-score < ______ should be treated for Osteoporosis.
Patients who have a T-score between ____ and _____ AND these 3 things should be treated for osteoporosis
2.5
1.0 + 2.5
Secondary cause associated with high fracture risk (ex total immobilization)
FRAX 10-year prob of hip fx >= to 3%
FRAX 10-year prob of any OP-related fx >=20%
What things makes osteoclasts more active? If osteoclasts are more active than osteoblasts, what happens to bones?
Sedentary lifestyle, lack of weight bearing activity, Hyperparathyroidism, Hyperthyroidism, estrogen deficiency, menopause, testosterone deficiency and Acidosis.
If osteoclasts are more active, then bone gets broken down at a faster rate than it gets restored.
Phosphates and biphosphonates _____ bone loss
Slow
Things that stop bone loss?
Increase bone gain?
Calcium, vit D, fosamax, calcitonin, Mild exercise,
Fluoride plus Ca, Vit D and calcitonin
Extensive weigh bearing exercise.
Will slide 21 be on the pharm test?
What type of bone disease is rickets?
Disorder of bone mineralization.
Osteopetrosis - what’s this?
Decreased osteoclast fxn (too much cortical bone, not any spongy bone)
Marble/dense bones, rugged Hersey spine, Erlenmeyer flask-shaped proximal humerus
S/S bone pain, anemia, optic/oculomotor nerves can be crushed by bone formation = blindness.
Why would Osteopetrosis cause anemia?
Loss of medullary bone where RBCs are produced.
Other than frequent fractures, what do you see in patients with Osteogenesis imperfecta?
Blue sclera, weak, discolored teeth, sensorineural hearing loss.
What is patho Phys of OI?
Defect in Type I collagen formation.
What bacteria is most common to cause osteomyelitis?
Kids?
SCD?
Old adults/immunocom?
Long term IV meds?
Staph aureus.
Kids GBs, H influenzae
SCD - salmonella
Old adults - Gram neg
Long term IV - mycobacterial and fungal
Exogenous vs endogenous osteomyelitis
Exogenous =- DM feet, open wounds/fx, post op infx
Endogenous = bacteremia, spine, pelvis and small bones, dialysis patient.s
Sequestra = _______
Involucrum = ______
Dead bone
Exudate from inflammatory response can lift periosteum off the underlying bone, disrupting the blood supply leading to bone death/necrosis (Sequestrum)
New bone.
Lifting of the periosteum also causes osteoblastic response of new bone formation
What is the most sensitive study for chronic osteomyelitis, malignancies and infx?
What study is best for early osteomyelitis?
FDG-PET Scan.
MRI
What is Marjolin’s ulcer?
A type of skin cancer at the site of chronic osteomyelitis.
What layer of cartilage is important for opposing compression?
Characteristics?
Middle zone
Increased metabolic activity, cell size, collagen size.
Osteophytes, narrowed joint space, synovitis and thickened joint capsule are characteristic findings of what?
Osteoarthritis
T/F: Osteoarthritis and an aging joint are the same.
False, they are pathologically different.
OA vs Aging
OA has mostly an INCREASE in everything (except proteoglycan and keratin sulfate)
Aging has a DECREASE in mostly everything except Keratan sulfate and chondrocyte size
OA = asymmetric joint involvement. Pain at rest, joint swelling.
RA = symmetric autoimmune, morning stiffness, hand and wrist
What gene is associated with RA?
HLA-DR4 gene
What is the most sensitive and specific test for RA?
Anticyclic citrullinated protein (Anti-CCP)
Rheumatoid arthritis is a _______-mediated ______ response involving _______ release by the ______ cells.
IL ______ and _____ are involved. This stimulates an increase in production of _____ which activates ______ to _____
T-cell mediated
Immune
Cytokine
Synovial
1 +6, TNF-alpha
RANKL
Osteoclasts
Destroy bone
Gout is an alteration in ________ metabolism which causes formation of _______.
These crystals trigger ________ which causes release _______.
Purine metabolism
Monosodium urate crystals
TNF-alfa
Chemokines and interleukins.
Diff diagnosis for elbow bursitis?
Tophaceous gout.
Difference between gout or pseudo gout?
Gout = MoNosodium Urate Crystals - Needle shape, Negative birefringent
Pseudo gout = Calcium PyroPhosPhate - Rhomboid shaped
Positive birefringent.
Clinical presentation signs of muscular dystrophy?
Large calf muscles and lower limb proximal muscle weakness.
Muscular dystrophy is malfunction of ________ and mutations of ______
Glycoproteins
Dystrophin
Rhabdo CK level
5x normal level or 1000u/L
Acute Renal Failure at 5000u/L
What 4 main things contribute to AKI in rhabdo?
-Tubular cell injury leads to Fenton reaction (oxidative stress)
-Low pH makes myoglobin and uric acid react with Tamm-Horsfall proteins causing tubular cast formation and intra-tubular obstruction
-Ferryl myoglobin, MB, free-heme and hemopexin cause cellular injury
-Exercise induced dehydration -> RAAS activation and renal vasoconstriction
What patient population are incomplete fractures in?
Kids - it just bends or buckles a little.
A pathological fracture happens in someone with _______ like _______
A pre existing condition
Tumors, osteoporosis, infx, anything that weakens bones.
3 phases of fx healing?
Inflammatory
Repair
Remodeling.
What two tissues heal with normal tissue and not scar tissue?
Bone and liver.
During which stage of fracture healing is the callus removed and trabeculae formed?
Remodeling stage (3rd).
During what phase of fx healing does capillary ingrowth happen?
Repair (2nd)
What things make osteoclasts less active? What happens when osteoclasts are less active?
Weight bearing activity
Estrogen
Testosterone
Calcitonin
Adequate vit D and Ca intake.
More bone is deposited than taken out - bone grows and strengthens.
A dialysis patient is most likely to get an ________ osteomyelitis.
A diabetic patient is most likely to get an ________ osteomyelitis.
A post op infection is an example of ______ osteomyelitis.
Endogenous.
Exogenous
Endogenous.
Types of fracture healing and what they are
Which are most common in casting vs surgical fixation?
Indirect - (secondary) casting. intramembranous and endochondral bone formation. Hallmark is the formation of a CALLUS.
Direct - (primary) adjacent bone cortices are in contact. Surgical fixation.
High levels of RANKL (caused by _________) mean increased osteo____ formation and decreased osteo_____ apoptosis.
Estrogen _______ OPG which _____ RANKL, which means that post menopausal women have ____ estrogen, and therefore ______ RANKL.
High OPG = _______ RANKL
IL1, 11, 17, TNF, prostaglandin E2, PTH, glucocorticoids
Clast
Clast
Stimulates
Decreases
Less
More
Low - inverse relationship.
OPG and RANKL expression have an _______ relationship.
medications/factors that increase RANKL expression would lead to bone ______
Inverse.
Breakdown
ESTROGEN and RANKL - bone protective or bone destructive? Why do post-menopausal women have decreased bone density?
Estrogen stimulates OPG which is a RANKL decoy receptor. When OPG is activated, RANKL is inactive, and osteoclasts are inactive, and bone formation occurs.
Without estrogen, RANKL takes over and increases osteoclast activity, breaking down bone.
Which has more bone mineral density LOSS - osteopenia or osteoporosis?
Osteopenia < osteoporosis
What is osteomalacia?
Metabolic bone disease - like Rickets but in adults.
Deficiency of Vit D and Ca. High PTH levels abnormal osteoid deposits. MSK pain between joints. Deformity.
Patho of muscular dystrophy? What lab values are elevated and why?
Dystrophin is a membrane stabilizing protein. muscular dystrophies have mutations in the gene that codes for Dystrophin.
Without dystrophin, muscle fibers are not anchored to the basement membrane and are easily torn apart. Repetition of this causes free Ca to enter muscle cells causing cell death and fiber necrosis.
Disruption of the muscle cell releases CK. Patients with MD have CK levels 10-100x normal.
Progressive weakness.
