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ABOS > Basic Science > Flashcards

Basic Science Flashcards

1
Q

exfix

factors inflencing the stiffness of a frame?

A

number 1 = reduction then diameter of screw

stiffness r to power of 4

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2
Q

anti-thrombotics

TXA: what’s the mechanism of action?

A

antifibrinolytic
Mechanism:
inhibits conversion of plasminogen to plasmin
prevents fribinolysis

prevents breaking down of clots. it stabilizes clots. Does NOT promote clots

tPA promotos fibrinolysis

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3
Q

anti-coagulation

Know: mechanisms, contraindications, things gone bad

A

A. Aspirin
B. Lovenox
C. Warfarin
D. Rivaroxaban (Xarelto), Apixaban (Eliquis)
E. Dabigatran

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4
Q

anticoagulation

Aspirin mechanism of action

A
  • inhibits the production of prostaglandins and thromboxanes through irreversible inactivation of the cyclooxygenase enzyme within platelets
  • Irreversible binds COX in platelets

thromboxane function
under normal conditions thromboxane is responsible for the aggregation of platelets that form blood clots

prostaglandins function
prostaglandins are local hormones produced in the body and have diverse effects including
the transmission of pain information to the brain
modulation of the hypothalamic thermostat
inflammation

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5
Q

anti-coagulation

Warfarin mechanism of action and reversal, when to stop pre-op?

A
  • Prevents Vit-K gamma carboxylation
    II,VII, IX, X & protein C & S
    * inhibits vitamin K 2,3-epoxide reductase
  • reversal Vit K: PO or IV (3 days); FFP immediate
  • stop 5 days pre-op

target INR 2-3 for orthopatients

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6
Q

Heparins

Heparin and LMWH (enoxaparin)
inhibits? reversal agent? excreted through?

A

Heparin: binds and enhances ability of antithrombin III to inhibit factors IIa, III, Xa

LMWH: inhibits Xa and thrombin (IIa); LMWH acts in several sites of the coagulation cascade, with its principal action being inhibition of factor Xa

protamine sulfate

kidneys!

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7
Q

DOACs

2 types: Factor Xa inhibitors and Direct thrombin inhibitors?
Reversals?

A
  • RivaroXaban, Apixaban, edoXaban: direct Xa inhibit. 12hr half line for apixaban. Reversal: AndeXanet alpha
  • daBigatran (Pradaxa): direct thrombin (IIa) inhibitor Reversal: Idarucizumab
  • Thrombin = IIa

mechanism of action of these drugs can be deduced from the name.
* Rivaro(Identifier)-xa(FactorXa)-ban(inhibitor)
* DaBigatran (Pradaxa): direct thromBin inhibitor

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8
Q

anticoagulants

indirect Factor Xa inhibitor

A

Fondaparinux: irreversibly binds X thru ATIII
(Indirect Xa inhibitor (works through ATIII))

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9
Q

osteoprogenitor cells: differentiation based on?

A

Strain and Oxygen.
High strain: fibroblast (think nonunion)
Medium strain, low O2 = chondrocyte
Low strain, High O2 = osteoblast/osteocyte

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10
Q

Bone cells

Osteoblast Development:
* under control of ? signaling?
* 3 key transcription factors

Chondrocyte development:
Adipocyte development

A

Blasts: Wnt Signaling
Key TF: B-catenin, Runx2, Osx

Chondrocytes: Sox9, “Sox sucks for making bone”

PPARy causes adipocytes (widest, looks fatest)

  • Osteoblasts are derived from undifferentiated mesenchymal stem cells, and RUNX2 is the multifunctional transcription factor that directs this process.
  • Wnt/Beta-catenin (B-catenin) pathways are involved in osteoblast differentiation.
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11
Q

Osteoblasts

control bone production via 2 receptors:
PTH: ultilizes ? as mediator for signaling, Pulsed PTH has what effect on bone?
Vitamin D

Osteoblasts produce?

A

PTH: ultilizes adenylyl cyclase as mediator for signaling
Pulsed PTH has anabolic effect on bone

  • Osteoblasts produce type I collagen (i.e., bone), alkaline phosphatase, osteocalcin, bone sialoprotein, and RANKL

osteoblasts make bone by producing nonmineralized matrix: Type I collagen, alkaline phosphatase

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12
Q

Osteoclast

inhibit osteoblasts via what messenger?? what is the effect of PTH and Calcitonin on this?

A

sclerostin:
- produced by osteocytes
- inhibits bone formation
- occurs via Wnt pathway antagonism
- can measure in blood, want low levels if supplementing patient with vitamind D
- PTH: increases sclerostin
- Calcitonin- decrease sclerostin

Former osteoblasts trapped in the matrix they produce
communicate via gap junctions in caliculi

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13
Q

osteoclasts

Osteoclasts are derived from ?.
? is produced by osteoblasts, binds to immature osteoclasts, and stimulates differentiation into active, mature osteoclasts that result in an increase in bone resorption.
Resorb: only ? matrix; occurs at ?; forms ?
how do they bind to bone?
? inhibits bone resorption by binding and inactivating ?

A
  • Osteoclasts are derived from hematopoietic cells in the macrophage lineage.
    * RANKL is produced by osteoblasts, binds to immature osteoclasts, and stimulates differentiation into active, mature osteoclasts that result in an increase in bone resorption.
  • resorb mineralized matrix, at ruffled border, forms howships lacunae
  • Bind to bone via: integrins - > vibronectin (sealing zone)
  • OPG inhibits bone resorption by binding and inactivating RANKL.

  • Osteocytes are former osteoblasts surrounded by newly formed matrix. They are important for control of extracellular calcium and phosphorous concentration, and are less active in matrix production than are osteoblasts.
    Osteoclasts bind to bone surfaces by means of integrins (vitronectin receptor), effectively sealing the space below, and then create a ruffled border and remove bone matrix by proteolytic digestion through the lysosomal enzyme cathepsin K.
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14
Q

Osteoclasts disorders:

carbonic anhydrase mutation leads to?
Cathespin K mutation leads to?

A

CA mutration = OSTEOPETROSIS
Catespin K mutation = pyknodysostosis

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15
Q

osteoclasts are regulated by 2 key molecules produced from osteoblasts?

A

Osteoprotegerin (OPG): prevents osteoclast activation by inactivating RANKL (osteoprotegrin Protects)
RankL: activates Osteoclastis

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16
Q

osteoclasts regulation

PTH can cause bone resorption via?
Osteoblasts van prevent resorption via?

A

PTH (receptor on osteoblast) – via RANKL
osteoblast prevents resoprtion via OPG

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17
Q

osteoclast regulation

calcitonin: where is it released from? what does it bind to and how how does it act? Effect on bone resorption and serum calcium. Opposes the effects of?

A

Calcitonin: released from parafollicular cells of the thyroid, binds to and inhibits osteoclasts, slowing bone resorption and reduces serum calcium.

Opposes effects of PTH

18
Q

intermittent vs chronic PTH effect on bone?

A

intermittent PTH builds bone, chronic PTH reduces bone

19
Q

metastatic pathway on bone destruction

what signaling is involved?

A

all about RANKL
“resorb with rank”
IL-1 and PTHrP production stimulates rank pathway

20
Q

bone matrix

Bone matrix is ? % inorganic (mineral) components and ? % organic components.
? constitutes the majority of the inorganic matrix.
Type ? collagen is 90% of the organic component

? is the most abundant noncollagenous protein in bone.

Tensile and compressive strength of bone?

A

inorganic:
Bone matrix is 60% inorganic (mineral) components
Calcium hydroxyapatite Ca10(PO4)6(OH)2 constitutes the majority of the inorganic matrix. Give compressive strength to bone

Organic: 40%
Type I collagen is 90% of the organic component

osteocalcin is the most abundant noncollagenous protein in bone. produced by blasts. Organic

Type 1 collagen = tensile strength
Proteoglycans = compressive strength

21
Q

wolff’s law: remodeling occurs?
hueter-volkmann law: compressive forces? tension?

A

Wolff’s law: Remodeling occurs in response to mechanical stress.

Hueter-Volkmann law: Compressive forces inhibit growth, whereas tension stimulates it.

22
Q

3 types of bone formation

A

enchondral formation, bone replaces a cartilage model. Long bones, physis, fracture callus

appositional formation, osteoblasts lay down new bone on existing bone; the groove of Ranvier supplies the chondrocytes. Periosteal bone enlargment (width)

Intramembranous formation occurs without a cartilage model; aggregates of undifferentiated mesenchymal differentiate into osteoblasts, which form bone. (embryonic flat bones, distraction osteogenesis) bones of the face, not really an orthothing

23
Q

endochondral bone fomation

all about zones.
what gets secreted by the chondrocytes? what is the effect?

PTH and PTrP have ?? properties

A

indian hedgehog

  • type x collagen and vegf are markers of differentiation, they are released from hypertrophic zone
  • PTH and PTH-related protein: have chondroprotective and chondroregenerative properties

chondrocytes produce cartilage which is absorbed by Clasts, osteoblasts lay down bone on cartilaginous framework, bone Replaces cartilage, not converts, forms primary trabecular bone

24
Q

Appositional growth:

Groove of Ranvier?
Perichondral ring

A
25
Q

Primary bone healing

what kind of healing?
occurs via?
occurs with what kind of constructs?

A

intramembranous
via haversian remodeling
with absolute stability constucts

strain less than 2%

26
Q

secondary bone healing

3 stages: describe each?
what tolerates greatest strain?

A

granulation tissue tolerates greatest strain before failure

NSAIDs adversely affect healing of fractures as well as of lumbar spinal fusions. COX-2 activity is required for normal enchondral ossification during fracture healing.

27
Q

Bone grafts

Osteoconductive
Osteoinductive
Osteogenic

A

Bone grafts have three properties.
Osteoconduction: acts as a scaffold for bone growth; cancellous autograft

osteoinduction involves growth factors that stimulate bone formation; DBM, BMP, TGF beta

osteogenic grafts contain primitive mesenchymal cells, osteoblasts, and osteocytes. must be autograft

28
Q

bone grafts

Fresh grafts have more?
cancellous grafts incorporated via?
calcium phosphate grafts have ?
calcium sulfate graft is?

A

Fresh grafts = higher immunogenicity
cancellous grafts incorporated via creeping substituion
CaPO4 highest compressive strength
Calcium sulfate, fastest to resorb, associated with serous wound drainage

Calcium phosphate–based grafts are capable of osteooconduction and osteointegration. They have the highest compressive strength of any graft material. Calcium sulfate is osteoconductive but rapidly resorbed

29
Q

Calcium phosphate–based grafts have what kind of properties? They have the highest ? of any graft material.

Calcium sulfate is ? but rapidly resorbed

A

Calcium phosphate–based grafts are capable of osteooconduction and osteointegration.
They have the highest compressive strength of any graft material.

Calcium sulfate is osteoconductive but rapidly resorbed

30
Q

Bone mass peaks between ? years of age. Physiologic bone loss affects ? bone.

A

Bone mass peaks between 16 and 25 years of age (3rd decade). Physiologic bone loss affects trabecular bone more than cortical bone.

31
Q

calcitonin:
PTH:
Vitamin D

A

Calcitonin: decreases calcium “tones down”
PTH: increases calcium, decreases phosphate (P thrashing hormone)

Vitamin D: vitamin D parallels PTH. Increase reabsorption of calcium in kidneys “PDH”
-1,25 Vit D is active form
-25 Vit D is laboratory study of choice to determine vitamin D deficiency

The primary homeostatic regulators of serum calcium are PTH and 1,25(OH)2D3. PTH results in increased serum Ca2+ level and decreased inorganic phosphate level.

32
Q

Renal Osteodystrophy

Renal osteodystrophy is a spectrum of disorders observed in chronic renal disease

unlikely to show up

A

The majority of cases are caused by phosphorous retention and secondary hyperparathyroidism.

33
Q

rickets and osteomalacia

essentially the same thing
what causes it?

A

Impaired mineralization
Rickets: of cartilage matrix (juvenile) zone of provisional calcification
Osteomalacia: of bone matrix adult

Rickets (in children) and osteomalacia (in adults) are caused by a failure of mineralization. In rickets, the width of the zone of provisional calcification is increased, which causes physeal widening and cupping.

34
Q

Osteoporosis:

prognosis?
affects what kind of bone?
how to diagnose?
medications?
what to pick on the boards when needs to initiate treatment?
What are the distractors?

A

Prognosis: prior fragility fx is strongest predictor of a future fragility fx from low energy trauma; 2 vertebral compression fractures is strongest predictor for further vertebral compression fx. 1 Vert compression fx increases risk of hip fx 5x

  • T score to treat, T score greater than -2.5
  • 25 vitamin-d levels will be low in patients w/
  • indication for treatment: any hip or vertebral fracture “fragility fracture” T score - 2.5,

medications:
- calcium 1200-1500mg/day
- vitD 800-1000u/d; want serum 25-OH-Vitamin D level 41 to 250 ng/ml
(Patients over 50)

On the boards:
- Pick a bisphosponate! if need to treat
- never pick calcitonin or start HRT (this is an ortho exam no endocrinology). Estrogen based (Raloxifene) reduces osteoclast activity
- Teriparatide (forteo): recombinant PTH (2nd line agent), intermittent use is anabolic on osteoblasts. contra indicated in Pagets and patients with previous bone mets due to risk of secondary osteosarcoma
- Denosumab (prolia): 2nd line, ig2 antibody to rank activation and inhibits formation and activation and survival of osteoclasts

clonazepam (increase sclerostin)
Osteoporosis is a quantitative defect in bone.
It is defined as a lumbar bone density of 2.5 or more standard deviations less than the peak bone mass of a healthy 25-year old (T-score).
don’t worry about FRAX or Z score for questions
fragility fx trumps all when it comes to treatment

35
Q

Bisphosphonates:
what cells do they inhibit?
nitrogen vs non nitrogren potency?
Risks?

A

Bisphosphonates directly inhibit osteoclastic bone resorption.

**Nitrogen-containing bisphosphonates are up to 1000-fold **more potent than non–nitrogen-containing bisphosphonates.
- Bisphosphonates function by inhibiting farnesyl pyrophosphate synthase in the mevalonate pathway.

They are associated with osteonecrosis of the jaw, and in animal models, they have reduced the rate of spinal fusion.

osteoclast down regulator

36
Q

Denosumab MOA

A

Denosumab is a monoclonal antibody that targets and inhibits binding of RANKL to the RANK receptor, which is found on osteoclasts.

37
Q

Loss of function of the ? gene results in osteoporosis

A

Loss of function of the OPG gene results in osteoporosis

38
Q

Scurvy results from ascorbic acid deficiency, which causes a decrease in chondroitin sulfate synthesis and ultimately defective ??

A

Scurvy results from ascorbic acid deficiency, which causes a decrease in chondroitin sulfate synthesis and ultimately defective collagen growth and repair.** Widening in the zone of provisional calcification is observed.**

39
Q

Both urinary hydroxyproline and pyridinoline cross-links are elevated when ?

A

Both urinary hydroxyproline and pyridinoline cross-links are elevated when there is bone resorption.

40
Q

Serum alkaline phosphatase increases when ?

A

Serum alkaline phosphatase increases when bone formation increases.

41
Q

most common cause of hypercalcemia?

A

The most common cause of hypercalcemia is malignancy. Initial treatment is with hydration, which causes a saline diuresis, along with loop diuretics.

42
Q

Premature arrest following growth plate injury is attributed to ?

A

Premature arrest following growth plate injury is attributed to vascular invasion across the physis.

ABOS (16 decks)

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