ethics and bone metabolism

Question 1

consent must include

Answer 1

1. diagnosis
2. description procedure
3. risks
4. alternatives
5. risk of nonoperative treatment

Question 2

physician self referral law (stark law)

Answer 2

can’t refer when financial relationship

Question 3

anti kick back statute

Answer 3

can’t receive anything of value in exchange for referral

Question 4

false claims act

Answer 4

can’t submit false claims to the government

Question 5

Emergency medical treatment and active labor act (EMTALA)

Answer 5

Medicare-participating hospitals must screen emergency conditions and treat or transfer if lack capacity to treat and transfer-receiving hospital cannot refuse.
25-66% of hand transfers inappropriate

Question 6

opioids

Answer 6

US consumes 80% global opioids

• leading cause of accidental death in young adults
• naloxone is opioid antagonist that causes opioids to detach from brain receptors

Question 7

bone metabolism

Answer 7

receptor activator of nuclear factor-Kb (RANK) binds to receptor activator of nuclear factor-Kb ligand (RANKL) and differentiates osteocytes and causes bone resorption.

• osteoprotegrin binds RANK to preserve bone
• parathyroid hormone and vit D increase RANK
• estrogen decreases RANK
• TGFb increases protegrin

Question 8

moth eaten bone appearance

Answer 8

hyperparathyroid, can be from renal failure or tumor

Question 9

vit D deficiency vs renal osteodystrophy vs hyperparathyroid

Answer 9

Ca Phos
vit D low low
renal low high
hyperparathyroid high low

Question 10

osteoporosis definition

Answer 10

-2.5 SD on DEXA scan (if fracture then severe)

Question 11

treatment osteoporosis

Answer 11

1200mg Ca
800-1000 IU vit D
- bisphosphonates decrease osteoclast activity (can’t use with renal impairment). can get osteonecrosis. recommend drug holiday 3-5 years.
- denosumab is anti-RANKL monoclonal antibody
- estrogens inhibit RANKL excretion (can increase cancer risk)
- tamoxifen - selective estrogen receptor modulator (increased VTE risk)
- PTH receptor agonists (“paratide” medications) stimulate osteoblast differentiation and activity. Use <2years.
- strontium ranelate - only dual mode agent. Inhibits osteoclasts and stimulates osteoblasts.

Question 12

heterotopic ossification

Answer 12

looks like normal bone without perisoteum

• induced by burns >20% BSA or brain/spinal cord injury.
• NSAIDS inhibit PGE2 -> decrease osteogenic differentiation
• radiation may help treat but increased risk sarcoma

Question 13

glucocorticoid injection in DM

Answer 13

• increased glucose for 5 days

- due to insulin antagonism

Question 14

impair healing steroids

Answer 14

impaired bone formation -> decrease OPG and RANKL

impaired wound healing mitigated with 25000 IU vitamin a pre-op and 3 days post op.

Question 15

effect of nicotine

Answer 15

• nicotine stimulates release of catecholamines and cause vasospasm
• carbon monoxide high affinity for hemoglobin displaces oxygen, reducing oxygen carrying capacity
• impaired osteoblast function and collagen synthesis
• must quit at least 4 weeks before surgery

Question 16

fracture stability

Answer 16

• absolute stability
• • compression plating to achieve
• • <2% strain across fracture site
• • allows for primary cortical healing through the Haversian system using cutting cones
• relative stability
• -2-10% strain
• • allow micromotion leading to endochrondral ossification through callus formation

Question 17

stages of healing

Answer 17

Immediately after injury, vessels constrict and aggregated platelets initiate healing through the release of platelet-derived growth factor (PDGF) and vasoactive agents (serotonin, histamine).

Chemokines attract inflammatory cells and initiate the inflammatory phase. The inflammatory phase is characterized by increased vascular permeability and cellular recruitment through thrombin activation. Recruited macrophages phagocytose debris, secrete collagenase, promote angiogenesis, and release growth factors that stimulate fibroblast proliferation. The inflammatory phase, which starts 10-15 minutes after injury, is completed by post-injury day three.

The proliferation phase starts 3-5 days after injury and is driven by fibroblasts drawn to the wound by PDGF. Fibroblasts begin collagen synthesis in addition to the production of elastin, fibronectin, glycosaminoglycan, and protease production. The proliferation phase lasts for six weeks and is followed by maturation. Maturation involves collagen remodeling through a balance of continued production and collagenase activity. Transition from type III to type I collagen and increasing collagen organization results in a wound with 80% of its original tensile strength at 6-12 weeks after injury.

Question 18

muscle contraction types

Answer 18

• concentric - muscle shortening
• eccentric - muscle lengthening
• isometric - tension changes while length remains the same
  isotonic - contraction related to change in muscle length while tension remains the same

Question 19

best donor site skin graft dressing

Answer 19

• calcium alginate, transparent film and hydrocolloids have fastest healing
• bismuth impregnated gauze, hydrocolloids and transparent film have lowest infection
• hydrocolloids and transparent film have lowest pain

Question 20

Dextran

Answer 20

branched polysaccharide osmotic agent that functions as a plasma expander by drawing fluids into the vasculature from interstitial spaces. It is also thought to bind directly to erythrocytes, platelets and vascular endothelium in a manner that decreases platelet adhesions. This is achieved by the following mechanisms: 1) increase in blood cell electronegativity to reduce RBC aggregation and platelet adhesion, 2) reduction of Factor VIII which reduces platelet function, 3) inhibition of alpha-2-antiplasmin resulting in net positive plasmin activity and subsequent clot fibrinolysis. It is dosed intravenously, processed in the kidneys and is excreted in the urine. While side effects are uncommon, they can be life threatening. They include anaphylaxis, volume overload, pulmonary edema, cerebral edema or platelet dysfunction.

Question 21

Chlorpromazine

Answer 21

centrally acting agent that exhibits a strong alpha-adrenergic blocking effect to decrease vasomotor tone and therefore decrease vasospasm. It is an antipsychotic drug often used to prevent anxiety. When used in the post-operative period it can prevent anxiety which, in turn, prevents vasospasm.

Question 22

Aspirin

Answer 22

inhibits cyclooxygenase, which irreversibly inhibits circulating platelets. Due to its irreversible binding to platelets it is effective for 8 to 10 days. Potential complications are dose dependent and include surgical site bleeding, hematoma, gastrointestinal bleeding, anaphylaxis and need for transfusion.

Question 23

Heparin

Answer 23

antithrombin III agonist (AT III) which accelerates the rate at which antithrombin III inactivates coagulation enzymes. Activated partial thromboplastin time (aPTT) must be monitored both before and during treatment to avoid supratherapeutic dosing. Potential complications include bleeding, heparin-induced thrombocytopenia, hyperkalemia, and hypersensitivity reactions.

Question 24

Low-molecular-weight heparin

Answer 24

factor Xa inhibitor. While it inhibits AT III, it is much weaker of an AT III inhibitor than unfractionated heparin and therefore is effective at preventing venous thrombosis, yet causes fewer hematomas. It has a longer half-life than unfractionated heparin, causes fewer cases of thrombocytopenia and requires no monitoring. That being said, the efficacy of low-molecular-weight heparin in preventing arterial thromboses is highly debated, making it a less common choice for prevention of small vessel thrombosis following replantation.