FR Review 10 - Spring Block 4 Material Other Than AAs Flashcards

1
Q

Differentiate osteoblasts from osteoclasts.

A

Osteoblasts: build bone
Osteoclasts: break down bone

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2
Q

List some non-pharmacologic interventions indicated for osteoporosis patients.

A

Smoke and alcohol cessation, fall prevention, regular weight bearing exercise, adequate intake of calcium and vitamin D

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3
Q

Describe the mechanism of action of vitamin D supplementation as it relates to osteoporosis.

A

Vitamin D is required for the intestinal absorption of calcium

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4
Q

What is the mainstay of osteoporosis therapy?

A

Bisphosphonates

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5
Q

Describe the mechanism of action of bisphosphonates.

A

Incorporated into bone in areas of active bone remodeling. There they decrease activity of osteoclasts allowing osteoblast activity to prevail

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6
Q

Describe the 30 minute rule of bisphosphonates and describe how Ibandronate is different.

A

Patients must take most bisphosphonates 30 minutes before eating and remain standing for 30 minutes after to allow the drug to travel easily down the esophagus and into the stomach –> risk for esophageal ulcers. Ibandronate requires 60 minutes standing.

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7
Q

What is the primary AE associated with bisphosphonates?

A

Long bone pain

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8
Q

Describe the mechanism of action of selective estrogen receptor modulators (SERM).

A

Agonize estrogen receptors on bone but antagonize estrogen receptors on uterine and breast tissue

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9
Q

What is the broad-view explanation as to why agonizing estrogen in bone helps osteoporosis?

A

Estrogen decreases osteoclast activity

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10
Q

Describe the mechanism of action of RANK-L inhibitors.

A

RANK binding to RANK-L receptors activates osteoclasts. Blocking RANK-L decreases bone breakdown.

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11
Q

Differentiate skeletal muscle relaxers from neuromuscular blockers.

A

Direct muscle relaxers: blocks release of Ca within the cell and thus blocking contraction
Indirect muscle relaxers: hyperpolarize neurons that innervate muscle groups to decrease spasm
Neuromuscular blockers: block Ach receptors in skeletal muscle system thereby preventing contraction

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12
Q

What acetylcholinesterase inhibitor drugs are used to reverse paralytics and what other disease are they used to treat?

A

Stigmines - neostigmine, ex –> also used to treat myasthenia gravis

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13
Q

What is an alternative to administering gasses for anesthesia?

A

Total propofol anesthesia usually administered with an opioid –> usually causes less N/V

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14
Q

Are anesthetic agents lipophilic or hydrophilic? State why.

A

Lipophilic –> need to get into the CNS

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15
Q

Describe the minimum alveolar concentration (MAC).

A

Minimum dose of a gas required to make 50% of the population not respond the pain. The lower the MAC, the more potent the drug.

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16
Q

What is propofol’s claim to fame?

A

Rapid on and rapid off

17
Q

What is the major AE of propofol?

A

Hypotension –> reduces vascular tone by 10-20%

18
Q

Why is propofol colored white and what are three reasons this is clinically significant?

A

The drug is not lipophilic so it is mixed with a soy-based lipid emulsion
Clinical - has egg so must be cautious in patients with egg allergies
Clinical - strict aseptic technique required because fat makes it more prone to bacteria
Clinical - the fat means it has calories that must be accounted for when calculating a patient’s nutrition administration

19
Q

How can the duration of action of a local anesthetic be prolonged?

A

Add a vasoconstrictor to the local anesthetic –> epinephrine

20
Q

In what areas of the body should local anesthetics with vasoconstrictors not be used?

A

Fingers, nose, penis, toes, and ears

21
Q

What is the most preferred local anesthetic?

A

Lidocaine

22
Q

Name and describe a rare life threatening AE of anesthetic gasses and state how it is treated.

A

Malignant hyperthermia –> sudden release of intracellular calcium results in muscle contraction, hyperkalemia, and hyperthermia.
Treated with dantrolene, insulin, and D5W –> future anesthesia must exclude gasses

23
Q

What are the ways nicotine replacement can be administered?

A

Many methods –> gum, patch, nasal spray, inhaler, lozenges

24
Q

How is the nicotine patch dose and how is it used?

A

21mg, 14mg, or 7mg. Wherever you start (based on how many cigarettes they smoke), have them on it for 3-4 weeks then taper down for 2 weeks at each lower dose.

25
Q

What is the mechanism of action of bupropion?

A

Dopamine agonist –> it gives the reward so the patient doesn’t need cigarettes for the reward

26
Q

What patients should not be prescribed bupropion?

A

Seizure patients and eating disorders –> hyponatremia decreases seizure threshold

27
Q

What is the mechanism of action of varenicline?

A

Antagonist and partial agonist of the nicotine receptor –> relieves withdrawal symptoms but provides little dopamine reward

28
Q

What are the two AEs of varenicline?

A

Weird dreams and SI

29
Q

What effect will smoking cessation have on a patient’s prescription medication doses?

A

Cigarette smoke is an inducer of CP 450. When a smoker suddenly stops, any drug that goes through CP 450 will require a lower dose

30
Q

In what type of vitamins do we worry about toxicity?

A

Fat soluble - A, D, E, K

31
Q

What AE associated with vitamin A supplementation do we need to know?

A

alopecia

32
Q

List and name the B vitamins discussed in class and describe what they are primarily known for.

A

B1: Thiamine - deficiency in chronic alcoholics
B3: Niacin - increase HDL
B6: Pyridoxine - supplemented in patients taking isoniazid for TB
B9: Folate - deficiency causes anemia
B12: Cyanocobalamin - deficiency causes pernicious anemia

33
Q

What drug can mask signs and symptoms of B12 deficiency/pernicious anemia?

A

Folate –> can return CBC values to normal but still result in further neuronal destruction and misdiagnosis. Pernicious anemia requires replacement of B12.

34
Q

Deficiency of what vitamin (other than B9) can ultimately lead to folate deficiency anemia and why?

A

Vitamin C protects stores of tetrahydrofolic acid (active form of folate). Vitamin C deficiency can lead to depletion of active folate and ultimately folate deficiency anemia.