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?

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
What is the mechanism of action of bupropion?
Dopamine agonist --> it gives the reward so the patient doesn't need cigarettes for the reward
26
What patients should not be prescribed bupropion?
Seizure patients and eating disorders --> hyponatremia decreases seizure threshold
27
What is the mechanism of action of varenicline?
Antagonist and partial agonist of the nicotine receptor --> relieves withdrawal symptoms but provides little dopamine reward
28
What are the two AEs of varenicline?
Weird dreams and SI
29
What effect will smoking cessation have on a patient's prescription medication doses?
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
In what type of vitamins do we worry about toxicity?
Fat soluble - A, D, E, K
31
What AE associated with vitamin A supplementation do we need to know?
alopecia
32
List and name the B vitamins discussed in class and describe what they are primarily known for.
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
What drug can mask signs and symptoms of B12 deficiency/pernicious anemia?
Folate --> can return CBC values to normal but still result in further neuronal destruction and misdiagnosis. Pernicious anemia requires replacement of B12.
34
Deficiency of what vitamin (other than B9) can ultimately lead to folate deficiency anemia and why?
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.