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Safe Prescribing Flashcards

1
Q

What types of subjects are included in Phase I clinical trials?

A

Health volunteers that do not have the target disease. About 20 to 80 participants. They are typically not taking any other meds.

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2
Q

How long does a patent last?

A

Usual patent lasts 9-11 years.

The patent can be extended (usually 3-5 years) if:
*The drug becomes available OTC (i.e. omeprazole).
*They implement a new delivery system (i.e. extended release formulation).
*New dosing regimen.
*New indications (i.e. new use, Canaglifilozon has 8 new indications, patent was extended until 2031)

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3
Q

Pharmacodynamics (PD)

A

The study of the biochemical and physiological effects of the drugs. What the drug does the the body/disease. The mechanism of action.

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4
Q

The pharmacodynamic profile of a medication is unchanged of the lifespan. True or False?

A

True. It works the same not matter the age.
Pharmacodynamics knows no age.

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5
Q

Pharmacokinetics - Define ADME

A

What the body does to the drug:

A - Absorption (skin, lungs, GI tract, praenteral)
D - Distribution (throughout the body, especially to the needed site of action
M - Metabolism (bio transformation, changing it from one form to another - liver, GI tract, other)
E- Elimination (kidney is the most common way a drug is eliminated from the body, GI tract, others)

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6
Q

Pharmacokinetics: True of False?

Age and gender significantly impact a medication’s pharmacokinetics.

A

Age and gender significantly impact a medication’s pharmacokinetics. True

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7
Q

Fick’s Law

A

The tendency of molecules to move from higher to lower concentration via random molecular motion. Typically occurs across a membrane or other permeable barrier.

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8
Q

Examples of permeable barriers

A

*blood brain
*mammary
*placenta
*cell membrane
*Vessels

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9
Q

Passive diffusion

A

Most common method of diffusion. Moving from higher to lower concentration

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10
Q

Examples of Drugs that cannot be given orally. Why?

A

Would be killed by the pH in the digestive tract, and the molecules (molecular weight) of these drugs is too big to be absorbed by the GI tract.

Unfractionated heparin
Insulin
LWMH - low molecular weight heparin

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11
Q

Why is Vancomycin only given parental? In what instance could PO Vanco be given?

A

Vanco molecules are too big to be given PO and would not be absorbed to fight an infection like cellulitis, etc?

PO Vanco could be given to treat a gut infection like CDiff and Enterocolitis. It would not need to be absorbed since it would be going directly to the site of infection.

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12
Q

What parameters need to be met for a drug need to be to be given PO (for oral drug absorption) so that it is absorbed by the gut?

A

*The molecular weight needs to be <1000 d, most 250-600 daltons
*It needs to be a lipid soluble substance (to pass through the gut wall
*Small intestine needs to be functional (this is where most drugs are absorbed). The stomach does a little bit of breakdown, but the duodenum (the first part of the small intestine) and the rest of the small intestine are the most common points of absorption.

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13
Q

Which scenario would a drug that is given PO have less efficacy?

A

History of gastric bypass surgery. This is because the duodenum and a portion of the small intestine is bypassed and so the drug would not be absorbed properly.

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14
Q

Area Under the Curve (AUC)

A

Area under the plot of drug plasma concentration against time after a single dose administration. This means:

The taller thinner curve means the drug peaked quicker and left the body sooner. This is indicative of a young healthy person.

The shorter fatter curve means the drug took longer to peak and longer to leave the body. This is indicative of an older adult.

Meaning, if you administer a sedating pain medication to a younger adult, they get higher pain control that lasts a short period of time. If you give that same medication to an older adult, the get less pain control, but the drowsy effect lasts longer.

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15
Q

Tmax

A

Time to maximum drug level observed. Time on the clock. Time to peak

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16
Q

Cmax

A

Measurement of Tmax (maximum or peak concentration of a drug observed after its administration). In other words, Cmax is if you were to measure the drug level, when would it be at its highest and what would that level be.

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17
Q

Tmax,Cmax

A

Is the maximum effect of the drug
The max clinical effect, and
The max adverse effect.

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18
Q

Basal insulin

A

Peak-less, Glargine or Detemir, keeps things level. It mimics what the pancreas does in a normal human body. 50% of insulin in the human body is basal.

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19
Q

All drugs of the same class have the same…

A

Pharmacodynamics

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20
Q

All drugs of the same class have the same…

A

Pharmacodynamics

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21
Q

What is a potential problem when insulin is at Cmax?

A

It can cause hypoglycemia. This using happens after a rapid acting insulin bonus. Therefore, hypoglycemia will occur when the rapid acting insulin hits Cmax.

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22
Q

Pharmacokinetics vs Pharmacodynamics

A

Pharmacokinetics (different) is what the body does to the drug. Therefore, the results can vary.

Pharmacodynamics (same, class effect) is what the drug does to the body. All drugs of the same class will work the same way.

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23
Q

Enteric coated

A

Releases in the small intestine and they take a while to kick in.

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24
Q

Volume distribution Drug blood concentration

A

The total amount of drug in the body/
Drug blood concentration

The amount of drug distributed uniformly in the body that produces the observed drug concentration

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25
Q

Why does Naproxen sodium work faster than, plain Naproxen or enteric coated sodium?

A

This is because the sodium molecule facilitates absorption

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26
Q

What organ makes albumin in the body? Why does the Albumin amount drop as we get older? Why does this matter when talking about drugs?

A

The liver. Our liver shrinks when we get older. Albumin is the most common plasma protein for highly protein-bound drugs to be attached to. (I.e. Coumadin, warfarin).

Example: Young adult between 20-30 will need more Coumidin or Warfarin than and older adult. Since the older adult has less albumin for the medicine to bind to, if you give them the same higher dose as the younger person, they will have the drug free roaming around the body.

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27
Q

Body fat increases in the average person as we age. Why is this important regarding drugs?

A

Many drugs are lipophilic and will hang out in the body fat, which makes meds hang around longer

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28
Q

What’s are the age related changes than can affect how drugs are processed?

A

% body weight as water decreases
Lean muscle mass decreases
% of body fat increases
Serum albumin decreases
Relative kidney weight decreases (the kidneys shrink)
Relative hepatic blood flow decreases (less able to do drug bio transformation in a timely manner)

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29
Q

In the older adult why will antibiotics not be well distributed?

A

Because an older adult has less extracellular water, so the antibiotics don’t distribute as well.

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30
Q

Protein-bound?

A

Means the 80% or more of the drug (i.e. warfarin, Heparin, carbamazepine, phenytoin) circulates via plasma protein (i.e. albumin)

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31
Q

Why does THC and PCP (angel dust) hang around in the body?

A

B/c it is highly lipid soluble.

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32
Q

How long does a person initiating oral bisphosphonate therapy need to be on alendronate to treat osteoporosis with history of fragility fracture and why?

A

3-5 years; this b/c the drug settles in the bone and hangs around a while. Bones hold on to meds for a long time (i.e. children in the 50s and 60s exposed to lead paint chips, lead was found in the bone for decades)

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33
Q

How long does a person initiating oral bisphosphonate therapy need to be on alendronate to treat osteoporosis with history of fragility fracture and why?

A

3-5 years; this b/c the drug settles in the bone and hangs around a while. Bones hold on to meds for a long time (i.e. children in the 50s and 60s exposed to lead paint chips, lead was found in the bone for decades)

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34
Q

How are a vast majority of drugs offloaded?

A

Through the kidney; Most oral drugs are fat soluble to get through the gut wall and then must be biotransformed to water soluble form to be offloaded through the kidney

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35
Q

Where are the primary biotransformation sites in the body?

A

Primary is the liver

Less active sites are:
GI tract
Lung
Skin
Kidney

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36
Q

Between a female and a male of the same height and weight, which accounts of 2/3 drug-induced liver toxicity and why?

A

The female, b/c the female’s liver is smaller which means she produces less hepatic enzymes. In addition, the female stores more fat, and therefore will store more of the fat soluble drug and needs to be expelled by the the liver.

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37
Q

First pass effect (AKA Pre systemic Elimination)

A

Biotransformation/excretion of oral drug by hepatic mechanisms, the result in minimal delivery into systemic circulation

Meaning the liver takes a portion of the drug and throws it away before it can reach systemic circulation

Drug dose are adjusted by the manufacturer through the phase clinical trials to accommodate first-pass effect

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38
Q

First pass effect and routes

A

Oral route is subject to first-pass effect, the IV route is not subject to first-pass effect. Therefore the oral dosage of the drug will be higher.

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39
Q

Bioavailability

A

Means how much of the drug is available after first-pass effect.

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40
Q

Which statins are best taken during the day? Why?

Which statins are best taken a nighttime? Why?

A

Simvastatin, pravastatin, lovastatin - because these statins have a shorter half-life and our bodies make LDL mostly at night

Atorvastatin and Rosuvastatin - because these statins have a longer half life they will be effective all day

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41
Q

Drug for community acquired pneumonia? Which for is better, Oral or parenteral?

A

Levofloxacin (Levaquin). They are equal; Both routes have 99% bioavailability.

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42
Q

Transdermal med requirements

A

*Molecular weight of <1000 daltons (higher won’t get through the skin)
*PH range 5-9 in aqueous medium (a pH too high or too low would burn the skin)
*No histamine- releasing action (would cause itchiness and hives)
*Relatively low daily drug requirement (not very much med can be transferred transdermally

43
Q

A transdermal med is similar to…

A

A slow IV drip

44
Q

Regardless of the route, all meds undergo first-pass effect T/F?

A

False; this is only oral and rectal

45
Q

Half-life

A

The time required for the amount of drug in the body to be reduced or eliminated by 1/2. Also, know as T1/2.

46
Q

How many half lives of the drug do you need on board to reach a steady state? How many drug free half lives to eliminate the drug from the body?

A

3-5 half lives for both; Meaning, if the drug has a 24 hour half life, it will take 3-5 days to reach the Cmax (max therapeutic effect) of the drug, and it will take 3-5 day for the drug to be eliminated from the body.

47
Q

Levothyroxine T1/2? How long would you wait to recheck TSH level to see if the dose needs to be tweaked if the person is in a euthyroid state?

A

If the person has hypothyroidism the T1/2 of is about 10-12 days. If the person has hyperthyroidism the T1/2 is 5 days. Euthyroid (normal thyroid state) T1/2 is 7 days.

Therefore, if the person is in a euthyroid state, we would want to recheck TSH as about 6 to 8 weeks. B/c with the person is in a euthyroid state, the half-life is 7 days.

48
Q

Penicillin half-life?

A

T1/2 is 1-2h

49
Q

Zolpidem half life?

A

T1/2 2 hours. This is a good sleep med, b/c for a sleep med you want something that works quickly and leaves quickly.

50
Q

Lead Half-life in blood, soft tissue, and bone?

A

Blood - 1 month
Soft tissue - 1-3 months
Bone - 20+ years

51
Q

Why would a dose for a child be the same for an older adult? (I.e Zyrtec)

A

Typically the T1/2 of meds is increased in older adults, and it is very short in children when compared to younger adults. This is because healthy children usually have really good kidneys and liver which results in a super active biotransformation process in their bodies, so they kick the meds out quicker.

52
Q

Drug effect versus half-life?

A

This is the effect of the medicine versus the medicine actually still being in the body. For example, Aspirin has a T1/2 of 0.25 hours, but it affects platelet function for 8-9 days. This is why the advice is to discontinue aspirin for 7-10 days prior to surgery.

53
Q

Triptan and liquid ibuprofen combo

A

Triptans are really good at treating non-headache symptoms such as photophobia and nausea. Liquid ibuprofen is easy on the stomach and better to treat pain. Together the combination is amazing.

54
Q

Receptor site locations:
Beta 1
Beta 2
Alpha 1

A

Beta 1 - one heart (mostly found in the heart), elevated heart rate
Beta 2 - In the airways going to two lungs, and Two arms, two legs, bronchodilation and tremors
Alpha 1 - Vascular bed (in the blood vessels) and also in the prostate, causes elevated blood pressure

55
Q

Agonist

A

Binds to a receptor, causes an effect similar to endogenous compound in the body

56
Q

If a person comes to the ER and receives 2 albuterol treatments, why will their hands be tremulous?

A

Because albuterol is a Beta-2 adrenergic agonist. Bronchodilates the airways to the lungs b/c there are Beta-2 receptors in those airways leading to the lungs. The hands, arms, and legs tremor b/c of the Beta-2 receptors in the arms and legs.

57
Q

Decongestant agonist like pseudoephedrine

A

This is an Alpha-1, beta-1, beta-2 agonist. In excessively high doses:
Alpha-1 - elevated blood pressure
Beta-1 - Elevated heart rate, because beta-1 agonist causes vasoconstriction
Beta- 2 - Mild bronchodilation

58
Q

Drugs with “terol”

A

These drugs activate the beta -2 receptors just like the catecholamines do, resulting in bronchodilation.

59
Q

beta-2 adrenergic agonist

A

Therefore, beta-2 adrenergic agonists (i.e. albuterol, salmeterol). Adrenergic (means adrenaline-like) is just like adrenaline

Therefore, Beta-2 adrenergic agonist activate the receptors in the airways going to the 2 lungs just like adrenaline would and epinephrine would resulting in bronchodilation

60
Q

adrenergic beta-2 agonist

A

Therefore, beta-2 adrenergic agonists. Adrenergic is just like adrenaline would

61
Q

Antagonist

A

an endogenous regulatory compound who’s action is blocked by the drug. Name reflects the receptor

62
Q

Olol and anolol. Difference? Of Atenolol, Metoprolol and Propranolol, which would you use of anxiety such as stage fright?

A

Olol = beta-1 blocker
Anolol= beta-1 and beta-2 blocker

You would use propranolol, b/c it is a beta-1 and beta-2 agonist. Beta-1 blocks the heart rate from increasing, and beta- would keep the the hands from tremoring.

63
Q

What beta blocker would you use in low dose with cardiovascular disease with concomitant COPD?

A

A beta-1 blocker only (i.e. Metoprolol). Because is only blocks the beta-1 receptor site. If you used something like propranolol it would block beta-2 as well preventing bronchodilation.

64
Q

What are Fluoroquinolones? And what do they interact with?

A

all “floxacin” suffix antimicrobials (i.e. ciprofloxacin) interact with metals ( iron, calcium, magnesium and aluminum, Antacids contain metals), resulting in 60-70% reduction of floxacin dose. If prescribed these meds together, they must be taken at least 2 hours apart.

I.e. A person being treated with Ciproflaxacin for a UTI who also takes ferrous sulfate for anemia. The antibiotic won’t work if the drugs are taken together.

This also applies to tetrycycline, doxycycline, and minocycline

65
Q

Why is it important to take Nitrofuratoin (Macrobid) used in treatment of UTI’s and Sertraline (Zoloft) with food? How much food?

A

The absorption of these medications increases with food. An actual meal that will sit in the stomach for a while.

Macrobid - 200-400% increase in the drug that’s absorbed due to delayed emptying, increased time to dissolve

Zoloft - 33% increase

66
Q

What is the problem with drugs and enteral feedings? What are some examples of this?

A

Enteral feedings contain a lot of Calcuim (Ca+), other metals and proteins. Drugs can bind to these components potentially leading to decreased absorption or chelation.

Phenytoin suspension - 71.6% dose absorption reduction w/ continuous enteral feeding, so you would need to increase the dose.

FQ antimicrobials - floxacin suffix - 27-67% reduction

67
Q

How do you get around dose reduction with feeding tubes and enteral feeding?

A

You would have to stop the feeding, wait a couple of hours, then administer the med, flush the tube, and then wait another hour to start it back up again. This is not reasonable, so it would be more reasonable to increase the dose.

68
Q

What are Narrow therapeutic index (NTI) drugs? How do you know if they are NTI drugs? Examples of these drugs.

A

NTI - medications that a little bit is not quite enough, but 1.5 times is too much. You would know if they are NTI drugs because you would be required to check a therapeutic level of the drug to a the effect level of the drug (i.e. TSH, INR (how long it takes for the blood to clot), PTT (time for blood to clot too)

The 1st reason is to check the level of the drug in the system:
Examples: Theophylline (older drug to treat asthma, emphysema and chronic bronchitis), digoxin (antiarrhythmic and BP support), Tricyclic antidepressants (TCAs), Carbamazepine ( seizures, nerve pain , and bipolar disorder), Lithium (bipolar mania)

The 2nd reason is to check the effect of the medication:
Levothyroxine - TSH level
Warfarin - INR level
Heparin - PTT level

69
Q

What is a WTI drug?

A

There is a huge range in possible dose. For example, Fluoxetine (Prozac, SSRI) the dose can be 10 mg to 80 mg.

70
Q

What is Cytochrome P450 (CYP450)? Where are the biotransformation sites of CYP450?

A

The major process where drugs are converted from lipophilic to hydrophilic state. It is more common source of drug-drug interactions.

Biotransformation sites of CYP450:
Liver (1st major site), Kidney, Placenta, Lung, Plasma, Intestinal mucosa (2nd major site)

71
Q

What are the important enzymes to CYP450? And of these, which is the biggest one.

A

Isoenzymes are the basic enzymes involved in biotransformation of the drug (lipophilic to hydrophilic). The important ones are: CYP1A2, CYP2D6, CYP2C9, CYP2E1, CYP219, CYP34A.

CYP34A-because nearly 50% of all prescription meds are bio transcribed by this one

72
Q

What is a substrate? Examples of CYP3A4 substrates?

A

A medication substrate that is going to seek out a given isoenzyme so it can go from that lipophilic to that hydrophilic state.

Sildenafil (Viagra), atorvastatin, Simvastatin, alprazolam (Xanax), etc

About 50% of all prescription meds are CYP450 3A4 substrates

73
Q

What is an inhibitor? Examples

A

These are drugs or substances that block the activity of an isoenzyme, limiting substrate excretions, allowing an increase in substrate levels, with a possible risk of substrate induced toxicity.

Erythromycin and clarithromycin. If you use these inhibitors with a substrate, the substrate level will increase.

For example:
Clarithromycin plus Simvastatin - can result in statin induced rhabdomyolisis (the breakdown of muscle tissue, and releasing of these toxins into the blood. Can severely damage the kidneys)

Clarithromycin plus alprazolam- can increase sedation and fall risk

Use Doxycycline instead

74
Q

What is an inhibitor? Examples

A

These are drugs or substances that block the activity of an isoenzyme, limiting substrate excretions, allowing an increase in substrate levels, with a possible risk of substrate induced toxicity.

Erythromycin and clarithromycin. If you use these inhibitors with a substrate, the substrate level will increase.

For example:
Clarithromycin plus Simvastatin - can result in statin induced rhabdomyolisis (the breakdown of muscle tissue, and releasing of these toxins into the blood. Can severely damage the kidneys)

Clarithromycin plus alprazolam- can increase sedation and fall risk

Use Doxycycline instead

75
Q

What is an inducer? Example

A

This accelerated the activity of the isoenzyme so that the substrate is pushed out the exit pathway, leading to a reduction in substrate level.

St. John’s Wort - when used with a 3A4 substrate can lead to reduced target drug levels and diminished therapeutic effect, possible treatment failure

I.e. St. John’s Wort with COC (combined oral contraceptive) use - this leads to the offloading of estrogen/progestin, leads to excessive spotting, potential contraceptive failure

76
Q

What is an inducer? Example

A

This accelerated the activity of the isoenzyme so that the substrate is pushed out the exit pathway, leading to a reduction in substrate level.

St. John’s Wort - when used with a 3A4 substrate can lead to reduced target drug levels and diminished therapeutic effect, possible treatment failure

I.e. St. John’s Wort with COC (combined oral contraceptive) use - this leads to the offloading of estrogen/progestin, leads to excessive spotting, potential contraceptive failure

Since about 50% of all medications are 3A4 substrates, St. John’s Wort will interact with all of them (reducing the substrate level =less effective med)

77
Q

Ciprofloxacin is what type of inhibitor? What does it interact with and why?

A

Ciprofloxacin is a CYP 1A2 inhibitor, it interacts with caffeine because it is a CYP1A2 substrate. Therefore, when taking the drug the caffeine cannot be offloaded

78
Q

Ciprofloxacin is what type of inhibitor? What does it interact with and why?

A

Ciprofloxacin is a CYP 1A2 inhibitor, it interacts with caffeine because it is a CYP1A2 substrate. Therefore, when taking the drug the caffeine cannot be offloaded

79
Q

What type of inhibitor is grapefruit juice? What does it interact with?

A

Grapefruit juice is a modest 3A4 inhibitor. I will interact with Atorvastatin, Lovastatin, and Simvastatin (3A4 drugs). It will not interact with all statins because they are not all biotransformed by the CYP450 3A4 isoenzyme.

The result of this is that if you take a 3A4 statin with grapefruit juice is will increase the statin 12.0 fold. Grapefruit juice will stay in the system for 24 hours plus.

80
Q

What is Pharmacogenetics?

A

Drug absorption, distribution, metabolism and excretion. This influences dose requirements and/or adverse effects.

81
Q

Pharmacodynamics

A

Genetic influences. Drug targets (receptor sites, transporters, metabolic pathways, etc). Influences drug efficacy. Therefore this is the body’s effect of on the drug.

82
Q

Pharmacodynamics genetic examples:

A

50 yo women with hx of SSRI use: “I tried citalopram and it reallly did not do anything. Sertraline works great.” In this example, it is about Pharmacodynamics because it is about the functioning of the receptor site.

83
Q

Pharmacokinetics example:

A

40 yo women on paroxetine (Paxil) 10 mg/day:
“I can hardly keep my eyes open.” This is medicine is known to be mildly sedating, but not like this. This is likely a PK issue. The women is a poor metabolizer of CYP450 2D6 drugs. The woman is not offloading the drug, perhaps?

84
Q

Pharmacogenomic drug Atomoxetine (Strattera) for ADHD. 1st drug that the FDA made a pharmacogenomic advisory for.

A

Northern European - poor sleep

East African ancestry - no problem with sleep

85
Q

Northern European vs East African

A

NE is a CYP2D6 poor metabolizer, and cannot offload the drug in a timely manner. Therefore, the effects of the drug will stick around longer. That person is “sensitive” to everything.

EA is a CYP2D6 extensive metabolizer, and offloads the drug too quickly. The drug wears off quickly. Sometimes these people are labeled “drug seeking.”

86
Q

Northern European vs East African

A

NE is a CYP2D6 poor metabolizer, and cannot offload the drug in a timely manner. Therefore, the effects of the drug will stick around longer. That person is “sensitive” to everything.

EA is a CYP2D6 extensive metabolizer, and offloads the drug too quickly. The drug wears off quickly. Sometimes these people are labeled “drug seeking.”

87
Q

Cardiotoxic Drug- induced effects

A

QT prolongation and increasing the risk of torsade(s) de point (TdP) which is a type of ventricular tachycardia.

88
Q

What is the QT interval?

A

It is the depolarization of the ventricles, followed by the repolarization of the ventricles

89
Q

Symptoms of torsade(s) de pointe (TdP)

A

Palpatations, dizziness, lightheadedness (for shorter periods), Fainting/Syncope (for longer periods), sudden cardiac death

90
Q

Symptoms of torsade(s) de pointe (TdP)

A

Palpatations, dizziness, lightheadedness (for shorter periods), Fainting/Syncope (for longer periods), sudden cardiac death

91
Q

With most TdP episodes, the patient will revert spontaneously to a normal sinus rhythm. T/F?

A

True.

92
Q

What is relationship of the length of the QT interval?

A

The longer the QT interval the higher the risk for TdP, V Tach, and sudden cardiac death.

Males - borderline is 430-450 ms
prolonged is > 450 Ms

Females - borderline 450-470 ms
Prolonged > 470 ms

93
Q

Meds with a known risk for TdP

A

Risk is increase for TdP b/c that prolong the QT interval. Examples: Amiodarone (older antarhhythmic)
Risperidone
Haldol

KR (known risk), CR (conditional risk), PR (potential risk)

94
Q

The QT-prolonging risk noted with select abnormal electrolytes is reversible with the electrolyte disturbance is corrected. T/F?

A

True

95
Q

Diuretics and TdP

A

Diuretics increase the risk of TdP, largely due to the depletion of electrolytes.

Loop diuretics - more K+ depleting

Thiazide diuretics - more Na+ depleting, and Ca++ sparing

96
Q

The coupling of multiple electrolytes disturbances in an individual increases the TdP risk. T/F?

A

True

97
Q

Other risk factors for TdP w/ use of QT prolonging meds…

A

*Hepatic and renal dysfunction, impact the offloading of the med

*Bradycardia - the lower the heart rate the longer the QT interval

*Advancing age - a non-modifiable risk factor >60-65 yrs

*Methadone - substance use disorder

*Fluoroquinolones

98
Q

In a comparison study, which of the following Fluoroquinolones demonstrated the most QT prolonging effect?
A. Ciprofloxacin
B. Levofloxacin
C. Moxifloxacin

A

Moxifloxacin

99
Q

The Fluoroquinolone most often cited in TdP episodes is:

A. Ciprofloxacin
B. Levofloxacin
C. Moxifloxacin

A

Ciprofloxacin, being that it is most commonly subscribed (i.e. it is so widely prescribed for Cdiff)

100
Q

The Fluoroquinolone most often cited in TdP episodes is:

A. Ciprofloxacin
B. Levofloxacin
C. Moxifloxacin

A

Ciprofloxacin, being that it is most commonly subscribed (i.e. it is so widely prescribed for Cdiff)

101
Q

The risk of TdP w macrolide antibiotics (erythromycin, clarithromycin, azithromycin) is greater in females than in males.
T/F?

A

True, about twice the risk b/c they are biologically starting with a longer QT interval, their liver is smaller, etc.

102
Q

The risk of TdP w macrolide antibiotics (erythromycin, clarithromycin, azithromycin) is greater in females than in males.
T/F?

A

True, about twice the risk b/c they are biologically starting with a longer QT interval, their liver is smaller, etc.

Go with doxycycline

103
Q

Torsade de Pointe Treatment

A

*Withdraw the offending med
*Correct the electrolytes (Mag will be given to shorten the QT interval
*Cardiac support - override ventricular pacing, IV isoproterenol, defibrillation

104
Q

Parenteral procainamide or amiodarone should be used to control ventricular dysrhythmias in the person with TdP. T/F?

A

False - these specifically should not be used due to the QT prolonging effects of those two antiarrhythmics

Advanced Pharm (2 decks)

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