29 April wk7-E Flashcards

1
Q

What is a rare but significant SE of statin therapy?

A

Myopathy: muscle pain and elevated serum CK

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2
Q

What cytochrome enzyme is at the heart of the interaction between some macrolides and statins?

A

CYP 3A4
Erythromycin inhibits this and statins are metabolized by it
Co-administration causes high levels of statins leading to toxicity including myopathy

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3
Q

CYP 450 inducers

A

Carbamazepine, Phenobarbital, Phenytoin, Rifampin, Griseofulvin

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4
Q

CYP 450 inhibitors

A

Cimetidine, Ciprofloxacin, Erythromycin, Azole antifungals, Grapefruit juice, Isoniazid, Ritonavir (protease inhibitors)

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5
Q

Carbamazepine and P450

A

inducer

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6
Q

Grapefruit juice and P450

A

inhibitor

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7
Q

Isoniazid and P450

A

inhibitor

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8
Q

Griseofulvin and P450

A

inducer

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9
Q

Ritonavir and P450

A

inhibitor

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10
Q

Phenobarbitol and P450

A

inducer

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11
Q

Phenytoin and P450

A

inducer

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12
Q

Erythromycin and P450

A

inhibitor

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13
Q

Cimetidine and P450

A

inhibtor

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14
Q

Ciprofloxacin and P450

A

inhibitor

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15
Q

Rifampin and P450

A

inducer

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16
Q

Azole antifungals and P450

A

inhibitor

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17
Q

Which macrolides affect CYP 3A4 and which do not?

A

Erythromycin and Clarithromycin inhibit

Azithromycin does not

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18
Q

Inhibitors of CYP 3A4

A

Erythromycin, Ketoconazole, Cyclosporine, HIV protease inhibitors, Grapefruit Juice

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19
Q

If patient is on a statin, what is a common drug interaction and which statin is best to avoid this?

A

Statins are metabolized by CYP 3A4
Interactions with drugs inhibiting it:
Erythromycin, Ketoconazole, Cyclosporine, HIV protease inhibitors, Grapefruit Juice
Best statin to avoid this is Pravastatin because it is metabolized by another enzyme

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20
Q

How does doxorubicin create cardio-toxicity?

A

Creates free-radicals that damage the heart leading to dilated cardiomyopathy

21
Q

Best method of preventing doxorubicin cardiomyopathy

A

Dexrazoxane

Iron-chelating agent that prevents formation of free radicals

22
Q

What is the general treatment approach for sustained ventricular arrhythmias after and MI?

A
Amiodarone first
If needed, Lidocaine or another class IB antiarrhythmic agent
23
Q

Amiodarone

A

Class III antiarrhythmic agent, blocks K+ channels prolonging AP duration and QT interval

24
Q

MOA of Digoxin and uses

A

Enhances vagal tone on the heart and slows conduction through AV node
Useful for arrhythmias originating above AV node but not for ventricular arrythmias

25
Q

Which of the antiarrhythmic agents is best suited for treating an abnormal rhythm originating from ischemic or damaged myocardium in the ventricle?

A

Class IB drugs because they bind preferentially to inactive channels whereas class IA drugs bind to open Na channels

26
Q

Clonidine is generally used for HTN, but can also be used for what?

A

ADHD in patients who failed other stimulant therapy

27
Q

What features help identify a Tourette’s tic from myoclonus?

A

Tics can be temporarily or partially suppressed and they are preceded by an urge to move. Myoclonus has neither feature.

28
Q

What is an essential tremor and how is it treated?

A

Intention tremor often of both hands appearing in middle adulthood
Treated with Propranolol

29
Q

Fluphenazine

A

Dopamine antagonist that can treat Tourette’s

30
Q

Alteplase, Tenecteplase

A

Fibrinolytics used to treat ACS to lyse clots
Bind to Fibrin in the clot and activate Plasminogen to Plasmin to lyse the Fibrin clot
Common SE is hemorrhage

31
Q

What is a classic sign of aortic dissection?

A

Widened mediastinum on x-ray

32
Q

What vessels are most affected by NO? Why does this help angina?

A

Large veins

Helps angina by redistributing blood to the veins and decreases preload on the heart and thereby decreases O2 demand

33
Q

Why are ACEI’s protective for the kidneys in DM?

A

DM leads to increased glomerular pressures leading to damage over time.
ACEI’s dilate the efferent arteriole decreasing filtering pressures and protecting the glomeruli.
ARB’s have a similar effect

34
Q

As DA administration goes from low to high dose, what receptors are activated and what effects?

A

Low: D1–vaso-D in renal and splanchnic vasculature
Med: B1–increased cardiac effects
High: alpha1–vasoconstriction to renal and visceral vasculature

35
Q

Dihydroergotamine

A

Treat acute migraine

May induce spastic angina by stimulating alpha and serotonin receptors

36
Q

Phentolamine

A

Non-selective alpha blocker

37
Q

Possible triggers of Prinzmetal’s angina?

A

Tobacco, cocaine, amphetamines, dihydroergotamine, statins

38
Q

Sodium Nitroprusside

A

IV vasodilator

39
Q

MOA for Nitrates

A

Converted in endothelial cells to NO that diffuses into SmM cells and activates guanylate cyclase to produce cGMP. cGMP reduces intracellular Ca reducing action of myosin light chain kinase and dephosphorylating myosin light chain causing muscle relaxation and vasodilation

40
Q

Describe events leading to muscle contraction starting with Ca release from ER.

A

Ca binds Troponin on Actin and moves Tropomyosin to reveal binding sites
Myosin binds Actin when it hydrolyzes ATP to ADP + P Power Stroke after releasing ADP+P
Myosin remains attached until ATP binds

41
Q

Indications for benzodiazepine use

A

Anxiolytic, sedation, anticonvulsant, muscle relaxant

42
Q

Chlorpheniramine

A

1st gen antihistamine

Lots of SE’s because not only blocks H receptors but many others

43
Q

Benzos should be avoided in conjunction with?

A

Alcohol, barbiturates, neuroleptics, 1st gen antihistamines

44
Q

Name 1st gen antihistamines and why they are so sedating

A
Diphenhydramine
Promethazine
Hydroxyzine
Chlorpheniramine
1st gen cross BBB and accumulate in CNS blocking H receptors and this causes sedation
45
Q

Bad SE of carbamazepine

A

Agranulocytosis or aplastic anemia

46
Q

MOA of Gabapentin

A

Blocks presynaptic Ca channels to reduce release of NT’s to treat seizures

47
Q

What seizure drug blocks PRESYNAPTIC Na channels?

A

Phenytoin

48
Q

Are GABA receptors pre or post synaptic?

A

Post synaptic

49
Q

When should you suspect malignant hyperthermia syndrome and what is the mechanism?

A

Patient recently under general anesthesia with an inhaled anesthetic presenting with fever and muscle rigidity, myoglobinemia, HTN, hyperkalemia, and elevated CK
Inherited predisposition where ryanodine receptors release too much Ca upon stimulation by anesthetics leading to rapid reuptake and use of ATP in sarcoplasmic reticulum leading to heat production and eventually damage to muscle and rhabdomyolysis
Dantrolene (muscle relaxant) treats by decreasing Ca release