3/15 pharm Flashcards

1
Q

Clearance can be impaired w/defects in which systems?

A

cardiac, renal, hepatic.

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2
Q

Clearance

-equation:

A
Cl = (rate of elim of drug)/(plasma drug conc.) 
Cl = (Vd)*(Ke)
Cl = (Q)*(Er)
Q = flow to that organ (ie. liver)
Er = extraction ratio
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3
Q

Loading dose

-equation

A

Loading dose = (Cp)(Vd) / (F)

Cp = target plasma concentration at steady state
F = bioavailability
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4
Q
Maintenance dose (MD)
-equation
A

MD = (Cp)(Cl)(t) / F

t = dosage interval (time between doses), if not administered continuously.
*If continuous, leave t out. You will also know its IV so F = 1. B/c only IV is continuous.

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5
Q

In liver or renal disease, does maintenance dose inc. or dec.?

A

Dec.

-less being cleared, so less dose needed.

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6
Q

Which drugs follow zero-order elimination?

-mnemonic?

A

-Phenytoin, Ethanol, and Aspirin (at high or toxic concentrations).

-PEA. (A pea is round, shaped like the “0” in
“zero-order.”)

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7
Q

Capacity-limited elimination

-0 or 1st order?

A

0 order elim.

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8
Q

Flow-dependent elimination

-0 or 1st order?

A

1st order elim.

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9
Q

Phase I drug metabolism

A

P450 system

-Reduction, oxidation, hydrolysis.

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10
Q

Phase II drug metabolism

A

Conjugation (Glucuronidation, Acetylation, Sulfation)

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11
Q

Which is most common P450 enzyme?

A

CYP3A4 = most common

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12
Q

Name 3 drugs that might cause trouble in a slow acetylator.

-which would also have a bimodal pop. distribution.

A
  • hydralazine, isoniazid, procainamade

* HIP: its not hip to be a slow acetylator.

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13
Q

What kind of antagonist is ketamine?

A

-ketamine (noncompetitive antagonist) on NMDA receptors.

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14
Q

Therapeutic index:

-equation:

A

TI = Toxic dose/Effective dose

*high therapeutic index is good b/c that means theres a big difference btwn toxic and effective doses.

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15
Q

Whats good, a high or low therapeutic index?

A

High.

-Safer drugs have higher TI values.

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16
Q

Is the therapeutic index the same as therapeutic window?

A

No, b/c the therapeutic window would never extend all the way until the toxic dose.

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17
Q

Some receptors that respond to autonomic neurotrasmitters/drugs receive NO nerve innervation (must get ligand through blood).
-can you name these uninnervated autonomic receptors?

A
  • muscarinic receptors on endothelium of blood vessels
  • adrenoreceptors on apocrine sweat glands
  • alpha-2 and beta adrenoreceptors in blood vessels.
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18
Q

para/pre, sym/pre: all release what?

A

ACh

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19
Q

All ganglia have what type of receptor?

A

Nicotinic: ligand-gated ion channels.

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20
Q

Do all sym/post release NE?

A

NO

  • adrenal medulla releases NE and epi.
  • sym/post release ACh that innervate sweat glands & piloerector muscles. These = sympathetic cholinergic.
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21
Q

sympathetic cholinergic

A

sym/post that releases ACh

-innervate sweat glands & piloerector muscles.

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22
Q

All glands have what receptors on them?

A

muscarinic

-even sweat glands that have sym/post innervation: these sym/posts dump ACh, not NE (sympathetic cholinergic).

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23
Q

adrenal medulla & sweat glands = part of sym nervous system but are innervated by _______ fibers.

A

cholinergic

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24
Q

Nicotinic ACh receptors

-what type of receptor is it?

A

-ligand-gated Na/K channels.

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25
Q

which receptors are more sensitive to activation, alpha or beta?

A

beta

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26
Q

Epi: acting more on alpha1 or beta2?

  • low dose =
  • high dose =
A
  • low dose - acts more on beta-2
  • high dose - acts more on alpha-1

*remember, beta-receptors are more sensitive.

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27
Q

Ciliary muscle innervation:

A
  • muscarinic
  • its NOT dual innervated.

*if there is an effect on accomodation, its a muscarinic (agonist or antagonist) drug

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28
Q

Cycloplega = what is it, what can cause it?

A

paralysis of ciliary muscles = M-antagonist

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29
Q

Gs => inc. cAMP => PKA => phosphorylates MLC kinase.

-whats the result?

A

smooth muscle relaxation

-hence beta-2 (Gs) causing smooth muscle relaxation in lungs.

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30
Q

Hemicholinium

  • mech:
  • use:
A
  • Prevents reuptake of choline so you have less in nerve terminal so you make less ACh and release less ACh.
  • NO CLINICAL USE.
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31
Q

NMJ

-what kind of receptor?

A

nicotinic, ACh.

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32
Q

Reserpine

A
  • inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicle packaging and release.
  • used in huntingtons.
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33
Q

guanethidine

A
  • like botulinum but for NE.

* not clinically used

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34
Q

Where do you find AChE?

A
  • AChE is only found in the synpatic cleft.
  • Not everywhere you find a M or N receptor.

*that means AChE inhibitor can not vasodilate b/c endothelial cell M3 receptors are not innervated = no synaptic cleft.

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35
Q

Can AChE inhibitors vasodilate?

A
  • AChE is only found in the synpatic cleft.
  • Not everywhere you find a M or N receptor.

*that means AChE inhibitor can not vasodilate b/c endothelial cell M3 receptors are not innervated = no synaptic cleft.

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36
Q

M agonists

-give pattern of what type of lung disease?

A

-obstructive, like COPD.

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37
Q

What an effect you can see via cholinomimetic drugs that you dont see w/parasym. nerve stimulation?

A

sweating

-b/c sweat glands have sym innervation but release ACh at the sweat glands M3 receptor.

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38
Q

Is bethanechol resistant or sensitive to AChE?

A
  • resistant to AChE.

- not the same exact structure as ACh so its not broken down by AChE!

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39
Q

Someone at movie and gets intense pain in their eyes.

A

-They’re in a dark room, their pupils dilate, the angle gets smaller, and this precipitates their glaucoma

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40
Q

Administer _______ to Cystic Fibrosis pt to get sweat so you can do sweat test

A

pilocarpine

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41
Q

Pilocarpine is resistant or sensitive to AChE?

A

resistant, just like bethanechol.

-not exactly the same structure as ACh so AChE doesn’t break it down.

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42
Q

myasthenic crisis

A

not enough ACh

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43
Q

cholinergic crisis

A

too much ACh

-can resemble myasthenic crisis

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44
Q

Which receptors do AChE inhibitors act at?

A

muscarinic & nicotinic

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45
Q

atropine OD

-which AChE inhibtor can you give?

A
  • physostigmine bc atropine gets into CNS and so does physostigmine.
  • physostigmine = a tertiary amine = not charged, lipid soluble.
46
Q

Myasthenia Gravis

  • how was it historically Dx?
  • how is it Dx now?
A

-historically: edrophonium.
-Myasthenia now diagnosed by anti-AChR Ab (anti-
acetylcholine receptor antibody) test.

47
Q

What to watch out for before giving cholinomimetic?

A

COPD, asthma, peptic ulcers.

48
Q

parathion

A

organophosphate

-irreversible AChE inhibtor.

49
Q

sarin

A

organophosphate
-irreversible AChE inhibtor.

*nerve gas

50
Q

organophosphate poisoning

-Tx:

A

-atropine (competitive inhibitor) + pralidoxime (regenerates AChE if given early).

51
Q

why isn’t atropine enough for organophosphate poisoning tx?

A

Atropine is a muscarinic antagonist.

  • it is NOT a nicotinic antagonist!
  • Nicotinic toxicity is treated by regenerating active cholinesterase w/pralidoxime.
52
Q

Which one gets desensitized, muscarinic or nicotinic?

A

nicotinic

  • muscarinic does NOT get desensitized.
  • succinylcholine acts on nicotinic.
53
Q

Glycopyrrolate

  • mech:
  • use:
A

muscarinic antagonist

  • Parenteral: preoperative use to reduce airway secretions.
  • Oral: drooling, peptic ulcer.
54
Q

Atropine

-uses:

A

Used to treat bradycardia & for ophthalmic applications.

55
Q

ACh

-its excitation of skeletal muscle & CNS mediated via which receptor?

A

nicotinic

56
Q

Jimson weed

-what effects?

A
  • atropine poisoning if you consume Jimson weed.

- aka Belladonna alkaloids.

57
Q

hexamethonium, mecamylamine

  • what are they?
  • use?
A
  • nicotinic (ganglion) blockers
  • They will be used in problems b/c they block baroreflex changes in heart rate.
  • If you use these you WIPE OUT the ANS, b/c all ganglia use Nn receptors.
  • just remember what the predominant tone on the system is at rest, and cancel out that tone.
58
Q

What resting tone does our heart have?

A

PARA

59
Q

Epi

-low dose effects:

A
  • B/c beta receptors are more sensitive, you will get primarily a beta response with a low dose of epi.
  • THIS IS KEY. At low dose acts like isoproterinol (nonselective beta agonist).
60
Q

Epi

-medium dose

A
  • alpha-1 gets involved.
  • alpha-1 and beta-2 antagonize each other.
  • so at medium dose epi looks like a beta-1 agonist. (like DOPUTAMINE, a selective beta-1 agonist)
61
Q

Epi

-high dose

A
  • alpha-1 will PREDOMINATE.
  • You will vasoconstrict and get inc. BP.
  • You will get tachy OR reflex brady. This looks just like NE.

*you can not distinguish NE and high dose EPI in cardiac parameters.

62
Q

NE vs high dose epi.

-differences:

A
  • If it bronchodilates, inc. lipolysis, inc. glycogenolysis, or inc. gluconeogenesis; then it MUST be EPI,
  • beta-2 does these things and NE does NOT act on beta-2.
63
Q

How do you unmask beta-2 action of epi?

A
  • give an alpha-1 blocker.

- alpha 1 is opposing beta-2.

64
Q

Can NE, under any circumstances, reduce BP?

A

NO

65
Q

Can epi, under any circumstances, reduce BP?

A

Yes, but only at low dose where beta-2 is activated but alpha-1 is not.

66
Q

Isoproterenol

-what does it do to pulse pressure?

A

nonselective beta-agonist.

  • inc inotropy = inc systolic.
  • inc vasodilation = dec diastolic
  • inc. pulse pressure.
67
Q

cardiac stress testing

-which drug is used?

A

dobutamine

68
Q

terbutaline

  • mech:
  • use:
A
  • beta-2 agonist

- reduce premature uterine contractions

69
Q

beta agonist

-can they cause hypo or hyperkalemia?

A

hypokalemia

-inc activity of Na/K pump which brings K into cells.

70
Q

name some mobile pool releasers

A

tyramine, amphetamine, ephedrine.

71
Q

Ephedrine

  • mech:
  • use:
A
  • releases stored catecholamines.

- Nasal decongestion, urinary incontinence, hypotension.

72
Q

Cocaine intox

-should you give beta-blockers?

A
  • No.
  • you never want to risk having unopposed alpha-1 action by blocking beta-2.
  • can get hypertensive crisis.
73
Q

amphetamine & cocaine

-predominantly the inc. in which chemical leads to addiction?

A

dopamine

74
Q

Clonidine

-uses

A

-ADHD, severe pain, and a variety of off-label indications (e.g., ethanol and opioid withdrawal).

75
Q

Whats the only anti-HTN drug w/approved analgesic use?

A

clonidine

76
Q

phentolamine vs phenoxybenzamine

-which one is irreversible?

A

phenoxybenzamine = irreversible

-both =nonselective alpha blockers

77
Q

Give ________ to patients on MAO inhibitors who eat

tyramine-containing foods

A

phentolamine

78
Q

Can tamulosin also be used for HTN like other alpha-1 blockers?

A

-No, tamulosin more specific for smooth muscle in urinary tract.

79
Q

Mirtazapine

  • mech:
  • use:
  • s/e:
A
  • alpha-2 blocker
  • depression
  • inc appetite, inc serum cholesterol, sedation.
80
Q

Beta-blocker OD

-tx:

A

glucagon

  • beta-1 & beta-2 both = Gs, they inc. cAMP.
  • glucagon also = Gs, so it inc. cAMP as well.
81
Q

beta-blockers

-can you use in a diabetic?

A

-Despite theoretical concern of masking hypoglycemia in diabetics, benefits likely outweigh risks; not contraindicated

82
Q

beat-blocker

-s/e:

A
  • Impotence
  • CV adverse effects
  • CNS adverse effects (seizures, sedation, sleep alterations)
  • dyslipidemia (metoprolol)
  • asthmatics/COPDers (may cause exacerbation)
83
Q

beta-1 selective blockers

-mnemonic?

A

A to M

84
Q

non-selective beta-blockers

-mnemonic?

A

N to Z

85
Q

pindolol

-why is it better to use in asthmatics?

A
  • partial non-selective agonist.

- it will also have some sympathetic effects, like slightly bronchodilating for instance.

86
Q

beta-blockers

-which ones are non-selective ALPHA & beta blockers?

A
  • carvedilol, labetalol

* dont end w/”olol”.

87
Q

Nebivolol

-what is unique about it?

A

Nebivolol combines cardiac-selective β1-adrenergic blockade with stimulation of β3-receptors, which activate nitric oxide synthase in the vasculature.

88
Q

Which drugs can cause cutaneous flushing?

-mnemonic?

A

VANC
-Vancomycin, Adenosine, Niacin, Ca2+ channel
blockers.

89
Q

Which drugs can cause Hyperglycemia?

-mnemonic?

A

Taking Pills Necessitates Having Blood Checked

  • Tacrolimus
  • Protease inhibitors
  • Niacin
  • HCTZ
  • β-blockers
  • Corticosteroids
90
Q

Which drugs can cause hypothyroidism?

A

Lithium, amiodarone, sulfonamides

91
Q

Which drugs can cause diarrhea?

-mnemonic?

A

Might Excite Colon On Accident

  • Metformin
  • Erythromycin
  • Colchicine
  • Orlistat
  • Acarbose
92
Q

Lanugo

  • what is it?
  • what disease is it seen in?
A

Fine body hair

-anorexia nervosa

93
Q

Parotitis

-bulimia or anorexia?

A

Both

-there is binge/purge type of anorexia.

94
Q

Does calcium bind troponin or tropomyosin?

A

-troponin C

95
Q

Prominent U wave

-hypo or hyperkalemia?

A

hypokalemia

96
Q

what happens to haptoglobin-Hb complex?

A

its hepatically cleared

97
Q

Winged scapula

-common causes?

A
  • mastectomy surgery & accidentally nick the long thoracic nerve.
  • stab wounds.
98
Q

clavicular fx

-where in clavicle?

A

middle 1/3

99
Q

ACL & PCL

-connect which two bones?

A

tibia & femur

100
Q

ACL & PCL

-which one more commonly injured?

A

ACL

101
Q

ACL or PCL

-which one attaches to medial condyle of femur?

A

PCL

*anterior lateral surface of medial epicondyle of femur.

102
Q

ACL or PCL

-which one attaches to the lateral condyle of femur?

A

ACL

*post. medial lateral femoral condyle.

103
Q

Where on femur does PCL attach?

A

medial condyle of femur.

104
Q

Where on femur does ACL attach?

A

lateral condyle of femur.

105
Q

Septic arthritis

  • usually due to what?
  • how do u treat it?
A

gonococcus

-ceftriaxone

106
Q

How does colchicine reduce acute inflammation of gouty arthritis?

A

inhibits neutrophil migration into inflamed areas.

107
Q

Which vitamin D is created upon exposure to sun?

A

D3 = cholecalciferol

108
Q

Major cause of morbidity in sarcoidodis?

A

pulm. fibrosis.

109
Q

medial or lateral cruciate ligament attached to its corresponding meniscus?

A

MCL.

110
Q

Ligation of sup. thyroid art:

-which nerve at risk?

A

-external branch of superior laryngeal n.

111
Q

Ligation of inf. thyroid art:

-which nerve at risk?

A

-recurrent laryngeal n.