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Step 1 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What does the PNS innervate?

A

cardiac and smooth muscle, gland cells, nerve terminals. The nerves come from the medulla and use Ach at pre and postganglionic receptors

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2
Q

What receptors does the SNS use to innverate sweat glands?

A

Ach for pregang

Ach for postgangiolinic M receptor

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3
Q

What receptors does the SNS use to innervate cardiac and smooth muscle, gland cells, and nerve terminals?

A

ACh for pregang

NE for alpha and beta receptors

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4
Q

What receptors does the SNS use to innervate renal vasculature, and smooth muscle

A

Ach for pregang

Dopamine for D1 receptors

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5
Q

What receptors does the Somatic system use to innervate skeletal muscle?

A

The voluntary motor nerve uses ACH at N receptors

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6
Q

What aspects of SNS are innervated by cholinergic fibers?

A
  1. adrenal medulla

2. sweat glands

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7
Q

What does botulinum toxin do?

A

prevents release of neurotransmitters at all cholinergic terminals

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8
Q

How do Nicotinic Ach receptors work?

A

ligand gated NaK channels. Nn found in autonomic ganglia and Nm found in neuromuscular

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9
Q

How do Muscarinic Ach receptors work?

A

GPCR that act via 2nd messengers. 5 subtypes M1-M5

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10
Q

What does alpha one receptor do?

A

VC - increases vascular SM contraction; increases pupillary dilator muscle contraction (mydriasis); increases intestinal and bladder sphincter muscle contraction

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11
Q

What does alpha 2 receptor do?

A

VD - decreases sympathetic outflow, decreases insulin release, decreases lipolysis, and increases platelet aggregation

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12
Q

What does beta 1 receptor do

A

increases heart rate, increases contractility, increases renin release, and increases lipolysis

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13
Q

What does beta 2 receptor do?

A

VD, BD, and decreases uterine tone
increases heart rate, increases contractility, increases lipolysis, increases insulin release, ciliary muscle relaxation, increases aqueous humor production

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14
Q

What does M1 receptor do?

A

CNS and ENS

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15
Q

What are the sympathetic receptors?

A

Alpha 1 and 2; Beta 1 and 2. They use NE

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16
Q

What are the Parasympathetic receptors?

A

M1-M3 using Ach

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17
Q

What does the M2 receptor do?

A

decreases heart rate and contractility or atria at SA node

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18
Q

What does M3 receptor do?

A

increase exocrine gland secretions, increases gut peristalsis, increases bladder contraction, bronchoconstriction, increased pupillary sphincter muscle contraction (miosis), ciliary muscle contraction (accommodation)

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19
Q

What does the D1 receptor do?

A

relaxes renal vascular SM to improve renal blood flow

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20
Q

What does the D2 receptor do?

A

modulates transmitter release especially in the brain

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21
Q

What does the H1 receptor do?

A

increases nasal and bronchial mucus production, contraction of bronchioles, pruritus, pain

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22
Q

What does the H2 receptor do?

A

increases gastric acid secretion

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23
Q

What does V1 receptor do?

A

increases vascular CM contraction

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24
Q

What does V2 receptor do?

A

increases H20 permeability and reabsorption in the collecting tubules of kidney

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25
Q

What 2nd messengers are used for the autonomic drug receptors?

A 
Alpha 1  - q
Alpha 2 - i
Beta 1 - s
Beta 2 - s
M1 - q
M2 - i
M2 - q
D1 - s
D2 - i
H1 - q
H2 - s
V1 - q
V2 - s
  • HAVe 1M & M for Gq (H1,A1,V1,M1, and M3)
  • MAD 2’s for Gi (M2, A2, D2)
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26
Q

How does the Gq receptor work?

A

PLC breaks down lipids to PIP2
PIP2 broken down into IP3 and DAG
IP3 increases Ca from Sr, Ca activates CAM kinase
DAG activates PKC

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27
Q

How does the G2 receptor work?

A

AC increases cAMP
cAMP activates PKA
PKA increases Ca in heart, and inhibits myosin light chain kinase in smooth muscle

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28
Q

How does Gi receptor work?

A

inhibits AC so no increase in cAMP

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29
Q

What are all the steps that take place at the cholinergic nerve terminal?

A
  1. Choline enters the axon w/ Na coupled transport
  2. Choline + AcetylCoA combine via ChAT to form Ach
  3. Ach is packaged into vesicles
  4. Ca stimulates release of ACh from vesicles into NMJ
  5. Ach has 4 fates: AchE degradation, Diffuse away, bind to postsynaptic receptor, and bind to autorecepto
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30
Q

What step does hemicholinium inhibit?

A

The entry of Choline and Na coupled transport into the axon

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31
Q

What step does Vesamicol inhibit?

A

The packaging of Ach into vesicles

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32
Q

What does black widow spider toxin do at the cholinergic nerve terminal?

A

activates releases of Ach

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33
Q

What are the steps that take place at the noradrenergic nerve terminal?

A
  1. Tyr is coupled to Na to enter axon
  2. Tyr to NE synthesis pathway
  3. NE is packaged into vesicles
  4. NE is releases via Ca stimulation
  5. NE has 5 fates: binds to the postsynpatic receptor, reuptake, binds to Alpha 2 autoreceptor
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34
Q

How do you make NE from Tyr?

A
  1. Tyr to dopa via Try hydroxylase
  2. Dopa to dopamine via Dopa decarboxylase
  3. Dopamine to NE via Dopamine Beta Hydroxylase
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35
Q

What does metyrosine inhibit at the adrenergic terminal?

A

Tyr hydroxylase

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36
Q

How does reserpine inhibit at the adrenergic terminal?

A

Dopamine Beta hydroxlase

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37
Q

What inhibits reuptake of NE at the terminal?

A

cocaine, TCAs, and amphetamine

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38
Q

What do amphetamines do at the adrenergic terminal?

A

inhibit reuptake of NE and activate release of NE

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39
Q

What do guanethidine and bretylium do at the adrenergic terminal?

A

inhibit release of NE

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40
Q

What are the 2 enzymes that metabolize NE?

A
  1. COMT - methylates NE
  2. MAO - oxidizes NE
    - both make NE unusable and excrete in urine and increases levels of byproduct in serum
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41
Q

How is release of NE from a sympathetic nerve ending modulated?

A
  1. By NE itself acting on presynaptic alpha 2 autoreceptor
  2. Ach binds to M2 receptors and inhibits release of NE
  3. AII binds to its receptor and activates release of NE
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42
Q

What are some direct cholinergic agonists?

A

Bethanechol, carbachol, pilocarpine, methacholine

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43
Q

What does bethanechol do?

A
  • activates bowel and bladder SM
  • resistant to AchE
    used for post op ileus, neurogenic ileus, and urinary retention
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44
Q

What does carbachol do?

A
  • think of it as a carbon copy of Ach

- used in glaucoma, pupillary constriction, and relief of intraocular pressure

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45
Q

What does pilocarpine do?

A
  • contracts ciliary muscle of eye (open angled glaucoma), pupillary sphincter
  • resistant to AchE
    used for potent stimulator of sweat, tears, and saliva. Open and closed angle glaucoma
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46
Q

What does methacholine do?

A

stimulates muscarinic receptors in airway when inhaled

- used for challenge test for Asthma dx

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47
Q

What are some indirect agonists or anticholinesterases?

A 
Neostigmine
Pyridostigmine
Edrophonium - Tensilon test
Physostigmine
Donepezil/Galantamine/Rivastigmine
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48
Q

What is the function of the indirect cholinergic agonists?

A

they increases endogenous Ach by inhibiting AchE

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49
Q

What is neostigmine used for?

A

Post op and neurogenic ileus, urinary retention, myasthenia gravis, reversal of NMJ blockade via succinycholine
- has NO CNS penetration

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50
Q

What is pyridostigmine used for?

A
  • myasthenia gravis (long acting),

- NO CNS penetration

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51
Q

What is edrophonium used for?

A

for Dx of myasthenia gravis b/c it’s short acting

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52
Q

What is physostigmine used for?

A
  • Anticholinergic toxicity (crosses BBB)

- fixes atropine overdose

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53
Q

What is donepezil/galantamine/rivastigmine used for?

A

Alzheimer’s disease

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54
Q

What is a caution you should take w/ all the cholinomimetic agents?

A

watch for exacerbation of COPD, asthma, and peptic ulcers when giving to susceptible patients

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55
Q

What is cholinesterase inhibitor poisoning typically do to and how does it present?

A
  • organophosphates such as parathion that irreverisibly inhibit AchE
  • causes DUMBBELSS
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56
Q

What is the treatment for organophosphate overdose?

A
  1. antidote = atropine

2. regenerator of active AchE = pralidoxime

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57
Q

What does DUMBBELSS stand for

A
  1. Diarrhea
  2. Urination
  3. Miosis
  4. Bronchospasm
  5. Bradycardia
  6. Excitation of skeletal muscle and CNS
  7. Lacrimation
  8. Sweating
  9. Salivation
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58
Q

What are the muscarinic antagonists?

A
  1. atropine, homatropine, tropicamide
  2. benztropine
  3. scopolamine
  4. ipratropium, tiotropium
  5. oxybutynin
  6. glycopyrrolate
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59
Q

What do atropine, homatropine, and tropicamide do?

A

produce mydriasis and cycloplegia

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60
Q

What does benztropine do?

A

treatment for parkinson’s (park my benz)

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61
Q

What does scopolamine do?

A

motion sickness so acts at the CNS

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62
Q

What does ipratropium and tiotropium do?

A

treats COP and asthma

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63
Q

What does oxybutynin do?

A

reduces urgency in mild cystitis and reduces bladder spasms

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64
Q

What other drugs can be used to reduce urgency?

A

tolterodine, darifenacin, solifenacin, trospium

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65
Q

What does glycopyrrolate do?

A

use parenteral for preop to reduce airway secretions

orally to stop drooling and peptic ulcers

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66
Q

What is atropine really used for?

A

to treat bradycardia and for ophthalmic applications

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67
Q

What effect does atropine have on eyes, airway, stomach, gut, and bladder?

A
  1. eyes - increase pupil dilation, cycloplegia
  2. airways- decreases secretions
  3. stomach - decrease acid secretion
  4. gut - decrease motility
  5. bladder- decrease urgency
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68
Q

What happens w/ atropine overdose?

A

it blocks DUMBBELSS

  • increases body temp (due to decreased sweating)
  • rapid pulse
  • dry mouth
  • dry, flushed skin
  • cycloplegia
  • constipation
  • disorientation
  • Can cause acute angle-closure glaucoma in elderly, urinary retention in men w/ prostatic hyperplasia and hyperthermia in infants
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69
Q

What other meds can cause anticholinergic side effects?

A
  1. 1st gen H blockers - diphenhydramine, doxylamine, chlorpheniramine
  2. traditional neuroleptics
  3. tricyclic antidepressants
  4. amantadine
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70
Q

What are the direct sympathomimetics?

A
  1. E
  2. NE
  3. Isoproterenol
  4. Dopamine
  5. Dobutamine
  6. Phenylephrine
  7. Albuterol, salmeterol, terbutaline, levalbuterol
  8. Ritodrine
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71
Q

What are the indirect sympathomimetics?

A
  1. amphetamine
  2. ephedrine
  3. cocaine (reuptake inhibitor)
    - all of these are indirect general agonists
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72
Q

MOA of epinephrine?

A

stimulates all receptors A1/2 and B1/2

  • at low doses it has no effect on BP
  • at high doses the alpha1 receptors overpower B2 so there is an increase in BP
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73
Q

When is epinephrine use?

A

anaphylaxis, glaucoma, asthma, hypotension

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74
Q

MOA of NE?

A

Alpha receptors&raquo_space; B1

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75
Q

When is NE used?

A

hypotension but decreases renal perfusion

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76
Q

MOA of isoproterenol?

A

B1 and B2 agonists

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77
Q

When is isoproterenol used?

A

torsade de pointes (tachycardia decreases QT interval), bradyarrhythmias ( but can worsen ischemia)

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78
Q

MOA of dopamine?

A

low dose - D1 receptor to increase renal blood flow
Med Dose - B1/2 receptor agonists
High dose - Alpha1/2 receptor agonists

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79
Q

When is dopamine used?

A

shock (renal perfusion), heart failure, inotropic and chronotropic

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80
Q

MOA of dobutamine?

A

Beta 1 agonists

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81
Q

When is dobutamine used?

A

heart failure, cardiac stress testing, inotropic and chronotropic

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82
Q

MOA of phenylephrine

A

Alpha 1&raquo_space; Alpha 2 so increases BP

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83
Q

When is phenylephrine used?

A

hypotension, ocular procedures (mydriatic), rhinitis (decongestant)

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84
Q

MOA of albuterol, salmeterol, terbutaline, and levalbuterol

A

B2&raquo_space; B1 agonists

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85
Q

When is albuterol used?

A

acute asthma

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86
Q

When is salmeterol used?

A

long term asthma or COPD control

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87
Q

when is terbutaline used?

A

to reduce premature utering contractions

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88
Q

MOA of ritodrine?

A

B2 agonists

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89
Q

When is ritodrine used?

A

reduces premature uterine contractions

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90
Q

What is amphetamine used for?

A

narcoplepsy, obesity, and ADHD

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91
Q

What is ephedrine used for?

A

nasal decongestion, urinary incontinence, hypotenion

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92
Q

What can cocaine do?

A

causes vasoconstriction and local anesthesia.

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93
Q

What drug is avoided w/ cocaine overdose?

A

B-Blockers because it can lead to an unopposed alpha 1 activation and extreme HTN

94
Q

What happens to HR and BP with NE use?

A

increases BP due to Alpha 1 and there is a reflexive bradycardia (decreased HR)

95
Q

What happens to HR and BP w/ E use?

A

increase in BP and HR because all four activated

96
Q

What happens to HR and BP w/ isoproterenol use?

A

little alpha effect but causes B2 mediated VD resulting in decrease BP and increased HR through B1 and reflex activity.

Widened pulse pressure as well

97
Q

What are some sympathoplegic drugs?

A

clonidine and alpha-methydopa, guanfacine

98
Q

MOA of clonidine and alpha-methyldopa

A

Alpha 2 agonists - decrease central sympathetic outflow

- decrease BP due to vasodilation

99
Q

Clonidine use?

A

low half life, used as a sleep aid for ADHD, used for HTN especially w/ renal disease

100
Q

When is alpha-methyldopa use?

A

HTN in pregnancy

101
Q

What are nonselective alpha blockers?

A

Phenoxybenzamine (IR)

Phentolamine (R)

102
Q

What are some adverse side effects w/ phenoxybenzamine and phentolamine?

A

orthostatic hypotention and reflexive tachycardia

103
Q

When is phenoxybenzamine used?

A

pheochromocytoma

104
Q

When is phentolamine used?

A

givens to pts on MAO inhibitors who eat tyramine-containing foods (aged)

105
Q

What are alpha1 selective blockers?

A

prazosin, terazosin, doxazosin, tamsulosin

106
Q

When are the alpha 1 selective blockers given?

A

HTN, urinary retention in BPH

107
Q

What are adverse side effects of alpha 1 selective blockers?

A

1st dose orthostatic hypotension, dizziness, headache

108
Q

What is tamsulosin a special alpha 1 selective blocker?

A

it works only at the prostate and has no effect on BP so safe to give to pts who have only BPH symptoms

109
Q

What is an alpha 2 selective blocker?

A

mirtazapine

110
Q

When is mirtazapine used and what are some side effects?

A

used - depression

ADE - sedation, increases serum cholesterol, and increases appetite

111
Q

What are beta blockers used for?

A
  1. Angina - decreased heart rate and contractility, resulting in decreased O2 consumption
  2. MI - decreased mortality
  3. SVT - decreased AV conduction velocity
  4. HTN - decreased CO and decreased renin secretion (due to B1 receptor blockade on JGA cells)
  5. CHF - slows progression of chronic failure
  6. Glaucoma (timolol) - decreases secretion of aqueous humor
112
Q

What are ADE of beta blockers?

A

impotence, exacerbation of asthma, CV effects such a bradycardia, AV block, CHF; CNS effects such as seizures, sedation, sleep alterations. Use w/ caution w/ diabetics b/c they can mask symptoms of low glucose

113
Q

What are B1 selective antagonists?

A

acebutolol, betaxolol, esmolol (short acting), atenolol, metoprolol
- they are advantageous in pts w/ comorbid pulmonary dz

114
Q

What are nonselective B antagonists?

A

Propranolol, timolol, nadolol, pindolol

115
Q

What are nonselective alpha and beta antagonists?

A

Carvediolol and labetaolol

116
Q

What are partial Beta agonists

A

Pindolol and acebutolol

117
Q

What are the Beta blockers of choice for MI

A

carvedilol and metoprolol

118
Q

What is the Beta blocker of choice for thryoid toxicosis?

A

propranolol

119
Q

What Beta blocker is given for esopheal varicies?

A

nadolol

120
Q

What do beta blockers do when treating aortic dissection?

A
  1. decrease BP

2. decrease slope of rise of BP

121
Q

For Michaelis-Menten kinetics, what is Vmax?

A
  • Vmax is directly related to enzyme concentration
122
Q

For Michaelis-Menten kinetics, what is km?

A
  • concentration of substrate at 1/2Vmax

- inversely related to affinity of enzyme for its substrate

123
Q

What is the y and x intercept for Lineweaver Burk plot?

A
  1. X-intercept: -1/km

2. Y-intercept: 1/vmax

124
Q

What is the slope of the LIneweaver Burk plot?

A

km/Vmax

125
Q

What happens when the y-intercept increases on the Lineweaver Burk plot?

A
  • Vmax decreases
126
Q

What happens when you go further right on the Lineweaver Burk plot?

A
  • the greater the Km and lower the affinity
127
Q

What effect do competitive inhibitors have on Michaelis Menten kinetics?

A
  1. Vmax is unchanged
  2. Km is increased
    - can be overcome by increasing substrate concentration
    - binds to the active site of the enzyme
    - decreases potency
128
Q

What effect do noncompetitive inhibitors have on Michaelis Menten kinetics?

A
  1. Vmax is decreased
  2. Km is unchanged
  3. Efficacy is decreased
  4. doesn’t resemble substrate, doesn’t bind to active site, and can’t be overcome by increasing substrate concentration
129
Q

What is bioavailability?

A
  • fraction of administered drug that reaches systemic circulation unchanged
  • for an IV dose = 100%
  • Orally: F typically 100% to incomplete absorption and first pass metabolism
130
Q

What is the volume of distribution of a drug?

A
  • theoretical fluid volume required to maintain the total absorbed drug amount at plasma concentration
131
Q

What is the Vd equation?

A

= amount of drug in the body/plasma drug concentration

132
Q

What can alter the Vd of plasma protein bound drugs

A
  • liver and kidney disease (decreased protein binding, increased Vd)
133
Q

What part of the body has a low Vd?

A
  • blood: usually contains large/charged molecules; plasma protein bound
134
Q

What part of the body has a medium Vd?

A

ECF: contains small hydrophilic molecules

135
Q

What part of the body has high Vd?

A

All tissue: contains small lipophilic molecules especially if bound to tissue protein

136
Q

What is the definition of half life?

A
  • time required to change the amount of drug in the body by 1/2 during elimination (or constant infusion)
137
Q

How many half lives does it take for a drug to reach steady state?

A
  • 4-5: 94% of drug at 4 half lives
    1. after 1 half life: 50% of drug is remaining
    2. after 2 half lives: 25% remaining
    3. after 3 half lives: 12.5% remaining
    4. after 4 half lives: 6.25% remaining
138
Q

what is the equation for half life?

A

= 0.7 *Vd/CL

139
Q

What is the definition of clearance?

A
  • relates the rate of elimination to the plasma concentration
  • may be impaired w/ defects in cardiac, hepatic, or renal function
140
Q

What is the loading dose equation

A

LD= VD*Css

141
Q

What is the maintenance dose equation?

A

MD = CL * Css

142
Q

What happens to maintenance and loading dose in liver and kidney disease?

A

maintenance dose is decreased but loading dose is unchanged

143
Q

T or F. Time to steady state depends on dosing frequency or size.

A

False. Depends only on half life

144
Q

What is zero order elimination?

A

rate of elimination is constant regardless of amount of drug eliminated per unit time

  • capacity limited elimination
  • Plasma concentration of drug decreases linearly w/ time
145
Q

What are examples of drugs that undergo zero order elimination?

A

PEA
Phenytoin
EtOH
ASA

146
Q

What is first order elimination?

A

aka Flow-dependent elimination

  • rate of elimination is directly proportional to the drug concentration – constant fraction of drug eliminated per unit time
  • plasma concentration of drug decrease exponentially w/ time
147
Q

What types of drugs are trapped in urine and cleared quickly?

A
  • ionized species

- neutral forms can be reabsorbed

148
Q

What are examples of weak acid drugs?

A

Phenobarbital
MTX
ASA

149
Q

What type of environments are weak acids trapped in?

A

basic = makes weak acids ionized

150
Q

How can you treat weak acid overdose?

A
  • bicarbonate - traps weak acids in urine
151
Q

What are examples of weak base drugs?

A

Amphetamines

152
Q

How are weak bases trapped in urine?

A

acidic environment

153
Q

How can you treat weak base overdose?

A

Ammonium chloride

154
Q

What type of rxns take place in phase 1 drug metabolism?

A

Reduction, oxidation, hydrolysis w/ CYP450

155
Q

What kind of metabolites form after first phase metabolism?

A
  • slightly polar, water soluble metabolites

often still active

156
Q

Who often loses phase 1 metabolism abilities?

A

Geriatric pts

157
Q

What types of rxns take place in phase 2 drug metabolism?

A

Conjugation - glucuronidation, acetylation, sulfation

158
Q

What kind of metabolites form after phase 2 metabolism?

A
  • very polar, inactive metabolites

- renally excreted

159
Q

What is efficacy?

A

maximal effect a drug can produce = Vmax

160
Q

What are some highly efficacious drugs?

A
  • analgesic (pain) meds, antibiotics, antihistamines, decongestants
  • partial agonists have less efficacy than full agonists
161
Q

What is potency?

A
  • amount of drug needed for a given effect

- increased potency leads to increased affinity for receptor

162
Q

What are some highly potent drugs?

A
  • chemotherapeutic, antihypertensive, and antilipid drugs
163
Q

What effect do competitive antagonsts have on potency or efficacy?

A
  • shift curve to right which decrease potency

- there is no change w/ efficacy

164
Q

What effect do noncompetitive antagonists have on potency or efficacy?

A
  • shift curve down which decreases efficacy

-

165
Q

What effect do partial agonists have on potency or efficacy?

A
  • acts at same site as full agonist but w/ reduced maximal effect = decreases efficacy
  • potency is a different variable and can be increased or decreased
166
Q

What is therapeutic index?

A
  • measurement of drug safety

= LD50/ED50 (median lethal dose/median effective dose)

167
Q

What types of drugs have a higher therapeutic index?

A
  • safer drugs
168
Q

What are examples of drugs w/ lower therapeutic index?

A

digoxin, lithium, theorphylline, and warfarin

169
Q

What is therapeutic window?

A
  • measure of clinical drug safety. range of minimum effective dose to minimum toxic dose
170
Q

What is the antidote/treatment for the following toxicities?

  1. Acetaminophen
  2. Salicylates
  3. Amphetamines
  4. ACE inhibitors, organophosphates
  5. Antimuscarinic, anticholinergic agents
A
  1. N-acetylcystein (replenishes GSH)
  2. NaHCO3 (alkalinizes urine), dialysis
  3. NH4Cl (acidify urine)
  4. atropine, pralidoxime
  5. Physostimgine salicylate, control hyperthermia
171
Q

What is the antidote/treament for the following toxicities?

  1. Beta blocerks
  2. Digitalis
  3. Iron
  4. Lead
  5. Mercury, arsenic, gold
A
  1. glucagon
  2. normalize K, Lidocaine, anti-dig Fab graments, Mg
  3. Deferoxamine, defersairox
  4. CaEDTA, dimercaprol, succimer, penicillamine
  5. dimercaprol, succimer
172
Q

What is the antidote/treament for the following toxicities?

  1. copper, arsenic, gold
  2. cyanide
  3. Methmeoglobin
  4. CO
  5. Methanol, ethylene glycol (antifreeze)
A
  1. penicillamine
  2. nitrite + thiosulfate, hydoxocobalamin
  3. methylene blue, Vitamin C
  4. 100% O2, hyperbaric O2
  5. Fomepizole > ethanol, dialysis
173
Q

What is the antidote/treament for the following toxicities?

  1. Opiods
  2. Benzodiazepines
  3. TCAs
  4. Heparin
  5. Warfarin
A
  1. naloxone/naltrexone
  2. Flumazenil
  3. NaHCO3 (plasma alkalinization)
  4. Protamine
  5. Vit K, Fresh frozen plasma
174
Q

What is the antidote/treament for the following toxicities?

  1. tPA, streptokinase, urkokinase
  2. theophylline
A
  1. aminocaproic acid

2. beta blocker

175
Q

What category of drugs are the following endings?

  1. azole
  2. cillin
  3. cycline
  4. navir
  5. triptan
A
  1. antifungal
  2. penicillin
  3. antiobiotic, protein synthesis inhibitor - tetracycline
  4. protease inhibitor
  5. 5HT agonists (migraine) : sumatriptan
176
Q

What category of drugs are the following endings?

  1. ane
  2. caine
  3. operidol
  4. azine
  5. barbital
A
  1. inhalational general anesthetic - halothane
  2. local anesthetic - lidocaine
  3. butyrophenone (neuroleptic) - haloperidol
  4. Typical antipsychotic - phenothiazine (neuroleptic, antiemetic) - chlorpromazine, thioridazine
  5. barbiturate - phenobabital
177
Q 
What category of drugs are the following endings?
1. zolam
2 azepam
3. etine
4. ipramine
5. triptyline
A
  1. benzodiazepine
  2. benzodiazepine
  3. SSRI - fluoxetine
  4. TCA
  5. TCA
178
Q

What category of drugs are the following endings?

  1. olol
  2. terol
  3. zosin
  4. oxin
  5. pril
A
  1. beta blocker
  2. beta agonist
  3. alpha 1 antagonists
  4. cardiac glycosides (inotropic agent)
  5. ACE inhibitor
179
Q

What category of drugs are the following endings?

  1. afil
  2. tropin
  3. tidine
  4. ivir
  5. navir
A
  1. erectile dysfunction
  2. pituitary hormone
  3. H2 antagonists
  4. Neuraminidase inhibitor
  5. protease inhibitor
180
Q

What category of drugs are the following endings?

  1. thromycin
  2. chol
  3. curium or curonium
  4. stigmine
  5. dipine
A
  1. Macrolide abx
  2. cholinergic agonist
  3. non depolarizing paralytic
  4. AChE inhibitor
  5. dihydropyridine CCB
181
Q

What category of drugs are the following endings?

  1. dronate
  2. glitazone
  3. prazole
  4. prost
  5. ximab
  6. zumab
A
  1. bisphosphonate
  2. PPAR- gamma activator
  3. proton pump inhibitor
  4. PG analog
  5. chiimeric monoclonal ab
  6. humanized monoclonal ab
182
Q

What drugs cause coronary vasospasm?

A

cocaine, sumatriptan, ergot alkaloids

183
Q

what drugs cause cutaneous flushing?

A

vancomycin, adenosine, niacin, CCB (VANC)

184
Q

what drugs cause dilated cardiomyopathy?

A

doxorubicine and daunorubicin

185
Q

What drugs cause torsades de pointes?

A

Class III (sotalol) and Class IA (DQP), macrolides, antipsychotics, and TCAs

186
Q

What can cause adrenocortical insufficiency?

A

HPA suppression secondary to glucocorticoid withdrawal

187
Q

What drugs can cause hot flashes?

A

tamoxifen

clomiphene

188
Q

What drugs can cause hyperglycemia?

A

Tacrolimus, protease inhibitors, niacin, HCTZ, Beta blockers, corticosteroids.
- taking pills necessitates having blood checked

189
Q

What drugs can cause hypothyroidism?

A

lithium, amiodarone, sulfonamide

190
Q

What drug causes acute cholestatic hepatitis and jaudice?

A

erythromycin

191
Q

What drugs can cause diarrhea?

A

Metformin, erthryomycin, colchicine, orlistat, acarbose

192
Q

What drugs can cause focal to massive hepatic necrosis?

A

Halothane, amanita phalloides (death cap mushroom), valproic acid, acetaminophen
- liver HAVAc

193
Q

What drug causes hepatitis?

A
  • INH
194
Q

What drugs cause pancreatitis?

A

didanosine, corticosteroids, alcohol, valproic acid, azathioprine, diuretics
- Drugs Causing A Violent Abdominal Distress

195
Q

What drugs cause pseudomembranous colitis?

A

Clindamycin, ampicillin, cephalosporins

- predispose to superinfxn by resistant C difficile

196
Q

What drugs cause agranulocytosis?

A

Dapson, clozapine, carbamazepine, colchicine, methimazole, PTU
- Drugs CCCrush Myeloblasts and Promyelocytes

197
Q

What drugs cause aplastic anemia?

A

Carbamazepine, methimazole, NSAIDS, benzene, chloramphenicol, PTU
- Can’t Make New Blood Cells Properly

198
Q

What drugs can direct coombs positive hemolytic anemia

A

Methyldopa and penicillin

199
Q

What drugs cause gray baby syndrome?

A

chloramphenicol

200
Q

What drugs cause hemolysis in G6PD deficiency?

A

INH, sulfonamides, dapsone, primaquine, aspirin, ibuprofen, nitrofurantoin

201
Q

What causes megaloblastic anemia?

A

Phenytoin, MTX, Sulfa drugs

202
Q

What causes thrombocytopenia?

A

heparin, cimetidine

203
Q

What causes thrombotic complications

A

OCPs

204
Q

What causes fat redistribution?

A

protease inhibitors and glucocorticoids

205
Q

What causes gingival hyperplasia?

A

Phenytoin, verapamil, cyclosporine, nifedipine

206
Q

What causes hyperuricemia (gout)?

A

Pyrazinamide, thiazides, furosemide, niazin, cyclosporine

207
Q

What causes myopathy?

A

Fibrates, niacin, colchicine, hydroxychloroquine, IFN alpha, penicillamine, statins, glucocorticoids

208
Q

What causes osteoporosis

A

corticosteroids and heparin

209
Q

What causes photosensivity

A

Sulfonamides, amiodarone, tetracyclines, and 5FU

210
Q

What causes Rash (SJS)?

A

anti-epileptic drugs (ethosiximide, carbamazepine, lamotrigine, phenytoin, phenobarbital)
- allopurinol, sulfa drugs, penicillin

211
Q

What causes SLE like symptoms?

A

sulfa drugs, hydralazine, INH, procainamide, phenytoin, etanercept

212
Q

What causes teeth discoloration?

A

tetracyclines

213
Q

What causes tendonitis, tendon rupture, and cartilage damage

A

fluroquinolones

214
Q

What causes cinchonism?

A

quinidine and quinine

215
Q

What causes parkinson like syndrome?

A

Antipsychotics, Reserpine, Metoclopramie

216
Q

What causes seizures?

A

INH (vit B6 deficiency), Bupropion, Imipenem/cilastatin, Tramadol, Enflurane, Metoclopramide
- I BITE My tongue

217
Q

What causes tardive dyskinesia

A

antipsychotics and metoclopramide

218
Q

What causes diabetes insipidues?

A

lithium and demeclocycline

219
Q

What causes fanconi syndrome?

A

expired tetracycline

220
Q

What causes hemorrhagic cystits?

A

cyclophosphamide and ifosfamide

221
Q

What causes interstitial nephritis?

A

Methicillin, NSAIDS, furosemide

222
Q

What causes SIADH?

A

Carbamazepine, cyclophosphamide, SSRIs

223
Q

What causes pulmonary fibrosis?

A

Bleomycin, Amiodarone, Busulfan, MTX

224
Q

What causes antimuscarinic reactions?

A

Atropines, TCAs, H1 blockers, Antipsychotics

225
Q

What causes disulfiram like reaction?

A

Metronidazole, certain cephalosporins, griseofulvin, procarbazine, 1st gen sulfonylureas

226
Q

What causes nephrotoxicity/ototoxicity?

A

Aminoglycosides, vanocmyin, loops diuretics, cisplatin

227
Q

What are you CYP inducers?

A
  1. Chronic alcohol use
  2. Modafinil
  3. St John’s wort
  4. Phenytoin
  5. Phenobarbital
  6. Nevirapine
  7. Rifampin
  8. Griseofulvin
  9. Carbamazepine
228
Q

What are CYP substrates?

A 
Anti-epileptics
Anti-depressants
Anti - psychotics
Anethetics
Theophylline
Warfarin
Statins
OCPs
229
Q

What are CYP inhibitors?

A
  1. Acute alcohol abuse
  2. Gemfibrozil
  3. Ciprofloxacin
  4. INH
  5. Grapefruit juice
  6. Quinindine
  7. Amiodarone
  8. Ketoconazole
  9. Macrolides
  10. Sulfonamides
  11. Cimetidine
  12. Ritonavir
230
Q

What are you sulfa drugs?

A

Probenecid, furosemide, acetazolamide, celecoxib, thiazides, sulfonamide abx, sulfasalazine, sulfonylureas

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