Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What receptors does the SNS use to innverate sweat glands?

A

Ach for pregang

Ach for postgangiolinic M receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

Ach for pregang

Dopamine for D1 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A

The voluntary motor nerve uses ACH at N receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What aspects of SNS are innervated by cholinergic fibers?

A
  1. adrenal medulla

2. sweat glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does botulinum toxin do?

A

prevents release of neurotransmitters at all cholinergic terminals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do Nicotinic Ach receptors work?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do Muscarinic Ach receptors work?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does alpha 2 receptor do?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does beta 1 receptor do

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does M1 receptor do?

A

CNS and ENS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the sympathetic receptors?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the Parasympathetic receptors?

A

M1-M3 using Ach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What does the M2 receptor do?

A

decreases heart rate and contractility or atria at SA node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does the D1 receptor do?

A

relaxes renal vascular SM to improve renal blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What does the D2 receptor do?

A

modulates transmitter release especially in the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What does the H1 receptor do?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What does the H2 receptor do?

A

increases gastric acid secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What does V1 receptor do?

A

increases vascular CM contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What does V2 receptor do?

A

increases H20 permeability and reabsorption in the collecting tubules of kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How does Gi receptor work?

A

inhibits AC so no increase in cAMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What step does hemicholinium inhibit?

A

The entry of Choline and Na coupled transport into the axon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What step does Vesamicol inhibit?

A

The packaging of Ach into vesicles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

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

A

activates releases of Ach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What does metyrosine inhibit at the adrenergic terminal?

A

Tyr hydroxylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How does reserpine inhibit at the adrenergic terminal?

A

Dopamine Beta hydroxlase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What inhibits reuptake of NE at the terminal?

A

cocaine, TCAs, and amphetamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What do amphetamines do at the adrenergic terminal?

A

inhibit reuptake of NE and activate release of NE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What do guanethidine and bretylium do at the adrenergic terminal?

A

inhibit release of NE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are some direct cholinergic agonists?

A

Bethanechol, carbachol, pilocarpine, methacholine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What does methacholine do?

A

stimulates muscarinic receptors in airway when inhaled

- used for challenge test for Asthma dx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are some indirect agonists or anticholinesterases?

A 
Neostigmine
Pyridostigmine
Edrophonium - Tensilon test
Physostigmine
Donepezil/Galantamine/Rivastigmine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is the function of the indirect cholinergic agonists?

A

they increases endogenous Ach by inhibiting AchE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is pyridostigmine used for?

A
  • myasthenia gravis (long acting),

- NO CNS penetration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is edrophonium used for?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is physostigmine used for?

A
  • Anticholinergic toxicity (crosses BBB)

- fixes atropine overdose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is donepezil/galantamine/rivastigmine used for?

A

Alzheimer’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is the treatment for organophosphate overdose?

A
  1. antidote = atropine

2. regenerator of active AchE = pralidoxime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are the muscarinic antagonists?

A
  1. atropine, homatropine, tropicamide
  2. benztropine
  3. scopolamine
  4. ipratropium, tiotropium
  5. oxybutynin
  6. glycopyrrolate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What do atropine, homatropine, and tropicamide do?

A

produce mydriasis and cycloplegia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What does benztropine do?

A

treatment for parkinson’s (park my benz)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What does scopolamine do?

A

motion sickness so acts at the CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What does ipratropium and tiotropium do?

A

treats COP and asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What does oxybutynin do?

A

reduces urgency in mild cystitis and reduces bladder spasms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What other drugs can be used to reduce urgency?

A

tolterodine, darifenacin, solifenacin, trospium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What does glycopyrrolate do?

A

use parenteral for preop to reduce airway secretions

orally to stop drooling and peptic ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is atropine really used for?

A

to treat bradycardia and for ophthalmic applications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are the indirect sympathomimetics?

A
  1. amphetamine
  2. ephedrine
  3. cocaine (reuptake inhibitor)
    - all of these are indirect general agonists
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

When is epinephrine use?

A

anaphylaxis, glaucoma, asthma, hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

MOA of NE?

A

Alpha receptors&raquo_space; B1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

When is NE used?

A

hypotension but decreases renal perfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

MOA of isoproterenol?

A

B1 and B2 agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

When is isoproterenol used?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

When is dopamine used?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

MOA of dobutamine?

A

Beta 1 agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

When is dobutamine used?

A

heart failure, cardiac stress testing, inotropic and chronotropic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

MOA of phenylephrine

A

Alpha 1&raquo_space; Alpha 2 so increases BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

When is phenylephrine used?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

MOA of albuterol, salmeterol, terbutaline, and levalbuterol

A

B2&raquo_space; B1 agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

When is albuterol used?

A

acute asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

When is salmeterol used?

A

long term asthma or COPD control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

when is terbutaline used?

A

to reduce premature utering contractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

MOA of ritodrine?

A

B2 agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

When is ritodrine used?

A

reduces premature uterine contractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What is amphetamine used for?

A

narcoplepsy, obesity, and ADHD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What is ephedrine used for?

A

nasal decongestion, urinary incontinence, hypotenion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What can cocaine do?

A

causes vasoconstriction and local anesthesia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?

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?

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?

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

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

Step 1 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions