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Drugs- Basic High Yield Stuff for Boards > Pharmacology 1 > Flashcards

Pharmacology 1 Flashcards

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1
Q

Zero Order Elimination Drugs(4)

A

“PEA” ( a pea is round- shaped like the “0”)

  1. Phenytoin
  2. Ethanol (causes hangover!!)
  3. Aspirin(at high or toxic concentrations)
  4. cisplatin

Constant amount of drug elimination per unit time

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2
Q 
Weak acids(3) eliminated in urine
How treat overdoses?
A
  1. Phenobarbital
  2. Methotrexate
  3. Aspirin

Trapped in basic environment.
Treat overdose w/ Bicarbonate

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3
Q 
Weak bases(2) eliminated in urine
How treat overdoses?
A
  1. amphetamines
  2. TCAs

Trapped in acidic environment
Treat overdose w/ Ammonium chloride

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4
Q

Notoriously slow Acetylators

Significance

A

Asians»White/Af. Am

increase drug concentration–> increase drug reactions

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5
Q

Drugs with lower Therapeutic Index(4)

Whats the formula for Therapeutic Index?

A
  1. Digoxin
  2. Lithium
  3. Theophylline
  4. Warfarin (monitor PT/INR)

TI= ToxD50/ED50
(in animal studies= LD50/ED50)

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6
Q

Diazepam is an agonist at GABA-R

What effect does Flumazenil have on the GABA receptor?

A

Competitive antagonist (resembles substrate)

  • decrease potency, no change in efficacy
  • can be overcome with increased concentration of agonist substrate
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7
Q

NE is an agonist at alpha-R

What effect does phenoxybenzamine have on the alpha-R?

A

Noncompetitive antagonist

  • decrease efficacy
  • can’t be overcome by increased agonist substrate concentration
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8
Q

Morphine is a full agonist at the u-R.

What effect does buprenorphine have on the u-R?

A

partial agonist

  • acts at same site as full agonist but with lower efficacy
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9
Q 
Sypathetic G-protein type:
a1
a2
B1
B2
B3
A 
a1- q
a2-i
B1-s
B2-s
B3-s
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10
Q 
Parasympathetic G-protein type:
M1
M2
M3
What type of receptor is nAch-R
A

M1-q
M2-i
M3-q

nAch-R: ligand-gated Na/K channel (Nn and Nm)

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11
Q

Dopamine G-protein type:
D1
D2

A

D1-s

D2-i

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12
Q

Histamine G-protein type:
H1
H2

A

H1-q

H2-s

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13
Q

Vasopressin G-protein type:
V1
V2

A

V1-q

V2-s

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14
Q

Mnemonic for G-proteins

A

“After QISSeS(kisses), you get a QIQ(kick) out of SIQ(sick) SQS (super qinky sex)”

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15
Q

Which receptors are Gs linked?

A

B1-3, D1, H2, V2

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16
Q

Which receptors are Gi linked?

A

M2, a2, D2

“MAD 2’s”

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17
Q

Which receptors are Gq linked?

A

H1, a1, V1, M1, M3

“HAVe 1 M&M”

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18
Q

Hemicholium (experimental rat drug):

MOA

A

inhib choline transporter

prevent choline uptake into cholinergic axon

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19
Q

Vesamicol(experimental rat drug):

MOA

A 
inhib vAchT
(prevent Ach transport into vesicle in cholinergic axon terminal)
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20
Q

Botulium:

MOA

A

inhib SNAP-25

prevent Ach vesicle fusion for NT release

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21
Q

Metyrosine:

MOA

A

inhib tyrosine hydroxylase

prevent tyrosine–>DOPA

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22
Q

Reserpine (anti-pysch):
MOA
Important adverse

A 
Inhib VMAT 
(prevent Dopamine transport into Noradrenergic vesicle)
* decrease BP b/c prevents NE storage-->loose a1 vasoconstriction
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23
Q

Bretylium & Guanethidine (never used):

MOA

A

inhib Noradrenergic vesicle fusion at synapse –> inhib NT release

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24
Q

Amphetamine & ephedrine:

MOA

A

increase fusion of vesicles at Noradrenergic synapse–> increase release of all Monoamines

  • Amphetamines use NET to enter presynaptic terminal, and use the VMAT to enter vesicle. This displaces NE from vesicle. Once NE reaches threshold concentration w/in terminal–>reverse NET and NE is expelled into Synaptic Cleft contributing to increased NE observed
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25
Cocaine & TCAs & Amphetamine: | MOA
inhib reuptake transporter & inhib DA transporter | -->many monoamine's reuptake inhibited--> Feel great and jacked up
26
ACEi effect on adrenergic-R in axon
inhib AT-II binding to "Release-modulating receptors" | -->prevent release of monoamines
27
Precursor to Tyramine (enzyme for conversion) Enzyme which degrades Tyramine Foods which contain Tyramine
- Tyrosine-->tyramine via tyrosine decarboxylase - degraded by MAO - Cheese and Wine
28
Describe D-D Tyramine & MAOi interaction
1. Excess tyramine enters presynaptic vesicles and displaces other NTs 2. increase active presynaptic NTs 3. increase NT diffusion in cleft 4. increase sympathetic stimulation 5. -->HYPERTENSIVE CRISIS
29
``` Buproprion: MOA Use (2) Adverse(4) Sexual effect? ```
-increase Ne/DA via unknown MOA Uses: 1. depression 2. smoking cessation 1. Tachycardia 2. insomnia 3. HA 4. seizures in ANOREXICS * NO SEXUAL SIDE EFFECTS
30
``` Describe the C. botulinum toxin: type of toxin MOA site of action Where do adults get toxin Where do babies get toxin Antidote ```
-heat-labile toxin (protease) cleaves SNARE -Toxin inhib Ach release at NMJ-->Flaccid paralysis -Adults= inject preformed toxin -Babies= ingest Honey spores-->Floppy Baby Tx: Anti-toxin
31
Can Dopamine cross BBB? | Can L-DOPA cross BBB?
No | Yes
32
Direct Cholinergic agonists: | Name (4)
1. BethaneCHOL 2. CarboCHOL 3. MethaCHOLine 4. Pilocarpine
33
``` Bethanechol: Action Effects Use (3) ACHE effect ```
"Bethany, call me to activate bowels and bladder" 1. Post-op ileum 2. neurogenic ileus (common in DM) 3. urinary retention - resistant to AchE
34
Carbachol: Description Use (1)
CARBon copy of AcetylCHOLine | 1. open-angle glaucoma (constricts pupil and relieves IOP)
35
Methacholine: MOA Use (1)
Stimulates mAchR in airways when inhaled | 1. Asthma challenge test (measure FEV1 and FVC)
36
Pilocarpine: MOA ACHE effect Use(4)
- Contract CiliaryM. and pupillary Sphincter - resistant to AchE 1. stim Sweat, tears, & saliva 2. Open angle glaucoma (ciliary m.) 3. Closed angle glaucoma (sphincter m.) 4. Sjogrens (xerostomia) "you cry, drool, and sweat on your PILOw"
37
another term for anti cholinesterase | overall effect
- indirect agonists | - increase Ach
38
3 anticholinesterases used to treat Alzheimers
1. Donepezil 2. Galantamine 3. Rivastigmine
39
Edrophonium: Use Half-life
Diagnosis Myesthenia Gravis historically (now diagnosed by anti-ache Ab test) very short acting
40
Neostigmine: Use(3) CNS penetration
1. post-op/neurogenic ileum & urinary retention (like bethanachol 2. Myasthenia gravis 3. Reversal of NMJ blockade (post-op) No CNS penetration (quaternary amine) "Neo CNS"
41
Physostigmine: Use CNS penetration
"PHYsostigmine 'PHYxes' atropine overdose 1. Anticholinergic toxicity CNS penetration (tertiary amine)
42
Pyridostigmine: Use CNS penetration Half-life
"PyRIDostiGMine gets RID of Myasthenia Gravis" 1. Myasthenia gravis (increase muscle strength) No CNS penetration (quaternary amine) Long-acting
43
2 drugs used to treat Myasthenia Gravis
1. NEOstiGMine 2. PyRIDostiGMine (neither cross BBB)
44
2 Contra/Caution for all cholinomimetic agents (both direct and indirect agonists)
1. COPD/Asthma exacerbation | 2. Peptic Ulcers (in susceptible patients)
45
Symptoms of Cholinesterase inhibitor poisoning | Who is the typical patient on Boards? Typical cause?
``` Farmer with organophosphate poisoning like parathion "DUMBBELSS" Diarrhea/N Urination Miosis Bronchospasm Bradycardia Excitation of Sk.Muscle/CNS Lacrimation Sweat Salivation -->Respiratory failure if untreated ```
46
Antidote for cholinesterase inhibitor poisioning (2)
1. atropine (competitive inhib) | 2. pralidoxime (regenerates AchE if given early)
47
3 drugs which produce Mydriasis and Cycloplegia
1. atropine 2. homatropine 3. tropicamide
48
Muscarinic antagonist to treat | Parkinson's/ Acute dystonia
Benztropine | "park my Benz"
49
2 uses for Glycopyrrolate
"'GI'copyR(resp)rolate" parenteral: pre-op reduction of airway secretions oral: drooling and peptic ulcers No cross BBB
50
2 muscarinic antagonists to treat Irritable bowel Synd
1. Hyoscyamine | 2. Dicyclomine
51
2 muscarinic antagonists to treat COPD/Asthma
1. Ipratropium 2. tiotropium "TIO PRAys to breath"
52
4 drugs to treat Overactive bladder/urge incontinence
" On the Darn Toilet, Sorry" 1. Oxybutynin 2. Trospium 3. Darifenacin 4. Tolterodine 5. Solifenacin
53
Drug to treat motion sickness
Scopolamine
54
``` Atropine Effects: Eye Airway Stomach Gut Bladder ```
``` dilate/cycloplegia decrease secretions in airway decrease stomach acid secretions decrease GI motility decrease urgency in cystitis ```
55
Atropine: Use Adverse
Blocks DUMBBeLSS in cholinesterase inhib poisoning. DOES NOT BLOCK 'E-EXCITATION OF SK.MUSCLE/CNS WHICH AR MEDIATED BY nACH-R 1. Hot as a hare (M3) 2. Dry as a bone (M3) 3. Red as a beet (M3) 4. Blind as a bat (M3) 5. Mad as a hatter (M1 in CNS
56
Atropine: | CONTRA (3)
1. Elderly (can cause Closed angle glaucoma via mydriasis) 2. Men with BPH (urinary retention) 3. infants (hyperthermia)
57
Effect of Jimson weed (Datura) | Chemicals causing effect (2)
Gardener's pupil MYDRIASIS due to plant alkaloids (ENLARGED FROM SPHINCTER PARALYSIS) 1. scopolamine 2. atropine
58
Albuterol/ Salmeterol: Receptor target Use
B2>B1 (COPD/Asthma) Albuterol (SABA) Slmeterol (LABA)
59
Dobutamine: Receptor target Use (2)
B1>B2, a 1. HF (inotropic>chronotropic) 2. cardiac stress testing
60
Dopamine: Receptor target Use (3) Dose dependent actions
D1=D2>B>a 1. unstable bradycardia 2. HF 3. shock ``` Low dose (Beta)-->inotropic and chronotropic effects High dose (alpha)-->vasoconstriction ```
61
Epinephrine: Receptor target Use(3) Dose dependent actions
B2/B1>a (methyl group addition from Ne-->Epi) 1. Anaphylaxis 2. Asthma 3. Open-angle glaucoma High dose-->alpha effect predominate
62
Fenoldopam: Receptor target Use(4) Potential adverse(2)
D1 ("FenolDOPAM") 1. post-op hypertension 2. hyeprtensive crisis 3. vasodiltor (coronary, peripheral, renal, and splanchnic) 4. promote naturesis Potentially cause hypotension and tachycardia
63
Isoproterenol: Receptor target Use potential adverse
B1=B2 1. electrophysiologic eval of tachyarrhythmias potentially can worsen ischemia
64
Midodrine: Receptor target Use(2) potential adverse
a1 1. autonomic insuff. 2. postural hypotension potentially exacerbate spine hypertension
65
Norepinephrine: Receptor target Use(2)
a1>>a2>B1 1. hypotension 2. septic shock
66
Phenylephrine: Receptor target Use(3)
a1>a2 1. hypotension (vasoconstriction) 2. ocular procedures (mydriatic) 3. rhinitis (decongestant)
67
Amphetamine: MOA(3) Use (3)
Indirect general agonist, reuptake inhib, release stored catecholamines 1. Narcolepsy 2. obesity 3. ADHD
68
Cocaine: MOA (2) Use(1)
Indirect general agonist, reuptake inhib 1. vasoconstrictor/ local anesthetic for Rhinoplasty
69
Cocaine: What should never be given if cocaine intoxication is suspected? Why?
BB | -->can lead to unopposed a1 activation-->extreme HTN
70
Ephedrine: MOA(2) Use (3)
indirect general agonist, releases stored catecholamines 1. Nasal decongestion 2. Urinary incontinence 3. Hypotension
71
Which dopamine receptor is generally in PNS? CNS? **exceptions to this rule do exist
PNS--> D1 (perpheral, coronary, renal, splanchnic circulations for widespread vasodilation) CNS-->D2
72
Low dose DA stimulates? | High dose DA stimulates?
``` low= D1 (vasodilation) high= a1(vasoconstriction) ```
73
Clonidine/ Guanfacine: MOA Use(3) Adverse (5)
a2-agonist (Gi) Use: 1. hypertensive urgency 2. ADHD 3. Tourette Adverse: 1. CNS depression 2. Bradycardia 3. Hypotension 4. Resp depression 5. Miosis
74
alpha-methyldopa: MOA Use (1) Adverse (2)
a2-agonist (Gi) Use: HTN in pregnancy Adverse: 1. Direct Coombs (autoimmune hemolytic anemia) 2. SLE-like syndrome (check anti-histone) ("Lupus is SHIPP-E, but not included)
75
Effects of a2 stimulation
Sympatholytic: 1. decrease SNS 2. decrease insulin release 3. decrease lipolysis 4. decrease aqueous humor prod. in eye 5. increase platelet aggregation
76
Nonselective a-blockers: Name (2) which is reversible vs. irreversible? Shared adverse (2)
1. Phenoxybenzamine- irreversible 2. Phentolamine- reversible "PhenTOLamine is TOLtally reversible" 1. Orthostatic Hypotension 2. Reflex tachycardia (via baroreceptors)
77
Phenozybenzamine: MOA Use(1)
nonselective, irreversible a-blocker 1. Pheochromocytoma (pre-op) to prevent Hypertensive crisis * classic question on boards!!!
78
Phentolamine: MOA Use(1)
nonselective, reversible a-blocker "PhenTOLamine is TOLtally reversible" 1. Give to patient on MAOi's who eats tyramine containing foods (prevent hypertensive crisis) * classic question on boards!!!
79
``` Prazosin Terazosin Doxazosin Tamsulosin: MOA Use (3) Adverse(3) ```
a1 selective blockers (all end in '-osin') 1. BPH urinary symptoms 2. PTSD ('P'razosin) 3. HTN (except tamsulosin Adverse: 1. 1st dose orthostatic hypotension 2. Dizzy/HA
80
Mirtazapine: MOA Use (1) & How Adverse (3)
a2 selective blocker Treat Depression (no (-)feedback--> increase 5-HT/NE/DA release) 1. sedation 2. increase cholesterol 3. increase appetite
81
BBs: | Name (12)-->"-olol"
1. Acebutolol (partial agonist) 2. Atenolol 3. Betaxolol 4. Carvedilol 5. Esmolol 6. Labetalol 7. Metoprolol 8. Nadolol 9. Nebivolol 10. Pindolol (partial agonist) 11. Propranolol 12. Timolol * A-M= B1 selective * N-Z= B2 selective * Nonselective a and B antagonists have modified suffixes: CarvedILOL & LabetALOL
82
BB effects on: Angina Pectoralis MI HTN
Angina: decrease HR-->decrease O2 consumption MI: decrease mortality HTN: decrease CO & decrease Renin secretion via block of JGA cells (B1-R)
83
BB: 2 drugs to treat SVT: MOA (supraventricular tachycardia)
Class II antiarrhythmics: 1. metoprolol 2. Esmolol decrease AV conduction velocity
84
BB: | 3 drugs to treat Heart Failure
1. Bisoprolol 2. Carvediol 3. Metoprolol decrease mortalilty
85
BB: 1 drug to treat glaucoma MOA
Timolol ('Timmy can BBarely see') decrease secretion of aqueous humor (B2=ciliary process)
86
BB: 2 drugs for variceal bleeding MOA(2)
1. Nadolol 2. Propranolol decrease hepatic venous pressure gradient decrease portal hypertension
87
BB: | Adverse(4)
1. Erectile dysfunction (not really true though) 2. CV- bradycardia, AV block, HF 3. CNS- seizures, sedation, sleep alterations 4. dyslipidemia (metoprolol 5. asthma/COPD exacerbations (Never use nonselective BB in these pts)
88
BB: 2 Contraindications Can diabetics use BB
1. Cocaine use: risk of unopposed a-adrenergic agonist activity 2. COPD/Asthma (nonselective BBs contra) Despite theoretical concern of masking hypoglycemia in DM, benefits likely outweigh risks (NOT A CONTRA)
89
BB: | 2 drugs which are partial agonists
1. acebutolol(B1 selective antagonist) (partial agonist) | 2. pindolol (B2 selective antagonist) (partial agonist)
90
BB-->Nebivolol: | MOA/Receptors involved
combines B1-block with B3-R stim -->increase NO release-->Sm. Muscle relaxes--> decrease TPR/Afterload
91
Importance of B1 selective blocking?
cardio selective decrease HR/contractility/CO/MVO2
92
3 important varicies | 2 BB drugs to treat vatical bleeding
1. esophageal--> 30% chance of killing patient 2. umbilical 3. rectal Tx: Propranolol, Nadolol
93
3 Ingested Seafood toxins
1. tetrodotoxin 2. ciguatoxin 3. Histamine from scombroid poisoning
94
``` Tetrodotoxin: geographic / source Action Symp (4) Treatment ```
- Japan/ pufferfish - highly potent, binds fast VGNa Channels in Cardiac/Nerve-->prevent depolarization - 1. N/D 2. Paresthesias 3 Dizzy 4. Weakness/Loss of Reflexes Treat: supportive
95
``` Ciguatoxin: geographic source(3) Action Symp Treatment ```
- 20% foodborne toxin in USA - barracuda, snapper, moray eel - Opens Na+ channels-->depol in all memb - Symp: mimic Cholinergic poisoning (N/V/D/abd. pain after fish) Treat: supportive
96
``` Scamboid Poisoning: Source(4) Action Symp/ Misdiagnosis Treatment ```
- Spoiled dark-meat fish (tuna, mahi-mahi, mackerel, bonito) - histadine-->histamine via Bacterial histidine decarboxylase -symp mimic Anaphylaxis (misdiagnosed as fish allergy) (burning of mouth, flushing, erythema, urticaria, itching-->broncospasms/angioedema/hypotension Treat: 1. Anti-histamines 2. Albuterol/Epi if needed

Drugs- Basic High Yield Stuff for Boards (20 decks)

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