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* DIT each session > Day 1.2 Pharm > Flashcards

Day 1.2 Pharm Flashcards

1
Q

What is the neurotransmitter for the nicotinic receptor?

A

ACh

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2
Q

What drug is a nicotinic receptor antagonist?

A

Hexamethonium

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3
Q

What does Hexamethonium block?

A

Nicotinic receptor antagonist- blocks ACh receptors at ALL autonomic ganglion- both sympathetic and parasympathetic

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4
Q

If hexamethonium blocks both SNS and PNS, how can you determine how it will affect an organ?

A

How it affects an organ depends on the dominant tone (SNS or PNS) in that organ. e.g. Dominant tone in vessels is SNS, so hexamethonium will act as a symp antagonist to blood vessels- so will decrease BP. (Most organs have dom PNS tone)

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5
Q

What is hexamethonium used for clinically?

A

Experimental only - to prevent vagal reflex response to changes in BP; prevents reflex bradycardia caused by NE

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6
Q

SNS to sweat glands: Preganglionic neurons go to what kind of receptor? Release which NT?

A

The sympathetic ganglion have a nicotinic receptor. ACh is the NT. All preganglionic neurons go to Nicotinic receptors.

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7
Q

SNS to sweat glands: Post-ganglionic neurons go to what kind of receptor? Release which NT?

A

Post-gang neurons go to sweat glands and synapse there with a Muscarinic receptor. ACh is the NT.

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8
Q

SNS to cardiac musc, smooth musc, gland cells, nerve terminals: Preganglionic neurons go to what kind of receptor? Release which NT?

A

The sympathetic ganglion have a nicotinic receptor. ACh is the NT. All preganglionic neurons go to Nicotinic receptors.

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9
Q

SNS to cardiac musc, smooth musc, gland cells, nerve terminals: Post-ganglionic neurons go to what kind of receptor? Release which NT?

A

Post-gang neurons go to cardiac musc, smooth musc, gland cells, and nerve terminals and synapse there with a adrenoceptor receptor (alpha or beta). NE is the NT.

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10
Q

SNS to renal vascular smooth musc: Preganglionic neurons go to what kind of receptor? Release which NT?

A

The sympathetic ganglion have a nicotinic receptor. ACh is the NT. All preganglionic neurons go to Nicotinic receptors.

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11
Q

SNS to renal vascular smooth musc: Post-ganglionic neurons go to what kind of receptor? Release which NT?

A

Post-gang neurons go to renal vascular smooth muscle and synapse there with a D1 receptor.

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12
Q

SNS to the adrenal medulla: what kind of receptor is at the adrenal medulla? Releases which NT?

A

There is a Nicotinic receptor at the adrenal medulla. The receptor is ACh. When stimulated, the adrenal medulla itself goes on to release NE and Epi

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13
Q

Somatic system: Nerves to skeletal muscle have what kind of receptor? What is the NT?

A

Nicotinic receptor; ACh is the NT.

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14
Q

PNS pre-ganglionis neurons go from the medulla all the way to the ganglion located right by the organ they will stimulate. What kind of receptor is in the ganglion? What is the NT?

A

The parasympathetic ganglion have a nicotinic receptor. ACh is the NT. All preganglionic neurons go to Nicotinic receptors.

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15
Q

PNS post-ganglionic nerves (short) go to cardiac and smooth muscle, gland cells, and nerve terminals. What is there receptor at these locations? What is the NT?

A

Muscarinic receptor; ACh is the NT.

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16
Q

What are the Nicotinic receptors (what kind of channel/protein)?

A

Ligand-gated Na+/K+ channels.
Nn for autonomic (SNS, PNS) ganglia
Nm for the NMJ (somatic)

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17
Q

What are the Muscarinic receptors (what kind of channel/protein)?

A

G-protein-coupled receptors, which act through 2nd messengers.
5 subtypes: M1, M2, M3, M4, M5

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18
Q

Cholinergic Nerve: What kind of NT does it produce?

A

ACh

ACh goes to a cholinocepor- either a M receptor or N receptor.

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19
Q

Noradrenergic Nerve: What kind of NT does it produce?

A

NE

Noradrenergic (SNS) goes to an adrenoceptor (alpha or beta receptor)

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20
Q

Cholinergic Nerve: how is ACh produced?

A

Choline is brought along with Na+ via the Na+ cotransporter. Choline is combined with Acetyl-CoA with the help of ChAT (choline acetyltransferase). Ca2+ helps release of ACh into synaptic cleft.

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21
Q

Cholinergic Nerve: What is the rate-limiting step in ACh synthesis?

A

Bringing choline in. (Via Na+ cotransporter)

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22
Q

Cholinergic Nerve: what inhibits choline from being brought into the cell?

A

Hemicholinium

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23
Q

Cholinergic Nerve: What inhibits release of ACh into the cleft?

A

Botulinum toxin, which causes flaccid paralysis (floppy baby)

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24
Q

Cholinergic Nerve: What toxin stimulates the release of ACh into the cleft?

A

Black widow spider toxin

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25
Q

What are the 4 fates of ACh once it’s in the synaptic cleft?

A
  1. Bind to the Ach cholinoceptor (either M or N) on the post-syn cell
  2. Bind to a pre-synaptic auto-receptor
  3. Be degraded (metabolized) by AChE (can block this with anti-AChE - the -stigmines)
  4. Diffuse away
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26
Q

Noradrenergic Nerve: How is NE produced?

A

Tyrosine is brought along with Na+ via the Na+ cotransporter. Tyrosine is converted to L-Dopa with the help of Tyrosine Hydroxylase. L-Dopa is converted to Dopamine, and Dopamine is converted to NE. Ca2+ helps release of NE into synaptic cleft.

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27
Q

Noradrenergic Nerve: What converts Tyrosine to L-Dopa?

A

Tyrosine Hydroxylase (imp in biochem!)

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28
Q

Noradrenergic Nerve: What drug blocks Tyrosine Hydroxylase? What happens if it’s blocked?

A

Metyrosine. Blocking Tyrosine Hydroxylase means that Tyrosine will not be converted into L-Dopa.

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29
Q

Noradrenergic Nerve: What are the two ways for NE to have effects on the pre-synaptic cell once it has been released?

A
  1. Can undergo reuptake

2. Can bind to release-modulating receptors (M2, Alpha2, AngII)

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30
Q

What are the 4 fates of NE once it has been released into the synaptic cleft?

A
  1. Bind to adrenoceptor (alpha1,2, beta1,2) on post-syn cell
  2. Bind to pre-syn autoreceptors (M2, alpha2, AngII)
  3. Undergo reuptake
  4. Be metabolized by COMT or MAO
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31
Q

Noradrenergic Nerve: What are the 3 auto-receptors for NE on the pre-synaptic cell, and what are their effects?

A

M2: inhibits release of more NE
Alpha2: inhibits release of more NE
Angiontensin II: stimulates release of more NE

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32
Q

Noradrenergic Nerve: What are the 3 things that prevent reuptake of NE? What is the effect of preventing reuptake?

A

Cocaine
TCAs
Amphetamine
When reuptake is inhibited, NE stays in the cleft for longer, so increased HR, BP, euphoria.

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33
Q

Noradrenergic Nerve: What drug blocks the conversion of Dopamine to NE?

A

Reserpine

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34
Q

Other than L-Dopa, what is Tyrosine converted to?

A

Thyroxine (thyroid hormone)

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35
Q

Other than Dopamine, what is L-Dopa converted to?

A

Melanin

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36
Q

Noradrenergic Nerve: What 2 drugs inhibit the release of NE into the cleft?

A

Guanethidine

Bretylium (anti-arrhythmic K+ chnl blocker)

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37
Q

Noradrenergic Nerve: What 3 drugs stimulate the release of NE into the cleft?

A

Amphetamines
Ephedrine (formerly OTC diet drug)
Tyramine

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38
Q

How is NE metabolized in the cleft?

A

Methylated by COMT (catechol-O-methyltransferase)

or oxidized by MAO (monoamine oxidase)

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39
Q

What inhibits MAOs?

A

MAO-Is. (MAO inhibitors). These are anti-depressants. Work by preventing metabolism of NE.

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40
Q

What are the two kinds of anti-depressants that work on NE?

A
  1. MAO-I prevent NE metabolism so more stays in cleft

2. TCAs inhibit reuptake so more NE stays in cleft

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41
Q

What should you not take if you’re on MAO-Is?

A

Tyramine. Tyramine stim’s release of NE into cleft. MAO-I inhibits metabolism of NE. So you have extra NE in cleft, plus you’re not metabolizing it - leads to HTN crisis. (MAO-I work in gut, where Tyramine will go if eaten)

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42
Q

What are the byproducts of NE breakdown? When are these seen in excess?

A

VMA, metanephrine, normetanephrine

Seen in pheochromocytoma, an adrenal tumor that releases excess NE and Epi.

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43
Q

Which drug reverses NMJ blockade (from paralytics)?

A

Neostigmine

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44
Q

What is the G-protein class for alpha1,2, beta 1,2?

A 
QISS:
alpha 1 = q
alpha 2 = i
beta 1 = s
beta 2 = s
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45
Q

What is the G-protein class for M1, M2, M3?

A

QIQ:
M1 = q
M2 = i
M3 = q

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46
Q

What is the G-protein class for D1, D2, H1, H2, V1, V2?

A 
SIQ, SQS
D1 = s
D2 = i
H1 = q
H2 = s
V1 = q
V2 = s
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47
Q

What is “HAV 1 M&M”

A

H1, alpha-1, V1
M1 and M3
all use Gq
(cutsies have 1 m&m)

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48
Q

What is MAD 2’s?

A

M2, alpha-2, D2

all use Gi

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49
Q 
Alpha-1: 
G-protein class and mjr fns
A

Gq
Increases vascular smooth musc contraction (so increases BP), increases pupillary dilator musc contraction (mydriasis), increases intestinal and bladder sphincter musc contraction

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50
Q

Alpha-2:

G-protein and mjr fns

A

Gi

Decreased symp outflow (so vasodilation, decreased BP), decreased insulin release

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51
Q

Beta-1:

G-protein and mjr fns

A

Gs
Incrs HR, contractility
Incrs renin rls, incrs lipolysis

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52
Q

Beta-2:

G-protein and mjr fns

A

Vasodilates! (but HR increases to compensate for the dilation)
So incrs HR, contractility
Bronchodilation
Increased lipolysis, increased insulin rls
decreased uterine tone

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53
Q

M1:

G-protein and mjr fns

A

Gq

CNS, enteric nervous system

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54
Q

M2:

G-protein and mjr fns

A

Gi
decreases HR
decreases contractility of atria

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55
Q

M3:

G-protein and mjr fns

A

Gq
Increased exocrine gland secretions (sweat, gastric acid), incrs gut peristasis, incrs bladder contraction
bronchoconstriction
increased pupillary sphincter musc contraction (miosis), cilairy musc contraction (accomodation)

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56
Q

D1:

G-protein and mjr fns

A

Gs

Relaxes renal vascular smooth musc (so increases circulation to the kidneys)

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57
Q

D2:

G-protein and mjr fns

A

Gi

modulates transmitter rls, esp in brain

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58
Q

H1:

G-protein and mjr fns

A

Gq

increases nasal and brochial mucus production, contracts bronchioles, pruritis and pain (allergic responses)

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59
Q

H2:

G-protein and mjr fns

A

Gs
Increased gastic acid secretion
(use H2 blockers like cimetidine, renitidine to block this)

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60
Q

V1:

G-protein and mjr fns

A

Gq

Increased vascular smooth muscle contraction

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61
Q

V2:

G-protein and mjr fns

A

Gs
Increased H20 permeability and reabs in the collecting tubules of the kidney
(V2 is found in the 2 kidneys)

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62
Q

What does the Gq protein do?

A

Gq activates phospholipase C, which converts lipids to PIP2.
PIP2 is cleaved to IP3 and DAG.
IP3 increases intracellular Ca2+ (Ca2+ finds to calmodulin and activates CaM-kinase)
DAG activates Protein Kinase C

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63
Q

What does the Gs protein do?

A

Gs = stimulatory.
Stimulates Adnylyl cyclase, which converts ATP to cAMP.
cAMP activates Protein Kinase A

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64
Q

What does the Gi protein do?

A

Gi = inhibitory
Inactivates Adenylyl cyclase, which decreases cAMP
Decreased cAMP means decreased Protein Kinase A.

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65
Q

How is phospolipase C activated

A

Either the Gq pathway, or can be activated when a hormone/growth factor binds to the tyrosine kinase receptor

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66
Q

What are the 2 pathways which can occur when a hormone or growth factor binds to a tyrosine kinase receptor?

A
  1. It can activate phospholipase C (leading to IP3, DAG)

2. It can activate the Ras pathway

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67
Q

What is the Ras pathway?

A

Hormone/growth factor binds to tyrosine kinase receptor, activating adaptor protein.
Adaptor protein activates Ras-activating protein, which activates Ras
Ras activates protein kinase 1.
PK1 activates PK2
PK2 activates PK3
PK3 affects target proteins/genes

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68
Q

Many bacterial toxins use one of the G-proteins- which one?

A

Use Gs, for the purpose of activating adenylyl cyclase (and making cAMP, activating PKA)

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69
Q

What is a 7-pass transmembrane receptor?

A

a G-protein

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70
Q

List the direct sympathomimetics

A

Epinephrine, NE, Isoproterenol, Dopamine, Dobutamine, Phenylephrine, Metaproterenol, Albuterol (levalbuterol), Salmeterol, Terbutaline, Ritodrine

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71
Q

What is the selectivity of epinephrine?

A

a1, a2, b1, b2. (selective for ALL sympathetic receptors).

at low doses, selective for b1 (mne: Blow)

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72
Q

Clinical use for epinephrine?

A

Anaphylactic shock
Open-angle glaucoma
Asthma
Hypotension (d/t shock)

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73
Q

What is the selectivity of NE?

A

a1, a2 > b1

no b2 effect

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74
Q

Clinical use for NE?

A 
Hypotension (but decrsd renal perfusion)- bc it causes vasoconstriction at a1
Septic shock (in shock have vasodilation, so use NE to counteract it)
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75
Q

What is the selectivity of Isoproterenol?

A

b1 = b2

ISOlated to beta; iso means equal

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76
Q

Clinical use for Isoproterenol?

A

AV block (rare)

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77
Q

Selectivity of Dopamine?

A

D1 = D2 > b > a

inotropic and chronotropic

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78
Q

Clinical use for Dopamine?

A

Shock (increases renal perfusion*), heart failure

*theoretically, not in actual practice

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79
Q

Selectivity for Dobutamine

A

B1 > B2

Inotropic and chronotropic (less so chronotropically tho)

80
Q

Clinical use for Dobutamine

A

Cardiogenic shock
Heart failure
Cardiac stress test (bc it increases HR and contractility)

81
Q

Phenylephrine selectivity?

82
Q

Clinical use for Phenylephrine?

A

Pupillary dilation, vasoconstriction, nasal decongestion (stops epistaxis- nosebleeds)

83
Q

What are the selective B2 agonists (B2 > B1)?

A 
MAST:
Metaproterenol
Albuterol
Salmeterol
Terbutaline
84
Q

Clinical use for Metaproterenol and Albuterol?

A

Use for acute asthma.

If it’s a cardiac pt, use levalbuterol- it doesn’t have B1 side effects, so it’s safer for heart pts

85
Q

Clinical use for Salmeterol?

A

Long-term treatment of asthma (and COPD)

86
Q

Clinical use for Terbutaline?

A

Reduce premature uterine contractions

Also given sub-q for asthma

87
Q

Selectivity of Ritodrine?

88
Q

Clinical use for Ritodrine?

A

Reduces premature uterine contractions

89
Q

Drug of choice for anaphylactic shock?

A

Epinephrine

90
Q

Drug of Choice for septic shock?

91
Q

Drug of Choice for cardiogenic shock?

A

Dobutamine

92
Q

Where do the indirect sympathomimetics work?

A

At the synapse- either promote release or inhibit reuptake.

93
Q

What are the indirect sympathomimetics?

A

Amphetamine
Ephedrine
Cocaine
(also Tyramine)

94
Q

How does amphetamine work?

A

releases stored catecholamines

95
Q

How does ephedrine work?

A

releases stored catecholamines

96
Q

How does Cocaine work?

A

Inhibits reuptake.

97
Q

Clinical use of amphetamines

A

Narcolepsy (keep pt awake)
Obesity (increase metabolism)
ADD
Mjr depressive disorder- use in gap before other anti-depressants start working

98
Q

Clinical use of Ephedrine

A

nasal decongestion
urinary incontinence
hypotension

99
Q

Clinical use of Cocaine

A

Vasoconstriction, local anesthesia (ENTs use it)

100
Q

Effect of NE on BP

NE = a1, a2 > b1

A

BP goes up (both alpha1 and beta1 effect)

101
Q

Effect of NE on HR

A

HR goes down d/t reflex bradycardia (bc BP went up)

102
Q

Effect of Epi on BP

Epi = nonselective, a1, a2, b1, b2

A

Systolic goes up d/t B1
Diastolic goes down d/t B2
Mean stays the same

103
Q

Effect of Epi on HR

A

HR increases d/t B1

104
Q

Effect of Isoproteronol on BP

Isoproterenol: B1 = B2

A

Systolic goes up, then down d/t B1
Diastolic goes down d/t B2 - B2 drops BP and there is no counteracting a1 vasoconstriction bc alphas are not affected
Overall, mean goes down

105
Q

Effect of Isoproterenol on HR

A

HR goes way up

d/t B1 stimulation, but also d/t the decreased BP causing reflex tachycardia

106
Q

What are the sympathoplegic drugs?

A

Clonidine

alpha-methyldopa

107
Q

What is the selectivity of the sympathoplegics?

A

Centrally acting alpha2 agonists.

Decrease central adrenergic outflow.

108
Q

Clinical use for sympathoplegics (clonidine and a-methyldopa)?

A

HTN, esp with renal dz (they don’t cause decrease in blood flow to the kidney)
alpha-methyldopa is used in pregnancy
not used bc must be dosed 3x daily (too frequent) and bc if you skip a dose get rebound HTN

109
Q

What are the beta blockers?

A

Acebutolol, betaxolol, esmolol, atenolol, metoprolol, propranolol, timolol, pindolol, labetolol

110
Q

What are the clinical uses of beta blockers?

A

HTN, Angina, MI, SVT, CHF, glaucoma

111
Q

How do beta blockers help HTN?

A

They decrease CO and decrease renin secretion (d/t b-receptor blockade on JGA cells)

112
Q

How do beta blockers help angina pectoris?

A

They decrease HR and contractility, resulting in decreased O2 consumption

113
Q

How do beta blockers help in MI? Which ones?

A

They decrease mortality- but only metoprolol and carvedilol

114
Q

How do beta blockers help SVT? Which ones?

A

Propranolol and (short-acting) esmolol. They decrease AV conduction velocity. They are class II anti-arrythmics

115
Q

How do beta blockers help CHF?

A

They slow the progression of chronic failure. Don’t use beta blockers in acute failure!

116
Q

How do beta blockers help glaucoma? Which one?

A

Timolol helps decrease the secretion of aqueous humor.

117
Q

What drugs can cause impotence/ED?

A

Anti-depressants / psych meds
Anti-histamines (H2 blockers)
BP drugs- Beta blockers, Ca2+ chnl blockers
Parkinson’s meds
Anti-androgen meds
Also, HTN and CV dz themselves can cause ED, so if you unmask them with another drug, they can be the cause

118
Q

What is the toxicity of beta blockers?

A 
Impotence/ED
exacerbation of asthma
cv effects: bradycardia, AV block, CHF
CNS effects: sedation, sleep alteration
use w caution in diabetics- they can get hypoglycemic but not feel it
119
Q

What are the non-selective beta blockers (B1 = B2)?

A 
Start w/ N-Z:
propranolol
timolol
nadolol
pindolol
labetolol
120
Q

What are the B1 selective antagonists? (B1 > B2)

A 
Start w/ A-M
Mne: A BEAM
Acebutolol (partial agonist)
Betaxolol
Esmolol (short acting)
Atenolol
Metoprolol
Use these for COPD and Asthma
121
Q

What are the non-selective alpha and beta antagonists?

A

carvedilol and labetalol

note: they end in -lol, but not in -olol like beta blockers

122
Q

What are the partial beta agonists?

A

Pindolol

Acebutolol

123
Q

Why should you not give a pt on cocaine a beta-blocker?

A

Cocaine stims a1 which increases BP as well as B2 which decreases BP. If you block the B2, you will only have the a1 unopposed, so you will get very very high BP.

124
Q

What is the drug of choice for aortic dissection? Why?

A

Beta blockers
They decrease BP, but also decrease the slope of the BP curve- so not only is BP decreased, the rate at which it rises is slower.

125
Q

What is the direction of flow of the aqueous humor?

A

Goes from posterior chamber (behind iris, in front of lens) to anterior chamber (in front of iris)

126
Q

What muscles are in the iris?

A

The dilator/radial muscle (a1 stimulation causes mydriasis)

The sphincter/circular/constrictor muscle (M3 causes miosis)

127
Q

What is the path of flow for the aqueous humor?

A

Beta receptors cause ciliary process to produce aqueous humor, secreted into posterior chamber (behind iris, but in front of lens)
Aq humor goes from behind iris to in front of iris, to anterior chamber.
Trabecular meshwork absorbs aq humor
Canal of schlemm collects aq humor from trabecular meshwork. Located at point where cornea changes to sclera.

128
Q

What is glaucoma?

A

Impaired flow of aq humor, leading to increased intraocular pressure, leading to optic disk atrophy with cupping

129
Q

What is open-angle glaucoma? (aka wide angle)

A

Obstructed outflow (drainage) of aq humor d/t problem with canal of schlemm. Can’t absorb/get rid of aq humor, so it builds up.
Common, silent/insidious, painless
assoc w myopia, age >40, black.

130
Q

What is closed-angle glaucoma (narrow angle, acute angle)

A

Obstruction of flow between the iris and cornea, so aq humor can’t go from the post to ant chamber trabecular meshwork to be absorbed. Iris is displaced forward bc of a large pressure build-up behind it.
Painful, emergency. Decreased vision, hard eye, frontal headache.

131
Q

What drugs should you NOT give in acute/narrow/closed angle glaucoma?

A

Do not give epinephrine or atropine- they cause mydriasis, which makes it worse.

132
Q

What is the cup to disk ratio?

A

Measurement for progression of glaucoma. Glaucoma has an increased cup:disk ratio, greater than 1:2 is bad. (More cupping is bad)

133
Q

What are the drug groups used in glaucoma?

A 
alpha-agonists
beta blockers
cholinomimetics
diuretics
prostaglandins
134
Q

What alpha-agonists are used to treat glaucoma?

A

Epinephrine and Brimonidine

135
Q

How does epinephrine help in glaucoma?

Side effects?

A

alpha-agonist
Decreases synthesis of aq humor d/t vasoconstriction.
SEff: mydriasis, stinging.
Use in open-angle only!!

136
Q

How does brimonidine help in glaucoma?

A

alpha-agonist
Decreases synth of aq humor
Does not cause pupillary or vision chgs

137
Q

What are the beta-blockers used in treatment of glaucoma?

A

Timolol, betaxolol, carteolol

138
Q

How do timolol, betaxolol, and carteolol help in glaucoma?

A

Beta-blockers
Decrease secretion of aq humor
No pupillary or vision chgs, but can have systemic beta effects- hypotension, bradycardia

139
Q

What diuretics are used to treat glaucoma?

A

Acetazolamide

Mannitol

140
Q

How does acetazolamide help in glaucoma?

A

It decreases aq humor secretion d/t decreased HCO3- bc it’s a carbonic anhydrase inhibitor.
Does not cause pupillary or vision chgs

141
Q

What cholinomimetics are used to treat glaucoma?

A 
Direct agonists: pilocarpine, carbachol
Indirect agonists (anti-AChE): physostigmine, echothiophate
142
Q

How do the cholinomimetics help in glaucoma?

A

They increase the outflow of aq humor.
Contract ciliary musc and open trabecular meshwork.
In emergencies, use pilocarpine- v effective at opening meshwork into canal of schlemm.
SEff: miosis, cyclospasm

143
Q

What prostaglandin is used to treat glaucoma?

A

Latanoprost (PGF-2a)

144
Q

How does Latanoprost/PGF-2a help treat glaucoma?

A

It increases outflow of aq humor

SEff: brown color of iris, increases eyelash length

145
Q

What are the effects of alpha blockers on a1 and a2 (generally)?

A

a1 causes vasoconstriction, so if you block it, will get vasodilation.
a2 causes vasodilation, so if you block it, will get vasoconstriction.

146
Q

What are the non-selective alpha blockers?

A

Phenoxybenzamine (irreversible- so non-competitive inhibitor)
Phentolamine (reversible- so competitive inhibitor)

147
Q

When would you use a non-selective alpha blocker?

A 
In pheochromocytoma (adrenal tumor which overproduces epi and NE).
You treat pheo w/ beta blockers, but BEFORE giving beta blockers, give phenoxybenzamine 1st. If you give beta blockers, you will get rid of B2 vasodilation and have unmasked alpha, so increased BP. So give alpha first to prevent this.
148
Q

What is the toxicity for non-selective alpha blockers?

A

Orthostatic HTN and reflex tachycardia

149
Q

What are the a1 selective alpha blockers?

A

Prazosin, terazosin, doxazosin

-zosin

150
Q

Clinical use of a1 blockers?

A

HTN, urinary retention in BPH

use tamsulosin esp for BPH

151
Q

Side effects of a1 blockers?

A

1st dose orthostatic HTN (so give at bedtime),

dizziness, headache

152
Q

What drug is an a2 selective blocker?

A

Mirtazapine

153
Q

What is mirtazapine used for? Side effects?

A

a2 blocker used for depression.
SEff: sedation, increased serum cholesterol, increased appetite
Use SEff to advantage: give to elderly depressed pt who is not sleeping or eating well.

154
Q

What happens if a large dose of Epi is given before an alpha blockade?

A

It vasoconstricts and therefore raises BP

155
Q

What happens if a large dose of Epi is given after an alpha blockade?

A

BP goes down. There is no longer a1 vasoconstriction, but Epi is still stimulating the B2 receptors to dilate the blood vessels.

156
Q

What effect predominates at LOW doses of Epi?

A

B2 predominates, so get vasodilation and decreased BP

At high doses, a1 vasoconstriction predominates

157
Q

What happens if Phenylephrine (a1>a2) is given before alpha blockade?

A

BP increased d/t a1 vasoconstriction

158
Q

What happens if phenylephrine (a1>a2) is given after alpha blockade?

A

BP stays the same.
Don’t have a1 stimulation, so doesn’t raise BP, but since there only effects on alpha and there are no effects on B2, it doesn’t lower the BP either.

159
Q

What is tamsulosin?

A

a1 antagonist- used to treat BPH by inhibiting smooth muscle contraction.
Selective for alpha1-A,D receptors (which are found in prostate in the urethral smooth muscle).
Does not relax the alpha1-B receptors of the vasculature, so will not affect the BP

160
Q

-afil

A

Erectile dysfunction

161
Q

-ane

A

inhalational general anesthetic

162
Q

-azepam

A

benzodiazepine

163
Q

-azine

A

phenothiazine (neuroleptic, antiemetic)

164
Q

-azole/-conazole

A

anti-fungal

165
Q

-barbital

A

barbituate

166
Q

-caine

A

local anesthetic

167
Q

-cillin

A

penicillin

168
Q

-cycline

A

abx, protein synth inhibitor

169
Q

-etine

170
Q

-ipramine

171
Q

-navir

A

protease inhibitor for HIV

172
Q

-olol

A

beta antagonist

173
Q

-operidol

A

butyrophenone (neuroleptic)

174
Q

-oxin

A

cardiac glycoside (inotropic agent)

175
Q

-phylline

A

methyxanthine (brochodilator)

176
Q

-pril

A

ACE inhibitor

177
Q

-terol

A

B2 agonist (albuterol)

178
Q

-tidine

A

H2 antagonist

cimetidine, ranitidine(zantac), NOT amatidine- that’s a parkinson’s drug

179
Q

-triptan

A

5HT-1b/1d agonists (for migranes)

180
Q

-triptyline

181
Q

-tropin

A

Pituitary hormone

182
Q

-zolam

A

Benzodiazapine

183
Q

-zosin

A

a1 antagonist

184
Q

-dronate

A

bisphosphonates (for osteoporosis)

185
Q

-sartan

A

Ang II receptor antagonist

186
Q

-chol

A

muscarinic agonist (cholinergic agonist)

187
Q

-stigmine

A

anti-cholinesterase (anti-AChE, indirect muscarinic agonist)

188
Q

-mustine

A

nitrosureas (cross BBB, for brain tumors)

189
Q

-curium, curonium

A

paralytics- non-depolarazing NMJ blockers (reversed w neostigmine)

190
Q

-statin

A

HMG CoA reductase inhibitors (reduce LDL)

191
Q

-glitazone

A

increase target cell response to insulin

192
Q

-bendazole

A

parasites, worms

193
Q

-dipine

A

dihydropyridine Ca2+ channel blocker

194
Q

-prost

A

Prostaglandin analog (for glaucoma)

195
Q

-mab

A

Monoclonal Ab

* DIT each session (34 decks)

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