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Year2 Renal > Exam I cholinergics and adrenergics > Flashcards

Exam I cholinergics and adrenergics Flashcards

1
Q

What drugs are choline esters and what type of compound are they

A

acetylcholine, carbachol and bethanechol

quarternary ammonium

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2
Q

why is bethanechol slower acting than carbachol and Ach

A

because it resists cholinesterases more

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3
Q

choline esters and alkaloids act as agonists or antagonists on cholinergic R?

A

agonists

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4
Q

what drugs are the alkaloids that act on chilinergic R

A

muscarine, nicotine and pilocarpine

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5
Q

describe structures and modes of absoprtion for muscarine and nicotine

A

nictoine is tertiary amine so absorbed at most sites

muscarine is quaternary amine and highly toxin if ingested because can enter brain

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6
Q

What Ach R are found in the nerves

A

M1 and the NN (dendrites) NM(NMJ)

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7
Q

What Ach R are in the CNS

A

M4 M5 and NN

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8
Q

What Ach R are in the Heart, and smooth m

A

M2

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9
Q

What Ach R are in the glands, smooth m and endothelium

A

M3

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10
Q

where are nACHR

A

skel muscle

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11
Q

What happens in vasculature in the presence of high levels of Ach

A

constriction

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12
Q

compare high doses Ach and low action on the heart

A

small cause vasodilation and dec in BP

large causes bradycardia and dec AV node conduction velocity and hypotension

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13
Q

Differentiate smooth m contraction caused by M2 Ach R and M3

A

M2 directly activates contraction

M3 reduces cMP formation and reduces relaxation caused by adrenergic effects

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14
Q

What Ach R predominate the brain and which ones the spinal cord

A

mACHR in brain and

spinal cord nACH R

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15
Q

What are the ACH effects on the GI and GU tracts

A

nausea, vomiting, diarrhea, voiding of urine

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16
Q

What are the side effects of too much muscarinic ACH

A

nausea, vomiting, diarrhea, urinary urgency, salivation, sweating, cutaneous vasodilation, bronchial constriction

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17
Q

How do we block negative sideeffects of choline esters and ilocarpine

A

atropin, antimuscarinic compounds

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18
Q

What are the major contraindications for mAchR agonists

A

asthma, hyperthyroidism, coronary insufficiency, acid-peptic disease

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19
Q

What are signs of acute toxicity of direct acting cholinergics

A

convulsions, coma and respiratory arrest

depolarization blockads–> respiratory paralysis, HTN and cardiac arrythmias

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20
Q

What is metacholine used for

A

to Dx hyperreactivity of broncial airway

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21
Q

What is Bethanechol used for

A

to Tx urinary retention and heartburn

selective mAchR agonist

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22
Q

What type of pharm agent is carbachol

A

nonspecific cholinergic agonist that is used for Tx of glaucoma
used to make miosis during surgery or ophthalmic examination

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23
Q

What is cevimeline

A

oral tablet used to treat xerostomia (dry mouth)

metabolized via p450 and eliminated in urine

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24
Q

What is pilocarpine used to treat

A

xerostomia, also head and neck cancer Tx related to xerostomia
miosis for opthalmic procedures and glaucoma
mAchR agonist

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25
Q

What is Varenicline used to Tx and how does it work

A

smoking cessation
partial agonists to a4b2 nAchR in brain
released dopamaine thought to curve craving

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26
Q

what are side effects of varenicline

A

nausea, neuropsychiatric symptoms like change in behavior, agitation, depressed mood, suicidal ideation

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27
Q

What are indirect acting cholinergic agonists

A

cholinesterase inhibitors

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28
Q

What are the chemical groups of Achesterase inhibitors

A

alcohol
carbamic acid esters
organophosphates

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29
Q

What is structure and mech of alcohol indirect-acting cholinergic agonists

A

alcohol group and quaternary ammonium group

bind to AchE is non-covalent and reversible

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30
Q

What are types of organophosphate indirect acting cholinergic agonists

A

echthiophate, parathion, malation, sarin, soman and tabun

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31
Q

Describe the binding of organophosphates

A

bind to AchE covalent and irreversible

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32
Q

Describe pharmakinetics of quaternary and charged AchE inhibitors

A

relatively insoluble in lipids and absorption from conjunctiva, skin and lungs is poor
parenteral admin
no CNS involvement
duration of effect determined by stability of inhibitor-enzyme complexx

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33
Q

describe pharmacokinetics of teriaty and uncharged AchE inhibitors

A

well absorbed everywhere
CNS distribution
more toxic than polar quaternary carbamates
e.g. physotigmine, donepezil, tacrine, rivastrigmine, galantamine

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34
Q

describe pharmacokinetics of organophosphates

A

lipid-soluble and readibly absored making dangerous to humans
distributed everywhere
includes CNS toxicity
coavalent and irreversible so usually biotransformation pathways

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35
Q

describe AchE inhibitors activity of CV system

A

SAN and PAN ganglia
PAN dominates so CO decreases
modest bradycardia, dec contractility of atria
decrease in BP

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36
Q

What are the main therapeutic uses of agents that stimulate AchR

A

galucoma, GI and urinar tracts, NMJ (myasthenia gravis)
heart (rarely for certain atrial arrhythmias
alzheimer disease

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37
Q

What do we use to reverse NMJ blocking in anestheia

A

AchE inhibitors

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38
Q

how do AchE inhibitors help with glaucoma

A

reduce intraocular pressure by stimulating mAchR of ciliary body causing contraction allowing outflow of aqueous humor

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39
Q

What are symptoms of anticholinergic overdose

A

cutaneous vasodilation, anhidrosis, anhydrotic hyperthermia, nonreactive mydriasis, delirium, hallucinations, reduction or elimination of the desire to urinate

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40
Q

What is used to reverse overdose of anticholinergic effects

A

physostigmine because crosses bbb

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41
Q

what happens when you combine a nondepolarizing NMJ blocking agent with AchE inhibitor

A

diminsh the blockade

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42
Q

What happens with succinylcholine and AchE inhibitors

A

enhance phase 1 block and antagonize phase 2 block

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43
Q

What happens with cholinergic agonists(direct) and AcheE inhibitor

A

enhance effects of cholinergic agonists

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44
Q

what happens when you combine beta blocker and AchE inhibitor

A

enhance bradycaric effects

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45
Q

what happens when you combine systemic corticosteroids with AchE inhibiors

A

enhance muscle weakness seen in patients with myasthenia gravis

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46
Q

what are the dominant initial signs of acute AchE inhibitiro intoxication

A

miosis, salivation, sweating, bronchial constriction, vomiting, diarrhea

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47
Q

how do you Dx deliberate poisoning

A

AchE activity measurement in RBC and plasma

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48
Q

What are cholinesterase regenerators used for

A

they restore stimulation of motor nerve after organophosphorus dosage that blocks the stimulus

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49
Q

What is pyridostigmine

A

a prophylactic for AchE inhibitor poisoning,

military use it if in area where might be exposed to nerve gas

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50
Q

what is the prototype antimuscarininc compound

A

atropine

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51
Q

where are tertiary amines of anticholinergic drugs targeted?

A

eye or central nervouse system

atropine, tropicamide, benztropine

52
Q

where are the quaternary amines of anticholinergic drugs targeted?

A

antimuscarinic effects in the periphery

ipratropium and glycopyrrolate

53
Q

what is the half life of atropine

A

2 hours

54
Q

is atropine reversible

A

yes

55
Q

what tissues are most sensitive to atropine

A

bronchial, sweat glands and salivary

56
Q

lwhat mAchR does atropine work on

A

all 5

57
Q

what drug is used to prevent motion sickness

A

scopolamine

58
Q

describe mode of action of antimuscarinic agents on the eye

A

weaken ciliary muscle causing inability to focus on nearby vision
and reduce lacrimal secretions

59
Q

describe atopine effects on respiratory system

A

smooth muscle and secretory glands of airway receive vagal innervations and contain mAchRs
case bronchodilation and reduce secretion

60
Q

describe effects of atropine on GU tract

A

relax smooth muscle of ureters and bladder wall

slow voiding

61
Q

what cholinergic antagonists are used for parkinsons

A

benztropine, trihexyphenidyl and procyclidine

62
Q

describe uses of atropine in anesthesia

A

paired with neostigmine to block parasympathetic effects during reversal of skel muscle relaxation

63
Q

What are the NE reuptake blockers

A

cocaine, Imipramine, venlafaxine

64
Q

What are the main catecholamines reuptake drugs that are NOT taken orally

A

epinephrine, norepinephrine
isoproterenol
dopamine
dobutamine

65
Q

what is the main alpha agonist drg

A

phenylephrine

66
Q

what are the beta 2 agonists

A

albuterol, salmeterol and formoterol

67
Q

what are the effects of alpha adrenergic drugs

A 
constriction of blood vessels(a1)
mydriasis (a1)
contraction of spleen and uterus (a1)
glycogenolysis of liver (a1)
ejaculation vas deferens (a1)
inhibit release of insulin (a2)
relaxation of intestinal smooth muscle (a2)
68
Q

what are the effects of beta adrenergic drugs

A

positive inotropic and chronotropic effects on the heart (b1)
stimulates release of renin (b1)
relaxation of bronchioles and uterus (b2)
relaxation of vas smooth m in skel m coronaries (b2)
metabolif effects, glycogenolysis and lipolysis
stimulates release of insulin (b2)
relaxation of detrusor and intestinal smooth m (b2)

69
Q

what are the cardiac effects of epinephrine

A 
\+ positive chronotropic effect
\+ inotropic effect
increased conduction in atria,
increased oxygen consumption
increased work of the heart
70
Q

what R does epinephrine have greatest affinity for

A

beta2

71
Q

descirbe the effects of epinephrine on blood vessels

A

low doses- beta2 causing relaxation

high doses- alpha 1, causing contraction

72
Q

what are the effects of epi on renal circulation

A

vasoconstriction

alpha 1

73
Q

what aa are vasodilated with epi

A

coronaries (beta2)

74
Q

how is epi used in asthma

A

bronchodilator (b2) vasoconstrictor (a1) and inhibitor of Ag-induced release of histamine (b2)

75
Q

what is a bad side effect of epi if used concurrently with halogenated hydrocarbons

A

arrhythmias

76
Q

what are the CNS side effects from epinephrine

A

fear, anxiety and headaches

77
Q

what conditions are contraindicated in use of epinephrine

A

HTN, shock, Hyperthyroidism, angina pectoris, asthmatics with degenerative heart disease

78
Q

What are the pharmacological effects of Norepi

A

agonist to a1 and 2 and b1

79
Q

what are the effects of norepi on the heart

A

direct, positive inotropic and chronotropic effects

indirectly causes a reflex of bradycardia

80
Q

what is the bradycardic reflex from nor epi stimulated by

A

vasoconstriction

81
Q

how to we prevent the reflex bradycardia seen after admin of norepi

A

atropine

82
Q

what R in blood vessels are activated by norepi

A

a1

83
Q

What is the net effect of Norepi on blood vessels

A

increased blood pressure

84
Q

what are the metabolic effects of norepi

A

a1 causes weak glycogenolysis and beta3 causes lipolysis

85
Q

what are the side effects of norepi on blood vessels

A

anxiety, slow forceful heart beat, headache

86
Q

What R does isopoterenol target

A

agonist B1 B2 and B3

87
Q

what are the effects of isoproterenol on heart

A

increased HR and force on contraction

88
Q

what are the effects of isopoterenol on blood vessels

A

vasodilation of blood vessels in skel m

89
Q

What is the net change in BP from isoproterenol

A

decreased in mean atrial BP

90
Q

what are the effects of isoporterenol on smooth m

A

relaxes bronchial and uterine smooth m

91
Q

what are the metabolic effects os isoporterenol

A

increased FFA because release insulin and opposes B2 glycogenolysis in liver

92
Q

what is isoproterenol used for in th ehar

A

hear block, intracardial injection
cardiogenic shock after MI
increases CO and blood flow

93
Q

what are the common sideeffects of isoproterenol

A

tachycardia, headache, flushing of skin

94
Q

what are the serious side effects of isproterenol

A

arrhythmias, anginal pain.

95
Q

what R does dopamine acticate

A

B1 and D1

at high also a1

96
Q

what are the effects of dopamine on the heart

A

mild positive inotropic and chronotropic effects compared to isopoterenol

97
Q

what are the effects of dopamine on blood vessels

A

vasodilation of mesenteric and renal vascular beds (dopamine R)

98
Q

how does dopamine help in schock

A

increase CO and enhance perfusion

99
Q

How is dopamine effective in CHF

A

increases CO without increases TPR

100
Q

What is Fenoldopam

A

synthetic dopamine D1 agonist

used to Tx HTN

101
Q

What is Bromocriptine

A

synthetic dopamine D2 agonist used to Tx parkinsons or prolactinemia

102
Q

What R does Dobutamine act on

A

selective B1 agonist

partial

103
Q

How is dobutamine effective for AMI

A

smaller effects on HR and systolic pressure

increases CO- lesser incidence of dopamine (especially for cardiogenic shock)

104
Q

what is the main contraindication for dobutamine

A

idiopathic hypertrophic subaortic stenosis

105
Q

What is different about metabolism of alpha adrenergic agonists “non-catecholamine” vs catecholamines

A

not metabolized as rapidly by COMT/MAO

106
Q

What R does phenyleprhine act on

A

a1

107
Q

What is phenylephrine used clinically for

A

nasal decongestant, infiltration with local anesthetics
pressor agent
paroxysmal atrial tachyardia inducing reflex bradycardia
glacoma
mydriasis(no effect on accomodation

108
Q

What is Midodrine used for

A

orally for orthostatic hypotensions that is disabling

109
Q

What are the main B2 agonists

A

albuterol, salmeterol, formoterol metaproterenol, terbutaline, ritodrine

110
Q

what are side effects of albuterol

A

muscle tremors, tachycardia, headaches, hypoglycemia, hypokalemia

111
Q

how do amphetamines work adrenergically

A

release NE from nerve endings and inhibit reuptake NE

112
Q

What are examples of pharm amphetamines

A

adderall (benzedrine)

dexedrine

113
Q

What are the CNS effects of amphetamines

A

increased alertness, confidence, ability to concentrate and decreased sense fatigue

114
Q

What are the CV effects of amphetamines

A

vasoconstriction, positive inotropic effect

115
Q

what are the smooth mm effects of amphetamines

A

mild constriction of sphincter of bladder

116
Q

what are the metabolic effects of amphetamines

A

last several hours

117
Q

what do we use amphetamines for clinically

A

nacrolepsy, ADHD and obesity (Anorexic effects)

118
Q

What are main side effects of amphetamines

A

CNS, insomnia delirium, anxiety
CV, arrhythmias anginal pain
GI: nausea vomiting

119
Q

What are signs of acute and chronic amphetamine toxicity

A

acute: convulsions, coma, death
chronic: abnormal mental state, weight loss, psychotic reactions

120
Q

How do we reverse amphetamines

A

are weak bases and therefore acidity-urine with ammonium chloride to prevent reabsorption

121
Q

what R does ephedrine and pseudoephedrine act on

A

mixed

B receptor and indirect actions (release NE)

122
Q

why are ephedrine and pseudoephedrine so long acting

A

not hydrolyzed by COMT or MAO

123
Q

What is ephedrine and pseudo ephedrine used for

A

pressor agent in spinal anesthesia, nasal decongestant, severe acture bronchospasm by parenteral admin

124
Q

What are sideeffects of ephedrine

A

anxiety, insomnia, palpitations

125
Q

What receptors do nasal decongestants act onact on

A

alpha 1 causing casoconstrictor

126
Q

What nasal decongestant should not be used in patients with HTN

A

otricin which is xylometazoline

127
Q

what nasal decongestant should not be used in children

A

tetrahydrozoline (tyzine and visine)

Year2 Renal (20 decks)

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