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pharmacodynamics > speth exam 2 > Flashcards

speth exam 2 Flashcards

1
Q

most muscarinic agonists have quaternary ______ that is essential for binding to acetylcholine receptors

A

nitrogen

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2
Q

how is glaucoma treated? what receptor is this acting on?

A

pilocarpine contracts the pupillary sphincter muscle which relaxes the iris by acting on the M3 receptor as an agonist

this allows for better flow of aqueous humor out of the eye to decrease intraocular pressure

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3
Q

pilocarpine is selective for _______ ____ receptors

A

muscarinic ACh receptors (M3)

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4
Q

list examples of muscarinic agonists (hint: there are 6)

A

acetylcholine
methacholine
carbachol
bethanechol
pilocarpine
cevimeline

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5
Q

list the 5 uses of muscarinic antagonists

A
  1. dilates pupil for retinal examination
  2. treats excessive motility of GI tract (diarrhea, IBS)
  3. treats urinary incontinence
  4. treats COPD and asthma
  5. treats motion sickness
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6
Q

overall, do muscarinic antagonists increase or decrease parasympathetic activity?

A

decrease parasympathetic activity

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7
Q

how are muscarinic antagonists used to dilate the pupil for retinal examination? what receptor is used for this?

A
  • increase sympathetic drive and decrease parasympathetic drive
  • M3 receptor is stimulated to cause relaxation of the pupillary sphinctor muscle which increases pupil size
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8
Q

what is mydriasis?

A

pupil dilation

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9
Q

how is excessive motility of the GI tract and the urinary tract treated?

A

muscarinic antagonists block overactivity of the parasympathetic nervous system (rest and digest)

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10
Q

how are COPD and asthma treated? (include drug and mechanism). is this a muscarinic or adrenergic mechanism?

A
  • can be both!
  • mucarinic antagonist: tiotropium Br (Spiriva) blocks ACh which causes bronchoconstriction
  • beta 2 adrenergic agonist
  • decreases parasympathetic stimulation for bronchodilation
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11
Q

how is motion sickness treated? (include drug, receptor, and mechanism)

A
  • scopolamine does not have quaternary nitrogen, so it is able to cross BBB and act on M1 muscarinic receptors
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12
Q

scopolamine causes ______ and ______

A

mydriasis and cycloplegia

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13
Q

what is cycloplegia?

A

paralysis of the ciliary muscle which results in dilation of the pupil and paralysis of accommodation (cannot see close objects)

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14
Q

what was atropine/belladonna used for in war? (explain the mechanism - hint: what does this block?)

A

atropine blocks acetylcholinesterase which causes a surge of acetylcholine

this causes bronchoconstriction and increased fluids in bronchial passages

this was useful for soldiers exposed to nerve gas (reduces flow of gas into lungs)

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15
Q

list the effects of anticholinergic agents using Dr. Speth’s mnemonic thing

A
  1. dry as a bone
  2. red as a beet
  3. hot as a hare
  4. blind as a bat
  5. mad as a hatter
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16
Q

what does “dry as a bone” mean in terms of anticholinergic agents?

A

causes very little peripheral dilation of cutaneous vessels

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17
Q

what does “red as a beet” mean in terms of anticholinergic agents?

A

causes flushing

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18
Q

what does “blind as a bat” mean in terms of anticholinergic agents?

A

inability to focus on things close up (cycloplegia)

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19
Q

what does “mad as a hatter” mean in terms of anticholinergic agents?

A

overdosing with antimuscarinic drugs can cause delirium

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20
Q

how long do atropine effects last?

A

6-10 days

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21
Q

what drug is closely related to atropine, treats motion sickness, causes anterograde amnesia, and is often used as a predatory drug? (hint: it is often called angel’s trumpet or natures poison?)

A

scopolamine

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22
Q

what is the source of scopolamine? (hint: it is known as the screaming plant in harry potter)

A

the mandrake mayapple

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23
Q

where is podophullum toxin found and what is it used for?

A
  • found in the mandrake mayapple (with scopolamine)
  • is an inhibitor of mitosis
  • source of anti-cancer and anti-viral drugs
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24
Q

what is tropicamide and what is it used for?

A
  • a synthetic agent that is similar to atropine and scopolamine but has a lower affinity for the receptor
  • this lower affinity allows for shorter duration of effects
  • used at the eye dr to dilate the pupils (effects only last 6 hours)
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25
Q

atropine effects last ____ days
scopolamine lasts ____ days
tropicamide lasts ____ hours - making it better for eye dilation exams

A

atropine = 6-12 days
scopolamine = 3-7 days
tropicamide = 6 hours
- will only have difficulty focusing and photophobia for 6 hours instead of days (this is why the dr uses this)

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26
Q

what are endogenous catecholamines?

A

hormones that act as neurotransmitters

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27
Q

what are the 3 uses of endogenous catecholamines?

A
  1. treats hypotension
  2. treats cardiogenic and septic shock
  3. treats anaphylaxis
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28
Q

how is shock treated

A

EPI and NE are given to increase BP (shock will decrease BP)

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29
Q

how is anaphylaxis treated?

A

By relaxing bronchiole smooth muscle

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30
Q

how is bradycardia treated?

A

NE and EPI are beta 1 agonists that increase HR

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31
Q

T or F: sympathetic agonists have similar functions to parasympathetic antagonists, and vice versa.

A

TRUE

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32
Q

what is the most potent catecholanine?

A

epinephrine

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33
Q

what receptor does epinephrine act on? what does this cause?

A
  • causes contraction/vasoconstriction of arteries (A1 and A2)
  • relaxes bronchial smooth muscle (B2)
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34
Q

what relaxes bronchial smooth muscle more: EPI or NE?

A

EPI

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35
Q

why is NE better than EPI for treating hypotension?

A
  • NE will only act on alpha1 receptors (causing contraction of arterial strips) and has a low potency at B2 adrenergic receptors (which causes relaxation of bronchioles/skeletal muscle beds)
  • EPI will interact with both A1 and B2
  • NE is used because you only want to constrict to increase BP, not dilate
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36
Q

what will happen when NE is pretreated with phenoxybenzamine?

A

phenoxybenzamine is a competitive antagonist
- dose response curve shifts to right

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37
Q

what happens with NE is pretreated with a non-competitive antagonist?

A

will get a lower maximum response

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38
Q

isoproterenol is a endogenous catecholamine that is a ____ selective agonist

A

beta selective agonist (beta 1 and 2)

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39
Q

where is isoproterenol potent and not potent? (what receptor and what does this do?)

A
  • most potent at B1 causing contraction of the heart
  • potent at B2 causing relaxation of bronchial smooth muscle
  • least potent for A1 (not good for contracting arteries)
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40
Q

phenylephrine is an ____ __ _____ receptor _____

A

phenylephrine is an alpha 1 adrenergic receptor agonist

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41
Q

what are the 5 uses of phenylephrine?

A
  1. treats nasal congestion
  2. treats hypotension
  3. treats shock
  4. induces mydriasis
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42
Q

phenylephrine drops in the eyes are an example of what?

A

a sympathetic agonist having similar effects to parasympathetic antagonist

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43
Q

how does phenylephrine treat hemorrhoids?

A

alpha 1 adrenergic agonist increases sympathetic stimulation

this increases vasoconstriction

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44
Q

what is an important aspect of the phenylephrine structure?

A

it has an alkyl chain with a methyl group

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45
Q

what is known as the “traitor” of sympathetic agonists? why is this?

A

alpha 2 adrenergic agonists are known as the “traitor” of sympathetic agonists.

This is because it causes inhibitory feedback. As EPI is released, the neuron will understand when there is too much, and will inhibit more release.

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46
Q

what are the uses of alpha 2 adrenergic receptor agonists? (hint: 3)

A
  1. treats hypertension
  2. treats ADHD
  3. treats neuropathic pain
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47
Q

how is hypertension treated by an alpha 2 adrenergic agonist?

A

inhibitory feedback of EPI release will decrease sympathetic drive

decreases BP, HR, CO, and vasoconstriction

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48
Q

amphetamine like drugs are used for what?

A

used as A2 adrenergic agonists to decrease ADHD symptoms

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49
Q

how is neuropathic pain treated by A2 adrenergic agonists?

A

any neuron with A2 adrenergic receptors will be inhibited (this includes pain fibers)

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50
Q

what are nonselective beta adrenergic receptor agonists used for?

A

treats heart block, bradycardia, and cardiac arrest

51
Q

how are nonselective beta adrenergic receptor agonists used to treat cardiac arrest, heart block, and bradycardia?

A

specifically acts on B1 (mostly)
shortens QRS T interval > speeds conduction of heart > restores normal sinus rhythm

52
Q

B1 adrenergic receptor agonists are used to treat:

A

cardiogenic shock

53
Q

B2 adrenergic receptor agonists are used to treat:

A

Asthma/bronchospasm
COPD

54
Q

explain the structure of adrenergic agonist drugs

A

all are amines that are metabolized into aldehydes and then metabolized into acids

the acids are “inactive” and no longer have affinity for receptor

55
Q

what is used as sedative/anesthetics in vet medicine and for ADHD symptoms?

A

clonidine - alpha 2 agonist

56
Q

is albuterol selective or nonselective? why?

A

selective for beta 2 adrenergic agonist, so you dont get adverse side effects of tachycardia and heart palpations

57
Q

is the fight or flight reaction mediated by sympathetic or parasympathetic nervous system?

A

sympathetic

58
Q

how is energy supplied to muscles for the fight or flight reaction?

A

glycogenolysis is stimulated by beta adrenergic receptors on the liver

they are stimulated to promote the glycogen stores to release glucose1phosphate into blood stream which supplies muscles with energy

59
Q

what are alpha adrenergic antagonists used to treat? (hint: 2)

A

treats benign prostatic hyperplasia
treats pheochromocytoma

60
Q

what is pheochromocytoma?

A

tumor of the adrenal medulla

61
Q

how is pheochromocytoma treated by alpha adrenergic antagonists?

A

too many chromatin cells secrete 80% EPI and 20% NE > increases sympathetic stimulation > causes hypertension and may cause stroke

use alpha adrenergic antagonists to decrease vasoconstriction

62
Q

what are the uses of beta adrenergic antagonists? (sorry there are 8 lol)

A
  1. treats tachycardia and angina post myocardial infarction
  2. treats essential tremors
  3. treats glaucoma
  4. treats heart failure
  5. treats hypertension
  6. treats migraine prophylaxis
  7. treats performance anxiety
  8. treats pheochromocytoma
63
Q

beta adrenergic _______ relaxes the workload of the heart after myocardial infarction

A

beta adrenergic antagonists

64
Q

how are beta blockers (beta adrenergic antagonists) used to treat hypertension?

A

juxtaglomergular cells on kidney release renin to stimulate pathway that creates angiotensin 2

beta blocker will decrease renin production and decrease cardiac output

65
Q

what beta blocker is used to treat performance anxiety? what receptor does it act on?

A

propranolol acts on Beta 1 to decrease HR

66
Q

what drug was used to steady the hands of ocular surgeons?

A

propranolol

67
Q

what do all beta blockers end in?

A

“olol”

68
Q

what are the benefits of selective antagonism?

A

non selective will block (for example) both A1 and A2 > can get more NE release because you are blocking inhibitory feedback

if you block only A1 (selective), you will have normal inhibition of NE release

69
Q

what is the most well known second messenger from GPCR signaling pathways? what enzyme is this created by?

A

cyclic AMP is the most well known second messenger

is created by adenylyl cyclase

70
Q

what is the most prominent excitatory neurotransmitter in the brain?

A

glutamate

71
Q

what is the most common GPCR receptor that has the most drugs made to target?

A

acetylcholine

72
Q

what is one of the most powerful vasopressor systems in the body?

A

the renin-angiotensin system

73
Q

what is the major function of the renin-angiotensin system?

A

to maintain fluid and electrolyte balance in the body

74
Q

originally, renin was thought to be a _______

A

hormone

75
Q

renin is an _______

A

enzyme

76
Q

where is renin released from?

A

kidney

77
Q

what does renin metabolize? (hint: first part of cascade in renin-angiotensin system)

A

angiotensinogen

78
Q

what is ACE?

A

angiotensin-converting enzyme

79
Q

how many amino acids does ACE remove from angiotensin 1? what does this create?

A

ACE removes 2 amino acids from the 10 amino acid chain of angiotensin 1

this creates an 8 AA chain which is angiotensin 2

80
Q

what is the primary hormone/neurotransmitter/neuropeptide of renin-angiotensin system?

A

angiotensin 2

81
Q

what happens to pressure when you have increased resistance to flow?

A

pressure increases

82
Q

ACE1 removes __ amino acids, while ACE2 removes __.

A

ACE = removes 2
ACE2 = removes 1

83
Q

AT2 acting on AT1R causes what?

A

increased BP and cardiofibrosis

84
Q

what receptor(s) does angiotensin 2 act on?

A

AT1 and AT2

85
Q

what is considered the “bad arm” of the renin-angiotensin system?

A

ACE, ANG2, AT1

86
Q

what is considered the “good arm” of the renin-angiotensin system?

A

ACE2, ANG1-7, MAS

87
Q

what is neprilysin (NEP)?

A

an endopeptidase that chops angiotensin 1 to remove last 3 amino acids, converting it directly to angiotensin 1-7

88
Q

what is valsartan?

A

NEP inhibitor

89
Q

list the 5 functions of angiotensin 2 (hint: all increase BP)

A
  1. increases sympathetic activity –> increases HR and blood pressure
  2. acts on kidney to promote reabsorption of sodium (and increase water retention) –> increases BP
  3. acts on adrenal cortex to release aldosterone –> increases sodium and water reabsorption into renal tubule
  4. acts on pituitary gland to secrete ADH/vasopressin –> causes vasoconstriction and promotes reabsorption of water from collecting duct of kidney
  5. increases arterial vasoconstriction
90
Q

where is the highest amount of ACE?

A

in the lung vasculature

91
Q

what is the ONLY precursor for angiotensin 2?

A

angiotensinogen

92
Q

what is the ONLY known function of angiotensinogen?

A

to be a precursor for angiotensin

93
Q

what are the 3 stimuli that cause renin release from the kidney?

A
  1. low blood pressure
  2. hyponatemia (low sodium in blood)
  3. increased sympathetic nervous system activity
94
Q

how does low BP cause renin release?

A

less stretch on the heart activates JG cells on kidney to secrete renin

95
Q

how does hyponatremia cause renin release?

A

macula densa cells are sensitive to sodium in urine

macula densa cells activate JG cells to secrete renin

96
Q

how does increased sympathetic nervous system activity cause renin release?

A

JG cells on arterial walls have B1 adrenergic receptors that recognize renin release to increase BP

97
Q

T or F: blood born angiotensin 2 can act on the brain

A

TRUE

98
Q

angiotensin 2 acts on ____ receptors on the brain

A

AT1

99
Q

angiotensin system acts on ______ organs which all have AT1 receptors

A

circumventricular organs

100
Q

when angiotensin 2 acts on the brain, what happens?

A

makes you thirsty, stimulates sympathetic nervous system, and releases vasopressin

101
Q

when ANG2 acts on the kidney, what happens?

A

fluid and salt retention

102
Q

when AG2 acts on the adrenal medulla, what happens?

A

aldosterone, EPI (80%), NE (20%), and ACTH are released

aldosterone promotes sodium retention to restore normonatremia

103
Q

when ANG2 acts on the liver, what happens?

A

creates a positive feedback and enzymatic reaction to release more angiotensinogen

104
Q

when ANG2 acts on the arterioles, what happens?

A

vasoconstriction and hypertrophy

105
Q

when ANG2 acts on the heart, what happens? what is a bad side effect from this?

A

increases rate and force of contraction

bad side effect: fibrosis from proliferation of fibroblasts

106
Q

when ANG2 acts on the anterior pituitary, what happens?

A

causes prolactin release

107
Q

overall, what does ANG2 do?

A

makes sure you have enough blood volume

108
Q

What kind of receptor is AT1?

A

G protein coupled receptor

109
Q

what 3 things happen from activation of the AT1 G protein coupled recepter?

A
  1. IP3 is released to cause influx of calcium for smooth muscle contraction
  2. diacylglycerol activates transcription factors to increase proteins
  3. Forms ROS (NOX - NADPH oxidase) which generates O2 and activates L type calcium channels to get more calcium into the cells to increase contractile force
110
Q

AT2 receptor is known as the ______ receptor but is NOT an angiotensin ______

A

known as the “anti-AT1 receptor” but is not an angiotensin antagonist

111
Q

what does the AT2 receptor cause?

A
  1. vasodilation
  2. apoptosis
  3. inhibition of growth
112
Q

CGP4412 is a _____ agonist for AT2 receptor

A

full agonist - DR SPETH FOUND THIS

113
Q

list the 5 groups of drugs that block the renin-angiotensin system

A
  1. KIREN
  2. OLOL
  3. PRIL
  4. SARTAN
  5. ONE (blocks aldosterone technically)
114
Q

renin inhibitor drugs that are rate limiting are known as what? (hint: they block the enzymatic activity of renin)

A

KIREN drugs

115
Q

beta blockers that decrease renin release by acting on B1 are known as what?

A

OLOL drugs

116
Q

ACE inhibitors are known as what?

A

PRILS

117
Q

ARBs (angiotensin receptor blockers (Blocks AT1)) are known as what?

A

SARTAN drugs

118
Q

why is it important that SARTAN drugs are AT1 selective?

A

AT2 does the opposite of AT1

119
Q

blockers of the renin-angiotensin-ALDOSTERONE system/mineralcorticoid receptor antagonists are known as what kind of drugs?

A

ONE drugs (spironolactone and eplerone)

120
Q

list therapeutic applications of ANG system inhibitors

A

 Hypertension/stroke prevention
 Diabetic nephropathy and retinopathy
 Polycystic kidney disease
 Cardiomyopathy/heart failure/left ventricular dysfunction/cardiac fibrosis/cardiac arrythmias (tachycardia) which is associated with clot formation
 Contraction of arteries  ischemia
 Hyperlipidemia
 Alzheimer’s (newer for ARBS)
 PTSD (increased BP) – ARBS on amygdala

121
Q

what is Giapreza (drug)

A

this is angiotensin 2 as a drug which is used for shock to increase BP

122
Q

List uses of muscarinic agonists

A
  • treat glaucoma
  • treat urinary leakage
123
Q

List uses of muscarinic antagonists

A
  • dilates pupil
  • treats excessive motility of GI tract
  • treats urinary incontinence
  • treats COPD and asthma
  • treats motion sickness
124
Q

List uses for endogenous catecholamines

A
  • treats hypotension
  • treats shock
    -treats anaphylaxis (relaxes bronchiole smooth muscle)
  • treats bradycardia

pharmacodynamics (2 decks)

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