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Block 2: Pharmacology > Lecture 1 > Flashcards

Lecture 1 Flashcards

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1
Q

(Drug Class)
Natural Catecholamine?

A

(Drug Name)
-Dopamine
-Epinephrine
-Norepinephrine

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2
Q

(Drug Class)
Indirect-acting Sympathomimetics?

A

(Drug Name)
-Cocaine
-Amphetamine

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3
Q

(Drug Class)
Mixed-action Sympathomimetics?

A

(Drug Name)
-Ephedrine
-Pseudoephedrine

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4
Q

(Nervous System)
Main 2 Systems?

A

-Peripheral (outside of Brain/Spinal Cord)
-Central (Brain + Spinal Cord)

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5
Q

(Nervous System)
Peripheral Nervous System?

A

(Outside of Brain/Spinal Cord)
-Autonomic (involuntary; homeostasis)
-Somatic (voluntary; movement)

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6
Q

(Nervous System)
Autonomic Nervous System?

A

(Involuntary; homeostasis)
-Parasympathetic (rest and digest)
-Sympathetic (fight or flight)

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7
Q

(Nervous System)
Autonomic we want to?

A

Preserve homeostasis

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8
Q

(Nervous System)
Somatic is?

A

Voluntary; movement

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9
Q

(Nervous System)
Autonomic target tissue?

A

Visceral organs, glands, smooth muscle

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10
Q

(Nervous System)
Somatic target tissue?

A

Skeletal Muscle

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11
Q

(Autonomic Nervous System)
Sympathetic Nervous System?

A

-Pre-ganglionic (short)
(spinal cord –> ganglia)
(ACh/Cholinergic)
-Post-ganglionic (long)
(ganglia –> site of action)
(multiple neurotransmitters but primary is adrenergic (norepinephrine)

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12
Q

(Autonomic Nervous System)
Sympathetic Pre-Ganglionic?

A

Short; Cholinergic

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13
Q

(Autonomic Nervous System)
Sympathetic Post-Ganglionic?

A

Long; Adrenergic

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14
Q

(Autonomic Nervous System)
Parasympathetic Nervous System?

A

-Pre-ganglionic (long)
(cholinergic/ACh)
-Post-ganglionic (short)
(cholinergic/ACh)

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15
Q

(Autonomic Nervous System)
Parasympathetic Pre-Ganglionic?

A

Long; Cholinergic/ACh

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16
Q

(Autonomic Nervous System)
Parasympathetic Post-Ganglionic?

A

Short; Cholinergic/ACh

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17
Q

(Effector Organ Response to Sympathetic Stimulation)
Heart?

A

(increases HR and blood flow to muscle)
-SA Node (accelerates)
-Contractility (increases)

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18
Q

(Effector Organ Response to Sympathetic Stimulation)
Blood Vessels?

A

-Skeletal muscle (relaxes/contracts)
-Coronary (relaxes/contracts)

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19
Q

(Effector Organ Response to Sympathetic Stimulation)
Lung?

A

(relax lung to breathe)
-Bronchial smooth muscle (relaxes)

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20
Q

(Effector Organ Response to Sympathetic Stimulation)
GI tract?

A

(stop digest food)
-Motility and tone (decreases)
-Sphincters (contracts)

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21
Q

(Effector Organ Response to Sympathetic Stimulation)
Skin?

A

(sweat)
-Sweat glands (thermoregulatory) (increases)
-Sweat glands (apocrine, stress) (increases)

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22
Q

(Effector Organ Response to Sympathetic Stimulation)
Metabolism/Other?

A

(breakdown for energy)
-liver (gluconeogenesis) (glycogeniolysis)

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23
Q

(Effector Organ Response to Sympathetic Stimulation)
Autonomic Nerve Endings?

A

-Parasympathetic (decrease ACh release)

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24
Q

(Effector Organ Response to Parasympathetic Stimulation)
No Parasympathetic Innervation to?

A

-Adrenal Medulla
-Sweat Glands
-Blood Vessels

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25
(Effector Organ Response to Parasympathetic Stimulation) Heart?
(decreases HR) -SA Node (decreases)
26
(Effector Organ Response to Parasympathetic Stimulation) Lungs?
(contract/secrete in lungs) -Bronchial smooth muscle (contracts) -Bronchial glands (increase)
27
(Effector Organ Response to Parasympathetic Stimulation) GI tract?
(digest food) -Motility and tone (contracts) -Sphincters (relaxes)
28
(Effector Organ Response to Parasympathetic Stimulation) Metabolism/Other?
-Liver (glycogen synthesis)
29
(Dual Innervation by ANS in an Organ) (Eye) Sympathetic Control?
(Fight or Flight) (Mydriasis) Eyes dilate to see better
30
(Dual Innervation by ANS in an Organ) (Eye) Parasympathetic Control?
(Miosis) Constricts --> aqueous humor release so it can repair eye
31
(Autonomic Nervous System) Efferent?
Signal going away from CNS
32
(Autonomic Nervous System) Afferent?
Signal going toward CNS
33
(Feedback Loops in the ANS: Baroreceptor Reflex) (Parasympathetic Output) No effect on?
Peripheral Resistance or Venous Tone
34
(Feedback Loops in the ANS: Baroreceptor Reflex) (Parasympathetic Output) Steps?
-Increase BP -Stretch BP -Increase firing to Vasomotor Center -Parasympathetic ACTIVATED -Decrease HR (and a little contractile force) -Decrease BP
35
(Feedback Loops in the ANS: Baroreceptor Reflex) (Sympathetic Output) Involved in?
-Normal physiological response -Pathophysiological responses (CHF) -Unwanted side effects (vasodilator)
36
(Feedback Loops in the ANS: Baroreceptor Reflex) (Sympathetic Output) Inhibition results in?
Orthostatic hypotension (BP drops when standing up)
37
(Feedback Loops in the ANS: Baroreceptor Reflex) (Sympathetic Output) Steps?
-Decrease BP -Decrease BR Firing to Vasomotor Cortex -Sympathetic ACTIVATED -Increase HR, resistance (constriction), contraction, venous tone
38
(Feedback Loops in the ANS: Baroreceptor Reflex) Parasympathetic Output?
Mainly HR and a little contractile force
39
(Feedback Loops in the ANS: Baroreceptor Reflex) Sympathetic Output?
When low BP (orthostatic hypotension)
40
(Cholinergic (ACh) Synapse Location) Both Parasympathetic and Sympathetic Ganglia all have?
Presynaptic Cholinergic Neurons
41
(Cholinergic (ACh) Synapse Location) All Parasympathetic target organs have?
Cholinergic synapses
42
(Cholinergic (ACh) Synapse Location) A few Sympathetic have Cholinergic Synapses?
-Sweat Glands -Vascular System
43
(Cholinergic (ACh) Synapse Location) ACh primary in?
-Adrenal Gland -Skeletal Muscle -All Ganglia
44
(Cholinergic (ACh) Synapse Location) Parasympathetic?
Cardiac and Smooth Muscle, Gland Cells, Nerve Terminals
45
(Cholinergic (ACh) Synapse Location) Sympathetic?
Sweat glands, vascular smooth muscle (few)
46
(Cholinergic (ACh) Synapse Location) Somatic?
Skeletal Muscle
47
(Cholinergic Juncture) Synthesis, Storage and Release?
-Choline transported into cell, Acetyl CoA originates from pyruvate -Acetyl CoA + Choline --> ACh via Choline Acetyl Transferase -ACh stored in vesicles -Ca increases and ACh is released -Binds to receptor (N or M) (depending on rec/location =effect)
48
(Cholinergic Juncture) ACh is produced outside of?
Vesicles then transported into vesicle
49
(Cholinergic Juncture) Ca?
ACh release from vesicle
50
(Cholinergic Juncture) Cholinoceptors?
Nicotine and Muscurine
51
(Cholinergic Juncture) Termination of Action?
-Excess ACh is mainly broken down via ACh Esterase -Choline is transported back into cell to be reused
52
(Cholinergic Juncture) Choline is pumped back in?
To make more ACh
53
(Cholinergic Juncture) ACh esterase enzyme?
Breaks down ACh
54
(Cholinergic Receptor Subtypes) What are the 2 types?
-Muscarinic (activated by Muscarine) -Nicotinic (activated by Nicotine)
55
(Cholinergic Receptor Subtypes) Muscarinic?
(M1-M5) -Activated by Muscarine -Slower (G Protein-Coupled Receptors (GPCR))
56
(Cholinergic Receptor Subtypes) Nicotinic?
(Nm,Nn, Nn-aBgt) -Activated by Nicotine -Faster (Ligand-Gated Ion Channels)
57
(Distribution of Nicotinic Receptors) Parasympathetic?
-Cardiac and Smooth Muscle -Gland Cells -Nerve Terminals
58
(Distribution of Nicotinic Receptors) Sympathetic?
-Sweat Glands, vascular smooth muscle (few) -Renal vascular smooth muscle -Cardiac and smooth muscle, gland cells, nerve terminals
59
(Distribution of Nicotinic Receptors) Somatic?
Skeletal Muscle
60
(Distribution of Nicotinic Receptors) Nicotinic Receptors are Ligand Gates and produce?
Fast Transmission (this is why in Ganglia and Skeletal Muscle)
61
(Nicotinic Receptor Channels) Nm?
(m for muscle contraction) -Neuromuscular juncture -Na+, Ca2+ channels -Skeletal muscle contraction
62
(Nicotinic Receptor Channels) Nn?
(n for neuronal) -Autonomic ganglia, Brain -Na+, Ca2+ channels -Ganglionic transmission
63
(Cholinomimetic Alkaloids: Muscarinic Agonists) What is the plant?
Amanita muscaria
64
(Distribution of Muscarinic Receptors) Parasympathetic?
-Cardiac and smooth muscle -Gland cells -Nerve terminalis
65
(Distribution of Muscarinic Receptors) Sympathetic?
-Sweat glands -Vascular smooth muscle (few)
66
(Distribution of Muscarinic Receptors) They mainly are?
Parasympathetic ONLY
67
(Muscarinic Receptors) Odds?
(M1, M3, M5) (Excitatory) -All increase calcium -Increase secretion
68
(Muscarinic Receptors) Evens?
(M2, M4) (Inhibitory) -Increase K, Hyperpolarize (No AP) -Decrease cAMP, decreasing SA node firing and slow HR
69
(GPCRs) Gs?
Stimulatory --> increases cAMP
70
(GPCRs) Gi?
Inhibitory --> decreases cAMP
71
(GPCRs) Gq?
"Different Stimulatory"--> increases IP3, DAG --> Ca
72
(Muscarinic Receptors) (Odd) M1?
(Excitatory) -Gq -PLC, IP3, DAG, increases intracellular Ca2+ -Nerves -Depolarization of neuron activation of myenteric plexus
73
(Muscarinic Receptors) (Odd) M3?
(Excitatory) -Gq -Similar to M1 PLC, IP3, DAG, increases intracellular Ca2+ -Glands, smooth muscle, endothelium, nerves -Contraction of GI and bronchial smooth muscle, increases GI secretion
74
(Muscarinic Receptors) (Odd) M5?
(Excitatory) -Gq -Similar to M1 (PLC, IP3, DAG, increases intracellular Ca2+) -CNS -Modulate neuroexcitability and vascular tone
75
(Muscarinic Receptors) (Odd) Gq?
Activates PLC --> increases IP3 and DAG --> increases Calcium
76
(Muscarinic Receptors) (Even) M2?
(Inhibitory) -Gi/Go -Inhibit adenylyl cyclase, activate K+ channels, inhibit Ca2+ channels -Heart, nerves, smooth muscle -Decreases SA node firing rate (negative chronotropic) decreases ventricular contractile force (negative inotropic)
77
(Muscarinic Receptors) (Even) M4?
(Inhibitory) -Gi/Go -Inhibit adenylyl cyclase, activate K+ channels, inhibit Ca2+ channels -Nerves, CNS -Modulate neuroexcitability
78
(Muscarinic Receptors) (Even) Gi?
Inhibitory --> Decreases cAMP
79
(Muscarinic Receptors) (Even) ACh -->?
ACh --> M2 --> Gi (GPCR) --> Inhibits adenylyl cyclase (decreasing cAMP), activates K, and decreases Ca --> decreases SA node and contraction
80
(Adrenergic Synapse Location) (At Target Organ) Sympathetic (D)?
Renal vascular smooth muscle
81
(Adrenergic Synapse Location) (At Target Organ) Sympathetic (NE)
(NE) Cardiac and smooth muscle, gland cells, nerve terminals
82
(Adrenergic Synapse Location) (At Target Organ) Mainly?
Sympathetic (fight or flight) (Norepinephrine)
83
(Noradrenergic Juncture) Synthesis, Storage and Release?
-Tyrosine transported into cells (A) --> combines with DOPA to create Dopamine --> Dopamine gets taken up into vesicle (B) (Dopamenergic) -Dopamine converts to Norepinephrine inside vesicle --> Ca release causes release of NE from vesicle (adrenergic)
84
(Noradrenergic Juncture) Dopaminergic?
Neuron just takes dopamine into vesicle
85
(Noradrenergic Juncture) Adrenergic?
Neurons take up dopamine into vesicle and convert it to NE
86
(Noradrenergic Juncture) (Termination of Action) Uptake 1?
NE is actively pumped back into presynaptic neuron (MOST IMPORTANT STEP) (some recycled into vesicles) (some is metabolized by monoamine oxidase (MAO))
87
(Noradrenergic Juncture) (Termination of Action) Uptake 2?
A smaller portion is transported into post-junctional cell and metabolized by catechol-O-methyl transferase (COMT)1
88
(Noradrenergic Juncture) (Termination of Action) Both Uptake 1 and Uptake 2 can degrade?
Catecholamines but not how action is terminated (Action is terminated by reuptake)
89
(Noradrenergic Juncture) (Termination of Action) Steps?
-Tyrosine transported into cells --> combines with DOPA to create dopamine --> dopamine gets taken up into vesicle --> dopamine converts to NE inside vesicle --> Ca release causes release of NE from vesicle --> NE binds to adrenoreceptor to have an effect (depends on location and receptor) --> excess of NE is terminated by reuptake via NET
90
(Adrenergic Receptor Subtypes) Odd?
(Adrenergic = sympathetic, think fight or flight) (Excitatory) -a1A -a1B -a1D
91
(Adrenergic Receptor Subtypes) Even?
(Adrenergic = sympathetic, think fight or flight) (Inhibitory) -B1 -B2 -B3
92
(Alpha Adrenergic Receptors) a1?
(excitatory increase Ca) -Gq -PLD, PLA2, PLC, IP3, DAG, increase intracellular Ca2+ -Vascular smooth muscle, heart, liver -Vasoconstriction, increases contractile force, glycogenolysis, gluconeogeneis (sympathetic mainly vascular smooth muscle)
93
(Alpha Adrenergic Receptors) a2?
-Gi -Inhibit adenylyl cyclase, activate K+ channels, inhibit Ca2+ channels -Pancreas islets (B cells), Nerve terminals, vascular smooth muscle -Decrease insulin secretion (parasympathetic decrease NT release)
94
(Beta Adrenergic Receptors) B1?
(1 HEART) -Gs -Stimulate adenylyl cyclase and L-type Ca2+ channels -Heart, juxtaglomerular cells -increase force and rate of contraction, increase renin secretion (sympathetic for Heart)
95
(Beta Adrenergic Receptors) B2?
(2 LUNGS) -Gs -Stimulate adenylyl cyclase -Smooth muscle (vascular, bronchial, GI), bronchial glands, liver -relaxation (vasodilation, bronchodilation), increase bronchial secretions glycogenolysis, gluconeogenesis, increase insulin secretion (sympathetic for BV and Lungs)
96
(Beta Adrenergic Receptors) B3?
-Gs -Stimulation of adenylyl cyclase -Adipose tissue -Lipolysis, NO release (Fat breakdown)
97
(Beta Adrenergic Receptors) All Gs?
Increase cAMP
98
(Factors Affecting Blood Pressure) Capacitance Venules?
Holds fluid on venous side and decreases BP
99
(Factors Affecting Blood Pressure) Preload?
Amount of blood to fill Heart/stretch
100
(Factors Affecting Blood Pressure) Afterload?
Resistance to blood being pushed out by Heart
101
(Factors Affecting Blood Pressure) Volume Kidneys?
Renin/Angio Sys
102
(Reuptake and Repackaging of NE) NET?
Norepinephrine transporter (brings NE into cell)
103
(Reuptake and Repackaging of NE) Vesicular Monoamine Transporter?
Transporter for NE to repackage into vesicle
104
(Drugs that Enhance Noradrenergic Transmission) Indirect-Acting Sympathomimetics?
-Cocaine (increases HR, increases contractility, increases activity of pacemakers, vasoconstriction) (can have negative effect on Heart) (Blocks NET so NE builds up in synapse)
105
(Drugs that Enhance Noradrenergic Transmission) (Indirect-Acting Sympathomimetics) Amphetamine Tyramine?
-Gets taken up by NET to get into cell, then VMAT imports into vesicle, this causes the vesicle to fill and dump everything into presynaptic terminus -Builds up NE in presynaptic --> Non-Vesicular Release
106
(Drugs that Enhance Noradrenergic Transmission) (Indirect-Acting Sympathomimetics) Ephedrine Pseudoephedrine?
-Displaces NE like Amphetamines but also effects receptor (think Epi and Amphetamines)
107
Indirect Acting Sympathomimetics?
-Cocaine -Amphetamines -Ephedrine (Mixed)
108
(Indirect Acting Sympathomimetics) Cocaine?
Blocks NET, builds up in synapse
109
(Indirect Acting Sympathomimetics) Amphetamines?
Gets into vesicle and causes release in Presynaptic --> builds causing NON-vesicular release
110
(Indirect Acting Sympathomimetics) Ephedrine (mixed)?
Causes Non-Vesicular Release AND acts on Adrenergic receptors
111
Natural Catecholamines?
-Epi -NE -Dopamine
112
Epinephrine: Mechanism of Action and Pharmacology?
-Fight or Flight Hormone (Adrenal Gland) -Activates ALL adrenergic receptors (a1, a2, B1, B2, and B3 receptors)
113
(Epinephrine: Mechanism of Action and Pharmacology) Effects?
-Cardiac (positive inotropic and chronotropic effect B1) -Vascular: Vasoconstriction (splanchnic) and vasodilation (skeletal muscle) B2 -Smooth muscle- relaxation of GI, uterine and bronchial -Metabolic- elevates serum glucose and free fatty acids
114
(Cardiovascular Effects of Adrenergic Agonists) Epinephrine (Systemically)?
-Pulse Rate (Increases HR (B1)) -Blood Press (wider = Heart is pumping stronger (increase contractility)) -Resistance (decrease in resistance)
115
(Cardiovascular Effects of Adrenergic Agonists) Epinephrine?
-Increase Vasoconstriction (A1) -Decreases peripheral resistance to skeletal (B2) -Net effect of activating A1 and B2 = decrease in resistance
116
Epinephrine: Clinical Use?
-Anaphylaxis -Septic shock -Cardiac arrest
117
(Epinephrine: Clinical Use) Anaphylaxis?
Can't breathe --> administer Epi --> activates B2 --> Bronchodilation to breathe again (peanut allergy/ can't breathe)
118
(Epinephrine: Clinical Use) Septic shock?
Decreases in BP --> Administer Epi --> activate A1 for vasoconstriction to increase BP
119
(Epinephrine: Clinical Use) Cardiac arrest?
Heart stopped beating --> activate B1 to increases pumping force of Heart
120
(Epinephrine: Adverse Effects) Exaggeration of physiological effects, including CNS reactions?
-Angina -Anxiety/fear -Cardiac arrhythmias (B1) -Dyspnea -Headache -Hypertension (A1) -Peripheral vasoconstriction -Tissue necrosis (END ARTERIES) -Tremor
121
(Norepinephrine: Mechanism of Action and Pharmacology) Receptor activation?
Activates all receptors (except B2)
122
(Norepinephrine: Mechanism of Action and Pharmacology) Effects?
-Similar to epinephrine, except do not see relaxation of smooth muscle from B2 activation (ex. bronchial smooth muscle) -No relaxation of skeletal smooth muscle vasculature (therefore, increases in BP are more exaggerated)
123
(Norepinephrine: Mechanism of Action and Pharmacology) Norepinephrine activates everything but B2, because B2 is for?
Skeletal Muscle Dilation
124
(Cardiovascular Effects of Adrenergic Agonists) (Norepinephrine) Pulse Rate?
Decreases HR due to increases in BP/Resistance. Parasympathetic gets activated and slows HR (NO B2)
125
(Cardiovascular Effects of Adrenergic Agonists) (Norepinephrine) Blood Pressure?
Increases BP and Pulse Pressure due to A1 causes vasodilation
126
(Cardiovascular Effects of Adrenergic Agonists) (Norepinephrine) Peripheral Resistance?
Increases resistance (No B2 just A1)
127
(Cardiovascular Effects of Adrenergic Agonists) (Norepinephrine) Dramatic increases in resistance?
Increase BP = Body responds by activating Parasympathetic to decrease HR
128
Norepinephrine: Clinical Use?
-Septic shock -Hypotension -Vasopressor support in other types of shock
129
(Norepinephrine: Clinical Use) Septic shock?
Septic= Vasodilation --> need to vasoconstrict to increase BP (first choice) (for low BP)
130
Norepinephrine: Pharmacokinetics and Adverse Effects?
-Kinetics (similar to epinephrine) -Adverse Effects (similar to epinephrine, except hypertension is more pronounced due to a1 stimulation without B2 balance)
131
(Dopamine) (Receptor Activation and Effects (outside CNS)) D1?
-Vasodilation, including renal vasculature, diuresis/natiruresis -Hypotension effect
132
(Dopamine) (Receptor Activation and Effects (outside CNS)) D2?
-Presynaptic receptors -Negative feedback to inhibit further norepinephrine, and possibly dopamine release
133
(Dopamine) (Receptor Activation and Effects (outside CNS)) B1?
Positive inotropic (CONTRACTION) and chronotropic (HEART RATE) effect (AT HIGH LEVELS OF DOPAMINE ONLY)
134
(Dopamine) (Receptor Activation and Effects (outside CNS)) a1?
-Seen only at high doses -Causes vasoconstriction (EVEN HIGHER LEVELS)
135
Dopamine: Clinical Use?
-Cardiogenic shock -Septic shock -Hypotension (High dose stimulates a1 and B1 just like Norepinephrine)
136
High Dose of Dopamine stimulates a1 and B1?
Just like Norepinephrine
137
Epinephrine?
-ALL receptors, decrease in resistance but increase HR = slight increase BP overall -Use: Anaphylaxis
138
Norepinephrine?
-ALL receptors BUT NOT B2 -No bronchial/skeletal dilation therefore more resistance and higher increase BP, decrease in HR -Use: Septic Shock
139
Dopamine?
-Vasodilation and decrease Norepinephrine -Increase dose = A1/B1 Activation -Use: Cardiogenic shock

Block 2: Pharmacology (5 decks)

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