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RW Principles > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is the preganglionic neurotransmitter, type and length for the sympathetic system?

A

Acetylcholine; cholinergic transmission (nicotinic receptor); short (because have to go to paravertebral/prevertabel which are near spinal cord)

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2
Q

What is the postganglionic neurotransmitter for the sympathetic system?

A

Noradrenaline; adrenergic transmission (adrenoreceptor); long

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3
Q

What is the preganglionic neurotransmitter, type and length for the parasympathetic system?

A

Acetylcholine; cholinergic transmission (nicotinic receptor); long (because ganglia are often in target tissue)

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4
Q

What is the postganglionic neurotransmitter, type and length for the parasympathetic system?

A

Acetylcholine; cholinergic transmission (muscarinic receptor); short

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5
Q

What are the 3 types of sympathetic outflow?

A
  • Prevertebral ganglia
  • Paravertebral
  • Adrenal gland directly (exception – only has a preganglionic neuron)
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6
Q

Where does the thoracolumbar outflow of the sympathetic system come from?

A

T1-L2/3

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7
Q

Where are paravertebral ganglia of the sympathetic system located?

A

In the sympathetic chain

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8
Q

Where are pre vertebral ganglia of the sympathetic system located?

A

Between the sympathetic chain and the target organ

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9
Q

There are 4 routes the axon of sympathetic system can take, what do 3 of them have in common?

A

All axons enter the paravertebral ganglion at the level of its originating spinal nerve

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10
Q

There are 4 routes the axon of sympathetic system can take, what are they?

A

After entering paravertebral ganglion they can:
• Synapse in this ganglion
• Ascend to a more superior or descend to a more inferior paravertebral ganglion and synapse there
• Or it can descend to a prevertebral ganglion and synapse there with the postsynaptic cell.
4th route is an exception: innervation of the adrenal medulla where the presynaptic neurons pass through paraverterbral ganglia, on through prevertebral ganglia and then synapse directly with suprarenal tissue

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11
Q

Which cranial nerves and pelvic splanchnic nerves are involved in the parasympathetic outflow?

A

CN III, VII, IX and X

S2-4

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12
Q

What is the overview of neurochemical transmission?

A
  1. Uptake of precursor into presynaptic cell
    • Brought in by channels
  2. Synthesis of transmitter (T)
  3. Storage of transmitter (T) in vesicles
  4. Depolarisation by action potential
  5. Ca2+ influx through voltage-activated Ca2+ channels caused by depolarisation
  6. Ca2+- induced release of transmitter (exocytosis)
    • Vesicles fuse with the presynaptic membrane and then release contents into cleft
    • Calcium interacting with membrane proteins allow the vesicles to fuse
  7. Receptor activation
  8. Enzyme-mediated inactivation of transmitter or
  9. Reuptake of transmitter
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13
Q

What are the two classes of adrenoreceptors?

A

alpha and beta

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14
Q

What kind of receptors are nicotinic ACh receptors?

A

ligand-gated ion channel

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15
Q

What kind of receptors are adrenoreceptors?

A

G-protein coupled

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16
Q

What kind of receptors are muscarinic ACh receptors?

A

G-protein coupled

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17
Q

What do G protein coupled receptors consist of?

A

Receptor with 7 transmembrane spans

Guanine nucleotide binding protein with 3 polypeptide subunits (α, β & γ)

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18
Q

What is happening with GPCR when they aren’t signalling?

A

The receptor is unoccupied
The G-protein α-subunit binds GDP
The effector is not modulated

19
Q

How is the signal turned on with a GPCR?

A

1) Agonist activated receptor
• G-protein moves over and couples with receptor
• GDP dissociates from the α subunit, and GTP binds
• 2) G-protein dissociates into separate α (red) and βγ (grey) subunits
• G-protein α subunit moves over and binds to effect and alters its activity
• 3) Agonist may dissociate from the receptor, but signalling can persist

20
Q

How is the signal of GPCR turned off?

A

1) The α-subunit acts as an enzyme (a GTPase) to hydrolyse GTP to GDP and Pi. The signal is turned off
2) The G-protein α-subunit recombines with the βγ subunit completing the ‘G-protein cycle

21
Q

What are the 2 types of cholinergic receptors?

A

Nicotinic and muscarinic

22
Q

What is the structure of nicotinic acetylcholine receptors?

A

Consist of five glycoprotein subunits which entirely spans the membrane and form a central, cation conducting, channel

23
Q

Excitatory Post-Synaptic Potential (EPSP)

A

Initial event of electrical excitation at cholinergic transmitters is a graded response therefore the more Ach that is released, the greater the rate of depolarisation

24
Q

Which drugs affect cholinergic transmission at ganglia?

A

Nicotine (Causes a HR increase because it stimulates recptors in the ganglia leading to excitation)
Hexamethonium (blocks autonomic function via channel open channel block - receptor tries to pass it but its gets stuck and blocks it)

25
Q

What kind of response to nicotinic receptors produce?

A

Excitatory

26
Q

Where are nicotinic receptors found?

A

Skeletal muscle and ganglia

27
Q

Where are muscarinic receptors found?

A

Parasympathetic neuroeffector junctions

28
Q

Where are adrenergic receptors found?

A

Sympathetic neuroeffector junctions

29
Q

Which G-protein do M1 receptors couple with, and what effect occurs?

A

Gq; Stimulation of phospholipase c –> Increased acid secretion

30
Q

Which G-protein do M2 receptors couple with, and what effect occurs?

A

Gi; Inhibition of adenylyl cyclase; opening of K+ channels –> decreased HR

31
Q

Which G-protein do M3 receptors couple with, and what effect occurs?

A

Gq; contraction of visceral smooth muscle and stimulation of phospholipase c –> Increased acid secretion;

32
Q

Which G-protein do B1 receptors couple with, and what effect occurs?

A

Gs; Stimulation of adenylyl cyclase –> increased HR and force

33
Q

Which G-protein do B2 receptors couple with, and what effect occurs?

A

Gs; Stimulation of adenylyl cyclase –> relaxation of bronchial and vascular smooth muscle

34
Q

Which G-protein do a1 receptors couple with, and what effect occurs?

A

Gq; Stimulation of phospholipase C –> Contraction of vascular smooth muscle

35
Q

Which G-protein do a2 receptors couple with, and what effect occurs?

A

Gi; Inhibition of adenylyl cyclase –> inhibition of NA release

36
Q

What effect does cocaine have on the ANS?

A

Structure similar to NA so uptake 1 in pre-synaptic terminal will bind cocaine. Cocaine occupies the NA receptor, so blocks the receptor to NA, therefore NA cant be moved out so the concentration of NA increases. Causes increased action on a1 so increased vasoconstriction and also arrhythmia

37
Q

What effect does amphetamine have on the ANS?

A

Also similar structure to NA, but it enters the noradrenic terminal where it locks the activity of the enzyme MAO which normally breaks NA down, so NA levels rise. Also causes increased action on a1 so increased vasoconstriction and also arrhythmia

38
Q

What effect does prazosin have on the ANS?

A

Selective competitive antagonist for α1 adrenorecptors, so blocks the effect of NA, which normally constricts. Therefore prazosin acts as a vasodilator so works as an anti-hypertensive agent

39
Q

What effect does atenolol have on the ANS?

A

Competitive antagonist for β2 adrenoreceptors (beta blocker) so antagonises the effects of adrenaline and NA, giving decreased heart rate and force. Effective as a anti-hypertensive agent and in angina

40
Q

What effect does salbutamol have on the ANS?

A

Selectively activates β2 adrenoreceptors (not B1, a1 or a2) so used as a bronchodilator in asthma to increase airflow

41
Q

What effect does atropine have on the ANS?

A

Competitive antagonist for all muscarinic Ach receptors (unspecifically), therefore used to reverse bradycardia (slowing of the heart) following MI, which is mediated by muscarinic receptors. Low doses of atropine paradoxically slow the a heart down so need a relatively high dose to have the desired effect of increasing the HR.

42
Q

What are the steps in noradrenergic transmission at sympathetic neuroeffector junctions?

A
  1. Synthesis of NA (multiple steps)
    - Precursor of NA is the dietary amino acid L-tyrosine
  2. Storage of NA by transporter (concentrates)
    - NA is concentrated in synaptic vesicles by vesicular mono-amit Transport (VMAT)
  3. Depolarization by action potential
    - Depolarisation open Ca channels and Ca conc increases intracellularly
  4. Ca2+ influx through voltage-activated Ca2+ channels
  5. Ca2+-induced release of NA
    - NA goes into synaptic cleft and activates post-synaptic adrenoreceptors
  6. Activation of adrenoceptor subtypes causing cellular response (tissue dependent)
  7. Reuptake of NA by transporters uptake 1 (U1) and uptake 2 (U2)
    - NA is not degraded in the cleft like Ach
    - Instead it is either repackaged into the pre-synaptic terminal by uptake 1, or reabsorbed into the effector cell by a distinct uptake process of Uptake 2
    • I.e. neuronal uptake of a transmitter vs. non-neuronal uptake
  8. Metabolism of NA by monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT)
    - Uptake 1: Re-uptaken into the pre-synaptic which results in metabolism by MAO which results in inactive metabolites
    • Uptake 2: Uptaken by the effector cells, it is inactivates by COMT were you again get inactive metabolites
43
Q

What are the steps for cholinergic transmission?

A
  1. Uptake of choline via transporter (co-transport or symport)
  2. Synthesis of ACh via choline acetyltransferase (CAT)
    • Choline combines with acetyl CoA produced in the mitochondria
    • This then forms Ach
    • Have a much higher conc of Ach intracellularly, than in the cytoplasm
  3. Storage of ACh via transporter (concentrates)
  4. Depolarization by action potential
  5. Ca2+ influx through voltage-activated Ca2+ channels
  6. Ca2+- induced release of ACh (exocytosis)
  7. Activation of ACh receptors (nicotinic at ganglia or muscarinic at neuroeffector junctions) causing cellular response
  8. Rapid degradation of ACh to choline and acetate by acetylcholinesterase (AChE) – terminates transmission
  9. Reuptake and reuse of choline

RW Principles (3 decks)

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