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106 > Pharmacology - ANS > Flashcards

Pharmacology - ANS Flashcards

1
Q

Nervous system - 5

A
  1. CNS connected to muscles & organs through PNS.
  2. ANS regulates functions like heart rate & BP.
  3. ANS is divided into: the sympathetic & parasympathetic.
  4. Sympathetic system: fight or flight
  5. Parasympathetic system: rest & digestion
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2
Q

ANS - 5

A
  1. ANS is self-governing, operates without conscious control.
  2. ANS consists of the sympathetic and parasympathetic systems, both of which are formed by two neurons, 1st releases ACH to activate second.
  3. Sympathetic system: second neuron releases noradrenaline to target organs
  4. Parasympathetic system: ACH binds to muscarinic receptors.
  5. Sympathetic system exceptions: sweat glands release ACH, & adrenal medulla releases adrenaline
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3
Q

ANS represented by two types of neurons: preganglionic & postganglionic: 4

A
  1. Sympathetic Nervous System: Preganglionic fibres are short & synapse in the ganglia, while the postganglionic fibres are long & innervate target organs.
  2. Parasympathetic Nervous System: The preganglionic fibres are long, & synapse near or within the target organ, where the second neuron’s soma is located.
  3. Preganglionic has small diameter & is myelinated, releasing ACh that binds to nicotinic receptors on the postganglionic neuron.
  4. Postganglionic neuron has a small, unmyelinated diameter & synapses near the target organ.
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4
Q

Autonomic ganglion - 3

A
  1. When ACh binds to nicotinic receptors, they undergo a conformational change, opening a channel that allows sodium (Na⁺) to enter & potassium (K⁺) to exit.
  2. This ion movement generates an excitatory postsynaptic potential (EPSP), can lead to an action potential, resulting in the release of neurotransmitters.
  3. These fast EPSPs contribute to the transmission of signals between neurons in the ANS
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5
Q

Cardiovascular regulation by the ANS - 2

A
  1. Sympathetic nervous system regulates heart rate & BP, controlling the contraction & relaxation of smooth muscle in blood vessels and organs.
  2. Most blood vessels do not have parasympathetic innervation.
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6
Q

Physiological consequences of ganglionic nicotinic receptor stimulation - 2

A
  1. Drugs which manipulate ganglia have S/Es on both sympa & para systems due to shared neurotransmitters & receptors.
  2. e.g. stimulating ganglia could increase heart rate but also trigger unwanted effects like increased sweating & salivation.
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7
Q

Q: What was the primary use of ganglionic blockers like Hexamethonium?

A

They were the first drugs used to control heart rate and blood pressure by blocking nicotinic receptors and inhibiting both the sympathetic and parasympathetic systems

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8
Q

What side effects did ganglionic blockers like Hexamethonium cause?

A

They reduced heart rate and blood pressure but also caused side effects such as reducing gut and intestinal tract activity.

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9
Q

Why were ganglionic blockers like Hexamethonium replaced by more targeted antihypertensives?

A

Due to their broad effects and significant side effects, they were replaced by antihypertensive drugs with fewer side effects.

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10
Q

Why is Hexamethonium rarely used today?

A

It has been replaced by better alternatives with fewer side effects.

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11
Q

What was Hexamethonium known for in the history of medicine?

A

Hexamethonium was the first effective antihypertensive drug.

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12
Q

What is the current use of modern local anesthetics like Lidocaine?

A

Lidocaine blocks sympathetic fibers for pain management in emergency situations, not for blood pressure control.

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12
Q

What neurotransmitter is primarily released by postsynaptic sympathetic fibers?

A

A: Noradrenaline (NA).

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13
Q

Where are the cell bodies of postsynaptic sympathetic fibers located, and where do their axons end?

A

The cell bodies are in the sympathetic ganglion, and their axons end in varicosities.

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14
Q

What happens at the varicosities of postsynaptic sympathetic fibers?

A

Noradrenaline is synthesized, stored, and released at the varicosities.

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15
Q

What are the exceptions to the release of noradrenaline in sympathetic fibers?

A

Sweat glands (which release acetylcholine) and renal vessels (which release dopamine).

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16
Q

What is the problem with blocking or modulating the system by targeting ganglia?

A

: It leads to undesirable effects due to the shared neurotransmitters and receptors across the sympathetic and parasympathetic systems.

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17
Q

Where is noradrenaline (NA) synthesized?

A

In postganglionic sympathetic fibers at the terminal structures called varicosities.

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18
Q

What is the precursor molecule for noradrenaline?

A

L-tyrosine.

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19
Q

What is the first step in the synthesis of noradrenaline?

A

Tyrosine → DOPA (via tyrosine hydroxylase).

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20
Q

What is the second step in the synthesis of noradrenaline?

A

: DOPA → Dopamine (via DOPA decarboxylase)

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21
Q

What is the final step in the synthesis of noradrenaline?

A

Dopamine → Noradrenaline (via dopamine β-hydroxylase).

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22
Q

How is the synthesis of noradrenaline regulated?

A

Through a feedback mechanism that inhibits the enzyme tyrosine hydroxylase, regulating its own synthesis.

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23
Q

Q: Where are the enzymes responsible for neurotransmitter synthesis made?

A

A: They are made in the cell body and transported to the nerve terminus.

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24
Q

Q: What neurotransmitter is released by the adrenal medulla instead of noradrenaline?

A

A: Adrenaline (epinephrine).

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25
Q

Q: What neurotransmitter is used by renal vessels instead of noradrenaline?

A

A: Dopamine.

26
Q

Q: What regulates the synthesis of noradrenaline?

A

A: A negative feedback mechanism on the initial step of synthesis.

26
Q

Q: What do sweat glands use for neurotransmission instead of noradrenaline?

A

A: Acetylcholine.

27
Q

Q: What drug inhibits the conversion of L-tyrosine to DOPA?

A

A: α-methyl-p-tyrosine (Metirosine).

27
Q

Q: What enzyme converts L-tyrosine to DOPA in the synthesis of noradrenaline?

A

A: Tyrosine hydroxylase.

28
Q

Q: What clinical condition is treated with Metirosine?

A

Pheochromocytoma, a catecholamine-secreting tumor.

29
Q

Q: What symptoms are associated with pheochromocytoma?

A

A: High blood pressure, rapid heartbeat, sweating, anxiety, and tremors.

30
Q

Q: What is the second step in the synthesis of noradrenaline?

A

A: The conversion of DOPA to dopamine via DOPA decarboxylase.

31
Q

Q: What drug inhibits DOPA decarboxylase to help manage Parkinson’s disease?

A

A: Carbidopa.

32
Q

Q: How does carbidopa aid in Parkinson’s treatment?

A

A: It prevents the breakdown of levodopa (L-DOPA) in the periphery, reducing side effects like high blood pressure and racing heart.

33
Q

Q: Why doesn’t carbidopa cross the blood-brain barrier?

A

A: To increase the availability of levodopa in the CNS and avoid peripheral side effects.

34
Q

Q: What is the clinical use of Metirosine?

A

A: To treat pheochromocytoma by inhibiting the synthesis of catecholamines.

35
Q

Q: How is carbidopa used in Parkinson’s disease treatment?

A

A: It is used in conjunction with levodopa to reduce peripheral side effects and improve brain access.

36
Q

Noradrenaline release -2

A
  1. Depolarization of nerve endings opens calcium channels, allowing calcium ions to enter the terminal.
  2. This influx of calcium triggers vesicle exocytosis, releasing noradrenaline (NA) and ATP.
37
Q

Q: What is the function of autoreceptors in the feedback mechanism?

A

: Released noradrenaline binds to alpha-2 adrenergic receptors on the presynaptic nerve fibers.

38
Q

Q: What does the binding of noradrenaline to alpha-2 adrenergic receptors trigger?

A

A: Activation of a negative feedback loop, inhibiting adenylyl cyclase.

39
Q

Q: What does the inhibition of adenylyl cyclase lead to in the feedback mechanism?

A

A: It prevents further calcium channel opening, limiting the release of additional noradrenaline.

40
Q

Noradrenaline (NA) Removal from Synaptic Cleft - 3

A
  1. Neuronal Epinephrine Transporter (NET) actively transports NA back into presynaptic nerve terminals, recycling most of it.
  2. NA is taken up into vesicles by Vesicular Monoamine Transporter (VMAT), where it is stored alongside ATP.
  3. ATP, with opposite charge to NA, helps prevent leakage from vesicles & is co-released with NA.
41
Q

Noradrenaline (NA) Removal - 2

A
  1. The free [NA] in the cytoplasm is kept low by Monoamine Oxidase (MAO), which breaks down NA into DOMA.
  2. Catechol-o-Methyl Transferase (COMT), found in both neuronal & non-neuronal tissues, metabolizes DOMA & NA, including circulating catecholamines in the liver.
42
Q

Drugs inhibiting NA: Guanethidine (G): - 4

A
  1. Guanethidine is a substrate for both the NET (neuronal epinephrine transporter) & VMAT (vesicular monoamine transporter).
  2. Accumulates in vesicles & stabilizes them, displacing noradrenaline (NA), leading to its release.
  3. The released NA is metabolized by monoamine oxidase (MAO).
  4. Overall Effect: Guanethidine blocks adrenergic neurons, reducing adrenergic activity , can cause excess NA in synaptic cleft, causing S/Es
43
Q

α1 receptors

A

α1 receptors: Cause vasoconstriction by activating Gq proteins, which increase Ca levels, leading to muscle contraction.

44
Q

α2 receptors:

A

α2 receptors: Inhibit release of neurotransmitters, by acting on Gi proteins. They reduce cAMP levels & block Ca entry, thus inhibiting neurotransmitter release.

45
Q

β1 receptors:

A

β1 receptors: Increase heart rate & the contractile force of the heart by activating Gs proteins, leading to increased cAMP & Ca, enhancing heart function.

46
Q

β2 receptors

A

β2 receptors: Cause vasodilation & bronchodilation by activating by increasing cAMP & Ca, relaxing smooth muscles in blood vessels & the lungs.

47
Q

β3 receptors

A

β3 receptors: Regulate lipolysis & energy expenditure in adipose tissue by increasing cAMP & activating protein kinase A (PKA).

48
Q

Adrenoceptors B1 & a2 on the heart - 6

A
  1. Stimulation of β1 receptors by NA increases Ca levels in cardiac myocytes
  2. Enhances contractility & pacemaker activity in the SA node
  3. Leads to increase in heart rate & force.
  4. Involves signalling cascade that activates Ca channels, & Ca is released from intracellular stores further strengthens the contraction.
  5. α2 receptors act as a negative feedback mechanism.
  6. When activated, inhibit release of NA from presynaptic fibres, reducing further stimulation of the heart.
49
Q

Adrenoceptors B2 & a1 on smooth muscle - 2

A
  1. In smooth muscle, stimulation of β2 receptors leads to a decrease in intracellular Ca, inhibition of myosin light-chain kinase (MLCK), & smooth muscle relaxation, resulting in vasodilation.
  2. This effect contrasts with the vasoconstriction caused by α1 receptor activation.
50
Q

Agonists for adrenoceptors - 3

A
  1. Agonists are agents that bind to a receptor and elicit a response.
  2. For sympathetic adrenoceptors these agonists are often referred to as:
    Sympathetic agonists, Adrenergic agonists or Sympathomimetic agonists
  3. Agonists can act in two ways:
    Directly: By binding to & activating the receptor.
    Indirectly: By influencing the release or availability of neurotransmitters (often called sympathomimetic).
51
Q

Antagonists of adrenoceptors - 4

A
  1. Adrenoceptor antagonists: These drugs block effect of noradrenaline or adrenaline by binding to the receptor but not producing a response.
  2. Alpha blockers (e.g., Prazosin): These block α receptors
  3. Beta blockers (e.g., Propranolol): These block β receptors
  4. Indirect antagonism: Noradrenaline activity can also be reduced by interfering with its synthesis
52
Q

Selective 1-antagonists - 4

A
  1. Selective alpha-1 blockers, (e.g. doxazosin, tamsulosin), used as antihypertensive drugs with fewer S/Es compared to non-selective blockers.
  2. These drugs help reduce BP by causing vasodilation.
  3. Tamsulosin is especially used for urinary retention.
  4. While these drugs cause postural hypotension & headaches, less likely to induce tachycardia compared to non-selective blockers.
53
Q

Phenoxybenzamine
Action a-antagonist

A

Phenoxybenzamine
Action a-antagonist
Use: Phaeochromo-cytoma
S/E: Hypotension, Flushing, Tachycardia, Nasal congestion, Impotence

54
Q

Phentolamine
Action: a-antagonist

A

Phentolamine
Action: a-antagonist
Use: (research)
S/E: Hypotension, Flushing, Tachycardia, Nasal congestion, Impotence

55
Q

Non-selective beta blockers (e.g., Propranolol - 4

A
  1. Affect beta-1, beta-2, & beta-3 receptors.
  2. Used for conditions like high BP, migraines, & glaucoma
  3. S/Es lung contraction (which can be problematic for asthma or COPD patients).
  4. Propranolol is also lipophilic and can cross the BBB
56
Q

Selective beta-1 blockers (e.g., Atenolol, Metoprolol)

A

Target beta-1 receptors in the heart, reducing heart rate & contractility with fewer effects on the lungs.

57
Q

Third-generation beta blockers (e.g., Carvedilol, Labetalol) - 2

A
  1. Block both beta-1 & alpha-1 receptors, providing dual benefits:
  2. reduced heart contraction & BP, making them useful for patients with hypertension & heart failure.
58
Q

Actions of β-antagonists
- 3

A
  1. Beta blockers reduce heart rate & contractility, leading to decreased cardiac output & reduced oxygen demand on the heart.
  2. Used to manage hypertension, angina, & heart failure.
  3. Additionally, beta blockers reduce renin release from the kidneys, contributing to a reduction in BP.
59
Q

Beta blocker: Propranolol -3

A
  1. In addition to heart effects, Propranolol can cross the BBB
  2. Used to treat migraines & tremors (by blocking skeletal muscle beta-receptors).
  3. However, their ability to prevent tremors has led to their ban in certain sports
60
Q

Unwanted effects of β-antagonists - 9

A
  1. Selective B-antagonists can reduce the S/Es
  2. Bronchoconstriction
  3. Cardiac failure
  4. Bradycardia
  5. Hypoglycaemia
  6. Fatigue
  7. Cold extremities
  8. Erectile dysfunction
  9. Lucid dreams

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