Exam 2 - ANS Physiology Flashcards

1
Q

Autonomic

A

Autonomic: Systems not under conscious control, such as Parasympathetic, sympathetic and enteric.

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2
Q

Sympathetic responses

A

Part of autonomic: Increased HR/BP, dilated bronchioles, shunt blood to needed muscles.

“Fight or flight”

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3
Q

parasympathetic response

A

Consereve energy, shunt blood to endocrine, GI, urogenital “Rest and digest”

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4
Q
  1. Note the function of chain ganglia, and how they are similar to PNS plexi.
A

The sympathetic chain ganglia (paravertebral ganglia) run along the sides of the spinal cord and serve as relay points for the sympathetic nerves. They allow for the rapid distribution of sympathetic signals throughout the body. In contrast, the PNS plexi (like the cardiac or celiac plexus) help distribute parasympathetic signals to specific organs

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5
Q

Sympathetic NS in terms of response, neurotransmitters, receptors, and anatomy.

A

Originates from the thoracolumbar region of the spinal cord. It has short preganglionic fibers that release ACh and long postganglionic fibers that release norepinephrine (NE) (except in the sweat glands and skeletal muscles where ACh is released). SNS has widespread effects throughout the body and uses adrenergic receptors (α1, α2, β1, β2, β3)

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6
Q

Parasympathetic NS in terms of response, neurotransmitters, receptors, and anatomy.

A

Originates from the craniosacral region (cranial nerves III, VII, IX, X, and sacral spinal nerves S2-S4). It has long preganglionic fibers that release ACh and short postganglionic fibers, which also release ACh. The PNS effects are more localized and involve muscarinic and nicotinic receptors

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7
Q

Define Parasympathomimetic (Cholinomimetic)

A

Drugs that mimic parasympathetic activation, typically by stimulating ACh receptors, increasing GI secretions, or slowing the heart

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8
Q

Define sympathomimetic

A

Drugs that mimic the effects of sympathetic activation (e.g., epinephrine, albuterol). They increase HR, BP, and bronchodilation.

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9
Q

Define parasympathoplegic

A

Drugs that inhibit parasympathetic activity, often by blocking muscarinic receptors (e.g., atropine)

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10
Q

Define Sympathoplegic (α and β blockers):

A

Drugs that inhibit sympathetic activity by blocking adrenergic receptors (e.g., propranolol, phentolamine

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11
Q

List the ANS receptors and receptor subtypes, including second messengers.

A

Cholinergic receptors: Nicotinic (ion channel, fast) and Muscarinic (G-protein-coupled, slow).

Adrenergic receptors: Alpha (α1, α2) and Beta (β1, β2, β3).

Second messengers like cAMP and IP3/DAG are involved in these signaling pathways. For example, β1 receptors increase cAMP to activate heart rate.

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12
Q

Name the major types and subtypes of autonomic receptors and the tissues in which they are
found

A

Alpha-1 receptors: Vascular smooth muscle (vasoconstriction).

Beta-1 receptors: Heart (increases HR and contractility).

Beta-2 receptors: Bronchioles (bronchodilation), skeletal muscle vasculature (relaxation)

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13
Q

Compare the autonomic and hormonal feedback loops in terms of mean arterial pressure
changes.

A

Autonomic regulation: Rapid, short-term adjustments in MAP through sympathetic vasoconstriction or parasympathetic reduction of HR.

Hormonal regulation: Slower, long-term adjustments through hormones like angiotensin II, aldosterone, and vasopressin, which affect blood volume and vascular tone

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14
Q

List innervation to skeletal muscle blood vessels

A

Skeletal muscle blood vessels are innervated by sympathetic fibers, where NE causes vasoconstriction (α1) while ACh from postganglionic sympathetic fibers causes vasodilation

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15
Q
  1. Describe the organ system effects of stimulation of the parasympathetic and sympathetic systems.
A

Sympathetic: Increases HR (β1), dilates bronchi (β2), and shunts blood to skeletal muscles (α1).

Parasympathetic: Decreases HR (M2), contracts bronchi (M3), increases GI motility and secretions (M3)

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16
Q
  1. Draw the structure of the neuron and the synapse.
A

A neuron consists of dendrites (receiving signals), a soma (cell body), an axon (transmitting signals), and synaptic terminals. The synapse is where neurotransmitter release occurs, crossing the synaptic cleft to affect the postsynaptic cell

17
Q
  1. List the six main classes of neurotransmitters and give examples of each.
A

Esters: Acetylcholine (ACh).

Monoamines: Norepinephrine (NE), dopamine.

Amino acids: Glutamate, GABA.

Purines: ATP.

Peptides: Substance P, endorphins.

Inorganic gases: Nitric oxide (NO

18
Q
  1. List three types of synapses described in lecture.
A

Chemical: Use neurotransmitters like ACh and GABA.

Electrical: Use gap junctions to directly pass ions between cells.

En passant: Found along the length of an axon, releasing neurotransmitters at multiple points

19
Q
  1. Recall the function of three CNS neurotransmitters in emotion.
A

Dopamine: Linked to pleasure and reward.

Serotonin: Affects mood, with low levels linked to depression.

GABA: Inhibitory neurotransmitter, promotes relaxation

20
Q
  1. Describe the possible fate of neurotransmitters in the synapse.
A

Neurotransmitters can diffuse away, be degraded by enzymes (e.g., AChE for acetylcholine), be reuptaken into the presynaptic neuron, or absorbed by surrounding cells

21
Q
  1. Note the difference between excitatory and inhibitory neurotransmitters.
A

Excitatory: Cause depolarization, making a neuron more likely to fire (e.g., glutamate).

Inhibitory: Cause hyperpolarization, making a neuron less likely to fire (e.g., GABA)

22
Q
  1. Describe the formation, transport, and enzymatic cleavage of acetylcholine
A
  • ACh is synthesized from acetyl-CoA and choline by choline acetyltransferase. It is stored in vesicles and released into the synapse. ACh is broken down by acetylcholinesterase (AChE) into acetate and choline, which is reabsorbed for recycling
23
Q
  1. Diagram the steps of ACh and NE in their transport, storage, release, and degradation. Include the proteins involved and their roles.
A

ACh: Synthesized in the cytoplasm, transported into vesicles, released via exocytosis, and degraded by AChE

NE: Synthesis: NE is synthesized from tyrosine via tyrosine hydroxylase to form dopamine, which is converted to NE in vesicles by dopamine-β-hydroxylase

Storage: NE is stored in vesicles by the vesicular monoamine transporter

Release: Triggered by calcium influx and released via SNARE proteins

Reuptake and Degradation: NE is reuptaken by norepinephrine transporter (NET) or degraded by monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT)

24
Q
  1. List targets for drug action in the synapse and examples.
A

AChE Inhibitors: Prevent ACh degradation (e.g., donepezil for Alzheimer’s)​

VMAT Inhibitors: Prevent NE storage (e.g., reserpine)​

NET Inhibitors: Block NE reuptake (e.g., cocaine or tricyclic antidepressants)​