Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Physiology ANS > Lecture 1 - Overview and Sympathetic NS > Flashcards

Lecture 1 - Overview and Sympathetic NS Flashcards

1
Q

What are the main neurotransmitters that are released by the sympathetic nervous system and parasympathetic nervous system?

A

Sympathetic NS: epinephrine, norepinephrine, dopamine

Parasympathetic NS: ACh

Note: ACh is involved with the sympathetic NS at the junction btwn pre and post ganglionic nerves, but is not the NT that ultimately mediates change at the end organs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are some cardiac effects of chronically overactive sympathetic activity?

A

Diastolic dysfunction (heart doesn’t fill as well)

Tachycardia

Tachyarrhythmias

Ischemia

Myocardial stunning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are some pulmonary effects of chronically overactive sympathetic activity?

A

Pulmonary edema (lungs can get leaky from intense and chronic right heart overactivity)

Pulmonary HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are some hematologic effects of chronically overactive sympathetic activity?

A

Hypercoagulation

Anemia

Bone marrow suppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are some endocrine effects of chronically overactive sympathetic activity?

A

Decreased thryoid function (will interfere with cell growth/repair)

Decreased growth hormone

Glucose intolerance (leads to hyperglycemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are some GI effects of chronically overactive sympathetic activity?

A

Hypo-perfusion

Decreased peristalsis

Ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are some immunological effects of chronically overactive sympathetic activity?

A

Immune suppression

Stimulation of bacterial cell growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are some metabolic effects of chronically overactive sympathetic activity?

A

Increased cellular metabolism

Hyperglycemia (tissues will be broken down to power high energy organs such as the heart and the brain - body eventually enters a catabolic state*)

Lipolysis

Electrolyte fluxes, due to increased cellular metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are some muscle effects of chronically overactive sympathetic activity?

A

Muscle cell death

Apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why do we administer glycopyrrolate prior to neostigmine?

A

Neostigmine inhibits ACh-ase which increases ACh presence throughout the body; this mimics an increase in global parasympathetic activity.

We give glycopyrrolate to mediate this global effect (acts as an anticholinergic/anti-ACh).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What part of the spinal cord does the sympathetic nervous system chain span?

A

T1-L2, through the intermediolateral nuclei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the organization of the sympathetic nervous system.

A

Sympathetic pre-ganglionic nerves emanate from T1-L2 of the spinal cord (sympathetic chain). These nerves are SHORT with the exception of the adrenal gland nerves.

Pre-ganglionic nerves synapse with post-ganglionic nerves that synapse to end organs.

Notable features: 2 nerve system, short pre, long post

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the sympathetic nervous system’s organization of the adrenal medulla.

A

*The only exception to the 2 nerve organization of the SNS. It is the only 1 nerve system of the SNS.

**The only SNS system that leads to a global response; functions more as a hormonal system

Pre-ganglionic fibers emanate from the thoracic region of the spine directly to the adrenal gland, which dumps epi and NE into the bloodstream**, causing global sympathetic response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the organization of the parasympathetic nervous system

A

AKA the cranio-sacral system.

Pre-ganglionic nerves emanate from the sacral portion of the spinal cord and the cranium.

These pre-g nerves are much longer than their SNS counterparts and synapse at post-ganglionic nuclei that are much closer to the end-organs they innervate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Sympathetic system - fast onset response or slow?

Parasympathetic system - fast onset response or slow?

A

Sympathetic: fast

Parasympathetic: slow

Partially due to the more focally concentrated effects of sympathetic nervous system (also due to evolution-derived response to danger)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the precursor to the primary sympathetic NS neurotransmitters?

A

Tyrosine

17
Q

What effects do alpha 1 post-synaptic receptors mediate?

A

Smooth muscle constriction (pupil dilation, lungs, blood vessels, uterus, sphincter tone of genitals and guts)

     >>Due to increase of intracellular Ca++ from ER release

Inhibition of insulin release (endocrine)

18
Q

What effects do alpha 2 post-synaptic receptors mediate?

A

Pre-synaptic receptors (on post-ganglionic cells)::

> Decrease intracellular Ca++ (via decreased adenylate cyclase activity)

  -This in turn, decreases NT exocytosis

> Feedback control

Post-synaptic receptors (on end organs):

> Smooth muscle constriction [similar to alpha 1 R’s)

> CNS effect: sedation, reduced central output –> main effect = vasodilation and smooth muscle relaxation due to decreased epi, NE release

     * *CNS effect: small group of alpha 2 receptors 
            - If you give adrenergic medication that crosses the BBB, this should be considered
19
Q

Clonidine: effects and mechanism of action

A

Effects:

> Anti-hypertensive

> Decrease HR

> Sedation (decrease anesthetic + analgesic requirements peri-op)

Action mechanism: selective CNS alpha 2 agonist

20
Q

Dexmedetomidine: effects and mechanism of action

A

Effects:

> Sedation without respiratory depression

> Analgesic

> Sympatholytic (ablates symp NS response)

Action mechanism: a lipophylic derivative of clonidine with higher affinity for alpha 2 receptors

21
Q

Where are beta 1 receptors primarily located?

What effects do beta 1 receptors have?

A

Beta 1 receptors are primarily located at post-synaptic ganglia in the heart.

Primary effects:

> Increased Ca++ (via increase in adenylate cyclase activity)

       -Causes NT exocytosis; increases epi, NE release

> Increased HR (chronotropy)

> Increased heart conduction rate (dromotropy)

> Increased heart contraction (inotropy)

22
Q

Where are beta 2 receptors primarily located?

What effects do beta 2 receptors have?

A

Beta 2 receptors are primarily located in post-synaptic ganglia in smooth muscles and glands.

Primary effects (think: opposite of alpha 1):

> Smooth muscle relaxation

> Gluconeogenesis (intracellular glucose storage increase due to insulin release)

> Insulin release

> Increased intracellular potassium due to Na-K pump stimulation

     **Implication: we can give hyperkalemic patients beta agonists (esp beta-2 specific ones) to drive plasma K+ back into cells
23
Q

Adrenergic agonist receptor activity for the followng:

Phenylephrine

Clonidine

Epinephrine

Ephedrine

Dopamine

Dobutamine

Albuterol

A

Phenylephrine (a1 selective)

Clonidine (a2 selective)

Epinephrine (a1 a2 b1 b2)

Ephedrine (a1 a2 b1 b2, NE release)

Dopamine (dopaminergic receptors, some adrenergic)

Dobutamine (b1 selective)

Albuterol (b2 selective)

24
Q

Ephedrine is an indirect agonist. Why is this important in patients that are chronic cocaine users?

A

The following can be generalized for pts with chronic exposure to/overactivity of adrenergic systems:

Indirect agonists increase endogenous NTs via increased release/decreased uptake/inhibition of NT metabolism.

Their effects depend on patients having adequate NT stores. In pts that have depleted adrenergic NT stores (such as chronic cocaine users), indirect agonists like ephedrine will not be as effective.

25
Q

How are sympathetic NTs broken down? (3 methods)

A

> Reuptake by presynaptic cell

> Breakdown of NT in the synapse back into tyrosine + side chains

> Breakdown by extrasynaptic enzymes (COMT and MAO)

 COMT: catechol-O-methltransferase

 MAO: mono-amine oxidases
26
Q

MAO inhibitors: what are they and why are these drugs not compatible with adrenergic drugs?

A

MAO inhibitors are primarily used as last resort anti-depressants and exert their effects by inhibiting MAO enzymes. Not as common now due to high profile incidences of serotonin syndromes in hospitals.

Its primary desired effects come from increase in dopamine due to inhibition of its breakdown by MAO (its part of the sympathetic family of neurotransmitters, even though it exerts a wide plethora of effects throughout cortical and subcortical structures).

MAO inhibitors are dangerous with adrenergic medication due to the potential for lethal sympathetic nervous system swings (remember that MAO is an important mechanisms of sympathetic NT destruction).

27
Q

why should we avoid using non-selective beta blocker for asthmatic patient?

A

Beta 2 inhibition leads to bronchoconstriction–> increased risk of asthma attack

Physiology ANS (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions