Autonomic Nervous System Flashcards Preview

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Flashcards in Autonomic Nervous System Deck (48):
1

What is Shy-Drager syndrome

1. Also called multiple system atrophy - things invlolved get smaller and disintegrate away

2. It is a progressive neurodegenerative disease

3. Initially it involves degeneration of the autonomic preganglionic neurons and in later stages can go on and affect other systems like in motor function and balance like in Parkinson disease

2

What is the difference in the architecture of the pathway of somatic and autonomic nervous system

The somatic nervous system directly connects from the CNS (brain and then the spinal cord) to the muscle whereas the autonomic nervous system has a CNS then a connection with a ganglion that lies outside of the CNS and then it connects to the sensory or the effector cell.

This is what defines the ANS

3

What are some of the other nervous system structure that have a ganglion and how is that different than the ANS

Sensory system also forms the ganglion except they do not form a synapse but at the ganglion is the cell body. (Ganglion with no interneuronal synapse)

4

Divisions of ANS

Sympathetic and parasympathetic nervous system: the two can be differentiated by the origin of their nerves

PNS:

1. These send out information through the cranial and sacral nerves. The cranial nerves are 3,7,9 and 10. Even though the distribution is throughout the body, the origin is only through the craniosacral system.

2. The ganglia are embedded in the target organs so fairly long preganlionic axon and short post ganglionic axon

SNS: Only comes from the thoracic and lumbar regions. Most of the ganglia occur outside the CNS, running along both sides of the spinal cord is the paraverteberal chain.

Then some ganglia occur in the preverteberal ganglia that innervate the viscera (gut) and the genitalia

In SNS we have realtively short preganglionic axon and long post ganglionic axon due to this architecture

5

Preganglionic transmission

There are some common aspects and some differences about preganglionic transmission for SNS and PNS

Common: Acetylcholine is the neurotranasmitter and the receptors for that are the nicotinic receptors.

SNS: The axon branches and connects with more than one ganglionic cell body, hence the output is diffused

PNS: 1 to 1 relationship for axons and cell bodies, hence the output is discrete

6

What is convergence and divergence

The cell body is the point of convergence where mutiple axons give input to the cell body whereas the axon itself is a point if divergence where they branch and give output to different cell bodies

7

What are the different nicotinic receptors

Not all of the nicotinic receptors are the same, curare blocks the nicotinic receptors on skeletal muscles but the preganglionic nicotinic receptors are blocked by hexamethonium

8

Structure of the  postganglionic transmission

The axons travel into the effector tissue, where they come in close apposition to the cells they form dilations called varicosities, they also interact with synpathetic axons as well and form a network of nerves on the effector tissues called the ground plexus

9

Neuroeffector junction 

Interestingly they dont make a synapse, the axon is covered with schwann cells except at vericosities where the vessicles are released at the junction (not a synapse).

There are prejunctional receptors for the contents of the vesicles and post junctional receptors are present on the effector cells

10

Explain the parasympathetic transmission at the vericosisites (cholinergic)

1. Choline ingested through the diet

2. Taken up by choline transporter

3. Enzyme Acetylcholine transferase makes choline into acetylcholine

4. When a nerve impusle travels along, the acetylcholine is released into the junction

5. There are different types of receptors on post junctional point (on the effector cells) 

Muscarinic  Excitatory receptors = M1, M3, M5 (present on smooth muscles and glands)

Muscarinic Inhibitory receptors = M2 and M4 (smooth muscles and cardiac muscles (vagus nerve))

6. Acetylcholine esterase on the effector cell breaks down acetyl choline

7. Choline is taken up by the transporter

8. There are also Inhibitory Prejunctional Autoreceptors that tend to modulate how much acetylcholine is released from the axon at the junction via negative feedback loop

 

 

11

Define the arginine associated PNS transmission

1. Arginine taken up by diet

2. Converted into NO

3. NO released at the junction

4. NO act on Guanylate Cyclase at the effector cell (it activates GC to make cGMP which is an inhibitory molecule)

5. Function is to relax vascular and smooth muscles

6. NO isnt broken down, it simply diffuses away

12

Sympathetic Noradrenergic Transmission

1. Tyrosine ingested through diet

2. Tyrosine hydroxylase converts it into DOPA

3. DOPA decarboxylase converts DOPA into dopamine

4. Dopamine beta hydroxylase acts on dopamine to produce norpeinephrine which is stored in the vesicles

5. Norepinephrine acts on adrenergic receptors, alpha 1 (smooth muscles and glands excitation), beta 1 (cardiac excitation and renin release), beta 3 and beta 2 (smooth muscles and gland relaxation)

6. Norepinephrine transporter on the prejunction takes up the norepinephrine

7. Alpha 2 Inhibitory Prejunction Receptors are also present at the prejunction complex to regulate the release of norepinephrine via negative feedback loop

13

What is the difference in the mechanism of action of epi and norepi

Epi works on all of the mentioned receptors, it works on alpha 1, beta 1, beta 3 and beta 2 whereas norepi doesnt work as effectively on beta 2 which functions to relax the smooth muscles and the glandular secretions

14

How do you terminate the activity of NE in the sympathetic junctions

NE transporter reuptakes the NE, hence it is not broken down

15

What are some of the other receptors involved in varicosities that are not present at the junction complex

There are muscarinin inhibitory receptors present at the other side of the varicosities, away from the junction complex so if acetylcholine is released it will inhibit the vericosity from releasing NE at the junction.

One of the other receptors present is the Angiotensin II receptor and the beta 2 receptor. If epi is released and binds to beta 2 receptor, or if angiotensin II is released, the vericosity is stimulated to released NE at the junction complex

16

Does the previous description define all of the sympathetic transmission

No, that describes 95% of the sympathetic transmission, the other 5% is exactly like the parasympathetic transmission involving acetylcholine mechanism

17

What does Epi, Isoproterenol, phenylepinephrine, Clonidine, Norepi, where are they located, their action and their effects 

18

Where does Epi and Norepi come from

Adrenal Medulla, the cells that release are chromaffin cells, these cells have all of the same enzymes as a sympathetic nerve cell except for 1 extra enzyme that converts norepi to epi which is:

Phenylethanolamine N-methyl transferase

 

19

How is adrenal medulla stimulated

Via a preganglionic axon which has a cholinergic nicotine synapse

20

Denervation supersensitivity

Over the course of time, with age and/or disease there can be degeneration of the nerve fibers to certain parts or tissues of the body. This process is called denervation. The body has mechanisms to compensate for the effects of denervation in several ways

Due to denervation, less neurotransmitter is released at the junction. To make of whatever neurotransmitter is available the sensitivity and number of receptors at the post junction site is increased. This is called post junction supersensitivity. This happens in both PNS and SNS

To make maximum use of neurotransmitter availale the reuptake of neurotransmitter can be dramatically reduced, this is called pre junctional supersensitivity. This happens only in SNS and the neurotransmitter involved is norepi

21

How did he describe the PSN and SNS

SNS as fight or flight and PNS as feed and breed

22

 What are some of the rules he talked about regarding parasympathetic nervous system

1. Always acts non vascular smooth muscles except for sphincters - cholinergic muscarinic junctions

2. Always relaxes sphincters (except the one in the eye since it is not a sphincter) - cholinergic 

3. Always inhibits cardiac activity - cholinergic

4. Always activates glands - cholinergic

5. Relaxes vascular smooth muscles - nitrergic

23

Rules for sympathetic nervous system

1. Contracts smooth muscle via alpha 1 receptors

2. Relaxes smooth muscles via beta 2 receptors

3. Excited heart and kidney via beta 1 receptors

4. Excites adipocytes via beta 3 receptros

5. Increase glandular secretions by alpha 1, beta 3 - muscarinic

24

What are the effects of PNS and SNS on the gut

PNS according to the feed and breed example will promote peristalsis so will give + signals to the gut via ACh but it will give - signals to the rectal sphincter so that it can relax and promot defecation

SNS according to the fight and flight model will have - signals to the gut via Epi and NE and beta 2 receptors but it will have + signals via NE and alpha 1 receptors in the rectum.

ACh reduces the amount of NO released and NE increases the amount of epi released

25

Baldder

Know the body of the baldder and the sphincter in the urethera

26

Erectile dysfunction

There is a structure in the  blood vessels which is called cavemous vessel which can fill up with blood during arousal leading to tumescence. 

Parasympathetic nerve firing makes more NO. The target of action of Viagra and other related drugs is that they inhibit phosphodiesterase type 5 so when NO acts of GC to make more cGMP, cGMP are not broken down by the phosphodiesterase type 5

27

Orthostatic hypotention or supine hypertension

When you stand up your blood pressure is still low, when you lay down your blood pressure is still high. This happens in shy drager syndrome

28

What is the name of the nerves that innervate arteriolar and venous smooth muscles and what are their types

Vasomotor nerves

Excitatoty nerves: will cause contraction of smooth muscles, the diameter will decrease

Inhibitory innervations: will cause relaxation of smooth muscles, decrease the diameter of the vessel

Arteriolar contraction increases resistance whereas the venous contraction increases venous return

29

3 reasons for changing vessel diameter

1. Changing local blood flow like erection, digestion etc

2. To change Total Peripheral Resistance since this should be different when we are standing or laying down

3. To change caridac output since 2/3rd of the blood is stored in the veins

30

What nerves cause changes in blood diameter

Sympathetic causes constriction by releasing NE that acts on alpha 1 receptors. Epi can cause vasodilation that acts on beta 2 (only released in fight or flight)

Parasympathetic = dilation by making NO

31

What determines the activity level of these nerves 

This refers to the tones. If the nerve is firing alot that means the nerve has a high firing tone. The vascular tone is determined by the neuronal tone. 

Cardiac tone is also determined by the net SNS and PNS activity. 

32

What intitates the baroreflex

There are stretch receptors called the baroreceptors in walls of the vessels that tell the brain to modula cardiovascular tone

1. Cardiopulomary receptors: These measure venous and hence often they are called the low pressure receptors becuase the venous pressure is usually 0 to 20 mm but more pressure means more nerve firing

These are located in the right atrium, vena cava and the pulomonary vessels. These stretch with more venous return

2. Arterial baroreceptors: high pressure receptors located in the aortic arch and carotid sinus. These assses the blood flow to the entire body  and the brain respectively

33

How is baroreflex regulated

34

Concept of selective resistance and how is it achieved

When the baroreflex happens there is selective constriction of blood vessels in the organs:

1. Renal resistance increases

2. Splanchnic arteriolar resistance increases

3. Cutaneous (skin) resistance increases

4. Skeletal muscles resistance increases

These effects are achieved mainly by alpha 1 receptors via NE release. It is important to know that in this process the adrenal medulla remains unstimulated. 

The heart and the brain are stimulated later

35

Massive activation of parasympathetics lead to vaso vagal syncope when the blood pressure drops to such an extent that the person faints. This happens due to emotional reasons

36

At what pressures does the baroreflex work

From 180 mm Hg to 60 mm Hg

37

What works below 60 mm Hg

Chemoreflex

38

Where are they located

In the aortic body and at the carotid body. They lie on top of the glossopharyngeal nerve and the vagus nerve. 

A dop in arterial pressure will cause an increase firing of chemoreceptors which cause an increase firing of the 2 nerves mentioned above so the heart will start beating faster

39

How is the nerve firing of the chemoreceptors different from that of baroreceptors

The stimulations coming out of the NTS is exactly the oppositive, it has inhibitory towards DMV and excitatoy towards C-1

 

40

What is the last ditch effort by the brain to bring back the blood pressure to normal if it stays below the 60 mm Hg

It is called the Central Ischemic Response where there is a discharge from the sympathetic center C1 to bring up the CO and MAP. Usually it is not very successful.

Another variant of this response is the Cushing reaction. In this reaction there is head injury which causes bleeding in the brain, bringing up the blood pressure in the brain. In order for the blood to profuse properly in the brain tissue the pressure in the arteries have to be higher than in the veins. Due to bleeding the pressure is higher in the veins which causes the C1 to increase sympathetic firing and cause a dramatic increase in blood pressure. So people with head injuries can often have a dramatic increase in blood pressure via Cushing Reaction

41

What are some examples of disturbances in neural control of circulation

1. Orthostatic hypotension 

2. Carotid Sinus Syndrome: abnormal drop in blood pressure when the carotid arteries are pressed like in a neck message or something, common in old age.

3. Vasovagal syncope

42

Short term, intermediate and long term

Nerves are short term, hormones are intermediate and structural or homeostatic changes are long term

43

What is he trying to explain here

Baroreceptor doesnt have a signficant effect on adrenal medulla, it only effects the sympathetic which cause high blood pressure via alpha 1 and beta 1 receptors

44

Anti Diuretic hormone

ADH is released from anterior pituitary gland

45

What organs are beta 1's important 

They are important in the heart and the kidneys

46

Renin Angiotensin system

SNS = Sympathetic nervous system

47

What is the main diuretic hormone made by the body

ANP: Atrial Natriuretic Hormone, made by the cardiac cells, increased plasma volume causes atrial stretching which causes ANP to be made and released by th atrial cardiomyocytes.

ANP acts on the kidneys to induce Na excretions which reduces plasma volume

48

What happens to the following in the case of failure of autonomic nervous system

1. Levels of NE and Dopa Beta Hydroxylase

2. ADH

3. ANP

4. ANG II

1. Levels will be low

2. Antonomous nervous system failure means that sympathetic nervous system is not working. There is nothing to tell the heart that it has to increase the cardiac output. This would lead to low blood pressure. The baroreflex will kick in and stimulate production of ADH so ADH levels will be high

3. Low

4. High to compensate for low blood pressue but the ANG II levels are regulated themselves by the sympathetic nerves so it can be either low or high depending on where the denervation has taken place