Autonomics Lectures

Front 1

Prevertebral vs Paravertebral sympathetic ganglia:

WTF?

Back 1

Paravertebral run along the spinal cord; Prevertebral are located elsewhere (i.e. mesenteric ganglion)

therefore, prevertebral ganglions will have longer preganglionic sympa fibers

Front 2

origin of parasympathetic fibers

Back 2

Cranial nerves 3,7,9,10

Sacral Cord (S2-S4)
-lower GI, bladder, sex organs, genitalia

Front 3

explain what's funny about sweat glands

Back 3

Sympathetic innervation with ACh used at the effector synapse; the ACh receptor is muscarinic (same AChR @ PS effector synapse)

Front 4

Neuromuscular J(x)
PS Effector J(x)
Autonomic Ganglia
Sweat Glands

Two of them use muscarinic receptors; two of them use nicotnic receptors. Which are which?

Back 4

Sweat/PS effector = M
NMJ/autonomic gang. = N

Front 5

Clinical use of systemic ACh agonists and antagonists...?

Back 5

ACh Agonists = too many side effects

ACh antagonists = many clinical uses, including anti-hypertensives

Front 6

enzyme that produces ACh

Back 6

CAT (cholineacetyl transferase)

Front 7

vasculature
eyes
heart
salivary glands
sweat glands
GI

Which organs are dominated by sympathetic drive? Which by PS drive? How can one simultaneously inhibit the dominant drive to each of these systems?

Back 7

vasculature: S
eyes: PS
heart: PS (S with pathology)
salivary glands: PS
sweat glands: S (but uses Muscarinic ACh receptor)
GI: PS

-Give anti-ACh (nicotinic) that affects autonomic ganglia (S + PS inhibition)

Front 8

G/U contraction
salivation/sweating
eye
gastric secretion

Assume a steady dose of anti-cholinergic drug is given: rank the aforementioned systems according to when they would first feel the effects of the drug.

Back 8

(most sensitive to least)
1. secretions/sweating
2. eye
3. G/U contraction
4. Gastric secretion

Front 9

name some clinical applications of anti-cholinergics acting at the level of the CNS

Back 9

Parkinson's
Motion sickness
Sedation
Anti-depressants (tricyclines)

Front 10

When anti-cholinergics are given, why would sweating decrease?

Back 10

Sweating = sympathetic terminals releasing ACh onto muscarinic receptors; anti-cholinergics will block M receptors

Front 11

AChEsterase Inhibitor is the antidote for someone suffering hallucination, circulatory collapse, ataxia, and dryness.

What got the person into trouble in the first place?

Back 11

Systemic block of ACh @ M receptors (anti-cholinergic poisoning)

Front 12

Describe the role of anti-cholinergics in myasthenia gravis treatment

Back 12

in MG, AChEi is given to increase [ACh] @ the NMJ; in order to prevent systemic [ACh] increase (and PS overdrive) in the body, anti-cholinergics are given

Front 13

How could anti-cholinergics help the following organs (list a pathology for each)?
lungs
heart
urinary
nose

Back 13

lungs - bronchospasm
heart - bradyarrythmia
urinary - urgency incontinence
nose - rhinitis / runny nose

Front 14

the classic muscarinic agonist: b_______

Describe it's application in OAGlaucoma and xerostomia treatment.

Back 14

the classic muscarinic agonist: _bethanicol_

OAGlaucoma: contract ciliary muscle, open Schlemm's canal, decrease IOP
Xerostomia: fixes dry mouth after H/N surgery

Front 15

renin secretion, pineal gland effects, uterine relaxation, increased conduction velocity of the heart

all of these are results of ________ stimulation

Back 15

adrenergic stimulation

(muscle relaxation, renin = BP rise)

Front 16

Classic Agonist/Antagonists for Sympathetic Receptors (A and B, not including subtypes)

Back 16

A agonist: phenylephrine
A antagonist: phentolamine
B agonist: isoproterenol
B antagonist: proterenol

this probably isn't important

Front 17

selectivity vs specificity in beta agonists (and antagonists): WTF?

Back 17

specific implies exclusive action; selective means drug acts at both sites, but far stronger at one site

Front 18

Beta1/2 (ant)agonists...name 'em

Back 18

B1 agonist: dobutamine
B1 antagonist: atenol
B2 agonist: terbutalmine
B2 antagonist: butoxamine

Front 19

Epinephrine is released at a 1:X ration to norepinephrine. This is a good thing, b/c EPI acts at _______

Back 19

1:4 ratio

EPI acts at B1 and B2 receptors (NE only acts at B1, which consists of heart/renal pretty much)

Front 20

experiment: NE decreases pulse rate; EPI increases pulse rate. Explain.

Back 20

NE acts equally @ heart and vasculature: TPR/diastolicBP increase-> baro reflex lowers pulse via PS output
EPI acts stronger @ B than A; TPR falls, but pulse pressure increases; vessel dilation in the muscles (B) overrides arteriole constriction (A)

Front 21

How does sympathetic drive inhibit the gut (alpha and beta mechanisms)?

Back 21

Alpha receptors @ PS nerve terminals inhibits ACh release

Beta receptors @ gut muscle causes relaxation

Front 22

NE and phentolamine are non-selective agonists and antagonists, respectively, for alpha receptors. Name the following selective drugs:
alpha 1 agonist:
alpha 1 antagonist:
alpha 2 agonist:

Back 22

alpha 1 agonist: methoxamine
alpha 1 antagonist: prozacin
alpha 2 agonist: a-CH3-NE

Front 23

illustrate the utility of a selective alpha 1 blocker with an example involving an anti-hypertensive drug

Back 23

non-selective alpha-blocker will also block alpha 2, which is critical in shutting off the sympathetic response (inhibits NE release); extra NE results in B1 stimulation of the heart, increasing cardiac output and heart rate

Front 24

explain the mechanism of epinephrine treatment in shock victims (reference alpha and beta receptors)

Back 24

A1 - vasoconstriction, decrease secretions and vascular permeability
B1 - cardiac output increases
B2 - bronchodilation

Front 25

orthostatic hypotension, tachycardiarrythmias, and bloodshot eyes can all be treated with which class of drugs?

Back 25

selective alpha 1 agonists

*stop taking the ortho'tension drug before sleep to avoid unecessary nocturnal TPR increase

**A agonist for tachycardiaarrythmia relies on triggering the baroreceptor reflex

Front 26

alpha 2 agonists are not used clinically for peripheral effects, but they can act centrally in the treatment of ______ (name some of the drugs)

Back 26

hypertension

clonidine/alpha-methyl-NE

Front 27

patients (especially the elderly) on alpha 1 antagonists are at risk of what common problem?

Back 27

orthostatic hypotension

Front 28

while arrythmia can be treated with an alpha agonist, it can also be treated with a selective beta ____ ____________

Back 28

beta 1 antagonist

Front 29

What is the mechanism underlying delaying of birth, slowing of peristalsis, and vasodilation via sympathetic stimulation?

Back 29

beta muscle relaxation

Front 30

Which step of bioamine synthesis is harnessed in Parkinson's treatment?

How is this treatment confined to the CNS?

Back 30

DOPA converted to Dopamine by DC (dopa decarboxylase) in the brain.

Confined to the CNS by a DC inhibitor that is unable to cross the BBB.

Front 31

What is the mechanism of action of indirect sympathomimetics (i.e. tyrinine, ephedrine, reserpine)?

What makes ephedrine unique?
What are the two main differences between reserpine and tyrinine?

Back 31

Uptake into nerve terminals and into NT vesicles in lieu of NE; NE displaced into synaptic cleft.

Ephedrine is mixed action (also a B2 agonist).

The speed/quality of uptake (reserpine is slower and irreversible) of drug into vesicles and which NTs can be displaced (reserpine works on all biogenic amines).

Front 32

Cocaine, Prozac, and Tricycline antidepressants mediate their effects by blocking the _____________ of biogenic amines at the ________.

Back 32

Block uptake of biogenic amines at the nerve terminal.

Cocaine DA
Tricycline 5-HT, NE
SSRI 5-HT

Front 33

The enzyme _______ produces epinephrine by placing a ________ group on NE.

Back 33

KMMT, methyl

Front 34

Discuss two different measures taken to ensure that exogenously-administered DOPA is converted to DA in the brain.

Back 34

1. Inhibit DOPA Decarboxylase (DC) with a drug that cannot cross the BBB.
2. Inhibit the catabolic enzyme COMT (kidneys/liver) so less DOPA gets shunted into a different pathway before reaching the brain.

Front 35

The biogenic amine degrading enzyme ______ comes in two forms, A and B. Inhibiting the A form can be particularly troublesome because it is responsible for the degradation of _____. The B form, on the other hand, is selective for the degradation of a single biogenic amine, _____.

Back 35

MAOa degrades NE; MAO blockers coupled with excess NE transmission can lead to sympathetic overdrive.
The B form degrades DA (potential Parkinson's drug).