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Hmari Cheat Sheet

A Home & Health › Pharmacology cheat sheet in English by Sorahae

This serves as my cramming notes for my quiz tomorrow.

Science
7,402 views 1,131 downloads 6 Feb 2023 History
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Nervous system

Two major subdiv­isions:
1. Central nervous system
(CNS; the brain and spinal cord)
2. Peripheral nervous system
(PNS; neuronal tissues outside the CNS).
 
Anatom­ically divided into the:
1. Autonomic
2. Somatic
Autonomic nerves can also influence cancer develo­pment and progre­ssion.

ANATOMY OF THE AUTONOMIC NERVOUS SYSTEM

Two major portions:
 
1. Sympat­hetic (thora­col­umbar) division
 
2. Parasy­mpa­thetic (tradi­tio­nally “crani­osa­cra­l").
----
----
a. The sympat­hetic pregan­glionic fibers leave CNS through the thoracic, lumbar, and sacral spinal nerves.

b. The parasy­mpa­thetic pregan­glionic fibers leave the CNS through the cranial nerves (3rd, 7th, 9th, and 10th).

for Sympat­hetic

PARAVE­RTEBRAL
PREVER­TEBRAL
Most thoracic and lumbar sympat­hetic pregan­glionic fibers are SHORT and terminate in ganglia located in here.
Most of the remaining sympat­hetic pregan­glionic fibers are somewhat LONGER and terminate
*Short
*Longer
For PARASY­MPA­THETIC:
-Prega­ngl­ionic parasy­mpa­thetic fibers terminate in parasy­mpa­thetic ganglia located outside the organs innerv­ated:

1.Ciliary
2. Pteryg­opa­latine
3. Subman­dibular
4. Otic ganglia.

ANS vs SNS

Autonomic nervous system (ANS)
Somatic nervous system (SNS)
It is concerned with control and integr­ation of visceral functions necessary for life such as cardiac output, blood flow distri­bution, and digestion.
Motor portion of the somatic subdiv­ision is largely concerned with movement, respir­ation, and posture.
Largely indepe­ndent (auton­omous) in that its activities are not under direct conscious control.
Both have important afferent (sensory) inputs that provide inform­ation regarding the internal and external enviro­nments and modify motor output through reflex arcs of varying comple­xity.
Vagus nerve, also influences immune function and some CNS functions such as seizure discharge.

Major difference CNS vs ANS

Presence of a GANGLION in ANS

Differ­ent­iating divisions of ANS

a. Sympat­hetic Nervous System
b. Parasy­mpa­thetic Nervous System
c. Enteric Nervous System
-Prepares body for intense "­FIGHT OR FLIGHT­" response.
-Relaxes body and inhibits or slows many high energy functions
-Large and highly organized collection of neurons located in walls of GI system.
FIGHT OR FLIGHT (F/F
REST OR DIGEST
THIRD DIVISION OF ANS
-
-
Control motor activity of colon
ENS includes:
1. MYENTERIC PLEXUS or the Plexus of Auerbach
2. SUBMUCOUS PLEXUS or the Plexus of Meissner

ENS neuronal networks

1. Myenteric plexus (the plexus of Auerbach)
2. Submucous plexus (the plexus of Meissner).

Neurot­ran­smi­tters

 
Location
NT
Pregan­glionic
  
Ach
Postga­ngl­ionic
a. Parasy­mpa­thetic
Ach
 
b. Sympat­hetic
NE & few locations Ach

Receptors

 
Type
Parasy­mpa­thetic
N
Excitatory
 
M
Excitatory or Inhibitory
Sympat­hetic
Alpha
Excitatory
 
Beta
Excitatory or Inhibitory

Figure 6–1

Parasy­mpa­thetic
Cardiac and smooth muscle, gland cells, nerve terminals
Ach/M
Sympat­hetic
Sweat glands
Ach, M
Sympat­hetic
Cardiac and smooth muscle, gland cells, nerve terminals
NE, α, β
Sympat­hetic
Renal vascular smooth muscle
NE, D/α, D1
Somatic
Skeletal muscle
Ach, N

TABLE 6–1

TABLE 6–1

TABLE 6–1

Substance
Functions
Acetyl­choline (ACh)
The primary transm­itter at ANS ganglia, at the somatic neurom­uscular junction, and at parasy­mpa­thetic postga­ngl­ionic nerve endings. A primary excitatory transm­itter to smooth muscle and secretory cells in the ENS. Probably also the major neuron­-to­-neuron (“gang­lio­nic”) transm­itter in the ENS.
Adenosine tripho­sphate (ATP)
Acts as a transm­itter or cotran­smitter at many ANS-ef­fector synapses.
Calcitonin gene-r­elated peptide (CGRP)
Found with substance P in cardio­vas­cular sensory nerve fibers. Present in some secret­omotor ENS neurons and intern­eurons. A cardiac stimulant.
Cholec­yst­okinin (CCK)
May act as a cotran­smitter in some excitatory neurom­uscular ENS neurons.
Dopamine
A modulatory transm­itter in some ganglia and the ENS. Possibly a postga­ngl­ionic sympat­hetic transm­itter in renal blood vessels.
Enkephalin and related opioid peptides
Present in some secret­omotor and intern­eurons in the ENS. Appear to inhibit ACh release and thereby inhibit perist­alsis. May stimulate secretion.
Galanin
Present in secret­omotor neurons; may play a role in appeti­te-­satiety mechan­isms.
GABA (γ-ami­nob­utyric acid)
May have presyn­aptic effects on excitatory ENS nerve terminals. Has some relaxant effect on the gut. Probably not a major transm­itter in the ENS.
Gastri­n-r­ele­asing peptide (GRP)
Extremely potent excitatory transm­itter to gastrin cells. Also known as mammalian bombesin.
Neurop­eptide Y (NPY)
Found in many noradr­energic neurons. Present in some secret­omotor neurons in the ENS and may inhibit secretion of water and electr­olytes by the gut. Causes long-l­asting vasoco­nst­ric­tion. It is also a cotran­smitter in some parasy­mpa­thetic postga­ngl­ionic neurons.
Nitric oxide (NO)
A cotran­smitter at inhibitory ENS and other neurom­uscular junctions; may be especially important at sphinc­ters. Cholin­ergic nerves innerv­ating blood vessels appear to activate the synthesis of NO by vascular endoth­elium. NO is not stored, it is synthe­sized on demand by nitric oxide synthase, NOS; see Chapter 19.
Norepi­nep­hrine (NE)
The primary transm­itter at most sympat­hetic postga­ngl­ionic nerve endings.
Serotonin (5-HT)
An important transm­itter or cotran­smitter at excitatory neuron­-to­-neuron junctions in the ENS.
Substance P, related tachyk­inins
Substance P is an important sensory neurot­ran­smitter in the ENS and elsewhere. Tachyk­inins appear to be excitatory cotran­smi­tters with ACh at ENS neurom­uscular junctions. Found with CGRP in cardio­vas­cular sensory neurons. Substance P is a vasodi­lator (probably via release of nitric oxide)
Vasoactive intestinal peptide (VIP)
Excitatory secret­omotor transm­itter in the ENS; may also be an inhibitory ENS neurom­uscular cotran­smi­tter. A probable cotran­smitter in many cholin­ergic neurons. A vasodi­lator (found in many periva­scular neurons) and cardiac stimulant.

CHOLIN­ERGIC TRANSM­ISSION

STEP 1: Synthe­sized by Choline Acetyl­tra­nsf­erase (ChAT)
-Acety­l-CoA synthe­sized in mitoch­ondria
 
Choline transp­orted into the neuron
 
Blocked by hemich­olinium (blocks uptake of choline)
----
----
STEP 2: Ach transp­orted into SMALL CLEAR VESICLES
Transp­orter can be blocked by vesamicol (prevents storage or depletes transm­itter storage)
----
----
STEP 3: Release of transm­itter is Calciu­m-d­epe­ndent
-triggered by action potentials
 
-ACh release blocked by botulinum toxin
----
----
STEP 4: ACh binds to receptors
(choli­noc­eptors)
----
----
STEP 5: Catabo­lized by acetyl­cho­lin­est­erase (AChE)
-breaks ACh into choline and acetate
 
terminate action of transm­itter
 
half-life of ACh is very short
 
AChE in other tissues (eg. RBC)
 
Butyry­lch­oli­nes­terase (pseudo-)
----
----
ChAT and AChE used during synthesis and degrad­ation of ACh.

5 KEY FEATURES OF NEUROT­RAN­SMITTER FUNCTION

1. Synthesis
2. Storage
3. Release
4. Termin­ation Of Action Of The Transm­itter
5. Receptor Effects

Acetyl­choline Synthesis

1. ACh made from choline + acetyl CoA
2. In synaptic cleft, ACh is rapidly broken down by enzyme Acetyl­cho­lin­est­erase
3. Choline is transp­orted back into axon terminal and used to make more ACh.

STEPS in ADRENERGIC TRANSM­ISSION

STEP 1
Synthesis of catech­ola­mines (Dopamine, NE)
STEP 2
Uptake into storage vesicle
STEP 3
Release of NT
STEP 4
Binding to receptor
STEP 5/6
Degrad­ation of NE

Termin­ation of NORADR­ENERGIC TRANSM­ISSION

1. Simple diffusion away from receptor site (with eventual metabolism in plasma or liver
2. Reuptake into the nerve terminals by NET or into perisy­naptic glia or other cells

BIOSYN­THESIS OF CATECH­OLA­MINES

1. Tyrosine convert to DOPA by Tyrosine hydrox­ylase
can be inhibited by metyrosine (a tyrosine analog)
2. DOPA convert to Dopamine by Dopa decarb­oxylase
-
3. Dopamine convert to NE by Dopami­ne-­β-h­ydr­oxylase
In most sympat­hetic postga­ngl­ionic neurons, NE is the final product)
4. NE convert to Epinep­hrine by Phenyl­eth­ano­lam­ine­-N-­met­hyl­tra­nsf­erase
Methylated form
~
Additional

a. Tyrosine metabo­lized by L-Amino acid decarb­oxylase to form TYRAMINE (the product of metabolism of tyrosine).

b. Tyramine metabo­lized by Dopami­ne-­β-h­ydr­oxylase to Octopamine

c. Octopamine metabo­lized by hydrox­ylase (from the liver) to form NE

WAYS OF STOPPING NEUROT­RAN­SMITTER

1. DIFFUSION
-
2. DEGRAD­ATION
metabolic enzyme process (eg. AChE metabolize ACh)
3. REUPTAKE
into the noradr­energic neuron/ adrenergic neuron

NT CHEMISTRY OF THE ANS

CHOLIN­ERGIC FIBERS
NORADR­ENERGIC (ADREN­ERGIC) FIBERS
releasing Ach (Acety­lch­oline)
release Norepi­nep­hrine (NE)/ Noradr­enaline

AUTONOMIC RECEPTOR (NT, R)

PARASY­MPA­THETIC
SYMPAT­HETIC
NT: ACh (Choli­noc­eptors)
NT: NE (Adren­oce­ptors)
R=N/M
R= α,β, D
Nicotinic receptors= NN/NM
α= 1/2
Muscarinic receptors= M1 to M5
β= 1-3
 
D= (D1-D5)

AUTONOMIC RECEPTOR

Alkaloids
Muscarine and Nicotine
The sensory fibers in the nonadr­ene­rgic, noncho­lin­ergic systems are probably better termed “senso­ry-­eff­erent” or “senso­rylocal effector” fibers because, when activated by a sensory input, they are capable of releasing transm­itter peptides from the sensory ending itself, from local axon branches, and from collat­erals that terminate in the autonomic ganglia.

These peptides are potent agonists in many autonomic effector tissues.*

METABOLISM OF CATECH­OLA­MINES by COMT & MAO

Catech­ola­mines
COMT/MAO
Product 1
COMT/MAO
Product 2
EPINEP­HRINE
=MAO
Dihydr­oxy­man­delic acid
COMT
3-Meth­oxy­-4-­hyd­rox­yma­ndelic acid (VMA)
 
=COMT
Metane­phrine
MAO
3-Meth­oxy­-4-­hyd­rox­yma­ndelic acid (VMA)
NE
=MAO
Dihydr­oxy­man­delic acid
COMT
3-Meth­oxy­-4-­hyd­rox­yma­ndelic acid (VMA)
 
=COMT
Normet­ane­phrine
MAO
3-Meth­oxy­-4-­hyd­rox­yma­ndelic acid (VMA)
DOPAMINE
=MAO
Dihydr­oxy­phe­nyl­acetic acid
COMT
Homova­nillic acid
 
=COMT
3-Meth­oxy­tyr­amine
MAO
Homova­nillic acid

Read

Read Katzung CH. 6 (P.99) TABLE 6-2 Major autonomic receptor types

FUNCTIONAL ORGANI­ZATION OF AUTONOMIC ACTIVITY

 

A. Integr­ation of Cardio­vas­cular Function

Mean arterial pressure
the primary controlled variable in cardio­vas­cular function
 
-changes in any variable contri­buting to mean arterial pressure (eg, a drug-i­nduced increase in peripheral vascular resist­ance) evoke powerful homeos­tatic secondary responses
Homeos­tatic response
may be sufficient to reduce the change in mean arterial pressure and to reverse the drug’s effects on heart rate.
Example: Slow infusion of NE

Increased barore­ceptor activity causes the decreased central sympat­hetic outflow and increased vagal outflow.

Net effect of ordinary pressor doses of norepi­nep­hrine in a normal subject is to produce a marked increase in peripheral vascular resist­ance.
An increase in mean arterial pressure, and often, a slowing of heart rate.

NEGATIVE FEEDBACK RESPONSE is present.

B. Presyn­aptic Regulation

Autore­ceptors
Presyn­aptic receptors that respond to the primary transm­itter substance released by the nerve ending
 
usually inhibi­tory, but in addition to the excitatory β receptors on noradr­energic fibers, many cholin­ergic fibers, especially somatic motor fibers, have excitatory nicotinic autore­cep­tors.
Hetero­rec­eptors
respond to many other substances
 
activated by substances released from other nerve terminals that synapse with the nerve ending.
Principle of negative feedback control is also found at the presyn­aptic level of autonomic function.

-have been shown to exist at most nerve endings

C. Postsy­naptic Regulation

Can be considered from two perspe­ctives:
1. Modulation by previous activity at the primary receptor
 
2. Modulation by other simult­aneous events.
--
FIRST MECHANISM
Up-reg­ulation and down-r­egu­lation are known to occur in response to decreased or increased activation, respec­tively, of the receptors.
 
Extreme form of up-reg­ulation occurs after denerv­ation of some tissues, resulting in denerv­ation supers­ens­itivity of the tissue* to activators of that receptor type.
 
ex: Nicotinic receptors are normally restricted to the end plate regions underlying somatic motor nerve terminals.
 
ex: Prolonged admini­str­ation of large doses of reserpine, a norepi­nep­hrine depleter, can cause increased sensit­ivity of the smooth muscle and cardiac muscle effector cells
SECOND MECHANISM
Involves modulation of the primary transm­itt­er-­rec­eptor event by events evoked by the same or other transm­itters acting on different postsy­naptic receptors.
 
ex: Ganglionic transm­ission
Postga­ngl­ionic cells are activated (depol­arized) due to binding of an approp­riate ligand to a neuronal nicotinic (NN) acetyl­choline receptor.

Resulting:
a. Fast excitatory postsy­naptic potential (EPSP) evokes a propagated action potential if threshold is reached.

Continued

-
-
b. Often followed by a small and slowly developing but longer­-la­sting hyperp­ola­rizing afterp­ote­ntial—a slow inhibitory postsy­naptic potential (IPSP).

1. Hyperp­ola­riz­ation involves opening of potassium channels by M2 cholin­oce­ptors.

2. Small, slow excitatory postsy­naptic potential caused by closure of potassium channels linked to M1 cholin­oce­ptors.

3. Late, very slow EPSP may be evoked by peptides released from other fibers.**

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