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109 Cards in this Set

  • Front
  • Back
What is the role of the ANS?
Being responsible for automatic, unconscious bodily functions such as:

(1) Control of HR
(2) Control of BP
(3) GI functions
(4) Genitourinary functions
What is a ganglia?
A relay station for PANS and SANS (between CNS and end organ).
What is an important anatomic difference between SANS and PANS?
Ganglia in the SANS lie in two paraventral chains adjacent to the vertebral column. Most ganglia of PANS are located in the organs innervated.
Mention the major receptor types and their locations for the ANS and somatic system.
(1) N_N: Cell bodies in ganglia of PANS, SANS, adrenal medulla
(2) N_M: Skeletal muscle motor end plate
(3) M (1-3): All organs and tissues innervated by postganglionic nn. of PANS and on thermoregulatory sweat glands innervated by the SANS.
Dopamine (DA) activates what receptors and where?
D1, causing vasodilation in renal and mesenteric vascular beds.
BP is a function of what?
What branch of the ANS are involved in the autonomic (neural) control of BP via feedback mechanisms?
Changes in mean blood pressure are detected by ____________.
Baroreceptors relay information to?
cardiovascular centers in the brain stem controlling PANS and SANS outflow.
Describe sequence of events from an increase in mean blood pressure.
Baroreceptor discharge to cardiovascular centers, increased PANS activity leading to bradycardia and decreased SANS activity leading to decreased heart rate, force of contraction and vasoconstriction.
How can you block the baroreceptor reflex?
You can block the ganglionic synapse with N_N receptor antagonists. Muscarinic antagonist can block reflex bradycardia. β1-antagonist can block reflex tachycardia.
Reflex bradycardia occurs through this receptor.
Reflex tachycardia occurs through this receptor.
What hormonal feedback loop is important in regulating BP?
Renin-Angiotensin-Aldosterone system
What makes the hormonal feedback system for BP respond?
Hypotension only. It decreases renal blood flow.
A patient is treated with an antihypertensive drug. What compensatory mechanisms in the body will kick in to reinstate homeostasis?
(1) ANS (neural)
• Baroceptor reflex → Tachycardia
(2) Endocrine feedback loop
• RAAS → Water, Na+ retention
(1) What is this called?
(2) How would a increased/decreased in BP look?
(3) How would a increased/decreased HR look?
What happens with SANS stimulation of the pupil?
α1 stimulation → Mydriasis through radial muscle contraction.

Remember: Gq coupled → Increased intracellular Ca++ (proportional to contractile force)
What happens with PANS stimulation (receptor and intracellularly) of the pupil?
M3 on sphincter and ciliary muscle.

This is Gq coupled, increasing calcium and miosis through sphincter muscle contraction. Ciliary muscle contraction relaxes suspensory ligaments of the lens and causes accomodation of the lens to view near objects.
These receptors induce H+ secretion in the stomach when stimulated by ACh.

(1) What receptor is this?
(2) What is it coupled to intracellularly?
(1) M1
(2) Gq, similarly to M3 in the eye for example.

("Gq increases Ca++, an important intracellular signal for exocytosis").
What happens to the eye if you use a muscarinic antagonist?
1. Mydriasis
2. Cycloplegia (paralysis of accomodation, you now accomodate to far vision)
What is cycloplegia?
Paralysis of accomodation, seen with muscarinic antagonism.
Blocking the PANS and stimulating the SANS can both cause mydriasis, how do you differentiate between the two?
With α1-agonists, there is mydriasis but without cycloplegia (solely dependent on PANS).
Acetylcholine can stimulate what receptor types?
Muscarinic and nicotinic
Hemicholinium does what?
Blocks the reuptake of choline into cholinergic nerves close to their neuroeffector junctions.
What enzyme condensates Choline and Acetyl-CoA to produce ACh?
Choline Acetyl Transferase
Botulinum toxin does what?
Binds synaptobrevin, preventing ACh release into the neuromuscular junction.
Choline is accumulated in cholinergic presynaptic nerve endings via an active transport mechanism linked to a ____ pump.
Botulinum toxin is used medically and cosmetically for what?
(1) Blepherospasm
(2) Strabismus
(3) Hyperhydrosis
(4) Dystonia
(5) Wrinkles
Some cholinergic nerve endings have presynaptic autoreceptors for ____ that on activation may elicit a negative feedback of transmitter release.
What do we call inhibitory drugs that have Acetylcholine Esterase as a target?
Indirect-acting cholinomimetics
Reversible AChE inhibitors include?
(1) Edrophonium
(2) Physostigmine
(3) Neostigmine, Pyridostigmine
(4) Donepezil, Tacrine
Irreversible AChE inhibitors include?
(1) Echothiophate
(2) Malathion
(3) Parathion
There are three major muscarinic responses in the body, list them.
(1) Heart: Decreased heart rate
(2) Secretions: Increased all types of secretions
(3) Smooth muscle: Contraction
What muscarinic receptors are found in the eye?
Sphincter - M3
Ciliary muscle - M3
What muscarinic receptors are found in the heart?
SA node - M2
AV node - M2
What muscarinic receptors are found in the lungs?
Bronchioles - M3
Glands - M3
What muscarinic receptors are found in the GI tract?
Stomach - M3
Glands - M1
Intestine - M3
What muscarinic receptors are found in the bladder?
• Detrusor → Contracts
• Trigone/sphincter → Relaxes

The result is voiding and urinary incontinence.
What muscarinic receptors are found in sphincters in the body?
• Causes relaxation EXCEPT LES which contracts.
What muscarinic receptors are found in glands?
• Causes secretion → Sweat (thermoregulatory), salivation, lacrimation
What happens when the PANS stimulates blood vessels through innervation?
There is no PANS innervation of blood vessels.
What muscarinic receptors are found in blood vessels?
M3 (however NOT innervated)
• Dilation via NO production by endothelium.
Stimulation of autonomic ganglia will result in what action in blood vessels?
Vasoconstriction. Vessels are solely innervated by the SANS.
What is special about the adrenal medulla and what does it do?
It acts like a specialized ganglion. It is innervated by the SANS and just like postganglionic neuron receives ACh stimulation via their N_N receptors, however, instead of extending axons to an end-organ, it just releases E into the blood.
Where do we find N_N receptors?
(1) Adrenal medulla
(2) Autonomic ganglia
Where are N_M receptors found? What is the result of stimulation?
Neuromuscular junction. Stimulation leads to twitching or hyperactivity of skeletal muscle.
An important property of N receptors is [...]
N receptors desensitize very quickly upon excessive stimulation.
Blood vessels are dominated by the ___________ while the GI tract is dominated by the ___________.
What happens in the GI tract if you "tickle" the autonomic ganglia?
GI tract is dominated by the PANS, so ganglionic stimulation causes increased motility and secretions.
These cholinergic receptors are Gq coupled and what happens upon stimulation of the receptors?
M1 (stomach) and M3 (widespread)

Increases phospholipase C activity, cleaving PIP2 into IP3 and DAG. IP3 mobilizes Ca++ from ER. Ca++ and DAG activate protein kinase C.
What cholinergic receptors are Gi coupled and how do they work?
M2 receptors, found in the heart (SA, AV node). It makes sense that it would be inhibitory, decreasing cAMP and causing negative chrono- and dromotropy.
What second messengers are generated upon stimulation of N_N and N_M receptors?
No 2nd messengers. Stimulation causes activation (opening) of Na/K channels.
List drugs that are direct-acting cholinomimetics.
(1) ACh
(2) Bethanechol
(3) Methacholine
(4) Pilocarpine
What is another word synonymous with cholinomimetics?
Muscarinic/Nicotinic agonists
What is another word synonymous with muscarinic agonists?
Clinical use of bethanechol?
• Ileus (tarmslyng, tarmgikt) postoperatively or neurogenic.
• Urinary retention in diabetic nephropathy or BPH.
Clinical use of methacholine?
Dx of asthma. It induces bronchial hyperreactivity.
Clinical use of pilocarpine?
• Glaucoma (topically)
• Xerostomia
To what degree can these different drugs resist Acetylcholinesterase degradation?

(1) ACh
(2) Bethanechol
(3) Methacholine
(4) Pilocarpine
(1) Highly hydrolyzed (+++)
(2) Resistant
(3) Somewhat (+)
(4) Resistant
What cholinergic receptors are stimulated with these drugs?

(1) ACh
(2) Bethanechol
(3) Methacholine
(4) Pilocarpine
(1) M and N
(2) M
(3) M > N
(4) M

("Methacholine er Metta med M")
What is another term synonymous with Acetylcholinesterase Inhibitors?
Indirect-Acting Cholinomimetics
What is the rational for clinical use of AChE inhibitors in Alzheimer's?
ACh neurons in Meynert's nucleus may degenerate in Alzheimers due to neuropathy (neurofibrillary tangles, amyloid plaques).
These drugs are Indirect-Acting Cholinomimetics (Acetylcholinesterase Inhibitors).
(1) Edrophonium
(2) Physostigmine
(3) Neostigmine, Pyridostigmine
(4) Donepezil, Tacrine
(5) Organophosphates
Clinical use of edrophonium?
• Dx of Myasthenia Gravis
• Used to differentiate myasthenia from cholinergic crisis
Clinical use of Physostigmine?
• Rx: Glaucoma
• Rx: Antidote in atropine overdose (enters CNS)
Clinical use of Neostigmine and Pyridostigmine?
• Rx: Ileus
• Rx: Urinary retention
• Rx: Myasthenia gravis
• Rx Reversal of nondepolarizing NM blockers (curare)
Clinical use of Donepezil and Tacrine?
• Rx: Alzheimers
Clinical use of Organophosphates?
• Rx: Glaucoma (Echothiophate)
What is the nature of the drugs found in insecticides and nerve gas?
AChE Inhibitors (irreversible)

Insecticides: Malathion, Parathion
Nerve gas: Sarin
Describe characteristics of AChE Inhibitors.
(1) Edrophonium - Ultra short acting
(2) Physostigmine - Tertiary amine (enters CNS)
(3) Neo-, Pyridostigmine - Quaternary amines (no CNS entry)
(4) Donepezil, Tacrine - Lipid soluble (CNS entry)
(5) Organophosphates - Lipid-soluble, irreversible inhibitors
How do human vs insects metabolize organophosphate insecticides?
What is the acute toxicity that results from organophosphate exposure? (General)
Excessive muscarinic and nicotinic stimulation.

• Diarrhea
• Urination
• Miosis
• Bradycardia
• Bronchoconstriction
• Lacrimation
• Salivation
• Sweating
• CNS stimulation

• Skeletal mm. excitation (twitching, fasciculations) followed by desensitization with paralysis.
• CNS stimulation
Excessive muscarinic (M2) stimulation of the heart may result in?
Increased PR interval with possibility of AV block.
How is organophosphate poisoning managed?
Regenerate AChE with Pralidoxime (2-PAM)

Rx of M: Atropine
How much time do you have from time of exposure to organophosphates until the time when AChE are truly irreversibly inhibited?
6-8 hours (couple of minutes for sarin)
How do irreversibly acting cholinomimetics work?
They phosphorylate the esteratic site on AChE, at serine hydroxyl groups. After some time, "aging" occurs where the R- portion of the drug disattaches from the P- part, which is now bound irreversibly to the enzyme. 2-PAM can be used before aging occurs.
What are symptoms of chronic exposure to irreversibly acting cholinomimetics?
• Peripheral neuropathy causing mm. weakness and sensory loss
• Demyelination not due to AChE inhibition

"Mimics MS"
What type of drug is atropine?
Muscarinic antagonist ("Prototype")
Atropine is a ___________ (tertiary/quaternary) amine.
tertiary; it enters the CNS
List effects of atropine in order of increasing dose.
(1) Decreased secretions (salivary, bronchiolar, sweat)
(2) Mydriasis and cycloplegia
(3) Hyperthermia (with vasodilation)
(4) Tachycardia
(5) Sedation
(6) Urinary retention, Constipation
(7) Behavioral excitation, Hallucinations
What are some other classes of drugs with antimuscarinic pharmacology (outside of atropine)?
(1) Antihistamines
(2) Tricyclic antidepressants
(3) Antipsychotics
(4) Quinidine
(5) Amantadine
(6) Meperidine
Treatment of acute intoxication with atropine?
Physostigmine and symptomatic treatment.
Clinical uses of atropine?
(1) Antispasmodic
(2) Antisecretory
(3) Management of AChE inhibitor OD
(4) Antidiarrheal
(5) Ophthalmology
List muscarinic antagonists.
(1) Atropine
(2) Tropicamide
(3) Iptratropium
(4) Scopolamine
(5) Benztropine, Trihexyphenidyl
Clinical uses of tropicamide?
Ophthalmology (topical)
Clinical uses of ipratropium?
Asthma and COPD (inhalational) - no CNS entry, no change in mucus viscosity
Clinical uses of scopolamine?
Used in motion sickness, causes sedation and short term memory block (anterograde)
Clinical uses of benztropine and trihexyphenidyl?
Lipid-soluble (CNS entry) used in parkinsonism and in acute extrapyramidal symptoms induced by antipsychotics.
Talk on ANS dominance.
For effector tissues with dual innervation, PANS is dominant. These include the SA and AV nodes of the heart, pupil, GI and GU muscles and sphincters. SANS is dominant only in terms of vascular tone and thermoregulatory sweat glands.
These drugs are ganglion blocking agents.
Hexamethonium and mecamylamine.
What is the effect og ganglion blockade on vessels, heart, eye, GI, bladder and glands?
(1) Arterioles - SANS (predominant) - Vasodilation, Hypotension
(2) Veins - SANS - Dilation, Decreased preload, Decreased CO
(3) Heart - PANS - Tachycardia
(4) Iris - PANS - Mydriasis
(5) Ciliary m. - PANS - Cycloplegia
(6) GI - PANS - Decreased tone and motility leading to constipation
(7) Bladder - PANS - Urinary retention
(8) Salivary glands - PANS - Xerostomia
(9) Sweat glands - SANS - Anhydrosis
True or false: Ganglionic blocking drugs do not prevent changes in HR elicited directly by beta1-agonists or M2-agonists.
What is the result of ganglion blockade when you administer a drug to a patient that produces hypotension?
The vasomotor center cannot relay stimuli via baroceptor reflex to the heart, so any reflex changes in HR is cancelled.
Describe catecholamine synthesis in adrenergic nerves.
Tyrosine to Dopa with the help of Tyrosine Hydroxylase (Vit C) to Dopamine with the help of DOPA Decarboxylase to NE with the help of Vesicular dopamine beta-hydroxylase. NE is stored in vesicles.
What molecule prevents transport of tyrosine into adrenergic nerves?
MAO inhibitors do what?
Inhibit MAO-A which normally degrade the NE mobile pool. Result is a larger NE pool.
What type of drug prevents reuptake of NE into the adrenergic nerve terminal?
Reuptake blockers
What is the role of reserpine and guanethidine?
Prevent exocytosis of NE-vesicles.
What receptor can modulate release of NE from adrenergic terminals?
Alpha2-receptors working through Gi proteins to inhibit the production and release of NE into the synaptic cleft.
What is the rate limiting step in the synthesis of NE?
Tyrosine hydroxylase step.
______ (beta/alpha) receptors are usually more sensitive to activators than _____ (beta/alpha) receptors. What is the significance of this?
beta; alpha

Since beta is more sensitive than alpha, administering drugs that have both effects will cause a beta-dominant response at low dosages while alpha responses will predominate at higher doses.
Where do we have α1-receptors? What is the result of stimulation in each organ.
• Eye (radial) - Mydriasis
• Arterioles (skin, viscera) - Contraction, Increased TPR, Increased diastolic P, Increased afterload
• Veins - Contraction, Increased preload, Increased systolic P
• Bladder trigone and sphincter - Contraction with urinary retention
• Male sex organs - Vas deferens - Ejaculation
• Liver - Increased glycogenolysis
• Kidney - Decreased renin release
What is the result of stimulation of β1, α1 and D1 in the kidney?
α1 - Decreased renin release
β1 - Increased renin release
D1 - Vasodilation
Where do we find α2 receptors and what is the response as a result of stimulation of the receptor?
• Prejunctional n. terminals - Decreased transmitter release, Decreased NE synthesis
• PLTs - Aggregation
• Pancreas - Decreased insulin secretion
Where do we find β1 receptors and what is the response as a result of stimulation of the receptor?
• Heart
- SA node → Increased HR
- AV node → Increased conduction velocity
- Atrial & Ventricular muscle → Increased force of contraction with oxygen consumption, Increased conduction velocity
- His-Purkinje → Increased automaticity and conduction velocity
• Kidney - Increased renin release
Where do we find β2 receptors and what is the response as a result of stimulation of the receptor?
• Blood vessels (all) → Vasodilation, Decreased TPR, Decreased Diastolic pressure, Decreased afterload
• Uterus → Relaxation
• Bronchioles → Dilation
• Skeletal muscle → Increased glycogenolysis
• Liver → Increased glycogenolysis
• Pancreas → Increased insulin secretion
True or false: β2 is mostly innervated.
False. It's mostly NOT innervated.
Where do we find D1 receptors (outside of the CNS) and what is the response as a result of stimulation of the receptor?
Renal, mesenteric, coronary vasculature - Causes vasodilation in kidney with increased RBF, increased GFR and increased Na+ secretion.