Autonomic Nervous System Flashcards

Question 1

Q

(T/F) While the CNS composes the brain and spinal cord (integrate and coordinate), the PNS composes of the somatic and autonomic nervous system.

Answer

A

True!

*PNS connects CNS to other parts of the body.

Question 2

Q

Somatic nervous system composes of somatic nerves (motor neurons), which are responsible for:

Answer

A

1) Contraction of skeletal muscles
2) Voluntary actions (conscious thought)

*spinal cord connected by motor neurons to muscles

Question 3

Q

Autonomic nervous system is responsible for:

Answer

A

Involuntary actions:

heart rate and heart muscle contractility
contraction of smooth muscles (blood vessel, lung airway, GI tract, eyes, urinary bladder)
gland secretion (lacrimation, salivation, GI tract secretion and sweat gland)

Question 4

Q

What are the two opposing systems autonomic nervous system is divided into?

Answer

A

1) Sympathetic nervous system
2) Parasympathetic nervous system

Question 5

Q

While the sympathetic nervous system arises from the __________, the parasympathetic nervous system arises from ___________ and _________.

Most ganglia of sympathetic nervous system are located in ______________ ____, while ganglia of parasympathetic nervous system are located in/near ______ _______.

Answer

A

Spinal cord T1-12 and L1-3
Brain stem (cranial nerves III, VII, IX, X); Spinal cord (Sacral 2-4)

Paraverterbral chain; target organs

Question 6

Q

(T/F) The sympathetic nervous system has long pre-ganglion fiber and short post-ganglion fiber. The opposite applies for the parasympathetic nervous system.

Answer

A

False!

Sympathetic nervous system: SHORT pre-ganglionic fiber, LONG post-ganglionic fiber

Parasympathetic nervous system: LONG pre-ganglionic fiber, SHORT post-ganglionic fiber

Question 7

Q

Which ANS triggers fight-or-flight responses and is activated in stress/frightening conditions?

Answer

A

The SYMPATHETIC nervous system

*activated in stress (physical/emotional)
*both fight or flight requires body movements (skeletal muscle contractions)

Question 8

Q

Briefly describe what happens to these during sympathetic activation:

1) Eyes
2) Brain
3) Heart
4) Blood vessels
5) Digestive tract
6) Lung airways (trachea, bronchi & bronchioles)
7) Stored energy
8) Sweat glands

Answer

A

1) Eyes: pupil dilates to see better

2) Brain: more alert for quicker reactions

3) Heart: beats harder and faster (more oxygen and nutrients to be circulated to contracting muscles)

4) Blood vessels: IN CONTRACTING MUSCLES dilates - more blood, oxygen and nutrients delivered to the muscles

5) Digestive tract: less active

6) Lung airways (trachea, bronchi and bronchioles): dilate for more oxygen to enter the lungs and the blood

7) Stored energy: in the LIVER, SKELETAL MUSCLES AND FAT tissues (in the form of glycogen n fat) breaks down providing more energy for contracting muscles.

8) Sweat glands: stimulated for heat loss and body temperature regulation.

Question 9

Q

What does the parasympathetic nervous system trigger?

Answer

A

It triggers the rest and digest responses including the three Ds: digestion, defecation and diuresis.

Question 10

Q

Briefly describe what happens to these during sympathetic activation:

1) Eyes
2) Heart
3) Digestive tract
4) Lung airways

What else?

Answer

A

1) Eyes: pupil constricts –> less light –> rest

2) Heart: beats slower –> less oxygen and nutrients need to be circulated

3) Digestive tract –> secretes digestive enzymes and CONTRACTS vigorously; promoting the digestion of food and nutrient absorption + storage

4) Lung airways: constrict –> less oxygen

At certain times, DEFECATION, URINATION or DILATATION of genital arteries occurs

Question 11

Q

What kinds of effects does the sympathetic nervous system have?

What kinds of effects does the para-sympathetic nervous system have?

Answer

A

Sympathetic: DIFFUSE effects (each pre-ganglionic fiber connects with MANY post-ganglionic fibers –> widespread activation)

Para-sympathetic: DISCRETE (localized) effects (each pre-ganglionic fiber connects with only A FEW post-ganglionic fibers)
*it can selectively decrease the heart rate and increase the GI tract activity

Question 12

Q

Parasympathetic activation is associated with energy ________.

Answer

A

Conservation!

*decreased heart rate, bp
*increased GI tract activity + secretions
*permission to empty bladder, open GI sphincter

Question 13

Q

(T/F) During fight-or-flight responses, the blood flow is redirected from skin and visceral regions to skeletal muscles.

Answer

A

True!

There is a VASODILATION of arteries in skeletal muscle.

Question 14

Q

Briefly answer the following questions about the synapse:

1) What is a synapse?

2) What is its function?

3) What is the function of pre-synaptic neuron?

4) What is the function of a post-synaptic neuron?

Answer

A

1) Synapse connects two neurons (in both CNS and PNS): in the PNS, the second neuron can be a target cell.

2) Its function is SIGNAL CONDUCTION. electrical –> chemical (NT) –> electrical

3) Synthesis, storage and release of NTs into cleft.

4) Receptors for NTs

Question 15

Q

(T/F) The somatic nervous system consists of chains of two neurons (nerve fibers) connected by synapses in ganglia.

Answer

A

False!

The AUTONOMIC nervous system consists of chains of two neurons (nerve fibers) connected by synapses in ganglia.

*when the 1st neuron is excited, it releases NTs in the 2nd neuron, exciting it (when the NTs bind the receptors), releasing NTs in the synapse.

Question 16

Q

While the NT of synapses between the pre-ganglionic fiber and the post is acetylcholine in both the sympathetic and parasympathetic nervous system, the NTs of synapses between post-ganglionic fiver and target organs differ.

List them.

Answer

A

Sympathetic system: Norepinephrine (NE) in most tissues, Acetylcholine (ACh) only in SWEAT GLANDS!

Parasympathetic system: Acetylcholine (ACh)

Question 17

Q

(T/F) The somatic nervous system has one neuron that directly connects the target tissue and releases ACh in the synapse.

Question 18

Q

What are the two types of cholinergic receptors?

Answer

A

1) Muscarinic (M) receptors (G-coupled protein receptors)

2) Nicotinic (N) receptors (ligand gated Na+ channels)

Question 19

Q

ACh is the neurotransmitter for?

Answer

A

1) All neurons originated in the CNS
- pre-ganglionic fibers (para/sympa)
- sympathetic fibers for adrenal medulla
- somatic nerve (motor neurons
/neuromuscular junction)

2) Post synaptic nerves for:
- parasympathetic nervous system
- sympathetic nervous system (only sweat
glands)

3) Some neurons in the CNS

Question 20

Q

There are three muscarinic (M) receptors, match them to where they are located:

1) M1
2) M2
3) M3

A) heart
B) smooth muscles and glands
C) some neurons (CNS, autonomic ganglia)

Answer

A

M1: some neurons (CNS, autonomic ganglia)

M2: heart

M3: smooth muscles and glands

Question 21

Q

Where are the nicotinic (N) receptors found in?

Answer

A

Autonomic ganglia, skeletal muscle (neuromuscular junctions) and some CNS neurons

Question 22

Q

What are the agonists and antgaonists of the muscarinic (M) receptors?

Answer

A

Agonists: ACh and muscarine
Antagonist: Atropine

Question 23

Q

For M3 receptors, what does an agonist do in:
1) Smooth muscle
2) Blood vessel
3) Glands

For M2 receptors, what does an agonist do in:
1) Atrial muscle
2) Peacemaker tissue (sinoatrial node)

Answer

A

For M3 receptors: M3 –> Gq –> IP3 (inositol triphosphate) –> Ca2+ release

1) Smooth muscle: stimulates contraction

2) Blood vessel: vasodilation

3) Glands: stimulates secretion

.

For M2 receptors: coupled to Gi –> inhibition of AC (adenylyl cyclase)

1) Atrial muscle: reduced cAMP –> reduced Ca2+ influx via Ca2+ channels —> reduced contractility

2) In peacemaker tissue: With Gβγ subunits, there is an activation of ACh-sensitive K+ channels (hyperpolarizes) and slows heart rate

Question 24

Q

Briefly describe how smooth muscle contraction occurs in 5 steps.

How does relaxation occur?

Answer

A

1) Initiated by Ca2+ release (0.1um –> 10 um)
2) Ca2+ binds to CALMODULIN
3) Ca2+/Calmodulin complex activates MYOSIN LIGHT CHAIN KINASE (MLCK)
4) The MLCK then phosphorylates MYOSIN
5) Myosin binds to ACTIN, triggering contraction

Relaxation: Ca2+ decreases or activation of MLC phosphatase (which counteracts MLCK)

Question 25

Q

How does Nitric Oxide (NO) cause relaxation in vascular smooth muscle resulting in vasodilation?

Answer

A

NO activates guanylyl cyclase (GC) which then activates cGMP.

cGMP can:
a) inhibit L-type Ca2+ channels
b) decrease MLCK
c) increase myosin light chain phosphatase

these all cause vascular smooth muscle relaxation (vasodilation)!

Question 26

Q

How/where is Nitric Oxide (NO) produced?

Answer

A

In the ENDOTHELIAL CELLS, nitric oxide synthase (NOS) turns L-arginine (L-arg) into NO.

Now, there is a generation of basal level of NO. This rapidly diffuses to smooth muscle causing relaxation!

Question 27

Q

(T/F) NO production can be further stimulated by ACh via M3 receptors on endothelial cells. This stimulates NOS to make more NO, resulting in a greater vasodilation of blood vessels.

Question 28

Q

What are nicotinic receptors? What do they do?

Answer

A

Ligand (ACh)-gated Na+ channels (pentamers)

When there is a Na+ influx, there is membrane depolarization (excitation), causing:

a) excitation of post-ganglionic nerves

b) Ca2+ release from Sarcoplasmic Reticulum (SR) –> skeletal muscle contraction

c) CNS: excitation of neurons

Question 29

Q

There are two different types of Nicotinic receptors, Nm and Nn. Though they are similar, they have different combinations of subunits.

Match them to their definitions:
1) Nm
2) Nn

A) found in SKELETAL MUSCLE + neuronmuscular endplates. Agonists: ACh, nicotine. Antagonist: Tubocutarine

B) found in POSTGANGLIONIC NEURONS, some presynaptic cholinergic terminals. Agonist: ACh, nicotine. Antagonist: Hexamethonium

Answer

A

Nm: found in SKELETAL MUSCLE + neuronmuscular endplates. Agonists: ACh, nicotine. Antagonist: Tubocutarine

Nn: found in POSTGANGLIONIC NEURONS, some presynaptic cholinergic terminals. Agonist: ACh, nicotine. Antagonist: Hexamethonium

Question 30

Q

What are the two types of ADRENERGIC RECEPTORS?

Answer

A

1) α receptors: α1 and α2
2) β receptors: β1 and β2

Question 31

Q

Describe α1 receptors (location + mechanism).

Answer

A

Located in the SMOOTH muscles (blood vessel, urinary bladder, eyes, etc), exocrine glands and CNS.

Mechanism:
Gq –> PL-C (phospholipase C) –> IP3 (inositol triphosphate) –> SR Ca2+ release —> CONTRACTION & SECRETION

Question 32

Q

Describe α2 receptors (location + mechanism).

Answer

A

Located in PRE-SYNAPTIC MEMBRANE where it inhibits further NE release (negative feedback “autoreceptor”)
Gi –> reduced cAMP/PKA –> reduced Ca2+ influx

Located in blood platelets
Gi –> reduced cAMP –> platelet AGGREGATION
*stops any potential bleeding during flight/fight

Question 33

Q

Describe β1 receptors (location + mechanism)

Answer

A

Increases cAMP in HEART and KIDNEY

Gs –> cAMP/PKA –> Ca2+ influx

Increased HEART RATE + CONTRACTILITY
RENIN SECRETION (in kidney cells)

Question 34

Q

Describe β2 receptors (location + mechanism)

Answer

A

Location: Smooth muscles (airway, blood vessels in skeletal muscle):

Gs –> cAMP –> inhibition of MLCK (myosin light chain kinase) –> relaxation of smooth muscle

Question 35

Q

Pupil size is regulated by the contraction of the iris muscle.

What are the two layers of the iris muscle?

Which receptors are located in each?

What happens when receptors are activated?

Answer

A

1) Circular (sphincter) muscle: M3 receptor: Pupil CONSTRICTS + MIOSIS

2) Radial (dilator muscle): α1 receptor: Pupil DILATES + MYDRIASIS

Question 36

Q

Describe the mechanisms on how the pupil dilates and constricts.

Answer

A

Parasympathetic activation –> ACh –> M3 receptor –> IP3/Ca2+ —> contraction —> pupil CONSTRICTS + MIOSIS

Sympathetic activation –> NE –> α1 receptor –> IP3/Ca2+ –> muscle contraction –> pupil DILATES & MYDRIASIS

Question 37

Q

What are the 6 steps of general mechanism of synaptic transmission?

Answer

A

1) SYNTHESIS of neurotransmitter from precursor; STORAGE in vesicles

2) EXCITATION (depolarization) of PRESYNAPTIC MEMBRANE: an action potential traveling down the neuron depolarizes the presynaptic nerve terminal

3) ACTIVATION of voltage-gated Ca2+ channels: Ca2+ entry

4) RELEASE of stored NTs: increased Ca2+ –> vesicle fusion with the plasma membrane –> release of NT into the synaptic cleft

5) ACTIVATION of receptors: NTs bind to postsynaptic receptors (ion channels/GPCRs)

6) REMOVAL OF TRANSMITTERS. Transmitter can be degraded by enzymes (6a) in the synaptic cleft or can be recycled into the presynaptic cell (6b) by reuptake transporters.

Question 38

Q

(T/F) Tyrosine turns into DOPA and then into DOPAMINE and then into NOREPINEPHRINE.

Question 39

Q

How is norepinephrine removed from the synaptic cleft?

Answer

A

1) MAO: monoAmine Oxidase (degrades NE)

2) COMT: catechol-O-methyltransferase (degrades NE)

Question 40

Q

NE synthesis is compartmentalized:

________ _______ transporter translocates dopamine into ________ vesicles.

In __________ neurons, intravesicular _______ __________ converts dopamine into norepinepherine, stored in vesicles until release.

Released NE can also be taken up into presynaptic terminals by the selective ____ transporter (NET akak uptake 1).

NE in the cytoplasm of the presynaptic neuron can further be taken up into synaptic vesicles by ________ or degraded by _____ _____ _____ ______.

Answer

A

Vescicular monoamine transporter (VMAT); synaptic

Adrenergic; dopamine-b hydrolase

NE

VMA; mitochondrion-associated monoamine oxidase (MAO).

Question 41

Q

Both norepinephrine and epinephrine are metabolized by _____ and _____ to the same metabolite, __________ acid, which is excreted in the urine.

Answer

A

MAO; COMT; vanillylmandelic acid

*by testing the VMA levels in the urine, we can test NE/E levels in the human body.

Question 42

Q

What is phenochromocytoma?

Answer

A

Phenochromocytoma (PCC); a tumor of chromaffin cells (phenochromocytes) in adrenal medulla.

Tumors secrete and release large amounts of epinephrine and norepinephrine into the blood.

It is a rare cause of hypertension.

Primary urinary excretion of VMA is markedly increased; diagnostic test.

Question 43

Q

Match the drugs affecting adrenergic neurotransmission to their definitions:

1) Alpha methyl tyrosine
2) Reserpine
3) Guanethidine
4) Cocaine, tricyclic antidepressants
5) Pargyline

A) inhibition of storage
B) reuptake inhibitors
C) synthesis inhibitors
D) MAO inhibitors
E) inhibition of release

Answer

A

Alpha methyl tyrosine: synthesis inhibitors

Reserpine: inhibition of storage

Guanethidine: inhibition of release

Cocaine, tricyclic antidepressants: reuptake inhibitors

Pargyline: MAO inhibitors

Question 44

Q

The effect of a neurotransmitter is determined by its ________ _______ present on target cells.

Answer

A

Receptor subtype

Question 45

Q

While sympathetic activation (NE/E) in α receptor causes __________, in a β receptor causes _________.

Answer

A

Contraction; relaxation

Question 46

Q

During filling of the bladder, ________ control predominates, causing relaxation of the _________ muscle ( β2) and contraction of the ________ _______ (α1).

During micturition, __________ control predominates causing contraction of the _______ muscle , and relaxation of ______ ______ (voluntary control)

Answer

A

Sympathetic; detrusor; internal sphincter

Parasympathetic; detrusor; external sphincter

Question 47

Q

A general rule is α1 and β1 ________, while α2 and β2 ________ smooth muscles, glands, and cardiac muscle.

Answer

A

stimulate; inhibit

Question 48

Q

Which one of the following statements is true?

1) Epinephrine has no selectivity for β (β1 = β2), but has high affinity for α1.

2) Norepinephrine has no selectivity for both α and β, so can potently activate all subtypes.

3) Epinephrine leads to vasoconstriction in arteries of skin tissues (α1) and vasodilation in skeletal muscle (β2).

4) Norepinephrine causes all blood vessels to dilate (α1 activation dominates, β2 not active).

Answer

A

3!

For 1: Epinephrine has no selectivity for both α and β, so can potently activate all subtypes.

For 2: Norepinephrine has no selectivity for α, but a low affinity for β2 (β1 > β2).

For 3: Norepinephrine causes all blood vessels to CONSTRICT (α1 activation dominates, β2 not active).

Question 49

Q

What are the four therapeutic uses of epinephrine?

Answer

A

1) Anaphylactic shock (relaxes airway smooth muscle β2+contracts vascular smooth muscle α1)

2) Cardiac arrest - not hear attack (stimulates cardiac contraction β1)

3) Reduce bleeding (vasoconstriction α1)

4) Delay absorption of local anesthetics (vasoconstriction α1)

Question 50

Q

What are the adverse effects of epinephrine?

Answer

A

Arrhythmias (b1)
Hypertension (a1)
Hyperglycemia (b1 in liver increases glucose)

Question 51

Q

Activation of a1 means smooth muscle contraction (a1 –> ip3 –> ca2+ release), this includes;

Answer

A

1) vascular smooth muscle (esp. blood vessels in extremities)

2) sphincters of digestive tract

3) inner sphincters of lower urinary tract

4) hair erector muscle

5) eye: contraction of radial iris muscle (mydriasis)

Question 52

Q

What is phenylephrine (PE)?

What are its clinical uses?

What are its adverse effects?

Answer

A

phenylephrine (PE) is an a1 agonist; its action is SMOOTH MUSCLE CONTRACTION (vasoconstriction)

Clinical uses:
1) superficial bleeding
2) nasal decongestion
3) hypotensive emergencies
4) mydriasis

Adverse effects: hypertension

Question 53

Q

What are prazoSIN and tamsuloSIN?

What are their clinical uses?

What are their adverse effects?

Answer

A

a1 reversible antagonist; its action is SMOOTH MUSCLE RELAXATION

Clinical uses:
1) hypertension (vasodilation)
2) urinary tract obstruction (men w benign prostatic hyperplasia): relaxes smooth muscles in internal sphincter of urethra + prostate gland

Adverse effects:
1) orthostatic hypotension + dizziness (excessive vasodilation in veins)
2) reflex heart rate increase (decrease in blood pressure causes sympathetic nervous system to increase heart rate)

Question 54

Q

Match what a2 receptor does in each location when activated:

1) Pre-synaptic neuron
2) Pancreatic islet cells
3) Blood platelets

A) promotes aggregation
B) inhibits further NE release
C) inhibits insulin secretion

Answer

A

1) Pre-synaptic neuron: inhibits further NE release

2) Pancreatic islet cells: inhibits insulin secretion

3) Blood platelets: promotes aggregation

*all due to reduced cAMP which reduces Ca2+ influx

Question 55

Q

What is clonidine?

What are its clinical uses?

What are its adverse effects?

Answer

A

clonidine is an a2 agonist. its action in pre-synaptic neuron is to decrease NE release in both PNS and CNS (causing reduced sympathetic outflow). this leads to VASODILATION in blood vessels as there is less vasoconstriction.

Clinical uses:
1) Hypertensive urgencies (Systolic BP > 180)
2) Diagnose phenochromocytoma (PCC) in patients. In health people, there is a reduced serum NE level!

Adverse effects:
1) dry mouth
2) sedation (a2-induced inhibition in CNS)

Question 56

Q

What is yohimbine?

What are its clinical uses?

What are its adverse effects?

Answer

A

it is an ALKALOID from bark of african yohimbe tree; it is an a2 antagonist and its action is to INCREASE PERFUSION OF CERTAIN TISSUES.

Clinical use:
1) erectile dysfunction (blockage of these receptors in corpus cavernosum artery; increased Ach release; vasodilation) *mechanism not fully understood

Adverse effect:
1) hypoglycemia (increases insulin secretion)

Question 57

Q

Match the non-selective alpha receptor antagonist to their definitions:

1) Phenoxybenzamine
2) Phentolamine

A) reversible a1 and a 2 blocker. use to relieve localized vasoconstriction and tissue ischemia.

B) irreversible a1 and a2 blocker. can be used orally, long term action (3-4 days). used to control hypertension in patients with PCC until removed.

Answer

A

1) Phenoxybenzamine: irreversible a1 and a2 blocker. can be used orally, long term action (3-4 days). used to control hypertension in patients with PCC until removed.

2) Phentolamine: reversible a1 and a 2 blocker. use to relieve localized vasoconstriction and tissue ischemia.

Question 58

Q

(T/F) Both phenoxybenzamine and phentolamine are used for chronic hypertension.

Answer

A

False!

Neither are used for chronic hypertension due to their adverse effects: reflex tachycardia, headache, and dizziness.

Question 59

Q

Both B1 and B2 receptors increase _______ but effects are ______ specific.

In heart and kidney, ____ is prevalent. This leads to ______ heart rate and renin secretion.

In smooth muscles, ___ is prevalent. This leads to an inhibition of ______, causing smooth muscle _________ (treats asthma and delays preterm labor).

Answer

A

cAMP; tissue

b1; increased

b2; MLCK (myosin light chain kinase); relaxation

Question 60

Q

What is dobutamine?

What are its clinical uses?

What are its adverse effects?

Answer

A

Dobutamine is a b1 agonist. It causes powerful increases in heart contractility + rate.

Clinical uses:
1) Cardiac arrest + during heart surgery
2) Acute heart failure (short term for cardiac pump failure)

Adverse effects:
1) Arrhythmias
2) Increased heart rate (increases O2 consumption –> ischemia/angia)

Question 61

Q

What is salbutamol?

What are its clinical uses?

What are its adverse effects?

Answer

A

Salbutamol is a b2 agonist. it causes a dilation of airway (bronchodilation).

Therapeutic uses:
1) relieve asthma caused by bronchospasm

Adverse effects:
1) tremor and anxiety
2) tachycardia (fast heart rate)

*selectivity is “relative” to all drugs: salbutamol in high dosages can activate b1 in heart –> tachycardia

Question 62

Q

What is isoproterenol?

What are its clinical uses?

What are its adverse effects?

Answer

A

Isoproterenol activates both b1 and b2. its action is cardiac stimulation (b1) and bronchodilation (b2).

Clinical uses:
1) cardiac disease (arrest, bradycardia, atrioventricular block)
2) no longer used for asthma

Adverse effects:
1) arrhythmias (b1)
2) hyperglycemia (b2-mediated glycogenolysis)

Question 63

Q

What are b-blockers?

What are their clinical uses?

What are their adverse effects?

Answer

A

b blockers are b1 and b2 antagonists. their action is to reduce heart activities (cardioprotection in heart disease)

Clinical uses:
1) Heart diseases (angina, myocardial infarction, heart failure, arrhythmias, hypertension)
2) Stage fright + anxiety (CNS effect)

Side effects:
Come only from B2 blockade! B2 blockers are not clinically useful!

Question 64

Q

What are atenolol and metoprolol?

Answer

A

Selective b1 blockers!

In heart it reduces heart rate + contractility and in kidneys it reduces renin secretion (treats hypertension)

Answer 62

A

Non selective b-blockers! blocks b1 and b2!

Blocking b2 (contraction in smooth muscle) causes bronchoconstriction and prolonged hypoglycemia.

Answer 63

A

It is a mixed acting antagonist. It blocks a1 and b1!

It treats CONGESTIVE HEART FAILURE!
- reduces heart rate (blocks b1)
- reduces blood pressure (blocks a1)
- reduces patient mortality

Answer 64

A

Non-specific blocker: blocks all subtypes (a1, a2, b1, and b2).

It is used to in the treatment of HYPERTENSIVE EMERGENCIES!
- decreases heart rate, contractility and peripheral vascular resistance (vasodilation)

Answer 65

A

1) Phenylephrine: a1 agonist

2) Clonidine: a2 agonist

3) Prazosin: a1 antagonist

4) Yohimbine: a2 antagonist

5) Phenoxybenzamine/Phentolamine: a1 and a2 antagonist

6) Dobutamine: b1 agonist

7) Salbutamol: b2 agonist

8) Isoproteronol: b1 and b2 agonist

9) Atenolol: b1 antagonist

10) Butoxamine: b2 antagonist

11) Propranolol: b1 and b2 antagonist

12) Labetolol: a1, a2, b1 and b2 antagonist

Answer 66

A

Direct acting sympathomimetics: a and b receptor agonists - directly acts on the receptors

Indirect acting sympathomimetics: works by increasing NE level! This can be done by reuptake inhibitors, MAO inhibitors, and displacement drugs.

Answer 67

A

1) Tyramine
2) Ephedrine
3) Amphetamine and related drugs

These bind to uptake 1 (aka NET) and reverse the mode of action, releasing NE stored in vesicles into cytoplasm/cleft!

Usually, NET would store the NE in the vesicles from the cleft!

Answer 68

A

1) Tyramine: found in foods (cheese, aged meats, soy, yeast, wine, beer + bananas). normally not absorbed significantly (rapid degradation by MAO). used with MAO inhibitors! not available for clinic use.

2) Ephedrine: an alkaloid from plant Ma Huang (chinese med). its derivative, pseudoephedrine and it are mixed acting agonists. they bind to a1 and increase NE release (vasoconstriction). used for treatment of nasal congestion. not available in US cos it can make methamphetamine.

3) Amphetamine: reverse uptake (1) to push out NE (or serotonin) into the cleft and prevent reuptake. net effect is unregulated release of large amounts of NTs into the synapse.

Answer 69

A

Adrenergic neurons (NE) arise in the locus ceruleus and have widespread projections to the cerebellum, hypothalamus, cerebral cortex!

Answer 70

A

3 is false!

To treat toxicity, you need to ACIDIFY the urine to maintain the charge on amphetamine (a weak base). This allows it to not be resorbed in kidney tubular cells, enhancing excretion.

Answer 71

A

Synthesizes, Degrades

Answer 72

A

Step 1: Choline is transported into the presynaptic nerve terminal by Na+-choline cotransporter.

Step 2: The cytosolic enzyme choline acetyltransferase catalyzes the formation of ACh from acetyl coenzyme A (AcCoA) and choline.

Step 3: Newly synthesized ACh is packaged into vesicles for storage.

Step 4: Nerve stimulation –> exocytosis and release

Step 5: Released ACh diffuses in the synaptic cleft and binds to post/pre-synaptic receptors.

Step 6: ACh in the synaptic cleft is degraded by membrane-bound acetylcholinesterase (AChE) into choline and acetate.

Answer 73

A

Hemicholinium: Inhibitor of choline uptake (step 1)

Vesamicol: Inhibitors of ACh storage (step 3)

Botulinum Toxic: Inhibitors of ACh release to the cleft (step 4)

Nerve gases: AChE inhibitors (step 6)

a-latrotoxin (black widow venom): Stimulates ACh release to cleft.

Answer 74

A

relaxes

skeletal muscle; urinary bladder; reduce

Adverse effects: Dry mouth + difficult swallowing.

Answer 75

A

Black widow bites (esp by female spiders with larger venom glands) causes a-latrotoxin to enter the body and stimulate ACh release to the cleft.

This results in excessive activation of ACh receptors and muscle contraction + pain.

Analgesic and anti-inflammatory meds can treat it.

Answer 76

A

Direct acting cholinomimetics are cholinergic receptor agonists. They directly bind and activate cholinergic receptors.

They include choline esters, plant alkaloids and synthetic drugs (cevimeline).

Answer 77

A

4!

Choline esters include acetylcholine and its analogs (carbachol + bethanechol). They are POORLY absorbed from the GI tract and NOT distributed to the CNS.

Acetylcholine and CARBACHOL activate both M and N receptors, while BETHANECHOL activates M only.

ONLY ACETYLCHOLINE IS hydrolyzed by cholinesterase (short-acting).

Answer 78

A

Muscarine: activate M receptors, come from poisonous mushrooms with no medical use

Nicotine: activate N receptors, come from tobacco plants. Chewing gum + transdermal patch for smoking cessation.

Pilocarpine: higher affinity for M receptors, come from pilocarpus. used in glaucoma.

Answer 79

A

The toxicity of muscarinic receptors when activated summarized.

Salivation
Lacrimation
Urination
Defecation
Gastrointestinal motility
Emesis (vomiting)
+ Bradycardia

*need M receptor antagonists to treat it.

Answer 80

A

Ciliary

Pupil; Anterior

Trabecular; Achlemm’s

Answer 81

A

Glaucoma is an eye disease associated with ELEVATED INTRAOCULAR PRESSURE. Damage to the eye nerve can lead to loss of vision and blindness.

Mechanisms: narrowing of anterior chamber angle
- reduced outflow
- increased intraocular pressure
- optic nerve damage

Answer 82

A

Pilocarpine: stimulates contraction of meridional ciliary muscle (M receptors). opens trabecular meshwork, faster drainage of aqueous humor and reduced pressure.

B-blockers: reduces secretion of aqueous humor and pressure.

Answer 83

A

Neostigmine and endrophonium are REVERSIBLE AChE inhibitors.

They reversibly inactivate AChE, causing increased levels of ACh. They stimulate N receptors at somatic neuromuscular junctions and M receptors.

Clinical uses:
- reverses skeletal muscle paralysis
- myasthenia gravis

Answer 84

A

An autoimmune neuromuscular disease caused by the blocking/destruction of the ACh receptors by antibodies at neuromuscular junctions.

Weakness in skeletal muscle; drooping eyelids; blurry vision; shortness of breath.

Answer 85

A

True!

If Neostigmine dose too low: with Edrophonium muscle strength improves.

Answer 86

A

Organophosphate compounds with high lipid solubility. They are extremely toxic! pesticides + nerve gases are examples.

Because AChE is inhibited, there is an excessive ACh at the synaptic cleft.

Answer 87

A

1) Excessive activation of M receptors (gland secretion + smooth muscle spasm)

2) Excessive activation of N receptors (inhibition of neuromuscular transmission –> muscle weakness)

3) CNS effects (seizuer, respiratory depression + coma)

Answer 88

A

1) Decontamination of patients
2) Pralidoxime to reactivate AChE
3) Atropine (M receptor antagonist)

Answer 89

A

Atropine: alkaloid that blocks M receptors (muscarinic antagonist). Has opposite effects to parasympathetic activation.

Clinical uses:
1) Prepare patients for surgery with general anesthesia (reduces salivatory + airway secretions)
2) Relieves urinary bladder spasm and internal spasm (inhibits muscle contraction)
3) Induces mydriasis during an eye exam
4) Treatment of bradycardia
5) Treatment of muscarinic poisoning

Adverse effects:
1) Dry eyes, mouth + constipation
2) Urinary secretion
3) Inhibition of sweating (reduced heat loss; hyperthermia)
4) Photophobia

Answer 90

A

Accommodation: ability of the eye to change its optical power to maintain a clear image or focus on an object as its distance varies. This is through the contraction of ciliary muscles.

Atropine inhibits accommodation by inhibition of ciliary muscle contraction, resulting in blurry vision.

Answer 91

A

Muscarinic antagonist. Also an alkaloid.

It has similar action as Atropine. It is used to prevent MOTION SICKNESS.

Answer 92

A

Muscarinic antagonist. Also an alkaloid.

It has similar action as Atropine. It is used to prevent MOTION SICKNESS.

It blocks ACh neurotransmission from vestibular apparatus to the vomiting center in brainstem; suppression of motion sickness.

Answer 93

A

Cholinergic (Nicotinic) Antagonist.

An alkaloid from curare plants.

It is a competitive blocker of N receptors in skeleton muscle (muscle relaxation + paralysis).

It was used to induce muscle relaxation during surgeries but newer drugs are available now!

Its effects can be reversed by AChE inhibitors.

Answer 94

A

A DEPOLARIZING antagonist. It is two covalently linked acetylcholine molecules.

It causes an excessive activation of N receptors (persistent cell depolarization + prevents subsequent contractions).

Its action: initial transient muscle contraction followed by a sustained muscle paralysis.

Clinical use: induce muscle relaxation during surgeries; facilitate airway intubation.

Its effects CAN NOT be reversed by AChE inhibitors.

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Autonomic Nervous System Flashcards

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