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Pharm > 03a: Cholinergic Drugs > Flashcards

03a: Cholinergic Drugs Flashcards

1
Q

Parasympathetic preganglionic fiber releases (X) messenger to bind (Y) receptor at synapse.

A 
X = ACh
Y = nicotinic
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2
Q

Sympathetic preganglionic fiber releases (X) messenger to bind (Y) receptor at synapse.

A 
X = ACh
Y = nicotinic
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3
Q

Parasympathetic post-gang fibers release (X) messenger to bind (Y) receptor on heart muscle.

A 
X = ACh
Y = muscarinic
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4
Q

Sympathetics oppose parasymp action on heart by releasing (X) messenger to bind (Y) receptor on (Z) cells.

A 
X = NE
Y = beta1
Z = myocardium
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5
Q

Sympathetics oppose parasymp action on GI tract by releasing (X) messenger to bind (Y) receptor on (Z) cells.

A 
X = NE
Y = alpha2
Z = post-gang parasymp neuron (terminal)
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6
Q

Parasympathetic post-gang fibers release (X) messenger to bind (Y) receptor to increase GI motility.

A 
X = ACh
Y = muscarinic
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7
Q

(Symp/parasymp) responsible for pupil dilation, aka (X).

A

Symp;

X = mydriasis

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8
Q

Predominant tone tends to be (parasymp/symp). List the key exceptions.

A

Parasymp;

  1. Blood vessels
  2. Sweat glands
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9
Q

(Cholinergics/adrenergics) responsible for predominant tone of salivary glands.

A

Cholinergics (parasymp)

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10
Q

(Cholinergics/adrenergics) responsible for predominant tone of blood vessels.

A

Adrenergics (symp)

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11
Q

(Cholinergics/adrenergics) responsible for predominant tone of sweat glands.

A

Cholinergics (but sympathetic NS!)

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12
Q

Iris radial muscle innervated by (symp/parasymp) and has (X) receptor.

A

Symp;

X = a1

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13
Q

(Symp/parasymp) relaxes bronchiolar smooth muscle. And (Symp/parasymp) contracts it. Which receptors involved?

A

Symp (beta2);

Parasymp (muscarinic - M2, M3)

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14
Q

Nicotinic receptor is a(n) (X)-gated (transporter/channel/ATPase). It transports (Y).

A

X = ligand;
Ion channel;

Y = Na, K, Ca

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15
Q

T/F: Nicotinic receptor is an excitatory receptor.

A

True

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16
Q

List the agonists of the nicotinic receptor. Star the muscle relaxant(s).

A
  1. Nicotine
  2. ACh
  3. Carbamoylcholine
  4. Succinylcholine*
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17
Q

List the antagonists of the nicotinic receptor. Star the muscle relaxant(s).

A
  1. Hexamethonium
  2. Tubocurarine*
  3. Atracurium*

(only have to know Tubocurarine)

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18
Q

ACh (does/doesn’t) penetrate cell membranes because of its structure as a(n) (X).

A

Doesn’t;

X = quaternary amine

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19
Q

ACh rapidly inactivated by (X) at which location(s)?

A

X = AChE (at synapse) and esterases (in blood)

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20
Q

(X), like ACh, is a quaternary amine and activates both N and M receptors. What’s a key difference between ACh and this agonist?

A

X = carbamylcholine

It’s an esterase-resistant analog of ACh

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21
Q

(X) is a nicotinic agonist that’s CNS-penetrating due to its structure as a(n) (Y).

A 
X = nicotine
Y = tertiary amine
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22
Q

Acute nicotine toxicity typically occurs via (X) route in children and (Y) route in adults.

A 
X = ingestion
Y = dermal contact (i.e. tobacco workers)
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23
Q

Acute nicotine toxicity: rapid onset of which symptoms initially?

A
  1. Abd pain, nausea, diarrhea
  2. Disturbed vision, confusion
  3. Weakness
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24
Q

T/F: Acute nicotine toxicity manifests in the respective symptoms due to overstimulated parasymp.

A

False - stimulates both parasymp and symp

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25
Q

Acute nicotine toxicity: central stimulation, in severe poisoning, will present with which symptoms?

A

Convulsions, coma, respiratory arrest

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26
Q

Acute nicotine toxicity: in severe poisoning, (tremors/paralysis) occurs via which mechanism(s)?

A

Paralysis;

  1. Na channel inactivation
  2. Desensitization of nicotinic receptors
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27
Q

List the treatment methods for acute nicotine toxicity.

A
  1. Activated charcoal (reduce GI absorption)
  2. Benzos (control seizures)
  3. IV fluids (increase/maintain BP)
  4. Atropine (if needed for bradycardia)
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28
Q

NMJ (neuromuscular junction) blocking agents have which general goal of action? What might these be used for?

A

Block ACh action at NMJ

  1. Tracheal intubation
  2. Set fractures
  3. Surgical muscle relaxant
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29
Q

Neuromuscular (NMJ) blocking agents can fall into which categories? State which type of inhibition is found in each.

A
  1. Depolarizing (non-competitive)

2. Non-depolarizing (competitive)

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30
Q

Tubocurarine is an example of (X) drug. What’s its mechanism?

A

X = muscle relaxant (non-depolarizing neuromuscular blocker)

Competitive inhibition of ACh binding to nicotinic receptors at skeletal muscle endplate

31
Q

When approximately (X)% of tubocurarine is bound, it is effective in (stimulating/preventing) (Y). What would this look like clinically?

A

X = 70
Preventing;
Y = ACh evoking muscle contraction

Flaccid paralysis of all skeletal muscle

32
Q

AChE inhibitors (assist/oppose) action of tubocurarine. How?When might these be used?

A

Opposes; increase endogenous ACh

Post-surgically to speed recovery

33
Q

Succinylcholine is an example of (X) drug. What’s its mechanism?

A

X = muscle relaxant (depolarizing neuromuscular blocker)

Bind nicotinic receptor (AGONIST) and evokes desensitization

34
Q

T/F: Effect of Succinylcholine cannot be reversed without synapse regeneration.

A

False - desensitized receptor can gradually reset (quick recovery) once agonist dissociates

35
Q

T/F: Succinylcholine is esterase-resistant.

A

False - rapidly hydrolyzed by plasma cholinesterase

36
Q

AChE inhibitors (assist/oppose) action of Succinylcholine. How?

A

Assist;

Increase endogenous ACh and further desensitize nicotinic receptors

37
Q

List the stages of block by neuromuscular depolarizing agents, such as (X).

A

X = Succinylcholine

  1. Fasciculation
  2. Phase I (depolarizing)
  3. Phase II (desensitizing)
38
Q

T/F: Block by neuromuscular depolarizing agents prevents muscle from repolarizing at all.

A

False - in Phase II, muscle repolarizes (channels are closed), but continues to exhibit flaccid paralysis

39
Q

Toxicity of nondepolarizing neuromuscular blocking agents, such as (X) involves:

A

X = tubocurarine

Histamine release (allergic rxn)

40
Q

Toxicity of depolarizing neuromuscular blocking agents, such as (X) involves:

A

X = succinylcholine

  1. Malignant hyperthermia
  2. Hyperkalemia
  3. Cardiac dysrhythmias
  4. Post-op muscle pain
41
Q

Malignant hyperthermia can be the result of a toxic dose of (X). This is prolonged in patients with (low/high) levels of which enzyme?

A

X = succinylcholine

Low; plasma cholinesterase

42
Q

(Low/high) levels of which ion are responsible for malignant hyperthermia?

43
Q

Toxicity via (X) neuromuscular blocking agent can result in (hyper/hypo)-kalemia via which mechanism?

A

X = succinylcholine
Hyperkalemia;

Excess K release through nicotinic receptor channels

44
Q

(X) falls into the class of denervating neurotoxins. It binds specifically to (Y) terminals.

A 
X = botulinum toxin
Y = cholinergic nerve
45
Q

T/F: Botulinum toxin has prolonged action (months).

46
Q

T/F: Nerve terminals can recover within minutes to hours of removal of botulinum toxin.

A

False - only via axonal sprouting

47
Q

List some adverse effects of botulinum toxin.

A
  1. Muscle weakness (potentially long-lasting)

2. Paralysis of respiratory muscles (can result in death)

48
Q

T/F: Although botulinum toxin has been FDA approved for certain uses, a 2008 FDA warning was issued for some cases of resp failure/death.

49
Q

T/F: there is no treatment for toxicity by botulism.

A

False - antitoxin exists (but doesn’t reverse toxicity in nerve terminal)

50
Q

Muscarinic receptor is a(n) (X) (transporter/channel/ATPase).

51
Q

List the subtypes of muscarinic receptors and the respective 2nd messenger pathways associated with each.

A
  1. M1, 3, 5: Increase PLC activity (and thus DAG, IP3)

2. M2, 4: Decrease cAMP (thus increase K and decrease Ca channel activation)

52
Q

List the muscarinic receptor agonists and star those that also bind nicotinic receptors (non-selective).

A
  1. ACh*
  2. Carbamoylcholine*
  3. Muscarine
  4. Pilocarpine
  5. Bethanchol (don’t need to know)
53
Q

List the clinical uses of ACh.

A

NONE! No clinical use

54
Q

Pilocarpine is a(n) (X) class drug with some selectivity for (Y) tissues/organs. How is it used clinically?

A 
X = muscarinic agonist (parasympathomimetic)
Y = salivary glands
  1. Orally (treat xerostomia)
  2. Topically (treat glaucoma)
55
Q

List clinical presentation of muscarinic agonist toxicity.

A
  1. Salivation
  2. Lacrimation
  3. Urination
  4. Diarrhea
  5. GI distress
  6. Emesis (vomiting)

(Plus bronchoconstriction, hypothension, bradycardia)

56
Q

Belladonna alkaloids are (X) agents/drugs. List some examples.

A

X = anti-muscarinic

  1. Atropine
  2. Scopolamine
57
Q

Anti-muscarinic agent would be used to treat (diarrhea/constipation) and (under/over)-active bladder.

A

Diarrhea; over-active

58
Q

Muscarinic (agonist/antagonist) used to reduce HR, by preventing vagal stimulation, during MI.

A

Antagonist

59
Q

Muscarinic (agonist/antagonist) used to treat AChE inhibitor poisoning.

A

Antagonist

60
Q

Clinical presentation of muscarinic antagonist toxicity.

A
  1. Dry as a bone
  2. Hot as a pistol
  3. Red as a beet
  4. Blind as a bat
  5. Mad as a hatter
61
Q

Treatment for patient presenting with muscarinic antagonist toxicity.

A

AChE inhibitor (physostigmine)

62
Q

List some conditions for which AChE inhibitors can serve as treatment.

A
  1. AD
  2. Myasthenia Gravis
  3. Post-surg paralytic ileus
  4. Urinary bladder atony
63
Q

List some conditions for which AChE inhibitors can serve as treatment.

A
  1. AD
  2. Myasthenia Gravis
  3. Post-surg paralytic ileus
  4. Urinary bladder atony
64
Q

List the major classes of AChE inhibitors. What’s the primary difference between them? Star the one used clinically.

A
  1. Alcohols
  2. Carbamate esters*
  3. Organophosphates

Duration of action

65
Q

List the major classes of AChE inhibitors. What’s the primary difference between them?

A
  1. Alcohols
  2. Carbamate esters
  3. Organophosphates

Duration of action

66
Q

T/F: Alcohols are rapidly reversible competitive inhibitors of AChE.

67
Q

MOA of carbamate esters: form (reversible/irreversible) (X) bond that lasts on the order of (sec/min/hours/days).

A

Reversible;
X = covalent

Hours (about 1-6)

68
Q

MOA of organophosphates: form (reversible/irreversible) (X) bond that lasts on the order of (sec/min/hours/days).

A

Irreversible
X = phosphate

Forever…

69
Q

MOA of organophosphates: form (reversible/irreversible) (X) bond that lasts on the order of (sec/min/hours/days).

A

Irreversible
X = phosphate

Forever…

70
Q

Sarin (nerve gas) poisoning likely due to (X) class of compounds. How might the individual present, clinically?

A

X = organophosphates (AChE inhibitors)

  1. SLUDGE (muscarinic toxicity)
  2. Neuromuscular block
  3. Resp failure
  4. Confusion, coma, convulsions
71
Q

Sarin (nerve gas) poisoning likely due to (X) class of compounds. How might the individual present, clinically?

A

X = organophosphates (AChE inhibitors)

  1. SLUDGE (muscarinic toxicity)
  2. Neuromuscular block
  3. Resp failure
  4. Confusion, coma, convulsions
72
Q

AChE inhibitor overdose/toxicity typically treated with (X). What’s the MOA?

A

X = Atropine

Blocks action at muscarinic (NOT NICOTINIC) receptors

73
Q

(X) is known as “cholinesterase regenerator” and is, in a way, better than atropine for treating (Y) toxicity. Why?

A 
X = Pralidoxime 
Y = AChE inhibitor (organophosphates)

Affects N and M receptor responses by binding organophosphates and causing them to release AChE (restores its function)

Pharm (16 decks)

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