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CPR Midterm > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Are pre- and/or post-gangionic neurons myelinated?

A

Pre-ganglionic are myelinated, post ganglionic are not

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2
Q

In general, where is the gangion and synapse located for the parasympathetic vs. sympathetic nervous systems

A

Parasympathetic: near the effector tissue Sympathetic: in the sympathetic chain, near the spinal cord

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3
Q

What are the 3 tissue types controlled by the autonomic nervous system?

A
  1. Cardiac tissue (muscle, nodes, and conduction system) 2. smooth muscle 3. glands
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4
Q

Contrast miosis and mydriasis. What autonomic nervous system causes each?

A

Miosis: pupil constriction due to contraction of the sphincter muscle, caused by parasymathetic innervation Mydriasis: pupil dialation due to contraction of the radial muscle, caused by sympathetic innervation

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5
Q

What are the neurotransmitters associated with the pre- and post-ganglionic synapses of the parasympathetic vs. sympathetic nervous systems?

A

Pre-ganglionic: ACh for both para and symp Post-ganglionic: ACh for para, Epinephrine and Norepinephrine for symp

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6
Q

Contrast the parasympathetic and sympathetic effects on blood vessel dilation/constriction.

A

Parasympathetic: weak (not significant) dilation Sympathetic: strong constriction to unnecessary tissues (skin and GI), dialation to liver and skeletal muscle

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7
Q

Name the peptides that sometimes coexist with ACh and NE in their respective post-ganglionic nerves.

A

Vasoactive intestinal peptide with ACh in parasympathetic Neuropeptide Y with NE in sympathetic

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8
Q

Where is ACh synthesized?

A

in the pre-synaptic terminal (Extra detail: after ACh is broken down in the synapse by AChE, the choline is transported back into the pre-synaptic neuron so it can be used to make more ACh.)

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9
Q

Where in a cholinergic synapse are nicotinic and muscarinic receptors found (if present)?

A

On the post-synaptic neuron

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10
Q

Identify the excitatory and inhibitory muscarinic receptors and contrast their effects.

A

M1, M3, M5: excitatory; stimulate IP3 and eventually increase intracellular Ca++ M2, M4: inhibitory; decrease cAMP, open K+ channels (hyperpolarizes the cell)

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11
Q

Name the 5 important molecules in the catecholamine synthesis pathway.

A
  1. tyrosine 2. L-dopa 3. dopamine 4. norepinephrine 5. epinephrine (last step only happens in adrenal medulla)
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12
Q

Identify the two types of nicotinic receptors, where they are found, and their general effects.

A

nAChRn (autonomic gangia - N for nerve) nAChRm (skeletal muscle - M for muscle) They cause stimulation and then blockade of their end tissue

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13
Q

What is the most important mechanism for termination of the action of NE?

A

Reuptake from the junctional space into the pre-synaptic nerve and storage vessels (requires ATP and Mg^2+) - Drugs like cocaine, tricyclic antidepressants, & methylphenidate inhibit this. (Impt exception: in blood vessels, excess NE is broken down by enzymes and/or diffused away.)

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14
Q

Describe the mechanism of reuptake blockers, and give examples (3).

A

They block reuptake of NE from the synpase (keeps stimulating the post-synaptic neuron) e.g.: cocaine, tricyclic antidepressants, methylphenidate

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15
Q

What class of drugs includes cocaine and methylphenidate?

A

Indirect acting sympathomimetic amines

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16
Q

What is the function of enzymes such as monoamine oxidase (in mitochondria) and catechol-O-methyl transferase (in cytoplasm)

A

Breaks down catecholamines (like NE) in synapse to terminate the effects.

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17
Q

what heart rate represents tachycardia? bradycardia?

A

tachy: 100
brady: 60

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18
Q

what effect do catecholamines have on action potential velocity?

A

increases action potential velocity. catecholamines include epinephrine and norepinephrine.

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19
Q

what arrhythmia is depicted here?

A

premature atrial contraction: the wave are normal but there is less distance between waves two and three

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20
Q

what arrhythmia is seen here?

A

supraventricular tachycardia the waves are regular but close together, really fast

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21
Q

what arrhythmia is seen here?

A

Accessory Pathway tachycardia: the delta wave is seen here which indicates that the signal has found another route to excite the ventricles before the normal path (example: WPW)

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22
Q

what arrhythmia is seen here?

A

Atrial tachycardia: there is a decreased PR interval

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23
Q

what arrhythmia is seen here?

A

atrial fibrillation: the QRS complex looks normal but there is no distinct P wave because there are too many atrial impulses

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24
Q

what arrhythmia is seen here?

A

atrial flutter: re-entry circuit that circulates in the atrium shows rapid, back-to-back atrial depolarization waves (ex. “saw-tooth” appearance)

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25
Q

what arrhythmia is seen here?

A

ventricular tachycardia: the ventricles are contracting too often so they can’t fill up all the way. therefore this lowers cardiac output.

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26
Q

what arrhythmia is seen here?

A

ventricular fibrillation with big coarse waves and small, frequent fine waves: the QRS is rapid and indistinguishable.

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27
Q

what is happening during ventricular fibrillation? what is the immediate treatment?

A

the ventricles are quivering and can’t pump enough blood to the body

CPR and defibrillate

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28
Q

what part of the cardiac cycle does long QT sydrome delay? what dangerous ECG pathology can this lead to?

A

delays repolarization. this can lead to Torsades de Pointes which can lead to ventricular tachycardia and death

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29
Q

whatare the three requirements for re-entry?

A
  1. unidirectioncal conduction block
  2. conduction time slows so the refractory tissue can recover (while other tissue is still depolarizing)
  3. adjacent cardiac tissue with many parallel pathways and different refractory periods
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30
Q

what arrhythmia is seen here?

A

bradycardia: distance between R peaks is extended (Hr approx 50)

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31
Q

what arrhythmia is seen here?

A

First degree heart block: fixed long PR interval

32
Q

where does a heart block occur? what does it cause (in terms of heart beat)?

A

as the signal travels from the AV node/His-Purkinje system to the ventricles.

causes a slow and irregular heart beat

33
Q

what arrhythmia is seen here?

A

second degree heart block type 1 (Wenckenbach): PR interval continues to get larger and larger and then the QRS is dropped

34
Q

what arrhythmia is seen here?

A

2:1 Mobitz type 2: the PR interval is stable and the P wave arrives regularly. For every two normal beats, 1 QRS complex is dropped.

35
Q

what arrhythmia is seen here?

A

third degree heart block: the P, QRS and T are all out of synchronization

36
Q

what are the class 1a antiarrhythmics?

A

Quinidine
Procainamide
Disopyramide

“The Queen Proclaims Diso’s pyramid.”

37
Q

name two class 1B antiarrhythmics

A

lidocaine
mexiletine
tocainide
phenytoin (also a seizure med)

38
Q

name the two class IC antiarrhythmics

A

flecainamide
propafenone (also a beta blocker)
“Can I have Fries Please?”

39
Q

what are class II antiarrhythmics? name three (there are 6 in FA)

A

beta blockers

**metoprolol, propanolol, **carvedilol
atenolol, timolol, esmolol

40
Q

what do class 3 antiarrhythmics block?

A

they block potassium channels (ie prolong depolarization)

41
Q

name 3 potassium channel blockers

A

amiodarone, ibutilide, dofetalide, sotalol

42
Q

what do class 1 antiarrhythmics block?

A

sodium channels

43
Q

what do class 2 antiarrhythmics block?

A

selective: only beta 1 receptors

non-selective: beta 1 and 2 receptors

44
Q

what do class 4 antiarrhythmics block?

A

calcium channels

45
Q

name the two calcium channel blockers

A

verapamil

diltiazam

46
Q

what does adenosine mainly treat?

A

paroxysmal supraventricular tachycardia

47
Q

what is used to treat bradyarrhythmias?

48
Q

what is used to treat atrial fibrillation?

A

ablation, beta blockers (propanolol), calcium channel blockers (verapamil), digoxin

49
Q

what are the primary indications for amiodarone?

A

ventricular tachycardia (with MI)

ventricular fibrillation

ventricular premature beats

Atrial fibrillation

Atrial flutter

50
Q

what are the primary indications for digoxin?

A

PSVT, atrial fibrillation, congestive heart failure

51
Q

what are the primary indications for procainamide?

A

WPW, PSVT, VT with MI, VF

52
Q

what is the primary indication for verapamil?

A

PSVT

(AV reentry, Afib)

53
Q

what is metoprolol used for?

A

hypertension mainly

also angina and CHF

54
Q

what are the primary indications for propanolol?

A

HTN, angina, a fib, a flutter, post-MI

55
Q

what are the primary indications for lidocaine?

A

VT with MI, VF

56
Q

Which class of antiarrhythmics is best for hypertension?

A

II- beta blockers

57
Q

Name four drugs that treat PSVT:

A

Adenosine, Digoxin, Procainamide, Verapamil

58
Q

Name three drugs that treat atrial fibrillation:

A

amiodarone, digoxin, propanolol

59
Q

alpha 1 receptor with G protein class?

A

vasoconstriction, mydriasis, intestinal and bladder sphincter muscle contraction

Gq

60
Q

alpha 2 receptor with G protein class?

A

decreasesd sympathetic outflow (autoregulation), decreased insulin release, decreased lipolysis, increased platelet aggregation

Gi (inhibitory)

61
Q

beta 1 receptors and G protein class?

A

incrased heart rate, increaseed contractility, increased renin release, increased lipolysis

Gs (stimulatory)

62
Q

beta 2 receptor and G protein class?

A

vasodilation, bronchodilation, increases heart rate, increases contractility, increased lipolysis, insulin release, decreased uterine tone (tocolysis), ciliary muscle relaxation, increased aqueous humor production

Gs

63
Q

M1 and G protein class?

A

CNS, enteric nervous system

Gq

64
Q

M2 and G protein class?

A

decrease heart rate and contractility of the atria

Gi

65
Q

M3 and G protein class?

A

increase exocrine gland secretions, increase gut peristalsis, increase bladder contraction, bronchoconstrition, increase pupillary sphincter muscle contracion (miosis), ciliary muscle relaxation (accomodation)

Gq

66
Q

D1 and G protein class?

A

relaxes renal vascular smooth muscle

Gs

67
Q

D2 and G protein class?

A

modulates transmitter release, especially in brain

Gi

68
Q

V1 and G protein class?

A

increased vascular smooth muscle contraction

Gq

69
Q

V2 and G protein class?

A

increased water permeability and reabsorption in the collecting tubules of kidney (V2 is found in the 2 kidneys)

Gs

70
Q

Which antiarrhythmic is best for “atrial fibrillation with atrioventricular conduction via accessory pathway”

hint: WPW

A

procainamide

slow conduction in accessory pathway connecting atrium and ventricle

71
Q

Which antiarrhythmic is best for patients with heart failure? why?

A

digoxin- (+) ionotroph

slows conduction, but increases contractility

72
Q

how to treat Vfib (ventricular fibrillation)

A

life threatening!

  1. cardioversion
  2. Epi + defibrillation
  3. lidocaine, amiodarone, procainamide, magnesium
  4. treat hyperkalemia
73
Q

how to treat torsades de pointes (long-QT syndrome)

A

pacing

magnesium

isoproterenol (B1 and B2 agonist, effects like epi)

74
Q

how to treat digitalis toxicity

A

stop digitalis

tx: digibind

magnesium

75
Q

What drug can you not give to WPW or SA/AV node dysfunction

A

digitalis, verapamil, diltiazem, amiodarone

76
Q

what drug do you not want to give to a pt with a history of MI or structural deformity

A

flecainide

can induce AV block

slows conduction of the electrical impulse within the heart, decreased contractility of the muscle,

77
Q

what drug can you not give to a pt with long QT interval

A

amiodarone, quinidine, procainamide, sotalol, ibutilide

lengthens QT interval

CPR Midterm (15 decks)

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