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Principles of Pharmacology and Immunology (PPI) > Quiz 2 Exam 2 > Flashcards

Quiz 2 Exam 2 Flashcards

Neuro

1
Q

What chemical was used in the first experiments that blocked the muscle response to nerve stimulation?

A

Curare (it was later found that curare blocked the Ach receptors so Ach could not bind)

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2
Q

What is retrograde neurotransmission?

A

This is when transmission goes in the opposite direction. NTs are released from the postsynaptic site and activate the presynaptic site.

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3
Q

What are the two broad categories of receptors located on the postsynaptic site?

A

Ionotropic (fast and ions) and Metabotropic (slow and G proteins 2nd messengers)

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4
Q

An action potential stimulates the release of ____________ into the cell which activates _______ channels. This then allows the secretory vesicles to bind to the presynaptic site and release the NTs into the cleft.

A

Na+
Ca2+

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5
Q

What is the neuromuscular junction?

A

These are the skeletal muscle neurons that are not apart of the ANS. They are activated by Acetylcholine (Ach) binding to nicotinic acetylcholine receptors and stimulate the release of Na+ which is part of muscle contraction.

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6
Q

Where is epinephrine made?

A

Adrenal glands

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6
Q

What are the 3 main groups of neurotransmitters?

A
  1. Biogenic Amines/ Catecholamines- dopamine, EPI, and NE
  2. Amino acids- glutamate and GABA
  3. Acetylcholine (Ach)
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7
Q

What is the amino acid precursor for catecholamines synthesis?

A

Tyrosine

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8
Q

What are the steps in converting tyrosine to dopamine, NE, and Epi?

A

Tyrosine ——-> DOPA via Tyrosine Hydroxylase

DOPA——–> Dopamine via Aromatic Amino Acid Decarboxylase (AADC)

Dopamine ——> NE via dopamine beta-hydroxylase (DBH)

NE travels in systemic circulation and reaches adrenals

NE ——-> Epi via PNMT

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9
Q

What is the rate limiting enzyme of catecholamine synthesis?

A

Tyrosine hydroxylase

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10
Q

What are two enzymes that metabolism catecholamines to their inactive versions?

A

Monoamine oxidase (MAO) and Catechol-O-methyltransferase (COMT)

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11
Q

What is the primary mechanism of inactivating catecholamines in the cleft?

A

Reuptake transporters. They remove catecholamines from the synapse and suck them back up into the presynaptic neuron.

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12
Q

What is the MOA of cocaine?

A

Cocaine blocks the reuptake of NE in the peripheral and dopamine in the reward pathway.

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13
Q

What is the MOA of amphetamines?

A

Amphetamines reverse the direction of the reuptake transporter therefore spitting more catecholamines out and not taking an back up. Overall, it increases the release of dopamine and NE.

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14
Q

What are presynaptic autoreceptors?

A

These are typically alpha2 and dopamine2 autoreceptors. There are feedback inhibitory receptors that sense how much NE or dopamine has been released and when it senses the limit, it tells the neuron to slow down and stop the release of the NTs.

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15
Q

What are the steps in the creation and breakdown of acetylcholine (Ach)?

A

Acetyl CoA + Choline ——-> Acetylcholine (Ach) via Choline Acetyltransferase (ChAT)

Acetylcholine (Ach)——–> Acetic acid + Choline via acetylcholinesterase (Ache)

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16
Q

What happens to choline after Ach is metabolizied?

A

It is taken back up into the presynaptic neuron.

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17
Q

What is myasthenia gravis?

A

Myasthenia gravis is an autoimmune disorder that results in the destruction of Nicotinic Acetylcholine Receptors in the neuromuscular junction. It is characterized by muscle weakness.

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18
Q

Curare (plant alkaloid) and a-bungarotoxin (snake venom) have what MOA?

A

These compounds block Ach receptors.

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19
Q

What is the MOA of botox/ botulinum toxins?

A

Botox destroys the presynaptic vesicles that hold Ach which leads to the inhibition of Ach release.

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20
Q

What is the MOA of black widow toxin?

A

Black widow toxin stimulates the release of Ach

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21
Q

What is the MOA of insecticides?

A

Insecticides inhibit Acetylcholinesterase leading to massive increases in Ach levels.

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22
Q

What is a disease state that uses acetylcholinesterase inhibitors to slow the progression of the disease?

A

Alzheimer’s

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23
Q

The effect of an alpha2 agonist would be to?

A. Inhibit release of NE
B. Inhibit reuptake of NE
C. Inhibit metabolism of NE
D. Increase the release of NE

A

A. Inhibit the release of NE

Alpha2 receptors are the autoreceptors that are the natural breaks for the release of NTs. Stimulating that receptor would inhibit the release of more NE.

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24
Q

Cocaine acts to?

A. Increase the synthesis of NE
B. Inhibit NE metabolism
C. Inhibit NE reuptake
D. Indirectly activate NE receptors
E. C and D

A

E. Inhibits NE reuptake and indirectly activates NE receptors

Cocaine’s MOA is to inhibit the reuptake of NE. Therefore it also indirectly allow more NE to activate its receptors.

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25
Q

What is the neurochemical pathology of Myasthenia gravis?

A. Loss of Ach neurons
B. Loss of acetylcholinesterase
C. Loss of nicotinic acetylcholine receptors
D. Impaired uptake of choline

A

C. Loss of nicotinic acetylcholine receptors

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26
Q

What would be the RX for myasthenia gravis?

A

Increase Ach transmission by inhibiting acetylcholinesterase enzyme.

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27
Q

What are the two parts of the peripheral nervous system?

A

Somatic and Autonomic

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28
Q

What does the somatic nervous system control?

A

Skeletal muscle (voluntary movements)

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29
Q

What does the autonomic nervous system include?

A

Sympathetic and parasympathetic

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30
Q

What does the autonomic nervous system innervate?

A

Cardiac muscle, smooth muscle throughout the body, and glands

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31
Q

What are the general lengths (short vs long) of the parasympathetic innervation to the ganglion and organs?

A

Long preganglionic neuron and short postganglionic neuron

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32
Q

What is the NTs used at the ganglion and at the organs in the parasympathetic system?

A

Acetylcholine for both!

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33
Q

What type of receptor does Acetylcholine bind to in the parasympathetic nervous system at the organs?

A

Muscarinic

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34
Q

Where in the spinal cord do the parasympathetic fibers originate from?

A

Cranial and sacral portions of the spine

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35
Q

Where in the spinal cord do the sympathetic fibers originate from?

A

Thoracic and lumbar portions of the spine

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36
Q

For sympathetic innervation, what is the general length (long vs short) of the ganglionic neurons?

A

The preganglionic are very short while the postganglionic are long.

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37
Q

What NTs is released at the ganglion in sympathetic innervation?

A

Acetylcholine

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38
Q

At the site of the organs, excluding the adrenal medulla and sweat glands, what NT is released with sympathetic innervation?

A

Norepinephrine and it binds to a/B adrenergic receptors

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39
Q

T or F: Almost all visceral organs are served by both the sympathetic and parasympathetic divisions, but always cause the opposite effects.

A

False. The first portion is correct but it is not every single time they cause the opposite effect. They mostly cause the opposite effects but not every time.

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40
Q

Know this chart

A
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41
Q

Does sympathetic or parasympathetic have control over the vagus nerve (X)?

A

Parasympathetic

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42
Q

In the sympathetic division, what innervation arises from the paravertebral ganglia?

A

Innervation of organs above the diaphragm.

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43
Q

In the sympathetic division, what innervation arises from the prevertebral ganglia?

A

Innervation of organs below to diaphragm.

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44
Q

How are sympathetic responses described?

A

Sympathetic responses are the ‘E’ situations like exercise, emergency, excitement, and embarrassment

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45
Q

How are the parasympathetic responses described?

A

Parasympathetic responses are described with SLUDD + 3 Ds

Salivation, lacrimation, urination, digestion, and defecation with decreased heart rate, decreased airway diameter, and decreased diameter of the pupils.

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46
Q

What NT is used in all ganglions regardless that it is sympathetic or parasympathetic?

A

Acetylcholine binding to nicotinic receptors

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47
Q

Why are sweat glands and SOME blood vessels in skeletal muscle the outliers in sympathetic innervation?

A

In general, the sympathetic nervous system used NE at organs but at sweat glands, acetylcholine is used and it binds to muscarinic receptors. This is similar to parasympathetic but it is innervated by the sympathetic system.

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48
Q

What is unique about the adrenal medulla and how it is innervated?

A

It is known that the adrenal medulla secretes epinephrine. It is innervated by the sympathetic nervous system but this innervation has no ganglion intermediate. Ach is released from the spinal cord portion and it binds to nicotinic receptors are the adrenal medulla. This stimulates the adrenal medulla to release Epi and NE into the blood stream.

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49
Q

Where are M2 (muscarinic 2) receptors located?

A

The heart (and some nerve endings but really the heart)

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50
Q

Where are M3 (muscarinic 3) receptors located?

A

Everywhere else like smooth muscle, glands, endothelium, but NOT the heart.

51
Q

What is the unique function of alpha 2 adrenergic receptors?

A

These are the autoreceptors that act as brakes in the presynaptic sites of the neuron. They reduce cAMP therefore reducing NT output.

52
Q

Do alpha1 and alpha2 have the same or different affinity for NE and EPI?

A

They have the same affinity for both meaning that both NE and Epi have the same potency at alpha 1 and alpha 2 receptors.

53
Q

Where are beta 1 receptors primarily located?

A

The heart

54
Q

Where are beta-2 receptors primarily located?

A

Smooth muscle, glands, liver, and lungs

55
Q

Do beta 2 and beta 3 receptors have the same or different affinity for NE and Epi?

A

Epi is much more potent than NE at the beta 2 receptor. Epi is slightly more potent than NE at the beta 3 receptor.

56
Q

Where are beta-3 adrenergic receptors located?

A

Adipose tissue and the bladder.

57
Q

Where are alpha-1 receptors located?

A

Effector tissues like smooth muscle and glands

58
Q

All beta receptors increase cAMP. What does the alpha-1 receptor do to downstream signalling?

A

Alpha-1 activation increases IP3 and DAG signalling

59
Q

All beta receptors increase cAMP. What does the alpha-2 receptor do to downstream signalling?

A

Alpha-2 decreases cAMP. This makes sense as this is mainly used as the autoreceptor in presynaptic neurons

60
Q

If the sympathetic system is activated, what happens to the radial muscle of the iris in the eye and what receptor is acted on to induce this change?

A

Contraction of the radial muscle resulting in a dilated pupil (myadriasis) and alpha-1

61
Q

If the parasympathetic system is activated, what happens to the sphincter muscle of the iris and what receptor is acted on to induce this change?

A

Contraction of the circular sphincter muscles causing a constricted pupil (miosis) and M3 (muscarinic 3)

62
Q

If the sympathetic nervous system is activated, what happens to the ciliary muscle in the eye and what receptor is acted on?

A

Ciliary muscle is used for the lens shape. If the sympathetic system is activated, the ciliary muscle relaxes for far vision and beta-2 is acted on.

63
Q

If the parasympathetic system is activated, what happens to the ciliary muscle of the eye and what receptor is acted on to induce this change?

A

Contraction for near vision via M3 receptor.

64
Q

If the sympathetic nervous system is activated, what happens to the SA node in the heart and what receptor is acted on?

A

Increase in heart rate and force of contraction via the beta-1 receptor

65
Q

If the parasympathetic system is activated, what happens to the SA node of the heart and what receptor is acted on to induce this change?

A

Decreased heart rate via M2

66
Q

Do both the parasympathetic and sympathetic systems innervate blood vessels?

A

NO! Only the sympathetic system innervates BVs! The parasympathetic system does not innervate BVs! (note: there are muscarinic cholinergic receptors on BVs so they can respond but there is no innervation)

67
Q

If the sympathetic nervous system is activated, what happens to the skeletal muscle blood vessels and what receptor is acted on?

A

Blood vessels in the skeletal muscle dilate via beta-2 receptors. This makes sense as we want to shunt blood to the muscle in order to run away from emergency.

68
Q

If the sympathetic nervous system is activated, what happens to the visceral (internal organs) blood vessels and what receptor is acted on?

A

Blood vessels to the viscera constrict via alpha-1 receptors. This makes sense as we want to shunt blood away for unnecessary functions during an emergency.

69
Q

Nitric Oxide (NO) is a potent vasodilator of the blood vessel endothelium and acts on what receptor?

A

M3. This is kind of the exception to the parasympathetic system not acting on the blood vessels.

70
Q

If the sympathetic nervous system is activated, what happens to the tracheal and bronchial smooth muscle and what receptor is acted on?

A

Tracheal and bronchial smooth muscle dilate via beta-2

71
Q

If the parasympathetic nervous system is activated, what happens to the tracheal and bronchial smooth muscle and what receptor is acted on?

A

Tracheal and bronchial smooth muscle constrict via M3

72
Q

If the sympathetic nervous system is activated, what happens to the detrusor muscle of the bladder and what receptor is acted on?

A

Relaxes detrusor muscle which inhibits urination via the Beta-3 receptor.

73
Q

If the parasympathetic nervous system is activated, what happens to the detrusor muscle of the bladder and what receptor is acted on?

A

Contracts detrusor muscle which activates urination via the M3 receptor.

74
Q

What drug class would be used to promote urination?

A

Muscarinic agonist

75
Q

What is a function in which the sympathetic and parasympathetic systems work together and do not oppose eachother?

A

Male erection (M3) and ejaculation (alpha-1)

76
Q

If the sympathetic nervous system is activated, what happens to sweat glands and what receptor is acted on?

A

This is the outlier! Sweat glands are only activated by the sympathetic nervous system via Muscarinic receptors meaning they respond to acetylcholine!

77
Q

If the parasympathetic nervous system is activated, what happens to salivary glands and what receptor is acted on?

A

Salivary glands are only activated by the parasympathetic nervous system and its activation increases salivary secretions via the M3 receptor.

78
Q

Most sites are under the predominant control of the parasympathetic systems. Conversely, which sites are under the primary control of the sympathetic system?

A

Arterioles and veins (this makes sense are the sympathetic system is the only one that controls blood pressure) and sweat glands. Both parasympathetic and sympathetic controls the genitals.

79
Q

What is the effect of a ganglionic blockade of arterioles and veins?

A

It is known that the predominant control of arterioles and veins is the sympathetic system. By blocking the ganglion here, we are blocking the effects of the sympathetic system. There the results of this would include vasodilation and hypotension.

80
Q

What is the effect of a ganglionic blockade to the heart?

A

It is known that the predominant control of the heart is the parasympathetic system. By blocking the ganglion here, we are the blocking the effect of the parasympathetic system to the heart. This would result in tachycardia.

81
Q

What is the effect of a ganglionic blockade of iris?

A

It is known that the predominant control of the iris of the eye is the parasympathetic system. By blocking the ganglion here, we are blocking the effect of the parasympathetic system to the iris. This would result in mydriasis (pupil dilation).

82
Q

What is the effect of a ganglionic blockade of the GIT?

A

Predominant control of GIT is the parasympathetic system. Blocking this results in reduced tone and motility.

83
Q

What is the effect of a ganglionic blockade of the salivary glands?

A

Predominant control of the salivary glands is parasympathetic. Blocking this would result in xerostomia (dry mouth)

84
Q

What is the effect of a ganglionic blockade of the sweat glands?

A

Predominant control of sweat glands is the sympathetic system. Blocking this would result in anhidrosis (lack of sweating).

85
Q

What do the autonomic reflex arcs regulate?

A

Regulate BP by adjusting HR, force of contraction, and vessel diameter.
Digestion by modifying motility and muscle tone.
Defecation and urination by regulating opening and closing of sphincters.

86
Q

What are the 5 things that only receive sympathetic input?

A

Adrenal medulla, Arrector pili muscles, blood vessels, kidneys, and sweat glands.

87
Q

What is Raynaud’s Syndrome?

A

This is when the fingers and toes become ischemic (lack of blood flow) after exposure to the cold.

88
Q

What is the cause of Raynaud’s Syndrome?

A

The reflex arc is too hyperreactive. There is too much activation of alpha-1 receptors. Treatment would include blocking alpha-1 receptors.

89
Q

Baroreceptors monitor blood pressure and chemoreceptors monitor blood acidity. If baroreceptors sense that blood pressure it too high, what happens?

A

Baroreceptors send signals to the cardiovascular center in the medulla oblongata in the brain. This tells the vagus nerve (parasympathetic) to decrease heart rate.

90
Q

If baroreceptors sense that blood pressure is too low, what happens?

A

Baroreceptors send signals to cardiovascular center in the medulla oblongata in the brain. This triggers the sympathetic nervous system within the spinal cord to increase heart rate, contractile force, venous tone, and peripheral vascular resistance.

91
Q

Explain the homeostatic response to a decrease in blood pressure.

A
  1. Decreased BP sensed by baroreceptors in arch of aorta and carotid sinus
  2. Decreases nerve impulses trigger cardiovascular center in medulla oblongata to increase sympathetic and decrease parasympathetic stimulation.
  3. Increases secretion of EPI and NE from adrenal medulla
  4. This increased stroke volume and HR to increase cardiac output and constricts blood vessels to increase vascular resistance
  5. Increases in blood pressure
  6. Homeostasis returns
92
Q

What is Horner’s Syndrome?

A

This is the unilateral loss of sympathetic outflow through the superior cervical ganglion. It affects the face. It is diagnosed through the cocaine test seen with a lack of response to the cocaine due to absence of endogenous NE at the synapse.

93
Q

Muscarinic and nicotinic agonist activate the ___________ system.

A

Parasympathetic

94
Q

Do smooth muscles, glands, and the heart respond to nicotine?

A

No! These are innervated by acetylcholine with muscarinic receptors for the parasympathetic system and NE and EPI with alpha and beta receptors in the sympathetic system.

95
Q

What two things responds to Ach and nicotine?

A

Skeletal muscle and ganglion. This makes sense as skeletal muscle responds to Ach binding to nicotinic M receptors and all ganglion respond to Ach and nicotinic N receptors.

96
Q

Do smooth muscle, glands, and the heart respond to muscarine?

A

Yes

97
Q

What are the two natural cholinomimetics (drugs that mimic Ach)?

A

Nicotine and Lobeline

98
Q

What are the 2 effects of nicotine on ganglionic transmission leading it to not be commonly used in a healthcare setting?

A
  1. Nicotine initially depolarizes the receptor
  2. Prolonged nicotine exposure produce a depolarization block

This is a biphasic effect

99
Q

What are the sympathetic effects of nicotine?

A

Nicotine acts on both sympathetic and parasympathetic as both systems responds to Ach and cholinomimetics like nicotine in the ganglia. So, in the sympathetic nervous system it would be your excitation responds like increased HR and BP and increased release of EPI from the adrenal.

100
Q

What are the parasympathetic effects of nicotine?

A

Nicotine acts on both sympathetic and parasympathetic as both systems responds to Ach and cholinomimetics like nicotine in the ganglia. The parasympathetic also responds to Ach at effector sites. So, in the parasympathetic system nicotine binding causes SLUDD + 3Ds like issues with GIT including nausea, vomiting, and diarrhea once systemically absorbed.

101
Q

What are the general peripheral nervous system responses to nicotine?

A

Increased HR, CO, BP, and cutaneous and coronary vasoconstriction

102
Q

What are the general central nervous system responses to nicotine?

A

Increased metabolic rate, decreased hunger and body weight, and nicotine withdrawal which produces the opposite of these effects. It also activates the reward circuit in the brain by activating dopaminergic neurons.

103
Q

What are the effects of nicotine poisioning?

A

Nausea, vomiting, dizziness, and respiratory failure due to paralysis. Reversed by a gastric lavage or activated charcoal as there is no nicotine antagonist for peripheral poisoning.

104
Q

What are the two prescription drugs used for nicotine withdrawal?

A

Varenicline (Chantix) and Bupropion (Zyban/ Wellbutrin)

105
Q

What is the MOA of varenicline (Chantix)?

A

This drug is a selective a4B2 receptor (type of nicotinic receptor) partial agonist. It provides modest activation of the dopamine reward pathway. By being a partial agonist, it produces some nicotinic agonist activity but blocks the rewarding effects of nicotine.

106
Q

What is the MOA of bupropion (Zyban/ Wellbutrin)?

A

This drug is an a4B2 receptor antagonist and a dopamine reuptake inhibitor. It reduces cravings by mildly activating the dopaminergic reward pathway.

107
Q

Overall, Varenicline and Bupropion prevent nicotine _________.

A

Craving

108
Q

In general, drugs used to combat addictions are taken in ________ or _________ and have ________ durations of action.

A

Orally or topically
Long

109
Q

Idiosyncrasy occurs at what relative dose?

A. Subtherapeutic
B. Therapeutic
C. Supratherapeutic
D. Can occur at any dose

A

B. Therapeutic. It occurs at a normal therapeutic dose and is specific and reproducible.

110
Q

A patient is having an acute response from a bee sting. What is mediating this response?

A. IgM
B. T cells
C. IgE
D. transporters

A

C. IgE mediated acute allergic reactions occur due to skins, pollens, and IV infusions

111
Q

A drug affects organ development in a fetus. When would this drug be most dangerous?

A. Between weeks 1-5
B. Between weeks 1-3
C. Between weeks 3-8
D. Between weeks 8-12

A

C. Between weeks 3-8.

112
Q

Which old pregnancy category means that risk cannot be ruled out due to animals studies that show no risk but no data in humans?

Category A, B, C, D, or X

A

Category C

113
Q

Which medication error category results in death?

Category A, B, I , or F

A

Category I

114
Q

Preterm babies are anything less than _______ weeks.

A

37

115
Q

A drug has a high molecular weight and high protein binding. It does not cross the placenta. Can it still harm the fetus?

A

Yes

116
Q

Which age is useful in determining organ function in premature infants?

A

Postmenstrual age

117
Q

Which statements are true about neonates?

A. Small surface area to volume ratio
B. High extracellular water content
C. Often needs higher doses for hydrophilic drugs
D. Codeine is the drug of choice for neonatal cough syndrome

A

B and C

Neonates have a high surface area to volume ratio. Codeine should not be used in neonates due to its active metabolite morphine.

118
Q

What disease are more common in men?

A

Gout, MIs, bladder and kidney cancer, and hearing loss

119
Q

What are some diseases that are more common in women?

A

Alzheimer’s disease, lupus, autoimmune disease, IBS, depression, fibromyalgia, cataracts, migraines, thyroid dysfunction

120
Q

Which statements are true about PK differences between males and females?

A. Women have higher ethanol concentration due to less alcohol dehydrogenase
B. Lipophilic medications last longer is men
C. Hydrophilic medication distribute into large plasma volumes in women
D. All of the above

A

A.

121
Q

What is the adjusted body weight formula?

A

ABS= IBW + 0.4 (TBW-IBW)

122
Q

Which PK characteristic would be affected if a patient has fatty liver disease due to class II obesity?

A. Absorption
B. Distribution
C. Metabolism
D. Excretion

A

C. Metabolism

123
Q

COPD is characterized partly by bronchitis and reduction in bronchial diameter. What autonomic receptor types could be targeted by potential therapeutics to treat this disorder? What would what be the actions of the drug to these receptors?

A

B2 agonist- active bronchial dilation
M3 antagonist- inhibit bronchial constriction

124
Q

Child swallows a potent, selective alpha-1 adrenergic agonist. What are the signs and symptoms that may occur?

A. Bronchodilation
B. Tachycardia
C. Mydriasis
D. Hypertension
E. Sweating

A

C and D. Alpha-1 receptors are located in the radial muscles of the eye causing pupil dilation (mydriasis) and in the visceral blood vessels causing obstruction resulting in hypertension. The other options are effects of sympathetic activation, but not due to the alpha-1 receptor.

125
Q

A tea caused the following symptoms… Pupil dilation, skin and oral mucous membranes dry, absent bowel sounds, and pulse of 120 bpm. The tea product likely contained a substance that mimicked what?

A. Muscarinic agonist properties
B. Muscarinic antagonist properties
C. Alpha adrenergic agonist properties
D. Alpha Adrenergic antagonist properties

A

B. Muscarinic antagonist properties

Sweat glands and salivary glands have muscarinic receptors on them. Bowel movement is done my M3 receptors. Pupil dilation is an alpha-1 receptor property which makes sense that it is activated since we shut off the muscarinic activity which would cause pupil constriction. Pulse increase is beta 1 so alpha agonist could not do that.

Principles of Pharmacology and Immunology (PPI) (7 decks)

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