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Spring 2018 > Pharm 1 > Flashcards

Pharm 1 Flashcards

1
Q

_ stimulates salivation by the submaxillary gland. _ blocks it

A

Pilocarpine

Atropine

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2
Q

Pilocarpine and atropine produce their effects by acting on _ proteins of _

A

Muscarinic acetylcholine receptor proteins of salivary glands

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3
Q

Which antagaonists can produce xerostomia?

A

Muscarinic

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4
Q

Like pilocarpine and atropine, _ and _ have the same relationship but with a chicken gastrocnemius muscle

A

Nicotine and curare

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5
Q

A and B with respect to Y compete based on what two things

A

How much of each is present

How well each can bind to receptor

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6
Q

Dissociation constant =

A

[R] [L] / [RL]

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7
Q

Interaction of a drug with a receptor is based on the law of _

A

Mass action

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8
Q

Kd happens at _ binding to the receptor

A

1/2

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9
Q

What is EC50?

A

The dose of the drug that produces 1/2 maximal effect

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10
Q

What is a dose response curve?

A

Dose on x, change on Y

Shows pharmacological effect

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11
Q

What are partial agonists?

A

Agonists that activate a low % of receptors and produce a partial effect

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12
Q

What is drug efficacy and what is drug potency?

A

Efficacy: ability to confer the response after binding

Potency: ability of a drug to confer an effect

Potency = affinity and efficacy

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13
Q

What are receptor gene families and why are they important in understanding pharmacology?

A

Receptors that differ in responsiveness to similar structures

One drug can elicit different effects in different contexts.

Explain why we need receptor specific agonists and antagonists and explains complexity of drug action

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14
Q

EC50 vs. Keq

A

EC50 produces 1/2 maximal EFFECT

Keq produces 1/2 maximal BINDING

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15
Q

Drugs with insufficient efficacy will be _ no matter how high their affinity

A

Partial agonists

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16
Q

Antagonists efficacy

A

0

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17
Q

4 types of signaling receptors

A

Ligand activated ion channels
G protein coupled
Ligand activated transcription factors
Tyrosine kinase receptors

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18
Q

40% of all drugs are agonists or antagonists of _

A

A G protein coupled receptor

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19
Q

The basis of transmission of nerve impulses is _

A

Activating and inhibiting ligand activated plasma membrane ion channels

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20
Q

Ca release from the ER is mediated by

A

IP3

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21
Q

4 steps in the G protein cycle

A
  1. Ligand binds to GPCR, GDP-GTP exchange
  2. complex falls apart into Galpha and GBetagamma
  3. Galpha hydrolyzes GTP to GDP and Pi
  4. Complex reassembles
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22
Q

Which parts of the GPCR are the major and minor parts

A

Major is Galpha

Minor is GBetagamma

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23
Q

What does adenylate Cyclase do

A

ATP -> cAMP + PPi

cAMP -> protein kinase A -> phosphorylation of many proteins causing many effects

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24
Q

Activation of glycogenolysis is mediated by _

A

PKA

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25
Q

How do GPCR liberate signaling molecules from within phospholipids

A

Activate phospholipases which free them up

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26
Q

_ is the source of eicosinoid signaling molecules and prostaglandins

A

Arachidonic acid

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27
Q

Cleavage of _ by phospholipase C yields DAG and _

A

PIP2

IP3

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28
Q

What turns off GPCR

A

Desensitization

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29
Q

Two fates of endocytosed receptor

A

Recycling

Degradation

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30
Q

How does signaling by receptor tyrosine kinase work? (Steps)

A 
Binding of ligand -> 
dimerization of receptor (homo/hetero) -> 
transphosphorylation of receptors -> 
docking of signaling molecules -> 
different cascades of signaling -> 
Change in gene expression in cells
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31
Q

STAT proteins mediate _

A

Biological response to cytokines

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32
Q

Class 1 vs class 2 nuclear receptors

A

Class 1: binds to ligand on complex, complex falls apart, forms homodimer, binds to DNA

Class 2: binds to target DNA or corepressors, switches from corepressor to coactivator

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33
Q

Patient factors influencing drug effects

A 
Body weight/composition
Age
Sex
Pregnancy
Environmental
Diet
Physiologic differences
Pathologic conditions
Genetic factors
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34
Q

Pharmacokinetic vs. pharmacodynamic tolerance

A

Kinetic: effective drug conc is diminished

Dynamic: response is diminished

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35
Q

Acute pharmacodynamic tolerance is called _

A

Tachyphylaxis

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36
Q

How does warfarin work?

A

Inhibits synthesis of vit. K dependent clotting factors (II, VII, IX, X)

Can lead to hemorrhaging

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37
Q

5 categories of drugs during pregnancy

A

A - no risks in humans
B - no risks in humans BUT animal studies bad OR no human studies, animal studies clear
C - no human and either no animal studies, or bad news animal studies
D - human fetal risk
X - human or animals BAD BAD. Risks outweigh benefit

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38
Q

Pharmacokinetic vs pharmacodynamic variations

A

Kinetic: response changes with drug concentration

Dynamic: diff response to drug

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39
Q

Most important oxidation polymorphic enzyme

A

CYP2D6

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40
Q

Why is CYP2D6 important

A

Poor metabolizers have higher incidence of bad effects (cevimeline isn’t metabolized as fast as it should be)

Need it to convert tamoxifen to endoxifen. W/o it, tamoxifen is less effective for breast cancer tx

Converts codeine to morphine

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41
Q

What do ryanodine receptors do?

Defect causes what

A

Mediate Ca mediated Ca release from SR in muscle

Malignant hyperthermia

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42
Q

% of americans that:
Take 1 prescription drug
At least 2
5+

A

70%
50%
20%

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43
Q

How does drug potentiation occur

A 
One drug:
-Enhances absorption
-Alters distribution
-Inhibits elimination
Of another drug.
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44
Q

Types of pharmaceutical interactions

A 
Antagonism
Potentiation
Unexpectation
Summation
Synergism
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45
Q

Pharmacokinetic interactions

A

Absorption
Distribution
Metabolism
Excretion

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46
Q

Most drugs metabolized in liver by _

A

Microsomal P450 enzymes

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47
Q

When does net efflux of K end

A

When the chemical force leading K outside is balanced by the electrical force bringing it back

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48
Q

Nernst equation

A

Vk = -60 mV log ([K]in/[K]out)

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49
Q

_ and _ are primarily responsible for maintaining homeostasis

A

Autonomic nervous sys
And
Endocrine

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50
Q

Synthesis of catecholamine NTMs

A 
Tyrosine
DOPA
Dopamine  -> norepinephrine -> epinephrine
      I
     V
Noradrenalin
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51
Q

Adrenergic vs cholinergic transmission at synapse. What happens to NTM

A

A: NE transported back into presynaptic terminal

C: Ach hydrolyzed in synapse

52
Q

Rate limiting step of catecholamine synthesis

A

Tyrosine hydroxylase (tyrosine -> L-DOPA)

53
Q

Alpha 1 receptors do what

Where are they

A

Increase Ca
Increase activity of myosin light chain kinase
Increase myosin light chain phosphorylation
Increase muscle contractility

Smooth muscle cells

54
Q

Increasing Ca in the smooth muscle cell will do what to the cell

A

Constrict

55
Q

Alpha 2 receptors are where and do what

A

Presynaptic termini

Inhibit epinephrine and NE release

56
Q

Beta 2 receptors on smooth muscle do what

A 
Increase PKA
Phosphorylation and inhibit MLCK
Lower Ca levels
Inhibit MLCK
Diminish phosphorylation of MLC
Decrease muscle contractility
57
Q

Beta 1 receptors on cardiac muscle cells do what

A

Activate PKA
Activate L type Ca channels
Increase Ca levels
Increase muscle contractility

58
Q

Drugs that activate B1 in heart are used to do what

A

Improve contractility of failing heart

59
Q

NE doesn’t activate _ receptors, but epinephrine does

A

B2

Epi activates a, B1 and B2

60
Q

Why use NE or epi with local anesthetic

A

Keep anesthetic around longer due to vasoconstriction

61
Q

Alpha1 receptor agonists do what

A

Produce contraction of vascular smooth muscle

-increase BP

62
Q

_ is sometimes used as a vasoconstrictor in conjunction with a local anesthetic

A

Levonordefrin

63
Q

3 reasons to use a vasoconstrictor with a local anesthetic?

Which is the most common and second most common

A
  1. Prolong duration of nerve block, increase success
  2. Diminish systemic toxicity of anesthetic
  3. Minimize blood loss during surgical procedure
64
Q

What do alpha2 receptor agonists do

A

Inhibit epi and NE release from presynaptic termini in CNS

65
Q

Beta1 agonists do what

A

Tx of heart failure and cardiogenic shock

66
Q

Beta2 receptor agonists do what

A

Produce smooth muscle relaxation. Treat asthma, relax uterine wall

67
Q

Adverse effects come from what 4 things

A

Too large a dose
Accidental intravascular injection
Heightened sensitivity
Patient with cardiovascular disease

68
Q

Alpha 1 antagonists are used to treat what

A

Hypertension
Hemodynamics shock
Raynaud’s disease

69
Q

3 alpha1 antagonists

A

Prazosin
Alfuzosin
Tamulosin

70
Q

_ is used to reverse soft tissue numbness after local anesthetic

It is a _

A

Phentolamine

Non-selective alpha adrenergic receptor antagonist

71
Q

Beta blockers are mostly used to block out _

What do they do

A

Beta1

Decrease heart rate and force of contraction

72
Q

Beta blockers diminish _ release from the kidney

A

Renin

73
Q

What is ISA and how does it affect beta blockers

A

Intrinsic sympathomimetic activity
(Partial agonists)

Low beta stimulation when using blockers. Don’t depress cardiac function as well but still attenuate agonist driven increases.

74
Q

Therapeutic uses of beta blockers

A 
Hypertension
Ischemic heart disease (reduce oxygen consumption by reducing CO)
Post MI
Congestive heart failure
Treat arrhythmias
75
Q

A patient taking a beta blocker could have what kind of conditions

A

Moderate, well controlled
Serious disease
Anything in between

76
Q

What can treat glaucoma

A

Beta blockers

77
Q

Two drugs are alpha and beta receptor antagonists

A

Labetalol

Carvedilol

78
Q 
Adverse effects of Beta blockers
Heart
Smooth muscle
Metabolic
CNS
A

Heart: bradycardia, AV block

Smooth muscle: reduce vasodilator responses, increase bronchospasms

Metabolic: hypoglycemia

CNS: depression, fatigue, sleep disturbances, hallucinations, dizziness

79
Q

Alpha blockers can cause _ hypotension

A

Orthostatic

80
Q

Who is at risk of a hypertensive episode after receiving local anesthetic with a vasoconstrictor?
Why?

A

Patient taking non-selective beta blocker

Doesn’t get B2 mediated vasodilation to counteract alpha mediated vasoconstriction

81
Q

-zosin

A

Alpha1 adrenergic receptor blocker

82
Q

-olol

A

Beta-adrenergic receptor blocker

83
Q

-ilol, -alol

A

Beta-adrenergic receptor blocker with alpha1 activity

84
Q

Two types of cholinergic receptors

A

Nicotinic and muscarinic

85
Q

Nicotinic AcCHRs bind what?

What kind of receptor is it?

Structure of receptor?

A

Bind nicotine

Ligand activated ion channel

Receptors contain 5 subunits and bind two molecules of agonist

86
Q

Difference in adult vs infant nicotinic receptors

A

Both have 2 alpha1, one Beta, one delta

Adult has one epsilon
Infant has one gamma

87
Q

How many muscarinic receptors are there

They are _ receptors

A

5

G protein coupled receptors

88
Q

M_, _, _ are linked to Galphaq

M_, _ are linked to Galphai

A

M1,3,5 G-alpha-q

M2,4 G-alpha-i

89
Q

How can we figure out whether an Ach receptor is nicotinic or muscarinic?

A

Ask whether we want to depolarize across a membrane (nicotinic) or activate G protein coupled receptor (musc)

90
Q

Two types of cholinergic agonists, how do they work

A

Direct: bind to nicotinic/muscarinic AcCh receptor or both

Indirect: cholinesterase inhibitor

91
Q

Acetylcholinesterase breaks Ach into _ and _

A

Acetate

Choline

92
Q

Which is hydrolyzed faster b/t ach and methacoline? What is the effect

A

Ach is hydrolyzed faster, shorter duration

93
Q

4 steps in neuromuscular transmission

A

Nicotinic Ach receptors activated, post-synaptic membrane de polarized

Local depolarization leads to action potential

Post synaptic depolarization leads to release of Ca from SR

Ca leads to muscle contraction

94
Q

How do troponin and tropomyosin work?

A

Ca binds to troponin complex
Troponin causes tropomyosin to shift exposing myosin binding sites
Myosin binds actin

95
Q

Muscle cross bridge cycle stops when

A

Ca levels drop

96
Q

Which muscarinic receptors are stimulatory, which are inhibitory

A

1,3,5 are stimulatory

2,4 are inhibitory

97
Q

_ receptors on the sphincter muscle mediate pupil constriction

A

M3 muscarinic

98
Q

Cardiac muscle contains _ receptors and parasympathetic innervation. Activation of these receptors _

A

M2

Reduce cardiac output

99
Q

Most arteries and veins in the body are innervated by _ nerves

A

Sympathetic adrenergic

100
Q

Vascular endothelial cells express _ receptors. When activated they produce vasodilation

A

M3

101
Q

_ on the bronchial muscle mediate muscle constriction

A

M3 muscarinic receptors

102
Q

Secretory glands are activated by _ receptors

A

M3

103
Q

_ receptors mediate detrusor muscle contraction (voids bladder)

A

M3

104
Q

3˚ vs 4˚ amine, which is better absorbed? Why?

A

3˚

Pass through biological membranes better

105
Q

Muscarinic agonists have what effect

A

SLUD

Salivation, lacrimation, urination, defecation

106
Q

Which anticholinesterases act in a completely irreversible manner

A

Malathion
Sarin
(Both organophosphate)

107
Q

Anticholinesterases produce an effect that is similar to _

A

Direct acting cholinergic agonists

108
Q

T/F anticholinesterases produce muscarinic mediated vasodilation

A

FALSE. They do not.

Not much parasymp innervation of vascular endothelium

109
Q

What is physostigmine and what does it do

A

Tertiary amine

Produces vasodilator effects through action in the CNS

110
Q

_ and _ (drugs) are frequently used to treat dry mouth

A

Pilocarpine

Cevimeline

111
Q

5 therapeutic used of cholinergic agonists and anticholinesterases

A
  1. Glaucoma
  2. Xerostomia
  3. Reversal of neuromuscular block
  4. ACE for treatment of Myasthenia Gravis
  5. ACE cross BBB to improve cognitive function in Alzheimer’s
112
Q

_ have the potential to cause significant CNS impairment

A

Antimuscarinics

113
Q

Antimuscarinics usually place the target under control by _

Except _

A

Symp NS

Sweat glands (both S and PS act on muscarinic)

114
Q

Anti-muscarinics cause _ in the eye

A

Pupil dilation

115
Q

Anti-muscarinics are used to produce _ in the lungs

A

Bronchodilation

116
Q

Heart and urinary respond how to antimuscarinics

A

Mild bradycardia

Urinary retention

117
Q

Quaternary amine anti-cholinergics are _ absorbed, have a _ therapeutic margin, and are _ tolerated

A

Poorly absorbed
Wide therapeutic margin
Well tolerated

118
Q

Anti-cholinergic toxidrome

A

Hot, blind, dry, mad

119
Q

_ receptors are important mediators in the CNS

A

Nicotinic Ach

120
Q

Desensitization especially happens at _ receptors

A

Ach

121
Q

Non-depolarizing blockers are competitive antagonists of _

A

Ach

122
Q

Non-polarizing vs polarizing blockers onset of action and duration

A

Depolarizing has rapid onset and shorter duration

123
Q

Intravenous infusion of neuromuscular blocking agents induces _

A

Flaccid paralysis

124
Q

Neuromuscular blockers are used how in dentistry

A

Muscle relaxation for surgery

125
Q

Adverse effects of neuromuscular blockers

A

Respiratory failure

Spring 2018 (18 decks)

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