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Spring 2018 > Pharm 2 > Flashcards

Pharm 2 Flashcards

1
Q

Local anesthetics are made of what 3 components

Why is each important

A

Aromatic - lipophilic

Ester or amide linkage - amides are favored. Esters broken down faster

Amine - basic crosses membrane, acidic binds to Na channel

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2
Q

Esters vs amides:

Half life

Where hydrolyzed/metabolized

How to tell which is which by name

A

Esters have shorter 1/2 life

Esters hydrolyzed by PsChEsterase

Amides metabolized by P450 in liver

Amides have i in name before caine (lidocaine), Esters don’t

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3
Q

Which type of bond in local anest. Is more allergic

A

Esters

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4
Q

Local anesthetics effect in axon

A

Interact with open and inactivated channel, blocking Na conductance

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5
Q

Why are the acidic and basic forms of a local anesthetic important

A

Basic form crosses membrane

Acidic form blocks sodium channel

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6
Q

Local anesthetics produce more rapid nerve block on axons with a _ firing rate because _

A

Rapid

They bind to open form of Na channel

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7
Q

Which functions are more disrupted by LA

A

Functions served by B/C fibers more than A

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8
Q

CNS neurons are _ sensitive than PNS neurons to local an

A

More

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9
Q

Which local an is especially cardiotoxic

A

Bupivacaine

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10
Q

Most amides last longer than esters, except 2:

A

Prilocaine

Articaine

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11
Q

2 ways an operator can cause excessive local an conc in blood

3 possible effects of overdose

A

Intravascular injection
Excessive quantities

Convulsions
Respiratory arrest
Cardiovascular collapse

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12
Q

Ideal anesthetic (7)

BRAUMS’S

A

Smooth and Rapid
Unconsciousness
Amnesia
Maintain physiologic functions while blocking reflexes
Skeletal muscle relaxation, NOT resp. Muscles
Block sensory stimuli
Recovery with no lasting effects

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13
Q

5 types of drugs in a cocktail, what do they do

A 
Antimuscarinics - minimize salivation
Analgesics - Preop pain relief, sedation
NOx / Opioids - reduce anest. Requirement
Anti-nicotinics - paralyze sk. Muscle
Antiemetics
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14
Q

Meyer Overton correlation:

Implication in body

A

Correlation b/t solubility in olive oil and anesthetic potency

Anesthesia begins when anesthetic reaches critical conc. In membrane lipids

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15
Q

What are 2 protein targets of general anesth.

Definitive target

A

Ligand activated ion channels
GABA receptors

No definitive target

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16
Q

Synaptic transmission is _ sensitive to anesthetics than action potentials

A

More

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17
Q

Which structures in the brain do anesthetics effect directly

A

Thalamus
Hippocampus
Limbic system

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18
Q

4 stages of general anesthesia

A

Analgesia
Excitement
Surgical anesthesia
Medullary paralysis

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19
Q

Blood : gas partition coefficient

Low vs high

A

Ratio of conc of anest. In blood phase to the conc. In gas phase when anesthetic is in equilibrium b/t two phases

Low - faster induction and recovery (NOx)

Higher - slower induction and recovery

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20
Q

MAC

What determines it

A

Minimum alveolar conc.

Olive oil solubility determines it

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21
Q

MAC and blood solubility of a good inhalation anesthetic agent

A

Low MAC

Low blood solubility

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22
Q

NOx has a low blood/gas and high MAC. What does this mean

A

Fast induction, recovery

Not potent, doesn’t produce full surgical anesthesia

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23
Q

3 common volatile anesthetics

General properties of the three?

A

Isoflurane
Desflurane
Sevoflurane

Low b/g (~0.5)
Single digit MAC

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24
Q

Barbiturates act as CNS depressants by doing what?

A

Binds to GABA
Activates chloride channels
Hyperpolarizes post synaptic membrane
Provides inhibitory influence on synaptic transmission

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25
Q

4 advantages of IV anesthetics like barbituates

A

Rapid distribution
Reduced cardiac depression
No risk of malignant hyperthermia
Eliminate risk of occupational exposure

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26
Q

3 barbituates used in dental settings

General qualities

A

Thiopental
Methoxhexital
Propofol

Fast acting, fast recovery (use with something else to keep them under)

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27
Q

Ketamine produces _ anesthesia.
What is it
Who gets it

A

Dissociative anesthesia
Anesthesia with analgesia and amnesia, minimal effect on respiratory funct.

Pt. Doesn’t seem anesthetized

Trauma patients, elderly pts

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28
Q

Pathway of pain receptors

A 
Sensory receptor (body in DRG/T.G.)
Dorsal root
Synapse
Cross spine
Thalamus
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29
Q

Aδ fibers vs C fibers

A

Aδ: faster, myelinated, first response to mechanical stimuli
Sharp pain

C: slower, unmyelinated, thermal, mechanical, chemical
Dull, aching, burning pain
5x more than Aδ

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30
Q

5 inflammatory mediators that facilitate transmission of pain

A 
Prostaglandins
Substance P
Tumor necrosis factor- α
Interleukin 1β
Ιnterleukin-6
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31
Q

Allodynia:

How?

A

Pain from normally painless stimuli

Tissue injury sensitizes pain response

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32
Q

3 places pain can be inhibited

Opioids affect which

A

Periphery
Signaling to CNS
CNS activity

Opioids do all 3

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33
Q

What affects whether a single neuron can initiate an action potential? 3 things

A

Number and types of post-synaptic receptors

Synchrony of signals

Frequency of signals

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34
Q

Cl, Na, K channels do what to let the ions pass?

Which way do they pass

A

Cl: channels that let in Cl HYPERpolarize

Na: channels that let in Na will DEpolarize

K: channels that let out K will HYPERpolarize

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35
Q

4 families of endogenous opioids

A

Pro-opiomelanocortin peptides
Pro-enkephalin peptides
Prodynorphin peptides
Endomorphins

Pro-OMC
Pro-EK
ProDynomorphin
Endomorphins

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36
Q

Three important opioid receptors

All 3 are _ receptors

They activate

A

μ
κ
δ

G-protein coupled receptors

Activate Gαi

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37
Q

_ is the natural agonist of the μ-opioid receptor

A

β-endorphin

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38
Q

2 natural agonists of δ opioid receptor

A

Met-enkephalin

Leu-enkephalins

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39
Q

Agonists of κ-opioid receptor

A

Dynorphin A/B

α/β Neo-endorphin

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40
Q

How do opioids affect GPCRs

A

Modulate nerve activity

Make it more difficult for nerve impulses to be conducted

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41
Q

Opioids can inhibit synaptic transmission on receptors where

A

Pre or post-synaptically

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42
Q

Majority of analgesic drugs act primarily at _ receptors

A

μ

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43
Q

μ receptors are found where

A 
Peri aqueduct always gray
Superficial dorsal horn of spinal cord
Nucleus accumbens
Amygdala
Cerebral cortex

MOSTLY PRE-SYNAPTIC

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44
Q

What exactly do opioids inhibit? Why is this strange

A

They inhibit the inhibitor

Helping to activate the pathway that produces CNS mediated inhibition of pain

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45
Q

Clinical effects of opioids

A 
Analgesia
Respiratory depression
Constipation
GI spasm
Physical dependence
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46
Q

Morphine is a strong _ agonist

A

μ

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47
Q

Which opioid has important effects on the motivational-affective component in limbic system

A

Morphine

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48
Q

Morphine is metabolized to what 2 molecules?

What’s the difference b/t the two

A

M-3-G - not active, doesn’t get to brain

M-6-G - more active than morphine, crosses BBB

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49
Q

Codeine metabolizes to what 2 things?

What are they like?

A

Morphine and codeine-6-glucuronide

They’re both active

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50
Q

Codeine is more effective than morphine when administered _

A

Orally

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51
Q

2 factors that make fentanyl more toxic and more therapeutic

A
  1. Fentanyl is more lipid soluble than morphine or heroin

2. Fentanyl binds tighter to μ opioid receptor than morphine or heroin

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52
Q

Therapeutic index of fentanyl

Why is it so dangerous

A

300 (morphine is 70)

People cutting it with other drugs
Prolonged respiratory depression
Harder to reverse tight binding

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53
Q

3 opioid antagonists that treat opioid toxicity

A

Naloxone
Naltrexone
Nalmefene

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54
Q

Opioids available for oral administration

A

Codeine
Hydrocodone
Oxycodone
Pentazocine

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55
Q

3 NSAIDS

A

Aspirin (acetylsalicylic acid)
Ibuprofen
Naproxen

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56
Q

Injured cells release _

Example

A

Alarmins

IL-33

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57
Q

How does histamine act

A

Through GPCR to produce local vasodilation and leaky capillaries

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58
Q

Histamine H1 receptor activity increases intracellular _

2 major effects from this

A

Ca++

  1. NO mediated relaxation of smooth muscle -> vasodilation
  2. MLCK mediated contraction of capillary endothelium
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59
Q

Anti-inflammatory drugs do what

A
  1. Attenuate inflammatory response

2. Attenuate pain

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60
Q

Which inflammatory mediator is the most important to attenuate

A

Prostaglandins

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61
Q

Pg is derived from _

4 main ones are

A

Arachidonic acid

PGE2
PGD2
PDF2
PGI2

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62
Q

2 enzymes that send arachidonic acid down the path toward pg

A

COX1

COX2

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63
Q

Inhibition of which COX is desirable/undesirable

A

inhibition of COX1 is bad

Inhibition of COX2 is desirable

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64
Q

Aspirin reduces what 4 things

Ibuprofen, naproxen?

Acetaminophen?

A

Pain
Fever
Inflammation
Thrombosis

Ibuprofen does 3 (not thrombosis)

Acetaminophen 2 (pain/fever only)

65
Q

Only _ is effective at preventing thrombotic events

A

Low dose aspirin

66
Q

Why do NSAIDS mess with the stomach

A

They block prostaglandins

Pgs stimulate mucus and bicarbonate secretion

67
Q

2 most common arthritis

A

Osteoarthritis

Rheumatoid

68
Q

Lupus erythematosus

A

Immune sys attacks healthy tissues, esp. joints

69
Q

What is osteoarthritis

A

Breakdown of articular hyaline cartilage in synovial joints

70
Q

Chondrocytes in inflamed vs healthy cartilage

A

Healthy - balanced b/t anabolic and catabolic

Inflamed - catabolic dominate, decreased collagen prod., increased prod. Of proteolytic enzymes

71
Q

2 important inflammatory mediators in arthritis

A

IL-1β

TNF-α

72
Q

Rheumatoid arthritis is _ mediated joint inflammation

A

Immunologically

73
Q

Rheumatoid a. Affects _ joints. These are joints that _

A

Diarthrodial

Join two opposing bone surfaces covered by hyaline cartilage

74
Q

Hyaline cartilage

Type of collagen?

A

Type II

75
Q

Ra starts initially with inflammation in the _

A

Synovium

76
Q

Synovitis leads to an overgrowth called the _.

What is it?

That leads to _ which leads to _

A

Pannus

Abnormal layer of fibrovcascular tiss or granulation tiss.

Fibrous ankylosis
Bony ankylosis

77
Q

Immune cells, osteoclasts, and chondrocytes make what that destroy bone and cartilage?

3 things

A

MMP

Cathepsins - cysteine proteases

ROS

78
Q

What causes rheumatoid arthritis

A

T-cell mediated response to immunological trigger

some alleles of MHC genes

79
Q

What cells (other than wonky MHC) are heavily implicated in AI disorders like RA

A

Th17

80
Q

Very important therapeutic target in AI disorders

A

TNFα

81
Q

5 types of antibodies that are associated with RA

CKCPC

A 
Anti collagen
Anti cardiolipin
Anti keratin
Anti calpastatin
Anti perinuclear factor
82
Q

Important DIAGNOSTIC marker of RA

A

Rheumatoid factor

83
Q

Antibodies directed against _ are frequently discovered in patients with RA.

Why else are they important?

A

Citrullinated proteins

Present in 80% of cases
# CCPs correlates with disease severity
Antibodies appear years before joints are affected
84
Q

_ catalyzes citrullination of peptides

A

Peptidyl arginine deaminase

85
Q

4 drugs to treat RA

A

NSAIDS
DMARDS (disease modifying anti rheumatic drugs)
Glucocorticoids
Pain meds (non-NSAIDS)

86
Q

A common DMARD is _.

It acts as an _

A

Methotrexate

Immunosuppressant

87
Q

How does methotrexate work

A

Potentiation of adenosine signaling as an immune modulator

88
Q

7 DMARDS - method of action of each

THA CALM

A
  1. Methotrexate
  2. Leflunomide - inhibits dihydroorotate dehydrogenase
  3. Hydroxychloroquine - inhibits TLRs on dendritic cells
  4. Cyclosporin - inhibits cytokine gene expression
  5. Azathioprine - inhibits DNA replication
  6. Tofacitinib - JAK kinase inhibitor
  7. Adalimumab - interferes with TNFα

THACALM

89
Q

TNF alpha results in what 5 changes

A 
Increased:
Inflammation
Cell infiltration
Angiogenesis
CRP in serum

And articular cartilage degradation

90
Q

TNFα is a _ that plays a major role in the _ response

A

Pleotropic cytokine

Immune/inflammatory response

91
Q

How does adalimumab work

A

It’s an anti-TNF IgG

92
Q

NTMs that act on GPCR will ultimately modify the activity of _

A

Synaptic proteins (pre or post)

93
Q

Glutamate can either act as a _ or a _

A 
Excitatory NTM (opens Na channel)
Neuromodulator (activates GPCR)
94
Q

Glycine receptors do what? What potentiates glycine receptors

A

Activate Cl- channels and produ e hyperpolarization

THC

95
Q

Positive and negative symptoms of schizo are lined to _

A

Positive: linked to excess dopamine

Negative: linked to prefrontal pathologies

96
Q

_ stimulation is the basis for hallucinatory effects of drugs

A

5-HT-receptor

97
Q

Dopamine hypothesis of schizo

A

Positive symptoms of schizo involve over activity of brain dopaminergic synapses

98
Q

-azine:

A

Phenothiazine-like antipsychotics

99
Q

Schizo has an over activity of the _ pathway (positive symptoms)

And a dysfunction of the _ pathway (negative and cognitive systems)

A

Over of Mesolimbic pathway

Dys of mesocortical pathway

100
Q

Two subtypes and 5 different dopamine receptors

What are the two subtypes linked to?

Antagonists of which are important drugs?

A

D1 like family (D1/D5)
-Linked to Gαs Inc. cAMP

D2 like family (D2, D3, D4)

  • Linked to Gαi dec. cAMP
  • antagonists are important
101
Q

Extrapyramidal effects of anti-psychotics

A

Parkinson’s like symptoms

102
Q

Why is antagonism of D2 and D4 receptors important

A

Important in producing therapeutic and adverse effects of anti-psychotics

103
Q

T/F atypical anti-psychotics don’t have extrapyramidal activity

A

TRUE

104
Q

Typical vs atypical antipsychotics

A

Typical: antagonists of D2, little activity on D4, varying on the rest

Atypical: antagonist of D4, stronger on 5-HT2, varying on H1, M1, α1

105
Q

NTMs that are deficient in depression

A

NE and serotonin

106
Q

Anti-depressants act in 3 ways:

A

Block transmitter reuptake
Inhibit MAO
Inhibit presynaptic autoreceptors

107
Q

Two types of reuptake blockers

A

Tricyclic antidepressants are non-specific blockers of transmitter reuptake and also muscarinic receptor antagonists

SSRIs are specific for serotonergic systems

108
Q

Side effects of SSRIs

A

First

  • nausea
  • anxiety
  • agitation
  • insomnia

Late

  • weight gain
  • weakness
  • sexual dysfunction
  • withdrawal syndrome
109
Q

SNRI:

4 common ones

A

Serotonin and NE reuptake inhibitors

Duloxetine (cymbalta)
Venlafaxine (Effexor)
Nefazodone (serzone)
Desvenlafaxine (pristiq)

110
Q

MAOs do what

A

Degrade dopamine etc

111
Q

Why block presynaptic autoreceptor

A

It’s feedback inhibition, won’t stop the NTM from being released

112
Q

3 serotonin receptor antagonists

A

Nefazodone
Trazodone
Mirtazapine

All are 5-HT2A receptor antagonists

113
Q

Parkinson’s disease is what

A

Degeneration of dopaminergic neurons projecting from substantia nigra to striatum

114
Q

What does L-DOPA do

A

Makes the remaining projections into the striatum provide more dopamine

115
Q

_ crosses BBB, but _ does not

A

L-DOPA

Dopamine

116
Q

L-DOPA treatment good for how long

A

3-4 years

117
Q

L-DOPA is given with _ to prevent what

A

Carbidopa

Nausea and vomiting

118
Q

In addition to LDOPA, Parkinson’s can be treated with _

A

Dopamine receptor agonists

119
Q

Epilepsy is caused by what

A

Inherited biochemical defect

Previously healed brain injury

120
Q

Ways to treat epilepsy (5)

A
  1. Phenytoin and others block high-frequency firing of action potentials
  2. Potentiate effects of GABA to dampen synaptic nerve impulses
  3. Blockade T-type Ca channels in thalamus
  4. Blockade of voltage-gated Ca channels
  5. Blockade of NMDA receptors
121
Q

How to potentiate GABA?

A
  1. Inhibition of GABA transaminase
    - metabolizes GABA
  2. Inhibition of GABA uptake
  3. Facilitation of Cl channel opening (Benzodiazepines)
122
Q

Dentists use _ to treat emergency seizures

A

Benzodiazepines

123
Q

5 effects of barbiturates and benzodiazepines in treating anxiety

A 
Anxiolysis
Sedation
Hypnosis
Anesthesia
Respiratory failure
124
Q

Sedation vs hypnosis vs anesthesia

A

Sedation is without loss of consciousness

Hypnosis is with impaired sensory responsiveness

Anesthesia is without possibility of arousal

125
Q

GABA A is a _

GABA B is a _

A

Ligand gated ion channel

G-protein coupled receptor

126
Q

Barbituates and benzodiazepines act by facilitating GABA mediated conductance of _ receptors

A

GABA A

127
Q

Barbituates increase _ of GABA mediated channel opening

Benzodiazepines increase _ of GABA mediated channel opening

This causes _ which eventually causes _

A

Duration

Frequency

Membrane hyperpolarization

CNS depression

128
Q

Effect of benzodiazepines vs barbiturates

A

Benzodiazepines - anti anxiety at doses that don’t incapacitate

Barbiturates knock out everything

129
Q

_ manages benzodiazepine overdoses

A

Flumazenil

130
Q

Hypnotics vs. benzodiazepines

A

Hyps are diff. Structure, but bind to same site

131
Q

Barbiturates are especially strong on _

A

The reticular formation

132
Q

In dentistry:
Sedative-hypnotic drugs = _
Drugs to treat anxiety = _
Drugs to treat anesthetic induced seizures = _

A

SH = barbiturates
anxiety = benzodiazepines with local an.
Anesthetic induced seizures = benzodiazepines

133
Q

3 things are used to treat bipolar

A

Anti-psychotic
Anti-convulsant
Anti-depression

134
Q

Sequence of events leading to infiltration of eosinophils in lung

A

Allergen -> mast cell -> Th2 -> infiltration of eosinophils

135
Q

Eosinophilic vs. non-eosinophilic asthma

A

E: eosinophils, basement membrane thickening, inhalation always corticosteroids

Non: new treatments

136
Q

_ is associated with eosinophilic asthma, _ is associated with neutrophilic asthma

A

Th2

Th17

137
Q

3 goals of asthma tx

A

Relieve bronchoconstriction
Inhibit airway inflammation
Prevent airway remodeling

138
Q

asthma vs COPD

A

A: bronchoconstriction part of allergic response, tx works, eosinophil recruitment

C: bronchoconstriction from change in vagal tone, tx doesn’t always help, neutrophil recruitment

139
Q

_ cells mediate inflammation and bronchoconstriction

A

Mast cells and their contents

140
Q

4 ways asthma drugs work

A

Snuff allergic response
Diminish number of immune cells in lung
Alter production of bronchoconstrictors
Attenuate activities of bronchoconstrictors and mucus producers

141
Q

β2 adrenergic receptor agonists do what

A

Produce relaxation of smooth muscle cells

142
Q

Best short acting β agonist

A

Albuterol

143
Q

Adverse effects of β2 agonists

A

Muscle tremor
Tachycardia
CNS problems (pain, restless, nervous)

144
Q

3 main functions of cortisol

A
  1. Carb and protein metabolism
  2. Lipid redistribution
  3. Hypertension
  4. Increased breakdown of bone/skin
  5. CNS - mood elevation
  6. ANTI-INFLAMMATORY agent
145
Q

Glucocorticoid inducible gene that plays an important role in attenuating inflammation

A

Annexin-A1

Lowers leukocytes

146
Q

Glucocorticoid Receptors do what to NF κB

A

Inhibit NFκB mediated transcription

147
Q

Glucocorticoids are used to mainly treat what two diseases

A

Chronic adrenal insufficiency

Suppress inflammation

148
Q

2 pts that don’t respond to ICS tx

A

Non-eosinophilic asthma

Glucocorticoid resistance

149
Q

In context of respiratory diseases, Anti-cholinergics refer to _

A

Antagonists of muscarinic acetylcholine receptors

150
Q

_ is a classic muscarinic antagonist

A

Atropine

151
Q

Blockade of M1 and M3 muscarinic receptor subtypes can lead to _

A

Bronchodilation

152
Q

Anti-cholinergics effect on airway

A

Inhibits smooth muscle contraction

Decreases mucus secretion

153
Q

_ is 1000x more potent bronchoconstrictor than histamine in the airway

A

Leukotriene

154
Q

Leukotrienes are made from _

A

Arachidonic acid (like prostaglandins)

155
Q

Singulair is a _

A

Leukotriene modifier

156
Q

T/F leukotriene modifiers treat COPD well

A

FALSE

157
Q

Xolair is what

A

Anti IgE

158
Q

Antihistamines block _

A

Vasodilation

159
Q

α1-adrenergic receptor agonists are _. They work by _

A

Decongestants

Constricting blood vessels

Spring 2018 (18 decks)

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