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Pharmacology > Module 2: Intro to Autonomics, Cholinomimetics, Cholinesterase Inhibitors, Cholinoreceptor blocking drugs, Cancer Chemotherapy > Flashcards

Module 2: Intro to Autonomics, Cholinomimetics, Cholinesterase Inhibitors, Cholinoreceptor blocking drugs, Cancer Chemotherapy Flashcards

1
Q

What drug prevents the transport of Choline into the presynaptic cleft by CHT?

A

Hemicholiniums

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2
Q

What drug inhibits the transport of Acetylcholine into the storage vesicle by VAT?

A

Vesamicol

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3
Q

This drug preents the release of Acetylcholine from the terminal buoton

A

Botulinum toxin

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4
Q

When is Acetylcholine released?

A

When Ca2+ channels in terminal membranes are opened

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5
Q

What terminates ACh?

A

Acetylcholinesterase

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6
Q

What prevents the conversion of Tyrosine to Dopamine?

A

Metyrosine

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7
Q

What specific enzyme does Metyrosine inhibit?

A

Tyrosine Hydroxylase

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8
Q

Dopamine gets transported into the vesicle via?

A

VMAT

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9
Q

This drug inhibits the transport of Dopamine via VMAT

A

Reserpine

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10
Q

This enzyme catalyzes the conversion of Dopamine to Norepinephrine

A

dopamine-beta-hydroxylase

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11
Q

What drugs inhibit the release of Norepinephrine when calcium channels open

A

Bretylium & guanethidine

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12
Q

After the release of norepinephrine, what transports it back to the cytoplasm?

A

NET

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13
Q

What inhibits NET?

A

Cocaine, Tricyclic Antidepressants

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14
Q

This ANS is tropotrophic, meaning its function is more on growth

A

Parasympathetic

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15
Q

This ANS is ergotrophic meaning it involves energy expenditure

A

Sympathetic

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16
Q

The sympathetic PREganglionic fibers are _____

and its POSTganglionic fibers are ____

A

PREganglionic SYMPATHETIC fibers are SHORT because they terminate at the ganglia in the PARAVERTEBRAL area.

POSTganglionic SYMPATHETIC fibers are LONG kasi nagsstart sya sa paravertebral area up to the end organ.

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17
Q

What is the spinal cord origin of the sympathetic nervous system?

A

THORACOLUMBAR (T1-L2)

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18
Q

What is the type of response exhibited by the sympathetic nervous system?

A

Diffused. It activates numerous receptors at the same time

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19
Q

What is the origin of the parasympathetic nervous system?

A

CRANIOSACRAL (CN 3, 7, 9, 10 & S2-S4)

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20
Q

Where do the preganglionic and post ganglionic fibers of the parasympathetic nervous system synapse?

A

Near the effector organ

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21
Q

What is the length of preganglionic and postganglionic fibers of the parasympathetic nervous system?

A

PRE: long
POST: short

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22
Q

this is a large and highly organized collection of neurons located in the walls of gastrointestinal system. This includes the Auerbach’s Plexus (myenteric plexus) and the Meissner’s Plexus (submucosal plexus).

A

Enteric Nervous System

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23
Q

What do you call the fibers that synthesize and release acetylcholine? ALL preganglionic ANS fibers are of this type

A

CHOLINERGIC FIBERS

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24
Q

What cells release a mixture of epinephrine and norepinephrine?

A

Adrenal Medullary cells. They are embryologically analogous to postganglionic sympathetic neurons

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25
Q

What are the key features of neurotransmitter function that are targets for pharmacologic therapy?

A 
Synthesis
Storage
Release
Termination of Action
Receptor Effects

SSRRT

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26
Q

Acetylcholine is synthesized in the cytoplasm from acetyl-CoA and Choline via what enzyme?

A

Choline Acetyltransferase

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27
Q

This is dependent on extracellular calcium and occurs when an action potential reaches the terminal and triggers sufficient influx of calcium ions via N-type calcium channels

A

Physiologic release of transmitter

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28
Q

What is the rate limiting step in cathecholamine transmitter synthesis?

A

Tyrosine to L-dopa via Tyrosine Hydroxylase

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29
Q

What are the cotransmitters released in the snaptic cleft together with the primary transmitter norepinephrine?

A

ATP, Dopamine-beta-hydroxylase, peptide

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30
Q

What are the 2 processes involved in the termination of noradrenergic transmission?

A

a. ) Simple Diffusion

b. ) reuptake into the nerve terminal by NET

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31
Q

These, in some cases, provide faster or slower action to supplement or modulate the effects of the primary transmitter. They also participate in feedback inhibition of the same and nearby nerve terminals

A

Cotransmitter

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32
Q

slowing of the heart and stimulation of digestive activity are typical actions of what ans?

A

Parasympathetic NS

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33
Q

Cardiac stimulation, increased blood sugar, cutaneous vasoconstriction are actions of what ans?

A

Sympathetic NS

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34
Q

What is the primary controlled variable in cardiovascular function?

A

Mean Arterial Pressure. Meaning, any changes in MAP evokes powerful homeostatic secondary responses to compensate for the directly evoked change.

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35
Q

The principle of negative feedback control is found at what level of autonomic function?

A

Presynaptic

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36
Q

These are presynaptic receptors that respond to the primary transmitter substance released by the nerve endings

A

Autoreceptors. They are usually INHIBITORY

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37
Q

Regulatory receptors that respond to many different substances are called

A

Heteroreceptors

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38
Q

This is an extreme form of up-regulation which occurs after DENERVATION of some tissues….

A

Denervation Supersensitivity

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39
Q

“Prolonged administration of large doses of reserpine, a norepinephrine depleter, can cause increased sensitivity of the smooth muscle and cardiac muscle effector cells served by the depleted sympathetic fibers.”

This is an example of what type of up-regulation?

A

Denervation Supersensitivity

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40
Q

This Muscarinic receptor is found in the CNS, specificcally in the cerebral cortex, hippocampus and striatum

A

M1

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41
Q

This muscarinic receptor is found in the heart, nerves, smooth muscle, autonomic nerve termincals

A

M2

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42
Q

This muscarinic receptor is found in glands, smooth muscle, endothelium

A

M3

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43
Q

This muscarinic receptor is found in the forebrain

A

M4

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44
Q

this muscarinic recptor is found in the substancia nigra

A

M5

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45
Q

What are the muscarinic receptors found in the CNS

A

M1, M4, M5

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46
Q

Functional response of this receptor includes:
Inc Smooth muscle contraction (eg bladder)
Inc Glandular secretion (salivary)
Inhibits Dopamine release and NO synthesis

A

M3

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47
Q

Functional response of this receptor includes:
Inc cognitive fxn
Inc secretions, Inc depolarization of autonomic ganglia
Dec dopamine release and locomotion

A

M1

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48
Q

Functional response of this receptor includes:

Analgesia
Facilitation of Dopamine Release

A

M4

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49
Q

Functional response of this receptor includes:
Slowing of the HR via slowed spontaneous SA node depolarization
Smoth muscle contraction
Neural inhibition of tremors; hypothermia; analgesisa

A

M2

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50
Q

Functional response of this receptor includes:

Dilation of cerebral arteries and arterioles
Facilitates dopamine release
Augment drug seeking behavior

A

M5

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51
Q

Where are nicotinic receptors found?

A

Skeletal NMJ
Autonomic Ganglia
CNS

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52
Q

Stimulation of this nicotinic receptor causes skeletal muscle contraction

A

Nm

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53
Q

Stimulation of this nicotinic receptor causes depolarization and secretion of cathecholamines

A

Nn

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54
Q

What are DIRECT-acting cholinoreceptor agonists?

These are lipid insoluble and do not cross the blood-brain barrier

A

Alkaloids or Choline esters

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55
Q

These are agonists that reversibly or irreversibly inhibits acetylcholinesterase or butyrylcholinesterases

A

Indirect-acting cholinoreceptor agonists

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56
Q

This acts on both nicotinic and muscarinic receptors and is rapidly metaboliozed by AChE and butyrylcholinesterases

A

Acetylcholine

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57
Q

This drug is resistant to AChE hydrolysis and has greater effect on muscarinic receptors though its potency is similar to ACh.

A

Metacholine

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58
Q

This drug has a longer duration of action than ACh and its effect on muscarinic receptors is greatest on the GIT and GUT. Least nicotinic effects in CVS.

This is used to constrict the pupils intraoperatively, preop and post op

A

Carbachol

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59
Q

This drug usually causes nausea/diarrhea after surgery

A

Carbachol. kasi greatest effect nya on GIT and GUT

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60
Q

What is the drug that is least susceptible to atropine?

A

Carbachol

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61
Q

What drug has the most nicotinic effect?

A

Carbachol

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62
Q

What drug has the least Gastrointestinal effect?

A

ACh and Methacholine

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63
Q

What drug has highes AChE susceptibility?

A

ACh

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64
Q

What drug has the least cardio effect?

A

Bethanecol

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65
Q

What drug do you give for a patient who has a bladder problem?

A

Carbachol, Bethanecol, Pilocarpine

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66
Q

These drugs are non-covalent inhibitors of the active site of AChE. These also target pseudocholinesterases

A

Competitive Anticholinesterases

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67
Q

These drugs binds and deactivates AChE

A

Non-competitive Anticholinesterases

68
Q

Rivastigmine is given to patients with ______ to improve cognition

A

Alzheimers

69
Q

Pyridostigmine is given to patients with ______ to increase the neurotransmitters leading to decrease in symptoms

A

Myasthenia Gravis

70
Q

Neostigmine and Pyridostigmine are examples of…

A

Carbamate Esters

71
Q

Diazinon and Parathion are examples of

A

Organophosphates

72
Q

This is used as diagnostic test for Myasthenia Gravis (tensilon test)

A

Edrophonium

73
Q

This drug is also used as treatment for Myasthenia Gravis. Also used for patients with Atonic Bladder

A

Neostigmine

74
Q

This drug is also used as tx for Alzheimers

A

Physostigmine

75
Q

This drug is used especially for patient with paralytic ileus

A

Pyridostigmine

76
Q

This is a cholinesterase reactivator.

A

Pralidoxime

77
Q

What is the MOA of Pralidoxime

A

regenerates cholinesterase via Pyridine-2-aldoxime methyl chloride (2PAM)

78
Q

This results from overfiring/ excessive actions of cholines

A

Cholinergic Crisis

79
Q

What drug do you give to patients suffering from Cholinergic crisis?

A

Atropine

80
Q

Cholinergic drug interaction with aminoglycosides may result to…

A

Inc risk of neuromuscular blockage

81
Q

Cholinergic drug interaction with depolarizing muscle relaxants may lead to…

A

prolongation of the block

82
Q

Cholinergic drug interaction with non-depolarizing muscle relaxants may lead to…

A

antagonism of the muscle relaxant effect

83
Q

These cholinergic antagonists block the effect of parasympa autonomic discharge at the receptor sites

A

Antimuscarinics

84
Q

these cholinergic antagonists block the action of ACh at the autonomic gangla

A

Antinicotinic

85
Q

Cholinergic antagonists may be used as preop medication for bronchoscopy because…

A

it decreases bronchial secretions

86
Q

What anticholinergic drug is used as tx for parkinsonism because it has antimuscarinic properties that improves tremors and rigidity

A

Biperiden

87
Q

What anticholinergic drugs are used for pupillary dilatation?

A

Atropine, Cyclopentolate, Tropicamide

88
Q

What anticholinergic drug is used for asthma?

A

Ipatropium

89
Q

What anticholinergic drug is used for diarrhea?

A

Lomotil

90
Q

What are the effects of antinicotinic agents in the CNS?

A

Sedation, tremor, choreiform movts, mental abberations

91
Q

What are the effects of antinicotinic agents in the Eyes?

A

Cycloplegia with loss of accomodation

92
Q

What are the effects of antinicotinic agents in the CVS?

A

Hypotension, Dec inotropic

93
Q

What are the effects of antinicotinic agents in the GIT?

A

motility inhibited, marked constipation

94
Q

What are the effects of antinicotinic agents in the GUT?

A

Urinary retention

95
Q

This hypothesis implies that a given dose kills a constant proportion of a cell population rather than a constant number of cells

A

Log-Kill Hypothesis

96
Q

What property of the tumor cells allows them to become resistant to chemotherapy and radiotherapy?

A

Genetic Instability

97
Q

What do you call the mammalian cellular genes that code for specific growth factors and their correspondin receptors. These are amplified and lead to constitutive overexpression in malignant cells

A

Oncogenes

98
Q

This is a class of genes that may be deleted or mutated and may give rise to the neoplastic phenotype

A

Tumor Suppressor Genes

99
Q

his is the best-established tumor supressor gene which plays an important rle in suppressing malignant transformation

A

p53

100
Q

This is the type of chemotherapy given to patients who present with advanced cancer for which no alternative treatment exists

A

Primary Chemotherapyy

101
Q

What are the goals of Primary Chemotherapy?

A

Relieve tumor related symptoms
Improve overall quality of life
Prolong time to tumor progression

102
Q

This is the main approach in treating patients with advanced metastatic diseases

A

Primary Chemotherapy

103
Q

This refers to the use of chemotherapy in patients who presents with localized cancer for which local therapies, such as surgey, exist but which are less than completely effective

A

Neoadjuvant chemotherapy

104
Q

What is the goal of Neoadjuvant chemotherapy?

A

Reduce the size of the primary tumor (for easier surgical resection)

105
Q

This is administered afer the surgery has been performed and its goal is to reduce the incidence of both local and systemic recurrence and improve overall survical of patients.

A

Adjuvant chemotherapy

106
Q

True or False: Cell kill is proportional regardless of tumor burden.

A

True

107
Q

True or false: The growth fraction of tumor increases exponentially with time.

A

False. Decreases

108
Q

Single drugs at clinically tolerable doses have been unable to cure cancer except for 2 types… What are these?

A

Choriocarcinoma and Burkitt’s Lymphoma

109
Q

What are the 3 reasons why combination chemotherapy is important?

A

1) provides maximal cell kill
2) provides a broader range of interaction bet drugs and tumor cells
3) may prevent or slow subsequent devt of drug resistance

110
Q

What are the 5 things to consider when choosing drugs for combination chemotherapy?

A

1) Efficacy
2) Toxicity
3) Optimum Scheduling
4) Mechanism of Interaction
5) Avoidance of Arbitrary Dose Changes

111
Q

What is CISPLATIN’s MOA? It is under what kind of drugs?

A

It is a Platinum Analogue

MOA: forms intrastrand and interstrand DNA cross-links; binds to nuclear and cytoplasmic proteins

112
Q

In general, Alkylating agents’ adverse effects are…

A

Nausea and Vomiting

113
Q

These drugs’ mechanism of resistance is via increased capability to repair DNA lesion

A

Alkylating Agents and Cisplatin

114
Q

These drugs’ mechanism of resistance is via formation of trapping agents

A

Bleomycine, Cisplatin, Anthracyclines

115
Q

These drug’s mechanism of resistance is via changes in target enzymes

A

Methotrexate

116
Q

What are the 6 mechanisms of resistance to anticancer drugs?

A
  1. )Increased DNA repair
  2. )Formation of trapping agents
  3. )Changes in target enzymes
  4. )Inactivation of anticancer drugs
  5. )Decreased drug accumulation
  6. )Decreased activation of prodrugs
117
Q

Toxic effects of anticancer drugs can sometimes be alleviated by this strategy

A

Rescue therapy

118
Q

After giving high doses of Methotexrate, this drug is given to rescue the normal cells. This drug bypasses the dihydrofolate reductase step in folic acid synthesis.

Rescue therapy for Methotexrate

A

Leucovorin

119
Q

This drug traps acrolein released from cyclophosphamide and thus reduces the incidence of hemorrhagic
cystitis.
Rescue therapy for Cyclophosphamide

A

Mercaptoethane sulfonate (mesna)

120
Q

This drug inhibits free radical formation and

affords protection against the cardiac toxicity of anthracyclines

A

Dexrazoxane

121
Q

These drugs lead to cross-linking

of bases, abnormal base-pairing, and DNA strand breakage

A

Alkylating agents

122
Q

These two drugs specifically alkylates guanine residues at N7

A

Cyclophosphamide & ifosfamide

123
Q

This drug is used for leukemia, non-Hodgkin’s lymphoma, breast and ovarian cancers, and neuroblastoma. This is also used as an immunosuppressant for lupus nephritis and polyarteritis nodosa

A

Cyclophosphamide

124
Q

This alkylating agent is used for testicular cancer

A

ifosfamide

125
Q

These 2 drugs adverse effects are:
↑ risk of transitional cell bladder CA
Hemorrhagic cystitis

A

Cyclophosphamide & ifosfamide

126
Q

What is the MOA of Mechlorethamine

A

spontaneously converts in the body to a reactive cytotoxic product

127
Q

Mechlorethamine is used for what kinds of cancer

A

Hodgkin’s and non-Hodgkin’s lymphoma

128
Q

What are the adverse effects of Mechlorethamine

A

Gastrointestinal distress
myelosuppression
Alopecia
sterility

129
Q

These Platinum Analogs testicular is used for carcinoma

cancers of the bladder, lung, and ovary

A

Carboplatin and Cisplatin

130
Q

This Platinum Analog is used for advanced colon cancer

A

Oxaliplatin

131
Q

What are the adverse effects of Cisplatin?

A

Neurotoxicity (peripheral neuritis + acoustic n damage)

Nephrotoxicity (may be reduced by mannitol + forced hydration)

132
Q

What are the adverse effects of Carboplatin?

A

myelosuppressant actions

133
Q

What are the adverse effects of Oxaliplatin?

A

Neurotoxicity

134
Q

This drug’s MOA is: Formation of hydrogen peroxide
& generation of free radicals that cause DNA strand scission
This is also used for Hodgkin’s and non-Hodgkin’s lymphoma

A

Procarbazine

135
Q

What are the adverse effects of Procarbazine?

A

Disulfiram-like reactions

leukemogenic.

136
Q

These are highly lipid soluble drugs used as adjuncts in the management of brain tumors

A

Nitrosureas: Carmustine and lomustine

137
Q

What is the adverse effect of Carmustine and lomustine?

A

CNS toxicity (seizures, ataxia, dizziness)

138
Q

This drug is sometimes used in chronic myelogenous leukemia (CML)
Its adverse effects are:
adrenal insufficiency, pulmonary fibrosis, and skin pigmentation

A

Busulfan

139
Q

This drug is used in regimens for Hodgkin’s lymphoma

Adverse effects:
alopecia, skin rash, gastrointestinal distress, myelosuppression, phototoxicity, and a flu-like syndrome

A

Dacarbazine

140
Q

These are structurally similar to endogenous compounds and have a dual effect: cytotoxic effects on neoplastic cells + immunosuppressant actions

A

ANTIMETABOLITES

141
Q

What phase of the cell cycle do antimetabolites target?

A

S phase of the cell cycle

142
Q 
MOA of this drug:
inhibitor of dihydrofolate reductase
leads to a decrease in the synthesis of:
-Thymidylate
-purine nucleotides
-amino acids
interferes with nucleic acid and protein metabolism
A

Methotrexate

143
Q

These drugs resist anti-cancer therapy by increasing DNA repair

A

Alkylating Agents and Cisplatin

144
Q

These drugs resist anti-cancer therapy by forming trapping agents

A

bleomycin, cisplatin, and the anthracyclines

145
Q

This drug resists anti-cancer therapy by changing its target enzymes

A

Methotrexate

146
Q

Give examples of nitrogen mustards

A

chlorambucil, cyclophosphamide,

mechlorethamine, ifosfamide

147
Q

These drugs are activated to toxic nucleotides that inhibit several enzymes involved in purine metabolism and are used as tx for acute leukemias & chronic myelocytic leukemia

A

Mercaptopurine (6-MP) and Thioguanine (6-TG)

148
Q

This inhibits thymidylate synthase via 5f-dUMP

A

5-Fluorouracil (5-FU)

149
Q

This drug is an inhibitor of DNA polymerases and is

most specific for the S phase of the cell cycle

A

CyTarabine (ARA-C)

150
Q

This drug is converted into the active diphosphate and
triphosphate nucleotide form. It inhibits ribonucleotide reductase. It is clinically used for pancreatic cancer and non-small cell lung cancer

A

Gemcitabine

151
Q

These drugs prevent the assembly of tubulin dimers into

microtubules and specifically targets the M phase of the cell cycle

A

Vinblastine, Vincristine, Vinorelbine

152
Q

These drugs induces DNA breakage through its inhibition of topoisomerase II and target late S phase and early G2 phases of the cell cycle

A

Etoposide and Teniposide

153
Q

These drugs are used for small cell lung cancer, Prostate cancer, Testicular cancer via inhibition of topoisomerase II

A

Etoposide and Teniposide

154
Q

These drugs damage DNA by inhibiting topoisomerase I

A

Toptecan and Irinotecan

155
Q

This drug is used as second-line therapy for advanced ovarian cancer. It can also be used for :
 small cell lung cancer
 Cervical cancer

A

Topotecan

156
Q

This drug is used for metastatic colorectal cancer

A

Irinotecan

157
Q

These drugs prevent microtubule disassembly into tubulin monomers and targets the prophase stage of the cell cycle

“taxes stabilizes society”

A

Paclitaxel and Doclitaxel

Hyperstabilizes mitotic spindle

158
Q

These drugs are used for breast, ovarian, lung, gastroesophageal, prostate, bladder, and head and neck cancers via hyperstabilizing mitotic spindles

A

Paclitaxel and Doclitaxel

159
Q

These drugs are anthracyclines that lock the synthesis of RNA and DNA and cause
DNA strand scission by the ff mechanisms:
 Intercalate between base pairs
 inhibit topoisomerase II
 Generate free radicals

A

Doxorubicin, Daunorubicin

160
Q

This is an anthracycline used for Hodgkin’s and non- Hodgkin’s lymphoma, myelomas, sarcomas, and
breast, lung, ovarian, and thyroid cancers

A

Doxorubicin

161
Q

This is an anthracycline used for acute leukemias

A

Daunorubicin

162
Q

This drugs is used for Childhood Tumors:
 Wilm’s Tumor
 Ewing sarcoma
 Rhabdomyosarcoma

A

Dactinomycin

163
Q

Drug that targets the g2 phase

A

bleomycin

164
Q

drugs that target the S phase

A 
irinotecan
methotrexate
hydroxyurea
cytarabine
6-thioguanine
5-fluorouacil
etoposide
165
Q

Drugs that target the M phase

A

vinblastine
vincristine
paclitaxel

166
Q

These are non-cell-cycle-specific drugs

A

Alkylating Agents
Antitumor antibiotics
Nitrosoureas

Pharmacology (12 decks)

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