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IPAP JUNIOR SEM. > PHARM III Drugs And Class And MOA > Flashcards

PHARM III Drugs And Class And MOA Flashcards

1
Q

Cylcobenzapine

Class, MOA, and C/U

A

CNS Depressant Muscle relaxant
Antispamodic

MOA: Structurally related to tricyclic antidepressants (TCA); causes a depressant effect on serotonergic neurons; has strong anticholinergic and antihistamine properties

C/U: short term local muscle spasms, ineffective at Tx of cerebral palsy or spinal cord injury
(SHORT TERM 2-3 weeks)

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2
Q

Orphanadrine

Class? MOA?? C/U??

A

CNS Depressant Muscle relaxant
Antispasmodic

MOA: Analog of diphenhydramine

Antihistamine and anticholinergic properties

Has euphorigenic and analgesic properties; Full mechanism is unknown

C/U: Treatment of muscle spasm associated with acute painful musculoskeletal conditions
Used short term (2-3 weeks)

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3
Q

Carisoprodol

Class? And MOA? C/U?

A

CNS Depressant Muscle relaxant
Antispasmodic

MOA:
Blocks interneuronal activity and depresses polysynaptic neuron transmission

Metabolized to meprobamate, which has anxiolytic and sedative effects

C/U: Relief of discomfort associated with acute, painful musculoskeletal conditions in adults
Used short term (2-3 weeks)

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4
Q

Metaxalone

Class and MOA, C/U?

A

CNS Depressant Muscle relaxant
Anitspasmodic

MOA: unknown; associated with general depression of the nervous system

C/U: Relief of discomforts associated with acute, painful musculoskeletal conditions
Appears to cause less drowsiness than others

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5
Q

Tizanidine

Class and MOA, C/U?

A

A2 agonist muscle relaxant

MOA: centrally acting α2 agonist (~clonidine)

Reduces spasticity by increasing presynaptic inhibition of motor neurons

1/10 to 1/15 of the blood pressure lowering ability as clonidine

Clinical Use:
Muscle spasticity
Short acting agent

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6
Q

Baclofen

Class and MOA, C/U ?

A

GABA Agonist

Mechanism of Action:
Orally active GABA-mimetic agent at the level of the spinal cord

Presynaptic inhibition by reducing calcium influx and reduces the release excitatory transmitters in both the brain and the spinal cord

May also reduce pain in patients with spasticity by inhibiting the release of substance P in the spinal cord

Clinical Use:
Anti-spastic agent
Drug of Choice for Multiple Sclerosis (MS)
At least as effective as diazepam in reducing spasticity and causes less sedation
Does not reduce overall muscle strength

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7
Q

Diazapam

Class and MOA

A

GABA Agonist

Mechanism of Action:
Bind to specific high affinity sites on the cell membrane separate but adjacent to the GABA receptor (allosteric binding)

Enhancement of the INHIBITORY effect of GABA on neuronal excitability (increase chloride influx)

Diazepam is an anxiolytic that may also be used as a spasmolytic: exerts both antispasmodic and antispasticity actions

C/U: Oral formulation used in Cerebral palsy, multiple sclerosis, temporary muscle spasms (of any origin)

Management of anxiety disorders, symptomatic relief of agitation, tremor, and acute delirium in alcohol withdrawal

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8
Q

Gabapentin

Class and MOA, C/U?

A

GABA Agonist

Mechanism of Action:
INHIBITION of voltage-dependent calcium channels

An analog of GABA, but does not directly impact GABA receptor

Clinical Use:
Generalized tonic-clonic seizures
Neuropathic pain and post herpetic neuralgia pain
Diabetic neuropathy (off-label)

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9
Q

Pregabalin

CLASS AND MOA, C/U ?

A

GABA Agonist

Mechanism of Action:
Inhibition of voltage-dependent calcium channels.

GABA derivative similar to gabapentin

Clinical Use:
Partial-onset seizure (adjunct)
Non-epileptic: neuropathic pain associated with diabetic neuropathy, restless leg syndrome, post-herpetic neuralgia, fibromyalgia, pain due to spinal cord injury, social phobia

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10
Q

Botulinim Toxin A

Class and MOA, C/U ?

A

Direct/peripherally acting MSK relxant

Mechanism of Action:
Inhibits the release of acetylcholine from cholinergic nerve fibers at neuromuscular junctions

Produced by the bacteria clostridium botulinum

Botulism is a rare but serious paralytic illness

Poisoned victim becomes gradually weaker as nerves lose their ability to stimulate muscle contraction

C/U: (Toxin A only)

headache ≥15 d/mo x 3 mo;
≥8 headaches/mo
or migraines w/o aura

ALso, Cervical dystonia and blepharospasm

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11
Q

Dantrolene Sodium

Class and MOA, C/U?

A

Direct/peripherally acting MSK relxant

Mechanism of Action: reduces skeletal muscle strength by interfering with excitation-contraction coupling in the muscle fibers

C/U:
IV: Drug of choice in the treatment of malignant hyperthermia (MH)

ORAL: Chronic spasticity resulting from upper motor neuron disorders (eg. Spinal cord injury, stroke, cerebral palsy, or MS)

Not indicated for skeletal muscle spasm resulting from rheumatic disorders (i.e., Chorea, Rheumatic Fever)

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12
Q

Dicyclomine

Class, MOA, and Clin Use

A

Antispasmodic Agent MSK relax

Antispasmodic Agents: Used in treatment of smooth muscle disorders (ie. irritable bowel syndrome)
All Centrally and Peripherally acting

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13
Q

Hyoscyamine

Class, MOA, C/U

A

Antispasmodic Agent MSK relax

Antispasmodic Agents: Used in treatment of smooth muscle disorders (ie. irritable bowel syndrome)
All Centrally and Peripherally acting

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14
Q

Succinylcholine

A

Short Acting NMB

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15
Q

Atracurium

A

Intermediate Acting NMB
(non depol)

Metz to laudanosine

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16
Q

Cisatracurium

A

Intermediate NMB

NONdepol

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17
Q

Rocuronium

A

Intermediate NMB

NONdepol

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18
Q

Vecuronium

A

Intermediate NMB

NONdepol

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19
Q

Pancuronium

A

Long acting Non Depol NMB

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20
Q

What is the MOA of antispastic agents

A

reduce muscle cramping and tightness in neurological disorders and spinal cord injury and disease

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21
Q

Methocarbamol

Class and MOA

A

CNS depressant MSK relaxant antispamodic

MOA: unknown; suppresses spinal polysynaptic reflexes

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22
Q

Butalbital in Fioricent and Fiorinal

Class, MOA, C/U

A

Acetaminophen combinations

MOA: short- to intermediate-acting barbiturate

Can be used to Tx migraines however, No randomized, placebo-controlled studies support the efficacy of butalbital containing products in treating migraine headaches

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23
Q

Midrin C-IV

Class, MOA, C/U

A

Combination drug of acetaminophen 325 mg, isometheptene 65 mg, dichloralphenazone 100 mg

Mechanism of Action:
-Acetaminophen: analgesic

-Isometheptene: sympathomimetic amine that produces vasoconstriction of arteries and veins

-Dichloralphenazone: 1:2 phenazone: chloral hydrate mixture
—Phenazone: analgesic
—Chloral hydrate: sedative/hypnotic

Clinical Use:
Alternative choice for patients with mild-to-moderate migraine headache attacks

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24
Q

Excedrin OTC

CLASS, MOA, C/U

A

Combination drug: acetaminophen 250 mg, aspirin 250 mg, caffeine 65 mg

Clinical Use: reasonable first-line treatment choice for mild-to-moderate migraine attacks or severe attacks that have been previously responsive

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25
Q

What is the MOA of ergotamine

A

Mechanism of Action: partial agonist activity at 5HT and D2 and alpha-adrenergic receptors

C/U: migraine relief

Caffeine: potentiates and increases ergotamine’s vasoconstrictive properties and absorption

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26
Q

What is the MOA and clin use of Digydroergotamine

A

Mechanism of Action: similar to ergotamine, with less potent α1-adrenergic vasoconstriction

C/U:

D.H.E. 45: IV
IV used in the treatment of status migrainosus (Raskin protocol)

D.H.E. subQ/IM/IV/nasal is a reasonable choice when the headache is moderate-to-severe or an adequate trial of NSAIDs or other non-opiate analgesics (including combo’s) have failed to provide adequate relief in the past*

D.H.E. IV plus anti-emetics IV is an appropriate treatment for patients with severe migraine

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27
Q

What is the MOA and C/U of triptans

A

Mechanism of Action:
5-HT1B/1D receptor agonists with additional activity at 5HT1F receptors
-5-HT1B cranial vasoconstriction
-5-HT1D peripheral neuronal inhibition (e.g., CGRP, substance P, etc.)
-5-HT1B/1D/1F inhibition of the trigeminocervical complex (i.e., decreased excitability)

Clinical Use: appropriate 1st line therapy for patients with moderate to severe migraine and are used for rescue therapy when nonspecific medications are ineffective

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28
Q

What is the MOA and C/U of Cyproheptadine

A

Tx of Seretonin Syndrome

1st generation antihistamine, and 5HT1A and 5HT2 antagonist

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29
Q

Sumatriptan/ Naproxen

MOA and C/U

A

Mechanism of Action: designed to target different vascular and inflammatory processes in a migraine

Clinical Considerations: combination provides superior relief to either component

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30
Q

Butorphanol

MOA and C/U

A

Mechanism of Action:

  • Partial agonist
  • Partial mμ and kappa receptor agonist

Formulations: IV, nasal spray

Clinical Use:

  • Pain management
  • Pain during labor (if epidural is not possible)
  • Off label: Migraine (as last resort)
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31
Q

Metoclopraminde

MOA and C/U

A

Antiemetic

Use for the Tx of N/V assoc. with migraine
Considered the best option

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32
Q

Chlorpromazine

MOA and C/U in migrianes

A

Typical Antipsychotic (1st Generation): dopamine and serotonin antagonist

Used an an antiemetic in migraine Tx

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33
Q

Prochlorperazine

MOA and C/U for Migraines

A

Typical Antipsychotic (1st Generation): dopamine and serotonin antagonist

Used as an antiemetic in Migraine Tx

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34
Q

Ondansetron

MOA and C/U with migraines

A

Seretonin antagonist

Antiemetic

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35
Q

Granisetron

MOA and C/U in migraines

A

5HT3 antagonist

Antiemetic

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36
Q

What is the MOA of CGRP Inhibitors

A

Inhibit Activation of trigeminovascular system results in decreased CGRP circulation

Reducing migraine and light sensitivity

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37
Q

Erenumab-aooe

Class and C/U

A

CGRP antagonists

Migraine prophylaxis in adults

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38
Q

Fremanezumab-vfrm

Class and C/U

A

CGRP antagonist

Migraine prophylaxis in adults

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39
Q

Galcanezumab-gnlm

Class and C/U

A

CGRP antagonists

Migraine prophylaxis in adults

Tx od episodic cluster HA

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40
Q

Amitryptyline

Class, and C/U in tension HA

A

TCA

DOC for Prophylaxis Tension HA

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41
Q

Verapamil

Class and C/U in HA

A

CCB

Considered the drug of choice in Maintenance Prophylaxis (Effective in ~ 70% of patient)

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42
Q

Prednisone

C/U in HA

A

Prophylactic Tx of Cluster HA

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43
Q

Insulin

MOA

A

Mechanism of Action:
Replaces (T1DM) or supplements (T2DM) endogenous insulin

Facilitates glucose uptake into insulin-sensitive peripheral tissues

Inhibits hepatic glucose output and glucagon secretion

Ultimately reduces glucose in circulation

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44
Q

Insulin Lispro

Drug class

A

Rapid acting insulin

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45
Q

Insulin Aspart

Drugg class

A

Rapid acting insulin

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46
Q

Insulin Glulisine

Drugg class

A

Rapid acting insulin

47
Q

Afrenza

Drug class

A

Inhaled insulin

48
Q

Humulin R

Drug class

A

Short acting Insulin

49
Q

U-500 insulin

C/U

A

Highly concentrated form of human regular insulin (i.e., 500 units/ml vs normal 100 units/ml)

Used in patients with severe insulin resistance (i.e., require insulin doses > 200 units/day)

50
Q

NPH (humulin N)

Drug class

A

Intermediate acting insulin

51
Q

NPH (Novolin N)

Drug class

A

Intermediate acting insulin

52
Q

Insulin glargine

Drug class

A

Long acting insulin

53
Q

Insulin Detemir

Drug class

A

Long acting insulin

54
Q

What is the MOA and C/U of Biguanides

A

Decreases hepatic glucose production (gluconeogenesis), glycogenolysis, and enhances insulin sensitivity in fat and peripheral (muscle) tissues (improves glucose uptake and utilization)

Slows intestinal absorption of sugars

Allows for an increased uptake of glucose into insulin-sensitive tissues

C/U: 1st line for T2DM
-Demonstrated improved cardiovascular outcomes

Polycystic ovary syndrome (PCOS)

55
Q

Metfromin

Drug class

A

Biguanide

56
Q

What is the MOA and C/U of Sulfonylreas

A

Mechanism of Action: binds to a specific sulfonylurea receptor (SUR) on the pancreatic β cell leading to stimulation of insulin secretion (2nd phase)

C/U T2DM

57
Q

Chlorpropamide

Drug class

A

1st gen Sulfonylureas

58
Q

Tolazamide

Drug class

A

1st gen sulfonylurea

59
Q

Tolbutamide

Drug class

A

1st gen Sulfonylurea

60
Q

Glipizide

Drug class

A

2nd gen sulfonylurea

61
Q

Glyburide

Drug class

A

2nd gen. sulfonylurea

62
Q

Glimepiride

Drug Class

A

2nd gen sulfonylurea

63
Q

What is the MOA and C/U of meglitinides

A

Stimulate insulin secretion from the β-cells of the pancreas, similarly to sulfonylureas (but different site)
Require the presence of glucose to stimulate insulin secretion

C/U; 2nd or 3rd line T2DM

64
Q

Nateglinide

Drug class

A

Meglitidines

65
Q

Repaglinide

Drug class

A

Meglitidines

66
Q

What is the MOA and C/U of thiazolidinediones (TZDs)

A

Mechanism of action:
Enhances insulin sensitivity in muscle and fat by increasing glucose transporter expression

Binds the peroxisome proliferator activator receptor-γ (PPAR-γ) enhancing insulin sensitivity at skeletal muscle, liver, and fat cell

Pioglitazone is also a partial agonist at PPAR-α (similar to fibric acid derivatives)

Clinical Use:
T2DM

67
Q

Pioglitazone

Drug class

A

TZDs

68
Q

Rosiglitazone

Drug class

A

TZD

69
Q

What is the MOA and C/U of DPP-4 Inh

A

Mechanism of Action:
Inhibits the enzyme DPP4, which prevents the degradation of endogenous incretins (GLP-1 and GIP) which increases insulin secretion, decreases glucagon secretion (glucose-dependent)

No effect on gastric emptying and satiety

Orally active

Clinical Use: T2DM

70
Q

Sitaglipin

Drug class

A

DPP-4 inhb

71
Q

Saxagliptin

Drug class

A

DPP-4 inhb

72
Q

Linagliptin

Drug class

A

DPP-4 inhb

73
Q

Alogliptin

Drug class

A

DPP-4 inhb

74
Q

What is the MOA and Clin use of GLP-1 agonists

A

Mechanism of Action:
Stimulates GLP-1 receptors which increases production of insulin secretion in response to high blood glucose levels

Suppresses postprandial glucagon secretion

Slows gastric emptying

Reduces food intake (i.e., increases satiety)

Stimulates β-cell proliferation, preservation, and function in animals

Clinical Use: T2DM

75
Q

Exanatide

Drug class

A

GLP-1

76
Q

Liraglutide

Drug class

A

GLP-1

77
Q

Semaglutide

Drug class

A

GLP-1

78
Q

Dulaglutide

Drug class

A

GLP-1

79
Q

What is the MOA and C/U of Sythentic Amylin Analogues

A

Mechanism of Action:
Suppress inappropriate high postprandial glucagon secretion

Increases satiety (may result in weight loss)

Slows gastric emptying: improves the rate of glucose appearance in the plasma

Clinical Use: adjunct to mealtime insulin therapy in T1DM and T2DM

80
Q

Pramlintide

Drug class

A

Synthetic amylin analogue

81
Q

What is the MOA and clin use of Alpha glucosidase inhibitors

A

Mechanism of Action:
Competitively inhibit α-glucosidase enzymes (maltase, isomaltase, sucrose, and glucoamylase) in the small intestine delaying the breakdown of sucrose and complex carbohydrates to glucose and other monosaccharides

Net effect is a reduction in the post-prandial blood glucose

Absorption of glucose, lactose, and fructose not affected

Clinical Use: T2DM

-Good for patients near target HbA1c levels with near normal FPG levels, but high postprandial levels

82
Q

Acarbose

Drug Class

A

Alpha glucosidase inhibitors

83
Q

Miglitol

Drug class

A

Alpha glucosidase inhibitors

84
Q

What is the MOA and C/U of SGLT2s

A

MOA: Inhibits the sodium glucose co-transporter 2 (SGLT2) transporter, which reduces reabsorption of filtered glucose and lowers the renal threshold for glucose, resulting in increased urinary glucose excretion

C/U: T2DM
Empagliflozin and Canagliflozin FDA approved for reducing CV events

85
Q

Canagliflozin

Drug class

A

SGLT2

86
Q

Dapagliflozin

Drug class

A

SGLT2

87
Q

Empagliflozin

Drug class

A

SGLT2

88
Q

What is Corticorelin Ovine Triflutate

A

Synth CRH used to Dx between pituitary (Cushing’s Disease) and ectopic production of adrenocorticotropic hormone (ACTH)

89
Q

What is the MOA and C/u of GNRH and LHRH

A

MOA: Sustained non-pulsatile administration results in suppression of ovarian and testicular steriodogensis due to decreased levels of LH and FSH

Pulsatile administration is required to stimulate the gonadotroph cell to produce and release LH and FSH

C/U :

Treat infertily

inhibit gonadal function in children with precocious puberty

CAn be used for transgenderes to block puberty

Tx of prostate cancer in men

ART in women

Ovarian supprsion in gyno d/.o

90
Q

What is Gonadorelin

A

Gonadotropin Releasing Hormone (GnRH)
Luteinizing Hormone-Releasing Hormone (LHRH)
Agents

91
Q

What is goderelin

A

Gonadotropin Releasing Hormone (GnRH)
Luteinizing Hormone-Releasing Hormone (LHRH)
Agents

92
Q

What is Leuprolide

A

Gonadotropin Releasing Hormone (GnRH)
Luteinizing Hormone-Releasing Hormone (LHRH)
Agents

93
Q

What is Nafarelin

A

Gonadotropin Releasing Hormone (GnRH)
Luteinizing Hormone-Releasing Hormone (LHRH)
Agents

94
Q

What is histrelin

A

Gonadotropin Releasing Hormone (GnRH)
Luteinizing Hormone-Releasing Hormone (LHRH)
Agents

95
Q

What is triptorelin

A

Gonadotropin Releasing Hormone (GnRH)
Luteinizing Hormone-Releasing Hormone (LHRH)
Agents

96
Q

What is the class and C/u of Ganirelix

A

GnRH Receptor Antagonists
Agent

Inhibition of premature LH surges in women undergoing controlled ovarian hyperstimulation procedures

97
Q

What is the class and C/u of Cetrorelix

A

GnRH Receptor Antagonists
Agent

Inhibition of premature LH surges in women undergoing controlled ovarian hyperstimulation procedures

98
Q

What is the class and C/u of degarelix

A

GnRH receptor antagonist

For men with advanced prostate cancer (dega is for the dicks)

99
Q

MOA and C/u of GHIH

A

Bind to pituitary somatostatin receptors and block growth hormone (GH) secretion

Also inhibits insulin, glucagon and gastrin secretion

Clinical Use:
Used to reduce symptoms caused by a variety of hormone-secreting tumors
—Acromegaly and control symptoms of secretory diarrhea caused by vasoactive intestinal peptide (VIP) [VIP-secreting tumors]

—Useful for the acute control of bleeding from esophageal varices (IV octreotide)

100
Q

What is the class and C/u for octreotide

A

GHIH, used for esophageal varicies

101
Q

What is the MOA and C/u of lanreotide

A

GHIH and used for acromegaly only

102
Q

MOA and C/u of Pegvisomant

A

Mechanism of Action:
Binds to growth hormone receptors on cell surfaces, where it blocks the binding of endogenous GH, thus interfering with GH signaling pathways

Decrease IGF-1 concentrations

Clinical Use:
Treatment of acromegaly resistant to or unable to tolerate other therapies

103
Q

What is thyrotropin alfa MOA and C/u

A

TSH

Clinical Use: diagnostic agent for detecting blood levels of thyroglobulin to exclude the diagnosis of residual or recurrent thyroid cancer following a thyroidectomy

104
Q

What is the Class and C/u of Follitropin alpha and beta

Also Urofollitropin and Lutropin alfa

A

FSH/LH

Clinical Use:
Ovulation induction (FSH)

Ovulation induction (LH) in infertile females with LH deficiency

Male Infertility (Spermatogenesis induction) (FSH)

105
Q

MOA and C/u of Dopamine Agonists

A

MOA: Effectively suppress prolactin release, shrinks pituitary prolactin-secreting tumors, lower circulating prolactin levels, and restore ovulation in 70% of women with microadenomas and 30% of women with
Adenomas

Adenomas that secrete excess prolactin usually retain the sensitivity to inhibition by dopamine exhibited by the normal pituitary

Clinical Use:
Treatment of hyperprolactinemia
Treatment of prolactin-secreting adenoma

Treatment of acromegaly (monotherapy or in combo with pituitary surgery, radiation, and/or octreotide administration)

106
Q

What is the class of bromocriptine

A

Dopamine agonist

107
Q

Class of Cabergoline

A

Dopamine agonist

108
Q

MOA and Clin/use of Conivaptan

A

Vasopressin antagonist

SIADH

109
Q

MOA and C/U of Tolvaptan

A

Vasopression antagonist

SIADH

110
Q

What is the Clin use of Pitocin

A

Labor stimulation and post partum bleeding

111
Q

What is the MOA and C/U of Methimazole

A

Mechanism of action:
Inhibits thyroid peroxidase, thus blocking iodination and synthesis of thyroid hormones

Preferred agent for Grave’s diseases for most patients unless in 1st trimester of pregnancy (PTU preferred in this case)

112
Q

What is the MOA and C/U of Propythiouracil

A

Mechanism of action:
Inhibits thyroid peroxidase, thus blocking iodination and synthesis of thyroid hormones

PTU may block T4 to T3 conversion in the peripheral as well

Used during the 1st trimester of pregnancy, thyroid storm, and in those experiencing adverse reactions to methimazole (other than agranulocytosis or hepatitis)

113
Q

What is the MOA and C/U of Iodides

A

Mechanism of action:
Acutely inhibits hormonal secretion within hours

Temporary inhibition of thyroid hormone synthesis

Reduces the thyroid gland’s vascularity (thereby increasing firmness) and decrease size prior to thyroidectomy

C/U
Short term preop or before rads

IPAP JUNIOR SEM. (43 decks)

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