PHARM III Drugs And Class And MOA Flashcards
Cylcobenzapine
Class, MOA, and C/U
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)
Orphanadrine
Class? MOA?? C/U??
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)
Carisoprodol
Class? And MOA? C/U?
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)
Metaxalone
Class and MOA, C/U?
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
Tizanidine
Class and MOA, C/U?
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
Baclofen
Class and MOA, C/U ?
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
Diazapam
Class and MOA
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
Gabapentin
Class and MOA, C/U?
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)
Pregabalin
CLASS AND MOA, C/U ?
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
Botulinim Toxin A
Class and MOA, C/U ?
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
Dantrolene Sodium
Class and MOA, C/U?
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)
Dicyclomine
Class, MOA, and Clin Use
Antispasmodic Agent MSK relax
Antispasmodic Agents: Used in treatment of smooth muscle disorders (ie. irritable bowel syndrome)
All Centrally and Peripherally acting
Hyoscyamine
Class, MOA, C/U
Antispasmodic Agent MSK relax
Antispasmodic Agents: Used in treatment of smooth muscle disorders (ie. irritable bowel syndrome)
All Centrally and Peripherally acting
Succinylcholine
Short Acting NMB
Atracurium
Intermediate Acting NMB
(non depol)
Metz to laudanosine
Cisatracurium
Intermediate NMB
NONdepol
Rocuronium
Intermediate NMB
NONdepol
Vecuronium
Intermediate NMB
NONdepol
Pancuronium
Long acting Non Depol NMB
What is the MOA of antispastic agents
reduce muscle cramping and tightness in neurological disorders and spinal cord injury and disease
Methocarbamol
Class and MOA
CNS depressant MSK relaxant antispamodic
MOA: unknown; suppresses spinal polysynaptic reflexes
Butalbital in Fioricent and Fiorinal
Class, MOA, C/U
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
Midrin C-IV
Class, MOA, C/U
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
Excedrin OTC
CLASS, MOA, C/U
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
What is the MOA of ergotamine
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
What is the MOA and clin use of Digydroergotamine
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
What is the MOA and C/U of triptans
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
What is the MOA and C/U of Cyproheptadine
Tx of Seretonin Syndrome
1st generation antihistamine, and 5HT1A and 5HT2 antagonist
Sumatriptan/ Naproxen
MOA and C/U
Mechanism of Action: designed to target different vascular and inflammatory processes in a migraine
Clinical Considerations: combination provides superior relief to either component
Butorphanol
MOA and C/U
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)
Metoclopraminde
MOA and C/U
Antiemetic
Use for the Tx of N/V assoc. with migraine
Considered the best option
Chlorpromazine
MOA and C/U in migrianes
Typical Antipsychotic (1st Generation): dopamine and serotonin antagonist
Used an an antiemetic in migraine Tx
Prochlorperazine
MOA and C/U for Migraines
Typical Antipsychotic (1st Generation): dopamine and serotonin antagonist
Used as an antiemetic in Migraine Tx
Ondansetron
MOA and C/U with migraines
Seretonin antagonist
Antiemetic
Granisetron
MOA and C/U in migraines
5HT3 antagonist
Antiemetic
What is the MOA of CGRP Inhibitors
Inhibit Activation of trigeminovascular system results in decreased CGRP circulation
Reducing migraine and light sensitivity
Erenumab-aooe
Class and C/U
CGRP antagonists
Migraine prophylaxis in adults
Fremanezumab-vfrm
Class and C/U
CGRP antagonist
Migraine prophylaxis in adults
Galcanezumab-gnlm
Class and C/U
CGRP antagonists
Migraine prophylaxis in adults
Tx od episodic cluster HA
Amitryptyline
Class, and C/U in tension HA
TCA
DOC for Prophylaxis Tension HA
Verapamil
Class and C/U in HA
CCB
Considered the drug of choice in Maintenance Prophylaxis (Effective in ~ 70% of patient)
Prednisone
C/U in HA
Prophylactic Tx of Cluster HA
Insulin
MOA
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
Insulin Lispro
Drug class
Rapid acting insulin
Insulin Aspart
Drugg class
Rapid acting insulin
Insulin Glulisine
Drugg class
Rapid acting insulin
Afrenza
Drug class
Inhaled insulin
Humulin R
Drug class
Short acting Insulin
U-500 insulin
C/U
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)
NPH (humulin N)
Drug class
Intermediate acting insulin
NPH (Novolin N)
Drug class
Intermediate acting insulin
Insulin glargine
Drug class
Long acting insulin
Insulin Detemir
Drug class
Long acting insulin
What is the MOA and C/U of Biguanides
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)
Metfromin
Drug class
Biguanide
What is the MOA and C/U of Sulfonylreas
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
Chlorpropamide
Drug class
1st gen Sulfonylureas
Tolazamide
Drug class
1st gen sulfonylurea
Tolbutamide
Drug class
1st gen Sulfonylurea
Glipizide
Drug class
2nd gen sulfonylurea
Glyburide
Drug class
2nd gen. sulfonylurea
Glimepiride
Drug Class
2nd gen sulfonylurea
What is the MOA and C/U of meglitinides
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
Nateglinide
Drug class
Meglitidines
Repaglinide
Drug class
Meglitidines
What is the MOA and C/U of thiazolidinediones (TZDs)
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
Pioglitazone
Drug class
TZDs
Rosiglitazone
Drug class
TZD
What is the MOA and C/U of DPP-4 Inh
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
Sitaglipin
Drug class
DPP-4 inhb
Saxagliptin
Drug class
DPP-4 inhb
Linagliptin
Drug class
DPP-4 inhb
Alogliptin
Drug class
DPP-4 inhb
What is the MOA and Clin use of GLP-1 agonists
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
Exanatide
Drug class
GLP-1
Liraglutide
Drug class
GLP-1
Semaglutide
Drug class
GLP-1
Dulaglutide
Drug class
GLP-1
What is the MOA and C/U of Sythentic Amylin Analogues
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
Pramlintide
Drug class
Synthetic amylin analogue
What is the MOA and clin use of Alpha glucosidase inhibitors
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
Acarbose
Drug Class
Alpha glucosidase inhibitors
Miglitol
Drug class
Alpha glucosidase inhibitors
What is the MOA and C/U of SGLT2s
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
Canagliflozin
Drug class
SGLT2
Dapagliflozin
Drug class
SGLT2
Empagliflozin
Drug class
SGLT2
What is Corticorelin Ovine Triflutate
Synth CRH used to Dx between pituitary (Cushing’s Disease) and ectopic production of adrenocorticotropic hormone (ACTH)
What is the MOA and C/u of GNRH and LHRH
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
What is Gonadorelin
Gonadotropin Releasing Hormone (GnRH)
Luteinizing Hormone-Releasing Hormone (LHRH)
Agents
What is goderelin
Gonadotropin Releasing Hormone (GnRH)
Luteinizing Hormone-Releasing Hormone (LHRH)
Agents
What is Leuprolide
Gonadotropin Releasing Hormone (GnRH)
Luteinizing Hormone-Releasing Hormone (LHRH)
Agents
What is Nafarelin
Gonadotropin Releasing Hormone (GnRH)
Luteinizing Hormone-Releasing Hormone (LHRH)
Agents
What is histrelin
Gonadotropin Releasing Hormone (GnRH)
Luteinizing Hormone-Releasing Hormone (LHRH)
Agents
What is triptorelin
Gonadotropin Releasing Hormone (GnRH)
Luteinizing Hormone-Releasing Hormone (LHRH)
Agents
What is the class and C/u of Ganirelix
GnRH Receptor Antagonists
Agent
Inhibition of premature LH surges in women undergoing controlled ovarian hyperstimulation procedures
What is the class and C/u of Cetrorelix
GnRH Receptor Antagonists
Agent
Inhibition of premature LH surges in women undergoing controlled ovarian hyperstimulation procedures
What is the class and C/u of degarelix
GnRH receptor antagonist
For men with advanced prostate cancer (dega is for the dicks)
MOA and C/u of GHIH
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)
What is the class and C/u for octreotide
GHIH, used for esophageal varicies
What is the MOA and C/u of lanreotide
GHIH and used for acromegaly only
MOA and C/u of Pegvisomant
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
What is thyrotropin alfa MOA and C/u
TSH
Clinical Use: diagnostic agent for detecting blood levels of thyroglobulin to exclude the diagnosis of residual or recurrent thyroid cancer following a thyroidectomy
What is the Class and C/u of Follitropin alpha and beta
Also Urofollitropin and Lutropin alfa
FSH/LH
Clinical Use: Ovulation induction (FSH)
Ovulation induction (LH) in infertile females with LH deficiency
Male Infertility (Spermatogenesis induction) (FSH)
MOA and C/u of Dopamine Agonists
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)
What is the class of bromocriptine
Dopamine agonist
Class of Cabergoline
Dopamine agonist
MOA and Clin/use of Conivaptan
Vasopressin antagonist
SIADH
MOA and C/U of Tolvaptan
Vasopression antagonist
SIADH
What is the Clin use of Pitocin
Labor stimulation and post partum bleeding
What is the MOA and C/U of Methimazole
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)
What is the MOA and C/U of Propythiouracil
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)
What is the MOA and C/U of Iodides
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
