Drugs to Know Exam 4 Flashcards
(90 cards)
1
Q
Somatropin
A
- MOA: recombinant form of human GH
- Uses: GH deficiency in children and adults and tx of children with genetic diseases associated with short stature
- ADE: edema and hyperglycemia (d/t decreased affect of insulin)
2
Q
Mecasermin
A
- MOA: recombinant human IGF-1
- Uses: pts with GH insensitivity who may be deficient in IGF-1
- ADE: hypoglycemia (give within 20 min of food)
3
Q
Octreotide
A
- MOA: somatostatin analog that inhibits GH secretion
- Uses: somatotroph adenomas
- ADE: significant GI disturbances, gallstones, and cardia conduction abnormalities
4
Q
Bromocriptine and Cabergoline
A
- MOA: dopamine D2 receptor agonist that inhibits prolactin release, but can reduce GH at high doses
- Uses: acromegaly and hyperprolactinemia
- ADE: nausea, vomiting
5
Q
Pegvisomant
A
- MOA: binds to GH receptor and prevents the receptor dimerization
- Uses: acromegaly
6
Q
Tolvaptan and Conicaptan
A
- MOA: vasopressin antagonist
- Uses: hyponatremia
- ADE: tolvaptan has significant risk of hepatotoxicity and liver failure
7
Q
Levothyroxine (T4)
A
- MOA: activation of nuclear receptors results in gene expression with RNA formation and protein synthesis
- Uses: hypothyroidism
- T1/2: 7 days
- administer on an empty stomach
- ADE: nervousness, heat tolerance, tachycardia, weight loss
8
Q
Liothyronine (T3)
A
- MOA: activation of nuclear receptors results in gene expression with RNA formation and protein synthesis
- faster acting and shorter half life than T4 so multiple daily doses
- Uses: myxedema coma (severe hypothyroidism)
- ADE: greater risk of cardiotoxicity
9
Q
Radioactive Iodine
A
- MOA: destroy all or most of thyroid follicular cells, it is rapidly absorbed, concentrated in the thyroid and incorporated in to follicles.
- Uses: treatment of thyrotoxicosis without surgery
- Contraindications: pregnancy/breast feeding
10
Q
Methimazole
A
- thioamides
- MOA: inhibits thyroid peroxidase –> prevents binding of iodide to tyrosine
- Dosing: once daily
- Contraindication: pregnancy
- ADE: agranulocytosis, severe hepatitis, goiter
11
Q
Lugol’s Solution and Potassium iodide
A
- iodides
- MOA: block release of T4 and T3, reduce size and vascularity of hyperplastic gland
- Uses: preoperative prep for surgery, NOT for long term use
- ADE: can cross placenta and can cause fetal goiter
- Wolff-Chaikoff effect: iodine overload is accompanied by auto-regulatory inhibition of thyroid hormone release
12
Q
Propylthiouracil
A
- thioamides
- MOA: inhibits thyroid peroxidase –> prevents binding of iodide to tyrosine
- Dosing: 3 times per day
- can be used in pregnancy
- ADE: agranulocytosis, severe hepatitis, goiter
13
Q
Jod-Basedow Phenomenon
A
- iodine induced hyperthyroidism
- auto-regulation is absent and excess iodine increases thyroid hormone synthesis
14
Q
Beta blockers and thyroid
A
- inhibits peripheral conversion of T4 to T3
- uses: treatment of thyrotoxicosis
15
Q
Glucocorticoids and thyroid
A
- inhibits peripheral conversion of T4 to T3
16
Q
Aspirin and NSAIDs and thyroid
A
- decrease protein binding and cause an increase in free thyroid hormone
17
Q
Amiodarone and thyroid
A
- inhibits T4 to T3 by increasing plasma iodine
- note: can also cause hyperthyroidism
18
Q
Prednisone, Hydrocortisone, Dexamethasone, and Fludricortisone
A
- Glucocorticoids
- hydrocortisone is tx of choice for Addison’s
- Prednisone is safe in pregnancy bc not converted to active in fetus
- ADE: hypertension, hypokalemia, hyperglycemia
19
Q
Ketaconazole
A
- inhibits glucocorticoid synthesis
- Uses: cushing’s syndrome
- ADE: fatigue, nausea, vomiting, HAs, mild liver dysfunction
- low dose: decreases androgen synthesis
- high dose: decreases all steroid hormone synthesis
20
Q
Leuprolide
A
- GnRH agonist –> will see initial surge of LH/FSH but will then turn off
- short acting used for ovulation stimulation
- sustained release formulations turn off GnRH and are used for prostate cancer, advanced breast cancer
- ADE: hot flashes, gynecomastia, osteoporosis, decreased libido
21
Q
GnRH antagonists
A
- end in -relix
- cause immediate drop in FSH and LH
- Aberelix for metastatic prostate palliation
- Degaralix - prostate cancer
- Ganirelix and cetrorelix for ovulation induction to control timing for IVF
- ADE: ovarian hyperstimulation syndrome - bloating, weight gain, dyspnea, venous thromboembolism, acute respiratory distress
22
Q
Clomiphene
A
- SERM (selective estrogen receptor modifier)
- MOA: block estrogen receptors in pituitary to increase FSH and LH
- Uses: induce ovulation
- ADE: multiple follicular growth, thickening of cervical mucus, hot flashes, mood swings, ovarian hyper stimulation is rare
23
Q
Tamoxifen
A
- SERM
- MOA: receptor antagonist in breast, agonist in endometrium and bone
- Uses: treatment and prevention of hormone sensitive breast cancer, palliative care in metastatic breast cancer, prevents osteoporosis
- ADE: higher risk of endometrial cancer, hot flashes, venous thrombosis, vaginal bleeding
24
Q
Raloxifene
A
- SERM
- MOA: partial estrogen agonist in bone
- Uses: prevention and treatment of osteoporosis in postmenopausal women
- can be used to prevent but not treat breast cancer
- ADE: hot flashes, venous thrombosis
25
Fulvestrant
- SERD
- MOA: pure estrogen receptor antagonist in all tissues
- Uses: treatment of women with breast cancer that have developed resistance to tamoxifen
- ADE: vasodilation (hot flash), headache, anti-estrogenic effects (osteoporosis)
- no risk of venous thrombosis or endometrial cancer
26
Anastrazole
- aromatase inhibitor
- indicated in postmenopausal women
- Used in treatment of breast cancer
- ADE: fatigue, arthralgia, increased risk of fx
- no risk of uterine cancer or venous thromboembolism
27
Finasteride
- 5-a reductase inhibitor
- Uses: treatment of symptoms resulting from benign prostate hyperplasia
- **pregnant women should not take
- ADE: decreased libido, erectile dysfunction, gynecomastia, risk of harm to exposed fetus
28
Bicalutamide
- androgen receptor antagonist
- used to prevent initial flare from leuprolide
- treatment of metastatic prostate cancers
29
Two predictable effects of increasing insulin:
- risk of hypoglycemia (beta blockers mask all symptoms except sweating)
- risk of weight gain
30
Lispro, Aspart and Glulisine
- rapid acting exogenous insulin
- MOA: forms weak hexamers which dissociate quickly into monomers
- short duration of about 4 hrs
- given just before or up to 15 min after meal, skip meal skip dose
31
Regular insulin (Humulin, Novolin)
- short acting
- MOA: binds to insulin receptor and is structurally similar to endogenous insulin + Zn+. Forms hexamers which slowly dissociate into monomers to delay absorption
- duration about 6-8 hrs
- give about 30 min before meal, skip meal skip dose
32
NPH
- intermediate insulin
- MOA: bound to protamine which needs to be cleaved before active
- duration of 12-18 hrs
- used for basal control, usually given with rapid or short acting for meal time control
33
Insulin glargine and insulin determir
- long acting, peakless insulins
- glargine - precipitates
- determir - attached to FA
- two should not be mixed in same syringe and must be given as separate injections
34
Chlorpropramide and Tolbutamide
- 1st gen sulfonylureas
- MOA: inhibit K channel causing Ca influx and insulin release
- must eat on time
- ADE: disulfram like rxn, hypoglycemia, SIADH, weight gain
- caution in hepatic and renal failure --> increased risk of hypoglycemia d/t decreased clearance
35
- Glyburide
- 2nd gen sulfonylurea
- MOA: inhibit K channel causing Ca influx and insulin release
- must eat on time
- ADE: hypoglycemia, weight gain
- caution in hepatic and renal failure --> increased risk of hypoglycemia d/t decreased clearance
36
Repaglinide
- MOA: inhibits K channel causing Ca influx and insulin release
- very rapid onset, take with meals (skip meal skip dose)
- ADE: hypoglycemia increased with renal failure, weight gain
37
Metformin
- MOA: decrease hepatic glucose production and increase insulin mediated peripheral glucose uptake --> does NOT promote insulin secretion
- 100% excreted by kidneys
- Use: initial drug in most T2DM
- affects fasting glucose more than post prandial
- advantages: no weight gain, no hypoglycemia
- ADE: lactic acidosis** in CHF, renal failure, alcohol abuse (reduce dose if GFR < 45, stop if < 30), also GI distress
- CI: DKA, metabolic acidosis, renal failure
38
Pioglitazone
- thiazolinediones
- MOA: insulin sensitizers, enhance sensitivity at peripheral targets, increase expression of GLUT4
- advantages: improves HDL, no hypoglycemia
- disadvantages: takes 6 weeks for max effect
ADE: edema, weight gain
- CI: CHF
39
Acarbose
- MOA: reversible inhibitor of alpha-glucosidase enzyme which decreases the digestion of carbs
- taken at beginning of meals
- uses: postprandial hyperglycemia
- advantages: skip meal skip dose, no weight gain
- ADE: GI distress
- CI: IBD. colonic ulceration, intestinal obstruction
- DI: to treat hypoglycemia use glucose rather than sucrose
40
Exenatide
- MOA: GLP-1 receptor agonist, increases post prandial insulin release and suppresses glucagon release
- use: adjunct in T2DM
- advantages: weight loss
- ADE: pancreatitis
- CI: gastroparesis
- DI: DPP-IV inhibitors
41
Sitagliptin
- MOA: inhibits DPP-4 enzyme to increase GLP-1 and increase insulin concentration
- uses: T2DM
- ADE: pancreatitis, delayed gastric emptying
- risk of hypoglycemia with SFU's
- CI: renal failure
42
Canagliflozin
- MOA: inhibits SLGT-2 to decrease reabsorption of glucose in the PCT
- use: T2DM
- ADE: hypovolemia, hypotension, hyperkalemia
- CI: renal failure
43
Glucagon
- use: treat severe hypoglycemia (in unconscious pts), overdose of beta blockers
44
Dextrose
- treat hypoglycemia if pt is on an alpha-glucosidase inhibitor (arcabose)
45
Octreotide
- MOA: long acting somatostatin analog that blocks release of inulin and glucagon
- uses: insulinomas
46
Diazoxide
- MOA: opens K channels and decreases insulin release
- uses: insulinomas
- ADE: opens K channels in cardiac and smooth muscle leading to cell hyperpolarization and vasodilation --> hypotension
47
Acyclovir
- anti-herpesvirus
- MOA: phosphorylated intracellularly by viral kinase to become inhibitors of viral DNA synthesis
- oral: genital herpes and adult varicella-zoster
- IV: herpes encephalitis, neonatal herpes, serious herpes or varicella
ADE: nausea, diarrhea, HA, renal toxicity or neurological effects
- don't give with other nephrotoxic agents
48
Docosanol
- topical fusion inhibitor
- prevents entry into cells and subsequent replication
- apply within 12 hrs of prodrome to reduce sx by 18 hrs
49
Cidofovir
- inhibitor and alternative substrate for viral DNA polymerase --> completely inhibits DNA synthesis
- phosphorylation is independent of viral enzyme
- ADE: dose dependent proximal tubular nephrotoxicity
- must administer with probencid
50
Foscarnet
- inhibits DNA, RNA, reverse transcriptase without requiring activation by phosphorylation
- broad spectrum
- ADE: nephrotoxicity, hypocalcemia
51
Oseltamivir (Tamiflu)
- competitively and reversibly interacts with active enzyme site to inhibit viral neuraminidase resulting in clumping of newly released virions
- flu a and b
- early administration is crucial - replication peaks at 24-72 hrs
52
Entecavir
- guanosine analog that competitively inhibits all 3 functions of hep B DNA polymerase
- ADE: exacerbation on discontinuation, lactic acidosis, hepatomegaly --> monitor liver function
53
Interferon therapy (pegylated interferon alpha)
- 2 is for hep B and C
- 2b is for hep C
- increases protein kinase which inhibits protein synthesis
- efficacy is enhanced by ribavirin
- ADE: flu-like sx, neutropenia
54
Ribivirin
- used in combo with interferon
- guanosine nucleotide analog
- ADE: VERY TOXIC pts should not conceive children for 6 months after stopping and healthcare workers exposed may have effects (HA, conjunctivitis, rhinitis, nausea)
55
Simeprevir
- tx for HVC genotype 1 in combo with peginterferon and ribivirin
- protease NS3/4A inibitor
- dont give with CYP3A4 inducers
- ADE: anemia, hepatotoxicity, fatigue
56
Daclastasvir
- NS5A inhibitor that affects replication and viral assembly
- tx of HCV
57
Ledipasvir
- NS5A inhibitor that affects replication and viral assembly
- tx of HCV
- very expensive
58
Ombitasvir
- NS5A inhibitor that affects replication and viral assembly
- tx of HCV
59
Sofosbuvir
- nucleotide polymerase inhibitor resulting in chain termination
- hep C
- administration with amioderone is not recommended d/t symptomatic bradycardia and fatal cardiac arrest
60
Dasabuvir
- non-nucleoside polymerase inhibitor that prevents viral replication
- less potent, best for genotype 1
- primarily used as an adjunct
61
Ritonavir
- protease inhibitor used in HIV that is used off label as a pharmacokinetic booster bc it is a strong CYP3A4 inhibitor
62
Raltegravir
- integrase strand transfer inhibitor
| - ADE: increase in creatine kinase, insomnia, HA, diarrhea, nausea
63
Maraviroc
- MOA: binds to host cell CCR5 receptor to block binding of viral gp120
- tropism testing required to ensure virus uses the CCR5 receptor
- substrate of CYP3A4
- ADE: URI, hepatotoxicity, hypotension, MI
64
Abacavir
- nucleoside reverse transcriptase inhibitor, competitive inhibition, require phosphorylation, require host kinases
- less active as single agents that other classes
- useful in resistant strains
- ADE: mitochondrial toxicity, lactic acidosis, hypersensitivity
65
Tenofovir
- nucleotide reverse transcriptase inhibitor, competitive inhibition, require phosphorylation, require host kinases
- ADE: mitochondrial toxicity, lactic acidosis,
66
Zidovudine
- nucleoside reverse transcriptase inhibitor, thymidine analog, competitive inhibition, require phosphorylation, require host kinases
- ADE: mitochondrial toxicity, lactic acidosis, insulin resistance. dyslipidemia, bone marrow suppression
67
Zidovudine
- nucleoside reverse transcriptase inhibitor, thymidine analog, competitive inhibition, require phosphorylation, require host kinases
- ADE: mitochondrial toxicity, lactic acidosis, insulin resistance. dyslipidemia, bone marrow suppression
- *generally used during labor and delivery to prevent transmission to the fetus and given to newborn for 6 wks*
68
Efavirenz
- non-nucleoside reverse transcriptase inhibitor, binds directly to HIV-1 reverse transcriptase and do not require host enzyme activation
- mixed CYP3A4 inducer/inhibitor
- ADE: *teratogenic*, skin rash, GI upset, CNS effects
69
Didanosine
- nucleoside reverse transcriptase inhibitor
| - ADE: mitochondrial toxicity, lactic acidosis, pancreatitis, peripheral neuropathy
70
Darunavir
- protease inhibitor to prevent HIV mature form
- CYP3A4 substrate
- ADE: hyperglycemia, lipodystrophy (buffalo hump), hepatotoxicity, GI intolerance
71
Ritonavir
- protease inhibitor
- CYP3A4 inhibitor
- used as a booster
- ADE: hyperglycemia, lipodystrophy (buffalo hump), hepatotoxicity, GI intolerance
72
Delavirdine
- non-nucleoside reverse transcriptase inhibitor, binds directly to HIV-1 reverse transcriptase and do not require host enzyme activation
- CYP3A4 inhibitor
- skin rash, GI upset
73
Cobicistat
- CYP3A4 inhibitor not active against HIV used to boost levels of other drugs
74
General ART
- 2 NRTI + protease inhibitor OR NNRTI
75
Latanoprost
- prostaglandin analog
- MOA: PGF2a analog that lowers IOP by facilitating aqueous outflow through accessory uveoscleral outflow
- caution: macular edema, bacterial keratitis
- ADE: may cause pigmentation of the iris, eyelash changes
- often first line therapy
76
Timolol and Betaxolol
- beta blocker
- MOA: inhibit the production of aqueous humor by decreasing intracellular cAMP
- Uses: glaucoma
- ADE: bradycardia, heart failure, depression, blurred vision, burning sensation
77
Acetazolamide, Dorzolamide, Brinzolamide
- CA inhibitor
- MOA: reduces formation of bicarb and reduces fluid transportation to decrease IOP
- Uses: glaucoma
- ADE: allergic reactions (sulfonamide related), abnormal taste, burning in eye, conjunctivitis
78
Dipiverfin (B2) and Brimonidine (A2)
- sympathomimetic
- MOA: decreases IOP by increasing uveoscleral outflow via beta 2
- ADE: hyperemia, systemic effects
79
Pilocarpine
- cholinergic agonist
- MOA: stimulates muscarinic receptors which increase outflow of aqueous fluid
- CI: cardiac failure, parkinson's, peptic ulcer disease
- ADE: clouding of corneal stroma, retinal detachment
- not commonly used
80
Cyclopentolate
- muscarinic antagonist
- MOA: causes mydriasis and paralysis of accommodation
- uses: angle closure glaucoma d/t anterior lens displacement, and to visualize internal structures of the eye
81
Phenylephrine
- sympathomimetic agent
| - MOA: alpha agonist that causes mydriasis
82
Dexamthasone and Prednisolone
- glucocorticoid
- MOA: anti-inflammatory
- uses: post operatively, age-related macular degeneration, do not use more than a week
ADE: cataracts, secondary infection, secondary open angle glaucoma, increase in IOP (all from long term use)
83
Olopatadine
- antihistamine
84
Antimuscarinic toxidrome
- fever, tachycardia, mydriasis, cycloplegia, flushing, dry skin, agitation, hallucinations, constipation
- antidote: physostigmine
- will not cause a change in BP
85
AChE inhibitors toxidrome
- increased BP, muscle fasciculations leading to paralysis, diaphoretic, pale, hyperkalemia
- atropine and pralidoxime
86
Insulin and potassium
- insulin shifts potassium into cells so can cause hypokalemia
87
Insulin and potassium
- insulin shifts potassium into cells so can cause hypokalemia
88
Iron
- antidote: deferoxamine
- sx: acute - necrotizing gastroenteritis, n/v, bloody diarrhea, shock, metabolic acidosis, hepatotoxicity
- iron is radiopaque
- some pts get sx from immune response to antidote --> histamine release and vasodilation
89
Lead
- antidote: BAL (dimercaprol), calcium disodium EDTA (after levels are lowered), succimer
- increased delta-ALA excreted in urine, less heme produced
- sx: fatigue, abdominal pain, anemia
- sources: paint, plumbing, imported food packaging, moonshine
90
Cyanide
- nitrate, sodium thiosulfate, hydroxocobalamin
- sx: HA, nausea, dyspnea, metabolic acidosis, hypotension, syncope, bitter almond odor
- suspect when: sudden collapse in lab, fire victim, artificial nail remover, *peach pit*, prolonged nitroprusside
- want to induce methemoglobinemia with sodium nitrite
