Random pharmacology Flashcards

1
Q

Fulvestrant

A
  • A “pure” estrogen antagonist

- Associated with a much lower risk of causing endometrial pathology, including cancer than raloxifene or toremifene

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2
Q

Ranolazine

A
  • MECHANISM: inhibits late phase of sodium current thereby reducing diastolic wall tension and oxygen consumption; does not affect HR or contractility
  • CLINICAL USE: angina refractory to other medical therapies
  • ADVERSE EFFECTS: constipation, dizziness, headache, nausea, QT prolongation
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3
Q

Cinacalcet

A
  • MECHANISM: sensitizes Ca2+ sensing receptor (CaSR) in parathyroid gland to circulating Ca2+, leads to decrease in PTH
  • CLINICAL USE: primary or secondary hyperparathyroidism
  • ADVERSE EFFECTS: hypocalcemia
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4
Q

Orlistat

A
  • MECHANISM: inhibits gastric and pancreatic lipase and leads to a decrease in breakdown and absorption of dietary fats
  • CLINICAL USE: weight loss
  • ADVERSE EFFECTS: steatorrhea, decreased absorption of fat-soluble vitamins
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5
Q

Ursodiol (ursodeoxycholic acid)

A
  • MECHANISM: nontoxic bile acid that increases bile secretion and decreases cholesterol secretion and absorption
  • CLINICAL USE: primary biliary cirrhosis, gallstone prevention or dissolution
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6
Q

Cladribine

A
  • MECHANISM: purine analog that works through multiple mechanisms (eg inhibition of DNA polymerase, DNA strand breaks); an antimetabolite
  • CLINICAL USE: hairy cell leukemia
  • ADVERSE EFFECTS: myelosuppression, nephrotoxicity, neurotoxicity
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7
Q

Cytarabine (arabinofuranosyl cytidine)

A
  • MECHANISM: pyrimidine analog that leads to the inhibition of DNA polymerase; an antimetabolite
  • CLINICAL USE: leukemias (AML), lymphomas
  • ADVERSE EFFECTS: myelosuppression with megaloblastic anemia (“CYTarabine causes panCYTopenia”)
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8
Q

Nitrosureas (carmustine, lomustine, semustine, streptozocin)

A
  • MECHANSIM: requires bioactivation; works as an alkylating agent; crosses blood brain barrier into the CNS where it crosslinks DNA
  • CLINICAL USE: brain tumors (including glioblastoma multiforme)
  • ADVERSE EFFECTS: CNS toxicity (convulsions, dizziness, ataxia)
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9
Q

Erlotinib

A
  • MECHANISM: EGFR tyrosine kinase inhibitor
  • CLINICAL USE: non-small cell lung cancer
  • ADVERSE EFFECTS: rash
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10
Q

Cetuximab

A
  • MECHANISM: monoclonal antibody against EGFR
  • CLINICAL USE: stage IV colorectal cancer (wild-type KRAS), head and neck cancer
  • ADVERSE EFFECTS: rash, elevated LFTs, diarrhea
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11
Q

Vemurafenib

A
  • MECHANISM: small molecule inhibitor of BRAF oncogene (+) melanoma
  • CLINICAL USE: metastatic melanoma
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12
Q

Leflunomide

A
  • MECHANISM: reversibly inhibits dihydroorate dehydrogenase, preventing pyrimidine synthesis; suppresses T cell proliferation
  • CLINCIAL USE: rheumatoid arthritis, psoriatic arthritis
  • ADVERSE EFFECTS: diarrhea, hypertension, hepatotoxicity, teratogenicity
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13
Q

Teriparatide

A
  • MECHANISM: recombinant PTH analog given subcutaneously daily, increases osteoblastic acitivity
  • CLINICAL USE: osteoporosis; causes increase in bone growth compared to antiresorptive therapies (eg bisphosphonates)
  • ADVERSE EFFECTS: transient hypercalcemia
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14
Q

Etanercept

A
  • MECHANISM: TNF-alpha inhibitor; fusion protein (receptor for TNF-alpha + IgG1, Fc), produced by recombinant DNA; acts as a TNF decoy receptor
  • CLINICAL USE: rheumatoid arthritis, psoriasis, ankylosing spondylitis
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15
Q

Infliximab, adalimumab

A
  • MECHANSIM: TNF-alpha inhibitor; anti-TNF-alpha monoclonal antibody
  • CLINICAL USE: inflammatory bowel disease, rheumatoid arthritis, psoriasis, ankylosing spondylitis
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16
Q

Rasburicase

A
  • MECHANISM: recombinant uricase that catalyzes metabolism of uric acid to allantoin
  • CLINICAL USE: prevention and treatment of tumor lysis syndrome
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17
Q

Cyclobenzaprine

A
  • MECHANISM: centrally acting skeletal muscle relaxant; structurally related to TCAs, similar to anticholinergic side effects
  • CLINICAL USE: muscle spasms
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18
Q

Varenicline

A
  • Atypical antidepressant
  • Nicotinic ACh receptor partial agonist
  • Used for smoking cessation
  • TOXICITY: sleep disturbance
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19
Q

Clomiphene

A
  • Selective estrogen receptor modulator
  • Antagonist at estrogen receptors in hypothalamus
  • Prevents normal feedback inhibition and increases release of LH and FSH from pituitary, which stimulates ovulation
  • Used to treat infertility due to anovulation (eg PCOS)
    May cause hot flashes, ovarian enlargement, multiple simultaneous pregnancies, visual disturbances
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20
Q

Tamoxifen

A
  • Selective estrogen receptor modulator
  • Antagonist at breast
  • Agonist at bone, uterus
  • Increase risk of thromboembolic events and endometrial cancer
  • Used to treat and prevent recurrence of ER/PR (+) breast cancer
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21
Q

Raloxifene

A
  • Selective estrogen receptor modulator
  • Antagonist at breast, uterus
  • Agonist at bone
  • Increase risk of thromboembolic events but no increased risk of endometrial cancer (vs tamoxifen)
  • Used primarily to treat osteoporosis
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22
Q

Anastrozole, letrozole, exemestane

A
  • Aromatase inhibitor
  • MECHANISM: inhibit peripheral conversion of androgens to estrogens
  • CLINICAL USE: ER(+) breast cancer in postmenopausal women
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23
Q

Mifepristone, ulipristal

A
  • Antiprogestin
  • MECHANISM: competitive inhibitors of progestins at progesterone receptors
  • CLINICAL USE: termination of pregnancy (mifepristone with misoprostol); emergency contraception (ulipristal)
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24
Q

Terbutaline, ritodrine

A
  • Beta-2 agonists that relax the uterus

- Used to decrease contraction frequency in women during labor

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25
Q

Danazol

A
  • MECHANISM: synthetic androgen that acts as partial agonist at androgen receptor
  • CLINICAL USE: endometriosis, hereditary angioedema
  • ADVERSE EFFECTS: weight gain, edema, acne, hirsutism, masculinization, decreased HDL levels, hepatotoxicity
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26
Q

Minoxidil

A
  • MECHANISM: direct arteriolar vasodilator

- CLINICAL USE: androgenetic alopecia, severe refractory hypertension

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27
Q

Bosentan

A
  • Pulmonary hypertension drug
  • MECHANISM: competitively antagonizes endothelin-1 receptors which leads to a decrease in pulmonary vascular resistance
  • CLINICAL NOTES: hepatotoxic (monitor LFTs)
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28
Q

Sildenafil

A
  • MECHANISM: inihibits cGMP PDE-5 and prolongs vasodilatory effect of NO
  • CLINICAL NOTES: used for pulmonary hypertension as well as erectile dysfunction
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29
Q

Epoprostenol, iloprost

A
  • Pulmonary hypertension drug
  • MECHANISM: PGI2 (prostacyclin) with direct vasodilatory effects on pulmonary and systemic arterial vascular beds, also inhibits platelet aggregation
  • ADVERSE EFFECTS: flushing, jaw pain
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30
Q

Fluticasone, budesonide

A
  • Inhaled corticosteroids used for asthma
  • Inhibit synthesis of virtually all cytokines
  • Inactivate NF-KB , the transcription factor that induces production of TNF-alpha and other inflammatory agents
  • 1st line therapy for chronic asthma
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31
Q

Omalizumab

A
  • Anti-IgE monoclonal therapy for asthma
  • Binds mostly unbound serum IgE and blocks binding to FcERI
  • Used in allergic asthma with increased IgE levels resistant to inhaled steroids and long acting beta-2 agonists
  • ADVERSE EFFECTS: anaphylaxis (mostly occurs on initial dose)
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32
Q

Tesamorelin

A
  • GHRH analog

- Used to treat HIV-associated lipodystrophy

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33
Q

Glycyrrhetic acid

A

Inhibits aldosterone synthase, which normally converts corticosterone to aldosterone and cortisol to cortisone

34
Q

Pegvisomant

A

Growth hormone receptor antagonist used to treat acromegaly

35
Q

Hyoscyamine, dicyclomine

A
  • Muscarinic antagonist
  • GI
  • Antispasmodic for irritable bowel syndrome
36
Q

Oxybutynin, solifenacin, tolterodine

A
  • Muscarinic antagonist
  • Genitourinary
  • Reduce bladder spasm and urge urinary incontinence (overactive bladder)
37
Q

Adverse effects of non-dihydropyridine Ca2+ blockers

A
  • Cardiac depression
  • AV block
  • Hyperprolactinemia
  • Constipation
38
Q

Adverse effects of dihydropyridine Ca2+ blockers

A
  • Peripheral edema
  • Flushing
  • Dizziness
  • Gingival hyperplasia
39
Q

Pindolol and acebutolol

A

Partial β agonists contraindicated in angina

40
Q

Which lipid lowering agent is associated with hyperuricemia

A

Niacin (B3)

41
Q

Which lipid-lowering agents ↑ triglycerides

A

Bile acid resins (cholestyramine, colestipol, colesevelam)

42
Q

Adverse effects of thionamides

A
  • Skin rash
  • Agranulocytosis
  • Aplastic anemia
  • Hepatotoxicity
  • Methimazole is a possible teratogen (can cause aplasia cutis)
43
Q

GH used to treat

A
  • GH deficiency

- Turner syndrome

44
Q

What does CUSHINGOID stand for

A
  • C → cataracts
  • U → ulcers
  • S → striae, skin thinning
  • H → hypertension, hirsutism
  • I → immunosuppression, infection
  • N → necrosis of femoral heads
  • G → glucose elevation
  • O → osteoporosis, obesity
  • I → impaired wound healing
  • D → depression/ mood changes
45
Q

Fludricortisone can cause what skin changes

A

Those associated with glucocorticoids + hyperpigmentation

46
Q

Adverse effects of proton pump inhibitors

A
  • ↑ risk of C difficile infection
  • Pneumonia
  • ↓ serum Mg2+ with long term use
47
Q

Adverse effects of aluminum hydroxide

A
  • Constipation and hypophosphatemia
  • Proximal muscle weakness
  • Osteodystrophy
  • Seizures
48
Q

Adverse effects of calcium carbonate

A
  • Hypercalcemia (milk-alkali syndrome)

- Rebound acid ↑

49
Q

Adverse effects of magnesium hydroxide

A
  • Diarrhea
  • Hyporeflexia
  • Hypotension
  • Cardiac arrest
50
Q

Adverse effects of sulfasalazine

A
  • Malaise
  • Nausea
  • Sulfonamide toxicity
  • Reversible oligospermia
51
Q

Adverse effects of ondansetron

A
  • Headache
  • Constipation
  • QT prolongation
52
Q

Adverse effects of ADP receptor inhibitors

A
  • Neutropenia (ticlopidine)

- TTP

53
Q

Cilostazol, dipyridamole

A
  • MECHANISM: phosphodiesterase III inhibitor; ↑ cAMP in platelets, resulting in inhibition of platelet aggregation; vasodilators
  • CLINICAL USE: intermittent claudication, coronary vasodilation, prevention of stroke or TIAs (combined with aspirin), angina prophylaxis
  • ADVERSE EFFECTS: nausea, headache, facial flushing, hypotension, abdominal pain
54
Q

Azathioprine and 6-mercaptopurine are activated by what enzyme

A

HGPRT

55
Q

Clinical use of azathioprine and 6-mercaptopurine

A
  • Preventing organ rejection, rheumatoid arthritis, IBD, SLE

- Used to wean patients off steroids in chronic disease and to treat steroid-refractory chronic disease

56
Q

Hemorrhagic cystitis caused by cyclophosphamide and isofamide can be prevented with what

A

Mesna and N-acetylcysteine. Thiol group binds to toxic metabolites.

57
Q

Used for treatment of c-KIT GI stromal tumors

A

Imantib

58
Q

Clinical uses of rituximab

A
  • Non-Hodgkin lymphoma
  • CLL
  • ITP
  • Rheumatoid arthritis
59
Q

Mannitol

A
  • MECHANISM: osmotic diuretic; ↑ tubular fluid osmolarity → ↑ urine flow, ↓ intracranial/ intraocular pressure
  • CLINICAL USE: drug overdose, elevated intracranial/intraocular pressure
  • ADVERSE EFFECTS: pulmonary edema, dehydration
  • Contraindicated in anuria, HF
60
Q

Contraindications of mannitol

A
  • Anuria

- HF

61
Q

Loop diuretics have what effect on the medulla

A

Abolish hypertonicity of medulla, preventing concentration of urine

62
Q

Loop diuretics stimulate release of

A

Stimulate PGE release (vasodilatory effect on afferent arteriole)

63
Q

What effect do loop diuretics have on Ca2+

A

↑ Ca2+ excretion

64
Q

Adverse effects of loop diuretics

A
  • Ototoxicity
  • Hypokalemia
  • Dehydration
  • Allergy (sulfa)/ metabolic Alkalosis
  • Nephritis (interstitial)
  • Gout

“OH DANG”

65
Q

What toxicity is more pronounced in ethacrynic acid than loop diuretics in general

A

Ototoxicity

66
Q

Potassium sparing diuretics

A
  • Spironolactone and eplerenone; triamterene and amilioride
  • Spironolactone and eplerenone → competitive aldosterone receptor antagonists in cortical collecting tubule
  • Tiramterene and amiloride → act at the same part of the tubule by blocking Na+ channels in the cortical collecting tubule
67
Q

Diuretics that ↓ pH

A
  • Carbonic anhydrase inhibitors: ↓ HCO3- reabsorption
  • K+ sparing: aldosterone blockade prevents K+ secretion and H+ secretion → hyperkalemia additionally leads to K+ entering all cells (via H+/K+ exchanger) in exchange for H+ exiting cells
68
Q

Diuretics that ↑ pH

A

Loop diuretics and thiazides cause alkalemia through several mechanisms

  • Volume contraction → ↑ AT II → ↑ Na+/H+ exchanger in PCT → ↑ HCO3- reabsorption (“contraction alkalosis”)
  • K+ loss leads to K+ exiting all cells (via H+/K+ exchanger) in exchange for H+ entering cells
  • In low K+ states, H+ (rather than K+) is exchanged for Na+ in cortical collecting tubule → alkalosis and “paradoxical aciduria”
69
Q

Adverse effects of ACE inhibitors

A
  • Cough
  • Angioedema (↑ bradykinin; contraindicated in C1 esterase inhibitor deficiency)
  • Teratogen (fetal renal malformations)
  • ↑ Creatinine (↓ GFR by preventing ATII mediated constriction of efferent arterioles)
  • Hyperkalemia
  • Hypotension
  • Used with caution in bilateral renal artery stenosis because ACE inhibtors will further ↓ GFR → renal failure
70
Q

Angiotensin II receptor blockers

A

Losartan, candesartan, valsartan

71
Q

Clinical use of leuprolide

A
  • Uterine fibroids
  • Endometriosis
  • Precocious puberty
  • Prostate cancer
  • Infertility
72
Q

Name estrogens

A
  • Ethinyl estradiol
  • DES
  • Mestranol
73
Q

Clinical use of estrogens

A
  • Hypogonadism or ovarian failure
  • Menstrual abnormalities
  • Hormone replacement therapy in postmenopausal women
  • Use in men with androgen dependent prostate cancer
74
Q

Adverse effects of estrogens

A
  • ↑ risk of endometrial cancer
  • Bleeding in postmenopausal women
  • Clear cell adenocarcinoma of vagina in females exposed to DES in utero
  • ↑ risk of thrombi
75
Q

Name progestins

A
  • Levonorgestrel
  • Medroxyprogesterone
  • Etonogestrel
  • Norethindrone
  • Megestrol
76
Q

Mechanism of progestins

A
  • Bind progesterone receptors
  • ↓ growth and ↑ vascularization of endometrium
  • Thicken cervical mucus
77
Q

Progestin challenge

A

Presence of withdrawal bleeding excludes anatomic defects (eg Asherman syndrome) and chronic anovulation without estrogen

78
Q

Mechanism of combined contraception

A
  • Estrogen and progestins inhibit LH/FSH and thus prevent estrogen surge
  • No estrogen surge → no LH surge → no ovulation
  • Progestins cause thickening of cervical mucus, thereby limiting access of sperm to uterus
  • Progestins also inhibit endometrial proliferation → endometrium is less suitable to the implantation of an embryo
79
Q

What can stimulate anabolism to promote recovery after burn or injury

A

Testosterone or methyltestosterone

80
Q

What causes premature closure of epiphyseal plates

A

Testosterone or methyltestosterone

81
Q

Used for PCOS to reduce androgenic symptoms

A

Ketoconazole → inhibits steroid synthesis (17,20-desmolase)

Spironolactone → inhibits steroid binding, 17alpha-hydroxylase, and 17,20-desmolase

82
Q

Minoxidil

A
  • MECHANISM: direct arteriolar vasodilator

- CLINICAL USE: androgenetic alopecia, severe refractory hypertension