Drugs to Know Exam 3 Flashcards
(138 cards)
1
Q
Actions of Angiotensin II
A
- raises BP by vasoconstriction and increased aldosterone biosynthesis and renal actions
- vasoconstriction –> increased stroke volume, cardiac output which increases systolic BP, constricts arterioles which increases diastolic BP
- aldosterone –> increases # of Na/K pump and Na channels in collecting tubule –> increasing Na and water reabsorption
- chronically active in HTN
2
Q
Aliskiren
A
- MOA: direct renin inhibitor
- Uses: currently only indicated in HTN
- ADE: hypokalemia, teratogenesis
3
Q
ACE inhibitors (-pril, -prilat)
A
- MOA: inhibit synthesis of angiotensin II
- Uses: first line in HTN, can be given in CHF
- ADE: hyperkalemia, hypotension (give low initial dose), angioedema, dry cough, decreased GFR avoid in renal artery stenosis pts
- Not used in MI
- Enalapril, Captopril, Lisinopril
- increase bradykinin
4
Q
Losartan and Valsartan
A
- MOA: angiotensin II receptor blockers
- Uses: same effect as ACE inhibitors but less side effects, CHF, MI
- ADE: hypotension and hypokalemia
- if pt has cough on ACE-I, switch to ARB
5
Q
Prostaglandins, ACE-I/ARB’s and NSAIDs
A
- Prostaglandins are vasodilatory at the afferent arteriole
- ACE-I/ARB causes dilation of the efferent arteriole, but GRF can be maintained by dilation of the afferent by PG
- NSAIDs block production of PG’s and will reduce GFR and urine output if pt is also on an ACE-I
- can cause hypertension or diuretic failure
6
Q
Verapamil and Diltiazem
A
- L-type Ca channel blockers with effects on cardiomyocytes
- *contraindicated in heart failure bc they decrease contractility and HR
- “VD brakes heart”
- also contraindicated in AV conduction defects
7
Q
Vascular smooth muscle contraction occurs when:
A
- increased intracellular Ca (bind calmodulin)
- Norepinephrine
- Angiotensin II
8
Q
Relaxation of vascular smooth muscle occurs when:
A
- decreased intracellular Ca
- cAMP inhibits MLCK
- cGMP activates MLC phosphatase
9
Q
Nifedipine and Amiodipine
A
- block Ca in smooth muscle of vasculature leading to relaxation of arterial smooth muscle but not venous
- causes a reflex increase in HR
- contraindicated in cardiac failure (but not as bad as VD)
10
Q
Acetazolamide
A
- carbonic anhydrase inhibitor
- works in proximal convoluted tubule (where 65% of Na is reabsorbed) to block CA which breaks down carbonic acid, so there is no H+ for the Na/H exchanger (NHE 3) so Na is not reabsorbed
- ADE: bicarb is depleted, metabolic acidosis, hypolakemia
- Uses: altitude sickness, restore acid-base balance, only used for diuretic if metabolic alkalosis is also present
- weak diuretic
11
Q
Furosemide and Ethacrynic Acid
A
- loop diuretic
- work in thick ascending loop by blocking the NKCC symporter
- Uses: manage hypercalcemia
- ADE: volume depletion, hypotension, hypokalemia, hypocalcemia, hypomagnesium, hyperuricemia resulting in gout, ototoxic
- NSAIDs can decrease response d/t decreased RBF
- strong diuretic
12
Q
Hydrochlorothiazide
A
- thiazide diuretic
- inhibit NCCT in distal tubule
- Uses: HTN, nephrogenic diabetes insipidus
- ADE: hypokalemia and hypomagnesemia, hypercalcemia, hyperuricemia
- only use in pts with good kidneys
- ** do not use with and anti-arrhythmic that prolongs QT interval –> Torsades de pointes
- average diuretic
13
Q
Amiloride and Triamterene
A
- K+ sparing diuretic
- block ENaC in the collecting tubule, preventing K loss
- ADE: acidosis and hyperkalemia
- DI: additive with other K sparing drugs
- weak diuretic
14
Q
Spironolactone
A
- aldosterone antagonist
- Uses: edema from heart failure, HTN, heart failure, hyperaldosteronism
- ADE: hyperkalemia, acidosis, gynecomastia
- DI: additive with other K sparing drugs (ACE-I, ARB, amiloride), non-steroidal anti-inflammatory drugs
15
Q
Mannitol
A
- osmotic
- acts mostly in proximal tubule, thin descending limb where water is permeable and prevents reabsorption
- Uses: reduce intraocular pressure, reduce intracranial pressure
- ADE: hypotension, confusion, HA, dehydration
- strong diuretic
16
Q
Vasopressin and Desmopressin
A
- vasopressin analogs
- Uses: diabetes insipidus
- ADE: water intoxication, increased BP, cardiac output, MI, hyponatremia, thrombotic risk
17
Q
Tolvaptan
A
- vasopressin antagonist
- uses: euvolemic and hypervolemic hyponatremia
- ADE: hypotenision, hypovolemia, hepatotoxic
18
Q
Phentolamine
A
- alpha antagonist
- first dose syncope, reflex tachycardia, edema
- don’t use with a PDE5 inhibitor
19
Q
Doxazosin
A
- alpha 1 antagonist
- first dose syncope, reflex tachycardia, edema
- don’t use with a PDE5 inhibitor
20
Q
Carvedilol and Labetolol
A
- alpha/beta antagonists
- contraindicated: decompensated heart failure, asthma, 2/3 degree AV block, sick sinus syndrome, bradycardia, cardiogenic shock, severe hepatic impairment
21
Q
Hydralazine
A
- direct vasodilator
- *can be used in pregnancy –> eclampsia
- used in combo with nitrates in heart failure
- not a first line agent, but used in pts who cannot use ACE-I
22
Q
Minoxidol
A
- direct vasodilator
- ADE: hypertrichosis (used for hair growth)
23
Q
Fenoldopam
A
- dopamine agonist
- dilates renal arteries
- used in severe hypertension
24
Q
Nitroglycerin and isosorbide mononitrate
A
- NO donor
- advantages: reduces preload more than afterload and improves myocardial oxygen supply
- disadvantages: tolerance develops quickly leading to dependence and withdrawal
- ADE: HA, reflex tachycardia, postural hypotension
- uses: angina, heart failure
- contraindications: pts on PDE5 inhibitors, hypotension, severe brady or tachycardia
25
Nitroprusside
- NO donor
- causes arterial and venous dilation from NO
- use: hypertensive emergency
- contraindications: compensatory hypertension, increased intracranial pressure
- monitor: cyanide and metHB --> cyanide toxicity at higher risk in hepatic impairment
26
Nesiritide
- NP analog
| - used in acute decompensated heart failure
27
Sacubitril
- Neprilysin inhibitor
| - increases bradykinin
28
Cilostazol
- PDE3 inhibitor
- increases intracellular cAMP
- used for peripheral vascular disease
29
Sildenafil, Tadalafil
- PDE5 inhibitors
- prevent the hydrolysis of cGMP to GMP to produce relaxation
- uses: erectile dysfunction, BPH and PAH
- ADE: hypotension, priapism, tachycardia, chest pain, MI
30
Milrinone
- PDE3 inhibitor, increases intracellular cAMP
| - used for inotropism
31
Alprostadil
- prostaglandin
| - used for erectile dysfunction
32
Epoprostanol
- prostaglandin
| - used for PAH
33
Bosentan and Macitentan
- Endothelin antagonists
| - used for PAH
34
Dobutamine
- B1>B2
- treatment of heart failure and cardiogenic shock
- significant increases in cardiac output
35
Procainamide and Quinidine
- class Ia Na channel blockers and decrease vagus
- slow/block phase 0 of action potential, increase refractory period, increase AP duration, decrease HR
- on EKG: increased QRS and QT
- used in ventricular tachycardia and A fib
- antimuscarinic effects may increase conduction through AV node
36
Amiodarone
- K channel blocker, also Na, B1, and Ca channels
- slow repolarization, prolong QT interval but torsades de pointes rare
- used in Afib/flutter, SVT, VT/VF, LVH, heart failure, post MI
- ADE: may mess with thyroid, inhibits CYP 3A4, smurf skin, optic neuritis, halo vision
- contraindicated: pts with cardiogenic shock, heart block, iodine allergy
- long half life
37
Ibutilide
- K channel blocker
- slow repolarization, prolong QT interval
- used to terminate Afib/flutter
- ADE: torsades de pointes may result
38
Adenosine
- slows SA nodal firing by opening K channels and hyperloarizing
- stops and restarts heart
39
Digoxin
- blocks Na/K ATPase, increases vagal tone, suppresses AV nodal conduction --> increases contractility and slows AV
- uses: control ventricular response in SVT and in pts with heart failure
- toxicity: less negative resting membrane leads to increased ectopy and DAD d/t increased intracellular Ca
40
Class II - beta blockers
- depress SA node, slow conduction through AV node
- prolong PR interval
- use: ventricular and SVT, slowing ventricular rate during A fib and flutter
41
Magnesium sulfate
- treatment of torsade de pointes caused by class Ia, III drugs which prolong the QT interval
42
Magnesium sulfate
- treatment of torsade de pointes caused by class Ia, III drugs which prolong the QT interval
43
Treatment of A fib
- 1: B-blocker - contraindicated by heart failure, hypotension, heart block
- 2: CCB (verapamil, diltiazem)
- 3: amioderone for pts with heart failure
- 4: digoxin for pts with heart failure
44
Wolf-Parkinson-White syndrome
- ventricular tissue also receives impulses from an accessory pathway (bundle of Kent)
- EKG: wide QRS, complex and short PR interval
45
Diphenhydramine, Hydroxyzine, Meclizine
- First gen H1 histamine inverse agonist
- ADE: sedation, weight gain, impaired cognition, respiratory suppression
- anticholinergic so causes mydriasis (bad in glaucoma)
- alpha 1 block so can cause hypotension
46
Loratadine and Desloratadine
- Second gen H1 histamine inverse agonist
47
Cetirizine, levocetirizine, Fexofenadine
- Second gen H1 histamine inverse agonist
- less CNS penetration so less drowsy and less weight gain than first gen
- can prolong QTc
48
Cimetidine
- H2 blocker to reduce H/H atpase activity
- ADE: CYP inhibitor that inhibits estradiol degradation and testosterone binding to its receptor --> gynecomastia, galactorrhea
- increased risk of pneumonia
49
Famotidine
- H2 blocker to reduce H/H atpase activity
50
Cromolyn
- Mast cell stabilizer
51
Olopatidine
- ophthalmic antihistamine
52
Azelastine
- ophthalmic/intranasal antihistamine
53
*Icatibant*
- Bradykinin antagonist
| - approved for use in hereditary angioedema and can be used for drug induced
54
Scromboid poisoning
- may occur when fish or swiss cheese aren't stored properly
- bacterial histidine decarboxylase converts histidine into histamine
- sx: n/v/d, urticaria, flushing, fever, fish tasted peppery
55
Bradykinin is deactivated by what?
- ACE --> ACE-I will increase bradykinin
56
Drug induced angioedema
- ACE-I
- DPP-IV inibitors
- Neprolysin inhibitors
- signs and symptoms d/t excess bradykinin
57
Alprostadil
- PGE1 agonist
- used for erectile dysfunction
- can be used to maintain patency of ductus arteriosus
58
Misoprostol
- PGE1 agonist
- uses: ulcer prophylaxis, cervical ripening, abortion
- contraindicated in pregnancy because will cause uterine contractions
- ADE: GI cramping and diarrhea
59
Dinoprostol
- PGE2 agonist
| - uses: cervical ripening, uterine contraction, evacuation of uterine content
60
Latanoprost
- PGF2a agonist for ophthalmic use
- increases aqueous humor outflow in cases of open angle glaucoma
- ADE: itchy, red eyes, change eye color, eyelash growth
61
Ketorolac
- COX1 > COX2 inhibitor
| - High risk of GI bleed, do not give for more than 5 days
62
Indomethacin
- COX1 > COX2 inhibitor
63
Aspirin
- irreversibly (unlike others) acetylates cyclooxygenase
- inhibits TXA2 in platelets
- benefits: antipyretic, anti-inflammatory, analgesia, anti-platelet aggregation
- tinnitus is cardinal sign of overdose as well as wide anion gap acidosis
- can cause Reye's syndrome - look for projectile vomiting
64
Naproxen
- COX1 > COX2 inhibitor
65
Meloxicam
- COX2 > COX1 inhibitor
66
Meloxicam
- COX2 > COX1 inhibitor
| - avoid giving in cardiac patients
67
Celecoxib
- COX2 > COX1 inhibitor
| - avoid giving in cardiac patients
68
Acetaminophen
- mechanism unknown
- therapeutic effects at level of CNS: antipyretic, analgesia
- ADE: minimal platelet effect, no respiratory effects, no renal effects
69
*N-acetylcystein*
- antidote to acetaminophen toxicity
70
Zileuton
- LOX inhibitor
71
Zileuton
- Lipooxygenase inhibitor
| - will produce more side effects that the receptor antagonist
72
*Carboprost*
- PGF2a agonist
- Gq coupled
- causes very powerful uterine contractions
* used to control post-partum bleeding*
- ADE: GI cramping and diarrhea
73
Side effects and contraindications of NSAIDs
- ADE: hypertension, diuretic failure, thrombosis
| - contraindications: active GI bleed, bad kidneys, pregnancy (d/t premature closure of ductus arteriosus)
74
Cobalamin/cyanocobalamin/hydroxocobalamin (B12)
- necessary for RBC formation
| - treatment of macrocytic anemia
75
*Erythropoietin*/ darbepoetin
- stimulates bone marrow to make cells
- given in end stage renal disease
- must make sure other ingredients for RBC production are sufficient
- ADE: HTN, thrombotic events and mortality if overshoot Hb/Hct
76
Ferrous sulfate/ iron dextran
- treatment for anemia (hypochromic microcytic)
77
Folic acid
- necessary for RBC formation
| - treatment of macrocytic anemia
78
Figrastim and Pegfilgrastim
- G-CSF analog
- treatment of neutropenias
- ADE: bone pain
79
Clopidogrel
- P2Y12 receptor antagonist
| - ADE: bleeding
80
Eptifibatide
- GPIIb/IIIa antagonist to prevent binding to vWF
- ADE: bleeding
- Contraindications: active bleeding, thrombocytopenia, prior stroke
- Monitor: for signs of bleeding, CBC and platelet count
81
Alteplase
- fibrinolytic
- activates plasmin to bind lysine on fibrin
- contraindications: at risk for major bleeding
- ADE: bleeding
82
Warfarin (Coumadin)
- Vitamin K antagonist
- impacts proteins C and S, 2, 7, 9, 10
- ADE: bleeding
- in those with C/S deficiencies: skin necrosis d/t clotting bc C and S are inactivated first
83
Phytonadione
- warfarin antidote
84
Heparins
- activate antithrombin III to inactivate factor Xa
- work quickly
- ADE: bleeding, osteoporosis for long term use, thrombocytopenia
85
Protamine
- antidote for heparin overdose
86
Rivaroxaban
- oral anti-Xa
- safe in HIT
- lower risk of bleed than warfarin
87
Oral dabigatran
- binds to active site of thrombin reversibly
- thought to result in less bleeding that others
- safe in HIT
88
PT/INR measures
warfarin activity
89
aPTT measures
heparin activity
| recheck 6 hrs after any bolus/ rate change then daily
90
PT/INR measures
warfarin activity
| - increased INR = too much = risk of bleeding
91
Proteins C and S
- endogenous anticoagulants
| - inherited deficiencies lead to excess clotting
92
*Proteins C and S*
- endogenous anticoagulants
| - inherited deficiencies lead to excess clotting
93
Hydrocortisone, Methylprednisolone, Prednisone, Dexamthasone
- glucocorticosteroid
- decreases antibody production and inflammation, inhibits PLA2
- negative feedback from long term use can cause adrenal atrophy
- early ADE: hyperglycemia, HTN, hypokalemia, decreased WBC margination without left shift, immune suppression
- late ADE: weight gain and fat redistribution (cushing), addisonian crisis upon abrupt discontinuation
94
Azathioprine/6MP
- inhibits lymphocyte proliferation by blocking purine synthesis
- metabolized by xanthine oxidase so fatal drug interaction can occur with allopurinol, a XO inhibitor (if you give, monitor CBC and drug levels)
- ADE: myelosuppression, hyperuricemia
95
Methotrexate
- inhibits dihydrofolate reductase interfering with DNA synthesis
- ADE: infection, diarrhea, megaloblastic anemia
96
Cyclosporin and Tacrolimus
- calcineurin inhibitors to block NFAT and reduce IL-2 production and inhibit auto-induction to block T-cell signaling
- ADE: nephrotoxicity, hyperglycemia, risk of infection
97
Sirolimus
- mTOR inhibitor
| - ADE: myelosuppression and risk of infection, nephrotoxic, hyperglycemia
98
Tofacitinib
- JAK3 inhibitor
- Do not give live vaccines while taking
- ADE: risk of infection, dyslipidemia
99
Adalimumab, Etanercept, Infliximab
- TNF-alpha inhibitors (either receptor analogs or antibodies)
- ADE: myelosuppression and risk of infection, risk of malignancy, no live vaccines
100
Rituximab
- anti CD20 antibody
- used in lymphomas
- ADE: infection, HACA abs, infusion reaction
101
Addisonian like state (Steroid discontinuation syndrome)
- hypoglycemia, n/v, ab pain, myalgia, hypotension, hypercalcemia
102
Live vaccines
measles, mumps, rubella, varicella and zoster
103
Rabies post-exposure schedule
- rabies Ig spread around wound immediately
- serial doses of vaccine on days 0, 3, 7 and 14
- must be on time!
104
Tetanus post-wound schedule
- For clean, minor wounds: if have had 3 or more doses of vaccine then nothing, if not/unknown then give Tdap or Td
- For other wounds: if 3 or more known doses then nothing, if not then give Tdap AND TIg
- TIG only used if the primary series or adult 3 doses not done
105
Cytarabine
- S-phase antimetabolite that competitively inhibits DNA polymerase
- single most effective agent against acute myeloid leukemia
- ADE: myelosuppression and pancytopenia
- given by continuous infusion
106
5-Fluorouracil
- S-phase antimetabolite which prevents the synthesis of thymidylate resulting in a thymineless death of cells
- cytotoxicity thought to be a result of combined effects on DNA and RNA mediated events
- leucovorin enhances activity instead of reducing toxicity
107
6-Metacaptopurine
- S-phase antimetabolite that inhibits enzymes of de novo purine nucleotide synthesis
- inactivated by xanthine oxidase so must monitor closely if you are going to also give a XO inhibitor such as allopurinol
108
Methotrexate
- S-phase antimetabolite that is structurally related to DHFR and interferes with DNA, RNA and protein synthesis
- non-proliferating cells are resistant
109
Premetrexed
- S-phase antimetabolite that inhibits thymidylate synthase
- ADE: myelosuppression, rash, mucositis, hand-foot syndrome
- supplement with folic acid and B12 to reduce toxicities
110
Etoposide
- topoisomerase II inhibitor
111
Irinotecan
- topoisomerase I inhibitor so S-phase specific
- dose limiting toxicity is diarrhea with or without neutropenia
- is metabolized to inactive form by glucuronidation so pts with Gilbert's syndrome (defect in UGT1A1 gene) will have a build up of active drug and increased toxicity
112
Paclitaxel
- promotes microtubule assembly resulting in an inability of the spindle to break down, inhibiting mitosis
- ADE: peripheral neuropathy, myalgias, neutropenia
113
Vincristine
- inihibts tubulin polymerization resulting in mitotic arrest during M phase
- metabolized by P450
- dose limiting neurotoxicity expressed as peripheral sensory neuropathy though ortho hypotension, urinary retention, constipation, ataxia, seizures and coma have been observed
114
Bleomycin
- antibiotic that binds to DNA and causes breaks, free radical formation and DNA synthesis inhibition
- cells accumulate in G2
- dose limiting toxicity is pulmonary symptoms
115
Leucovorin
- bypasses DHFR and reduces toxicity of methotrexate without diminishing anti-tumor activity
116
Hydroxyurea
- inhibits ribonucleoside reductase and inhibits DNA synthesis
- has radiation sensitizing activity by maintaining cells in G1-S boundary and interfering with DNA repair
117
Cyclophosphamide
- alkylates reavtive amines, oxygens, or phosphates on DNA
- works on rapidly proliferating tissue
- must be activated by liver to cytotoxic form by CYP450
- releases a nephrotoxic and urotoxic metabolite acrolein which can cause severe hemorrhagic cystitis
- Mesna used to conjugate acrolein in the urine and pts should stay hydrated
- beware of water intoxication
- ADE: carcinogenic, vesicant, toxic effects on reproduction
118
Ifosfamide
- alkylates reavtive amines, oxygens, or phosphates on DNA
- works on rapidly proliferating tissue
- releases a nephrotoxic and urotoxic metabolite acrolein which can cause severe hemorrhagic cystitis
- Mesna used to conjugate acrolein in the urine and pts should stay hydrated
- beware of water intoxication
- ADE: carcinogenic, vesicant, toxic effects on reproduction
119
Carboplatin and Cisplatin
- platinum analogs that work similar to alkylating agents
- extensively cleared by kidney
- toxicity: otoxic, neprhotoxic (cisplatin less toxic of the two)
120
Doxorubicin
- Generates free radicals
- metabolized in liver
- causes irreversible cardiomyopathy
- acute cardiotoxicity: 2-3 days arrhythmias and conduction abnormalities, transient and asymptomatic
- chronic: cardiomyopathy associated with heart failure
121
Busulfran
- alkylates reavtive amines, oxygens, or phosphates on DNA
- works on rapidly proliferating tissue
- causes pulmonary fibrosis
- leukocyte may continue to fall for a month after use is stopped
- ADE: carcinogenic, vesicant, toxic effects on reproduction
122
Alemtuzumab
- CD52
123
Bevacizumab
- VEGF inhiitor
- ADE: risk of bleeding and poor wound healing
- enhances ability of cytotoxics to reach tumor
124
Erlotinib
- EGFR inhibitor
| - diarrhea and rash in 50% of pts
125
Imantinib
- BCR-ABL inhibitor
- ADE: promotes fluid retention leading to edema and peri-orbital swelling
- first kinase inhibitor to be approved
- used in CML with >90% remission rates
126
Rituximab
- CD20
127
Bortezomib
- proteasome inhibitor that induces arrest at G2-M
| * Toxicities: NEUROPATHY*
128
Cardilzomib
- protease inhibitor
129
Tamoxifen
- SERM, competitive inhibitor of estradiol binding to receptor
- antagonistic effects in breast cancer, estrogenic effects on non-breast tissue
- increases risk of thrombotic events with age
- ADE: hot flashes, atrophy of vagina, hair loss, n/v
130
Raloxifene
- SERM
131
Trastuzumab
- HER2/neu
- first monoclonal ab approved for treatment of a solid tumor
- ADE: cardiac failure, fever, chills, nausea, dyspnea
132
Vemurafenib
- BRAF inhibitor
| - 30-60% of patients have cutaneous events
133
Anastrazole
- blocks the function of the armoatase enzyme that converts androgens to estrogens
- generally well tolerated, less effects than tamoxifen with no risk of thrombotic effects
134
Leuprolide
- GnRH analog --> initally FSH/LH rise until they get turned off by feedback loop
135
Cetuximab
- antibody that binds to the extracellular domain of EGFR
| - diarrhea and rash in 50% of pts
136
Thalidomide
- makes flipper babies
| - anti-angiogenic and immunomodulatory
137
Temsirolimus
- mTOR inhibitor
| - ADE: rash, mucositis, anemia, fatigue
138
Side effects common to -mabs
- infusion reactions, HTN, heart failure
