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Drugs Flashcards

1
Q

MOA of mannitol

A

osmotic diuretic - increased tubular fluid osmolarity, producing increase urine flow, decreases intracranial/intraocular pressure
- uses : drug overdose, and increased ICP/IOP

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2
Q

ADE of mannitol

A

pulmonary edema, dehydration,

- CI in anuria and CHF

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3
Q

MOA of Acetazolamide

A

CA inhibitor causing self limited NaHCO3 diuresis and decreases total body HCO3- stores
- uses: glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness, pseudotumor cerebri

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4
Q

ADE of acetazolamide

A

Hyperchloremia metabolic acidosis, parethesias, NH3 toxicity, sulfa allergy

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5
Q

MOA of loop diuretic (furosemide, ethancrynic acid, torsemide)

A

inhibitis NaK2Cl cotransporter in thick ascending limb

  • abolishes hypertonicity of medulla, preventing concentration of urine
  • stimulates PGE release (vasodilatory effect on affferent arteriole)
  • increases Ca excretion (loops lose Ca)
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6
Q

ADE of furosemide

A

OH DANG - otoxicity, hypokalemia, dehydration, allergy (sulfa), nephritis (interstitial), gout

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7
Q

use of ethacrynic acid

A

Diuresis in pts allergic to sulfa drugs. It’s a phenoxyacetic acid derivative.
- NEVER use to treat gout

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8
Q

MOA of HCTZ

A

Thiazide diuretic - inhibits NaCl reabsorption in early distal tubule.

  • decreases diluting capacity of nephron, decreases Ca excretion
  • uses: HTN, CHF, idiopathic hypercalciuria, nephrogenic DI, osteoporosis (saves Ca)
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9
Q

ADE of HCTZ

A

-GLUC
hypokalemia metabolic alkalosis, hyponatremia
- hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia
- sulfa allergy

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10
Q

MOA of Spironolacton and eplerenone

A

competitive aldosterone receptor antagonists in cortical collecting tubule

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11
Q

MOA of triamterene and amiloride

A

block eNa Channels in CCT

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12
Q

ADE of K sparing diuretics

A

Hyperkalemia (can lead to arrhythmias)

Endocrine effects w/ spironolactone (gynecomastia and antiandrogen effects)

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13
Q

Diuretics and effect on urine NaCl

A

all increase urine NaCl except acetazolamide, serum NaCl may decrease as a result

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14
Q

Diuretics and effect on urine K

A
  • increases w/ loop/thiazides

serum K may decrease as a result

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15
Q

Diuretics and effects on blood pH

A
  1. decrease (acidemia) - CA inhibitors and K sparing diuretics
  2. increase (alkalemia) - loop and thiazides
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16
Q

mechanism via which loops/thiazides causes blood alkalemia

A
  1. volume contraction - increases ATII = increases Na/H exchange in PT = increase HCO3- reabsorption
  2. K loss leads to K exiting all cells in exchange for H entering cells
  3. low K state, H is exchanged for Na in cortical collecting tubule = alkalosis and paradoxical aciduria
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17
Q

Diuretics and effects on urine Ca

A
  1. increase in loop b/c of decreased paracellular Ca reabsorption
  2. decrease w/ thiazide - enhanced paracellular Ca reabsorption in DT
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18
Q

MOA of ACE inhibitors

A
  • decreases ATII and GFR by preventing constriction of efferent arterioles.
  • levels of renin increase, prevent inactivation of bradykinin (potent vasodilator)
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19
Q

ADE of ACE inhibitor

A

Cough, Angioedema, Teratogen (renal malformations), increase Creatinine, Hyperkalemia, Hypotension

  • CI in C1 esterase inhibitor deficiency
  • avoid in bilateral renal artery stenosis b/c it will further decrease GFR and lead to renal failure
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20
Q

MOA of ARBs

A

ATII receptor blockers

- no increase in bradykinin so no cough or angioedema

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21
Q

MOA of CCB

A

block voltage dependent L type calcium channels of cardiac and SM = decrease contractility

  • Vascular SM think dihydropyridine
  • Heart think verapamil > dilitazem
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22
Q

What are dihydropyridine CCB’s used for?

A
  1. HTN
  2. Angina - including Prinzmetal
  3. Raynaud
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23
Q

What are the non-dihydropyridine CCB’s used for?

A
  1. HTN
  2. Angina
  3. Atrial fibrillation/flutter
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24
Q

What is Nimodipine used for?

A

Subarachnoid hemorrhage - prevents cerebral vasospasm

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25
Q

ADE of CCBs

A

Cardiac depression, AV block, peripheral edema, flushin, dizziness, hyperPRL, constipation

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26
Q

MOA of Hydralazine

A

Increase cGMP = SM relaxation. Vasodilates arteriole > veins

- decreases afterload

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27
Q

When is hydralazine used?

A

severe HTN, CHF

  • First line therapy for HTN in pregnancy, w/ methyldopa
  • usually co-administered w/ a beta blocker to prevent reflex tachycardia
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28
Q

ADE of hydralazine

A 
Compensatory tachycardia (contraindicated in angina/CAD)
Fluid retention, Nausea, HA, angina, SLE syndrome
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29
Q

What is commonly used to treat hypertensive emergeny?

A

Nitroprusside, nicardipine, clevidipine, labetalol, and fenolodpam

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30
Q

MOA of nitroprusside

A

short acting; increases cGMP via direct release of NO

- worry about cyanide toxicity (treat w/ sulfur)

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31
Q

MOA of fenolodopam

A

D1 receptor agonist = coronary, peripheral, renal, and splanchnic vasodilation
- decreases BP and increases natriuresis

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32
Q

MOA of nitroglycerin and isosorbide dinitrate

A

Vasodilate by increasing NO in vascular SM - increase cGMP and SM relaxation.
- likes to dilate veins&raquo_space; arteries. Decreases preload

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33
Q

uses for nitroglycerin and isosorbide dinitrate

A

angina, acute coronary syndrome, pulmonary edema

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34
Q

ADE of Nitroglycerin and isosorbide nitrate

A
  • reflex tachycardia (treated w/ beta blocker), hypotension, flushing, HA
  • development of tolerance for vasodilating action during work week and loss of tolerance over the weekend leads to tachycardia, dizziness, and HA upon reexposure
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35
Q

What is the goal for antianginal therapy?

A

reduce myocardial O2 consumption by decreasing

  1. EDV
  2. BP
  3. HR
  4. contractility
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36
Q

What effects do nitrates have on the body?

A
  1. decrease EDV, HR, ejection time, MVO2

1. increase contractility and HR - both reflex exposure

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37
Q

What effect do beta blockers have on the body?

A
  1. decrease contractility, BP, HR, MVO2

2. increase EDV and ejection time

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38
Q

What effect do nitrate combined w/ beta blockers have on the body?

A
  1. decrease BP, HR, and MVO2

2. not a huge effect on EDV, contractility, ejection time

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39
Q

What beta blockers are contraindicated in angina?

A

pindolol and acebutolol - both are partial Beta agonists

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40
Q

MOA of statins

A

inhibit conversion of HMG-CoA to mevalonate (cholesterol precursor)

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41
Q

lipid effects of statins

A

decreases LDL mainly
increases HDL
decreases TG

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42
Q

ADE of statins

A 
Liver toxicity (increased LFTS)
rhabdomyolysis (especially when used w/ fibrates and niacin)
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43
Q

MOA of Niacin (vitamin B3)

A

inhibits lipolysis in fat tissue, decreases hepatic VLDL synthesis

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44
Q

lipid effects of niacin

A

decrease LDL and increase HDL

slight decrease in TG

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45
Q

ADE of niacin

A

red, flushed face - decreased by aspirin or long term use
Hyperglycemia (acanthosis nigricans)
Hyperuricemia (worsens gout)

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46
Q

MOA of bile acid resins - cholestryramine, colestipol, colesevelam

A

Prevents intestinal absorption of bile acids; liver must use cholesterol to make more

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47
Q

Lipid effects of bile acid resins

A

decrease LDL

slightly increases HDL and TG

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48
Q

ADE of bile acid resins

A

bad taste, GI discomfort, decreases absorption of fat soluble vitamins, cholesterol gallstones

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49
Q

MOA of ezetimibe

A

prevent cholesterol absorption at small intestine brush border

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50
Q

lipid effects of ezetimibe

A

decreases LDL

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51
Q

ADE of ezetimibe

A

rare increase in LFT, diarrhea

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52
Q

MOA of fibrates (gemfibrozil, clofibrate, bezafibrate, fenofibrate)

A

upregulates LPL = increases TG clearance

- Activates PPAR-alpha to induced HDL synthesis

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53
Q

lipid effects of fibrates

A

decreases TG a lot

decrease LDL, increase HDL

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54
Q

ADE of fibrates

A

myositis, liver toxicity (LFTs), cholesterol gallstones (esp w/ concurrent bile acid resins)

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55
Q

Pharmacokinetics of digoxin

A

75% bioavailable
20-40% protein bound
half life = 40 hours
urinary excretions

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56
Q

MOA of digoxin

A
  • direct inhibition of NaKATPase = indirect inhibition of NaCa exchanger = increases IC Ca => positive inotropy. Stimulates vagus nerve = decreases HR
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57
Q

clinical use of digoxin

A

CHF to increase contractility

Atrial fibrillation - decrease conduction at AV node and depression at SA node

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58
Q

ADE of digoxin

A
  1. cholinergic = N/V, diarrhea, blurry yellow vision
  2. ECG = increase PR, decrease QT, ST scooping, T wave inversion, arrhythmia, AV block
    - hyperkalemia indicates poor prognosis
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59
Q

What factors predispose to digoxin toxicity

A
  1. renal failure = decreased excretion
  2. hypokalemia - allows digoxin to bind to K site at NaKATPase
  3. Verapamil, amiodarone, quinidine (decrease digoxin clearance, displaces it from tissue binding site)
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60
Q

Antidote for digoxin toxicity

A

slowly normalize K, cardiac pacer, anti-digoxin Fab fragments, Mg

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61
Q

What are the classes of antiarrhythmics?

A

No Bad Boys Keep Clean

  • class I - Na channel blockers
  • class II - Beta blockers
  • class III - K channel blockers
  • class IV - CCB
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62
Q

What do type I antiarrhythmics do?

A
  • slow or block conduction especially in depolarized cells
  • decrease slope of phase 0 depolarization and increase threshold for firing of abnormal pacemaker cells
  • hyperkalemia causes increased toxicity for all class I drugs
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63
Q

What are the class IA antiarrhythmics and their toxicities?

A

DQP - disopyramide, quinidine, procainamide

  1. Disopyramide: heart failure
  2. Quinidine - cinchonism
  3. Procainamide - SLE syndrome
    - Thrombocytopenia, torsades de pointes due to increase QT interval
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64
Q

MOA of Class IA antiarrhythmics

A

increase AP duraion, increase ERP, increase QT interval

- used to treat atrial and ventricular arrhythmia especially re-entrant and ectopic SVT and VT

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65
Q

What are the class IB antiarrhythmics and their ADEs?

A
  1. Lidocaine
  2. Mexiletine
  3. Phenytoin
  4. Tocainide
    - CNS stimulation/depression, CV depression
    Lettuce, Tomato, Mayo, Pickles
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66
Q

MOA of class IB antiarrhythmics

A

decrease AP duration

  • perferentially affect ischemic or depolarized Purkinije and ventricular tissue
  • used to treat acute ventricular arrhythmias (especially post MI), digitalis induced arrhythmias
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67
Q

What are the class IC antiarrhythmics and ADEs?

A
  1. Flecainide
  2. Propafenone
    - Fries Please
    - proarrhythmic, especially post MI (contraindicated, also CI in structural and ischemic heart disease)
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68
Q

MOA of Class IC antiarrhytmics

A
  • significantly prolongs refractory period in AV node
  • minimal effect on AP duration
  • used to treat SVTS, including atrial fibrillation
  • last resort in refractory VT
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69
Q

MOA of Class II antiarrhythmics

A

Beta blockers

  • decrease SA and AV nodal activity by decrease cAMP, decreases Ca current. Suppress abnormal pacemakers by decreasing slope of phase 4.
  • AV node is particularly sensitive = increase PR interval
  • esmolol is very short acting
  • used to treat SVT, slowing ventricular rate during atrial fibrillation and atrial flutter
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70
Q

ADE of Class II antiarrythmics

A

impotence, exacerbation of COPD and asthma
- CV effects (bradycardia, AV block, CHF)
- CNS effects (sedation, sleep alterations)
- may mask signs of hypoglycemia.
Metoprolol can causes dyslipidemia
Propranolol can exacerbate vasospasm in Prinzmetal angina.
- Beta blockers are contraindicated in cocaine users (risk of unopposed alpha adrenegic receptor agonist activity).
- treat overdose w/ glucagon

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71
Q

What are you Class III antiarrhythmics

A

Amiodarone, Ibutilide, Dofetilide, Sotalol (AIDS)

- used for atrial fibrillation, atrial flutter, ventricular tachycardia (amiodarone, sotalol)

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72
Q

MOA of class III antiarrhythmics

A

Increase AP duration, increase ERP

  • used when other antiarrhythmics fails
  • increase QT interval
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73
Q

ADE of Sotalol

A

torsades de pointes, excessive beta blockade

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74
Q

ADE of Ibutilide

A

torsade de pointes

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75
Q

ADE of amiodarone

A

pulmonary fibrosis, liver toxicity, hypo/hyperTH - check LFT, PFT, and TFT

  • corneal deposits, skin deposits (blue/gray) resulting in photodermatitis, neuro problems, constipation
  • CV Effects (bradycardia, heart block, CHF)
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76
Q

MOA of class IV antiarrhythmics

A

-Verapamil and dilitiazem
decreases conduction velocity, increase ERP, increase PR interval
- used to prevent nodal arrhythmias, rate control in atrial fibrillation

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77
Q

ADE of class IV antiarrhythmics

A

constipation, flushing, edema,

- CV effects = CHF, AV block, sinus node depression

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78
Q

MOA of adenosine

A

increase K out of cells = hyperpolarizes cell and decreases Ca current.

  • DOC of dx of SVT.
  • Very short acting
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79
Q

ADE of adenosine

A

flushing, hypotension, chest pain

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80
Q

What can block the effects of adenosine?

A

theophylline and caffeine

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81
Q

MOA of Mg

A

effective in torsades de pointes and digoxin toxicity

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82
Q

MOA of leuprolide

A

GnRH analog w/ agonist properties when used in pulsatile fashion
- antagonist when used in continuous fashion = downregulates GnRH receptors in pituitary = decreased FSH and LH

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83
Q

uses of leuprolide

A 
infertility (pulsatile)
Prostate cancer (continuous - use w/ flutamide)
uterine fibroids (continuous)
Precocious puberty (continuous)
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84
Q

ADE of leuprolide

A

antiandrogen, N/V

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85
Q

MOA fo estrogens

A

binds estrogen receptors

  • used for hypogonadism/ovarian failure, menstrual abnormalities, HRT in postmenopausal women,
  • used in men w/ androgen dependent prostate cancer
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86
Q

ADE of estrogens

A

increase risk of endometrial cancer, bleeding in postmenopausal women, clear cell adenocarcinoma of vagina in females exposed to DES in utero, increased risk of thrombi.

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87
Q

What are contraindications for estrogens?

A

ER positive breast cancer, history of DVTs

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88
Q

MOA of clomiphene

A

antagonists at E-receptors in hypothalamus

- prevents normal feedback inhibition and increases release of LF and FSH from pituitary = stimulates ovulation.

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89
Q

What is clomiphene used to treat

A

infertility due to anovulation (PCOS)

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90
Q

ADE of clomiphene

A

hot flashes, ovarian enlargement, multiple simultaneous pregnancies, and visual disturbances

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91
Q

MOA of tamoxifen

A

antagonist on breast tissue

Agonist at uterus and bone - associated w/ endometrial cancer and thromboemolic events

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92
Q

Tamoxifen use

A

treat and prevent recurrences of ER + breast cancer

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93
Q

MOA of raloxifene

A

Agonist on bone - hence used to treat osteoporosis b/c decreases bone resorption
Antagonist at uterus
- worry about thromboembolic events

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94
Q

Uses of hormone replacement therapy

A

relief of prevent menopausal symptoms and osteoporosis

  • unopposed estrogen replacement therapy increases risk of endometrial caner so progesterone is added.
  • possible increased CV risk
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95
Q

MOA of anastrozole/exemestane

A

Aromatase inhibitors used in postmenopausal women w/ breast cancer

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96
Q

MOA of progestins

A

bind progesterone receptors to decrease growth and increase vascularization of endometrium
- used in OCP and treatment of endometrial cancer and abnormal uterine bleeding

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97
Q

MOA of mifepristone

A

competitive inhibitor of progestins at progesterone receptos

- used to terminate pregnancy, usually gived w/ misoprostol (PGE1)

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98
Q

ADE of mifepristone

A

heavy bleeding, GI effects, ab pain

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99
Q

MOA of oral contraceptions

A

E and Progestin inhibit LH/FSH and thus prevent estrogen surge. No E surge = no LH surge = no ovulation.
1. Progestins causes thickening of cervial mucus limiting acess of sperm to uterus. Also inhibits endometrial proliferation, making endometrium less suitable for the implantation of embryo.

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100
Q

what are OCP contraindications

A

Smokers >35 years old, pts w/ history of thromboembolism and stroke, pts w/ history of E-dependent tumor

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101
Q

MOA of terbutaline

A

Beta 2 agonists that relaxes the uterus, used to decrease contractions frequency in women during labor

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102
Q

MOA of Danazol

A

synthethic androgen that acts as partial agonist at androgen receptors
- used to treat endmetriosis and hereditary angioedema

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103
Q

ADE of danazol

A

wt gain, edema, acne, hirsutism, masculinization, decreased HDL levels, liver toxicity

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104
Q

MOA of Testosterone and methylT

A

agonist at androgen receptors
- treats hypogonadism and promotes development of secondary sexual characteristics, stimulates anabolism to promote recovery after burn or injury

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105
Q

ADE of T and methyl-T

A

causes masculinization of females

  • decreases intratesticular T in males by inhibiting release of LH (via negative feedback) = gonadal atrophy
  • premature closure of epiphyseal plates
  • increases LDL and decreases HDL
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106
Q

MOA of finasteride

A

5 alpha reductase inhibitor (less DHT conversion)

  • useful in BPH
  • also promotes hair growth so used to treat male pattern baldness
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107
Q

MOA of flutamide

A

nonsteroidal competitive inhibitor of androgens at the T receptor
- used in prostate carcinoma

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108
Q

MOA of ketoconazole

A

inhibits steroid synthesis - inhibits 17,20 desmolase

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109
Q

MOA of spironolactone for repro

A

inhibits steroid binding, 17alpha hydroxlase and 17,20 desmolase

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110
Q

What are uses of ketoconazole and spironolactone for repro

A

PCOS and prevents hirsutism

- both have side effects of gynecomastia and amenorrhea

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111
Q

MOA of tamsulosin

A

alpha 1 antagonist used to treat BPH by inihibiting SM contraction. Selective for alpha 1A,D receptors found on prostate va vascular alpha 1B receptors

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112
Q

MOA of sildenafil and vardenafil

A

inhibit PDE 5 = increases cGMP = SM relaxation in corpus cavernosum, increases blood flow and penile erection

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113
Q

ADE of sildenafil and vardenail

A

HA, flushing, dyspepsia, impaired blue-green color vision

- RISK of life threatening hypotension in patients taking nitrates

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114
Q

What is the treatment strategy for DM1 and DM2? gestational DM

A

DM1 - low sugar diet, insulin replacement
DM2 - dietary modification and exercise for wt loss, oral agents, non-insulin injectables, insulin replacements
Gestational DM - dietary modifications, exercise, insulin replacement if lifestyle modification fails

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115
Q

What are the rapid acting insulins?

A

Lispro
Aspart
Glulisine

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116
Q

MOA of rapid acting insulins?

A

bind insulin receptor

  1. liver = increase glucose stored as glycogen
  2. muscle = increase glycogen, protein synthesis, and K uptake
  3. Fat = increase TG storage
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117
Q

ADE of rapid acting insulins?

A

hypoglycemia, rare HSR rxn

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118
Q

What are the uses for regular insulin and intermediate insulin (NPH)?

A
  1. regular - DM1, 2, GDM, DKA (IV), hyperkalemia (+ glucose), stress hyperglycemia
  2. DM1, DM2, GDM
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119
Q

What are the long acting insulins?

A

Glargine and detemir

- used for DM1, 2, and GDM (basal glucose control)

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120
Q

MOA of biguanides (metformin)

A

decreases gluconeogenesis
increases glycolysis
increase peripheral glucose uptake (insulin sensitivity)
- 1st line therapy for DM2. can be used in pts w/out islet function

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121
Q

ADE of metformin

A 
GI upset
Lactic acidosis (contraindicated in renal failure)
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122
Q

What are you sulfonylureas?

A

1st Gen = tolbutamide, chlorpropamide

2nd Gen = glyburide, glimepiride, glipizide

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123
Q

MOA of sulfonylureas

A

Close K channel in beta cell membrane = cell depolarizes triggering insulin release via increase Ca influx
- stimulates release of endogenous insulin in DM2, requires islet function so can’t be used in DM1

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124
Q

ADE of sulfonylureas

A

risk of hypoglycemia increases w/ renal failure
- 1st gen have disulfiram like effects
= 2nd gen have hypoglycemia

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125
Q

MOA of glitazones/thiazolidinediones

A

increase insulin sensitivty in peripheral tissue

  • binds PPAR-gamma nuclear transcription regulator
  • used on monotherapy in DM2 or combined
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126
Q

ADE of glitazones/thiazolidinedions

A

wt gain, edema, liver toxicity, heart failure

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127
Q

MOA of alpha glucosidase ihibitors = acarbose, miglitol

A

inhibits intestinal brush border alpha glucosidase
- delayed sugar hydrolysis and glucose absoprtion = decrease postprandial hyperglycemia
ADE = GI disturbances

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128
Q

MOA of Amylin analog = pramlintide

A

decrease gastric emptying , decrease glucagon

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129
Q

MOA of GLP-1 analog = Exenatide, Liraglutide

MOA of DPP-4 inhibitors = Linagliptin, saxagliptin, sitagliptin

A

Increase insulin and decrease glucagon release

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130
Q

ADE of pramlintide

A

hypoglycemia, nausea, diarrhea

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131
Q

ADE of exenatide and liraglutide

A

N/V, pancreatitis

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132
Q

ADE of gliptins

A

mild urinary and respiratory infxns

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133
Q

MOA of PTU and methimazole

A

blocks thyroid peroxidase = inhibits oxidation of I, organification of I = inhibits TH synthesis
- Know that PTU also blocks 5’deiodinase which decreases peripheral conversion of T4 to T3.
- used in HyperTH
Also know that PTU is used in pregnancy

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134
Q

ADE of PTU and methimazole

A

Skin rash, agranulocytosis (rare), aplastic anemia

  • PTU = liver toxicity so check LFTs
  • Methimazole = teratogen - can cause aplastic cutis
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135
Q

MOA of levothyroxin and triiodothyronine

A

Thyroxine replacement

- used in hypoTH and myxedema

136
Q

ADE of levothyroxine and triidothyronine

A

tachycardia, heat intolerance, tremors, arrhythmia

137
Q

use of GH

A

GH deficiency and Turner syndrome

138
Q

use of somatostatin (octreotide)

A

acromegaly, carcinoid, gastrinoma, glucagonom, esophageal varicies, VIPoma

139
Q

use of oxytocin

A

stimulates labor, uterine contractions, milk let down, controls uterine hemorrhage

140
Q

use of ADH

A

pituitary (central) DI

141
Q

MOA of demeclocycline

A 
ADH antagonist (member of tetracycline family)
used in SIADH
142
Q

ADE of demeclocycline

A

nephrogenic DI, photosensitivty, abnormalities of bone and teeth

143
Q

MOA of glucocorticoids

A

metabolic, catabolic, anti-inflammatory, immunosuppressive effects mediated by interaction w/ response elements and inhibition of TF such as NFkB

144
Q

ADE of glucorticoids

A

Iatrogenic Cushing syndrome - buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy brusiability, osteoporosis, adrenocortical atrophy, PUD, diabetes if chronic use.
- can get adrenal insufficiency when drug stopped abruptly after chronic use

145
Q

ADE of octreotide

A

Nausea, cramps, steatorrhea

146
Q

MOA of H2 blockers - cimetidine, ranitidine, famotidine, nizatidine

A

reversible block of H2 receptors to decrease H secretion by parietal cells
- used to treat peptic ulcer, gastritis, mild reflux

147
Q

ADE of cimetidine

A
  1. potent inhibitor of CYP450
  2. anti-androgenic effect; PRL release, gynecomastia, impotence, decreased libidio in males
  3. can cross BBB - confusion, dizziness, headache
  4. can cross placenta
    - both this and ranitidine decrease renal excretion of Cr
148
Q

MOA of PPIs- prazoles

A

irreversibly inhibits H/K ATPase in stomach parietal cells

- used for peptic ulcer, gastritis, esophageal reflux, and ZE syndrome

149
Q

ADE of PPIs

A

increased risk of C. difficile infxn, pneumonia.

Hip fractures, decreases serum Mg w/ long term use

150
Q

MOA of bismuth and sucralfate

A

bind to ulcer base, providing physical protection and allowing HCO3- secretion to reestablish pH gradient in mucous layer
- use to heal ulcers and traveler’s diarrhea

151
Q

MOA of Misoprostol

A

PGE1 analog. increases production and secretion of gastric mucous barrier and decreases acid production

152
Q

uses of misoprostol

A
  1. prevents NSAID induced peptic ulcers
  2. maintenance of a PDA
  3. induces labor by ripening cervix
153
Q

Antacid use

A

can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying
- all can cause hypokalemia

154
Q

Overuse of Aluminum hydroxide leads to what?

A

constipation, hypophosphatemia

proximal muscle weakness, osteodystrophy, and seizures

155
Q

overuse of Calcium carbonate leads to what?

A

hypercalcemia and rebound acid increase

- can chelate and decrease effectiveness of other drugs like tetracycline

156
Q

overuse of MgOH leads to what?

A

diarrhea, hyporeflexia, hypotension, cardiac arrect

- Mg = must go to bathroom

157
Q

MOA of osmotic laxative = MgOH, Mg citrate, PEG, lactulose

A
  1. provide osmotic load to draw water out
  2. Lactulose = treats hepatic encephalopathy b/c gut flora degrade it into lactic acid and acetic acid that promote nitrogen excretion as NH4+
    - these overall are used to treat constipation
158
Q

ADE of osmotic laxatives

A

diarrhea, dehydration, may be abused by bulimics

159
Q

MOA of infliximab

A

TNF-alpha mab

– treats CD, UC, RA, AS, and psoriasis

160
Q

ADE of infliximab

A

infxn incluidng reactivation of latent TB, fever, hypotension

161
Q

MOA of sulfasalazine

A

combo of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory)
- used to treat CD and UC

162
Q

ADE of sulfasalazine

A

malaise, nausea, sulfonamide toxicity, reversible oligospermia

163
Q

MOA of ondansetron

A

5HT3 blocker, decreases vagal stimulation. Powerful central acting antiemetic
- control vomiting posteroperatively and in pts undergoing cancer chemotherapy

164
Q

ADE of ondansetron

A

HA, constipation

165
Q

MOA of metoclopramide

A

D2 receptor block - increases resting tone, contractility, LES tone, motility

    • doesn’t influence colon transport time
  • used to treat diabetic and post surgery gastroparesis, antiemetic
166
Q

ADe of metoclopramide

A
  1. increase parkinsonian effects
  2. relestness, drowsiness, fatigue, depression, nausea, diarrhea
  3. drug interaction w/ digoxin and diabetic agents
  4. CI - in pts w/ small bowl obstruction or PD
167
Q

What are the 1st gen histamine 1 blockers?

A

Diphenhydramine, dimenhydrinate, chlorpheniramine

168
Q

What are the 2nd gen histamine 1 blockers?

A

loratadine, fexofenadine, desloratadine, cetirizine

  • used for allergies
  • think ends in “-adine”
169
Q

Uses 1st gen histamine 1 blockers

A

allergy, motion sickness, sleep aid

170
Q

ADE of 1st gen H1 blockers

A

sedation, antimuscarinic, anti-alpha adrenergic (orthostatic hypotension)

171
Q

MOA of guaifenesin

A

expectorant - thins respiratory secretions, doesn’t suppress cough reflex

172
Q

MOA of n-acetylcysteine

A

Mucolytic - loosens mucous plugs in CF patients.

173
Q

MOA of dextromethorphan

A

antitussive - blocks NMDA glutamate receptors
- synthetic codeine analog
- has mild opoid effect when used in excess, mild abuse potential
use Naloxone for overdose.

174
Q

MOA of pseudoephedrine and phenylephrine

A

alpha agonists nasal decongestants

  • used to decrease hyperemia, edema, and nasal congestion
  • opens obstructed eustachian tubes
  • worried about HTN.
175
Q

MOA of albuterol, salmeterol, formoterol

A

Beta 2 agonists, relaxes bronchial SM

  1. Albuterol - for acute exacerbation
  2. Sal and form - long acting agents for prophylaxis, adverse effect are tremor and arrhythmia
176
Q

MOA of theophylline

A

causes bronchodilation by inhibiting PDE = increase cAMP levels

  • narrow therapeutic index
  • metabolized by CYP450
177
Q

ADE of theophylline

A

narrow TI = cardiotoxicity, neurotoxicity

- blocks effect of adenosine

178
Q

MOA of ipratropium

A

competitive block of muscarinic receptors, preventing bronchoconstriction
- also use for COPD

179
Q

MOA of beclomethasone and fluticasone

A
  • inhibits cytokine synthesis
  • inactivates NFkB
  • 1st line therapy for chronic asthma
180
Q

MOA of Montelukast and Zafirlukast

A
  • blocks LT receptor

- especially good for Aspirin induced asthma

181
Q

MOA of zileuton

A

5LOX pathway inhibitor

- blocks conversion of arachidonic acid to LT

182
Q

MOA of omalizumab

A

Anti-IgE Mab

  • binds mostly unbound serum IgE and blocks binding to FceRI
  • Used in allergic asthma resistant to inhaled steroids and long acting Beta agonists
183
Q

MOA of methacholine

A

muscarinic receptor agonists

- used in bronchial provocation challenge to help dx asthma

184
Q

MOA of bosentan

A

Used to treat pulmonary arterial HTN

- competitively blocks endothelin -1 receptor and decreases pulmonary vascular resistance

185
Q

MOA of Heparin

A

cofactor for activation of antithrombin - decreases thrombin and factor Xa.
- it has a short half-life

186
Q

Uses of heparin

A

Immediate anticoagulation for PE, acute coronary syndrome, MI, DVT. Used during pregnancy b/c doesn’t cross placenta

187
Q

What do you monitor when someone is on heparin?

A

PTT

188
Q

ADE of heparin

A

bleeding, thrombocytopenia (HIT), osteoporosis, drug-drug interactions.

189
Q

What do you give to rapidly reverse heparin toxicity?

A

Protamine sulfate - it’s a positively charged molecule that binds negatively charged heparin)

190
Q

What is good about LMW heparins? (enoxaparin, dalteparin)

A

act more on factor Xa, have better bioavailability, and longer half life.
- they can be given subcutaneously and without lab monitoring

191
Q

What is the bad thing about LMW heparins?

A

they can’t be easily reversed

192
Q

What is heparin induced thrombocytopenia?

A

development of IgG antibodies against heparin bound to platelet factor 4. This Ab-heparin-PF4 complex activates platelets leading to thrombosis and thrombocytopenia

193
Q

What are argatroban and bivalirudin and their MOA?

A
  1. deriatives of hirudin, anticoagulants used by leeches.
  2. inhibit thrombin directly
    - used instead of heparin for anticoagulating patients w/ HIT
194
Q

MOA of warfarin (coumadin)

A

interferes w/ normal synthesis and gamma carboxylation of vitamin K dependent clotting factors 2, 7, 9, 10 and proteins C and S.

195
Q

What is monitored in pts on warfarin?

A

PT - extrinsic pathway. INR values

196
Q

Where is warfarin metabolized and tell me about its half life?

A
  • metabolized by CYP450

- long half life

197
Q

When is warfarin used?

A

Chronic anticoagulation (after STEMI, venous thromboemobolism prophylaxis, and prevention of stroke in atrial fibrillation)

198
Q

When is warfarin not used?

A

in pregnant women b/c warfarin can cross the placenta

199
Q

ADE of warfarin

A

Bleeding, teratogenic, skin/tissue necrosis, drug drug interactions

200
Q

What do you give for rapid reversal of warfarin overdose?

A

FFP

- then give vitamin K

201
Q

MOA of apixaban and rivaroxaban

A

direct factor Xa inhibitors

202
Q

What are the uses of apixaban and rivaroxaban

A

treatment and prophylaxis of DVT and PE (rivaroxaban), stroke prophylaxis in pts w/ atrial fibrillation

203
Q

ADE of apixaban and rivaroxaban

A

bleeding

- they have no reversal agent

204
Q

Why is the onset of action of warfarin slow?

A

action is limited on half lives of normal clotting factors

205
Q

What is the site of action of warfarin and heparin?

A
  1. warfarin - work in liver

2. heparin - works in blood

206
Q

What is the structural difference b/w warfarin and heparin?

A
  1. warfarin - small lipid soluble molecul

2. heparin - large anionic acidic polymer

207
Q

MOA of alteplase, reteplase, tenecteplase

A

directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots.

208
Q

What do the thrombolytics do PT, PTT, and platelet count?

A
  1. increase both PT and PTT

2. no change in platelet count

209
Q

When are the thrombolytics used?

A

early MI, early ischemic stroke, direct thrombolysis of severe PE

210
Q

ADE of thrombolytics

A

bleeding
- they are CI in pts w/ active bleeding, hx of intracranial bleeding, recent surgery, known bleeding diatheses, or severe hypertension

211
Q

What do you treat thrombolytic toxicity w/?

A

aminocaproic acid - inhibitor of fibrinolysis

- FFP and cryoprecipitate can also be used to correct factor deficiencies

212
Q

MOA of Aspirin

A

irreversibly inhibits COX 1 and 2 by covalent acetylation.

- platelets can’t make new enzymes so effect lasts until new platelets are produced.

213
Q

What effect do aspirin have on blood mearsuring things?

A
  1. increases bleeding time
  2. decreases TXA2 and PGs
  3. no effect on PT and PTT
214
Q

uses for aspirin

A

antipyretic, antiinflammatory, analgesic, antiplatelet (decreases aggregation)

215
Q

ADE of aspirin

A
  1. gastric ulceration
  2. tinnitus - CN 8
  3. chronic use can lead to ARF, intersitital nephritis, and upper GI bleeding
  4. Reye syndrome in kids w/ viral infxn
216
Q

What will aspirin overdose cause?

A

initially a respiratory alkalosis, then superimposed by metabolic acidosis

217
Q

MOA of clopidogrel, ticlopidine, prasugrel, ticagrelor

A

inhibits platelet aggregation by irreversibly blocking ADP receptors
- inhibits fibrinogen binding by preventing GpIIb/IIIa from binding to fibrinogen

218
Q

Uses of the ADP receptor inhibitors?

A

acute coronary syndrome, coronary stenting

- there is decreased incidence/recurrence of thrombotic stroke

219
Q

ADE of ADP receptor inhibitors?

A

neutropenia w/ ticlopidine

- TTP and HUS may be seen

220
Q

MOA of cilostazol and dipyridamole

A

phosphodiesterase III inhibitor = increases cAMP in platelets thus inhibiting platelet aggregaion
- also a vasodilator

221
Q

uses for cilostazol and dipryidamole

A

intermittent claudication, coronary vasodilation, prevention of stroke or TIA (combined w/ ASA), angina prophylaxis

222
Q

MOA of abciximab, eptifibatide, tirofiban

A

bind to Gp IIb/IIIa on activated platelets preventing aggregation

223
Q

What are uses of Gp IIb/IIIa inhibitors?

A

unstable angina, percutaneous transluminal coronary angioplasty

224
Q

ADE of Gp IIb/IIIa inhibitors?

A

bleeding, thrombocytopenia

225
Q

At what step in the cell cycle do the following drugs interfere?

  1. Vinca alkaloids and taxols
  2. Bleomycin
  3. Etoposide
  4. Antimetabolites
A
  1. M phase - affect microtubules
  2. G2 phase
  3. 2 and G2 phase - inhibits DNA synthesis
  4. S phase - inhibit nucleotide syntehsis
226
Q

What are you antimetabolite cancer drugs?

A
  1. MTX
  2. 5FU
  3. Cytarabine
  4. Azathioprine, 6MP, 6TG
227
Q

MOA of MTX

A

folic acid analog that inhibits DHF reducatse = decreases dTMP = decreases DNA and protein synthesis

228
Q

What are the uses of MTX?

A
  1. cancer - leukemias, lymphomas, choriocarcinomas, sarcomas

2. others - abortions, ectopic pregnancy, RA, psoriasis, IBD

229
Q

ADE of MTX

A
  • myelosuppression which is reversible w/ leucovorin rescue
  • Macrovesicular fatty change in liver
  • mucositis
  • teratogenic
230
Q

MOA of 5FU

A

pyrimidine analog bioactivated to 5F-dUMP which covalently complexes folic acid.
- this complex inhibits thymidylate synthase = decreased dTMP = decreased DNA and protein synthesis

231
Q

Uses of 5FU?

A

colon cancer, pancreatic cancer, basal cell carcinoma (topical use)

232
Q

ADE of 5FU?

A

myelosuppresion

  • overdose: rescue w/ uridine
  • photosensitivity
233
Q

MOA of cytarabine

A

pyrimidine analog that inhibits DNA polymerase

- used in leukemias and lymphomas

234
Q

ADE of cytarabine

A

leukopenia, thrombocytopenia, megaloblastic anemia

- essentially PANCYTOPENIA

235
Q

MOA of azathioprine, 6MP, 6TG

A

purine (thiol) analogs that decrease de nove purine synthesis
- activated by HGPRT

236
Q

uses for azathioprine, 6MP, 6TG

A

preventing organ rejection, RA, SLE (azathioprine)

- leukemia, IBD (6MP, 6TG)

237
Q

ADE of azathioprine, 6MP, 6TG

A
  • all lead to BM, GI and liver toxicity
  • Azathioprine and 6MP = both metabolized by xanthine oxidase thus both increase toxicity w/ allopurinol which inhibits their metabolism.
238
Q

What are you antitumor Abx?

A
  1. dactinomycin
  2. Doxorubicin, daunorubicin
  3. Bleomycin
239
Q

MOA of dactinomycin

A

intercalates DNA

240
Q

uses for dactinomycin

A

Wilms tumor, Ewing sarcoma, rhabdomyosarcoma = thinkg kid tumors!

241
Q

MOA of doxorubicin and daunorubicin

A

generates free radicals and intercalates in DNA causing breaks and decreasing replication

242
Q

ADE of doxorubicin/daunorubicin

A
  1. cardiotoxicity = dilated cardiomyopathy
  2. myelosuppression
  3. alopecia
  4. toxic to tissues following extravasation
243
Q

What is used to prevent anthracycine cardiotoxicity?

A

dexrazoxane - Fe chelating agent

244
Q

MOA of bleomycin

A

induces free radical formation which causes breaks in DNA strands

245
Q

uses of bleomycin

A

testicular cancer and Hodgkin lymphoma

246
Q

ADE of bleomycin

A

pulmonary fibrosis, skin changes, mucositis, minimal myelosuppression

247
Q

What are you alkylating agents for cancer treatment?

A
  1. cyclophosphamide and ifosfamide
  2. nitrosoureas
  3. busulfan
248
Q

MOA of cyclophosphamide and ifosfamide

A

covalently X link (interstrand) DNA at guanine N7

- requires bioactivation in liver

249
Q

ADE of clyclophosphamide and ifosfamide

A
  • myelosuppression

- hemorrhagic cystitis - can be partially prevents w/ mesna

250
Q

What is mesna?

A

used to treat hemorrhagic cystisis

- the thiol group of mesna binds toxic metabolites

251
Q

MOA of nitrosureas - carmustines, semustine, streptozocin

A
  • requires bioactivation
  • cross BBB and cross links DNA
  • used to treat brain tumors
252
Q

ADE of nitroureas

A

CNS toxicity - convulsions, dizziness, ataxia

253
Q

MOA of busulfan

A

cross links DNA

- used treat CML and ablate pt’s BM before BMT

254
Q

ADE of busulfan

A

severe myelosuppression

  • pulmonary fibrosis
  • hyperpigmentation
255
Q

MOA of vincristine/blatine

A

bind Beta tubulin and inhibit polymerization into microtubules - prevent formation of mitotic spindle needed for M phase

256
Q

ADE of vincristine

A
  1. neurotoxicity (areflexia, peripheral neuritis)

2. paralytic ileus

257
Q

ADE of vinblastine

A

BM suppression

258
Q

MOA of paclitaxel/taxols

A

hyperstabilize polymerized MT in M phase so that mitotic spindle can’t break down (anaphase can’t occur)
- used to treat ovarian and breast carcinomas

259
Q

ADE of taxols

A

myelosuppression, alopecia, HSR

260
Q

MOA of cisplatin and carboplatin

A

cross links DNA

261
Q

uses of cisplatin and carboplatin

A

testicular, bladder, ovary, and lung carcinomas

262
Q

ADE of cisplatin and carboplatin

A
  • nephrotoxicity and acoustic nerve damage
263
Q

What can you prevent the nephrotoxicity with?

A

amifostine (free radical scavenger) and chloride diuresis

264
Q

MOA of etoposide and teniposide

A

inhibits topoisomerase II –> increases DNA degradation

265
Q

uses of etoposide and teniposide

A

solid tumors, leukemias, lymphomas

266
Q

ADE of etoposide and teniposide

A

myelosuppression, GI irritation, alopecia

267
Q

MOA of irinotecan and topotecan

A

inhibits topoisomerase I and prevent DNA unwinding and replication

268
Q

uses for the -tecans?

A

colon cancer - irinotecan

ovarian and small cell lung cancers - topotecan

269
Q

ADE of -tecans?

A

severe myelosuppression, diarrhea

270
Q

MOA of hydroxyurea

A

inhibits ribonucleotide reductase = decreases DNA synthesis

- S phase specific

271
Q

uses for hydroxyurea

A

melanoma, CML, SCD to increase HbF

272
Q

MOA of trastuzumab (herceptin)

A

HER2 (tyrosine kinase receptor) mab

- used to kill breast cancer cells that overexpress HER2

273
Q

ADE of trastuzumab

A

cardiotoxicity

274
Q

MOA of imatinib

A

Y kinase inhibitor of bcr-abl (CML) and c-Kit (common in GI stromal tumors)

275
Q

ADE imatinib

A

fluid retention

276
Q

MOA rituximab

A

CD20 mab

277
Q

Uses of rituximab

A

Non-hogdkin lymphoma, RA (w/ MTX), and ITP

278
Q

ADE of rituximab

A

increase risk of progressive multifocal leukoencephalopathy

279
Q

MOA of vemurafenib

A

small molecule inhibitor of forms of B-raf kinase w/ the V600E mutation
- used to treat metastic melanoma

280
Q

MOA of bevacizumab

A

VEGF mab

- treated for solid tumors to prevent angiogenesis

281
Q

ADE of bevacizumab

A

hemorrhage and impaired wound healing

282
Q

MOA of zanamivir and oseltamivir

A

inhibits influzena neruaminidase –> stops release of progeny virus
- can be used to treat both influenza A and B

283
Q

MOA of ribavarin

A

inhibits synthesis of Guanine nucleotides by competitively inhibiting IMP DH
- used for RSV and Hep C treatment

284
Q

ADE of ribavarin

A

hemolytic anemia, severe teratogen

285
Q

MOA of acyclovir, famciclovir, valacyclovir

A
  • monophosphorylated by HSV/VZV thymidine kinase and not phosphorylated in uninfected cell
  • all guanosine analog
  • triphosphate formed by cellular enzymes. They preferentially inhibits viral DNA polymerase by chain termination
286
Q

What are the uses for acyclovir, famciclovir, and valacyclovir for the herpes infxns?

A
  1. can use them to treat HSV, VZV
  2. weak activity against EBV
  3. no activity against CMV
  4. used for HSV induced mucocutaneous and genital lesions as well as for encephalitis
  5. Prophylaxis in ICPs
  6. no effect on latent forms of HSV and ZVZ
    * valcyclovir is a prodrug for acyclovir = has better oral bioavailability
287
Q

ADE for acyclovir, famiciclovir, and valacyclovir

A

obstructive crystalline nephropathy and ARF if not adequately hydrated

288
Q

mechanism of resistance for acyclovir, famiciclovir, and valacyclovir

A

mutated viral thymidine kinase

289
Q

MOA of ganciclovir

A

5’monophosphate formed by CMV viral kinase

  • Guanonsine analog
  • triphosphate formed by cellular kinases and preferentially inhibits viral DNA polymerase
290
Q

ADE of gancicloir

A

pancytopenia, renal toxicity

- more toxic to host enzymes than acyclovir

291
Q

Mechanism of resistance to ganciclovir

A

mutated CMV DNA polymerase or lack of viral kinase

292
Q

When is ganciclovir used?

A

CMV, especially in ICP.

* Valganciclovir is a prodrug and has better oral bioavailability

293
Q

MOA of Foscarnet

A

viral DNA polymerase inhibit that binds to the pyrophosphate binding site of the enzyme.
- doesn’t require activation of viral kinase!!!

294
Q

when is foscarnet used?

A
  1. CMV retinitis in ICP pts when ganciclovir fails

2. acyclovir resistant HSV

295
Q

ADE of foscarnet

A

renal failure

296
Q

mechanism of resistance of foscarnet

A

mutated DNA polymerase

297
Q

MOA of cidofovir

A

preferentially inhibits viral DNA polymerase

- doesn’t require phosphorylation by viral kinase!!!!

298
Q

when is cidofovir used?

A

CMV retinitis in ICP pts, acyclovir resistant HSV

- it has a long half life

299
Q

ADE of cidofovir

A

renal toxicity

300
Q

What do you give w/ cidofovir to decrease the renal toxicity?

A

coadminister with probenecid and IV saline to decrease toxicity

301
Q

What is normal HIV therapy?

A

HAART - give when pts presents w/ AIDS defining illness, low CD4 cell counts, or high viral load
1. regimen consists of 3 drugs to prevent resistance
Give pt 2 NRTIs + 1 NNRTI or 1 protease inhibitor or 1 integrase inhibitor

302
Q

What are you HIV protease inhibitors?

A 
think -navir
Atazanavir
Darunavir
Fosamprenavir
Indinavir
Lopinavir
Ritonavir
Saquinavir
303
Q

MOA of the HIV protease inhibitors

A
  1. assembly of virions depends on HIV-1 protease (from pol gene) which normally cleaves the polypeptide products of HIV mRNA into their functional parts.
  2. Protease inhibitors prevent maturation of new virions
304
Q

ADE of protease inhibitors

A
  1. Hyperglycemia, GI intolerance (nausea, diarrhea), lipodystrophy
  2. Indinavir - nephropathy, hematuria, kidney stones
  3. Ritonavir can boost other drug concentrations b/c it inhibits CYP450
305
Q

What are the HIV NRTIs?

A 
Abavacir
Didanosine
Emtricitabine
Lamivudine
Stavudine
Tenofovir
Zidovudine
306
Q

MOA of NRTIs

A

competitively inhibits nucleotide binding to reverse transcriptase and terminates DNA chain (lacks a 3’OH group)

  • Tenofovir is a nucleotide; all the others are nucleosides and need to be phosphorylated to be active
  • Zidovudine is used for general prophylaxis and during pregnancy to decrease risk of fetal transmission
307
Q

ADE of NRTIs

A
  1. bone marrow suppression - can be reversed w/ G-CSF and EPO
  2. Peripheral neuropathy
  3. lactic acidosis w/ nucleosides
  4. Rash -
  5. Anemia - zidovudine
  6. pancreatitis - didanosine and stavudine
308
Q

What are the HIV NNRTIs?

A

efavirenz, nevirapine, delavirdine

309
Q

MOA of HIV NNRTIs

A

binds to reverse transcriptase at site different from NRTI

- don’t require phosphorylation to be active or compete w/ nucleotides!!!!

310
Q

ADE of NNRTIs

A
  1. rash and liver toxicity common to all
  2. Efavirenz - vivid dreams and CNS symptoms
  3. Delavirdine and efavirenz are CI in pregnancy
311
Q

MOA of raltegravir

A

inhibits HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase

312
Q

ADE of raltegravir

A

Hypercholesteremia

313
Q

MOA of enfurvirtide

A

binds gp41 inhibiting HIV viral entry

314
Q

MOA of maraviroc

A

binds CCR5 on surface of T cells/monocytes inhibiting interaction w/ gp120

315
Q

ADE of enfuviritide

A

skin reaction at injection sites

316
Q

MOA of interferons

A

glycoproteins normally made by virus infected cells, exhibiting a wide range of antiviral and antitumoral properties

317
Q

When is IFN alpha used

A 
chronic Hep B and C
Kaposi sarcoma
Hairy cell leukemia
condyloma acuminatum
RCC
malignant melanoma
318
Q

When is IFN beta used

A

Multiple sclerosis

319
Q

When is IFN gamma used

A

chronic granulomatous diease

320
Q

ADE of Interferons

A

neutropenia and myopathy

321
Q

What Abx should be avoided in pregnancy and why?

A
  1. Sulfonamides - kernicterus
  2. Aminoglycosides - ototoxicity
  3. Fluoroquinolones - cartilage damage
  4. Clarithomycin - embryotoxic
  5. Tetracyclines - discolored teeth, inhibition of bone growth
  6. chloramphenicol - gray baby
322
Q

What antifungal and antiviral should be avoided in pregnancy?

A
  1. Ribavirin - teratogenic
  2. Griseofulvin - teratogenic
  3. Delavirdine and efavirenz
323
Q

MOA of Cox 2 inhibitors

A
  • reversibly inhibits COX2 which is found in inflammatory cells and vascular endothelium and mediates inflammation and pain
  • spares COX1 which helps maintain the gastric mucosa thus should not have the corrosive effects of other NSAIDS on the GI lining
  • spares platelet functions as TXA2 production is dependent on COX 1
324
Q

When are COX 2 inhibitors used?

A

RA, OA, pts w/ gastritis or ulcers

325
Q

ADE of COX 2 inhibitors

A

increase risk of thrombosis, sulfa allergy

326
Q

MOA of acetaminophen

A

reversibly inhibits COX mostly in CNS

- inactivated peripherally

327
Q

When is acetaminophen used?

A

antipyretic, analgesic but not anti-inflammatory

- used instead of ASA to avoid Reye syndrome in kids w/ viral infxn

328
Q

ADE of acetaminophen

A
  • overdose produces hepatic necrosis
  • it’s metabolite (NAPQI) depletes GSH and forms toxic tissue adducts in lvier
  • N-acetylcysteine is the antidote - generates GSH
329
Q

MOA of bisphosphonates

A

Pyrophosphate analog that binds hydroxyapatite in bone, inhibiting osteoclast activity

330
Q

uses of bisphosphonates

A

Osteoporosis, hyperCa, Paget disease of bone

331
Q

ADE of bisphosphonates

A

corrosive esophagitis, osteonecrosis of jaw

332
Q

MOA of allopurinol

A

inhibits Xanthine oxidase to decrease conversion of xanthine to uric acid

  • also used in tumor lysis associate urate nephropathy
  • increases concentrations of 6MP and azathioprine
333
Q

What can’t you give at the same time as allopurinol?

A
  • salicylates b/c all but the highest doses depress uric acid clearance. Even high doses (5-6g/day) have only minor uricouric activity
334
Q

MOA of febuxostat

A

inhibits xanthine oxidase

335
Q

MOA of probenecid

A

inhibits reabsorption of uric acid in PCT

- also inhibits secretion of penicillin

336
Q

What are the chronic gout drugs?

A

Allopurinol, febuxostat, probenecid

337
Q

MOA of colchicine

A

binds and stabilizes tubulin to inhibit MT polymerization, impairing leukocyte chemotaxis and degranulation

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