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1

MOA of mannitol

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

2

ADE of mannitol

pulmonary edema, dehydration,
- CI in anuria and CHF

3

MOA of Acetazolamide

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

4

ADE of acetazolamide

Hyperchloremia metabolic acidosis, parethesias, NH3 toxicity, sulfa allergy

5

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

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)

6

ADE of furosemide

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

7

use of ethacrynic acid

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

8

MOA of HCTZ

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)

9

ADE of HCTZ

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

10

MOA of Spironolacton and eplerenone

competitive aldosterone receptor antagonists in cortical collecting tubule

11

MOA of triamterene and amiloride

block eNa Channels in CCT

12

ADE of K sparing diuretics

Hyperkalemia (can lead to arrhythmias)
Endocrine effects w/ spironolactone (gynecomastia and antiandrogen effects)

13

Diuretics and effect on urine NaCl

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

14

Diuretics and effect on urine K

- increases w/ loop/thiazides
serum K may decrease as a result

15

Diuretics and effects on blood pH

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

16

mechanism via which loops/thiazides causes blood alkalemia

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

17

Diuretics and effects on urine Ca

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

18

MOA of ACE inhibitors

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

19

ADE of ACE inhibitor

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

20

MOA of ARBs

ATII receptor blockers
- no increase in bradykinin so no cough or angioedema

21

MOA of CCB

block voltage dependent L type calcium channels of cardiac and SM = decrease contractility
- Vascular SM think dihydropyridine
- Heart think verapamil > dilitazem

22

What are dihydropyridine CCB's used for?

1. HTN
2. Angina - including Prinzmetal
3. Raynaud

23

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

1. HTN
2. Angina
3. Atrial fibrillation/flutter

24

What is Nimodipine used for?

Subarachnoid hemorrhage - prevents cerebral vasospasm

25

ADE of CCBs

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

26

MOA of Hydralazine

Increase cGMP = SM relaxation. Vasodilates arteriole > veins
- decreases afterload

27

When is hydralazine used?

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

28

ADE of hydralazine

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

29

What is commonly used to treat hypertensive emergeny?

Nitroprusside, nicardipine, clevidipine, labetalol, and fenolodpam

30

MOA of nitroprusside

short acting; increases cGMP via direct release of NO
- worry about cyanide toxicity (treat w/ sulfur)

31

MOA of fenolodopam

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

32

MOA of nitroglycerin and isosorbide dinitrate

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

33

uses for nitroglycerin and isosorbide dinitrate

angina, acute coronary syndrome, pulmonary edema

34

ADE of Nitroglycerin and isosorbide nitrate

- 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

35

What is the goal for antianginal therapy?

reduce myocardial O2 consumption by decreasing
1. EDV
2. BP
3. HR
4. contractility

36

What effects do nitrates have on the body?

1. decrease EDV, HR, ejection time, MVO2
1. increase contractility and HR - both reflex exposure

37

What effect do beta blockers have on the body?

1. decrease contractility, BP, HR, MVO2
2. increase EDV and ejection time

38

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

1. decrease BP, HR, and MVO2
2. not a huge effect on EDV, contractility, ejection time

39

What beta blockers are contraindicated in angina?

pindolol and acebutolol - both are partial Beta agonists

40

MOA of statins

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

41

lipid effects of statins

decreases LDL mainly
increases HDL
decreases TG

42

ADE of statins

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

43

MOA of Niacin (vitamin B3)

inhibits lipolysis in fat tissue, decreases hepatic VLDL synthesis

44

lipid effects of niacin

decrease LDL and increase HDL
slight decrease in TG

45

ADE of niacin

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

46

MOA of bile acid resins - cholestryramine, colestipol, colesevelam

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

47

Lipid effects of bile acid resins

decrease LDL
slightly increases HDL and TG

48

ADE of bile acid resins

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

49

MOA of ezetimibe

prevent cholesterol absorption at small intestine brush border

50

lipid effects of ezetimibe

decreases LDL

51

ADE of ezetimibe

rare increase in LFT, diarrhea

52

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

upregulates LPL = increases TG clearance
- Activates PPAR-alpha to induced HDL synthesis

53

lipid effects of fibrates

decreases TG a lot
decrease LDL, increase HDL

54

ADE of fibrates

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

55

Pharmacokinetics of digoxin

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

56

MOA of digoxin

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

57

clinical use of digoxin

CHF to increase contractility
Atrial fibrillation - decrease conduction at AV node and depression at SA node

58

ADE of digoxin

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

59

What factors predispose to digoxin toxicity

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)

60

Antidote for digoxin toxicity

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

61

What are the classes of antiarrhythmics?

No Bad Boys Keep Clean
- class I - Na channel blockers
- class II - Beta blockers
- class III - K channel blockers
- class IV - CCB

62

What do type I antiarrhythmics do?

- 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

63

What are the class IA antiarrhythmics and their toxicities?

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

64

MOA of Class IA antiarrhythmics

increase AP duraion, increase ERP, increase QT interval
- used to treat atrial and ventricular arrhythmia especially re-entrant and ectopic SVT and VT

65

What are the class IB antiarrhythmics and their ADEs?

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

66

MOA of class IB antiarrhythmics

decrease AP duration
- perferentially affect ischemic or depolarized Purkinije and ventricular tissue
- used to treat acute ventricular arrhythmias (especially post MI), digitalis induced arrhythmias

67

What are the class IC antiarrhythmics and ADEs?

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

68

MOA of Class IC antiarrhytmics

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

69

MOA of Class II antiarrhythmics

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

70

ADE of Class II antiarrythmics

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

71

What are you Class III antiarrhythmics

Amiodarone, Ibutilide, Dofetilide, Sotalol (AIDS)
- used for atrial fibrillation, atrial flutter, ventricular tachycardia (amiodarone, sotalol)

72

MOA of class III antiarrhythmics

Increase AP duration, increase ERP
- used when other antiarrhythmics fails
- increase QT interval

73

ADE of Sotalol

torsades de pointes, excessive beta blockade

74

ADE of Ibutilide

torsade de pointes

75

ADE of amiodarone

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)

76

MOA of class IV antiarrhythmics

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

77

ADE of class IV antiarrhythmics

constipation, flushing, edema,
- CV effects = CHF, AV block, sinus node depression

78

MOA of adenosine

increase K out of cells = hyperpolarizes cell and decreases Ca current.
- DOC of dx of SVT.
- Very short acting

79

ADE of adenosine

flushing, hypotension, chest pain

80

What can block the effects of adenosine?

theophylline and caffeine

81

MOA of Mg

effective in torsades de pointes and digoxin toxicity

82

MOA of leuprolide

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

83

uses of leuprolide

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

84

ADE of leuprolide

antiandrogen, N/V

85

MOA fo estrogens

binds estrogen receptors
- used for hypogonadism/ovarian failure, menstrual abnormalities, HRT in postmenopausal women,
- used in men w/ androgen dependent prostate cancer

86

ADE of estrogens

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.

87

What are contraindications for estrogens?

ER positive breast cancer, history of DVTs

88

MOA of clomiphene

antagonists at E-receptors in hypothalamus
- prevents normal feedback inhibition and increases release of LF and FSH from pituitary = stimulates ovulation.

89

What is clomiphene used to treat

infertility due to anovulation (PCOS)

90

ADE of clomiphene

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

91

MOA of tamoxifen

antagonist on breast tissue
Agonist at uterus and bone - associated w/ endometrial cancer and thromboemolic events

92

Tamoxifen use

treat and prevent recurrences of ER + breast cancer

93

MOA of raloxifene

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

94

Uses of hormone replacement therapy

relief of prevent menopausal symptoms and osteoporosis
- unopposed estrogen replacement therapy increases risk of endometrial caner so progesterone is added.
- possible increased CV risk

95

MOA of anastrozole/exemestane

Aromatase inhibitors used in postmenopausal women w/ breast cancer

96

MOA of progestins

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

97

MOA of mifepristone

competitive inhibitor of progestins at progesterone receptos
- used to terminate pregnancy, usually gived w/ misoprostol (PGE1)

98

ADE of mifepristone

heavy bleeding, GI effects, ab pain

99

MOA of oral contraceptions

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.

100

what are OCP contraindications

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

101

MOA of terbutaline

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

102

MOA of Danazol

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

103

ADE of danazol

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

104

MOA of Testosterone and methylT

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

105

ADE of T and methyl-T

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

106

MOA of finasteride

5 alpha reductase inhibitor (less DHT conversion)
- useful in BPH
- also promotes hair growth so used to treat male pattern baldness

107

MOA of flutamide

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

108

MOA of ketoconazole

inhibits steroid synthesis - inhibits 17,20 desmolase

109

MOA of spironolactone for repro

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

110

What are uses of ketoconazole and spironolactone for repro

PCOS and prevents hirsutism
- both have side effects of gynecomastia and amenorrhea

111

MOA of tamsulosin

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

112

MOA of sildenafil and vardenafil

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

113

ADE of sildenafil and vardenail

HA, flushing, dyspepsia, impaired blue-green color vision
- RISK of life threatening hypotension in patients taking nitrates

114

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

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

115

What are the rapid acting insulins?

Lispro
Aspart
Glulisine

116

MOA of rapid acting insulins?

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

117

ADE of rapid acting insulins?

hypoglycemia, rare HSR rxn

118

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

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

119

What are the long acting insulins?

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

120

MOA of biguanides (metformin)

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

121

ADE of metformin

GI upset
Lactic acidosis (contraindicated in renal failure)

122

What are you sulfonylureas?

1st Gen = tolbutamide, chlorpropamide
2nd Gen = glyburide, glimepiride, glipizide

123

MOA of sulfonylureas

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

124

ADE of sulfonylureas

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

125

MOA of glitazones/thiazolidinediones

increase insulin sensitivty in peripheral tissue
- binds PPAR-gamma nuclear transcription regulator
- used on monotherapy in DM2 or combined

126

ADE of glitazones/thiazolidinedions

wt gain, edema, liver toxicity, heart failure

127

MOA of alpha glucosidase ihibitors = acarbose, miglitol

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

128

MOA of Amylin analog = pramlintide

decrease gastric emptying , decrease glucagon

129

MOA of GLP-1 analog = Exenatide, Liraglutide
MOA of DPP-4 inhibitors = Linagliptin, saxagliptin, sitagliptin

Increase insulin and decrease glucagon release

130

ADE of pramlintide

hypoglycemia, nausea, diarrhea

131

ADE of exenatide and liraglutide

N/V, pancreatitis

132

ADE of gliptins

mild urinary and respiratory infxns

133

MOA of PTU and methimazole

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

134

ADE of PTU and methimazole

Skin rash, agranulocytosis (rare), aplastic anemia
- PTU = liver toxicity so check LFTs
- Methimazole = teratogen - can cause aplastic cutis

135

MOA of levothyroxin and triiodothyronine

Thyroxine replacement
- used in hypoTH and myxedema

136

ADE of levothyroxine and triidothyronine

tachycardia, heat intolerance, tremors, arrhythmia

137

use of GH

GH deficiency and Turner syndrome

138

use of somatostatin (octreotide)

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

139

use of oxytocin

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

140

use of ADH

pituitary (central) DI

141

MOA of demeclocycline

ADH antagonist (member of tetracycline family)
used in SIADH

142

ADE of demeclocycline

nephrogenic DI, photosensitivty, abnormalities of bone and teeth

143

MOA of glucocorticoids

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

144

ADE of glucorticoids

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

ADE of octreotide

Nausea, cramps, steatorrhea

146

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

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

147

ADE of cimetidine

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

MOA of PPIs- prazoles

irreversibly inhibits H/K ATPase in stomach parietal cells
- used for peptic ulcer, gastritis, esophageal reflux, and ZE syndrome

149

ADE of PPIs

increased risk of C. difficile infxn, pneumonia.
Hip fractures, decreases serum Mg w/ long term use

150

MOA of bismuth and sucralfate

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

MOA of Misoprostol

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

152

uses of misoprostol

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

153

Antacid use

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

Overuse of Aluminum hydroxide leads to what?

constipation, hypophosphatemia
proximal muscle weakness, osteodystrophy, and seizures

155

overuse of Calcium carbonate leads to what?

hypercalcemia and rebound acid increase
- can chelate and decrease effectiveness of other drugs like tetracycline

156

overuse of MgOH leads to what?

diarrhea, hyporeflexia, hypotension, cardiac arrect
- Mg = must go to bathroom

157

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

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

ADE of osmotic laxatives

diarrhea, dehydration, may be abused by bulimics

159

MOA of infliximab

TNF-alpha mab
-- treats CD, UC, RA, AS, and psoriasis

160

ADE of infliximab

infxn incluidng reactivation of latent TB, fever, hypotension

161

MOA of sulfasalazine

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

162

ADE of sulfasalazine

malaise, nausea, sulfonamide toxicity, reversible oligospermia

163

MOA of ondansetron

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

164

ADE of ondansetron

HA, constipation

165

MOA of metoclopramide

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

ADe of metoclopramide

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

What are the 1st gen histamine 1 blockers?

Diphenhydramine, dimenhydrinate, chlorpheniramine

168

What are the 2nd gen histamine 1 blockers?

loratadine, fexofenadine, desloratadine, cetirizine
- used for allergies
- think ends in "-adine"

169

Uses 1st gen histamine 1 blockers

allergy, motion sickness, sleep aid

170

ADE of 1st gen H1 blockers

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

171

MOA of guaifenesin

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

172

MOA of n-acetylcysteine

Mucolytic - loosens mucous plugs in CF patients.

173

MOA of dextromethorphan

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

174

MOA of pseudoephedrine and phenylephrine

alpha agonists nasal decongestants
- used to decrease hyperemia, edema, and nasal congestion
- opens obstructed eustachian tubes
- worried about HTN.

175

MOA of albuterol, salmeterol, formoterol

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

MOA of theophylline

causes bronchodilation by inhibiting PDE = increase cAMP levels
- narrow therapeutic index
- metabolized by CYP450

177

ADE of theophylline

narrow TI = cardiotoxicity, neurotoxicity
- blocks effect of adenosine

178

MOA of ipratropium

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

179

MOA of beclomethasone and fluticasone

- inhibits cytokine synthesis
- inactivates NFkB
- 1st line therapy for chronic asthma

180

MOA of Montelukast and Zafirlukast

- blocks LT receptor
- especially good for Aspirin induced asthma

181

MOA of zileuton

5LOX pathway inhibitor
- blocks conversion of arachidonic acid to LT

182

MOA of omalizumab

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

MOA of methacholine

muscarinic receptor agonists
- used in bronchial provocation challenge to help dx asthma

184

MOA of bosentan

Used to treat pulmonary arterial HTN
- competitively blocks endothelin -1 receptor and decreases pulmonary vascular resistance

185

MOA of Heparin

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

186

Uses of heparin

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

187

What do you monitor when someone is on heparin?

PTT

188

ADE of heparin

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

189

What do you give to rapidly reverse heparin toxicity?

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

190

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

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

191

What is the bad thing about LMW heparins?

they can't be easily reversed

192

What is heparin induced thrombocytopenia?

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

193

What are argatroban and bivalirudin and their MOA?

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

194

MOA of warfarin (coumadin)

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

195

What is monitored in pts on warfarin?

PT - extrinsic pathway. INR values

196

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

- metabolized by CYP450
- long half life

197

When is warfarin used?

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

198

When is warfarin not used?

in pregnant women b/c warfarin can cross the placenta

199

ADE of warfarin

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

200

What do you give for rapid reversal of warfarin overdose?

FFP
- then give vitamin K

201

MOA of apixaban and rivaroxaban

direct factor Xa inhibitors

202

What are the uses of apixaban and rivaroxaban

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

203

ADE of apixaban and rivaroxaban

bleeding
- they have no reversal agent

204

Why is the onset of action of warfarin slow?

action is limited on half lives of normal clotting factors

205

What is the site of action of warfarin and heparin?

1. warfarin - work in liver
2. heparin - works in blood

206

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

1. warfarin - small lipid soluble molecul
2. heparin - large anionic acidic polymer

207

MOA of alteplase, reteplase, tenecteplase

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

208

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

1. increase both PT and PTT
2. no change in platelet count

209

When are the thrombolytics used?

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

210

ADE of thrombolytics

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

211

What do you treat thrombolytic toxicity w/?

aminocaproic acid - inhibitor of fibrinolysis
- FFP and cryoprecipitate can also be used to correct factor deficiencies

212

MOA of Aspirin

irreversibly inhibits COX 1 and 2 by covalent acetylation.
- platelets can't make new enzymes so effect lasts until new platelets are produced.

213

What effect do aspirin have on blood mearsuring things?

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

214

uses for aspirin

antipyretic, antiinflammatory, analgesic, antiplatelet (decreases aggregation)

215

ADE of aspirin

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

What will aspirin overdose cause?

initially a respiratory alkalosis, then superimposed by metabolic acidosis

217

MOA of clopidogrel, ticlopidine, prasugrel, ticagrelor

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

218

Uses of the ADP receptor inhibitors?

acute coronary syndrome, coronary stenting
- there is decreased incidence/recurrence of thrombotic stroke

219

ADE of ADP receptor inhibitors?

neutropenia w/ ticlopidine
- TTP and HUS may be seen

220

MOA of cilostazol and dipyridamole

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

221

uses for cilostazol and dipryidamole

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

222

MOA of abciximab, eptifibatide, tirofiban

bind to Gp IIb/IIIa on activated platelets preventing aggregation

223

What are uses of Gp IIb/IIIa inhibitors?

unstable angina, percutaneous transluminal coronary angioplasty

224

ADE of Gp IIb/IIIa inhibitors?

bleeding, thrombocytopenia

225

At what step in the cell cycle do the following drugs interfere?
1. Vinca alkaloids and taxols
2. Bleomycin
3. Etoposide
4. Antimetabolites

1. M phase - affect microtubules
2. G2 phase
3. 2 and G2 phase - inhibits DNA synthesis
3. S phase - inhibit nucleotide syntehsis

226

What are you antimetabolite cancer drugs?

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

227

MOA of MTX

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

228

What are the uses of MTX?

1. cancer - leukemias, lymphomas, choriocarcinomas, sarcomas
2. others - abortions, ectopic pregnancy, RA, psoriasis, IBD

229

ADE of MTX

- myelosuppression which is reversible w/ leucovorin rescue
- Macrovesicular fatty change in liver
- mucositis
- teratogenic

230

MOA of 5FU

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

231

Uses of 5FU?

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

232

ADE of 5FU?

myelosuppresion
- overdose: rescue w/ uridine
- photosensitivity

233

MOA of cytarabine

pyrimidine analog that inhibits DNA polymerase
- used in leukemias and lymphomas

234

ADE of cytarabine

leukopenia, thrombocytopenia, megaloblastic anemia
- essentially PANCYTOPENIA

235

MOA of azathioprine, 6MP, 6TG

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

236

uses for azathioprine, 6MP, 6TG

preventing organ rejection, RA, SLE (azathioprine)
- leukemia, IBD (6MP, 6TG)

237

ADE of azathioprine, 6MP, 6TG

- 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

What are you antitumor Abx?

1. dactinomycin
2. Doxorubicin, daunorubicin
3. Bleomycin

239

MOA of dactinomycin

intercalates DNA

240

uses for dactinomycin

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

241

MOA of doxorubicin and daunorubicin

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

242

ADE of doxorubicin/daunorubicin

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

243

What is used to prevent anthracycine cardiotoxicity?

dexrazoxane - Fe chelating agent

244

MOA of bleomycin

induces free radical formation which causes breaks in DNA strands

245

uses of bleomycin

testicular cancer and Hodgkin lymphoma

246

ADE of bleomycin

pulmonary fibrosis, skin changes, mucositis, minimal myelosuppression

247

What are you alkylating agents for cancer treatment?

1. cyclophosphamide and ifosfamide
2. nitrosoureas
3. busulfan

248

MOA of cyclophosphamide and ifosfamide

covalently X link (interstrand) DNA at guanine N7
- requires bioactivation in liver

249

ADE of clyclophosphamide and ifosfamide

- myelosuppression
- hemorrhagic cystitis - can be partially prevents w/ mesna

250

What is mesna?

used to treat hemorrhagic cystisis
- the thiol group of mesna binds toxic metabolites

251

MOA of nitrosureas - carmustines, semustine, streptozocin

- requires bioactivation
- cross BBB and cross links DNA
- used to treat brain tumors

252

ADE of nitroureas

CNS toxicity - convulsions, dizziness, ataxia

253

MOA of busulfan

cross links DNA
- used treat CML and ablate pt's BM before BMT

254

ADE of busulfan

severe myelosuppression
- pulmonary fibrosis
- hyperpigmentation

255

MOA of vincristine/blatine

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

256

ADE of vincristine

1. neurotoxicity (areflexia, peripheral neuritis)
2. paralytic ileus

257

ADE of vinblastine

BM suppression

258

MOA of paclitaxel/taxols

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

ADE of taxols

myelosuppression, alopecia, HSR

260

MOA of cisplatin and carboplatin

cross links DNA

261

uses of cisplatin and carboplatin

testicular, bladder, ovary, and lung carcinomas

262

ADE of cisplatin and carboplatin

- nephrotoxicity and acoustic nerve damage

263

What can you prevent the nephrotoxicity with?

amifostine (free radical scavenger) and chloride diuresis

264

MOA of etoposide and teniposide

inhibits topoisomerase II --> increases DNA degradation

265

uses of etoposide and teniposide

solid tumors, leukemias, lymphomas

266

ADE of etoposide and teniposide

myelosuppression, GI irritation, alopecia

267

MOA of irinotecan and topotecan

inhibits topoisomerase I and prevent DNA unwinding and replication

268

uses for the -tecans?

colon cancer - irinotecan
ovarian and small cell lung cancers - topotecan

269

ADE of -tecans?

severe myelosuppression, diarrhea

270

MOA of hydroxyurea

inhibits ribonucleotide reductase = decreases DNA synthesis
- S phase specific

271

uses for hydroxyurea

melanoma, CML, SCD to increase HbF

272

MOA of trastuzumab (herceptin)

HER2 (tyrosine kinase receptor) mab
- used to kill breast cancer cells that overexpress HER2

273

ADE of trastuzumab

cardiotoxicity

274

MOA of imatinib

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

275

ADE imatinib

fluid retention

276

MOA rituximab

CD20 mab

277

Uses of rituximab

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

278

ADE of rituximab

increase risk of progressive multifocal leukoencephalopathy

279

MOA of vemurafenib

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

280

MOA of bevacizumab

VEGF mab
- treated for solid tumors to prevent angiogenesis

281

ADE of bevacizumab

hemorrhage and impaired wound healing

282

MOA of zanamivir and oseltamivir

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

283

MOA of ribavarin

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

284

ADE of ribavarin

hemolytic anemia, severe teratogen

285

MOA of acyclovir, famciclovir, valacyclovir

- 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

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

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

ADE for acyclovir, famiciclovir, and valacyclovir

obstructive crystalline nephropathy and ARF if not adequately hydrated

288

mechanism of resistance for acyclovir, famiciclovir, and valacyclovir

mutated viral thymidine kinase

289

MOA of ganciclovir

5'monophosphate formed by CMV viral kinase
- Guanonsine analog
- triphosphate formed by cellular kinases and preferentially inhibits viral DNA polymerase

290

ADE of gancicloir

pancytopenia, renal toxicity
- more toxic to host enzymes than acyclovir

291

Mechanism of resistance to ganciclovir

mutated CMV DNA polymerase or lack of viral kinase

292

When is ganciclovir used?

CMV, especially in ICP.
* Valganciclovir is a prodrug and has better oral bioavailability

293

MOA of Foscarnet

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

294

when is foscarnet used?

1. CMV retinitis in ICP pts when ganciclovir fails
2. acyclovir resistant HSV

295

ADE of foscarnet

renal failure

296

mechanism of resistance of foscarnet

mutated DNA polymerase

297

MOA of cidofovir

preferentially inhibits viral DNA polymerase
- doesn't require phosphorylation by viral kinase!!!!

298

when is cidofovir used?

CMV retinitis in ICP pts, acyclovir resistant HSV
- it has a long half life

299

ADE of cidofovir

renal toxicity

300

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

coadminister with probenecid and IV saline to decrease toxicity

301

What is normal HIV therapy?

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

What are you HIV protease inhibitors?

think -navir
Atazanavir
Darunavir
Fosamprenavir
Indinavir
Lopinavir
Ritonavir
Saquinavir

303

MOA of the HIV protease inhibitors

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

ADE of protease inhibitors

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

What are the HIV NRTIs?

Abavacir
Didanosine
Emtricitabine
Lamivudine
Stavudine
Tenofovir
Zidovudine

306

MOA of NRTIs

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

ADE of NRTIs

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

What are the HIV NNRTIs?

efavirenz, nevirapine, delavirdine

309

MOA of HIV NNRTIs

binds to reverse transcriptase at site different from NRTI
- don't require phosphorylation to be active or compete w/ nucleotides!!!!

310

ADE of NNRTIs

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

311

MOA of raltegravir

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

312

ADE of raltegravir

Hypercholesteremia

313

MOA of enfurvirtide

binds gp41 inhibiting HIV viral entry

314

MOA of maraviroc

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

315

ADE of enfuviritide

skin reaction at injection sites

316

MOA of interferons

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

317

When is IFN alpha used

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

318

When is IFN beta used

Multiple sclerosis

319

When is IFN gamma used

chronic granulomatous diease

320

ADE of Interferons

neutropenia and myopathy

321

What Abx should be avoided in pregnancy and why?

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

What antifungal and antiviral should be avoided in pregnancy?

1. Ribavirin - teratogenic
2. Griseofulvin - teratogenic
3. Delavirdine and efavirenz

323

MOA of Cox 2 inhibitors

- 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

When are COX 2 inhibitors used?

RA, OA, pts w/ gastritis or ulcers

325

ADE of COX 2 inhibitors

increase risk of thrombosis, sulfa allergy

326

MOA of acetaminophen

reversibly inhibits COX mostly in CNS
- inactivated peripherally

327

When is acetaminophen used?

antipyretic, analgesic but not anti-inflammatory
- used instead of ASA to avoid Reye syndrome in kids w/ viral infxn

328

ADE of acetaminophen

- 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

MOA of bisphosphonates

Pyrophosphate analog that binds hydroxyapatite in bone, inhibiting osteoclast activity

330

uses of bisphosphonates

Osteoporosis, hyperCa, Paget disease of bone

331

ADE of bisphosphonates

corrosive esophagitis, osteonecrosis of jaw

332

MOA of allopurinol

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

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

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

334

MOA of febuxostat

inhibits xanthine oxidase

335

MOA of probenecid

inhibits reabsorption of uric acid in PCT
- also inhibits secretion of penicillin

336

What are the chronic gout drugs?

Allopurinol, febuxostat, probenecid

337

MOA of colchicine

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