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Step1 > Everything needs a Medication > Flashcards

Everything needs a Medication Flashcards

1
Q

low potency first generation neuroleptics

A

chlopromazine, thioridazine

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2
Q

high potency first generation neuroleptics

A

trifluoperazine, fluphenazine, haloperidol

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3
Q

antispychotic MOA

A

block D2 receptors

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4
Q

Side effects of first gen neuroleptics

A

acute dystonia first, akasthisa, parkinson, tardive

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5
Q

atypical antpsychotics MOA

A

partial D2 antagonists and have varying effects on other neurotransmitters. Tend to decreased positive and negative symptoms

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6
Q

olanzapine SE

A

obestity

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7
Q

clozapine SE

A

agranulocytosis- moniter WBC weekly

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8
Q

risperidone SE

A

hyperprolactinemia

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9
Q

lithium SE

A

tremor, nephrogenic DI, hypothyroid, Ebsteins anomaly

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10
Q

why does lithium cause DI

A

it impairs the principle cells in the collecting tubule causing no water to be reabsorbed. Otherwise, it is reabsorbed in the PCT with Na

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11
Q

buspirone- MOA, uses

A

partial agonist of serotonin receptors, slow onset of action but used for GAD. Does not cause addiction, tolerance, or sedation. Does not interact with alcohol

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12
Q

SSRI MOA and SE

A

can induce mania in patients with bipolar disorder, can have SIADH and sexual dysfunction, it is a serotonin repute inhibitor because it blocks the SERT. Can have some GI distress

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13
Q

SNRI MOA and SE

A

inhibit SERT and NEt transporters to increase SE and NE in the synapse. Increase BP and stimulant effects and sedation and nausea

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14
Q

fluoxetine use

A

bulimia

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15
Q

venlafaxine use

A

social anxiety, panic disorder, PTSD, OCD

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16
Q

serotonin syndrome

A

increase in serotonin with clonus hyperrflexia, hypertonia, tremor and seize, hyperthermia, diaphoresis, diarrhea, and agitation

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17
Q

treatment for serotonin syndrome

A

cyproheptadine- antihistamine with anti SE properties

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18
Q

TCA- MOA and SE

A

block reuptake of NE and SE. It can cause sedation from alpha 1 effects and postural hypotension and atropine like side effects (ALICE), can prolong QT interval. Can have confusion and hallucination in elderly

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19
Q

TCA overdose

A

convulsions, coma, cardiotoxic from Na blockade in the heart leading to arrhythmia. treat with sodium bicarb.

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20
Q

MOAI MOA and SE

A

nonselective MAO inhibition and increase levels of neurotransmitters like NE, DA and Se. can have hypertensive crisis after ingestion of tyramine. CNS stimulation.

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21
Q

how long do you have to wait before starting antidepressants after starting and MAOI

A

2 week washout period to prevent serotonin syndrome

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22
Q

bupropion MOA

A

increased DA nd NE. for smoking cession.

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23
Q

what patients are contraindicated for bupropion

A

anorexic and bulimic patients have seizures

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24
Q

mirtazapine MOA

A

alpha 2 agonist which increases NE and SE. H1 antagonist. Sedation and increased appetite and weight gain.

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25
Q

who do you use mirtazapine in

A

old anorexic people who have insomnia

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26
Q

trazadone

A

block SE, alpha 1, and H1 receptors. weakly inhibits SE uptake. Used for insomnia and high doses can have antidepressant effect.

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27
Q

trazadone side effect

A

priapism

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28
Q

varenicline

A

nicotinic receptor partial agonist- used for smoking cessation. can have sleep disturbance

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29
Q

fluoxetine, paroxetine, sertaline, citopram

A

SSRi

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30
Q

venlafaxine, desvenlafaxine, duloxetine, levomulnacipran, milnacipran

A

SNRI

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31
Q

amitrytiline, notripyline, imipramine, desipramine, clomipramine, doxepinm amoxapine

A

TCA

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32
Q

trancyclopromine, phenelzeine, isocarboxazid

A

MOAI- nonselective

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33
Q

selegine

A

selective for MAO B which is for parkinsons

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34
Q

cyclosporine MOA

A

calcinuerin inhibitor- prevents IL2 transcription

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35
Q

cyclosporine toxicity

A

nephrotoxic so can have increased risk and damage with p450 inhibitors

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36
Q

tacrolimus MOA

A

prevents IL2 transcription and calcineuin inhibitor

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37
Q

tacrolimus SE

A

increased risk of diabetes and neurotoxic and nephrotoxic

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38
Q

sirolimus MOA

A

prevents response of IL2- MTOR inhibitor

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39
Q

sirolimus SE

A

not nephrotoxic but can cause pancytopenia

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40
Q

daclizumab and basiliximab MOA

A

monoclonal block of IL2-

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41
Q

azathioprine MOA

A

precursor of 6MP stops lymphocyte proliferation by blocking nucleotide synthesis

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42
Q

azothioprine SE

A

degrades by xanthine oxidase which is blocked by allopurinol. It messes with purine synthesis

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43
Q

mycophenolate MOA

A

reversibly inhibits IMP dehydrogenase to prevent the purine synthesis in B and T cells

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44
Q

mycophenoplate SE

A

can cause invasive CNS lymphoma or infection

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45
Q

corticosteroids MOA

A

inhibit NFKB suppress B and T cell function by decreasing transcription of many cytokines. Induce apoptosis of T lymphocytes

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46
Q

corticosteroid SE

A

Cushing from long term use

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47
Q

aldesleukin

A

IL2- used for RCC and melanoma

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48
Q

epoetin alfa

A

increased risk of HTN and clots but used for anemia from CKD. Anemias especially in renal failure

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49
Q

filgrastim

A

recovery of bone marrow

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50
Q

sargramostim

A

recovery of bone marryo

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51
Q

IFN alpha use

A

chronic heaptitis B and C. Kaposi sarcoma and malignant melanoma

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52
Q

IFN beta use

A

multiple sclerosis

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53
Q

IFN gamma use

A

chronic granulomatous disease

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54
Q

romiplostin and eltrobopag

A

thrombocytopenia

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55
Q

oprelvekin

A

IL11- thrombocytopenia

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56
Q

alemtuzumab target, use

A

CD52- CLL

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57
Q

bevacizumab- target and use

A

VEGF- colon cancer and renal cell carcinoma

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58
Q

cetuximab- target and use

A

EGFR-colon cancer and HEENT

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59
Q

rituximab target and use

A

CD20 B cell marker-B cell Hodgekin lymphoma, CLL, RA, ITP,

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60
Q

trastuzumab target and use

A

Her2neu used for breast cancer

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61
Q

adalimumab- target and use

A

soluble TNF alpha- IBD, RA, AS, and psoriasis- can reactivate TB because TNF alpha is what keeps TB sequestered

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62
Q

etancerpt– use and target

A

decoy TNF alpha receptor-IBD, RA, AS, and psoriasis

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63
Q

eculizumab- use and target

A

completment proein C5- paroxysmal nocturnal hemoglobinuria

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64
Q

natalizumab use and target

A

alpha 4 integrin- MS and crohn- risk of PML

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65
Q

abciximab use and target

A

platelet glycoprotein IIB/IIIa- antiplatelet agent for prevention of ischemic complications in patients undergoing percutaneous intervention- IIb multipled by IIIa is equal to absiximab

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66
Q

denosumab use and target

A

RANKL- osteoporosis inhibits osteoclast maturation and mimics osteoprotergin- effects clasts not blasts

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67
Q

omalizumab use and target

A

IGE- allergic asthma prevents allergic response

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68
Q

palivizumab use and target

A

RSV F protein- RSV prophylaxis for high risk infants

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69
Q

ranibizumab and bevacuzimab

A

VEGF for neovascular age related macular degeneration

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70
Q

Dala dala sturctural analog that binds penicillin binding proteins and blocks transpeptidase cross linkingg of peptidoglycan in cell wall

A

PCN

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71
Q

what does PCN cover

A

gram posiitive and used for gram negative cocci and spirochetes, penicillinase senstive

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72
Q

adverse reactions to PCN

A

hypersensitivity reactions and direct coombs positive hemolytic anemia

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73
Q

what is the resistance mechanism to PCN

A

cleaves the beta lactam ring, and penicillinase in bacteria

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74
Q

what is the mechanism of action for amoxicillin, ampicillin, and aminopenicillin

A

daladlala analog and PBP blocker

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75
Q

amoxicillin, ampicillin, and aminopenicillin clinical use

A

Hib, h pylori, ecoli, listeria, proteus, salmonella, shigella

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76
Q

amoxicillin, ampicillin, and aminopenicillin- adverse effects

A

hypersensitivity reactions rash, and psuedomembranous colitis

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77
Q

amoxicillin, ampicillin, and aminopenicillin- mechanism of resistance

A

penicillinase in bacteria that cleave the beta lactam ring

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78
Q

MOA of dicloxacillin, naficillin, oxacilin

A

narrow spectrum but works the same as PCN- bulky R group which blocks access of beta lactase to beta lactic ring

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79
Q

dicloxacillin, naficillin, oxacilin- clinical use

A

staph aureus, MRSA and resistant because of altered penicillin binding protein target site

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80
Q

dicloxacillin, nficillin, oxacilin- adverse effects

A

hypersensitivity reactions, interstitial nephritis

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81
Q

piperacillin and ticarcilin MOA

A

extended spectrum PCN MOA

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82
Q

piperacillin and ticarcilin- clinical use

A

pseudomonas and gram negative rods

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83
Q

piperacillin and ticarcilin- adverse effects

A

hypersensitivity reaction

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84
Q

amoxicillin- is it oral or IV

A

oral bioavailability

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85
Q

what are the beta lactase inhibitors

A

clavulinic acid, sulbactam, tazobactam,

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86
Q

what is the MOA of cephalosporins

A

beta lactase drugs that inhibit cell wall synthesis but are less susceptible to penicilinases

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87
Q

first generation cephalosporins

A

cefazolin, cephalexin

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88
Q

what do first generation cephalosporins cover

A

proteus, kleb, cefazolin can prevent staph aureus

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89
Q

what are the second generation cephalosporins

A

cefaclor, cefotaxime, ceftazidime

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90
Q

what do the second generation ceph cover

A

enterobacter, hib, neusseria, seratia, ecoli, kleb,

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91
Q

what are the third generation ceph

A

ceftriaxone, cefotaxime, ceftazidime- resistant to other beta lactams

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92
Q

what do the third gen ceph cover

A

ceftriazone cover meningitis, gonorrhea, disseminated lyme, ceftazidime- psudomonas

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93
Q

what are fourth generation cep

A

cefepime

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94
Q

what do the fourth gen ceph cover

A

gram negative with increased pseudomonas activity and other gram positive organisms

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95
Q

what are the fifth gen ceph

A

ceftaroline

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96
Q

what do fifth gen ceph cover

A

broad gram positive and gram negative coverage MRSA and does not cover pseudomonas

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97
Q

what are the adverse effects of cephalosporins

A

hypersensitive reactions, autoimmune hemolytic anemia, disulfiram like reaction, vitamin K deficiency, exhibit cross reactivity with PCN, and increased nephrotoxicity

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98
Q

what is the mechanism of resistance for cephalosporins

A

structural changes to penicillin binding proteins

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99
Q

penems MOA

A

beta lactamase resistant carbapenenm alswyas given with dilation to decreased inactivation in the renal tubules

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100
Q

penems use

A

gram positive cocci, gram negative rods, anaerobes- wide spectrum limit use to life threatening infections or after other drugs have failed. Meropenum has decreased risk of seuzres

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101
Q

penems adverse reactions

A

GI distress, skin rash and seizures

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102
Q

which carbapenem is used for pseudomonas

A

ertapenem

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103
Q

aztreonam MOA

A

less susceptible to beta lactase, prevents peptidoglycancross linking by binding to penicillin binding protein 3. Synergistic with aminoglycosides

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104
Q

aztreonam clinical use

A

gram negative rods

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105
Q

aztreonam adverse effects

A

non-toxic sometimes GI upset

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106
Q

vancomycin MOA

A

inhibits cell wall peptidoglycan formation by binding data data portion of cell wall precursors.

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107
Q

vancomycin clinical use

A

gram postivie bugs, serious multi drug resistant like MRSA, diff, enterococcus, staph pi, can be used orally for cdiff

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108
Q

vancomycin adverse effects

A

nephrotoxic, ototoxic, thrombophlebitits, diffuse flushing can pretreat with antihistamines

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109
Q

vancomycin resistance

A

occurs if there is a modification of dala dala to dala dlac

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110
Q

what are the 30s inhibitors

A

aminoglycosides and tetracyclines

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111
Q

what are the 50s inhibitos

A

chloramphenicol, clindamycin, erythromycin, linezolid

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112
Q

what are the aminoglycosides

A

gentamycin, neomycin, amikacin, tobramycin, streptomycin

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113
Q

what are the amino glycoside MOA

A

irreversible inhibition of initiation complex through binding of 30S submit. Causes misreading of mRNA and blocks translocation. Requires O2 for uptake and ineffectie against anaerobes

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114
Q

what is the use of aminoglycosides

A

severe gam negative rods, beta lactam antibiotics

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115
Q

what is neomycin used for

A

bowel surgery

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116
Q

what are the adverse effects of aminoglycosides

A

nephrotoxic, neuromuscular blcok, ototoxicity, teratogen

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117
Q

what is the mechanism of resistance to aminoglycosides

A

bacterial transferase enzumes inactivate the drug by acetylation, phopshorylation, or adenylation

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118
Q

what is the MOA of tetracyclines

A

bind to 30S and prevent attachment of aminoacyltTNA. limited CNS penetration. Doxycylcine is eliminated fecally and can be used with renal failure

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119
Q

what can you not eat with tetracyclines

A

milk and magnesium and iron containing prep

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120
Q

what is the clinical use of tetracyclines

A

borrelia burgdorferi, mycoplasma pneumoniae, ability ot acculate intracelluluar for rickettsia, chlamydia, and acne

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121
Q

what are the adverse effects of tetracylcines

A

GI distress, discolored teeth and inhibition of bone growth in children, photosensitivity,

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122
Q

tetracycline resistance

A

decreased uptake, or increased efflux out of the bacterial ells by plasmid encoded transport pumps

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123
Q

choloramphenicol MOA

A

blcoks peptidyltransferase at 50S ribosomal subunit

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124
Q

choloramphenicol clinical use

A

memingitis, rocky mountain spotted fever,

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125
Q

choloramphenicol adverse effects

A

anemia, aplastic anemia, grey baby syndome

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126
Q

choloramphenicol resistance

A

plasmid encoded acetyltrasnferase inactivates the drug

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127
Q

clindamycin MOA

A

blocks peptide transfer at 50S ribosomal subunit

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128
Q

clindamycin clinical use

A

anaerobic infections in aspiration pneumo, lung abscesses, and oral infections and invasive group A strep

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129
Q

clindamycin adverse effects

A

pseudomembranous colitis fever, diarrhea

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130
Q

linezolid MOA

A

inhibit protein synthesis by binding to 50S subunit and preventing formation of initiation complex

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131
Q

linezolid clinical use

A

gram positive MRSA and VRE

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132
Q

linezolid adverse effects

A

bone marrow suppression and peripheral neuropathy, and serotonin syndrome

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133
Q

linezolid mechanism of resistance

A

point mutation of ribosomal RNA

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134
Q

what are the macrolides

A

azithromycin, clarithromycin, erythromycin

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135
Q

macrolide MOA

A

inhibit portein sun by binding the 23S until of 50S

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136
Q

macrolide clinical use

A

atypical penumonia, STI, gram positive cocci, pertusis

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137
Q

macrolide adverse effects

A

GI motility, arryhtmia, prolonged QT, actue cholestatic hepatitis, rash, eosinophilia, increased serum concentration of thyophilline, oral anticoagulants

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138
Q

do any macrocodes do anything to P450

A

clarithromycin and erythromycin inhibit P450

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139
Q

macrolide mechanism of resistance

A

methylation of 23S rRNA binding site prevents binding of the drug

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140
Q

what are the sulfonamides

A

sulfamethoxazole, and sulfadiazine

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141
Q

what is the MOA of sulfonamides

A

inhibit dihydropteroate synths thus inhibiting folate synthesis, bacteriostatic combined with TMP

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142
Q

sulfonamides clinical use

A

gram positive and gram negative- nocardia, chlamydia, SMX for simple UTI

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143
Q

sulfonamides adverse effects

A

HSN reaction, G6PD deficienct, nephrotoxic, photosensitive, kernictursi, displace other drugs from albumin

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144
Q

sulfonamides resistance

A

altered enzyme, decreased uptake or altered PABA

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145
Q

dapsone MOA

A

similar to sulfonamides with inhibiting dihydropeteroate synthase and inhibit folate synthesis

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146
Q

dapsone clinical use

A

leprosy, PJP

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147
Q

dapsone adverse effects

A

hemolysis with G6PD

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148
Q

TMP MOA

A

inhibits bacterial dihydropfolate reductase

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149
Q

TMP clinical use

A

combination with sulfonamides SMX for sequential block of folate synthesis. Como use for uTI< shigella, salmonella, PJP, and toxoplasmosis prophylaxis

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150
Q

TMP adverse effects

A

megaloblastic anemia, leukopenia, granulocytopenia

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151
Q

nitrofuritan MOA

A

stop bacterial ribosomes, UTI, sad in pre, does not over proteus

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152
Q

polymyxin MOA

A

cationic detergent tend to be topical and use for resistat gram negative it is neurotoxic and nephrotoxic

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153
Q

what are the FQ/ what do they end it

A

floxacin

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154
Q

FQ MOA

A

inhibit prokaryotic enzymes topoisomerase II and IV.

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155
Q

what is the clinical use of FQ

A

gram negative rods of urinary tract infections and GI tract so pseudomonas, neisseria,

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156
Q

adverse effect of Fq

A

GI upset, superinfectiosn ,skin rash, cramps and mylgias. long QT fronte to tendon rupture and increased risk if they are taking prednisone

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157
Q

resistance to FQ

A

chomosome encoded mutation in DNA gyrase or plasmid or efflux pump

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158
Q

daptomycin MOA

A

lipopetide that disrupts cell membrane of gram positive cocci

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159
Q

daptomycin clinical use

A

staph skin infections MRSA, VRE, bacteria, endocarditis,

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160
Q

adverse effects of daptomycin

A

myopathy, rhabdomyolysis

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161
Q

what is daptomycin contraindicated in

A

it binds surfactant so its not used in pneumonia

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162
Q

metronidazole MOA

A

forms toxic free radical metabolies in the bacterial cell that damages the DNA

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163
Q

Metronidazole clinical use

A

giardia, entamoeba, trichomonas, gardernerall, anaerobes used with PPI and clarithromycin for h pylori triple therapy

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164
Q

treatment of anaerobes above the diaphragm

A

clinda

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165
Q

treatment of anaerobes below the diaphragm

A

metronidazole

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166
Q

adverse effect of metronidazole

A

disulfrram raction (flushing tachy and hypotension) with alcohol, headache, metallic taste

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167
Q

rifampin MOA, adverse effects and resistance

A

inhibits DNA dependent RNA polymerase,there can be hepatotoxicity, induce P450 system and orange body fluid, and resistant bed on if there is altered binding to RNA polymerase

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168
Q

isoniazid-MOA, adverse effects and resistance

A

it decreases the synthesis of mycelia acids, bacterial catalase peroxidase needed to convert INH to active metabolite, there is decreased mycelia acid. It can be used as solo prophylaxis against TB. Can also be used in mono therapy against latent TB. It is hepatotoxic and inhibits P450, and drug induced SLE, have to give B6 to the patients- resistance is the mutation in KatG which codes for the mycelia acid

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169
Q

pyrazinamide-MOA, adverse effects and resistance

A

mechanism is uncertain, it is a prodrug, works best at acidic pH, hyperuriciemia, hepatotoxic

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170
Q

ethambutol-MOA, adverse effects and resistance

A

decreased carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase. It causes optic neuropathy and red green color blind

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171
Q

streptomycin-MOA, adverse effects and resistance

A

interferes with the 30S subunit and its is second line for TB. it causes tinnitus, vertigo, ataxia, nephrotoxicity

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172
Q

prophylaxis for endocarditis and undergoing dental procedure

A

amoxicillin

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173
Q

prophylaxis for exposure to gonorhea

A

ceftriaxone

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174
Q

prophylaxis for recurrent UTI

A

tmp SMX

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175
Q

prophylaxis for exposure to meningitis

A

cegtriazone, ciprofloxacin, rifampin

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176
Q

prophylaxis for pregnant woman carrying group B strep

A

intrapartum PCN G

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177
Q

prophylaxis for prevention of gondola conjunctivitis of the newborn

A

erythromycin

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178
Q

prophylaxis for prevention of post surgical infection by staph aureis

A

cefazolin

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179
Q

prophylaxis for strep pharnygitis prior rheumatic fever

A

PCN

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180
Q

prophylaxis for exposure to syphilis

A

PCN

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181
Q

treatment of MRSA

A

vanc, daptomycin, linezolid, tigecycline, ceftaroline

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182
Q

VRE treatment

A

linezolid and streptogrammin (pristin)

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183
Q

amphotericin B-MOA, adverse effects and resistance

A

binds ergosterol, pores then are formed, fever chills, hypotension, nephrotoxic, anemia, phlebitis, decreased nephrotoxic, it is all from the similarity to the cholesterol

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184
Q

nystatin-MOA, adverse effects and resistance

A

it is only used topically, it binds ergosterol and pores are formed in the cell, swish in swallow for oral thrush or topical

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185
Q

flucytosine-MOA, adverse effects and resistance

A

inhibits DNA and RNA biosythesis by coversion to 5FY by cytosine deaminase- bone marrow suppression

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186
Q

azoles-MOA, adverse effects and resistance

A

inhibits fung sterol synthesis by inhibiting the P450 enzyme that converts lanosterol to ergosterol- local and less serious myoses- it inhibits testosterone so gives gynecomastia, liver dysfunction from inhibition of cytochrome P450

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187
Q

terbinafine-MOA, adverse effects and resistance

A

inhibits the final enzyme squalene epoxidase- dermatophytes- GI upset, headaches, hepatotoxic, taste disturbance

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188
Q

echinocandins-MOA, adverse effects and resistance-ALL END IN FUNGIN

A

inhibit cell wall synthesis by inhibiting synthesis of beta glucan- used for invasive aspergillosis or candida-GI upset, flushing, and histamine

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189
Q

griseofulvin-MOA, adverse effects and resistance

A

interfere with microtubule function and disrupts mitosis, and deposits in keratin containing tissues- oral treatment for superficial dermatophyte infections. It is teratogenic, carcinogenic, confusion, headaches,increased cytochrome P450, and warfarin metabolism

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190
Q

what do you use to treat mites or louse

A

permethrin blocks the Na channels leading to neurotoxic, and malthion (ACH) and lindane (GABA)

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191
Q

chloroquine-MOA, adverse effects and resistance

A

blocks detoxification of heme to hemozoin. Heme accumulates and is toxic to plasmodia- it treats plasmodium falciparum, resistance is due to membrane pump, if its life threatening its better to use quinine- retinopathy, pruritis

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192
Q

antihelminthic therapy

A

mebendazole, pyrantel pamoate, ivermectin, diethycarbamazine, praziquantal

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193
Q

oseltamivir, zanamivir-MOA, adverse effects and resistance and what it treats

A

inhibit the release of virus from infected cells and spreads within the respiratory tract, Also slows mucosal penetration by the virus in the respiratory tract- inhibit neuraminidase and it is for flu- it is only good in the first 48 hours, and it is resistance against it so only use it in high risk patients

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194
Q

acyclovir, famciclovir, valacyclovir-MOA, adverse effects and resistance and what it treats

A

guanosine analogs, monophosphorylated by HSV/VZV thymidine kinase, and not phosphorylated in uninfected cells, few adverse effects. Triphosphate formed by cellular enzymes. Preferentially inhibit viral DNA polymerase by chain termination. Incorporated into cellular DNA. HSV and VZV and weak activity against EBV. No activity against CMV. Used for HSV induced mucocutanou and genital lesions as well as encephalitis. Prophylaxis in immunocompromised patients. No effect on latent forms of HSV and VZV. Valacyclovir has more oral availability because of its prodrug. Famciclovir is used for HSV encephalitis and herpes zoster. It can cause obstructive crystal neuropathy, and acute renal failure if not well hydrated- resistance is with mutated thymidine kinase

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195
Q

ganciclovir-MOA, adverse effects and resistance and what it treats

A

5’ monophosphate formed by CMV viral kinase guanosine analog- triphosphate cellular kinases- inhibits viral DNA polymerase- CMV especially in immunocompromised.- bone marrow suppression with leukopenia and neutropenia and thrombocytopenia- renal toxicity is also seen- combined with TMP SMX gets even more bone marrow suppression

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196
Q

valganciclovir how is it different from ganciclovir

A

it is a prodrug form so it has increased bioavailability

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197
Q

foscarnet-MOA, adverse effects and resistance and what it treats

A

viral DNA/RNA polymerase inhibitor and HIV reverse transcriptase inhibitor and binds pyrophosphate binding site of the enzyme- CMV retinitis in immunocompromiezed when ganciclovir fails. It is nephotroxic and can cause electrolyte abnormalities with increased seizures. It is resistant if the viral DNA polymerase is mutated

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198
Q

cidofovir-MOA, adverse effects and resistance and what it treats

A

it preferentially inhibits viral DNA polymerase. does not require phosphorylation. CMV retinitis and it is only in immunocompromised patients that are acyclovir resistant HSV- has long half life and and is nephrotoxic and you administer fluids with it

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199
Q

NRTIs-MOA, adverse effects and resistance and what it treats

A

competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain. It can cause bone marrow suppression and peripheral neuropathy, and lactic acidosis, anemia, and pancreatitis,

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200
Q

which HIV drug is contraindicated if the patient has HLA B5701 mutation

A

abacavir- hypersensitivity reaction

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201
Q

which drug is used for general prophylaxis for HIV and pregnancy to decrease transmission

A

zidovudine

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202
Q

NNRTI-MOA, adverse effects and resistance and what it treats

A

bind to reverse transcriptase at site different than NRTI, and it does not require phosphorylation to be avtive or compete with nucleotide- rash, hepatotoxic,

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203
Q

efaverintz

A

vivid dreams and CNS symptoms

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204
Q

what NNRTIs are not able to be used during pregnancy

A

efavirenze and delaviridine

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205
Q

what is the common lingo for NNRTI

A

vir somewhere in the name

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206
Q

protease inhibitors–MOA, adverse effects and resistance and what it treats

A

assembly of visions of HIV protease (pol) genre which cleaves the polypeptide produces of HIV mRNA into their functional parts, so protease inhibitors prevent maturation of new viruses- can cause GI tolerance, hyperglycemia, lipodystrophy, cushing like, nephropathy, hematuria,

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207
Q

what medication is contraindicated in with protease inhibitors

A

rifampin because it can decrease the amount in the blood

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208
Q

what is the ending of all protease inhibitors

A

navir ending

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209
Q

can boost other drug concentrations by inhibiting cytochrome p450- which of the protease inhibitors is this

A

ritonavir

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210
Q

integrase inhibitors-MOA, adverse effects and resistance and what it treats

A

inhibits the HIV viral genome integration into host cell chromosome by reversibly inhibiting HIV integrase- increase creatine kinase

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211
Q

what do integrase inhibitors end in

A

tegravir

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212
Q

enfuvirtide- MOA, and toxicity

A

binds gp41 and inhibits entry into the HIV and there is skin reaction at injection site

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213
Q

maraviroc- MOA

A

bins CCR5 on the surface of T cells and monocytes to inhibit the interaction with p120 and it is only used if CCR5

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214
Q

interferon- MOA

A

glycoproteins normally synthesized by virus infected cells, exhibiting a wide range of antiviral and antitumoral properties. had proline synthesis

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215
Q

what is interferon alpha used for

A

chornic HCV and HBV, kaposi sarcoma, hairy cell leukemia, condyloma acuminatum, RCC, and malignant melanoma

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216
Q

what is interferon beta used for

A

multiple sclerosis

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217
Q

what is interferon gamma used for

A

chronic granulomatous disease

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218
Q

ribavirin- MOA and use and adverse effects

A

inhibit synthesis of guanine nucelotides by competitively inhibiting inosine monophosphate dehydrogenase- Chronic HCV, RSV and adverse effect of hemolytic anemia and severe teratogen

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219
Q

sofosbuvir- MOA and use and adverse effects

A

inhibits HCV RNA dependent RNA polymerase and acts as a chain terminator- chronic HCV in comnination with ribavirn and peg interferon alpha- feature and headache and nausea but not used alone

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220
Q

simeprevir- MOA and use and adverse effects

A

HCV protease inhibitor prevents viral replication- chronic HCV in combination with ledipasvir. do not use as mono therapy, photosensitive, rash,

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221
Q

chlorohexidine infection control what does it do

A

denature proteins and disrupts cell membranes non sporadical.

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222
Q

iodine and iodophors infection control what does it do

A

halogenation of DNA, RNA, and proteins may be sporadical

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223
Q

antimicrobials to avoid in pregnancy and what does it cause- sulfonamides

A

kernicterus

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224
Q

antimicrobials to avoid in pregnancy and what does it cause- aminoglycosides

A

ototoxic

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225
Q

antimicrobials to avoid in pregnancy and what does it cause- FQ

A

cartilage damage

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226
Q

antimicrobials to avoid in pregnancy and what does it cause-clarithromycin

A

embryotoxic

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227
Q

antimicrobials to avoid in pregnancy and what does it cause- tetracyclines

A

discolored teeth and inhibition of bone growth

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228
Q

antimicrobials to avoid in pregnancy and what does it cause- ribavirin

A

teratogenic

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229
Q

antimicrobials to avoid in pregnancy and what does it cause- griseofulvin

A

teratogenic

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230
Q

antimicrobials to avoid in pregnancy and what does it cause- chloramphenicol

A

gray baby syndrome

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231
Q

tyramine

A

normally degraded by MAO. Increased levels of tyramine in patients taking MAO inhibitors, and if they ingest tyramine, they will have excess tyramine enter the presynaptic vesicles and displaces other NT so it increases active presynaptic NT and increased infusion of NT into the synaptic cleft. Increased sympathetic stimulation It can result in a hypertensive crisis

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232
Q

bethanechol

A

activates the bowel and bladder smooth muscle- used for postoperative ileum and urinary retention. Can have HR and increased secretion

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233
Q

carbachol

A

it is like acetylcholine- constricts pupil and relieves intraocular pressure in open-angle glaucoma

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234
Q

methacholine

A

It stimulates muscarine receptors in airway when inhaled. Challenge for diagnosis of astham

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235
Q

pilocarpine

A

contracts ciliary muscle of the eye for open angle glaucoma, it constricts the pupillary sphincter for close agle- potent stimulater of sweat, tears, and saliva

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236
Q

what are the acetlycholinesterase used for AD

A

donepezil, galantamine, rivastigmine they all increase the amount of acetylcholine

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237
Q

edrophonium

A

used for MG but is short acting so can be used to test to see for dosage. it is an acetylcholinesterase

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238
Q

neostigmine

A

increase acetylcholine has no CNS penetration. It is good for post operative ileum, neurogenic ileum, and urinary retention , MG, and reversal of NMJ blockade

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239
Q

physostigmine

A

increase Ach, it is good for atropine overdose. it does cross the BBB

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240
Q

pyridostigmine

A
  • increase ACh, and it is used for treat myasthenia gravis and it does not penetrate the PNS
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241
Q

which Ache do cross the BBB

A

physostigmine

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242
Q

what patients do you need to watch out for with cholinomimetic agents

A

COPD exacerbation, asthma, and peptic ulcers

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243
Q

farmer that has diarrhea, urination, mitosis, bronchospasm, bradycardia, excitation of skeletal muscle, and CNS, and lacrimation, sweating, and salivation- wha t was the farmer poisoned with and what treats it

A

Organophosphate poisoning and treat with atropine for competitive inhibition and pralidoxime is for regeneration of AchE

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244
Q

atropine, homatropine, tropicamide

A

eye- produce mydriasis and cycloplegia-muscarinic antagonist

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245
Q

benztropine

A

parkinsons and acute dystonia-muscarinic antagonist

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246
Q

glycopyrrolate

A

GI and respiratory- parenteral for preoperative use to reduce airway secretion. Oral drooling an peptic ulcer-muscarinic antagonist

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247
Q

hyoscyamine, and dicyclomine

A

GI- antispasmodics for IBS- muscarinic antagonist

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248
Q

ipratropium, tiotripium

A

COPD and asthma, blocks PNS stimulation by the vagus to stop muscarinic stimulation

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249
Q

oxybutynin, solifenacin, darfenicin

A

reduce bladder spams and urger urinary incontinence-muscarinic antagonist

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250
Q

scopolamine

A

CNS, motion sickness- some effect can be blurry vision, dry mouth, urinary retention, and constipation

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251
Q

atropine

A

muscarinic antagonist used to treat bradycardia, ophthalmic applications, and organophosphate poisoning. In the eye it causes dilation, decreases secretions, acid secretion decreases, decreased gut motility, decreased urgency

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252
Q

what are the side effects of muscarinic antagonists

A

hot as a hare, dry as a bone, red as a beat, blind as a bat, mad as a hatter

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253
Q

how can you naturally get atropine poisoning

A

jimson weed- mydriasis due to plant alkaloids

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254
Q

elderly with acute delirium what drugs might be causing it

A

atropine, diphenhydramine, doxcline, chlorophenamine, neuroepileptics, TCA, amantidine

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255
Q

albuterol and salmetrerol- activation of G receptors, an applications

A

B2>B1- acute asthma or COPD

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256
Q

dobutamine

A

B1>B2 and a- it is a positive ionotrope, and increase CO, decreased LV pressure. positive chronotrope to increased HR and increased myocardial consumption can worsen myocardial ischemia- Use in heart failure and has a move inotropic than chronotropic effect. Severe HF or LV issue or cardio shock

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257
Q

dopamine

A

D1=D2>B>a- unstable bradycardia. HF, shock, inotropic and chronotropic effects at lower doses due to beta effects, vasoconstriction at high doses due to alpha effects

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258
Q

epinephrine

A

B>a- anaphylaxis, asthma, open angle glaucome- alpha effects predominate at high doses significantly stronger effect at beta2 receptor than NE

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259
Q

fenoldopam

A

d1- postoperative hypertension, HTN crisis, vasodilator of the coronary, peripheral, renal and splanchnic, promotes nature’s, can cause hypotension and tachycardia

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260
Q

isoproterenol

A

B1=B2- increased cardiac contractility and decreased vascular resistance and decrease MAP- can worsen ischemia

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261
Q

midodrine

A

a1- autonomic insufficiency and postural hypotension- may exacerbate HTN laying down

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262
Q

NE

A

a1>a2>B1- hypotension, septic shock

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263
Q

phenylephrine

A

a1>a2- Gq to IP3 and increase Ca and protein kinase C- hypotension vasoconstrictor, ocular procedures (dilation or mydriasis)- rhinitis as a decongestant

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264
Q

amphetamine

A

indirect general agonist, reuptake inhibitor, releases stored catecholamines- narcolepsy, obesity, ADHD

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265
Q

cocaine

A

indirect general agonist, reputake inhibitor- causes vasoconstriction and local anesthesia- never give beta blockers if cocaine intoxication in suspected because can lead to unopposed alpha 1 activation and extreme hypotension

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266
Q

ephedrine

A

indirect general agonist, releases stored catecholamines- nasal decongestion, urinary incontinence, hypotension

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267
Q

NE vs isoproterenol

A

NE increases systolic and diastolic BP as a result of alpha 1 mediated vasoconstriction. increased mean arterial presses and reflex bradycardia,Isoproterenol is no longer used has little alpha effect but causes beta2 mediated vasodilation, resulting in decreased MAP and increased HR through B1 and relax activity

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268
Q

clonidine and guanfacine- applications and adverse effects

A

hypertensive urgency used in ADHD, Tourettes- It can cause CNS depression, bradycardia, hypotension, respiratory depression, miosis

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269
Q

alpha methyldopa- applications and adverse effects

A

hypertension in pregnancy- it can cause direct Coombs and positive hemolysis and SLE like syndrome

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270
Q

phenoxybenzamine- applications and adverse effects

A

pheochromocytoma to prevent catecholamine crisis- non selective alpha blocker, stop HTN from pheochromocytoma- can cause orthostatic hypotension and reflex tachycardia- alpha blocker irreversible

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271
Q

phentolamine- applications and adverse effects

A

give to patients on Mao inhibitors who eat tyramine containing food- can cause orthostatic hypotension and reflex tachycardia- it is a reversible alpha blocker

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272
Q

alpha1 selective blockers end in what

A

osin

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273
Q

prazosin, terazosin, doxasocin, tamsulosin- applications and adverse effects

A

treats urinary symptoms of BPH, PTSD< and hypertension besides tamsulosin. It can cause first dose orthostatic hypotension, dizziness and headache from the decreased brain perfusion.

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274
Q

why is tamsulosin different than other selective alpha 1 blockers

A

it is specific for prostate ones

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275
Q

the osins cause orthostatic hypotension from

A

the decreased venous return, decreased CO, decreased BP causing the increase in sympathetic tone

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276
Q

what are the beta 1 selective blockers and what is it used for

A

acebutolol, atenolol, betazolol, esmolol, metoprolol- it is used for CHF, HTN

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277
Q

how does naming indicate which are beta 1 selective

A

A to M is the start of the names

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278
Q

which are non selective and whats the receptors and whats the naming

A

B1 and B2- nadolol, pindolol, propranolol, timolol- N to z

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279
Q

which are nonselective a and B antagonist and what are the naming

A

carvediol, labetalol- slightly different suffixes instead of olol

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280
Q

nebivolol

A

combines cardiac selective B1 blockade with stimulation of B3 receptors which activate NO synthase in the vasculature-

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281
Q

why are beta blockers used in angina

A

decrease HR and contractility, results in decreased O2 consumption

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282
Q

why are beta blockers used in MI

A

decreased mortality from arrythmia

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283
Q

why are beta blockers used in SVT and which are used

A

metoprolol, esmolol- decreased AV conduction velocity- class II antiarrythmics

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284
Q

why are beta blockers used in HTN

A

decreased cardiac output, decreased renting section due to Beta1 blockade on JGA cells

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285
Q

why are beta blockers used in HF and which drugs

A

decreased mortality and bisoprolol, varvediol, metoprolol

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286
Q

why are beta blockers used in glaucoma and what drug

A

decreased secretion of aqueous humor- timolol

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287
Q

why are beta blockers used in vatical bleeding and what drugs

A

decreased hepatic venous pressure gradient and portal hypertension

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288
Q

what are the adverse effects of beta blockers

A

erectile dysfnction, cardiovascular adverse effects like bradycardia, AV block, HF, and seizures, sedation, sleep alterations, dyslipidemia, and asthma and COPD exacerbations

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289
Q

what can beta blocker not be used concurrently with

A

cocaine because of unopposed beta blockade

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290
Q

what drugs to give with HF

A

beta blocker, ACE inhibitor, and angio II block,and aldosterone antagonist like spirolactone

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291
Q

tetrodoxin- source of toxin, action, symptoms, and treatment

A

pufferfish, highly potent toxin binds fast voltage gated Na channels in cardiac/nerve tissue, preventing depolarization- nausea, diarrhea, paresthesias, weakness, dizziness, loss of reflexes- primarily supportive

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292
Q

ciguatoxin- source of toxin, action, symptoms, and treatment

A

from reef fish like snapper, barracuda, snapper, and moray eel- opens NA channels causing depolarization- symptoms mimic cholinergic posioning- primarily supportive

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293
Q

histamine Scombroid posioning– source of toxin, action, symptoms, and treatment

A

spoiled dark meat fish such as tuna, mahi, mackerel, and bonito- bacterial histidine decarboxylase converts histidine to histamine frequently misdiagnosed as fish allergy- mimics anaphylaxis, bring sensation of mouth, facail flushing, erythema, itching, urticaria, may go to angioedema, hypotension, and bronchospasm, treatment is antihistamines, albuterol, and epinephrine if needed

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294
Q

what is the treatment for acetaminophen toxicity

A

NAC that replenishes the glutathione

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295
Q

what is the treatment for ache inhibitors and organophosphates tox

A

atropine>pralidozime

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296
Q

what is the treatment for amphetamines tox

A

ammonium chloride to acidify urine

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297
Q

what is the treatment for antimuscarinic toxicty and anticholergic agents

A

physostigmine, control hyperthermia

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298
Q

what is the treatment for arsenic tox

A

dimercaprol succimer

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299
Q

what is the treatment for benzodiazepines tox

A

flumazenil

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300
Q

what is the treatment for beta blocker tox

A

saline ,atropine glucagon

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301
Q

what is the treatment for CO tox

A

hyperbaric O2

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302
Q

what is the treatment for copper tox

A

pencillamine trientine

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303
Q

what is the treatment for cyanide tox

A

nitrite+thiosulfate, hydroxycolbalamin

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304
Q

what is the treatment for digitalis tox

A

anti dig fab fragments

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305
Q

what is the treatment for gold tox

A

penicllamine, dimercaprol, succimer

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306
Q

what is the treatment for heparin tox

A

protamine sulfate

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307
Q

what is the treatment for iron tox

A

deferozamine, deferasirox, deferiprone

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308
Q

what is the treatment for lead tox

A

EDTA, dimercaprol, succimer, penicillamine

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309
Q

what is the treatment for mercury tox

A

dimercaprol, succimer

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310
Q

what is the treatment for methanol and ethylene glycol tox

A

fomepizole or ethanol

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311
Q

what is the treatment for methemoglobin

A

methylene blue and vitamin C

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312
Q

what is the treatment for opioids

A

naloxone

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313
Q

what is the treatment for salicylate tox

A

alkalinize urine- bicarb

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314
Q

what is the treatment for TCA tox

A

bicarb

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315
Q

what is the treatment for warfarin

A

vitamin K and FFP

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316
Q

drug reactions causing: coronary vasospasm

A

cocaine, sumatriptan, ergot alkaloids

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317
Q

drug reactions causing: cutaneous flushing

A

vancomycin, adenosine, niacin, Ca channel blocker, echinocandins

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318
Q

drug reactions causing: dilated cardiomyopathy

A

anthracyclines (doxyrubacin and donarubicin) prevent with dexrazocane

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319
Q

drug reactions causing: torsades des pointes

A

antiarrythmics (class I1 and II), macrolides, antipsychotics, haloperidol, antiemetics like ondansetron

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320
Q

adenoctorical insufficiency drug reactions

A

withdrawal of long term steroids

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321
Q

drug reactions: hot flashes

A

tamoxifen and clomiphene

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322
Q

drug reactions: hyperglycemia

A

tacrolimus, protease inhibitors, niacin, HCTZ, corticosteroids

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323
Q

drug reactions: hypothyroid

A

lithium, amioderone, sulfonamides

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324
Q

drug reactions: acute cholestatic hepatitis, jaundice

A

erythromycin

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325
Q

drug reactions: diarrhea

A

acmprosate, acarbose, cholinesterase inhibitors, colchicine, erythromycin, ezetimibe, metformin, misoprostol, orlistat, pramlinitide, quinidine, SSRI

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326
Q

drug reactions: focal massive hepatic necrosis

A

halothane, amnita phalloidea, valproic acid, acerominophin- tender liver, increased LFT fever anorexia, rash, arthralgia,

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327
Q

drug reactions: hepatitis

A

rifampin, isoniazid, pyrazinamide, sttins, fibrates

328
Q

drug reactions: pancreatitis

A

didanosine, corticosteoriids, alcohol, vampiric acid, drugs, azothiprine, diuretics, furosemide and HCTZ

329
Q

drug reactions: pill induced esophagitits

A

tetracyclines, bisphophonates, potassium cholride

330
Q

drug reactions: pseudomembranous colitis

A

clindamycin, ampicillin, cephalosporins

331
Q

drug reactions: agranulocytosis

A

clozapine, carbamazepine, proylthiouracil, methimazole, colchicine, ganciclovir

332
Q

drug reactions: aplastic anemia

A

carbamazepine, methimazole, NSAIDs, benzen, chloramphenicol, propylthiouracil-

333
Q

drug reactions: direct Coombs- positive hemolytic anemia

A

methyldopa, PCN

334
Q

drug reactions: Grey baby

A

chloramphenicol

335
Q

drug reactions: hemolysis of G6Pd

A

isoniazid, sulfonamides, dapsone, primaquine, aspirin, ibuprofen, nitrofurantoin

336
Q

drug reactions: megaloblastic anemia

A

phenytoin, methotrexate, sulfa drugs

337
Q

drug reactions: thrombocytopenia

A

heparin

338
Q

drug reactions: thrombotic complications

A

OCPs, hormone replacement therapy

339
Q

drug reactions: fat redistribution

A

protease inhibitors, glucocorticoids

340
Q

drug reactions: gingival hyperplasia

A

phenytoin, Ca channel blockers, cyclosporine

341
Q

drug reactions: hyperuricemia (gout)

A

pyrazinamide, thiazides, furosemide, niacin, cyclosporine

342
Q

drug reactions: myopathy

A

fibrates, niacin, colchicine, hydroxychloroquine, interferon alpha, penicillamine,statines, glucocoriticoids

343
Q

drug reactions: osteoporosis

A

corticosteroids, heparin

344
Q

drug reactions: photosensitivity

A

sulfomanides, amiodarone, tetracyclines, 5-FU

345
Q

drug reactions: Stevens-Johnson Syndrome

A

anti-epileptic drugs like lamotrigine, allopurinol, sulfa drugs, penicillin

346
Q

drug reactions: SLE-like syndrome

A

sulfa drugs, hydralazine, isoniazid, procainamide, phenytoin, etanercept

347
Q

drug reactions: teeth discoloration

A

tetracyclines

348
Q

drug reactions: tendentious and tendon rupture, and cartilage damage

A

FQ

349
Q

drug reactions: cinchonism

A

quinidine, quinine

350
Q

drug reactions: Parkinson-like syndrome

A

antipsychotics, reserpine, metoclopramide

351
Q

drug reactions: seizures

A

isoniazid (B6 deficiency), bupropion, imipenem/cisplatin, tramadol, enflurane

352
Q

drug reactions: tradeoff dyskinesia

A

antipsychotics, metoclopramide

353
Q

drug reactions: diabetes insipidus

A

lithium, demeclocyline

354
Q

drug reactions: Fanconi syndrome- secreted everything from the PCT

A

tenofovir, ifosfamide

355
Q

drug reactions: hemorrhagic cystitis

A

cyclophosphamide, ifosfamide- treat with mensa before treating

356
Q

drug reactions: interstitial nephritis

A

methcilin, NSAIDs, furosemide

357
Q

drug reactions: SIADH

A

carbamazepine, cyclophosphamide, SSRI

358
Q

drug reactions: dry cough

A

ACE inhibitors

359
Q

drug reactions: pulmonary fibrosis

A

methotrexate, nitrofurantoin, carmustine, bleomycin, busulfan, amioderone

360
Q

drug reactions: antimuscarinic

A

atropine, TCA,H1 blocker, atipsychotics

361
Q

drug reactions: disulfiram reactions

A

metronidazole, certain cephalosporins, griseofulvin, procarbazine, first generation sulfonylureas

362
Q

drug reactions: nephrotoxicity

A

aminoglycosides, vancomycin, loop diuretics, cisplatin, Cisplatin toxicity will respond to amifostine

363
Q

Cytochrome P450 inducer

A

chronic alcohol use, st johns wart, phenyltoin, phenobarbitl, nevirapine, rifampin, griseofulvin, carbamazepine- Guiness Coronas, and PBRS induce Chronic Alcholism

364
Q

Cytochrome P450 inhibitors

A

Ciprofloxacine, ritonavir, amnioderone, cimetidine, ketoconazole, acute alcohol, macrolides, isoniazid, grapefruit, ompeprazole, sulfonamides- CRACK AMIGOS

365
Q

sulfa drugs

A

sulfonamide, sulfasalazine, probenacid, furosemide, acetazolamide, celecoxib, thiazides, sulfonylureas

366
Q

what do patients with sulfa allergies present with

A

fever, UTI, SHS, hemoyltic anemia, thrombocytopenia, agranulocytosis, urticaria- range from mild to life threatening

367
Q

azol

A

ergosterol syntehsis inhibitor

368
Q

bendazole

A

antiparasitic/antihelminthic

369
Q

cillin

A

peptidoglycan synthesis inhibitor

370
Q

cycline

A

protein synthesis inhibitor

371
Q

ivir

A

neuraminidase inhibitors

372
Q

navir

A

protease inhibitor

373
Q

ovir

A

DNA polymerase inhibitor

374
Q

thromycin

A

macrolide antibiotic

375
Q

ane

A

inhaled general anesthetic

376
Q

azine

A

typical antipsychotic

377
Q

barbital

A

barbituate

378
Q

caine

A

local anesthetic

379
Q

etine

A

SSRI

380
Q

ipramide, triptyline

A

TCA

381
Q

triptan

A

5HT agonists

382
Q

zepam, zolam

A

benzodiazepine

383
Q

chol

A

cholinergic agonist

384
Q

curium, curonium

A

nondepolarizing paralytic

385
Q

olol

A

beta blocker

386
Q

stigmine

A

AChE inhibitor

387
Q

terol

A

beta 2 agonist

388
Q

zosin

A

alpha 1 antagonist

389
Q

afil

A

PDE5 inhibitor

390
Q

dipine

A

dihydropyridine Ca channel blocker

391
Q

pril

A

ACE inhibitor

392
Q

sartan

A

ARB

393
Q

statin

A

HMG COA reductase inhibitor

394
Q

xaban

A

direct factor Xa inhibitor

395
Q

dronate

A

bisphosphonate

396
Q

glitazone

A

PPAR gamma activator- down regulates receptor transcription

397
Q

prazole

A

proton pump inhibitor

398
Q

prost

A

prostaglandin analog

399
Q

tidine

A

H2 antagonist

400
Q

tropin

A

pituitary hormone

401
Q

ximab

A

chimeric monoclonal antibody

402
Q

zumab

A

humanized monoclonal antibody

403
Q

SA node location

A

near the SVC and RA wall

404
Q

AV node location

A

near the coronary sinus and tricuspid valve

405
Q

what supplies the nodes in a right dominant heart

A

right circumflex artery

406
Q

what supplies the nodes in a left dominant heart

A

the left circumflex artery

407
Q

enlargment of what part of the heart can cause dysphagia and hoarsness

A

the left atrium can enlarge causing compression of the recurrent laryngeal nerve or the esophagus

408
Q

what is Fick’s principle

A

rate of O2 consumed/ arterial O- pulmonary O

409
Q

what happens to diastole when HR increases

A

it shortens which means less O2 to the heart

410
Q

how do you calculate resistance

A

R=8viscosityL/pi r4

411
Q

how do you calculate resistance in parallel

A

1/rt=1/r1+1/r2….

412
Q

how do you calculate resistance in series

A

rt=r1+r2+r3

413
Q

what vessels have the largest cross sectional area

A

capillaries

414
Q

what is the force of contraction directly proportional to

A

EDV

415
Q

what decrease the contractility

A

MI damage, beta blockers, CCB (non dihydro), dilated cardiomyopathy

416
Q

what accounts for the total peripheral resistance

A

arterioles

417
Q

what accounts for the blood storage capacity

A

venous system

418
Q

normal heart split

A

it is pul being delayed because of inspiration increasing the venous return

419
Q

wide split

A

RBBB or pulmonary stenosis causes a longer split with inspiration

420
Q

fixed split

A

L to R shunt increases the blood volume on the R side all the time so its always split

421
Q

paradoxical split

A

aortic valve is delayed during normal expiration which leads to increased split during expiration but closer split on inspiration. It is from LBBB or aortic stenosis

422
Q

Phase 0 of myocardial AP and pacemaker AP

A

Na channels open in myocardium and Ca channels open in AP of SA node

423
Q

Phase 1 in myocardium and pacemaker AP

A

inactivation of NA channels and K begin to open- only in myocardium

424
Q

Phase 2 in myocardium and pacemaker AP

A

plateau phase with CA and it balances the K efflux and opens Ca is released from the SR- myocardium only

425
Q

Phase 3 in myocardium and pacemaker AP

A

rapid repole with massive K efflux due to opening of voltage gated K channels and Ca channels closing in myocardium. In SA node its basically the same with K coming in and Ca being closed

426
Q

Phase 4 in myocardium and pacemaker AP

A

high K permeability leading to resting potential in myocardium. In SA there is slow spontaneous Na flow through funny channels leading to the depole and the rising +values to threshold

427
Q

speed of conduction after the SA node

A

purkinje>atria>ventricles>AV node

428
Q

IF its positive in I and II leads then what

A

normal

429
Q

if AVR is positie then

A

abnormal

430
Q

HTN treatment

A

thiazides, ACE, ARB, dihydropyridine CCB

431
Q

HTN with HF treatment

A

diuretics, ACE, ARB, beta blocker, aldosterone antagonists

432
Q

HTN with DM treatment

A

ACE inhibitors, ARB, CCB, thiazides, beta blockers- ace inhibitors/ARB are protective against diabetic neprhopathy

433
Q

HTN in pregnancy treatment

A

hydralazine, labetalol, methyldopa, nifedipine

434
Q

dihydropyradines act on what and are which ones

A

all end in dipine

435
Q

nondihydropyridines are which ones

A

diltiazam, and verapamil

436
Q

what is the MOA of CCB

A

block voltage dependent L type channels of cardiac and smooth muscle- decreased smooth muscle contractility-

437
Q

which CCBs work stronger on the vascular smooth muscle

A

amlodipine, nifedine>diltiazam>verapamil

438
Q

which CCB work stronger on heart

A

verapamil> diltiazam>amlodipine-nigedipine

439
Q

clinical use of CCB

A

hypertension, agnina, raynaus

440
Q

use of nimodipine

A

subarachnoid hemorhage

441
Q

clevedipine use

A

hypertensive emergency and urgency

442
Q

what are the nondihydropyradines used for

A

HTN, angina, a fib or flutter

443
Q

what are the adverse effects of non-dihydropyradines

A

cardiac depression, AV block, hyperprolactinmeia, constipation

444
Q

what are the adverse effects of dihydropyradines

A

peripheral edema, flushing, diziness, gingival hyperplasia

445
Q

what can happen if using verapamil and beta blockers

A

can cause a combination negative chronotropic effect, effect yielding severe bradycardia and hypotension

446
Q

hydralazine MOA, clinical use, and adverse effects

A

increased cGMP, smooth muscle relaxation, increase vasodilation of arteries > veins and after load is reduced. Severe hypertension, HF, safe to use during pregnancy, coadminstered with beta blocker because of tachycardia. Compensatory tachycardia, fluid retention, headache, angina, lupus like syndrome

447
Q

what drugs are used for hypertensive emergency

A

clevidipine, fenoldopam, labetalol, nicardipine, nitriprusside

448
Q

nitroprusside what are the mechanisms and adverse effects

A

short acting but increased cyclic GMP, direct release of NO can cause cyanide toxicity

449
Q

fenoldopam- mechanisms and adverse effects

A

dopamine D1 receptor agonist- cornary, peripheral, renal, and splanchnic, and vasodilation. decreased BP. increased nantruresis, post op for anti hypertension, Cau cause hypotension and tachycardia.

450
Q

what does nitroprusside do to the heart

A

decreased LV, and after load so SV is maintained can be used in hypertensive heart failure

451
Q

nitrate dosing

A

do not dose overnight because there is a tolerance

452
Q

nitrate moa, clinical use, adverse effects

A

vasodilate by increased NO in vascular smooth muscle, and increase in cGMP and smooth muscle relaxation. Delate the veins>arteries and decrease preload. Angina, acute coronary syndrome, pulmonary edema- reflex tachycardia, hypotension, fishing headache- development of tolerance during the work week- tachy and dizzy and headache with re-exposure. decrease GTP and increase GMP and so decrease activation of myosin light chain kinase so diaphoresis of MLC so vascular relaxation

453
Q

ranolazine- MOA, clinical use, adverse effects

A

inhibits the late phase of sodium current reducing diastolic wall tension and oxygen consumption, does not affect heart rate or contractility. Angina refractory to other medical therapies. Constipation, dizziness, headache, nausea, QT prolongation

454
Q

what does HMG-Coa reducatse do to LDL, HDL, triglycerides

A

decreased LDL, increased HDL, decreased TAG

455
Q

what is the MOA of statins

A

inhibit conversion of HMG oa to mevalonate a cholesterol precursos, and decreased mortality in CAD patients, increased LDL receptor recycling

456
Q

what is the adverse effects of statins

A

hepatotoxic, increased LFT, myopathy with fibrates, and increased CK

457
Q

what are the bile acid resins and what do they do to LDL, HDL, triglycerides

A

cholestyramine, colestipol, colsesvelam- decreased LDL, increased HDL, increased TAG

458
Q

what is the MOA of the bile acid resins

A

prevent intestinal reabsorption of bile acids, liver must use cholesterol to make more- can help to get rid of gall stones

459
Q

what are the adverse effects of bile acid resins

A

GI upset, decreased absorption, fat soluble vitamins decrease

460
Q

what does ezetimibe do to LDL, HDL, triglycerides

A

decreased LDL only

461
Q

what is the mOA of ezetimibe

A

prevent cholesterol absorption at small intestine brush border so stop cholesterol absorption through the intestine

462
Q

what is the side effect of ezetimibe

A

increase in LFT and diarrhea

463
Q

fibrates do what to LDL, HDL, triglycerides

A

decrease LDL, increase HDL, really decrease TAG

464
Q

fibrates MOA

A

upregulate LPK and increase TG clearance. Activates PPAR alpha to induces HDL synthesis. Inhibit cholesterol 7 alpha hydroxylase so decayers cholesterol solubility

465
Q

fibrates are used for what

A

good for TAG pancreatitis and because it lowers TAGs it increases gallstones

466
Q

what are the adverse effects of TAGs

A

myopathy, increased risk of statins, cholesterol gallstones

467
Q

niacin do what to LDL, HDL, triglycerides

A

decrease LDL, increase HDL, decrease TG

468
Q

niacin MOA

A

inhibits lipolysis in adipose tissues reduces hepatic VLDL synthesis

469
Q

niacin adverse effect

A

red flushed face which is by decreased NSAIDs, hyperglycemia, hyperuriciemia

470
Q

why is there increased flushing from niacin

A

increased prostaglandins

471
Q

why do fibrates increase the risk of myopathy with statins

A

fibrates inpair hepatic clearance of statins and increased blood levels of statin. also increase risk with niacin, and ezetimide

472
Q

what does fish oil do

A

antagonize VLDL

473
Q

digoxin MOA

A

stops Na/K ATPase so increase Na in the cell so increase Ca in the cell so increase contraction

474
Q

clinical use of digoxin

A

HP, atrial fib, decrease conviction of AV node and depression of SA node

475
Q

what are the adverse effects of digoxin

A

nausea, vomitting diarrhea, yellow vision .arrhymias, av block- can lead to hyperkalemia, renal failure, hypokalemia, drugs that displace digoxin from tissue binding sites and decrease clearance

476
Q

what are the class IA antiarrythmics, MOA, clinical use, and adverse effects

A

quinidine, procainamide, disopyramide- increased AP duration, and increased refractory period. Can have cinchonism headache, tinitis, SLE, heart failure, thrombocytopenia, increased QT and torsades

477
Q

what are the class IB antiarrythmics, MOA, clinical use, and adverse effects

A

lidocaine, mexiletine- decreased AP duration, preferentially affects ischemic or depolarized purkinje and ventricular tissue. Can be from acute centricualr arrhythmias, digitalis induces arrhythmias, post MI. CNS stimulation, depression, cardiovascular depression

478
Q

what are the class IC antiarrythmics, MOA, clinical use, and adverse effects

A

flecainamide, propafenone- strongest binding, terminate tachycardia angina- significantly prolongs ERP in AV node and accessory bypass tracts. No effect of ERP in purkinge and ventricular tissue. minimal effect on AP duration. Used for SVT, including atrial fibrillation. Proarrythmic especially post-MI- contraindicated in strugural and ischemic heart disease

479
Q

NA channel by strength

A

1C>1A>1B- so increased HR and to increased NA blockade- 1 C mose use dependent due to slow dissociative. 1B is the fastest to dissociate

480
Q

Class II antiarryhtmics MOA, clinical use, and adverse effects

A

metoprolol, propanolol, esmolol, atenolol, timolol, carvediol- decrease SA and AV nodal activity by decrease cAMP, decreased Ca currents. Suppress abnormal pacemakers by decreased slope of phase 4. Ave node particualrly sensitive to increase PR interval. Impotence exacerbation of COPD and asthma, cardiovascular effects of bradycardia and heart block, HP, sedation, sleep alternations, mast hypoglycemia-

481
Q

what can cause dyslipidemia

A

metoprolol

482
Q

prinzmetal angina can be aggravated by which beta blocker

A

propanolol

483
Q

how do you treat a beta blocker overdose

A

glucagona

484
Q

what are the class III antiarryhtmics , MOA, clinical use, and adverse effects

A

amiodorone, ibutilide, dofetilide, sotalol- K blocker through atrial fib, atrial flutter, ventricular tachycardia-

485
Q

adverse effects of sotalol

A

torsades des pointes excesssive beta blockage

486
Q

adverse effects of ibutilide

A

torsades

487
Q

adverse effects of amnioderone

A

pulmonary fibrosis, hepatotoxic, hypothyroid, hyperthyroid, hapten cuasing corneal deposits, blue grey skin deposits leading to phodermatitis, neurologic effects- bradycardia, heart block, HF

488
Q

what do you check when starting amnioderone

A

PFT, LFT, TFT

489
Q

what are the class IV antiarrythmics, MOA, clinical use, and adverse effects

A

verapamil, diltiazam- decreased conduction velocity, preven nodal arrythmias, rate control of fib. constipation, flushing, emema, vurdiovacualr effects- HF, AV block, sinus dpression

490
Q

where in the SA nodal AP does class Iv antiarryhtmics work

A

phase 4 depolarization

491
Q

adenosine MOA and what does it do

A

increase K out of cells, hyper polarize the cells and decrase intracellular CA. Drug of choice on diagnosing termination of certain forms of SVT. very short acting- blunted by theophylline and caffeine both are receptor antagnoists- flushing, hypotension, chest pain, sense of impending doom, bronchospasm- see a pause of EKG

492
Q

what does Mg do to arryhtias

A

effective against torsades and K is also used to treat for decreased ectopic pacemakers- for hypokalemia

493
Q

what should you check levels of with arryhtmias

A

K and Mg

494
Q

Propyluracil and methimazole- MOA

A

block thyroid peroxidase and inhibit the oxidation of iodide and organification of iodine, inhibit thyroid hormone synthesis. Propyluracil also blocks the 5 deiodinase and decrease peripheral conversion of t4 to t3

495
Q

Propyluracil and methimazole- clinical use

A

hyperthyroidism

496
Q

Propyluracil and methimazole- adverse effets

A

skin rash, agranulocytosis, aplastic anemia, hepatotoxic

497
Q

what can methimazole cause during pregnancy

A

cutis aplasia

498
Q

levothyroxine and triiodothyronine which goes with which

A

levothyroxine- T4

triidothyronine T3

499
Q

what are the side effects of levothyroxine and triiodothyronine

A

tachycardia, heat intolerance, tremor, arrhythmias

500
Q

convivaptan and tolvaptan

A

it is block ADH at V2- SIADH treatment

501
Q

desmopressin

A

central DI

502
Q

GH as a drug

A

for turner or GH deficiency

503
Q

oxytocin use as drug

A

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

504
Q

somatostatin as drug

A

acromegaly, carcinoid syndrome, gastrinoma, glucagonoma, esophageal varices- can stop bleeding out and GnRH release

505
Q

demeclocylcine MOA

A

ADH antagonist- from tetracycline family

506
Q

demeclocylcine clinical use

A

SIADH

507
Q

demeclocylcine side effects

A

neprhogenic DI, photosensitivity, abnormal bone and teeth

508
Q

glucocorticoids- MOA

A

metabolic carabolic anti-inflammatory, and immunosuppressive effects mediated with response elements, inhibit phospholipase A2, inhibition of transcription factors such as NfKB

509
Q

glucocorticoids- clinical use

A

adrenal insufficiency, inflammation, immunosuppression, asthma

510
Q

glucocorticoids- adverse effects

A

iatrogenic cushing, adrenocrotical atrophy, peptic ulcers, steroid diabets, steroid psychosis, cataracts. adrena insufficiency when the drug is quickly removed

511
Q

fludrocortisone MOA

A

synthetic analog of aldosterone with little glucocorticoid effects

512
Q

fludrocortisone clinical effects

A

mineralocorticoids replacement in 1 degree adrenal insufficiency

513
Q

fludrocortisone adverse effects

A

similar cushing, edema, exacerbation of heart failure, hyperpigmentation

514
Q

cinacalcet MOA

A

sensitizes Ca sensing receptor in parathyroid gland to circulating Ca and decreae PTH

515
Q

cinacalcet clincal use

A

first or second hyperparathyroidism

516
Q

cinacalcet adverse effects

A

hypocalcemia

517
Q

H2 blockers- name

A

dine

518
Q

H2 blockers- MOA and use

A

reversible block of hiatime H3 receptors and decreased H section by parietal cells- used for peptic ulcers, gastritis, mild refluc

519
Q

adverse effects of H2 blockers-

A

cimetidine is a potente hihibitor of P450 and it is antiandrogenic effe can cross the BBB and placenta.

520
Q

PPI- name

A

prazole

521
Q

PPI- MOA and use

A

irreverisly inhibits the H/K ATPASe in stomach pareital cels os it blocks the final common pathyway for gastric acid secretion

522
Q

ppi adverse effects

A

increased risk of diff infection, pneumonia, decreased serum Mg

523
Q

aluminum hydroxide- adverse effeccts

A

constipation, hypophosphatemia and proximal msucle weakness, osteodystrophy, and seizures

524
Q

calcium carbonate adverse effects

A

hypercalcemia, milk alkali, and increased rebound acid secretion can decrease effectiveness of tetracyclines

525
Q

magnesium hydroxide adverse effects

A

diarrhea, hyporeflexia, hypotension, cardiac arrest

526
Q

bismuth, sulcrafate

A

bind to ulcer base to provide physical protection and allow bicarb secretion to reestablish pH gradient in the mucous layer

527
Q

misoprostol

A

PGE1 analo- increase poductio and secretion of gastric mucous carrier and reduce acid production. prevents NSAID induced peptic ulcers- induces labor and diarrhea- abortifactan

528
Q

octreotide

A

long acting somatitsiin analog inhibits the secretion of various splanchnic vasodilatory hormones acute parcel bleeds, acromegaly, VIPoma, carcinoid tumors, nausea, cramps, steatorrhea, increased cholestsis from CCK inhibitorn

529
Q

osmotic laxatives- which

A

magnesium hydroxide, magnesium citrate, polyethylen glycol, lactulose

530
Q

MOA of osmotic laxatives

A

proived osmotic load to draw water into GI lumen. Constipation and the use and it can be used for hepatic encephalopathy

531
Q

sulfasalazine

A

a combination of antibacterial and amsnosalcillic acid which his anti inflammatory- activated by colonic bacteria used for UC and crohn, can cause malaise , nausea, sulfonamide toxicity, and oligospermia

532
Q

loperamide

A

agonist of the mu opiod receptor to slow gut motility

533
Q

ondansetron

A

%ht receptor antagonist and decrease vagal stimulation. powerful central acting anti-emetic. Control vomiting, and chemo- can cause headache, constipatin ,QT prolongation

534
Q

metoclopramide

A

D2 recptor antagonist increased resting tone contractility and LES tone, motility does not influence colonic transport time. Diabeticc and post surgery gastroparesis, antiemetic. Increased parkinson effects, tadive dyskinesia, restlessness, drowsiness, fatigue, depression, diahrrea, can interact with digoxin and diabetic agetns.

535
Q

orlistat

A

inhibits gastric pancreatic lipase which decreases the breakdown and absorption of dietary fats. It cause weight loss, steatorrhea, decreased absorption of ADEK

536
Q

ursodiol

A

nontoxinc bile acid to increase bile acid secretion and decrease cholesterol secretion and absorption. Primary biliary cirrhosis, gallstone prevention or dissolution

537
Q

heparin MOA

A

it lowers the activity of thrombin and factor Xa and has a short half life and potentiates action of ATIII

538
Q

what are the low molecular weight heparins

A

enoxaparin, dalteparin, fondaparinux

539
Q

what does LMWH act on

A

it acts more on Xa- can bind ATIII but once active in Xa to stop thrombin to prothrombin

540
Q

HIT

A

development of IgG antibodies against heparin bound platelet factor 4, an antibody PF4 complex activates platelets and thrombosis and thrombocytopenia form- direct thrombin inhibitors like argatroban

541
Q

bivalirudin- MOA

A

it directly inhibits activity of free and clot associated thrombin.

542
Q

warfarin MOA

A

interferes with gamma carboxylation of vitamin K dependent clotting factors II, VII, Ix, X and protein C and S. Metabolism by polymorphisms in the gene for vitamin K epoxide reductase complex. Has effect on extrinsic pathway and increased PT.

543
Q

wafarin dverse effects

A

skin and tissue necroses, drug drug interactions. and protein C and S have shorter half lies, and this leads to early transient hypercoagulbility with warfarin use. Skin and tissue necrosis within the first few days of large doses due to small vessel microthrombi

544
Q

which one, heparin or warfarin should be given in pregnancy

A

heparin because its polar and water soluble

545
Q

apixaban and rivaroxaban- MOA- Xa in the name

A

bind to and directly inhibit factor Xa.

546
Q

alteplase, reteplase, streptokinase, tenecteplase-MOA

A

directly inhibit conversion of plasminogen to plasmic which cleaves thrombin and fibrin clots. Increased Pt and PTT but no change in the platelet count.

547
Q

adverse effects or who do you not use thrombolytics in

A

risk of inter cranial hemorrhage and asymetric pupils, irregular breathing, decreased consciousness and bleeding and active surgery, severe HTN.

548
Q

what do you treat toxicity of thrombolytics with

A

aminocaproic acid

549
Q

clopidogrel, prasigrel, ticagrelor, ticlodipine- MOA- gre in the name

A

inhibit platelt aggregation by irrversible blocking ACP receptors to prevent the expression of IIb/IIIa o platelets. this prevents platelet aggregation

550
Q

cilostazol and dypyridamole MOA

A

PGIII inhibitior so increased CAMP in the platelets leading to decreased aggregation and vasodialtion so good for PAD and intermittent claudication

551
Q

abciximab, eptifibatide, tirofiban MOA

A

bind BpII/IIIa on activated platelets, preventing aggregation is made from Fab fragments

552
Q

when do the microtubule inhibitors work in the cell cycle

A

M phase

553
Q

azothioprine and 6-MP- MOA

A

purine thiol analongs to decrease de novo purine synthesis and activated by HGPRT.

554
Q

azothioprine and 6MP clinical use

A

preventing organ rejection, RA, IBD, SLE

555
Q

what increases the toxicity of azothioprine and 6MP

A

its from xanthine oxidase and this increased toxicity with allopurinol or febuxostat

556
Q

cladribine- MOA

A

purine analog and mucltiple mechanisms like inhibitors or DNA polymerase and DNA strand breaks

557
Q

cladribine clinical use

A

hairy cell leukemia

558
Q

cytarabine- arabinofuranosyl cytidine- MOA

A

pyrimidine analog and inhibit of DNA polymerase

559
Q

cytarabine- arabinofuranosyl cytidine- adverse effects

A

pancytopenia

560
Q

5-FU MOA

A

purimidine analog bioactivated 5-FdUMP which covalentlly complexes folic acid. This complex inhibits thymbdilate synthase

561
Q

5-FU has what effect with leucovorin

A

it is enhanced by it

562
Q

methotrexate MOA

A

folic acid analog that competitively inhibits dihydrofolate reductase and decreased DNA synthesis. Can have mouth ulcers

563
Q

methotrexate has what effect with leucovorin

A

it is decreased effect with it. It is the rescue

564
Q

bleomycin MOA

A

induce free radical formation and breaks in DNA strands

565
Q

bleomycin adverse effects

A

pulmonary fibrosis and skin hyperpigmentation

566
Q

dactinomycin MOa

A

intercalates DNA

567
Q

what are the uses of dactomycin

A

used for childhood tumors

568
Q

doxarubicin and daunorubicin MOA

A

generate free radicals and intercalate DNA and breaks in DNA and decreased replication

569
Q

doxarubicin and daunorubicin adverse effects

A

cardiotoxicity, dilated cardiomyopathy. use ironchelator to prevent the cardiotoxicity

570
Q

busulfan MOA

A

cross links DNA

571
Q

busulfan adverse effects

A

severe myelosuppression and pulmonary fibrosis and hyperpigmentation

572
Q

cyclophosphamide, ifofamide MOA

A

cross like DNA at guanine N7 require bioactivation by liver that screws up the DNA replication

573
Q

cyclophosphamide, ifofamide- adverse effects

A

hemorrhagic cystitis blocked by mensa or NAC

574
Q

carmustine, iomustine, semustine, treptozocin- MOA

A

require bioactivation and crosses the BBB- cross links the DNA

575
Q

carmustine, iomustine, semustine, treptozocin- adverse effects

A

CNS toxicity

576
Q

paclitaxel and other taxols- MOA

A

hyperstabalize polymerized microtibules in the M phase so that mitotic spindle cannot break down so anaphase cannot occur

577
Q

paclitaxel and taxols- adverse effects

A

hypersensitivity

578
Q

vincristine, vinblastine- MOA

A

vinca alkaloids that bind beta tubular and inhibit its polymerization into microtubules and prevent mitotic spindle formation so M phase arrest

579
Q

vincristine, vinblastine adverse effect

A

neurotoxicity wit hareflexia, peripheral neuritis, constipation like paralytic ileus

580
Q

cisplatin, carboplatin MOA

A

Cross link DNA

581
Q

cisplatin, carboplatin adverse effects

A

can cause hearing loss form damage to organ of Corti. and there is nephrotoxicity and can be prevented with amifostine and chloride diuresis

582
Q

etoposide and teniposide MOA

A

inhibits topoisomerase II and increased DNA degradation

583
Q

etoposide and teniposide adverse effects

A

myelosuppression and alopecia

584
Q

podophyllin MOA

A

used in genital warts has the same Moa and block DNA too 2

585
Q

irinotecan and topotecan MOA

A

inhibit topoisomerase I and prevent DNA unwinding and replication

586
Q

irinotecan and topotecan adverse effects

A

severe myelosuppression and diarrhea

587
Q

hydroxyurea MOA

A

inhibits ribonucelotide reductase and decrease DNA synthesis so S phase

588
Q

hydroxyurea other use

A

increased fetal hemoglobin which is protective against sickling

589
Q

prednisone and prednisolone MOA

A

bdinind to intracytopalsmic steroid receptor to block gene transcription

590
Q

prednisone and prednisolone adverse effects

A

cushing like, weight gain, central obesity, muscle breakdown, cataracts, acne, osteoporosis, hypertension, PUD, hyperglycemia, psychosis

591
Q

bevacizumab MOA

A

monoclonal antibody against VEGF inhibits angiogenesis

592
Q

bevacizumab adverse effects

A

hemorrhage, blood clots, impaired wound healing

593
Q

erlotinib mOA

A

EGFR tyrosine kinase

594
Q

erlotinib adverse effects

A

rash

595
Q

cetuximab MOA

A

monoclonal antibody against EGFR

596
Q

cetuximab adverse effect

A

rash, elevated LFT, diarrhea

597
Q

imatinib MOA

A

tyrosine kinase inhibitor of BCR-ABL and c-kit.

598
Q

imatinib uses

A

CML and GI stromal tumor

599
Q

imatinib adverse effects

A

fluid retention

600
Q

retuximab MOA

A

monoclonal antibody against Cd20 which is found on most B cell neoplasms

601
Q

retuximab clinical use

A

non-hodgekin lymphoma, CLL, ITP, RA

602
Q

retuximab adverse effects

A

increased risk of progressive multifocal leukoencepthalopathy

603
Q

tamoxifn/raloxifene MOA

A

selective estrogen receptor modulators- receptor antagonists in breast and agonists in bone. Block he binding of estrogens to the ER positive cells.

604
Q

adverse effects of tamoxifen

A

partial agonist in endometrium which increases the risk of endometrial cancer hot flashes

605
Q

adverse effects of raloxifene

A

no increase in endometrial carcinoma because it is an estrogen receptor antagonist in endometrial tissue but it helps prevent breast cancer and treat with/prevent osteoporosis

606
Q

trastuzumab MOA

A

monoclonal antibody against HER-2 a tyrosine kinase receptor. Helps kill cancer cells that overexposes HEr2, and through inhibitor of HER2 initiated cellular signaling and antibody dependent cytotoxicity

607
Q

what are the adverse effects of trastuzumab

A

ardiotoxic

608
Q

vemurafenib MOA

A

small molecule inhibitor of BRAF oncogene and positive for melanoma- mutation BRAF inhibiton

609
Q

vemurafenib clinical use

A

melanoma

610
Q

epinephrine and brimonide

A

decreased aqueous humor and synthesis via vasscondstriction- adverse effects of a1 do not sued in closed angle glucaoma

611
Q

timolol, betaxolol, carteolol

A

decreased aqueous humor and no pupillary or vision changes

612
Q

acetazolamide

A

decreasd aqueous humor synthesis veal inhibitor of carbonic anhydrase also hits the PCT

613
Q

polocarpine and carbachol- direct cholinomemetics

A

increased outflow of quakes tumor via contraction of ciliary muscle and opening of trabecular meshwork- mitosis and contraction or pupillary sphincter and cylclospasm

614
Q

indirect cholinomimetics of M3- its physostigmine and echothiphate

A

use pilocaripin in emergenices- but increases the outflow of aqueous humor via contraction of ciliary muscles and opening of traveler network

615
Q

bimatoprost and iatoprost

A

increase the outflow of aqueous humor

616
Q

adverse effects of bimatoprost and iatoprost

A

darkens iris and eyelash growth

617
Q

opiod analgesics MOA

A

act as agonist at opiod receptors to modulate synaptic transition open K channels and close Ca channels- decreased synaptic transmission inhibit release of ACh, NE, and 5-HT, glutamate, and substance P

618
Q

what are the opioids used in diarrhea

A

loperamide and diphenoxylate

619
Q

what are the adverse effects of opiods

A

addiction, respiratory depression, constiaption, mioisis, additive CNS depression with other drugs tolerance does not develop to mitosis and constipation. toxicity treat with naloxone

620
Q

what happens if there is morphine tolerance

A

active metabolites can cause build up and deterioration-called morphine 6 gloconamide

621
Q

pentazocine MOA

A

kappa opiod receptor agonist and mu receptor antagonist

622
Q

pentazocine adverse effects

A

can cause opioid withdrawal symptoms if patient is also taking full opiod antagonist competition for opiod receptors

623
Q

butorphanol MOA

A

kappa receptor agonist with mu receptor partial agonist produces adalgesia

624
Q

tramadol MOA

A

very weak opioid agents but also inhibitors 5HT and NE repute so it can be used to treat chronic pain, but it can cause serotonin syndrome

625
Q

ethosuxamide MOA and use

A

it blocks the T type Ca channels and it causes GI , fatigue, urticaria, SJS, and it can be used for abssence seizure

626
Q

Benzos

A

increased frequency of GAB channel opening- sedation, tolerance, dependency, and respiratory depression

627
Q

phenobarbitol

A

increased GABA opening for longer- it has sedation, tolerance, dependence and induction of P450-

628
Q

phenyotin

A

blcoks NA channel with zero order kinetics

629
Q

phenytoin adverse effects

A

neurologic nystagmus, diplopia, ataia, sedation, peripheral neuropathy, hirsuitism, gingival hyperplasia, DRESS, DLE, megaloblastic anemia, P450 induction

630
Q

carbamazepine

A

blocks NA channels- diplopia, blood dyscrasia, treatment, SIASH, SJS, induce cytoP450

631
Q

valporic acid

A

increaed NA channel inactivation and increased GABa- GI distress, pancreatitis, neural tube, tremor, weight gain, contraindicated inpregnanacy

632
Q

vigabatrin

A

increased GAB inactivation

633
Q

gabapentin

A

inhibit CA channels and designed by GABA analot- sedation and ataia- it is perioheral neuropathy and postherpetic neuralgia

634
Q

topiramate

A

blcoks NA channels and increased GABA action- sedation, mental dulling, kidney stones, and weight loss. migraine prevention

635
Q

lamtotrigine

A

blcoks voltage gated NA channels can cause SJS

636
Q

levetiracetam

A

may modular GABA or glutamate

637
Q

tiagabine

A

increase GABA uptake

638
Q

what is the alternate use of phenobarbitol

A

it is used to increase output of conjugated bilirubin in Criggler Najjar II

639
Q

zolpedemi, zaleporn, eszopilon

A

act as BZ1 subtype of GABA receptor effects revers by flmazenil and it sleep cycle affected as compared with benzodiazepine hypnotics. It is used for insomnia- it has ataxia headaches and confsion- short duration because of rapid metabolism by liver enzymes. Can only modedest day after psychomotor depression and few amnesic effects decreased dependence and not as bad on old people

640
Q

ramelteon

A

is a melatonin agonist better for geriatric because no adverse effects

641
Q

anesthetics what happens if lipid solubility is increased

A

more potent because it crosses the BBB better so MAC is lower

642
Q

anesthetic what happens if the inhaled has a higher partition or decreased blood solubility

A

faster induction/onset

643
Q

which inhales anesthetic is hepatotoxic

A

halothane

644
Q

which inhaled anesthetic is nephrotoxic

A

methoxyflurane

645
Q

which inhaled anesthetic is proconvilsant

A

enflurane

646
Q

what are the parameter changes with inhaled anesthetics

A

myocardial depression, respiratory depression, nausea, increased cerebral blood flow, decreased cerebral metabolic demand

647
Q

malignant hyperthermia

A

life threatening condition in which inhaled anesthetics or succinylcholine induce fever and severe muscle contractions. Sucesptibility is often inherited as autosomal dominant with variable penetrance. Mutations in voltage sensitive ryandine receptor to cause increased CA release from SR. treat with dantrolene a ryanodine receptor antagonist

648
Q

barbituates IV- thiopental-what does it do to blood flow

A

it decreases cerebral blood flow

649
Q

midazolam- barb for anesthesia- what does it do to blood flow

A

it decreases repertory depression, decrease BP, anterograde amnesia

650
Q

ketamine- what MOA and what does it do to blood flow

A

PCP analog so block NMDA receptor and causes cardio tim and increased cerebral blood flow

651
Q

propofol- MOA what does it do to blood flow

A

it is for sedation and it potentiates GABA.

652
Q

which are the ester local anesthetics

A

procaine, cocaine, tetracaine, and benzocaine- this is for allergic reactions

653
Q

which are the amide LAs

A

lidocaine, mepivacaine, bupivacian- amides

654
Q

MOA of LA

A

it is for block of NA channels and it can penetrate the membrane to prevent depolarization.

655
Q

what order does LA unnerve the fibers- types

A

small diameter fibers>large diameter

656
Q

order of loss of fibers of LA

A

it is pain, temperature, touch, pressure

657
Q

which LA is cardiotoxic

A

bupivacaine

658
Q

what LA can cause methylglobulinemia

A

its benzocaine

659
Q

succinylcholine

A

strong Ach receptor agnost and produces sustained depolariation to prevent the muscle contraction

660
Q

what is the phase I of the reversal of the succinylcholine block

A

it is no antidote block is potentates by cholinesteraseinhibitors

661
Q

what is the phase II of the reversal of the succinylcholine block

A

it can be reversed because there are some Ach receptors- desnsitized

662
Q

what are the complications with succinylcholine

A

hypercalcemia, heperkalemia, malignant hyperthermia

663
Q

nondepoalizing NMJ blcokers- curare

A

all compete for ACh receptors- neostigmine can revere it.

664
Q

dantrolene

A

prevents release of Ca from SR form skeletal muscle by binding to ryanodine receptor. malignant hyperthermia reatmuc. Neuroleptic malign syndrome

665
Q

baclofen

A

activates GABA receptors the spinal cord levels- inducing skeletal muscle relaxation- muscle spasms- can be used for MS and acute low back pain with muscle spasms

666
Q

cyclobenzaprine

A

centally acting skeletal muscle relaxant. related to TCA and similar anticholinergic side effects- muscle sparsms

667
Q

dopamine agonists

A

ropinerole and pramipexole- direct stimulation of dopamine receptors

668
Q

amantadine

A

increase dopamine availability- can cause lived reticularis

669
Q

levodopa

A
  • increase blocks, peripheral conversion of L dopa to dopamine by inhibiting dopa decarboxylase and reduce side effects of peripheral L dopa conversion into dopamine
670
Q

entacapone, tolcapone

A

prevent peripheral L dopa degradation in 3-O methyldoma by inhibiting COMT- COMT inhibitors help prevent peripheral breakdown of L dopa used for its on off effects

671
Q

selegine

A

blocks onversion of dopamine into DOPAc by selectively inhibiting MAO-B

672
Q

tolcapone

A

lbcoks conversion of dopamine to 3-OMD by inhibiting central COMT

673
Q

benztropine

A

antimuscarinic that improves tremor but little effect on bradykinesia

674
Q

riluzole

A

used for ALS for increased survival and decreased glutamate excitiotixicity via unclear mechanism

675
Q

triptans

A

5HT agonist that inhibits trigeminal nerve activation and prevents vasoactive peptide release and induce vasoconstriction. coronary vasospasm

676
Q

what are synthetic prostaglandins used for

A

pulmonary HTN, and Raynauds, inhibit platelet aggregation, adhesion to vase endothlium, and vasodialte and increased vascular permeability, and stimulater leukocyte chemotaxis

677
Q

aceotminophen MOA

A

it reversibly inhibits COS and mostly in CNS inactivates peripherally

678
Q

acetominophen adverse effects

A

overdose produces heaptic necosis NAPQI the metabolite depletes glutathione and forms toxic byproducts in the liver.

679
Q

what does NAC do

A

it regenerates glutatione

680
Q

aspirin MOA

A

NSAID that irreversibly inhibits COX and by covalent acetylation and decreased synthesis of TXA2 and prostaglading and increased BT and no effect on PT and PTT effects last until new platelets are produced

681
Q

what is the aspirin adverse effects

A

gastric ulcers, tinnitus from CNVIII, chronic acan lead to renal failure, interstitial nephritis

682
Q

what is the metabolic pH change from ASA

A

it is respiratory alkalosis early then goes to mexed metabolic acidosis and respiratory alkalosis

683
Q

celecoxib MOA

A

reveribly inhibtis specifically the cos isfoomr 2 which is found in inflammatory cel and vascular endothelium and mediates inflammation nan pain spacres COX1 an maintain gastric mucosa so less corrosive effect

684
Q

adverse effects of celecoxib

A

thrmobosis and sulfa allergy

685
Q

NSAID MOA

A

reversibley inhibit COZ and block prostaglandin synthesis

686
Q

adverse effects of NSAIDs

A

interstitial nephritis, gastric ulcer, renal ischemia from prostaglandin dilation of the afferent arteriole

687
Q

what are the NSAIDs

A

ibuprofen, naproxen, indometicin, ketorolac, diclofenac, meloxicam, piroxicam

688
Q

leflunomide MOA

A

reversible inhiits dihydroorate dyhydrogenase to prevent pyrimiden synthes inad prevent T cell proliferation

689
Q

leflunomide used for

A

RA and psoriatic arthritis

690
Q

adverse effects of leflunomide

A

diarrhea, HTN, hepatotoxic, and teratogenicity

691
Q

bisphosphinates MOA

A

pyrophosphate analogs, bind hydroxyapetitis in blone to prevent clast activity

692
Q

bisphosphinates adverse effects

A

esophagitis, osteonecrosis of the jaw and atypical stress fracture

693
Q

teriparatide MOA

A

recombinant PTH analog given subcutaneously daily to increase blast activity

694
Q

teriparatide adverse effects

A

transiet hypercalcemia- used before bisphosphinates before starting

695
Q

what are the acute gout drugs

A

NSAIDS, glucocorticoids, colchicine

696
Q

what are the chronic gout drugs

A

allourinaol, febuxostate, pegloticase, probenacid

697
Q

allopurinol

A

competitive inhibitor of xanthine oxidase to decreased conversion. sued in lymphoma and leukemia to prevent tumor lysis syndrome and increased concentration os azothiprine and ^MP from decreased metabolism

698
Q

febuxostats

A

inhhibits xanthine oxidase

699
Q

pegloticase

A

recombinant fricassee that catalyzes metabolism of uric acid to allantoin which is more water soluble

700
Q

probenacid

A

inhiits resorbiton of uric acid in proximal convoluted tubules for uric acid calculi

701
Q

colchicine

A

binds and stabalizes tubulin to inhibit microtubules polymerization, impairing neutrophil chemotzis and degranulation acute and prophylactic use

702
Q

colchicine side effects

A

GI mucosa is disrupted leading to diarrhea nausea, and abdominal pain and vomiting

703
Q

lubar punitive goes through what ligament

A

the ligament flavum

704
Q

what has to be checked before starting TNF alpha inhibitors

A

TB test

705
Q

etanercept

A

it is a fusion protein that is the receptor for TNF alpha so its used for RA, psoriasis, AS

706
Q

infliximab and adalimumab

A

it is an anti-TNFalpha monoclonal antibody used for IBD, RA, AS, and psoriasis

707
Q

rasburicase

A

recombinat fricassee that catalyzes metabolism of uric acid to allantoin, and prevention of tumor lysis syndrome

708
Q

what are the first generation antihistamines

A

diphenhydramine, dimenhydrinate, hydroxyzine, chlorpheiramine

709
Q

what are the adverse effects of first generation antihistamines

A

sedation, antimuscarinic anti alpha adrenergic

710
Q

what are the side effects of first generation antihistamines on old people

A

cholinergic seide effects like blurry vision, glaucoma, delrium, retention, alpha 1 falls, serotinergic weight gain ,and appetitie stimulation

711
Q

second generation antihistamines- what are they

A

loratadine, fexofenadine, desloratadine, cetirizine

712
Q

second generation antihistamines adverse effects

A

far less sedating than first generation because of decreased entry into the CNS

713
Q

what is guaifensin

A

expectorant thins respiratory secretions does not suppress cough reflex

714
Q

what is N-acetylcysteine

A

mucolytic liquifies mucus in COPD patients by disrupting disulfide bonds used as an antidote for acetaminophen overdose

715
Q

dextromethrophan

A

antitussive antagonizes NMDA gluatate receptors and codein analog. Mild opiod effect in excess. Can have contraption or serotonin syndrome

716
Q

what is the adverse effects of dextromethrophan

A

constipation, sedation if high and serotonin syndrome

717
Q

pseudo ephedrine and phenylephrine

A

alpha adrenergic agonist used as nasal decongestants. short term for nasal congestion.

718
Q

adverse effects of pseudo ephedrine and phenylephrine

A

hypertension, can also cause CNS stimulation/anxiety and pseudoephedrine

719
Q

bosentan MOA

A

compeittive antagonism of endothelin 1 receptors and decreased pulmonary vascular resistance.

720
Q

bosentan side effects

A

hepatotixic, moniter LFP and decreased arterial pulmonary pressure and lessens RVH

721
Q

sildalafil

A

inhibits cGMP PDE5 and prolongs vasodilatory effects of NO

722
Q

epoprostenol and iloprost

A

PGi3 prostacyclin with direct vasodilatory effecton pulmonary and systemic arterial vascular bests. inhibits platelet aggregation

723
Q

Beta 2 agonists- albuterol, salmeterol, formoterol-MOA

A

increased cAMP by Gs

724
Q

albuterol

A

relaxes the bronchial smooth muscle by short acting beta 2 and used for acute

725
Q

salmetrerol and formoterol

A

long acting for prophylaxis adverse effects of armor and arrythmia

726
Q

inhaled corticosteroids like flutixaon and budesonide

A

inhibit the syndrther os all xytokines and inactivate NF-KB the transcription factor that induces TNF alpha and other inflammatory agents. first line for chronic asthma

727
Q

ipratropium

A

blocks muscarinic receptors compeititvely and it prevents bronchoconstriciton also used for COPS

728
Q

tiotropium

A

it is a long term inhibitor of muscarinic receptors prevents bronchoconstriction

729
Q

montelukast and zafrilukast

A

block leukotriene receptors epxiaclly good for aspirin induced asthma- receptor blocker in LOX pathway

730
Q

zileuton

A

5 lox pathway inhibits blocks conversion of arachadoinc acid to leukotrienes hepatotoxic

731
Q

omalizumab

A

binds mostyl unbound serum IgE and blocks binding to FcERI used in allergic asthma with increased IgE levels resistant to inhaled steroids and long acting beta 2 agonists

732
Q

theophylline

A

bronchi dilation by inhibiting phosphodiesterase increased cAMP and decreased CAMP hydrolysis. Usage limited for narrow TI cardio and neurotoxic metabolized by cytochrome P450 and blocks action of adenosine

733
Q

methacholine

A

muscarinic 3 agonist and bronchial challenge test to induce and activate asthma in suceptible patients

734
Q

mannitol MOA

A

osmotic diuretic and increased tubular fluid osmolarity and increased urine flow and decreased intraocular pressure and intracranial pressure

735
Q

why do you use mannitol and what are the adverse effects

A

used for drug overdose, elevated inter cranial pressure or intraocular pressure, and causes pulmonary edema, and dehydration, contraindicated in anuria, HF

736
Q

acetazolamide MOA

A

carbonic anhydrase inhibitor causing self-limited NaHCO3 diuresis and decreased total body HCO3 stores. works at PCT to alkalinize the urine works at the PCT

737
Q

acetazolamide clinical use and adverse effects

A

used for glaucoma, urinary alkalization, metabolic alkalosis, altitude sickness, and pseudotumore cerebra and closed angle glaucoma. Adverse effects are proximal renal tubular acidosis, paresthesias, NH3 toxicity, sulfa allergy, somnolence, alkaline urine, metabolic acidosis, dehydration and decreased K and Na

738
Q

loop diuretics which ones are they and their MOA

A

sulfonamide Loop diuretics, inhibit cotransport ssystem of NA/K/Cl of thick ascending limb. Abolism hypertonicity of the medulla and prevent concentration of the urine. stimulate PGE release and vasodilatory effect, and inhibited by nSAIDs and increased Ca excretion- furosemide, bumetanide, torsemide

739
Q

loops clinical use and adverse effects

A

used for edematous states, HF ,cirrhosis, nephrotic syndrome, pulmonary edema, and hypertension, and hypercalcemia. it is ototoxic, hypokalemia, dehydration, allergy like sulfa drugs, metabolic alkalosis, nephritis, and gout

740
Q

ethacrynic acid MOA

A

nonsulfonamide inhibitor to the same thing as loops

741
Q

ethacrynic acid clinical use and adverse effects

A

diuresis in pateints allergic to sulfa drugs and similar to furosemide but more ototoxic

742
Q

which are the thiazide diuretics

A

hydrocholorthiazide, chlorthalidone, metolazone, imatomapide

743
Q

what is the MOA of thiazides

A

it inhibits NaCLe reabsorption at the DCT and it decreases the diluting capacity of the nephron and decreases Ca excretion. can cause stones but increased Ca leads to decreased fractures

744
Q

thiazide clinical use

A

HTN (first line), HF, idiopathic hypercalciuria, nephrogenic DI, and osteoporosis

745
Q

adverse effects of thiazide diuretics

A

hypokalemia, metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcimia, sulfa allergy

746
Q

what happens to the electrolytes with thiazide diuretics

A

INCREASED CA, INCREASED URIC ACID, INCREASED glucose, increased cholesterol, increased TG, decreased Na, decreased K and decreased Mg

747
Q

what are the potassium sparing diuretics

A

spirolactone, eplernone, trimeterene, amiloride

748
Q

Moa of K sparing diuretics

A

spirolactone and eplerenone are competitive aldosterone receptor antagonists in the cortical collecting tubule. Triameterene and amiloride act at the same part of the tubule by blocking Na channels in the cortical collecting tubule.

749
Q

what is the clinical use of the K sparing diuretics

A

hyperaldosteronism, K depleteion, HF, hepatic ascites, nephrogenic DI,regression of fibrosis and remodeliing in HF

750
Q

what K sparing diuretics is specific usual for hepatic ascites

A

spirolactone

751
Q

what K sparing diuretics is specific usual for nephrogenic DI

A

amiloride

752
Q

what are the adverse effects of potassium sparing diuretics

A

hyperkalemia, arrthmyias from this, endocrine effects like gynecomastia and anti androgen for spirolactone

753
Q

what happens to urine NaCl with diruetics

A

increased with all diuretics

754
Q

what happens to urine K with diuretics

A

it increases with loops and thiazides

755
Q

what diuretics decrease urine pH

A

carbonic anhydrase inhibitors like acetazolamide

756
Q

what diuretics increase blood Ph

A

loops, thiazides cause alklemia through volume contraction, and K loss, low K state

757
Q

what diuretics increase urine Ca so decrease serum Ca

A

loops

758
Q

what diuretics decrease urine Ca so increase serum Ca

A

thiazides

759
Q

what is common ending for ACE inhibitors

A

it is pril

760
Q

what is the MOA of Ace inhibitors

A

inhibit ACE conversion to ATII and so decrease GFr by preventing the constriction of efferent arterioles. increased Rening from loss of feedback. There is a decreased GFr from the dilation of the efferent arteriole. Prevents inactivation of bradykinin

761
Q

what is the clinical use of ACE inhibitors

A

hypertesnion,HF< protenuria, diabetic neprhopathy, heart remodelling prevention. slows GBM thickening in the diabetic patient

762
Q

what are the adverse effects of ACE inhibitors

A

cough ,angioedema, teratogen (detal renal malformation), increased creatinine from decreased GFR, hyperkalemia, hypotension,

763
Q

why can’t you use Ace inhibitors with bilateral renal artery stenossi

A

used with caution in bilateral renal artery stenosis because ACE inhibitors with further decrease in GFr can lead to renal failure See rigns of renal stenosis if patient has TIA or coronary atheroscelosis, so decreased RPF and decreased GFR, and increased renin so constricted efferent arteriole to increase GFr, and this is blocked by the perils because they stop the feedback

764
Q

angiotensin II receptor blockers end in what and MOA

A

losartan, candesartan, and valsartan. selectively block binding of ATII or AT1 receptors effects are similar to ace inhibitors but ARBs do not increase bradykinin

765
Q

artans clinical use and adverse effects

A
  • clinical use- hypertension, HF, proteinuria, diabetic neprhopathy with intolerance to ACE inhibitors from cough and angioedema.
  • adverse effects0 hyperkalemia, and decreased GFR, hypotension, and teratogenic
766
Q

aliskiren MOA

A

direct renin inhibitor, blocks conversion of angiotensinogen to antiotensin I

767
Q

aliskiren clinical use and adverse effects

A
  • clincial use- hypertension

- adverse effects- hyperkalemia, decreased GFR, hypotension, contraindicated in patients taking ACE inhibitors or arbs

768
Q

leuprolide MOA

A

GnRH analog with agonist properties when used n pulsatile fashion antagonist hwhen used in continuous fashion to down regulate GnRH and decrease Lh and FSh

769
Q

leuprolide clinical use

A

uterine fibroids, endometriosis, precocious puberty, prostate cancer, infertility. Pulsatile is for infertility the others are continuous use for suppression

770
Q

what are the synthetic estrogens

A

ethinyl estradiol, DES, and mestranol

771
Q

estrogens MOA

A

bind estrogen receptors

772
Q

estrogens use

A

hypogonadism, ovarian failure, menstrual abnormalities, hormone replacement therapy in postmenopausal women, use in men with androgen-depent prostate cancer

773
Q

estrogens adverse effects

A

increased risk of endometrial cancer, bleeding in postmenopausal women, and increased risk of clear cell if DES in utero, and increased risk of thrombi

774
Q

what is estrogen contraindicated in

A

ER positive breast cancer and history of DVT

775
Q

selective estrogen reecptor modulators- which ones

A

clomiphene, tamoxifen, raloxifene

776
Q

clomiphen

A

antagonist at estrogen receptors in the hypothalamus. Prevents normal feedback inhibition increased release of LH and FSH from pituitary which stimulates ovulation. Used to treat infertility due to involution from PCOS. May cause hot flashes, ovarian enlargement, multiple simultaneous pregnancies, visual disturbances

777
Q

tamoxifen

A

antagonist at breast, uterus; agonist at the bone and uterus. Increased risk of thromboembolic events and endometrial cancer. Used to treat and prevent recurrence of ER/PR positive breast cancer

778
Q

raloxifene

A

antagonist breast, uterus, increased risk of thromboembolic events but not increased risk of endometrial cancer. It is used to treat osteoporosis as ell

779
Q

what are the aromatase inhibitors

A

anastozole, letrozole, exemestane

780
Q

anastozole, letrozole, exemestane- MOA

A

inhibit peripheral conversion of androgens to estrogen

781
Q

anastozole, letrozole, exemestane- clinical use

A

Er+ breast cancer in postmenopausal women

782
Q

HRT

A

used for relief or prevention of menopausal symptoms- hot flashes and vaginal atrophy and osteoporosis and it increases estrogen and decrease osteoclast activity.

783
Q

what does estrogen do in the bone

A

it decreases osteoclast activity and increases osteoblast activity

784
Q

what happens with unopposed estrogen replacement therapy

A

increased risk of endometrial cancer, so progesterone is added. Possible increased cardiovascular risk

785
Q

what are the synthetic progestins

A

levonogestrel, medroxyprogesterone, etongestrel, norethindron, megrestrol, and RU486, and mifepristol

786
Q

what are the MOA of progestins

A

bind the progesterone receptors to decrease growth, increased vascularization of the nedometrium and thickened cervical mucus

787
Q

what is the clinical use of progestins

A

contraception (forms in crude pill, intrauterine device, implant, depot injection), and endometrial cancer, abnormal uterine bleeding

788
Q

progestin challenge

A

prsence with withdrawal beleeding excluded anatomic defeats (ashram syndrome) and chronic anovulation without estrogen

789
Q

what is the mOA of the mini pull and IUD

A

thickens the cervical mucus

790
Q

what is the progestin shot or implant MOA

A

it decreases the GnRH and it decreases ovulation

791
Q

what is the MOA of combined contraception

A

progestins and ethinyl estradiol in a pill, patch or ring. Estrogens and progestins inhibit the LH/FSH and prevent estrogen surge. if there is no LH surge then there is no ovulation

792
Q

what does the progestin part of the OCP do

A

it is to thicken tehe cervical mucus and limit the access of sperm to the uterus.. Progestin also inhibit endometrial prolideration making the endometrium less suitable to implantation

793
Q

what are the contraindications for OCPs

A

smokers>35 and increased risk of cardiovascular events, patients with increased risk of cardiovascular disease and including history of venous thromboembolism, CAD, and migraine, breast cancer

794
Q

copper IUD MOA

A

produces local inflammatory reaction toxic to sperm and ova, preventing fertilization and implantation and is hormone free

795
Q

copper IUD clinical use

A

long-acting reversible contraception most effective emergency contraception

796
Q

copperIUD and adverse effects

A

heavier or longer menses, dysmenorrhea, and risk of PID with insertion so it is contraindicated in active pelvic infection

797
Q

terbutaline, ritodrine

A

beta 2 agonists that relax the uterus and used to decreased contraction frequency in women in labor- called tocolytics

798
Q

danazol MOA and use

A

synthetic androgen that acts as partial agonist at androgen receptors the use is endometriosis, and hereditary angioedema

799
Q

what are the adverse effects of danazol

A

weight gain, edema, acnes, hirsutism, masculinization, decreased HDL, and hepatotoxic

800
Q

testosterone and methyltestosterone- MOA

A

agonists at the androgen receptors

801
Q

testosterone and methyltestosterone- clinical use

A

treat hypogonadism and promote the development of secondary sex characteristics and stimulater anabolism to promote recovery after burn or injury

802
Q

testosterone and methyltestosterone- adverse effects

A

causes masculinization in females and decreased intratesticular testosterone in males by inhibiting release o LH (via negative feedback), and gonadal atrophy. Premature closure of the epiphyseal plates and increased Ldl and decreased HDL

803
Q

anti androgens which are they

A

finasteride, flutamide, ketoconazole, spirolactone

804
Q

finasteride

A

five alpha reductase inhibitor and it decreases the conversion of testosterone to DHT, and used for SPH and male-pattern baldness

805
Q

flutamide

A

nonsteroidal competitive inhibitor at androgen receptors. Used for prostate cancer

806
Q

ketoconazole

A

inhibits steroid synthesis at 17,20 desmolase

807
Q

spirolactone

A

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

808
Q

what are the uses of spirolactone and ketoconazole

A

used for PCOS to reduce androgenic symptoms. Both have side effects of gynecomastia and amenorrhea

809
Q

tamsulosin

A

alpha 1 antagonist used to treat BPH by inhibiting smooth muscle contraction, selective for alpha AD receptors (fond o the prostate) and it is not hitting the alpha receptors as much

810
Q

what are the phosphodiesterase type 5 inhibitors

A

sildenafil, vardenafil, tadalafil

811
Q

what is the MOA of sildenafil, vardenafil, tadalafil

A

inhibit PDE-5 and increased CGMP and prolonged smooth muscle relaxation in response to NO and increases blood flow to the corpus vacernosum of the penis and decreases pulmonary vascular resistance.

812
Q

what is the clinical use of sildenafil, vardenafilm tadalafil

A

erectile dysfunction, pulmonary HTN

813
Q

what is tadafil especially used for

A

BPH

814
Q

what is sildenafil, vardenafilm tadalafil adverse effects

A

headache, flushign, dypepsia, cyanopia blue tinted vision.

815
Q

what is the associated risk with nitrates and sildenafil, vardenafilm tadalafil

A

nitrates increase the cGMP and enhance the inhibiton of PDE and this leads to no degraation of PDE and enhanced effects leading to unopposed dilation and hypotension

816
Q

minoxidil

A

direct arteriolar vasodilatory and it treats androgenic alopeica and severe refractory hypertension

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